MasterOfCellTypes.bib

@article{poulin_defining_2014,
  title = {Defining {{Midbrain Dopaminergic Neuron Diversity}} by {{Single-Cell Gene Expression Profiling}}},
  volume = {9},
  issn = {2211-1247},
  doi = {10.1016/j.celrep.2014.10.008},
  abstract = {Summary
Effective approaches to neuropsychiatric disorders require detailed understanding of the cellular composition and circuitry of the complex mammalian brain. Here, we present a paradigm for deconstructing the diversity of neurons defined by a specific neurotransmitter using a microfluidic dynamic array to simultaneously evaluate the expression of 96 genes in single neurons. With this approach, we successfully identified multiple molecularly distinct dopamine neuron subtypes and localized them in the adult mouse brain. To validate the anatomical and functional correlates of molecular diversity, we provide evidence that one Vip+ subtype, located in the periaqueductal region, has a discrete projection field within the extended amygdala. Another Aldh1a1+ subtype, located in the substantia nigra, is especially vulnerable in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease. Overall, this rapid, cost-effective approach enables the identification and classification of multiple dopamine neuron subtypes, with distinct molecular, anatomical, and functional properties.},
  timestamp = {2016-04-19T22:21:29Z},
  number = {3},
  urldate = {2016-04-19},
  journal = {Cell Reports},
  author = {Poulin, Jean-Francois and Zou, Jian and Drouin-Ouellet, Janelle and Kim, Kwang-Youn~A. and Cicchetti, Francesca and Awatramani, Rajeshwar B.},
  month = nov,
  year = {2014},
  pages = {930--943}
}

@article{fujimura_ccr2_2015,
  title = {{{CCR2}} inhibition sequesters multiple subsets of leukocytes in the bone marrow},
  volume = {5},
  issn = {2045-2322},
  doi = {10.1038/srep11664},
  timestamp = {2015-08-17T18:09:49Z},
  urldate = {2015-08-17},
  journal = {Scientific Reports},
  author = {Fujimura, Naoki and Xu, Baohui and Dalman, Jackson and Deng, Hongping and Aoyama, Kohji and Dalman, Ronald L},
  month = jul,
  year = {2015},
  pages = {11664}
}

@article{schmidt_identification_2012,
  title = {Identification of the {{Cortical Neurons}} that~{{Mediate Antidepressant Responses}}},
  volume = {149},
  issn = {0092-8674},
  doi = {10.1016/j.cell.2012.03.038},
  abstract = {Summary
Our understanding of current treatments for depression, and the development of more specific therapies, is limited by the complexity of the circuits controlling mood and the distributed actions of antidepressants. Although the therapeutic efficacy of serotonin-specific reuptake inhibitors (SSRIs) is correlated with increases in cortical activity, the cell types crucial for their action remain unknown. Here we employ bacTRAP translational profiling to show that layer 5 corticostriatal pyramidal cells expressing p11 (S100a10) are strongly and specifically responsive to chronic antidepressant treatment. This response requires p11 and includes the specific induction of Htr4 expression. Cortex-specific deletion of p11 abolishes behavioral responses to SSRIs, but does not lead to increased depression-like behaviors. Our data identify corticostriatal projection neurons as critical for the response to antidepressants, and suggest that the regulation of serotonergic tone in this single cell type plays a pivotal role in antidepressant therapy.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {5},
  urldate = {2014-10-21},
  journal = {Cell},
  author = {Schmidt, Eric~F. and Warner-Schmidt, Jennifer~L. and Otopalik, Benjamin~G. and Pickett, Sarah~B. and Greengard, Paul and Heintz, Nathaniel},
  month = may,
  year = {2012},
  pages = {1152--1163},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/CE4VR943/S0092867412004722.html:}
}

@article{westra_mixupmapper_2011,
  title = {{{MixupMapper}}: correcting sample mix-ups in genome-wide datasets increases power to detect small genetic effects},
  issn = {1367-4803, 1460-2059},
  shorttitle = {{{MixupMapper}}},
  doi = {10.1093/bioinformatics/btr323},
  abstract = {Motivation: Sample mix-ups can arise during sample collection, handling, genotyping or data management. It is unclear how often sample mix-ups occur in genome-wide studies, as there currently are no post-hoc methods that can identify these mix-ups in unrelated samples. We have therefore developed an algorithm (MixupMapper) that can both detect and correct sample mix-ups in genome-wide studies that study gene expression levels.
Results: We applied MixupMapper to five publicly available human genetical genomics datasets. On average, 3\% of all analyzed samples had been assigned incorrect expression phenotypes: in one of the datasets 23\% of the samples had incorrect expression phenotypes. The consequences of sample mix-ups are substantial: when we corrected these sample mix-ups, we identified on average 15\% more significant cis-expression quantitative trait loci (cis-eQTLs). In one dataset, we identified three times as many significant cis-eQTLs after correction. Furthermore, we show through simulations that sample mix-ups can lead to an underestimation of the explained heritability of complex traits in genome-wide association datasets.
Availability and implementation: MixupMapper is freely available at http://www.genenetwork.nl/mixupmapper/
Contact: lude@ludesign.nl
Supplementary Information: Supplementary information is available online at http://www.genenetwork.nl/mixupmapper/},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2015-02-19},
  journal = {Bioinformatics},
  author = {Westra, H.-J. and Jansen, R. C. and Fehrmann, R. S. N. and {te Meerman}, G. J. and {van Heel}, D. and Wijmenga, C. and Franke, L.},
  month = jun,
  year = {2011},
  pages = {btr323},
  pmid = {21653519}
}

@article{wang_lipoprotein_2012,
  title = {Lipoprotein {{Lipase}} in the {{Brain}} and {{Nervous System}}},
  volume = {32},
  doi = {10.1146/annurev-nutr-071811-150703},
  abstract = {Lipoprotein lipase (LPL) is rate limiting in the provision of triglyceride-rich lipoprotein-derived lipids into tissues. LPL is also present in the brain, where its function has remained elusive. Recent evidence implicates a role of LPL in the brain in two processes: (a) the regulation of energy balance and body weight and (b) cognition. Mice with neuron-specific deletion of LPL have increases in food intake that lead to obesity, and then reductions in energy expenditure that further contribute to and sustain the phenotype. In other mice with LPL deficiency rescued from neonatal lethality by somatic gene transfer wherein LPL in the brain remains absent, altered cognition ensues. Taking into consideration data that associate LPL mutations with Alzheimer's disease, a role for LPL in learning and memory seems likely. Overall, the time is ripe for new insights into how LPL-mediated lipoprotein metabolism in the brain impacts CNS processes and systems biology.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-11-28},
  journal = {Annual Review of Nutrition},
  author = {Wang, Hong and Eckel, Robert H.},
  year = {2012},
  keywords = {cognition,energy balance,fatty acids,lpl,metabolism,triglycerides},
  pages = {147--160},
  pmid = {22540257}
}

@article{shay_conservation_2013,
  title = {Conservation and divergence in the transcriptional programs of the human and mouse immune systems},
  volume = {110},
  issn = {1091-6490},
  doi = {10.1073/pnas.1222738110},
  abstract = {Much of the knowledge about cell differentiation and function in the immune system has come from studies in mice, but the relevance to human immunology, diseases, and therapy has been challenged, perhaps more from anecdotal than comprehensive evidence. To this end, we compare two large compendia of transcriptional profiles of human and mouse immune cell types. Global transcription profiles are conserved between corresponding cell lineages. The expression patterns of most orthologous genes are conserved, particularly for lineage-specific genes. However, several hundred genes show clearly divergent expression across the examined cell lineages, and among them, 169 genes did so even with highly stringent criteria. Finally, regulatory mechanisms--reflected by regulators' differential expression or enriched cis-elements--are conserved between the species but to a lower degree, suggesting that distinct regulation may underlie some of the conserved transcriptional responses.},
  language = {eng},
  timestamp = {2015-12-18T20:22:22Z},
  number = {8},
  journal = {Proceedings of the National Academy of Sciences of the United States of America},
  author = {Shay, Tal and Jojic, Vladimir and Zuk, Or and Rothamel, Katherine and Puyraimond-Zemmour, David and Feng, Ting and Wakamatsu, Ei and Benoist, Christophe and Koller, Daphne and Regev, Aviv and {ImmGen Consortium}},
  month = feb,
  year = {2013},
  keywords = {Animals,Gene Expression Profiling,Humans,Immune System,Lymphocyte Activation,Mice,T-Lymphocytes,Transcription; Genetic},
  pages = {2946--2951},
  pmid = {23382184},
  pmcid = {PMC3581886}
}

@article{kim_gene_2001,
  title = {A {{Gene Expression Map}} for {{Caenorhabditis}} elegans},
  volume = {293},
  issn = {0036-8075, 1095-9203},
  doi = {10.1126/science.1061603},
  abstract = {We have assembled data from Caenorhabditis elegans DNA microarray experiments involving many growth conditions, developmental stages, and varieties of mutants. Co-regulated genes were grouped together and visualized in a three-dimensional expression map that displays correlations of gene expression profiles as distances in two dimensions and gene density in the third dimension. The gene expression map can be used as a gene discovery tool to identify genes that are co-regulated with known sets of genes (such as heat shock, growth control genes, germ line genes, and so forth) or to uncover previously unknown genetic functions (such as genomic instability in males and sperm caused by specific transposons).},
  language = {en},
  timestamp = {2016-03-16T01:52:12Z},
  number = {5537},
  urldate = {2016-03-16},
  journal = {Science},
  author = {Kim, Stuart K. and Lund, Jim and Kiraly, Moni and Duke, Kyle and Jiang, Min and Stuart, Joshua M. and Eizinger, Andreas and Wylie, Brian N. and Davidson, George S.},
  month = sep,
  year = {2001},
  pages = {2087--2092},
  pmid = {11557892}
}

@article{herculano-houzel_isotropic_2005,
  title = {Isotropic {{Fractionator}}: {{A Simple}}, {{Rapid Method}} for the {{Quantification}} of {{Total Cell}} and {{Neuron Numbers}} in the {{Brain}}},
  volume = {25},
  issn = {0270-6474, 1529-2401},
  shorttitle = {Isotropic {{Fractionator}}},
  doi = {10.1523/JNEUROSCI.4526-04.2005},
  abstract = {Stereological techniques that estimate cell numbers must be restricted to well defined structures of isotropic architecture and therefore do not apply to the whole brain or to large neural regions. We developed a novel, fast, and inexpensive method to quantify total numbers of neuronal and non-neuronal cells in the brain or any dissectable regions thereof. It consists of transforming highly anisotropic brain structures into homogeneous, isotropic suspensions of cell nuclei, which can be counted and identified immunocytochemically as neuronal or non-neuronal. Estimates of total cell, neuronal, and non-neuronal numbers can be obtained in 24 h and vary by \ensuremath{<}10\% among animals. Because the estimates obtained are independent of brain volume, they can be used in comparative studies of brain-volume variation among species and in studies of phylogenesis, development, adult neurogenesis, and pathology. Applying this method to the adult rat brain, we show, for example, that it contains \ensuremath{\sim}330 million cells, of which 200 million are neurons, and almost 70\% of these are located in the cerebellum alone. Moreover, contrary to what is commonly assumed in the literature, we show that glial cells are not the majority in the rat brain.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {10},
  urldate = {2014-11-14},
  journal = {The Journal of Neuroscience},
  author = {Herculano-Houzel, Suzana and Lent, Roberto},
  month = sep,
  year = {2005},
  keywords = {cerebellum,cortex,evolution,glia,morphometry,neuron},
  pages = {2518--2521},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/QGI6ME99/2518.html:},
  pmid = {15758160}
}

@article{papapetropoulos_multiregional_2006,
  title = {Multiregional gene expression profiling identifies {{MRPS6}} as a possible candidate gene for {{Parkinson}}'s disease},
  volume = {13},
  issn = {1052-2166},
  abstract = {Combining large-scale gene expression approaches and bioinformatics may provide insights into the molecular variability of biological processes underlying neurodegeneration. To identify novel candidate genes and mechanisms, we conducted a multiregional gene expression analysis in postmortem brain. Gene arrays were performed utilizing Affymetrix HG U133 Plus 2.0 gene chips. Brain specimens from 21 different brain regions were taken from Parkinson's disease (PD) (n = 22) and normal aged (n = 23) brain donors. The rationale for conducting a multiregional survey of gene expression changes was based on the assumption that if a gene is changed in more than one brain region, it may be a higher probability candidate gene compared to genes that are changed in a single region. Although no gene was significantly changed in all of the 21 brain regions surveyed, we identified 11 candidate genes whose pattern of expression was regulated in at least 18 out of 21 regions. The expression of a gene encoding the mitochondria ribosomal protein S6 (MRPS6) had the highest combined mean fold change and topped the list of regulated genes. The analysis revealed other genes related to apoptosis, cell signaling, and cell cycle that may be of importance to disease pathophysiology. High throughput gene expression is an emerging technology for molecular target discovery in neurological and psychiatric disorders. The top gene reported here is the nuclear encoded MRPS6, a building block of the human mitoribosome of the oxidative phosphorylation system (OXPHOS). Impairments in mitochondrial OXPHOS have been linked to the pathogenesis of PD.},
  language = {eng},
  timestamp = {2016-03-15T01:06:46Z},
  number = {3},
  journal = {Gene Expression},
  author = {Papapetropoulos, Spiridon and Ffrench-Mullen, Jarlath and McCorquodale, Donald and Qin, Yujing and Pablo, John and Mash, Deborah C.},
  year = {2006},
  keywords = {Adult,Aged,Aged; 80 and over,Aging,biomarkers,Female,Gene Expression Profiling,Gene Expression Regulation,Humans,Male,Middle Aged,Mitochondrial Proteins,Oligonucleotide Array Sequence Analysis,oxidative phosphorylation,Parkinson Disease,Ribosomal Protein S6,RNA; Messenger,Substantia nigra},
  pages = {205--215},
  file = {Papapetropoulos et al_2006_Multiregional gene expression profiling identifies MRPS6 as a possible.pdf:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/CN2IQ2ED/Papapetropoulos et al_2006_Multiregional gene expression profiling identifies MRPS6 as a possible.pdf:application/pdf},
  pmid = {17193926}
}

@article{severson_midbrain_2003,
  title = {Midbrain serotonergic neurons are central {{pH}} chemoreceptors},
  volume = {6},
  issn = {10976256},
  language = {English},
  timestamp = {2016-03-24T10:05:47Z},
  number = {11},
  urldate = {2016-03-24},
  journal = {Nature Neuroscience},
  author = {Severson, Christopher A and Wang, Wengang and Pieribone, Vincent A and Dohle, Carolin I and Richerson, George B},
  month = nov,
  year = {2003},
  note = {1139},
  keywords = {Chemoreceptors,Mesencephalon,Neurons},
  pages = {1139+}
}

@article{nordentoft_m_absolute_2011,
  title = {{{ABsolute}} risk of suicide after first hospital contact in mental disorder},
  volume = {68},
  issn = {0003-990X},
  doi = {10.1001/archgenpsychiatry.2011.113},
  abstract = {Context~Estimates of lifetime risk of suicide in mental disorders were based on selected samples with incomplete follow-up.Objective~To estimate, in a national cohort, the absolute risk of suicide within 36 years after the first psychiatric contact.Design~Prospective study of incident cases followed up for as long as 36 years. Median follow-up was 18 years.Setting~Individual data drawn from Danish longitudinal registers.Participants~A total of 176~347 persons born from January 1, 1955, through December 31, 1991, were followed up from their first contact with secondary mental health services after 15 years of age until death, emigration, disappearance, or the end of 2006. For each participant, 5 matched control individuals were included.Main Outcome Measures~Absolute risk of suicide in percentage of individuals up to 36 years after the first contact.Results~Among men, the absolute risk of suicide (95\% confidence interval [CI]) was highest for bipolar disorder, (7.77\%; 6.01\%-10.05\%), followed by unipolar affective disorder (6.67\%; 5.72\%-7.78\%) and schizophrenia (6.55\%; 5.85\%-7.34\%). Among women, the highest risk was found among women with schizophrenia (4.91\%; 95\% CI, 4.03\%-5.98\%), followed by bipolar disorder (4.78\%; 3.48\%-6.56\%). In the nonpsychiatric population, the risk was 0.72\% (95\% CI, 0.61\%-0.86\%) for men and 0.26\% (0.20\%-0.35\%) for women. Comorbid substance abuse and comorbid unipolar affective disorder significantly increased the risk. The co-occurrence of deliberate self-harm increased the risk approximately 2-fold. Men with bipolar disorder and deliberate self-harm had the highest risk (17.08\%; 95\% CI, 11.19\%-26.07\%).Conclusions~This is the first analysis of the absolute risk of suicide in a total national cohort of individuals followed up from the first psychiatric contact, and it represents, to our knowledge, the hitherto largest sample with the longest and most complete follow-up. Our estimates are lower than those most often cited, but they are still substantial and indicate the continuous need for prevention of suicide among people with mental disorders.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {10},
  urldate = {2014-12-16},
  journal = {Archives of General Psychiatry},
  author = {{Nordentoft M} and {Mortensen P} and {Pedersen C}},
  month = oct,
  year = {2011},
  pages = {1058--1064}
}

@article{zhang_rna-sequencing_2014,
  title = {An {{RNA-Sequencing Transcriptome}} and {{Splicing Database}} of {{Glia}}, {{Neurons}}, and {{Vascular Cells}} of the {{Cerebral Cortex}}},
  volume = {34},
  issn = {0270-6474, 1529-2401},
  doi = {10.1523/JNEUROSCI.1860-14.2014},
  abstract = {The major cell classes of the brain differ in their developmental processes, metabolism, signaling, and function. To better understand the functions and interactions of the cell types that comprise these classes, we acutely purified representative populations of neurons, astrocytes, oligodendrocyte precursor cells, newly formed oligodendrocytes, myelinating oligodendrocytes, microglia, endothelial cells, and pericytes from mouse cerebral cortex. We generated a transcriptome database for these eight cell types by RNA sequencing and used a sensitive algorithm to detect alternative splicing events in each cell type. Bioinformatic analyses identified thousands of new cell type-enriched genes and splicing isoforms that will provide novel markers for cell identification, tools for genetic manipulation, and insights into the biology of the brain. For example, our data provide clues as to how neurons and astrocytes differ in their ability to dynamically regulate glycolytic flux and lactate generation attributable to unique splicing of PKM2, the gene encoding the glycolytic enzyme pyruvate kinase. This dataset will provide a powerful new resource for understanding the development and function of the brain. To ensure the widespread distribution of these datasets, we have created a user-friendly website (http://web.stanford.edu/group/barres\_lab/brain\_rnaseq.html) that provides a platform for analyzing and comparing transciption and alternative splicing profiles for various cell classes in the brain.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {36},
  urldate = {2015-06-15},
  journal = {The Journal of Neuroscience},
  author = {Zhang, Ye and Chen, Kenian and Sloan, Steven A. and Bennett, Mariko L. and Scholze, Anja R. and O'Keeffe, Sean and Phatnani, Hemali P. and Guarnieri, Paolo and Caneda, Christine and Ruderisch, Nadine and Deng, Shuyun and Liddelow, Shane A. and Zhang, Chaolin and Daneman, Richard and Maniatis, Tom and Barres, Ben A. and Wu, Jia Qian},
  month = mar,
  year = {2014},
  keywords = {alternative splicing,astrocytes,microglia,oligodendrocytes,transcriptome,vascular cells},
  pages = {11929--11947},
  pmid = {25186741}
}

@article{lesnick_genomic_2007,
  title = {A genomic pathway approach to a complex disease: axon guidance and {{Parkinson}} disease},
  volume = {3},
  issn = {1553-7404},
  shorttitle = {A genomic pathway approach to a complex disease},
  doi = {10.1371/journal.pgen.0030098},
  abstract = {While major inroads have been made in identifying the genetic causes of rare Mendelian disorders, little progress has been made in the discovery of common gene variations that predispose to complex diseases. The single gene variants that have been shown to associate reproducibly with complex diseases typically have small effect sizes or attributable risks. However, the joint actions of common gene variants within pathways may play a major role in predisposing to complex diseases (the paradigm of complex genetics). The goal of this study was to determine whether polymorphism in a candidate pathway (axon guidance) predisposed to a complex disease (Parkinson disease [PD]). We mined a whole-genome association dataset and identified single nucleotide polymorphisms (SNPs) that were within axon-guidance pathway genes. We then constructed models of axon-guidance pathway SNPs that predicted three outcomes: PD susceptibility (odds ratio = 90.8, p = 4.64 x 10(-38)), survival free of PD (hazards ratio = 19.0, p = 5.43 x 10(-48)), and PD age at onset (R(2) = 0.68, p = 1.68 x 10(-51)). By contrast, models constructed from thousands of random selections of genomic SNPs predicted the three PD outcomes poorly. Mining of a second whole-genome association dataset and mining of an expression profiling dataset also supported a role for many axon-guidance pathway genes in PD. These findings could have important implications regarding the pathogenesis of PD. This genomic pathway approach may also offer insights into other complex diseases such as Alzheimer disease, diabetes mellitus, nicotine and alcohol dependence, and several cancers.},
  language = {eng},
  timestamp = {2016-03-03T22:52:23Z},
  number = {6},
  journal = {PLoS genetics},
  author = {Lesnick, Timothy G. and Papapetropoulos, Spiridon and Mash, Deborah C. and Ffrench-Mullen, Jarlath and Shehadeh, Lina and {de Andrade}, Mariza and Henley, John R. and Rocca, Walter A. and Ahlskog, J. Eric and Maraganore, Demetrius M.},
  month = jun,
  year = {2007},
  keywords = {Axons,Case-Control Studies,Genetic Predisposition to Disease,Genomics,Humans,Neural Pathways,Parkinson Disease,Polymorphism; Single Nucleotide},
  pages = {e98},
  pmid = {17571925},
  pmcid = {PMC1904362}
}

@article{sommeijer_synaptotagmin-2_2012,
  title = {Synaptotagmin-2 {{Is}} a {{Reliable Marker}} for {{Parvalbumin Positive Inhibitory Boutons}} in the {{Mouse Visual Cortex}}},
  volume = {7},
  doi = {10.1371/journal.pone.0035323},
  abstract = {BackgroundInhibitory innervation by parvalbumin (PV) expressing interneurons has been implicated in the onset of the sensitive period of visual plasticity. Immunohistochemical analysis of the development and plasticity of these inhibitory inputs is difficult because PV expression is low in young animals and strongly influenced by neuronal activity. Moreover, the synaptic boutons that PV neurons form onto each other cannot be distinguished from the innervated cell bodies by immunostaining for this protein because it is present throughout the cells. These problems call for the availability of a synaptic, activity-independent marker for PV+ inhibitory boutons that is expressed before sensitive period onset. We investigated whether synaptotagmin-2 (Syt2) fulfills these properties in the visual cortex. Syt2 is a synaptic vesicle protein involved in fast Ca2+ dependent neurotransmitter release. Its mRNA expression follows a pattern similar to that of PV throughout the brain and is present in 30\textendash{}40\% of hippocampal PV expressing basket cells. Up to now, no quantitative analyses of Syt2 expression in the visual cortex have been carried out.Methodology/Principal FindingsWe used immunohistochemistry to analyze colocalization of Syt2 with multiple interneuron markers including vesicular GABA transporter VGAT, calbindin, calretinin, somatostatin and PV in the primary visual cortex of mice during development and after dark-rearing.Conclusions/SignificanceWe show that in the adult visual cortex Syt2 is only found in inhibitory, VGAT positive boutons. Practically all Syt2 positive boutons also contain PV and vice versa. During development, Syt2 expression can be detected in synaptic boutons prior to PV and in contrast to PV expression, Syt2 is not down-regulated by dark-rearing. These properties of Syt2 make it an excellent marker for analyzing the development and plasticity of perisomatic inhibitory innervations onto both excitatory and inhibitory neurons in the visual cortex.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {4},
  urldate = {2014-11-28},
  journal = {PLoS ONE},
  author = {Sommeijer, Jean-Pierre and Levelt, Christiaan N.},
  month = apr,
  year = {2012},
  keywords = {Syt2},
  pages = {e35323},
  file = {PLoS Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/JNZ4XI9R/infodoi10.1371journal.pone.html:}
}

@article{arion_distinctive_2015,
  title = {Distinctive transcriptome alterations of prefrontal pyramidal neurons in schizophrenia and schizoaffective disorder},
  copyright = {\textcopyright{} 2015 Nature Publishing Group},
  issn = {1359-4184},
  doi = {10.1038/mp.2014.171},
  abstract = {Schizophrenia is associated with alterations in working memory that reflect dysfunction of dorsolateral prefrontal cortex (DLPFC) circuitry. Working memory depends on the activity of excitatory pyramidal cells in DLPFC layer 3 and, to a lesser extent, in layer 5. Although many studies have profiled gene expression in DLPFC gray matter in schizophrenia, little is known about cell-type-specific transcript expression in these two populations of pyramidal cells. We hypothesized that interrogating gene expression, specifically in DLPFC layer 3 or 5 pyramidal cells, would reveal new and/or more robust schizophrenia-associated differences that would provide new insights into the nature of pyramidal cell dysfunction in the illness. We also sought to determine the impact of other variables, such as a diagnosis of schizoaffective disorder or medication use at the time of death, on the patterns of gene expression in pyramidal neurons. Individual pyramidal cells in DLPFC layers 3 or 5 were captured by laser microdissection from 36 subjects with schizophrenia or schizoaffective disorder and matched normal comparison subjects. The mRNA from cell collections was subjected to transcriptome profiling by microarray followed by quantitative PCR validation. Expression of genes involved in mitochondrial (MT) or ubiquitin\textendash{}proteasome system (UPS) functions were markedly downregulated in the patient group (P-values for MT-related and UPS-related pathways were \ensuremath{<}10-7 and \ensuremath{<}10-5, respectively). MT-related gene alterations were more prominent in layer 3 pyramidal cells, whereas UPS-related gene alterations were more prominent in layer 5 pyramidal cells. Many of these alterations were not present, or found to a lesser degree, in samples of DLPFC gray matter from the same subjects, suggesting that they are pyramidal cell specific. Furthermore, these findings principally reflected alterations in the schizophrenia subjects were not present or present to a lesser degree in the schizoaffective disorder subjects (diagnosis of schizoaffective disorder was the most significant covariate, P\ensuremath{<}10-6) and were not attributable to factors frequently comorbid with schizophrenia. In summary, our findings reveal expression deficits in MT- and UPS-related genes specific to layer 3 and/or layer 5 pyramidal cells in the DLPFC of schizophrenia subjects. These cell type-specific transcriptome signatures are not characteristic of schizoaffective disorder, providing a potential molecular\textendash{}cellular basis of differences in clinical phenotypes.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2015-05-15},
  journal = {Molecular Psychiatry},
  author = {Arion, D. and Corradi, J. P. and Tang, S. and Datta, D. and Boothe, F. and He, A. and Cacace, A. M. and Zaczek, R. and Albright, C. F. and Tseng, G. and Lewis, D. A.},
  month = jan,
  year = {2015}
}

@article{weisheit_postnatal_2006,
  title = {Postnatal development of the murine cerebellar cortex: formation and early dispersal of basket, stellate and {{Golgi}} neurons},
  volume = {24},
  issn = {1460-9568},
  shorttitle = {Postnatal development of the murine cerebellar cortex},
  doi = {10.1111/j.1460-9568.2006.04915.x},
  abstract = {The cerebellar cortex consists of a small set of neuronal cell types interconnected in a highly stereotyped way. While the development of cerebellar cortical projection neurons, i.e. Purkinje cells, and that of granule cells has been elucidated in considerable detail, that of cerebellar cortical inhibitory interneurons is still rather fragmentarily understood. Here, we use mice expressing green fluorescent protein (GFP) from the Pax2 locus to analyse the ontogenesis of these cells. Numbers of Pax2-positive inhibitory interneuronal precursors increase following a classical sigmoidal growth curve to yield a total of some 905.000~\ensuremath{\pm}~77.000~cells. Maximal cell increase occurs at about postnatal day (P)5.4, and some 75\% of all inhibitory interneurons are generated prior to P7. Conjoint analysis of the developmental accruement of Pax2-GFP-positive cells and their cell cycle distribution reveals that, at least at P0 and P3, the numerical increase of these cells results primarily from proliferation of a Pax2-negative precursor population and suggests that Pax2 expression begins at or around the final mitosis. Following their terminal mitosis, inhibitory cerebellar cortical interneurons go through a protracted quiescent phase in which they maintain expression of the cell cycle marker Ki-67. During this phase, they translocate into the nascent molecular layer, where they stall next to premigratory granule cell precursors without penetrating this population of cells. These observations provide a quantitative description of cerebellar cortical inhibitory interneuron genesis and early differentiation, and define Pax2 as a marker expressed in basket and stellate cells, from around their final mitosis to their incipient histogenetic integration.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-11-20},
  journal = {European Journal of Neuroscience},
  author = {Weisheit, Gunnar and Gliem, Michael and Endl, Elmar and Pfeffer, Peter L. and Busslinger, Meinrad and Schilling, Karl},
  month = jul,
  year = {2006},
  keywords = {basket cell,cerebellum,development,Golgi neuron,inhibitory interneuron,Pax2,proliferation,stellate cell},
  pages = {466--478},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/IAE7TBCK/abstract.html:}
}

@article{cahoy_transcriptome_2008,
  title = {A {{Transcriptome Database}} for {{Astrocytes}}, {{Neurons}}, and {{Oligodendrocytes}}: {{A New Resource}} for {{Understanding Brain Development}} and {{Function}}},
  volume = {28},
  issn = {0270-6474, 1529-2401},
  shorttitle = {A {{Transcriptome Database}} for {{Astrocytes}}, {{Neurons}}, and {{Oligodendrocytes}}},
  doi = {10.1523/JNEUROSCI.4178-07.2008},
  abstract = {Understanding the cell\textendash{}cell interactions that control CNS development and function has long been limited by the lack of methods to cleanly separate neural cell types. Here we describe methods for the prospective isolation and purification of astrocytes, neurons, and oligodendrocytes from developing and mature mouse forebrain. We used FACS (fluorescent-activated cell sorting) to isolate astrocytes from transgenic mice that express enhanced green fluorescent protein (EGFP) under the control of an S100\ensuremath{\beta} promoter. Using Affymetrix GeneChip Arrays, we then created a transcriptome database of the expression levels of \ensuremath{>}20,000 genes by gene profiling these three main CNS neural cell types at various postnatal ages between postnatal day 1 (P1) and P30. This database provides a detailed global characterization and comparison of the genes expressed by acutely isolated astrocytes, neurons, and oligodendrocytes. We found that Aldh1L1 is a highly specific antigenic marker for astrocytes with a substantially broader pattern of astrocyte expression than the traditional astrocyte marker GFAP. Astrocytes were enriched in specific metabolic and lipid synthetic pathways, as well as the draper/Megf10 and Mertk/integrin \ensuremath{\alpha}v\ensuremath{\beta}5 phagocytic pathways suggesting that astrocytes are professional phagocytes. Our findings call into question the concept of a ``glial'' cell class as the gene profiles of astrocytes and oligodendrocytes are as dissimilar to each other as they are to neurons. This transcriptome database of acutely isolated purified astrocytes, neurons, and oligodendrocytes provides a resource to the neuroscience community by providing improved cell-type-specific markers and for better understanding of neural development, function, and disease.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2015-08-08},
  journal = {The Journal of Neuroscience},
  author = {Cahoy, John D. and Emery, Ben and Kaushal, Amit and Foo, Lynette C. and Zamanian, Jennifer L. and Christopherson, Karen S. and Xing, Yi and Lubischer, Jane L. and Krieg, Paul A. and Krupenko, Sergey A. and Thompson, Wesley J. and Barres, Ben A.},
  month = feb,
  year = {2008},
  keywords = {Aldh1L1,astrocyte,astroglia,culture,Draper,GeneChip,gene profiling,Megf10,Mertk,Mfge8,microarray,neuron,oligodendrocyte,phagocytosis,transcriptome},
  pages = {264--278},
  pmid = {18171944}
}

@article{defelipe_new_2013,
  title = {New insights into the classification and nomenclature of cortical {{GABAergic}} interneurons},
  volume = {14},
  issn = {1471-0048},
  doi = {10.1038/nrn3444},
  abstract = {A systematic classification and accepted nomenclature of neuron types is much needed but is currently lacking. This article describes a possible taxonomical solution for classifying GABAergic interneurons of the cerebral cortex based on a novel, web-based interactive system that allows experts to classify neurons with pre-determined criteria. Using Bayesian analysis and clustering algorithms on the resulting data, we investigated the suitability of several anatomical terms and neuron names for cortical GABAergic interneurons. Moreover, we show that supervised classification models could automatically categorize interneurons in agreement with experts' assignments. These results demonstrate a practical and objective approach to the naming, characterization and classification of neurons based on community consensus.},
  language = {eng},
  timestamp = {2016-05-29T09:57:25Z},
  number = {3},
  journal = {Nature Reviews. Neuroscience},
  author = {DeFelipe, Javier and L{\'o}pez-Cruz, Pedro L. and Benavides-Piccione, Ruth and Bielza, Concha and Larra{\~n}aga, Pedro and Anderson, Stewart and Burkhalter, Andreas and Cauli, Bruno and Fair{\'e}n, Alfonso and Feldmeyer, Dirk and Fishell, Gord and Fitzpatrick, David and Freund, Tam{\'a}s F. and Gonz{\'a}lez-Burgos, Guillermo and Hestrin, Shaul and Hill, Sean and Hof, Patrick R. and Huang, Josh and Jones, Edward G. and Kawaguchi, Yasuo and Kisv{\'a}rday, Zolt{\'a}n and Kubota, Yoshiyuki and Lewis, David A. and Mar{\'\i}n, Oscar and Markram, Henry and McBain, Chris J. and Meyer, Hanno S. and Monyer, Hannah and Nelson, Sacha B. and Rockland, Kathleen and Rossier, Jean and Rubenstein, John L. R. and Rudy, Bernardo and Scanziani, Massimo and Shepherd, Gordon M. and Sherwood, Chet C. and Staiger, Jochen F. and Tam{\'a}s, G{\'a}bor and Thomson, Alex and Wang, Yun and Yuste, Rafael and Ascoli, Giorgio A.},
  month = mar,
  year = {2013},
  keywords = {Algorithms,Animals,Bayes Theorem,Cerebral Cortex,Cluster Analysis,gamma-Aminobutyric Acid,Humans,interneurons,Terminology as Topic},
  pages = {202--216},
  pmid = {23385869},
  pmcid = {PMC3619199}
}

@article{molnar_towards_2006,
  title = {Towards the classification of subpopulations of layer {{V}} pyramidal projection neurons},
  volume = {55},
  issn = {0168-0102},
  doi = {10.1016/j.neures.2006.02.008},
  abstract = {The nature of cerebral cortical circuitry has been increasingly clarified by markers for the identification of precise cell types with specific morphology, connectivity and distinct physiological properties. Molecular markers are not only helpful in dissecting cortical circuitry, but also give insight into the mechanisms of cortical neuronal specification and differentiation. The two principal neuronal types of the cerebral cortex are the pyramidal and GABAergic cells. Pyramidal cells are excitatory and project to distant targets, while GABAergic neurons are mostly inhibitory non-pyramidal interneurons. Reliable markers for specific subtypes of interneurons are available and have been employed in the classification and functional analysis of cortical circuitry. Until recently, cortical pyramidal neurons have been considered a homogeneous class of cells. This concept is now changing as the powerful tools of molecular biology and genetics identify molecular tags for subtypes of pyramidal cells such as: Otx-1 [Frantz, G.D., Bohner, A.P., Akers, R.M., McConnell, S.K., 1994. Regulation of the POU domain gene SCIP during cerebral cortical development. J. Neurosci. 14, 472\textendash{}485; Weimann, J.M., Zhang, Y.A., Levin, M.E., Devine, W.P., Brulet, P., McConnell, S.K., 1999. Cortical neurons require Otx1 for the refinement of exuberant axonal projections to subcortical targets. Neuron 24, 819\textendash{}831]; SMI-32, N200 and FNP-7 [Voelker, C.C., Garin, N., Taylor, J.S., Gahwiler, B.H., Hornung, J.P., Moln{\'a}r, Z., 2004. Selective neurofilament (SMI-32, FNP-7 and N200) expression in subpopulations of layer V pyramidal neurons in vivo and in vitro. Cereb. Cortex 14, 1276\textendash{}1286]; ER81 [Hevner, R.F., Daza, R.A., Rubenstein, J.L., Stunnenberg, H., Olavarria, J.F., Englund, C., 2003. Beyond laminar fate: toward a molecular classification of cortical projection/pyramidal neurons. Dev. Neurosci. 25 (2\textendash{}4), 139\textendash{}151; Yoneshima, H., Yamasaki, S., Voelker, C., Moln{\'a}r, Z., Christophe, E., Audinat, E., Takemoto, M., Tsuji, S., Fujita, I., Yamamoto, N., 2006. ER81 is expressed in a subpopulation of layer 5 projection neurons in rodent cerebral cortices. Neuroscience, 137, 401\textendash{}412]; Lmo4 [Bulchand, S., Subramanian, L., Tole, S., 2003. Dynamic spatiotemporal expression of LIM genes and cofactors in the embryonic and postnatal cerebral cortex. Dev. Dyn. 226, 460\textendash{}469; Arlotta, P., Molyneaux, B.J., Chen, J., Inoue, J., Kominami, R., Macklis, J.D., 2005. Neuronal subtype-specific genes that control corticospinal motor neuron development in vivo. Neuron 45 (2), 207\textendash{}221]; CTIP2 [Arlotta, P., Molyneaux, B.J., Chen, J., Inoue, J., Kominami, R., Macklis, J.D., 2005. Neuronal subtype-specific genes that control corticospinal motor neuron development in vivo. Neuron 45 (2), 207\textendash{}221]; Fez1 [Molyneaux, B.J., Arlotta, P., Hirata, T., Hibi, M., Macklis, J.D., 2005. Fez1 is required for the birth and specification of corticospinal motor neurons. Neuron 47 (6), 817\textendash{}831; Chen, B., Schaevitz, L.R., McConnell, S.K., 2005. Fez1 regulates the differentiation and axon targeting of layer 5 subcortical projection neurons in cerebral cortex. Proc. Natl. Acad. Sci. U.S.A. 102 (47), 17184\textendash{}17189]. These genes outline the numerous subtypes of pyramidal cells and are increasingly refining our previous classifications. They also indicate specific developmental programs operate in cell fate decisions. This review will describe the progress made on the correlation of these markers to each other within a specific subtype of layer V neurons with identified, stereotypic projections. Further work is needed to link these data with observations on somatodendritic morphology and physiological properties. The integrated molecular, anatomical and physiological characterisation of pyramidal neurons will lead to a much better appreciation of functional cortical circuits.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-11-05},
  journal = {Neuroscience Research},
  author = {Moln{\'a}r, Zolt{\'a}n and Cheung, Amanda F. P.},
  month = jun,
  year = {2006},
  keywords = {Callosum,Corticospinal projections,ER81,Fez1,FNP-7,N200,OTX-1,Pyramidal neurons,SMI-32},
  pages = {105--115},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/ETCJS3R2/S0168010206000447.html:}
}

@article{abbas_deconvolution_2009,
  title = {Deconvolution of blood microarray data identifies cellular activation patterns in systemic lupus erythematosus},
  volume = {4},
  issn = {1932-6203},
  doi = {10.1371/journal.pone.0006098},
  abstract = {Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease with a complex spectrum of cellular and molecular characteristics including several dramatic changes in the populations of peripheral leukocytes. These changes include general leukopenia, activation of B and T cells, and maturation of granulocytes. The manifestation of SLE in peripheral blood is central to the disease but is incompletely understood. A technique for rigorously characterizing changes in mixed populations of cells, microarray expression deconvolution, has been applied to several areas of biology but not to SLE or to blood. Here we demonstrate that microarray expression deconvolution accurately quantifies the constituents of real blood samples and mixtures of immune-derived cell lines. We characterize a broad spectrum of peripheral leukocyte cell types and states in SLE to uncover novel patterns including: specific activation of NK and T helper lymphocytes, relationships of these patterns to each other, and correlations to clinical variables and measures. The expansion and activation of monocytes, NK cells, and T helper cells in SLE at least partly underlie this disease's prominent interferon signature. These and other patterns of leukocyte dynamics uncovered here correlate with disease severity and treatment, suggest potential new treatments, and extend our understanding of lupus pathology as a complex autoimmune disease involving many arms of the immune system.},
  language = {eng},
  timestamp = {2015-08-17T22:23:09Z},
  number = {7},
  journal = {PloS One},
  author = {Abbas, Alexander R. and Wolslegel, Kristen and Seshasayee, Dhaya and Modrusan, Zora and Clark, Hilary F.},
  year = {2009},
  keywords = {B-Lymphocytes,Case-Control Studies,Humans,Lupus Erythematosus; Systemic,Lymphocyte Activation,T-Lymphocytes},
  pages = {e6098},
  pmid = {19568420},
  pmcid = {PMC2699551}
}

@article{ugrumov_neurons_2014,
  title = {Neurons expressing individual enzymes of dopamine synthesis in the mediobasal hypothalamus of adult rats: {{Functional}} significance and topographic interrelations},
  volume = {277},
  issn = {0306-4522},
  shorttitle = {Neurons expressing individual enzymes of dopamine synthesis in the mediobasal hypothalamus of adult rats},
  doi = {10.1016/j.neuroscience.2014.06.051},
  abstract = {Besides dopaminergic (DA-ergic) neurons having all enzymes of DA synthesis, tyrosine hydroxylase (TH) and aromatic l-amino acid decarboxylase (AADC), ``monoenzymatic'' neurons expressing only one of them were found in the brain, mostly in the mediobasal hypothalamus (MBH). The aim of this study was to test our hypothesis that DA is synthesized by monoenzymatic neurons, i.e. l-3,4-dihydroxyphenylalanine (l-DOPA), which produced in the monoenzymatic TH neurons is transported in the monoenzymatic AADC neurons for DA synthesis. Incubation of MBH in Krebs-Ringer solution with l-leucine, a competitive inhibitor of l-DOPA uptake, was used to prevent a hypothetical l-DOPA capture into AADC-containing neurons. Incubation of the substantia nigra containing DA-ergic neurons under the same conditions served as the control. According to our data, the l-leucine administration provoked a decrease of DA concentration in MBH and in the incubation medium but not in the substantia nigra and respective incubation medium, showing a decrease of cooperative synthesis of DA in MBH. This conclusion was supported by an observation of higher concentration of l-DOPA in the incubation medium under perfusion of MBH with Krebs-Ringer solution containing tolcapone, an inhibitor of catechol-O-methyltransferase, and l-leucine than under perfusion with the same solution, but without l-leucine. Functional interaction between monoenzymatic TH and AADC neurons was indirectly confirmed by finding in electron microscopy their close relations in MBH. Besides monoenzymatic AADC neurons, any AADC-possessing neurons, catecholaminergic and serotoninergic, apparently, could participate in DA synthesis together with monoenzymatic TH neurons. This idea was confirmed by the observation of close topographic relations between monoenzymatic TH neurons and those containing both enzymes, i.e. DA-ergic, noradrenergic or adrenergic. Thus, monoenzymatic neurons possessing TH or AADC and being in close topographic relations can synthesize DA in cooperation.},
  timestamp = {2016-04-25T19:44:34Z},
  urldate = {2016-04-25},
  journal = {Neuroscience},
  author = {Ugrumov, M. and Taxi, J. and Pronina, T. and Kurina, A. and Sorokin, A. and Sapronova, A. and Calas, A.},
  month = sep,
  year = {2014},
  keywords = {aromatic l-amino acid decarboxylase,dopaminergic neuron,hypothalamus,l-DOPA,rat,Tyrosine hydroxylase},
  pages = {45--54},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/2ZMCG8J2/S0306452214005363.html:}
}

@article{gerstung_combining_2015,
  title = {Combining gene mutation with gene expression data improves outcome prediction in myelodysplastic syndromes},
  volume = {6},
  copyright = {\textcopyright{} 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  doi = {10.1038/ncomms6901},
  abstract = {Cancer is a genetic disease, but two patients rarely have identical genotypes. Similarly, patients differ in their clinicopathological parameters, but how genotypic and phenotypic heterogeneity are interconnected is not well understood. Here we build statistical models to disentangle the effect of 12 recurrently mutated genes and 4 cytogenetic alterations on gene expression, diagnostic clinical variables and outcome in 124 patients with myelodysplastic syndromes. Overall, one or more genetic lesions correlate with expression levels of \textasciitilde{}20\% of all genes, explaining 20\textendash{}65\% of observed expression variability. Differential expression patterns vary between mutations and reflect the underlying biology, such as aberrant polycomb repression for \hspace{0pt}ASXL1 and \hspace{0pt}EZH2 mutations or perturbed gene dosage for copy-number changes. In predicting survival, genomic, transcriptomic and diagnostic clinical variables all have utility, with the largest contribution from the transcriptome. Similar observations are made on the TCGA acute myeloid leukaemia cohort, confirming the general trends reported here.},
  language = {en},
  timestamp = {2015-08-17T19:08:22Z},
  urldate = {2015-08-17},
  journal = {Nature Communications},
  author = {Gerstung, Moritz and Pellagatti, Andrea and Malcovati, Luca and Giagounidis, Aristoteles and Porta, Matteo G. Della and J{\"a}dersten, Martin and Dolatshad, Hamid and Verma, Amit and Cross, Nicholas C. P. and Vyas, Paresh and Killick, Sally and Hellstr{\"o}m-Lindberg, Eva and Cazzola, Mario and Papaemmanuil, Elli and Campbell, Peter J. and Boultwood, Jacqueline},
  month = jan,
  year = {2015},
  keywords = {Biological sciences,Cancer,Genetics}
}

@article{bowyer_evaluating_2015,
  title = {Evaluating the {{Stability}} of {{RNA-Seq Transcriptome Profiles}} and {{Drug-Induced Immune-Related Expression Changes}} in {{Whole Blood}}},
  volume = {10},
  issn = {1932-6203},
  doi = {10.1371/journal.pone.0133315},
  abstract = {Methods were developed to evaluate the stability of rat whole blood expression obtained from RNA sequencing (RNA-seq) and assess changes in whole blood transcriptome profiles in experiments replicated over time. Expression was measured in globin-depleted RNA extracted from the whole blood of Sprague-Dawley rats, given either saline (control) or neurotoxic doses of amphetamine (AMPH). The experiment was repeated four times (paired control and AMPH groups) over a 2-year span. The transcriptome of the control and AMPH-treated groups was evaluated on: 1) transcript levels for ribosomal protein subunits; 2) relative expression of immune-related genes; 3) stability of the control transcriptome over 2 years; and 4) stability of the effects of AMPH on immune-related genes over 2 years. All, except one, of the 70 genes that encode the 80s ribosome had levels that ranked in the top 5\% of all mean expression levels. Deviations in sequencing performance led to significant changes in the ribosomal transcripts. The overall expression profile of immune-related genes and genes specific to monocytes, T-cells or B-cells were well represented and consistent within treatment groups. There were no differences between the levels of ribosomal transcripts in time-matched control and AMPH groups but significant differences in the expression of immune-related genes between control and AMPH groups. AMPH significantly increased expression of some genes related to monocytes but down-regulated those specific to T-cells. These changes were partially due to changes in the two types of leukocytes present in blood, which indicate an activation of the innate immune system by AMPH. Thus, the stability of RNA-seq whole blood transcriptome can be verified by assessing ribosomal protein subunits and immune-related gene expression. Such stability enables the pooling of samples from replicate experiments to carry out differential expression analysis with acceptable power.},
  timestamp = {2015-08-17T22:42:46Z},
  number = {7},
  urldate = {2015-08-17},
  journal = {PLoS ONE},
  author = {Bowyer, John F. and Tranter, Karen M. and Hanig, Joseph P. and Crabtree, Nathaniel M. and Schleimer, Robert P. and George, Nysia I.},
  month = jul,
  year = {2015},
  pmid = {26177368},
  pmcid = {PMC4503719}
}

@article{platt_crispr-cas9_2014,
  title = {{{CRISPR-Cas9 Knockin Mice}} for {{Genome Editing}} and {{Cancer Modeling}}},
  volume = {159},
  issn = {0092-8674},
  doi = {10.1016/j.cell.2014.09.014},
  abstract = {Summary
CRISPR-Cas9 is a versatile genome editing technology for studying the functions of genetic elements. To broadly enable the application of Cas9 in~vivo, we established a Cre-dependent Cas9 knockin mouse. We demonstrated in~vivo as well as ex~vivo~genome editing using adeno-associated virus (AAV)-, lentivirus-, or particle-mediated delivery of guide RNA in neurons, immune cells, and endothelial cells. Using these mice, we simultaneously modeled the dynamics of KRAS, p53, and LKB1, the top three significantly mutated genes in lung adenocarcinoma. Delivery of a single AAV vector in the lung generated loss-of-function mutations in p53 and Lkb1, as well~as homology-directed repair-mediated KrasG12D mutations, leading to macroscopic tumors of adenocarcinoma pathology. Together, these results suggest that Cas9 mice empower a wide range of biological and disease modeling applications.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-11-19},
  journal = {Cell},
  author = {Platt, Randall~J. and Chen, Sidi and Zhou, Yang and Yim, Michael~J. and Swiech, Lukasz and Kempton, Hannah~R. and Dahlman, James~E. and Parnas, Oren and Eisenhaure, Thomas~M. and Jovanovic, Marko and Graham, Daniel~B. and Jhunjhunwala, Siddharth and Heidenreich, Matthias and Xavier, Ramnik~J. and Langer, Robert and Anderson, Daniel~G. and Hacohen, Nir and Regev, Aviv and Feng, Guoping and Sharp, Phillip~A. and Zhang, Feng},
  month = oct,
  year = {2014},
  pages = {440--455},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/AE3VNUBX/S0092867414011635.html:}
}

@article{jang_neural_2014,
  title = {Neural stem cells derived from epiblast stem cells display distinctive properties},
  volume = {12},
  issn = {1873-5061},
  doi = {10.1016/j.scr.2013.12.012},
  abstract = {Pluripotent stem cells can be derived from preimplantation and postimplantation mouse embryos. Embryonic stem cells (ESCs) derived from blastocysts are in a ``naive'' pluripotent state and meet all of the criteria for pluripotency, including the ability to generate live pups through tetraploid complementation. Epiblast stem cells (EpiSCs) derived from postimplantation epiblasts are in a ``primed'' pluripotent state. ESCs and EpiSCs show different phenotypes and gene expression patterns, and EpiSCs are thought to be less pluripotent than ESCs. In this study, we addressed whether EpiSCs can be differentiated into specialized cell types in vitro. To do this, we first derived EpiSCs from E5.5\textendash{}6.5 mouse embryos containing the Oct4-GFP transgene. We found that EpiSCs expressed pluripotency markers and differentiated into all three germ layers in intro and in vivo. Interestingly, EpiSCs also efficiently differentiated into a homogenous population of neural stem cells (NSCs) in vitro. The EpiSC-derived NSCs (EpiSC-NSCs) expressed NSC markers (Nestin, Sox2, and Musashi), self-renewed for more than 20 passages, and differentiated into neuronal and glial neural cell subtypes in vitro. We then transplanted the EpiSC-NSCs into the neonatal mouse brains, and found that they were able to survive and differentiate into robust neurons and glial cells in the mouse brains, demonstrating that primed pluripotent EpiSCs efficiently form functional NSCs. We compared the global gene expression patterns of NSCs differentiated from EpiSC-NSCs, ESCs, and brain tissue and found that the expression patterns of most genes, including pluripotency and NSC specificity, were similarly clustered, but that the developmental process-related genes were distantly clustered. Moreover, the global gene expression pattern of brain-derived NSCs was more similar to that of ESC-derived NSCs than that of EpiSC-derived NSCs. Taken together, these results indicate that although NSCs, regardless of their origins, display very similar in vitro and in vivo differentiation properties, their global gene expression profiles may differ, depending on the pluripotency state, i.e., naive or primed.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-11-20},
  journal = {Stem Cell Research},
  author = {Jang, Hyo Jin and Kim, Jong Soo and Choi, Hyun Woo and Jeon, Iksoo and Choi, Sol and Kim, Min Jung and Song, Jihwan and Do, Jeong Tae},
  month = mar,
  year = {2014},
  pages = {506--516},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/332WCSAR/S1873506113001906.html:}
}

@article{kabanova_gene_2009,
  title = {Gene expression analysis of human red blood cells},
  issn = {1449-1907},
  doi = {10.7150/ijms.6.156},
  language = {en},
  timestamp = {2015-08-14T20:57:12Z},
  urldate = {2015-08-14},
  journal = {International Journal of Medical Sciences},
  author = {Kabanova, Sveta},
  year = {2009},
  pages = {156}
}

@article{arena_influence_2016,
  title = {Influence of white matter {{MRI}} hyper-intensities on acute l-dopa response in patients with {{Parkinson}}'s disease},
  volume = {24},
  issn = {1353-8020},
  doi = {10.1016/j.parkreldis.2016.01.017},
  abstract = {Objective
To determine whether brain white matter hyperintensities (WMH) influence l-dopa response in Parkinson's disease (PD) patients.
Methods
We prospectively evaluated 60 PD patients with an acute l-dopa challenge test, and assessed motor performance with the Movement Disorders Society revised Unified Parkinson's Disease Rating Scale (MDS-UPDRS) during ``ON'' and ``OFF'' medication states. Magnetic resonance images were examined using a visual semi-quantitative rating scale for quantification and distribution analysis of WMH. l-dopa challenge test response was correlated to extent and location of WMH, to determine a potential association between them.
Results
Subjects with greater deep WMH burden, showed less response to l-dopa on axial motor symptoms (R~=~-0.35; p~\&lt;~0.027), when tested with Part III of the MDS-UPDRS before and after acute levodopa challenge.
Conclusions
Results suggest WMH may affect response to l-dopa on axial function of PD patients, which could be due to either non-dopaminergic (cortico-basal ganglia) motor pathway disruption, or postsynaptic nigrostriatal pathway involvement.},
  timestamp = {2016-04-19T00:33:55Z},
  urldate = {2016-04-19},
  journal = {Parkinsonism \& Related Disorders},
  author = {Arena, J. E. and Cerquetti, D. and Rossi, M. and Chaves, H. and Rollan, C. and Dossi, D. E. and Merello, M.},
  month = mar,
  year = {2016},
  keywords = {Levodopa,Parkinson's disease,White matter disease},
  pages = {126--128},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/PFE566FU/S1353802016300177.html:}
}

@article{zuckerman_self-directed_2013,
  title = {A {{Self-Directed Method}} for {{Cell-Type Identification}} and {{Separation}} of {{Gene Expression Microarrays}}},
  volume = {9},
  issn = {1553-734X},
  doi = {10.1371/journal.pcbi.1003189},
  abstract = {Gene expression analysis is generally performed on heterogeneous tissue samples consisting of multiple cell types. Current methods developed to separate heterogeneous gene expression rely on prior knowledge of the cell-type composition and/or signatures - these are not available in most public datasets. We present a novel method to identify the cell-type composition, signatures and proportions per sample without need for a-priori information. The method was successfully tested on controlled and semi-controlled datasets and performed as accurately as current methods that do require additional information. As such, this method enables the analysis of cell-type specific gene expression using existing large pools of publically available microarray datasets., Gene expression microarrays are widely used to uncover biological insights. Most microarray experiments profile whole tissues containing mixtures of multiple cell-types. As such, gene expression differences between samples may be due to different cellular compositions or biological differences, highly limiting the conclusions derived from the analysis. All current approaches to computationally separate the heterogeneous gene expression to individual cell-types require that the identity, relative amount of the cell-types in the tissue or their individual gene expression are known. Publically available microarray-based datasets, which include thousands of patient samples, do not usually measure this information, rendering existing separation methods unusable. We developed a novel approach to estimate the number of cell-types, identities, individual gene expression and relative proportions in heterogeneous tissues with no a-priori information except for an initial estimate of the cell-types in the tissue analyzed and general reference signatures of these cell-types that may be easily obtained from public databases. We successfully applied our method to microarray datasets, yielding highly accurate estimations, which often exceed the performance of separation methods that require prior information. Thus, our method can be accurately applied to any heterogeneous dataset, where re-examination and analysis of the individual cell-types in the heterogeneous tissue can aid in discovering new aspects regarding these diseases.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {8},
  urldate = {2015-03-05},
  journal = {PLoS Computational Biology},
  author = {Zuckerman, Neta S. and Noam, Yair and Goldsmith, Andrea J. and Lee, Peter P.},
  month = aug,
  year = {2013},
  pmid = {23990767},
  pmcid = {PMC3749952}
}

@article{adler-wailes_effects_2008,
  title = {Effects of {{Ritonavir}} on {{Adipocyte Gene Expression}}: {{Evidence}} for a {{Stress}}-related {{Response}}},
  volume = {16},
  copyright = {2008 North American Association for the Study of Obesity (NAASO)},
  issn = {1930-739X},
  shorttitle = {Effects of {{Ritonavir}} on {{Adipocyte Gene Expression}}},
  doi = {10.1038/oby.2008.350},
  abstract = {To understand the molecular mechanisms underlying the development of dyslipidemia and lipodystrophy that occurs after administration of aspartic acid protease inhibitors, we examined transcriptional profiles using cDNA microarrays in 3T3-L1 adipocytes exposed to 10 \ensuremath{\mu}mol/l ritonavir for 2\textendash{}21 days. The expression levels of \ensuremath{\sim}12,000 transcripts were assessed using the MgU74Av2 mouse microarray chip. Ritonavir altered gene expression of inflammatory cytokines, stress response genes localized to endoplasmic reticulum, oxidative stress genes, apoptosis-related genes, and expression of genes involved in cell adhesion and extracellular matrix remodeling. Microarray analysis also identified a novel gene downregulated by ritonavir, Cidea, whose expression levels may affect free-fatty acid metabolism. These changes suggest a unique, stress-related pattern in adipocytes induced by chronic exposure to the protease inhibitor, ritonavir.},
  language = {en},
  timestamp = {2016-02-22T19:37:30Z},
  number = {10},
  urldate = {2014-09-08},
  journal = {Obesity},
  author = {Adler-Wailes, Diane C. and Guiney, Evan L. and Koo, Jashin and Yanovski, Jack A.},
  month = oct,
  year = {2008},
  note = {00013},
  pages = {2379--2387}
}

@article{wang_rna-seq_2009-1,
  title = {{{RNA-Seq}}: a revolutionary tool for transcriptomics},
  volume = {10},
  issn = {1471-0056},
  shorttitle = {{{RNA-Seq}}},
  doi = {10.1038/nrg2484},
  abstract = {RNA-Seq is a recently developed approach to transcriptome profiling that uses deep-sequencing technologies. Studies using this method have already altered our view of the extent and complexity of eukaryotic transcriptomes. RNA-Seq also provides a far more precise measurement of levels of transcripts and their isoforms than other methods. This article describes the RNA-Seq approach, the challenges associated with its application, and the advances made so far in characterizing several eukaryote transcriptomes.},
  timestamp = {2016-03-15T06:20:37Z},
  number = {1},
  urldate = {2016-03-15},
  journal = {Nature reviews. Genetics},
  author = {Wang, Zhong and Gerstein, Mark and Snyder, Michael},
  month = jan,
  year = {2009},
  pages = {57--63},
  pmid = {19015660},
  pmcid = {PMC2949280}
}

@article{butovsky_identification_2014,
  title = {Identification of a unique {{TGF}}-\ensuremath{\beta}-dependent molecular and functional signature in microglia},
  volume = {17},
  copyright = {\textcopyright{} 2013 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1097-6256},
  doi = {10.1038/nn.3599},
  abstract = {Microglia are myeloid cells of the CNS that participate both in normal CNS function and in disease. We investigated the molecular signature of microglia and identified 239 genes and 8 microRNAs that were uniquely or highly expressed in microglia versus myeloid and other immune cells. Of the 239 genes, 106 were enriched in microglia as compared with astrocytes, oligodendrocytes and neurons. This microglia signature was not observed in microglial lines or in monocytes recruited to the CNS, and was also observed in human microglia. We found that TGF-\ensuremath{\beta} was required for the in vitro development of microglia that express the microglial molecular signature characteristic of adult microglia and that microglia were absent in the CNS of TGF-\ensuremath{\beta}1\textendash{}deficient mice. Our results identify a unique microglial signature that is dependent on TGF-\ensuremath{\beta} signaling and provide insights into microglial biology and the possibility of targeting microglia for the treatment of CNS disease.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-10-15},
  journal = {Nature Neuroscience},
  author = {Butovsky, Oleg and Jedrychowski, Mark P. and Moore, Craig S. and Cialic, Ron and Lanser, Amanda J. and Gabriely, Galina and Koeglsperger, Thomas and Dake, Ben and Wu, Pauline M. and Doykan, Camille E. and Fanek, Zain and Liu, LiPing and Chen, Zhuoxun and Rothstein, Jeffrey D. and Ransohoff, Richard M. and Gygi, Steven P. and Antel, Jack P. and Weiner, Howard L.},
  month = jan,
  year = {2014},
  pages = {131--143},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/D2UPKABG/Butovsky et al. - 2014 - Identification of a unique TGF-β-dependent molecul.html:;Butovsky et al_2014_Identification of a unique TGF-β-dependent molecular and functional signature.pdf:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/GMQ56F4P/Butovsky et al_2014_Identification of a unique TGF-β-dependent molecular and functional signature.pdf:application/pdf}
}

@article{jansen_gene_2015,
  title = {Gene expression in major depressive disorder},
  copyright = {\textcopyright{} 2015 Nature Publishing Group},
  issn = {1359-4184},
  doi = {10.1038/mp.2015.57},
  abstract = {The search for genetic variants underlying major depressive disorder (MDD) has not yet provided firm leads to its underlying molecular biology. A complementary approach is to study gene expression in relation to MDD. We measured gene expression in peripheral blood from 1848 subjects from The Netherlands Study of Depression and Anxiety. Subjects were divided into current MDD (N=882), remitted MDD (N=635) and control (N=331) groups. MDD status and gene expression were measured again 2 years later in 414 subjects. The strongest gene expression differences were between the current MDD and control groups (129 genes at false-discovery rate, FDR\ensuremath{<}0.1). Gene expression differences across MDD status were largely unrelated to antidepressant use, inflammatory status and blood cell counts. Genes associated with MDD were enriched for interleukin-6 (IL-6)-signaling and natural killer (NK) cell pathways. We identified 13 gene expression clusters with specific clusters enriched for genes involved in NK cell activation (downregulated in current MDD, FDR=5.8 \texttimes{} 10-5) and IL-6 pathways (upregulated in current MDD, FDR=3.2 \texttimes{} 10-3). Longitudinal analyses largely confirmed results observed in the cross-sectional data. Comparisons of gene expression results to the Psychiatric Genomics Consortium (PGC) MDD genome-wide association study results revealed overlap with DVL3. In conclusion, multiple gene expression associations with MDD were identified and suggest a measurable impact of current MDD state on gene expression. Identified genes and gene clusters are enriched with immune pathways previously associated with the etiology of MDD, in line with the immune suppression and immune activation hypothesis of MDD.},
  language = {en},
  timestamp = {2015-08-17T19:14:39Z},
  urldate = {2015-08-17},
  journal = {Molecular Psychiatry},
  author = {Jansen, R. and Penninx, B. W. J. H. and Madar, V. and Xia, K. and Milaneschi, Y. and Hottenga, J. J. and Hammerschlag, A. R. and Beekman, A. and {van der Wee}, N. and Smit, J. H. and Brooks, A. I. and Tischfield, J. and Posthuma, D. and Schoevers, R. and {van Grootheest}, G. and Willemsen, G. and {de Geus}, E. J. and Boomsma, D. I. and Wright, F. A. and Zou, F. and Sun, W. and Sullivan, P. F.},
  month = may,
  year = {2015}
}

@misc{[guest_[bioc]_2013,
  title = {[{{BioC}}] affy code archeology: expresso behavior for	liwong/invariantset},
  shorttitle = {[{{BioC}}] affy code archeology},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2014-12-02},
  author = {[guest, David Eby},
  year = {Thu Jan 24 22:41:22 CET 2013},
  file = {snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/34G3UUHS/050500.html:}
}

@article{weyer_developmental_2003,
  title = {Developmental and cell type-specific expression of the neuronal marker {{NeuN}} in the murine cerebellum},
  volume = {73},
  copyright = {Copyright \textcopyright{} 2003 Wiley-Liss, Inc.},
  issn = {1097-4547},
  doi = {10.1002/jnr.10655},
  abstract = {NeuN is a 46/48-kD nuclear protein antigen used widely to identify postmitotic neurons in both research and diagnostics. It is expressed by neurons throughout the nervous system of a variety of species, including birds, rodents, and man (Mullen et al. [1992] Development 116:201\textendash{}211). When we sought to use NeuN to follow the developmental progression of murine cerebellar interneurons, we observed that expression of this antigen in the cerebellum was restricted to granule neurons and a small population of cells present in the lower molecular layer of the adult cerebellum. In an attempt to identify these cells, we combined immunostaining for NeuN with a panel of cell type-specific markers to unambiguously identify neurons that express NeuN in the adult and developing cerebellum. In contrast to postmitotic granule neurons, NeuN was not expressed by any other immunocytochemically identified cerebellar interneurons, which comprised basket and stellate cells, Golgi neurons, unipolar brush cells, and Lugaro cells. NeuN-positive cells in the molecular layer failed to express any cell type-specific markers tested. They may represent ectopic granule cells; alternatively, they may represent a hitherto unknown population of cerebellar cells. In vitro experiments suggest that NeuN expression is related closely to granule cell axogenesis. This approach also revealed that the level of NeuN expression could be modulated by chronically depolarizing these cells. Thus, whereas NeuN expression per se is a reliable marker of proliferative capacity, levels of NeuN expression may also be indicative of the physiological status of a postmitotic neuron. \textcopyright{} 2003 Wiley-Liss, Inc.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {3},
  urldate = {2014-10-27},
  journal = {Journal of Neuroscience Research},
  author = {Weyer, Anja and Schilling, Karl},
  month = aug,
  year = {2003},
  keywords = {cerebellum,granule cell,lineage,NeuN,nuclear antigen},
  pages = {400--409},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/K8T92W35/abstract.html:}
}

@article{hegarty_midbrain_2013,
  title = {Midbrain dopaminergic neurons: {{A}} review of the molecular circuitry that regulates their development},
  volume = {379},
  issn = {0012-1606},
  shorttitle = {Midbrain dopaminergic neurons},
  doi = {10.1016/j.ydbio.2013.04.014},
  abstract = {Dopaminergic (DA) neurons of the ventral midbrain (VM) play vital roles in the regulation of voluntary movement, emotion and reward. They are divided into the A8, A9 and A10 subgroups. The development of the A9 group of DA neurons is an area of intense investigation to aid the generation of these neurons from stem cell sources for cell transplantation approaches to Parkinson's disease (PD). This review discusses the molecular processes that are involved in the identity, specification, maturation, target innervation and survival of VM DA neurons during development. The complex molecular interactions of a number of genetic pathways are outlined, as well as recent advances in the mechanisms that regulate subset identity within the VM DA neuronal pool. A thorough understanding of the cellular and molecular mechanisms involved in the development of VM DA neurons will greatly facilitate the use of cell replacement therapy for the treatment of PD.},
  timestamp = {2016-03-24T09:37:42Z},
  number = {2},
  urldate = {2016-03-24},
  journal = {Developmental Biology},
  author = {Hegarty, Shane V. and Sullivan, Aideen M. and O'Keeffe, Gerard W.},
  month = jul,
  year = {2013},
  keywords = {dopaminergic neurons,Floor plate,Neurogenesis,Specification,Ventral midbrain},
  pages = {123--138}
}

@article{de_jong_seasonal_2014,
  title = {Seasonal changes in gene expression represent cell-type composition in whole blood},
  volume = {23},
  issn = {0964-6906},
  doi = {10.1093/hmg/ddt665},
  abstract = {Seasonal patterns in behavior and biological parameters are widespread. Here, we examined seasonal changes in whole blood gene expression profiles of 233 healthy subjects. Using weighted gene co-expression network analysis, we identified three co-expression modules showing circannual patterns. Enrichment analysis suggested that this signal stems primarily from red blood cells and blood platelets. Indeed, a large clinical database with 51 142 observations of blood cell counts over 3 years confirmed a corresponding seasonal pattern of counts of red blood cells, reticulocytes and platelets. We found no direct evidence that these changes are linked to genes known to be key players in regulating immune function or circadian rhythm. It is likely, however, that these seasonal changes in cell counts and gene expression profiles in whole blood represent biological and clinical relevant phenomena. Moreover, our findings highlight possible confounding factors relevant to the study of gene expression profiles in subjects collected at geographical locations with disparaging seasonality patterns.},
  timestamp = {2015-08-18T00:22:35Z},
  number = {10},
  urldate = {2015-08-18},
  journal = {Human Molecular Genetics},
  author = {{De Jong}, Simone and Neeleman, Marjolein and Luykx, Jurjen J. and {Ten Berg}, Maarten J. and Strengman, Eric and {Den Breeijen}, Hanneke H. and Stijvers, Leon C. and Buizer-Voskamp, Jacobine E. and Bakker, Steven C. and Kahn, Ren{\'e} S. and Horvath, Steve and {Van Solinge}, Wouter W. and Ophoff, Roel A.},
  month = may,
  year = {2014},
  pages = {2721--2728},
  pmid = {24399446},
  pmcid = {PMC3990170}
}

@article{edgar_meta-analysis_2014,
  title = {Meta-analysis of human methylomes reveals stably methylated sequences surrounding {{CpG}} islands associated with high gene expression},
  volume = {7},
  copyright = {http://creativecommons.org/licenses/by/2.0/},
  issn = {1756-8935},
  doi = {10.1186/1756-8935-7-28},
  abstract = {DNA methylation is thought to play an important role in the regulation of mammalian gene expression, partly based on the observation that a lack of CpG island methylation in gene promoters is associated with high transcriptional activity. However, the CpG island methylation level only accounts for a fraction of the variance in gene expression, and methylation in other domains is hypothesized to play a role. We hypothesized that regions of very high stability in methylation would exist and provide biological insight into the role of methylation both within and outside CpG islands.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-10-27},
  journal = {Epigenetics \& Chromatin},
  author = {Edgar, Rachel and Tan, Powell Patrick and Portales-Casamar, Elodie and Pavlidis, Paul},
  month = oct,
  year = {2014},
  pages = {28},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/TWNCR9ZX/abstract.html:}
}

@article{yuan_cell-surface_2011,
  title = {Cell-{{Surface Marker Signatures}} for the {{Isolation}} of {{Neural Stem Cells}}, {{Glia}} and {{Neurons Derived}} from {{Human Pluripotent Stem Cells}}},
  volume = {6},
  doi = {10.1371/journal.pone.0017540},
  abstract = {Background
Neural induction of human pluripotent stem cells often yields heterogeneous cell populations that can hamper quantitative and comparative analyses. There is a need for improved differentiation and enrichment procedures that generate highly pure populations of neural stem cells (NSC), glia and neurons. One way to address this problem is to identify cell-surface signatures that enable the isolation of these cell types from heterogeneous cell populations by fluorescence activated cell sorting (FACS).

Methodology/Principal Findings
We performed an unbiased FACS- and image-based immunophenotyping analysis using 190 antibodies to cell surface markers on na{\"\i}ve human embryonic stem cells (hESC) and cell derivatives from neural differentiation cultures. From this analysis we identified prospective cell surface signatures for the isolation of NSC, glia and neurons. We isolated a population of NSC that was CD184+/CD271-/CD44-/CD24+ from neural induction cultures of hESC and human induced pluripotent stem cells (hiPSC). Sorted NSC could be propagated for many passages and could differentiate to mixed cultures of neurons and glia in vitro and in vivo. A population of neurons that was CD184-/CD44-/CD15LOW/CD24+ and a population of glia that was CD184+/CD44+ were subsequently purified from cultures of differentiating NSC. Purified neurons were viable, expressed mature and subtype-specific neuronal markers, and could fire action potentials. Purified glia were mitotic and could mature to GFAP-expressing astrocytes in vitro and in vivo.

Conclusions/Significance
These findings illustrate the utility of immunophenotyping screens for the identification of cell surface signatures of neural cells derived from human pluripotent stem cells. These signatures can be used for isolating highly pure populations of viable NSC, glia and neurons by FACS. The methods described here will enable downstream studies that require consistent and defined neural cell populations.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {3},
  urldate = {2014-11-05},
  journal = {PLoS ONE},
  author = {Yuan, Shauna H. and Martin, Jody and Elia, Jeanne and Flippin, Jessica and Paramban, Rosanto I. and Hefferan, Mike P. and Vidal, Jason G. and Mu, Yangling and Killian, Rhiannon L. and Israel, Mason A. and Emre, Nil and Marsala, Silvia and Marsala, Martin and Gage, Fred H. and Goldstein, Lawrence S. B. and Carson, Christian T.},
  month = mar,
  year = {2011},
  pages = {e17540},
  file = {PLoS Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/3CM3NRJU/infodoi10.1371journal.pone.html:}
}

@article{stuart_gene-coexpression_2003,
  title = {A {{Gene-Coexpression Network}} for {{Global Discovery}} of {{Conserved Genetic Modules}}},
  volume = {302},
  copyright = {American Association for the Advancement of Science},
  issn = {0036-8075, 1095-9203},
  doi = {10.1126/science.1087447},
  abstract = {To elucidate gene function on a global scale, we identified pairs of genes that are coexpressed over 3182 DNA microarrays from humans, flies, worms, and yeast. We found 22,163 such coexpression relationships, each of which has been conserved across evolution. This conservation implies that the coexpression of these gene pairs confers a selective advantage and therefore that these genes are functionally related. Manyof these relationships provide strong evidence for the involvement of new genes in core biological functions such as the cell cycle, secretion, and protein expression. We experimentallyconfirmed the predictions implied bysome of these links and identified cell proliferation functions for several genes. By assembling these links into a gene-coexpression network, we found several components that were animal-specific as well as interrelationships between newly evolved and ancient modules.
Twenty-two thousand pairs of genes that are coexpressed in organisms as diverse as yeast, flies, worms, and humans are used to construct a genetic network and predict the functions of proteins.
Twenty-two thousand pairs of genes that are coexpressed in organisms as diverse as yeast, flies, worms, and humans are used to construct a genetic network and predict the functions of proteins.},
  language = {en},
  timestamp = {2016-03-16T01:51:57Z},
  number = {5643},
  urldate = {2016-03-16},
  journal = {Science},
  author = {Stuart, Joshua M. and Segal, Eran and Koller, Daphne and Kim, Stuart K.},
  month = oct,
  year = {2003},
  pages = {249--255},
  pmid = {12934013}
}

@article{doyle_application_2008,
  title = {Application of a {{Translational Profiling Approach}} for the {{Comparative Analysis}} of {{CNS Cell Types}}},
  volume = {135},
  issn = {0092-8674},
  doi = {10.1016/j.cell.2008.10.029},
  abstract = {Summary
Comparative analysis can provide important insights into complex biological systems. As demonstrated in the accompanying paper, translating ribosome affinity purification (TRAP) permits comprehensive studies of translated mRNAs in genetically defined cell populations after physiological perturbations. To establish the generality of this approach, we present translational profiles for 24 CNS cell populations and identify known cell-specific and enriched transcripts for each population. We report thousands of~cell-specific mRNAs that were not detected in whole-tissue microarray studies and provide examples that demonstrate the benefits deriving from comparative analysis. To provide a foundation for further biological and in~silico studies, we provide a resource of 16 transgenic mouse lines, their corresponding anatomic characterization, and translational profiles for cell types from a variety of central nervous system structures. This resource will enable a wide spectrum of molecular and mechanistic studies of both well-known and previously uncharacterized neural cell populations.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {4},
  urldate = {2014-10-20},
  journal = {Cell},
  author = {Doyle, Joseph P. and Dougherty, Joseph D. and Heiman, Myriam and Schmidt, Eric F. and Stevens, Tanya R. and Ma, Guojun and Bupp, Sujata and Shrestha, Prerana and Shah, Rajiv D. and Doughty, Martin L. and Gong, Shiaoching and Greengard, Paul and Heintz, Nathaniel},
  month = nov,
  year = {2008},
  keywords = {MOLNEURO},
  pages = {749--762},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/3QX8C6NX/S0092867408013664.html:;Doyle et al_2008_Application of a Translational Profiling Approach for the Comparative Analysis.pdf:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/XSTE7KNZ/Doyle et al_2008_Application of a Translational Profiling Approach for the Comparative Analysis.pdf:application/pdf}
}

@article{fomchenko_recruited_2011,
  title = {Recruited {{Cells Can Become Transformed}} and {{Overtake PDGF-Induced Murine Gliomas In Vivo}} during {{Tumor Progression}}},
  volume = {6},
  doi = {10.1371/journal.pone.0020605},
  abstract = {Background
Gliomas are thought to form by clonal expansion from a single cell-of-origin, and progression-associated mutations to occur in its progeny cells. Glioma progression is associated with elevated growth factor signaling and loss of function of tumor suppressors Ink4a, Arf and Pten. Yet, gliomas are cellularly heterogeneous; they recruit and trap normal cells during infiltration.

Methodology/Principal Findings
We performed lineage tracing in a retrovirally mediated, molecularly and histologically accurate mouse model of hPDGFb-driven gliomagenesis. We were able to distinguish cells in the tumor that were derived from the cell-of-origin from those that were not. Phenotypic, tumorigenic and expression analyses were performed on both populations of these cells. Here we show that during progression of hPDGFb-induced murine gliomas, tumor suppressor loss can expand the recruited cell population not derived from the cell-of-origin within glioma microenvironment to dominate regions of the tumor, with essentially no contribution from the progeny of glioma cell-of-origin. Moreover, the recruited cells can give rise to gliomas upon transplantation and passaging, acquire polysomal expression profiles and genetic aberrations typically present in glioma cells rather than normal progenitors, aid progeny cells in glioma initiation upon transplantation, and become independent of PDGFR signaling.

Conclusions/Significance
These results indicate that non-cell-of-origin derived cells within glioma environment in the mouse can be corrupted to become bona fide tumor, and deviate from the generally established view of gliomagenesis.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {7},
  urldate = {2014-10-21},
  journal = {PLoS ONE},
  author = {Fomchenko, Elena I. and Dougherty, Joseph D. and Helmy, Karim Y. and Katz, Amanda M. and Pietras, Alexander and Brennan, Cameron and Huse, Jason T. and Milosevic, Ana and Holland, Eric C.},
  month = jul,
  year = {2011},
  pages = {e20605},
  file = {PLoS Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/FRWBCV32/infodoi10.1371journal.pone.html:}
}

@article{hebenstreit_rna_2011,
  title = {{{RNA}} sequencing reveals two major classes of gene expression levels in metazoan cells},
  volume = {7},
  copyright = {Copyright \textcopyright{} 2011 EMBO and Macmillan Publishers Limited. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits distribution, and reproduction in any medium, provided the original author and source are credited. This license does not permit commercial exploitation without specific permission.},
  issn = {1744-4292, 1744-4292},
  doi = {10.1038/msb.2011.28},
  abstract = {The expression level of a gene is often used as a proxy for determining whether the protein or RNA product is functional in a cell or tissue. Therefore, it is of fundamental importance to understand the global distribution of gene expression levels, and to be able to interpret it mechanistically and functionally. Here we use RNA sequencing (RNA-seq) of mouse Th2 cells, coupled with a range of other techniques, to show that all genes can be separated, based on their expression abundance, into two distinct groups: one group comprised of lowly expressed and putatively non-functional mRNAs, and the other of highly expressed mRNAs with active chromatin marks at their promoters. These observations are confirmed in many other microarray and RNA-seq data sets of metazoan cell types.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2015-03-26},
  journal = {Molecular Systems Biology},
  author = {Hebenstreit, Daniel and Fang, Miaoqing and Gu, Muxin and Charoensawan, Varodom and {van Oudenaarden}, Alexander and Teichmann, Sarah A.},
  month = jan,
  year = {2011},
  keywords = {bimodal,ChIP‐seq,expression levels,RNA‐FISH,RNA‐seq},
  pages = {497},
  pmid = {21654674}
}

@article{figlewicz_culture_2000,
  title = {Culture {{Models}} of {{Neurodegenerative Disease}}},
  volume = {919},
  issn = {1749-6632},
  doi = {10.1111/j.1749-6632.2000.tb06873.x},
  abstract = {Abstract:  In order to investigate how mutant SOD1 protein or environmental exogenous stressors lead to the death of motor neurons, we have established several in vitro model systems. We describe some features of the various models in order to demonstrate the advantages and shortcomings of each system.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-12-17},
  journal = {Annals of the New York Academy of Sciences},
  author = {Figlewicz, D. A. and Dong, L. and Mlodzienski, M. and Turcotte, J. C.},
  year = {2000},
  pages = {106--118},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/68EK5EAD/full.html:}
}

@article{bourque_male/female_2011,
  title = {Male/{{Female Differences}} in {{Neuroprotection}} and {{Neuromodulation}} of {{Brain Dopamine}}},
  volume = {2},
  issn = {1664-2392},
  doi = {10.3389/fendo.2011.00035},
  abstract = {The existence of a sex difference in Parkinson's disease (PD) is observed as related to several variables, including susceptibility of the disease, age at onset, and symptoms. These differences between men and women represent a significant characteristic of PD, which suggest that estrogens may exert beneficial effects against the development and the progression of the disease. This paper reviews the neuroprotective and neuromodulator effects of 17\ensuremath{\beta}-estradiol and progesterone as compared to androgens in the nigrostriatal dopaminergic (NSDA) system of both female and male rodents. The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mice model of PD and methamphetamine toxicity faithfully reproduce the sex differences of PD in that endogenous estrogen levels appear to influence the vulnerability to toxins targeting the NSDA system. Exogenous 17\ensuremath{\beta}-estradiol and/or progesterone treatments show neuroprotective properties against NSDA toxins while androgens fail to induce any beneficial effect. Sex steroid treatments show male and female differences in their neuroprotective action against methamphetamine toxicity. NSDA structure and function, as well as the distribution of estrogen receptors, show sex differences and may influence the susceptibility to the toxins and the response to sex steroids. Genomic and non-genomic actions of 17\ensuremath{\beta}-estradiol converge to promote survival factors and the presence of both estrogen receptors \ensuremath{\alpha} and \ensuremath{\beta} are critical to 17\ensuremath{\beta}-estradiol neuroprotective action against MPTP toxicity.},
  timestamp = {2016-03-12T01:00:35Z},
  urldate = {2016-03-12},
  journal = {Frontiers in Endocrinology},
  author = {Bourque, M{\'e}lanie and Dluzen, Dean E. and {Di Paolo}, Th{\'e}r{\`e}se},
  month = sep,
  year = {2011},
  pmid = {22654803},
  pmcid = {PMC3356083}
}

@article{heiman_molecular_2014,
  title = {Molecular adaptations of striatal spiny projection neurons during levodopa-induced dyskinesia},
  volume = {111},
  issn = {0027-8424, 1091-6490},
  doi = {10.1073/pnas.1401819111},
  abstract = {Levodopa treatment is the major pharmacotherapy for Parkinson's disease. However, almost all patients receiving levodopa eventually develop debilitating involuntary movements (dyskinesia). Although it is known that striatal spiny projection neurons (SPNs) are involved in the genesis of this movement disorder, the molecular basis of dyskinesia is not understood. In this study, we identify distinct cell-type\textendash{}specific gene-expression changes that occur in subclasses of SPNs upon induction of a parkinsonian lesion followed by chronic levodopa treatment. We identify several hundred genes, the expression of which is correlated with levodopa dose, many of which are under the control of activator protein-1 and ERK signaling. Despite homeostatic adaptations involving several signaling modulators, activator protein-1\textendash{}dependent gene expression remains highly dysregulated in direct pathway SPNs upon chronic levodopa treatment. We also discuss which molecular pathways are most likely to dampen abnormal dopaminoceptive signaling in spiny projection neurons, hence providing potential targets for antidyskinetic treatments in Parkinson's disease.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {12},
  urldate = {2014-10-21},
  journal = {Proceedings of the National Academy of Sciences},
  author = {Heiman, Myriam and Heilbut, Adrian and Francardo, Veronica and Kulicke, Ruth and Fenster, Robert J. and Kolaczyk, Eric D. and Mesirov, Jill P. and Surmeier, Dalton J. and Cenci, M. Angela and Greengard, Paul},
  month = mar,
  year = {2014},
  pages = {4578--4583},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/WCJDSG86/4578.html:},
  pmid = {24599591}
}

@book{escartin_imaging_2014,
  title = {Imaging and monitoring astrocytes in health and disease},
  isbn = {978-2-88919-393-6},
  abstract = {Astrocytes  are key cellular partners to neurons in the brain. They play an  important role in multiple processes such as neurotransmitter recycling,  trophic support, antioxidant defense, ionic homeostasis, inflammatory  modulation, neurovascular and neurometabolic coupling, neurogenesis,  synapse formation and synaptic plasticity. In addition to their crucial  involvement in normal brain physiology, it is well known that astrocytes  adopt a reactive phenotype under most acute and chronic pathological  conditions such as ischemia, trauma, brain cancer, epilepsy,  demyelinating and neurodegenerative diseases. However, the functional  impact of astrocyte reactivity is still unclear.~  During the  last decades, the development of innovative approaches to study  astrocytes has significantly improved our understanding of their  prominent role in brain function and their contribution to disease  states. In particular, new genetic tools, molecular probes, and imaging  techniques that achieve high spatial and temporal resolution have  revealed new insight into astrocyte functions in situ.   This  Research Topic provides a collection of cutting-edge techniques,  approaches and models to study astrocytes in health and disease. It also  suggests new directions to achieve discoveries on these fascinating  cells.},
  language = {en},
  timestamp = {2016-03-24T08:35:16Z},
  publisher = {{Frontiers Media SA}},
  author = {Escartin, Carole and Murai, Keith},
  month = nov,
  year = {2014}
}

@article{aghajanian_l-trypophan_1974,
  title = {l-{{Trypophan}} as a selective histochemical marker for serotonergic neurons in single-cell recording studies},
  volume = {81},
  issn = {0006-8993},
  doi = {10.1016/0006-8993(74)90954-8},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-11-18},
  journal = {Brain Research},
  author = {Aghajanian, G. K. and Haigler, H. J.},
  month = dec,
  year = {1974},
  pages = {364--372},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/5T77UDI2/0006899374909548.html:}
}

@article{moran_whole_2006,
  title = {Whole genome expression profiling of the medial and lateral substantia nigra in {{Parkinson}}'s disease},
  volume = {7},
  issn = {1364-6745},
  doi = {10.1007/s10048-005-0020-2},
  abstract = {We have used brain tissue from clinically well-documented and neuropathologically confirmed cases of sporadic Parkinson's disease to establish the transcriptomic expression profile of the medial and lateral substantia nigra. In addition, the superior frontal cortex was analyzed in a subset of the same cases. DNA oligonucleotide microarrays were employed, which provide whole human genome coverage. A total of 570 genes were found to be differentially regulated at a high level of significance. A large number of differentially regulated expressed sequence tags were also identified. Levels of mRNA sequences encoded by genes of key interest were validated by means of quantitative real-time polymerase chain reaction (PCR). Comparing three different normalization procedures, results based on the recently published GeneChip Robust Multi Array algorithm were found to be the most accurate predictor of real-time PCR results. Several new candidate genes which map to PARK loci are reported. In addition, the DNAJ family of chaperones is discussed in the context of Parkinson's disease pathogenesis.},
  language = {eng},
  timestamp = {2016-06-05T05:38:44Z},
  number = {1},
  journal = {Neurogenetics},
  author = {Moran, L. B. and Duke, D. C. and Deprez, M. and Dexter, D. T. and Pearce, R. K. B. and Graeber, M. B.},
  month = mar,
  year = {2006},
  keywords = {Aged,Aged; 80 and over,Female,Gene Expression Profiling,Gene Expression Regulation,Genome; Human,Humans,Male,Middle Aged,Molecular Sequence Data,Oligonucleotide Array Sequence Analysis,Parkinson Disease,Reproducibility of Results,Substantia nigra},
  pages = {1--11},
  pmid = {16344956}
}

@article{gillies_sex_2014,
  series = {Sex Differences in Neurological and Psychiatric Disorders},
  title = {Sex differences in {{Parkinson}}'s disease},
  volume = {35},
  issn = {0091-3022},
  doi = {10.1016/j.yfrne.2014.02.002},
  abstract = {Parkinson's disease (PD) displays a greater prevalence and earlier age at onset in men. This review addresses the concept that sex differences in PD are determined, largely, by biological sex differences in the NSDA system which, in turn, arise from hormonal, genetic and environmental influences. Current therapies for PD rely on dopamine replacement strategies to treat symptoms, and there is an urgent, unmet need for disease modifying agents. As a significant degree of neuroprotection against the early stages of clinical or experimental PD is seen, respectively, in human and rodent females compared with males, a better understanding of brain sex dimorphisms in the intact and injured NSDA system will shed light on mechanisms which have the potential to delay, or even halt, the progression of PD. Available evidence suggests that sex-specific, hormone-based therapeutic agents hold particular promise for developing treatments with optimal efficacy in men and women.},
  timestamp = {2016-03-14T21:03:22Z},
  number = {3},
  urldate = {2016-03-14},
  journal = {Frontiers in Neuroendocrinology},
  author = {Gillies, Glenda E. and Pienaar, Ilse S. and Vohra, Shiv and Qamhawi, Zahi},
  month = aug,
  year = {2014},
  keywords = {Neuroprotection,Nigrostriatal dopaminergic pathways,Parkinson’s disease,Sex differences,Sex hormones},
  pages = {370--384}
}

@article{perrone-bizzozero_increased_2011,
  title = {Increased {{Expression}} of {{Axogenesis-Related Genes}} and {{Mossy Fibre Length}} in {{Dentate Granule Cells}} from {{Adult HuD Overexpressor Mice}}},
  volume = {3},
  issn = {, 1759-0914},
  doi = {10.1042/AN20110015},
  abstract = {The neuronal RNA-binding protein HuD plays a critical role in the post-transcriptional regulation of short-lived mRNAs during the initial establishment and remodelling of neural connections. We have generated transgenic mice overexpressing this protein (HuD-Tg) in adult DGCs (dentate granule cells) and shown that their mossy fibres contain high levels of GAP-43 (growth-associated protein 43) and exhibit distinct morphological and electrophysiological properties. To investigate the basis for these changes and identify other molecular targets of HuD, DGCs from HuD-Tg and control mice were collected by LCM (laser capture microscopy) and RNAs analysed using DNA microarrays. Results show that 216 known mRNAs transcripts and 63 ESTs (expressed sequence tags) are significantly up-regulated in DGCs from these transgenic mice. Analyses of the 3\ensuremath{'}-UTRs (3\ensuremath{'}-untranslated regions) of these transcripts revealed an increased number of HuD-binding sites and the presence of several known instability\textendash{}conferring sequences. Among these, the mRNA for TTR (transthyretin) shows the highest level of up-regulation, as confirmed by qRT\textendash{}PCR (quantitative reverse transcription\textendash{}PCR) and ISH (in situ hybridization). GO (gene ontology) analyses of up-regulated transcripts revealed a large overrepresentation of genes associated with neural development and axogenesis. In correlation with these gene expression changes, we found an increased length of the infrapyramidal mossy fibre bundle in HuD-Tg mice. These results support the notion that HuD stabilizes a number of developmentally regulated mRNAs in DGCs, resulting in increased axonal elongation.},
  language = {en},
  timestamp = {2015-08-28T03:37:51Z},
  number = {5},
  urldate = {2015-08-28},
  journal = {ASN Neuro},
  author = {Perrone-Bizzozero, Nora I. and Tanner, Daniel C. and Mounce, Joanna and Bolognani, Federico},
  month = jan,
  year = {2011},
  keywords = {axonal outgrowth,dentate granule cell,gene profiling,HuD,post-transcriptional mechanisms,RNA-binding protein},
  pages = {AN20110015},
  pmid = {22004431}
}

@article{tong_gene_2011,
  title = {Gene expression profile of steroid-induced necrosis of femoral head of rats},
  volume = {89},
  issn = {1432-0827},
  doi = {10.1007/s00223-011-9516-y},
  abstract = {The key to treating steroid-induced necrosis of femoral heads (SINFH) is early diagnosis. Dramatic improvements in diagnosis could be made if the pathogenesis of SINFH was more fully understood; however, the underlying mechanism of this disease is currently unknown. To explore the potential mechanism of SINFH, we performed gene array analysis on a rat model of the disease and compare the expression profile with that of normal rats. A quantitative RT-PCR and immunohistochemistry (IHC) assays were used to confirm the microarray results. Compared to the control group, 190 genes in the experimental group were differentially expressed, with 52 up-regulated and 138 down-regulated. Of these genes, 102 are known (deposited in GenBank), while 88 of them are unknown. The known genes can be divided into several families according to their biological functions, such as oxidative stress, apoptosis, signal transduction, angiogenesis, extracellular matrix, lipid metabolism, and transcription related genes. The results of quantitative RT-PCR and IHC were consistent with gene chip results. Our findings indicate that many genes involved in diverse signaling pathways were differentially expressed between SINFH rats and normal rats. Furthermore, our findings suggest that the development of SINFH is a complicated and dynamic process affected by multiple factors and signaling pathways and regulated by various genes.},
  language = {eng},
  timestamp = {2016-02-22T19:37:30Z},
  number = {4},
  journal = {Calcified Tissue International},
  author = {Tong, Peijian and Wu, Chengliang and Jin, Hongting and Mao, Qiang and Yu, Nanze and Holz, Jonathan D. and Shan, Letian and Liu, Hui and Xiao, Luwei},
  month = oct,
  year = {2011},
  note = {00001 PMID: 21833848},
  keywords = {Animals,Biological Markers,Bone and Bones,Bone marrow,Cluster Analysis,Disease Models; Animal,Femur Head Necrosis,Gene Expression Profiling,Glucocorticoids,Male,Microarray Analysis,Rats,Rats; Wistar,Steroids,Time Factors},
  pages = {271--284}
}

@article{li_automated_2014,
  title = {Automated identification of cell-type-specific genes in the mouse brain by image computing of expression patterns},
  volume = {15},
  copyright = {2014 Li et al.; licensee BioMed Central Ltd.},
  issn = {1471-2105},
  doi = {10.1186/1471-2105-15-209},
  abstract = {PMID: 24947138},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2015-02-27},
  journal = {BMC Bioinformatics},
  author = {Li, Rongjian and Zhang, Wenlu and Ji, Shuiwang},
  month = jun,
  year = {2014},
  pages = {209},
  pmid = {24947138}
}

@article{linington_augmentation_1988,
  title = {Augmentation of demyelination in rat acute allergic encephalomyelitis by circulating mouse monoclonal antibodies directed against a myelin/oligodendrocyte glycoprotein.},
  volume = {130},
  issn = {0002-9440},
  abstract = {In this study the authors have developed a model with which can be studied directly the influence of circulating anti-myelin antibody on the clinical and pathologic course of inflammatory T-cell-mediated experimental allergic encephalomyelitis (EAE) in the rat. EAE was induced by passive transfer of either myelin basic protein (MBP)-activated spleen cells derived from sensitized donors or long-term-cultured MBP-specific T-cell lines. At the onset of the disease, monoclonal antibodies against a myelin/oligodendrocyte glycoprotein (MOG) were injected intravenously. This antigen is exposed on the surface of central nervous system myelin and oligodendrocytes. Intravenous injection of the antibody in the course of T-cell-mediated transfer EAE augmented the severity and duration of clinical signs and resulted in the formation of large, confluent demyelinated plaques.},
  timestamp = {2016-03-23T08:46:27Z},
  number = {3},
  urldate = {2016-03-23},
  journal = {The American Journal of Pathology},
  author = {Linington, C. and Bradl, M. and Lassmann, H. and Brunner, C. and Vass, K.},
  month = mar,
  year = {1988},
  pages = {443--454},
  pmid = {2450462},
  pmcid = {PMC1880661}
}

@article{nikolic_subfraction_2002,
  title = {A subfraction of {{B220}}+ cells in murine bone marrow and spleen does not belong to the {{B}} cell lineage but has dendritic cell characteristics},
  volume = {32},
  copyright = {\textcopyright{} WILEY-VCH Verlag GmbH, Weinheim, Fed. Rep. of Germany},
  issn = {1521-4141},
  doi = {10.1002/1521-4141(200203)32:3<686::AID-IMMU686>3.0.CO;2-I},
  abstract = {Although CD45R\,/\,B220 is commonly used as a pan-B cell marker in the mouse, not all B220+ cells belong to the B cell lineage. Here we report the characterization of a subpopulation ofB220+CD19\textendash{} cells in murine bone marrow, which failed to express markers that are present in early CD19\textendash{} B cell precursors. Instead, these cells expressed low levels of MHC class II and CD11c, which are typically found on dendritic cells (DC). Moreover, these B220+CD19\textendash{}CD11c+ cells expressed Gr-1, indicating that they are related to the recently identified murine plasmacytoid DC or their progenitors. Therefore, we evaluated surface marker expression of the B220+CD19\textendash{}CD11c+ cells in lymphoid tissues of C57BL\,/\,6 mice, recombinase activating gene-1 deficient mice, lacking mature B and T lymphocytes, and mice with a targeted disruption of the Ig H chain \ensuremath{\mu} membrane exon (\ensuremath{\mu}MT), lacking mature B lymphocytes. When comparing bone marrow and spleen, we found that the surface profiles of B220+CD19\textendash{}CD11c+ cells were remarkably similar, indicating that they are in a comparable maturation or activation stage in the two lymphoid compartments. In addition, the almost complete absence of peripheral B220+ B-lineage cells in \ensuremath{\mu}MT mice allowed the anatomical localization of the B220+CD19\textendash{}CD11c+ cells to the red pulp and the T cell areas in the spleen. Taken together, our findings indicate that the mouse bone marrow contains a recirculatingpopulation of B220+CD19\textendash{} CD11c+ plasmacytoid DC, the development of which is largely independent of the presence of mature T and B cells.},
  language = {en},
  timestamp = {2015-09-01T00:21:51Z},
  number = {3},
  urldate = {2015-09-01},
  journal = {European Journal of Immunology},
  author = {Nikolic, Tatjana and Dingjan, Gemma M. and Leenen, Pieter J. M. and Hendriks, Rudolf W.},
  month = mar,
  year = {2002},
  keywords = {B lymphocyte,Bone marrow,CD45R,Dendritic cell,RAG-1},
  pages = {686--692},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/2CW5U7IK/full.html:;Full Text PDF:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/P94D52MQ/Nikolic et al. - 2002 - A subfraction of B220+ cells in murine bone marrow.pdf:application/pdf}
}

@article{usoskin_unbiased_2015,
  title = {Unbiased classification of sensory neuron types by large-scale single-cell {{RNA}} sequencing},
  volume = {18},
  copyright = {\textcopyright{} 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1097-6256},
  doi = {10.1038/nn.3881},
  abstract = {The primary sensory system requires the integrated function of multiple cell types, although its full complexity remains unclear. We used comprehensive transcriptome analysis of 622 single mouse neurons to classify them in an unbiased manner, independent of any a priori knowledge of sensory subtypes. Our results reveal eleven types: three distinct low-threshold mechanoreceptive neurons, two proprioceptive, and six principal types of thermosensitive, itch sensitive, type C low-threshold mechanosensitive and nociceptive neurons with markedly different molecular and operational properties. Confirming previously anticipated major neuronal types, our results also classify and provide markers for new, functionally distinct subtypes. For example, our results suggest that itching during inflammatory skin diseases such as atopic dermatitis is linked to a distinct itch-generating type. We demonstrate single-cell RNA-seq as an effective strategy for dissecting sensory responsive cells into distinct neuronal types. The resulting catalog illustrates the diversity of sensory types and the cellular complexity underlying somatic sensation.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2015-01-13},
  journal = {Nature Neuroscience},
  author = {Usoskin, Dmitry and Furlan, Alessandro and Islam, Saiful and Abdo, Hind and L{\"o}nnerberg, Peter and Lou, Daohua and Hjerling-Leffler, Jens and Haeggstr{\"o}m, Jesper and Kharchenko, Olga and Kharchenko, Peter V. and Linnarsson, Sten and Ernfors, Patrik},
  month = jan,
  year = {2015},
  pages = {145--153},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/WUUDCV83/nn.3881.html:}
}

@article{shen_identification_2006,
  title = {Identification and {{Validation}} of {{Differences}} in {{Protein Levels}} in {{Normal}}, {{Premalignant}}, and {{Malignant Lung Cells}} and {{Tissues Using High-Throughput Western Array}} and {{Immunohistochemistry}}},
  volume = {66},
  issn = {0008-5472, 1538-7445},
  doi = {10.1158/0008-5472.CAN-04-1444},
  abstract = {The identification of proteins, which exhibit different levels in normal, premalignant, and malignant lung cells, could improve early diagnosis and intervention. We compared the levels of proteins in normal human bronchial epithelial (NHBE) and tumorigenic HBE cells (1170-I) by high-throughput immunoblotting (PowerBlot Western Array) using 800 monoclonal antibodies. This analysis revealed that 87 proteins increased by \ensuremath{>}2-fold, and 45 proteins decreased by \ensuremath{>}2-fold, in 1170-I compared with NHBE cells. These proteins are involved in DNA synthesis and repair, cell cycle regulation, RNA transcription and degradation, translation, differentiation, angiogenesis, apoptosis, cell adhesion, cytoskeleton and cell motility, and the phosphatidylinositol 3-kinase signaling pathway. Conventional Western blotting using lysates of normal, immortalized, transformed, and tumorigenic HBEs and non\textendash{}small cell lung cancer cell lines confirmed some of these changes. The expression of several of these proteins has been then analyzed by immunohistochemistry in tissue microarrays containing 323 samples, including normal bronchial epithelium, hyperplasia, squamous metaplasia, dysplasias, squamous cell carcinomas, atypical adenomatous hyperplasia, and adenocarcinomas from 144 patients. The results of the immunohistochemical studies correlated with the Western blotting findings and showed gradual increases (caspase-8, signal transducers and activators of transcription 5, and p70s6K) or decrease (E-cadherin) in levels with tumor progression. These results indicate that the changes in proteins detected in this study may occur early in lung carcinogenesis and persist in lung cancer. In addition, some of the proteins detected by this approach may be novel biomarkers for early detection of lung cancer and novel targets for chemoprevention or therapy. (Cancer Res 2006; 66(23): 11194-206)},
  language = {en},
  timestamp = {2016-02-12T21:27:20Z},
  number = {23},
  urldate = {2016-02-12},
  journal = {Cancer Research},
  author = {Shen, Jie and Behrens, Carmen and Wistuba, Ignacio I. and Feng, Lei and Lee, J. Jack and Hong, Waun Ki and Lotan, Reuben},
  month = jan,
  year = {2006},
  keywords = {biomarkers,Cellular models in prevention research,Intermediate or pre-neoplastic markers and risk factors,Lung cancer,Premalignant lesions,prevention research,Proteomics},
  pages = {11194--11206},
  pmid = {17145864}
}

@article{maier_correlation_2009,
  series = {Systems Biology - Nobel Symposium 146},
  title = {Correlation of {{mRNA}} and protein in complex biological samples},
  volume = {583},
  issn = {0014-5793},
  doi = {10.1016/j.febslet.2009.10.036},
  abstract = {The correlation between mRNA and protein abundances in the cell has been reported to be notoriously poor. Recent technological advances in the quantitative analysis of mRNA and protein species in complex samples allow the detailed analysis of this pathway at the center of biological systems. We give an overview of available methods for the identification and quantification of free and ribosome-bound mRNA, protein abundances and individual protein turnover rates. We review available literature on the correlation of mRNA and protein abundances and discuss biological and technical parameters influencing the correlation of these central biological molecules.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {24},
  urldate = {2014-12-23},
  journal = {FEBS Letters},
  author = {Maier, Tobias and G{\"u}ell, Marc and Serrano, Luis},
  month = dec,
  year = {2009},
  keywords = {Genomics,mRNA,Protein,Proteomics,Quantitative,Systems biology},
  pages = {3966--3973}
}

@article{obaid_compensation_2015,
  title = {Compensation of {{CD55 Underexpression}} on {{Red Blood Cells}} of \ensuremath{\beta}-{{Thalassemia Major Patients}}},
  volume = {39},
  issn = {0363-0269},
  doi = {10.3109/03630269.2015.1029588},
  abstract = {\ensuremath{\beta}-Thalassemia (\ensuremath{\beta}-thal), is an autosomal recessive disorder caused by mutations at the \ensuremath{\beta} gene locus. \ensuremath{\beta}-Thalassemia major (\ensuremath{\beta}-TM) is a severe form of the disease, characterized by severe hypochromic and hemolytic anemia with an increased need for transfusion. Hemolysis is caused by intoxication, whereas mechanical removal of the affected cells caused by macrophage. Immunological implications are also reported and occur via antibodies and complement. We found previously that complement inhibitor receptor CD55 is underexpressed in these patients. This study concerns the compensatory mechanisms of this diminished expression upon flow cytometry analysis of CD55 and CD59 on the red blood cells (RBCs) of \ensuremath{\beta}-thal patients. This study was conducted on 24 patients and 10 healthy controls. Full history and transfusion data was obtained, then a complete blood count (CBC) and flow cytometry analysis of CD55 and CD59 on erythrocytes were carried out. Within our 24 patients, we found a diminished expression of CD55 with a normal expression of CD59. The percentage of cells that express CD55 was significantly different from that of the controls. The mean fluorescence intensity (MFI) of CD55 and CD59 with correlation studies reveals that different factors affect the underexpression of CD55 and also revealed compensatory changes of the defect to minimize the hemolysis occurring in \ensuremath{\beta}-thal patients. Compensation of CD55 underexpression in the deficient patients occurred when an increase in the MFI of both the receptor CD55, on the positive cells, and another complement inhibitor receptor CD59.},
  timestamp = {2015-08-17T19:21:57Z},
  number = {3},
  urldate = {2015-08-17},
  journal = {Hemoglobin},
  author = {Obaid, Jamil M. A. S. and {Abo El-Nazar}, Salma Y. and Ghanem, Amal M. and El-Hadidi, Abeer S. and Mersal, Basma H. M.},
  month = apr,
  year = {2015},
  pages = {184--189}
}

@article{vawter_gender-specific_2003,
  title = {Gender-{{Specific Gene Expression}} in {{Post-Mortem Human Brain}}: {{Localization}} to {{Sex Chromosomes}}},
  volume = {29},
  copyright = {\textcopyright{} 2003 Nature Publishing Group},
  issn = {0893-133X},
  shorttitle = {Gender-{{Specific Gene Expression}} in {{Post-Mortem Human Brain}}},
  doi = {10.1038/sj.npp.1300337},
  abstract = {Gender differences in brain development and in the prevalence of neuropsychiatric disorders such as depression have been reported. Gender differences in human brain might be related to patterns of gene expression. Microarray technology is one useful method for investigation of gene expression in brain. We investigated gene expression, cell types, and regional expression patterns of differentially expressed sex chromosome genes in brain. We profiled gene expression in male and female dorsolateral prefrontal cortex, anterior cingulate cortex, and cerebellum using the Affymetrix oligonucleotide microarray platform. Differentially expressed genes between males and females on the Y chromosome (DBY, SMCY, UTY, RPS4Y, and USP9Y) and X chromosome (XIST) were confirmed using real-time PCR measurements. In situ hybridization confirmed the differential expression of gender-specific genes and neuronal expression of XIST, RPS4Y, SMCY, and UTY in three brain regions examined. The XIST gene, which silences gene expression on regions of the X chromosome, is expressed in a subset of neurons. Since a subset of neurons express gender-specific genes, neural subpopulations may exhibit a subtle sexual dimorphism at the level of differences in gene regulation and function. The distinctive pattern of neuronal expression of XIST, RPS4Y, SMCY, and UTY and other sex chromosome genes in neuronal subpopulations may possibly contribute to gender differences in prevalence noted for some neuropsychiatric disorders. Studies of the protein expression of these sex-chromosome-linked genes in brain tissue are required to address the functional consequences of the observed gene expression differences.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-12-04},
  journal = {Neuropsychopharmacology},
  author = {Vawter, Marquis P},
  month = oct,
  year = {2003},
  keywords = {DBY,RPS4Y,SMCY,USP9Y,UTY,VCX,VCY,XIST},
  pages = {373--384},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/XGIP7D66/1300337a.html:}
}

@article{simunovic_gene_2009,
  title = {Gene expression profiling of substantia nigra dopamine neurons: further insights into {{Parkinson}}'s disease pathology},
  volume = {132},
  issn = {0006-8950},
  shorttitle = {Gene expression profiling of substantia nigra dopamine neurons},
  doi = {10.1093/brain/awn323},
  abstract = {Parkinson's disease is caused by a progressive loss of the midbrain dopamine (DA) neurons in the substantia nigra pars compacta. Although the main cause of Parkinson's disease remains unknown, there is increasing evidence that it is a complex disorder caused by a combination of genetic and environmental factors, which affect key signalling pathways in substantia nigra DA neurons. Insights into pathogenesis of Parkinson's disease stem from in vitro and in vivo models and from postmortem analyses. Recent technological developments have added a new dimension to this research by determining gene expression profiles using high throughput microarray assays. However, many of the studies reported to date were based on whole midbrain dissections, which included cells other than DA neurons. Here, we have used laser microdissection to isolate single DA neurons from the substantia nigra pars compacta of controls and subjects with idiopathic Parkinson's disease matched for age and postmortem interval followed by microarrays to analyse gene expression profiling. Our data confirm a dysregulation of several functional groups of genes involved in the Parkinson's disease pathogenesis. In particular, we found prominent down-regulation of members of the PARK gene family and dysregulation of multiple genes associated with programmed cell death and survival. In addition, genes for neurotransmitter and ion channel receptors were also deregulated, supporting the view that alterations in electrical activity might influence DA neuron function. Our data provide a `molecular fingerprint identity' of late\textendash{}stage Parkinson's disease DA neurons that will advance our understanding of the molecular pathology of this disease.},
  timestamp = {2016-06-07T06:30:45Z},
  number = {7},
  urldate = {2016-06-07},
  journal = {Brain},
  author = {Simunovic, Filip and Yi, Ming and Wang, Yulei and Macey, Laurel and Brown, Lauren T. and Krichevsky, Anna M. and Andersen, Susan L. and Stephens, Robert M. and Benes, Francine M. and Sonntag, Kai C.},
  month = jul,
  year = {2009},
  pages = {1795--1809},
  pmid = {19052140},
  pmcid = {PMC2724914}
}

@article{kharchenko_bayesian_2014,
  title = {Bayesian approach to single-cell differential expression analysis},
  volume = {11},
  issn = {1548-7091},
  doi = {10.1038/nmeth.2967},
  abstract = {Single-cell data provides means to dissect the composition of complex tissues and specialized cellular environments. However, the analysis of such measurements is complicated by high levels of technical noise and intrinsic biological variability. We describe a probabilistic model of expression magnitude distortions typical of single-cell RNA sequencing measurements, which enables detection of differential expression signatures and identification of subpopulations of cells in a way that is more tolerant of noise.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {7},
  urldate = {2015-01-14},
  journal = {Nature methods},
  author = {Kharchenko, Peter V. and Silberstein, Lev and Scadden, David T.},
  month = jul,
  year = {2014},
  pages = {740--742},
  pmid = {24836921},
  pmcid = {PMC4112276}
}

@article{holtman_glia_2015,
  title = {Glia {{Open Access Database}} ({{GOAD}}): {{A}} comprehensive gene expression encyclopedia of glia cells in health and disease},
  copyright = {\textcopyright{} 2015 Wiley Periodicals, Inc.},
  issn = {1098-1136},
  shorttitle = {Glia {{Open Access Database}} ({{GOAD}})},
  doi = {10.1002/glia.22810},
  abstract = {Recently, the number of genome-wide transcriptome profiles of pure populations of glia cells has drastically increased, resulting in an unprecedented amount of data that offer opportunities to study glia phenotypes and functions in health and disease. To make genome-wide transcriptome data easily accessible, we developed the Glia Open Access Database (GOAD), available via www.goad.education. GOAD contains a collection of previously published and unpublished transcriptome data, including datasets from isolated microglia, astrocytes and oligodendrocytes both at homeostatic and pathological conditions. It contains an intuitive web-based interface that consists of three features that enable searching, browsing, analyzing, and downloading of the data. The first feature is differential gene expression (DE) analysis that provides genes that are significantly up and down-regulated with the associated fold changes and p-values between two conditions of interest. In addition, an interactive Venn diagram is generated to illustrate the overlap and differences between several DE gene lists. The second feature is quantitative gene expression (QE) analysis, to investigate which genes are expressed in a particular glial cell type and to what degree. The third feature is a search utility, which can be used to find a gene of interest and depict its expression in all available expression data sets by generating a gene card. In addition, quality guidelines and relevant concepts for transcriptome analysis are discussed. Finally, GOAD is discussed in relation to several online transcriptome tools developed in neuroscience and immunology. In conclusion, GOAD is a unique platform to facilitate integration of bioinformatics in glia biology. GLIA 2015},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2015-05-05},
  journal = {Glia},
  author = {Holtman, Inge R. and Noback, Michiel and Bijlsma, Marieke and Duong, Kim N. and {van der Geest}, Marije A. and Ketelaars, Peer T. and Brouwer, Nieske and Vainchtein, Ilia D. and Eggen, Bart J. L. and Boddeke, Hendrikus W. G. M.},
  month = mar,
  year = {2015},
  keywords = {astrocytes,bioinformatics,microglia,oligodendrocytes,RNA-seq,transcriptome analysis},
  pages = {n/a--n/a}
}

@article{min_variability_2010,
  title = {Variability of gene expression profiles in human blood and lymphoblastoid cell lines},
  volume = {11},
  issn = {1471-2164},
  doi = {10.1186/1471-2164-11-96},
  abstract = {Background
Readily accessible samples such as peripheral blood or cell lines are increasingly being used in large cohorts to characterise gene expression differences between a patient group and healthy controls. However, cell and RNA isolation procedures and the variety of cell types that make up whole blood can affect gene expression measurements. We therefore systematically investigated global gene expression profiles in peripheral blood from six individuals collected during two visits by comparing five of the following cell and RNA isolation methods: whole blood (PAXgene), peripheral blood mononuclear cells (PBMCs), lymphoblastoid cell lines (LCLs), CD19 and CD20 specific B-cell subsets.

Results
Gene expression measurements were clearly discriminated by isolation method although the reproducibility was high for all methods (range \ensuremath{\rho} = 0.90-1.00). The PAXgene samples showed a decrease in the number of expressed genes (P \ensuremath{<} 1*10-16) with higher variability (P \ensuremath{<} 1*10-16) compared to the other methods. Differentially expressed probes between PAXgene and PBMCs were correlated with the number of monocytes, lymphocytes, neutrophils or erythrocytes. The correlations (\ensuremath{\rho} = 0.83; \ensuremath{\rho} = 0.79) of the expression levels of detected probes between LCLs and B-cell subsets were much lower compared to the two B-cell isolation methods (\ensuremath{\rho} = 0.98). Gene ontology analysis of detected genes showed that genes involved in inflammatory responses are enriched in B-cells CD19 and CD20 whereas genes involved in alcohol metabolic process and the cell cycle were enriched in LCLs.

Conclusion
Gene expression profiles in blood-based samples are strongly dependent on the predominant constituent cell type(s) and RNA isolation method. It is crucial to understand the differences and variability of gene expression measurements between cell and RNA isolation procedures, and their relevance to disease processes, before application in large clinical studies.},
  timestamp = {2015-08-18T00:27:20Z},
  urldate = {2015-08-18},
  journal = {BMC Genomics},
  author = {Min, Josine L and Barrett, Amy and Watts, Tim and Pettersson, Fredrik H and Lockstone, Helen E and Lindgren, Cecilia M and Taylor, Jennifer M and Allen, Maxine and Zondervan, Krina T and McCarthy, Mark I},
  month = feb,
  year = {2010},
  pages = {96},
  pmid = {20141636},
  pmcid = {PMC2841682}
}

@article{kim_three_????,
  title = {Three {{Types}} of {{Cortical Layer}} 5 {{Neurons That Differ}} in {{Brain}}-wide {{Connectivity}} and {{Function}}},
  issn = {0896-6273},
  doi = {10.1016/j.neuron.2015.11.002},
  abstract = {Summary
Cortical layer 5 (L5) pyramidal neurons integrate inputs from many sources and distribute outputs to cortical and subcortical structures. Previous studies demonstrate two L5 pyramid types: cortico-cortical (CC) and cortico-subcortical (CS). We characterize connectivity and function of these cell types in mouse primary visual cortex and reveal a new subtype. Unlike previously described L5 CC and CS neurons, this new subtype does not project to striatum [cortico-cortical, non-striatal (CC-NS)] and has distinct morphology, physiology, and visual responses. Monosynaptic rabies tracing reveals that CC neurons preferentially receive input from higher visual areas, while CS neurons receive more input from structures implicated in top-down modulation of brain states. CS neurons are also more direction-selective and prefer faster stimuli than CC neurons. These differences suggest distinct roles as specialized output channels, with CS neurons integrating information and generating responses more relevant to movement control and CC neurons being more important in visual perception.},
  timestamp = {2015-12-08T23:25:44Z},
  urldate = {2015-12-08},
  journal = {Neuron},
  author = {Kim, Euiseok~J. and Juavinett, Ashley~L. and Kyubwa, Espoir~M. and Jacobs, Matthew~W. and Callaway, Edward~M.},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/RSDPQKJS/S0896627315009812.html:}
}

@article{trabzuni_widespread_2013,
  title = {Widespread sex differences in gene expression and splicing in the adult human brain},
  volume = {4},
  copyright = {\textcopyright{} 2013 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  doi = {10.1038/ncomms3771},
  abstract = {There is strong evidence to show that men and women differ in terms of neurodevelopment, neurochemistry and susceptibility to neurodegenerative and neuropsychiatric disease. The molecular basis of these differences remains unclear. Progress in this field has been hampered by the lack of genome-wide information on sex differences in gene expression and in particular splicing in the human brain. Here we address this issue by using post-mortem adult human brain and spinal cord samples originating from 137 neuropathologically confirmed control individuals to study whole-genome gene expression and splicing in 12 CNS regions. We show that sex differences in gene expression and splicing are widespread in adult human brain, being detectable in all major brain regions and involving 2.5\% of all expressed genes. We give examples of genes where sex-biased expression is both disease-relevant and likely to have functional consequences, and provide evidence suggesting that sex biases in expression may reflect sex-biased gene regulatory structures.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2015-05-07},
  journal = {Nature Communications},
  author = {Trabzuni, Daniah and Ramasamy, Adaikalavan and Imran, Sabaena and Walker, Robert and Smith, Colin and Weale, Michael E. and Hardy, John and Ryten, Mina and {North American Brain Expression Consortium}},
  month = nov,
  year = {2013},
  keywords = {Biological sciences,Genetics,neuroscience}
}

@article{baquet_brain-derived_2005,
  title = {Brain-{{Derived Neurotrophic Factor Is Required}} for the {{Establishment}} of the {{Proper Number}} of {{Dopaminergic Neurons}} in the {{Substantia Nigra Pars Compacta}}},
  volume = {25},
  issn = {0270-6474, 1529-2401},
  doi = {10.1523/JNEUROSCI.4601-04.2005},
  abstract = {Brain-derived neurotrophic factor (BDNF) has been implicated in regulating neuronal survival, differentiation, and synaptic plasticity. Reduced expression of BDNF within the substantia nigra accompanies the deterioration of dopaminergic neurons in Parkinson's disease (PD) patients. Analysis of the effects of long-term BDNF absence from the CNS has been difficult because of the early postnatal lethality of BDNF-/- mice. Mice with a floxed BDNF allele were bred with Wnt1-Cre mice to generate Wnt-BDNFKO mice that lack BDNF from the midbrain-hindbrain (MHB). These mice are viable but exhibit hindlimb clutching and poor rotarod performance. Tyrosine hydroxylase (TH)-positive neuron numbers in the substantia nigra pars compacta (SNC) were estimated using stereological methods, revealing a persistent \ensuremath{\sim}23\% reduction of these cells at postnatal day 21 (P21) in Wnt-BDNFKO mice compared with controls. The diminishment of TH-expressing neurons was present at birth and continued through P120. This deficit appears selective for the dopaminergic population, because at P21, total neuron number within the SNC, defined as neuronal nuclei protein-positive cells, was not significantly reduced. Interestingly, and similar to observations in PD patients, SNC neuron subpopulations are not equally affected. Calbindin- and calretinin-expressing SNC populations show no significant difference between Wnt-BDNFKO mice and controls. Thus, BDNF depletion from the MHB selectively leads to reduced TH expression in a subpopulation of neurons, but it remains unclear whether these cells are lost.},
  language = {en},
  timestamp = {2015-08-27T18:55:09Z},
  number = {26},
  urldate = {2015-08-26},
  journal = {The Journal of Neuroscience},
  author = {Baquet, Zachary C. and Bickford, Paula C. and Jones, Kevin R.},
  month = jun,
  year = {2005},
  keywords = {BDNF,Cre-lox,mouse,neurotrophin,Parkinson's disease,stereology,substantia nigra pars compacta},
  pages = {6251--6259},
  pmid = {15987955}
}

@article{nakazawa_gabaergic_2012,
  title = {{{GABAergic}} interneuron origin of schizophrenia pathophysiology},
  volume = {62},
  issn = {0028-3908},
  doi = {10.1016/j.neuropharm.2011.01.022},
  abstract = {Hypofunction of N-methyl-D-aspartic acid-type glutamate receptors (NMDAR) induced by the systemic administration of NMDAR antagonists is well known to cause schizophrenia-like symptoms in otherwise healthy subjects. However, the brain areas or cell types responsible for the emergence of these symptoms following NMDAR hypofunction remain largely unknown. One possibility, the so-called ``GABAergic origin hypothesis,'' is that NMDAR hypofunction at GABAergic interneurons, in particular, is sufficient for schizophrenia-like effects. In one attempt to address this issue, transgenic mice were generated in which NMDARs were selectively deleted from cortical and hippocampal GABAergic interneurons, a majority of which were parvalbumin (PV)-positive. This manipulation triggered a constellation of phenotypes\textemdash{}from molecular and physiological to behavioral\textemdash{}resembling characteristics of human schizophrenia. Based on these results, and in conjunction with previous literature, we argue that during development, NMDAR hypofunction at cortical, PV-positive, fast-spiking interneurons produces schizophrenia-like effects. This review summarizes the data demonstrating that in schizophrenia, GABAergic (particularly PV-positive) interneurons are disrupted. PV-positive interneurons, many of which display a fast-spiking firing pattern, are critical not only for tight temporal control of cortical inhibition but also for the generation of synchronous membrane-potential gamma-band oscillations. We therefore suggest that in schizophrenia the specific ability of fast-spiking interneurons to control and synchronize disparate cortical circuits is disrupted and that this disruption may underlie many of the schizophrenia symptoms. We further argue that the high vulnerability of corticolimbic fast-spiking interneurons to genetic predispositions and to early environmental insults\textemdash{}including excitotoxicity and oxidative stress\textemdash{}might help to explain their significant contribution to the development of schizophrenia.},
  timestamp = {2016-03-17T04:53:52Z},
  number = {3},
  urldate = {2016-03-17},
  journal = {Neuropharmacology},
  author = {Nakazawa, Kazu and Zsiros, Veronika and Jiang, Zhihong and Nakao, Kazuhito and Kolata, Stefan and Zhang, Shuqin and Belforte, Juan E.},
  month = mar,
  year = {2012},
  pages = {1574--1583},
  pmid = {21277876},
  pmcid = {PMC3090452}
}

@article{qin_expression_2007,
  title = {The expression pattern of nuclear receptors during cerebellar development},
  volume = {236},
  copyright = {Copyright \textcopyright{} 2007 Wiley-Liss, Inc.},
  issn = {1097-0177},
  doi = {10.1002/dvdy.21060},
  abstract = {The cerebellum is essential for fine control of movement and posture, and it has been a useful model for studying many aspects of neural development because of its relatively simple anatomy and developmental program. However, the roles of nuclear receptors (NRs) underlying formation of the cerebellum and maintenance of cerebellar functions are still poorly characterized. As a contribution to the Nuclear Receptor Signaling Atlas (NURSA), we employed immunohistochemistry to investigate the expression pattern of 18 NRs in the cerebellum. Ten receptors were demonstrated to be expressed in the postnatal day 21 (P21) cerebellum. Among them, five receptors (COUP-TFI, COUP-TFII, ROR\ensuremath{\alpha}, ER\ensuremath{\beta}, and ERR\ensuremath{\gamma}) were expressed at all stages (embryonic stage, P0, P7, and P21) examined. Interestingly, COUP-TFI and COUP-TFII show differential anterior-posterior expression patterns during cerebellar development. Taken together, our results suggest that members of the nuclear receptor superfamily might play importantly physiological roles in the cerebellum. Developmental Dynamics 236:810\textendash{}820, 2007. \textcopyright{} 2007 Wiley-Liss, Inc.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {3},
  urldate = {2014-11-06},
  journal = {Developmental Dynamics},
  author = {Qin, Jun and Suh, Jae Mi and Kim, Bum-Jun and Yu, Cheng-Tai and Tanaka, Toshiya and Kodama, Tatsuhiko and Tsai, Ming-Jer and Tsai, Sophia Y.},
  month = mar,
  year = {2007},
  keywords = {anterior-posterior expression patterns,cerebellum,COUP-TFI,COUP-TFII,ERRγ,ERβ,expression pattern,nuclear receptors,NURSA,RORα},
  pages = {810--820},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/F96P5HNA/full.html:}
}

@article{rossner_global_2006,
  title = {Global {{Transcriptome Analysis}} of {{Genetically Identified Neurons}} in the {{Adult Cortex}}},
  volume = {26},
  issn = {0270-6474, 1529-2401},
  doi = {10.1523/JNEUROSCI.0468-06.2006},
  abstract = {The enormous cellular complexity of the brain is a major obstacle for gene expression profiling of neurological disease models, because physiologically relevant changes of transcription in a specific neuronal subset are likely to be lost in the presence of other neurons and glia. We solved this problem in transgenic mice by labeling genetically defined cells with a nuclear variant of GFP. When combined with laser-directed microdissection, intact RNA from unfixed, freeze-dried sections can be isolated, which is a prerequisite for high-quality global transcriptome analysis. Here, we compared gene expression profiles between pyramidal motor neurons and pyramidal somatosensory neurons captured from layer V of the adult neocortex. One striking feature of motor neurons is the elevated expression of ribosomal genes and genes involved in ATP synthesis. This suggests a molecular adaptation of the upper motor neurons to longer axonal projections and higher electrical activity. These molecular signatures were not detected when cortical layers and microareas were analyzed in toto.
Additionally, we used microarrays to determine the global mRNA expression profiles of microdissected Purkinje cells and cellularly complex cerebellar cortex microregions. In summary, our analysis shows that cellularly complex targets lead to averaged gene expression profiles that lack substantial amounts of cell type-specific information. Thus, cell type-restricted sampling strategies are mandatory in the CNS. The combined use of a genetic label with laser-microdissection offers an unbiased approach to map patterns of gene expression onto practically any cell type of the brain.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {39},
  urldate = {2014-10-21},
  journal = {The Journal of Neuroscience},
  author = {Rossner, Moritz J. and Hirrlinger, Johannes and Wichert, Sven P. and Boehm, Christine and Newrzella, Dieter and Hiemisch, Holger and Eisenhardt, Gisela and Stuenkel, Carolin and {von Ahsen}, Oliver and Nave, Klaus-Armin},
  month = sep,
  year = {2006},
  keywords = {cerebellum,cortex,GFP,microarrays,microdissection,transcriptome},
  pages = {9956--9966},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/QU9BC8JD/9956.html:},
  pmid = {17005859}
}

@article{brun_clinical_2010,
  title = {Clinical and biochemical features of aromatic {{L}}-amino acid decarboxylase deficiency},
  volume = {75},
  issn = {0028-3878, 1526-632X},
  doi = {10.1212/WNL.0b013e3181e620ae},
  abstract = {Objective: To describe the current treatment; clinical, biochemical, and molecular findings; and clinical follow-up of patients with aromatic l-amino acid decarboxylase (AADC) deficiency.
Method: Clinical and biochemical data of 78 patients with AADC deficiency were tabulated in a database of pediatric neurotransmitter disorders (JAKE). A total of 46 patients have been previously reported; 32 patients are described for the first time.
Results: In 96\% of AADC-deficient patients, symptoms (hypotonia 95\%, oculogyric crises 86\%, and developmental retardation 63\%) became clinically evident during infancy or childhood. Laboratory diagnosis is based on typical CSF markers (low homovanillic acid, 5-hydroxyindoleacidic acid, and 3-methoxy-4-hydroxyphenolglycole, and elevated 3-O-methyl-l-dopa, l-dopa, and 5-hydroxytryptophan), absent plasma AADC activity, or elevated urinary vanillactic acid. A total of 24 mutations in the DDC gene were detected in 49 patients (8 reported for the first time: p.L38P, p.Y79C, p.A110Q, p.G123R, p.I42fs, c.876G\ensuremath{>}A, p.R412W, p.I433fs) with IVS6+ 4A\ensuremath{>}T being the most common one (allele frequency 45\%).
Conclusion: Based on clinical symptoms, CSF neurotransmitters profile is highly indicative for the diagnosis of aromatic l-amino acid decarboxylase deficiency. Treatment options are limited, in many cases not beneficial, and prognosis is uncertain. Only 15 patients with a relatively mild form clearly improved on a combined therapy with pyridoxine (B6)/pyridoxal phosphate, dopamine agonists, and monoamine oxidase B inhibitors.},
  language = {en},
  timestamp = {2016-03-22T22:07:39Z},
  number = {1},
  urldate = {2016-03-22},
  journal = {Neurology},
  author = {Brun, L. and Ngu, L. H. and Keng, W. T. and Ch'ng, G. S. and Choy, Y. S. and Hwu, W. L. and Lee, W. T. and Willemsen, M. a. a. P. and Verbeek, M. M. and Wassenberg, T. and R{\'e}gal, L. and Orcesi, S. and Tonduti, D. and Accorsi, P. and Testard, H. and Abdenur, J. E. and Tay, S. and Allen, G. F. and Heales, S. and Kern, I. and Kato, M. and Burlina, A. and Manegold, C. and Hoffmann, G. F. and Blau, N.},
  month = jun,
  year = {2010},
  pages = {64--71},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/2QCGS3FT/64.html:},
  pmid = {20505134}
}

@article{hoheisel_microarray_2006,
  title = {Microarray technology: beyond transcript profiling and genotype analysis},
  volume = {7},
  copyright = {\textcopyright{} 2006 Nature Publishing Group},
  issn = {1471-0056},
  shorttitle = {Microarray technology},
  doi = {10.1038/nrg1809},
  abstract = {Understanding complex functional mechanisms requires the global and parallel analysis of different cellular processes. DNA microarrays have become synonymous with this kind of study and, in many cases, are the obvious platform to achieve this aim. They have already made important contributions, most notably to gene-expression studies, although the true potential of this technology is far greater. Whereas some assays, such as transcript profiling and genotyping, are becoming routine, others are still in the early phases of development, and new areas of application, such as genome-wide epigenetic analysis and on-chip synthesis, continue to emerge.},
  language = {en},
  timestamp = {2016-02-13T03:37:43Z},
  number = {3},
  urldate = {2016-02-13},
  journal = {Nature Reviews Genetics},
  author = {Hoheisel, J{\"o}rg D.},
  month = mar,
  year = {2006},
  pages = {200--210}
}

@article{kuhn_population-specific_2011,
  title = {Population-specific expression analysis ({{PSEA}}) reveals molecular changes in diseased brain},
  volume = {8},
  copyright = {\textcopyright{} 2011 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1548-7091},
  doi = {10.1038/nmeth.1710},
  abstract = {Human diseases are often accompanied by histological changes that confound interpretation of molecular analyses and identification of disease-related effects. We developed population-specific expression analysis (PSEA), a computational method of analyzing gene expression in samples of varying composition that can improve analyses of quantitative molecular data in many biological contexts. PSEA of brains from individuals with Huntington's disease revealed myelin-related abnormalities that were undetected using standard differential expression analysis.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {11},
  urldate = {2015-03-10},
  journal = {Nature Methods},
  author = {Kuhn, Alexandre and Thu, Doris and Waldvogel, Henry J. and Faull, Richard L. M. and Luthi-Carter, Ruth},
  month = nov,
  year = {2011},
  pages = {945--947}
}

@article{molyneaux_neuronal_2007,
  title = {Neuronal subtype specification in the cerebral cortex},
  volume = {8},
  copyright = {\textcopyright{} 2007 Nature Publishing Group},
  issn = {1471-003X},
  doi = {10.1038/nrn2151},
  abstract = {In recent years, tremendous progress has been made in understanding the mechanisms underlying the specification of projection neurons within the mammalian neocortex. New experimental approaches have made it possible to identify progenitors and study the lineage relationships of different neocortical projection neurons. An expanding set of genes with layer and neuronal subtype specificity have been identified within the neocortex, and their function during projection neuron development is starting to be elucidated. Here, we assess recent data regarding the nature of neocortical progenitors, review the roles of individual genes in projection neuron specification and discuss the implications for progenitor plasticity.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {6},
  urldate = {2014-11-05},
  journal = {Nature Reviews Neuroscience},
  author = {Molyneaux, Bradley J. and Arlotta, Paola and Menezes, Joao R. L. and Macklis, Jeffrey D.},
  month = jun,
  year = {2007},
  pages = {427--437},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/XSAQDK6R/nrn2151.html:}
}

@article{huffaker_novel_2009,
  title = {A novel, primate-specific, brain isoform of {{KCNH2}} impacts cortical physiology, cognition, neuronal repolarization and risk for schizophrenia},
  volume = {15},
  issn = {1078-8956},
  doi = {10.1038/nm.1962},
  abstract = {Organized neuronal firing is critical for cortical processing and is disrupted in schizophrenia. Using 5' RACE in human brain, we identified a primate-specific isoform (3.1) of the K+-channel KCNH2 that modulates neuronal firing. KCNH2-3.1 mRNA levels are comparable to KCNH2-1A in brain, but 1000-fold lower in heart. In schizophrenic hippocampus, KCNH2-3.1 expression is 2.5-fold greater than KCNH2-1A. A meta-analysis of 5 clinical samples (367 families, 1158 unrelated cases, 1704 controls) shows association of SNPs in KCNH2 with schizophrenia. Risk-associated alleles predict lower IQ scores and speed of cognitive processing, altered memory-linked fMRI signals, and increased KCNH2-3.1 expression in post-mortem hippocampus. KCNH2-3.1 lacks a domain critical for slow channel deactivation. Overexpression of KCNH2-3.1 in primary cortical neurons induces a rapidly deactivating K+ current and a high-frequency, non-adapting firing pattern. These results identify a novel KCNH2 channel involved in cortical physiology, cognition, and psychosis, providing a potential new psychotherapeutic drug target.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {5},
  urldate = {2014-11-28},
  journal = {Nature medicine},
  author = {Huffaker, Stephen J. and Chen, Jingshan and Nicodemus, Kristin K. and Sambataro, Fabio and Yang, Feng and Mattay, Venkata and Lipska, Barbara K. and Hyde, Thomas M. and Song, Jian and Rujescu, Daniel and Giegling, Ina and Mayilyan, Karine and Proust, Morgan J. and Soghoyan, Armen and Caforio, Grazia and Callicott, Joseph H. and Bertolino, Alessandro and Meyer-Lindenberg, Andreas and Chang, Jay and Ji, Yuanyuan and Egan, Michael F. and Goldberg, Terry E. and Kleinman, Joel E. and Lu, Bai and Weinberger, Daniel R.},
  month = may,
  year = {2009},
  pages = {509--518},
  pmid = {19412172},
  pmcid = {PMC2756110}
}

@article{aguzzi_microglia_2013,
  title = {Microglia: {{Scapegoat}}, {{Saboteur}}, or {{Something Else}}?},
  volume = {339},
  copyright = {Copyright \textcopyright{} 2013, American Association for the Advancement of Science},
  issn = {0036-8075, 1095-9203},
  shorttitle = {Microglia},
  doi = {10.1126/science.1227901},
  abstract = {Microglia are resident immune cells in the brain and spinal cord. These cells provide immune surveillance and are mobilized in response to disparate diseases and injuries. Although microglial activation is often considered neurotoxic, microglia are essential defenders against many neurodegenerative diseases. It also seems increasingly likely that microglial dysfunction can underlie certain neurological diseases without an obvious immune component.},
  language = {en},
  timestamp = {2016-03-27T06:46:32Z},
  number = {6116},
  urldate = {2016-03-27},
  journal = {Science},
  author = {Aguzzi, Adriano and Barres, Ben A. and Bennett, Mariko L.},
  month = jan,
  year = {2013},
  pages = {156--161},
  pmid = {23307732}
}

@article{nielsen_immunodetection_2006,
  title = {Immunodetection of the serotonin transporter protein is a more valid marker for serotonergic fibers than serotonin},
  volume = {59},
  copyright = {Copyright \textcopyright{} 2006 Wiley-Liss, Inc.},
  issn = {1098-2396},
  doi = {10.1002/syn.20240},
  abstract = {Tracking serotonergic pathways in the brain through immunodetection of serotonin has widely been used for the anatomical characterization of the serotonergic system. Immunostaining for serotonin is also frequently applied for the visualization of individual serotonin containing fibers and quantification of serotonin positive fibers has been widely used to detect changes in the serotonergic innervation. However, particularly in conditions with enhanced serotonin metabolism the detection level of serotonin may lead to an underestimation of the true number of serotonergic fibers. The serotonin transporter (SERT) protein, on the other hand, is less liable to metabolism and for that reason we hypothetized that SERT immunostaining is a more stable marker of serotonergic fibers. Rats were pretreated with monoamine oxidase (MAO) inhibitor and compared with placebo treated rats. Brains were double immunostained for serotonin and SERT protein and colocalization was quantified in several brain areas by confocal microscopy. In comparison with untreated rats, MAO inhibitor treated rats had a significantly higher number (almost 200\% increase) of serotonin immunopositive fibers whereas no difference was observed in the number of the SERT positive fibers. Colocalization between serotonin and SERT positive fibers was close to 100\% in MAO inhibitor treated animals but only 30\% in untreated rats. We conclude that the rapid metabolism of serotonin leads to an underestimation of immunodetected serotonergic fibers and that in many instances, SERT immunostaining may be a better indicator of serotonergic fibers. Synapse 59:270\textendash{}276, 2006. \textcopyright{} 2006 Wiley-Liss, Inc.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {5},
  urldate = {2014-11-19},
  journal = {Synapse},
  author = {Nielsen, Kirsten and Brask, Dorte and Knudsen, Gitte M. and Aznar, Susana},
  month = apr,
  year = {2006},
  keywords = {colocalization,confocal microscopy,fluorescence immunostaining,serotonin metabolism,SLC6A4},
  pages = {270--276},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/K4ACZMF9/abstract.html:}
}

@article{richard_comparison_2014,
  title = {Comparison of gene expression microarray data with count-based {{RNA}} measurements informs microarray interpretation},
  volume = {15},
  copyright = {2014 Richard et al.; licensee BioMed Central Ltd.},
  issn = {1471-2164},
  doi = {10.1186/1471-2164-15-649},
  abstract = {Although numerous investigations have compared gene expression microarray platforms, preprocessing methods and batch correction algorithms using constructed spike-in or dilution datasets, there remains a paucity of studies examining the properties of microarray data using diverse biological samples. Most microarray experiments seek to identify subtle differences between samples with variable background noise, a scenario poorly represented by constructed datasets. Thus, microarray users lack important information regarding the complexities introduced in real-world experimental settings. The recent development of a multiplexed, digital technology for nucleic acid measurement enables counting of individual RNA molecules without amplification and, for the first time, permits such a study.
PMID: 25091430},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2015-01-12},
  journal = {BMC Genomics},
  author = {Richard, Arianne C. and Lyons, Paul A. and Peters, James E. and Biasci, Daniele and Flint, Shaun M. and Lee, James C. and McKinney, Eoin F. and Siegel, Richard M. and Smith, Kenneth GC},
  month = aug,
  year = {2014},
  keywords = {gene expression,microarray,NanoString,nCounter},
  pages = {649},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/WD93V875/649.html:},
  pmid = {25091430}
}

@article{graeber_microglia:_2010,
  title = {Microglia: biology and pathology},
  volume = {119},
  issn = {1432-0533},
  shorttitle = {Microglia},
  doi = {10.1007/s00401-009-0622-0},
  abstract = {The past 20 years have seen a gain in knowledge on microglia biology and microglia functions in disease that exceeds the expectations formulated when the microglia "immune network" was introduced. More than 10,000 articles have been published during this time. Important new research avenues of clinical importance have opened up such as the role of microglia in pain and in brain tumors. New controversies have also emerged such as the question of whether microglia are active or reactive players in neurodegenerative disease conditions, or whether they may be victims themselves. Premature commercial interests may be responsible for some of the confusion that currently surrounds microglia in both the Alzheimer and Parkinson's disease research fields. A critical review of the literature shows that the concept of "(micro)glial inflammation" is still open to interpretation, despite a prevailing slant towards a negative meaning. Perhaps the most exciting foreseeable development concerns research on the role of microglia in synaptic plasticity, which is expected to yield an answer to the question whether microglia are the brain's electricians. This review provides an analysis of the latest developments in the microglia field.},
  language = {eng},
  timestamp = {2016-03-15T02:13:13Z},
  number = {1},
  journal = {Acta Neuropathologica},
  author = {Graeber, Manuel B. and Streit, Wolfgang J.},
  month = jan,
  year = {2010},
  keywords = {Animals,Central Nervous System,Central Nervous System Diseases,Humans,microglia,Models; Neurological},
  pages = {89--105},
  pmid = {20012873}
}

@article{xiu_il-10_2015,
  title = {{{IL}}-10 induces the development of immunosuppressive {{CD14}}+{{HLA-DRlow}}/|[minus]| monocytes in {{B}}-cell non-{{Hodgkin}} lymphoma},
  volume = {5},
  copyright = {\textcopyright{} 2015 Nature Publishing Group},
  doi = {10.1038/bcj.2015.56},
  abstract = {The biological role of monocytes and macrophages in B-cell non-Hodgkin lymphoma (NHL) is not fully understood. We have previously reported that monocytes from patients with B-cell NHL have an immunosuppressive CD14+HLA-DRlow/- phenotype that correlates with a poor prognosis. However, the underlying mechanism by which CD14+HLA-DRlow/- monocytes develop in lymphoma is unknown. In the present study, we found that interleukin (IL)-10, which is increased in the serum of patients with B-cell NHL, induced the development of the CD4+HLA-DRlow/- population. Using peripheral blood samples from patients with B-cell NHL, we found that absolute numbers of CD14+ monocytic cells with an HLA-DRlow/- phenotype were higher than healthy controls and correlated with a higher International Prognostic Index score. IL-10 serum levels were elevated in lymphoma patients compared with controls and were associated with increased peripheral monocyte counts. Treatment of monocytes with IL-10 in vitro significantly decreased HLA-DR expression and resulted in the expansion of CD14+HLA-DRlow/- population. We found that lymphoma B cells produce IL-10 and supernatants from cultured lymphoma cells increased the CD14+HLA-DRlow/- population. Furthermore, we found that IL-10-induced CD14+HLA-DRlow/- monocytes inhibited the activation and proliferation of T cells. Taken together, these results suggest that elevated IL-10 serum levels contribute to increased numbers of immunosuppressive CD14+HLA-DRlow/- monocytes in B-cell NHL.},
  language = {en},
  timestamp = {2015-08-17T18:02:21Z},
  number = {7},
  urldate = {2015-08-17},
  journal = {Blood Cancer Journal},
  author = {Xiu, B. and Lin, Y. and Grote, D. M. and Ziesmer, S. C. and Gustafson, M. P. and Maas, M. L. and Zhang, Z. and Dietz, A. B. and Porrata, L. F. and Novak, A. J. and Liang, A.-B. and Yang, Z.-Z. and Ansell, S. M.},
  month = jul,
  year = {2015},
  pages = {e328}
}

@article{barnes_transcription_2011,
  title = {Transcription and pathway analysis of the superior temporal cortex and anterior prefrontal cortex in schizophrenia},
  volume = {89},
  copyright = {Copyright \textcopyright{} 2011 Wiley-Liss, Inc.},
  issn = {1097-4547},
  doi = {10.1002/jnr.22647},
  abstract = {The molecular basis of schizophrenia is poorly understood; however, different brain regions are believed to play distinct roles in disease symptomology. We have studied gene expression in the superior temporal cortex (Brodmann area 22; BA22), which may play a role in positive pathophysiology, and compared our results with data from the anterior prefrontal cortex (BA10), which shows evidence for a role in negative symptoms. Genome-wide mRNA expression was determined in the BA22 region in 23 schizophrenics and 19 controls and compared with a BA10 data set from the same subjects. After adjustments for confounding sources of variation, we carried out GeneGO pathway enrichment analysis in each region. Significant differences were seen in age-related transcriptional changes between the BA22 and the BA10 regions, 21.8\% and 41.4\% of disease-associated transcripts showing age association, respectively. After removing age associated changes from our data, we saw the highest enrichment in processes mediating cell adhesion, synaptic contact, cytoskeletal remodelling, and apoptosis in the BA22 region. For the BA10 region, we observed the strongest changes in reproductive signalling, tissue remodelling, and cell differentiation. Further exploratory analysis also identified potentially disease-relevant processes that were undetected in our more stringent primary analysis, including autophagy in the BA22 region and the amyloid process in the BA10 region. Collectively, our analysis suggests disruption of many common pathways and processes underpinning synaptic plasticity in both regions in schizophrenia, whereas individual regions emphasize changes in certain pathways that may help to highlight pathway-specific therapeutic opportunities to treat negative or positive symptoms of the disease. \textcopyright{} 2011 Wiley-Liss, Inc.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {8},
  urldate = {2015-08-07},
  journal = {Journal of Neuroscience Research},
  author = {Barnes, Michael R. and Huxley-Jones, Julie and Maycox, Peter R. and Lennon, Mark and Thornber, Amy and Kelly, Fiona and Bates, Stewart and Taylor, Adam and Reid, Juliet and Jones, Neil and Schroeder, J{\"o}rn and Scorer, Carol A. and Davies, Ceri and Hagan, Jim J. and Kew, James N.C. and Angelinetta, Claire and Akbar, Tariq and Hirsch, Steven and Mortimer, Ann M. and Barnes, Thomas R.E. and {de Belleroche}, Jackie},
  month = aug,
  year = {2011},
  keywords = {amyloid,autophagy,BA10,BA22,synaptic plasticity},
  pages = {1218--1227}
}

@article{ray_analysis_2010,
  title = {Analysis of {{Alzheimer}}'s disease severity across brain regions by topological analysis of gene co-expression networks},
  volume = {4},
  copyright = {2010 Ray and Zhang; licensee BioMed Central Ltd.},
  issn = {1752-0509},
  doi = {10.1186/1752-0509-4-136},
  abstract = {Alzheimer's disease (AD) is a progressive neurodegenerative disorder involving variations in the transcriptome of many genes. AD does not affect all brain regions simultaneously. Identifying the differences among the affected regions may shed more light onto the disease progression. We developed a novel method involving the differential topology of gene coexpression networks to understand the association among affected regions and disease severity.
PMID: 20925940},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-11-18},
  journal = {BMC Systems Biology},
  author = {Ray, Monika and Zhang, Weixiong},
  month = oct,
  year = {2010},
  pages = {136},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/GKQ33R5P/136.html:},
  pmid = {20925940}
}

@article{wienecke_spinal_2014,
  title = {Spinal {{Cord Injury Enables Aromatic}} l-{{Amino Acid Decarboxylase Cells}} to {{Synthesize Monoamines}}},
  volume = {34},
  issn = {0270-6474, 1529-2401},
  doi = {10.1523/JNEUROSCI.3838-13.2014},
  abstract = {Serotonin (5-HT), an important modulator of both sensory and motor functions in the mammalian spinal cord, originates mainly in the raphe nuclei of the brainstem. However, following complete transection of the spinal cord, small amounts of 5-HT remain detectable below the lesion. It has been suggested, but not proven, that this residual 5-HT is produced by intraspinal 5-HT neurons. Here, we show by immunohistochemical techniques that cells containing the enzyme aromatic l-amino acid decarboxylase (AADC) occur not only near the central canal, as reported by others, but also in the intermediate zone and dorsal horn of the spinal gray matter. We show that, following complete transection of the rat spinal cord at S2 level, AADC cells distal to the lesion acquire the ability to produce 5-HT from its immediate precursor, 5-hydroxytryptophan. Our results indicate that this phenotypic change in spinal AADC cells is initiated by the loss of descending 5-HT projections due to spinal cord injury (SCI). By in vivo and in vitro electrophysiology, we show that 5-HT produced by AADC cells increases the excitability of spinal motoneurons. The phenotypic change in AADC cells appears to result from a loss of inhibition by descending 5-HT neurons and to be mediated by 5-HT1B receptors expressed by AADC cells. These findings indicate that AADC cells are a potential source of 5-HT at spinal levels below an SCI. The production of 5-HT by AADC cells, together with an upregulation of 5-HT2 receptors, offers a partial explanation of hyperreflexia below a chronic SCI.},
  language = {en},
  timestamp = {2016-03-22T22:33:21Z},
  number = {36},
  urldate = {2016-03-22},
  journal = {The Journal of Neuroscience},
  author = {Wienecke, Jacob and Ren, Li-Qun and Hultborn, Hans and Chen, Meng and M\o{}ller, Morten and Zhang, Yifan and Zhang, Mengliang},
  month = mar,
  year = {2014},
  keywords = {5-HTP,AADC,motoneuron,serotonin,spasticity,supersensitivity},
  pages = {11984--12000},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/EIUNK5AI/11984.html:},
  pmid = {25186745}
}

@article{tan_microrna-128_2013,
  title = {{{MicroRNA}}-128 governs neuronal excitability and motor behavior in mice.},
  volume = {342},
  issn = {0036-8075, 1095-9203},
  doi = {10.1126/science.1244193},
  abstract = {The control of motor behavior in animals and humans requires constant adaptation of neuronal networks to signals of various types and strengths. We found that microRNA-128 (miR-128), which is expressed in adult neurons, regulates motor behavior by modulating neuronal signaling networks and excitability. miR-128 governs motor activity by suppressing the expression of various ion channels and signaling components of the extracellular signal\textendash{}regulated kinase ERK2 network that regulate neuronal excitability. In mice, a reduction of miR-128 expression in postnatal neurons causes increased motor activity and fatal epilepsy. Overexpression of miR-128 attenuates neuronal responsiveness, suppresses motor activity, and alleviates motor abnormalities associated with Parkinson's\textendash{}like disease and seizures in mice. These data suggest a therapeutic potential for miR-128 in the treatment of epilepsy and movement disorders.
Not Too Much, Not Too Little
The microRNA miR128 is expressed in brain neurons of the mouse. Lek Tan et al. (p. 1254) now find that miR128 is crucial to stable brain function. Mice deficient in miR128 developed hyperactivity and were susceptible to fatal seizures, whereas overexpression of miR128 correlated with reduced motor activity and reduced susceptibility to proconvulsive drugs. Experiments using ex vivo\textendash{}isolated adult brain tissues suggested that miR-128 controlled motor activity by governing the signaling network that determines the intrinsic excitability and signal responsiveness of neurons.},
  language = {en},
  timestamp = {2015-08-28T03:44:15Z},
  number = {6163},
  urldate = {2014-10-21},
  journal = {Science},
  author = {Tan, Chan Lek and Plotkin, Joshua L. and Ven\o{}, Morten T. and {von Schimmelmann}, Melanie and Feinberg, Philip and Mann, Silas and Handler, Annie and Kjems, J\o{}rgen and Surmeier, D. James and O'Carroll, D{\'o}nal and Greengard, Paul and Schaefer, Anne},
  month = jun,
  year = {2013},
  pages = {1254--1258},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/ECC4RFQM/1254.html:},
  pmid = {24311694}
}

@article{baxter_selective_2013,
  series = {Behavioral Neuroscience at 30},
  title = {Selective immunotoxic lesions of basal forebrain cholinergic cells: {{Effects}} on learning and memory in rats},
  volume = {127},
  issn = {0735-7044},
  shorttitle = {Selective immunotoxic lesions of basal forebrain cholinergic cells},
  doi = {10.1037/a0033939},
  abstract = {Male Long-Evans rats were given injections of either 192 IgG-saporin, an apparently selective toxin for basal forebrain cholinergic neurons (LES), or vehicle (CON) into either the medial septum and vertical limb of the diagonal band (MS/VDB) or bilaterally into the nucleus basalis magnocellularis and substantia innominata (nBM/SI). Place discrimination in the Morris water maze assessed spatial learning, and a trial-unique matching-to-place task in the water maze assessed memory for place information over varying delays. MS/VDB-LES and nBM/SI-LES rats were not impaired relative to CON rats in acquisition of the place discrimination, but were mildly impaired relative to CON rats in performance of the memory task even at the shortest delay, suggesting a nonmnemonic deficit. These results contrast with effects of less selective lesions, which have been taken to support a role for basal forebrain cholinergic neurons in learning and memory. (PsycINFO Database Record (c) 2013 APA, all rights reserved). (journal abstract)},
  timestamp = {2016-03-24T09:50:24Z},
  number = {5},
  urldate = {2016-03-24},
  journal = {Behavioral Neuroscience},
  author = {Baxter, Mark G. and Bucci, David J. and Gorman, Linda K. and Wiley, Ronald G. and Gallagher, Michela},
  month = oct,
  year = {2013},
  keywords = {192 IgG-saporin,Animal Learning,basal forebrain cholinergic cells,Brain Lesions (Experimental),Cholinergic Nerves,Forebrain,immunotoxic lesions,Immunotoxin,Learning,Memory,Rats},
  pages = {619--627}
}

@article{demars_cortical_2014,
  title = {Cortical parvalbumin and somatostatin {{GABA}} neurons express distinct endogenous modulators of nicotinic acetylcholine receptors},
  volume = {7},
  copyright = {2014 Demars and Morishita; licensee BioMed Central Ltd.},
  issn = {1756-6606},
  doi = {10.1186/s13041-014-0075-9},
  abstract = {Inhibition from GABAergic interneurons in brain circuits is a critical component of cognitive function. This inhibition is regulated through a diverse network of neuromodulation. A number of recent studies suggest that one of the major regulators of interneuron function is nicotinic acetylcholinergic transmission and dysregulation of both systems is common in psychiatric conditions. However, how nicotinic modulation impacts specific subpopulations of diverse GABAergic interneurons remains in question. One potential way of conferring specificity to the convergence of GABAergic and nicotinic signaling is through the expression of a unique family of nicotinic acetycholine receptor modulators, the Lynx family. The present study sought to identify members of the Lynx family enriched in cortical interneurons and to elucidate subpopulations of GABAergic neurons that express unique nicotinic modulators.},
  language = {en},
  timestamp = {2015-10-06T02:40:47Z},
  number = {1},
  urldate = {2015-10-06},
  journal = {Molecular Brain},
  author = {Demars, Michael P. and Morishita, Hirofumi},
  month = oct,
  year = {2014},
  keywords = {GABA,Lynx1,Lynx family,Lypd6,mouse,Nicotinic acetylcholine receptor,Parvalbumin,Somatostatin,Visual cortex},
  pages = {75},
  pmid = {25359633}
}

@article{gautier_affyanalysis_2004,
  title = {affy\textemdash{}analysis of {{Affymetrix GeneChip}} data at the probe level},
  volume = {20},
  issn = {1367-4803, 1460-2059},
  doi = {10.1093/bioinformatics/btg405},
  abstract = {Motivation: The processing of the Affymetrix GeneChip data has been a recent focus for data analysts. Alternatives to the original procedure have been proposed and some of these new methods are widely used.
Results: The affy package is an R package of functions and classes for the analysis of oligonucleotide arrays manufactured by Affymetrix. The package is currently in its second release, affy provides the user with extreme flexibility when carrying out an analysis and make it possible to access and manipulate probe intensity data. In this paper, we present the main classes and functions in the package and demonstrate how they can be used to process probe-level data. We also demonstrate the importance of probe-level analysis when using the Affymetrix GeneChip platform.},
  language = {en},
  timestamp = {2016-02-13T04:42:12Z},
  number = {3},
  urldate = {2016-02-13},
  journal = {Bioinformatics},
  author = {Gautier, Laurent and Cope, Leslie and Bolstad, Benjamin M. and Irizarry, Rafael A.},
  month = dec,
  year = {2004},
  pages = {307--315},
  pmid = {14960456}
}

@article{mistry_gene-expression_2007,
  title = {Gene-{{Expression Patterns}} in {{Whole Blood Identify Subjects}} at {{Risk}} for {{Recurrent Tuberculosis}}},
  volume = {195},
  issn = {0022-1899, 1537-6613},
  doi = {10.1086/510397},
  abstract = {Background. The majority of patients with tuberculosis who comply with appropriate treatment are cured. However, \ensuremath{\sim}5\% subsequently have a repeat disease episode, usually within 2 years of successful combination therapy. Presently, there is no way of predicting which patients will experience a relapse.
Methods. We identified 10 subjects who had previously experienced recurrent tuberculosis and carefully matched them to cured subjects who had had only 1 episode of tuberculosis, to patients with active tuberculosis, and to latently infected healthy subjects. We compared their ex vivo whole-blood gene-expression profiles by use of DNA array technology and confirmed the results by use of quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR).
Results. The 4 clinical tuberculosis groups exhibited distinct patterns of gene expression. The gene-transcript profiles of the patients with recurrent tuberculosis were more similar to those of the patients with active tuberculosis than to those of the cured or latently infected subjects. Discriminant analysis of a training data set showed that 9 genes were sufficient to classify the subjects. We confirmed that measurement of the expression of these genes by qRT-PCR can accurately discriminate between subjects in a test set of samples.
Conclusions. A simple test based on gene-expression patterns may be used as a biomarker of cure while identifying patients who are at risk for relapse. This would facilitate the introduction of new tuberculosis drugs.},
  language = {en},
  timestamp = {2015-08-18T01:35:29Z},
  number = {3},
  urldate = {2015-08-18},
  journal = {Journal of Infectious Diseases},
  author = {Mistry, Rohit and Cliff, Jacqueline M. and Clayton, Christopher L. and Beyers, Nulda and Mohamed, Yasmin S. and Wilson, Paul A. and Dockrell, Hazel M. and Wallace, Don M. and {van Helden}, Paul D. and Duncan, Ken and Lukey, Pauline T.},
  month = jan,
  year = {2007},
  pages = {357--365},
  pmid = {17205474}
}

@article{bankston_oligodendroglia_2013,
  title = {Oligodendroglia and neurotrophic factors in neurodegeneration},
  volume = {29},
  issn = {1673-7067},
  doi = {10.1007/s12264-013-1321-3},
  abstract = {Myelination by oligodendroglial cells (OLs) enables the propagation of action potentials along neuronal axons, which is essential for rapid information flow in the central nervous system (CNS). Besides saltatory conduction, the myelin sheath also protects axons against inflammatory and oxidative insults, and loss of myelin results in axonal damage and ultimately neuronal loss in demyelinating disorders. However, accumulating evidence indicates that OLs also provide support to neurons via mechanisms beyond the insulating function of myelin. More importantly, an increasing volume of reports indicates defects of OLs in numerous neurodegenerative diseases, sometimes even preceding neuronal loss in pre-symptomatic episodes, suggesting that OL pathology may be an important mechanism contributing to the initiation and/or progression of neurodegeneration. This review focuses on the emerging picture of neuronal support by OLs in the pathogenesis of neurodegenerative disorders through diverse molecular and cellular mechanisms, including direct neuron-myelin interaction, metabolic support by OLs, and neurotrophic factors produced by and/or acting on OLs.},
  timestamp = {2016-03-24T08:50:50Z},
  number = {2},
  urldate = {2016-03-24},
  journal = {Neuroscience bulletin},
  author = {Bankston, Andrew N. and Mandler, Mariana D. and Feng, Yue},
  month = apr,
  year = {2013},
  pages = {216--228},
  pmid = {23558590},
  pmcid = {PMC4020141}
}

@article{hashimoto_neural_1996,
  title = {A neural cell-type-specific expression system using recombinant adenovirus vectors},
  volume = {7},
  issn = {1043-0342},
  doi = {10.1089/hum.1996.7.2-149},
  abstract = {We demonstrated neural cell-type-specific gene expression using an adenovirus vector, which is useful for delivering foreign genes into quiescent neural cells. We produced eight recombinant replication-defective adenoviruses carrying the lacZ reporter gene driven by various promoters, including those of the L7/PCP2 gene (highly restricted expression in cerebellar Purkinje cells), and the myelin basic protein (in oligodendrocytes) gene. We demonstrated in vitro and in vivo promoter-driven, neural cell-type-specific gene expression by recombinant adenoviruses. The genes were transferred into these recombinant adenoviruses and expressed with high levels of efficiency in vitro and in vivo. In primary culture, the recombinant adenoviruses AdexL7-NL-LacZ and AdexMBP-NL-LacZ appeared to be expressed in a Purkinje cell and oligodendrocyte-specific manner. Introduction of 10(8) pfu of these viruses into the adult rat cerebellum by stereotactic injection yielded neural cell-type-specific expression without apparent toxicity to the animals. Thus, adenovirus vectors are useful for cell-type-specific therapeutic uses and in studies requiring neural cell-type-specific gene expression.},
  language = {eng},
  timestamp = {2016-03-23T09:10:26Z},
  number = {2},
  journal = {Human Gene Therapy},
  author = {Hashimoto, M. and Aruga, J. and Hosoya, Y. and Kanegae, Y. and Saito, I. and Mikoshiba, K.},
  month = jan,
  year = {1996},
  keywords = {Adenoviruses; Human,Animals,Cells; Cultured,cerebellum,Female,gene expression,Genes; Reporter,Genetic Vectors,Gene Transfer Techniques,Humans,Lac Operon,Mice,Mice; Inbred ICR,Myelin Basic Protein,Nerve Tissue Proteins,Oligodendroglia,Purkinje cells,Rats,Rats; Sprague-Dawley,Recombinant Fusion Proteins},
  pages = {149--158},
  pmid = {8788166}
}

@article{speicher_new_2005,
  title = {The new cytogenetics: blurring the boundaries with molecular biology},
  volume = {6},
  copyright = {\textcopyright{} 2005 Nature Publishing Group},
  issn = {1471-0056},
  shorttitle = {The new cytogenetics},
  doi = {10.1038/nrg1692},
  abstract = {Exciting advances in fluorescence in situ hybridization and array-based techniques are changing the nature of cytogenetics, in both basic research and molecular diagnostics. Cytogenetic analysis now extends beyond the simple description of the chromosomal status of a genome and allows the study of fundamental biological questions, such as the nature of inherited syndromes, the genomic changes that are involved in tumorigenesis and the three-dimensional organization of the human genome. The high resolution that is achieved by these techniques, particularly by microarray technologies such as array comparative genomic hybridization, is blurring the traditional distinction between cytogenetics and molecular biology.},
  language = {en},
  timestamp = {2016-03-16T07:16:25Z},
  number = {10},
  urldate = {2016-03-16},
  journal = {Nature Reviews Genetics},
  author = {Speicher, Michael R. and Carter, Nigel P.},
  month = oct,
  year = {2005},
  pages = {782--792}
}

@article{bradl_oligodendrocytes_2010,
  title = {Oligodendrocytes: biology and pathology},
  volume = {119},
  issn = {0001-6322},
  shorttitle = {Oligodendrocytes},
  doi = {10.1007/s00401-009-0601-5},
  abstract = {Oligodendrocytes are the myelinating cells of the central nervous system (CNS). They are the end product of a cell lineage which has to undergo a complex and precisely timed program of proliferation, migration, differentiation, and myelination to finally produce the insulating sheath of axons. Due to this complex differentiation program, and due to their unique metabolism/physiology, oligodendrocytes count among the most vulnerable cells of the CNS. In this review, we first describe the different steps eventually culminating in the formation of mature oligodendrocytes and myelin sheaths, as they were revealed by studies in rodents. We will then show differences and similarities of human oligodendrocyte development. Finally, we will lay out the different pathways leading to oligodendrocyte and myelin loss in human CNS diseases, and we will reveal the different principles leading to the restoration of myelin sheaths or to a failure to do so.},
  timestamp = {2016-03-15T00:49:10Z},
  number = {1},
  urldate = {2016-03-15},
  journal = {Acta Neuropathologica},
  author = {Bradl, Monika and Lassmann, Hans},
  month = jan,
  year = {2010},
  pages = {37--53},
  pmid = {19847447},
  pmcid = {PMC2799635}
}

@article{kohli_whole_2015,
  title = {Whole blood defensin {{mRNA}} expression is a predictive biomarker of docetaxel response in castration-resistant prostate cancer},
  volume = {8},
  issn = {1178-6930},
  doi = {10.2147/OTT.S86637},
  abstract = {This study tested the potential of circulating RNA-based signals as predictive biomarkers for docetaxel response in patients with metastatic castration-resistant prostate cancer (CRPC). RNA was analyzed in blood from six CRPC patients by whole-transcriptome sequencing (total RNA-sequencing) before and after docetaxel treatment using the Illumina's HiSeq platform. Targeted RNA capture and sequencing was performed in an independent cohort of ten patients with CRPC matching the discovery cohort to confirm differential expression of the genes. Response to docetaxel was defined on the basis of prostate-specific antigen levels and imaging criteria. Two-way analysis of variance was used to compare differential gene expression in patients classified as responders versus nonresponders before and after docetaxel treatment. Thirty-four genes with two-fold differentially expressed transcripts in responders versus nonresponders were selected from total RNA-sequencing for further validation. Targeted RNA capture and sequencing showed that 13/34 genes were differentially expressed in responders. Alpha defensin genes DEFA1, DEFA1B, and DEFA3 exhibited significantly higher expression in responder patients compared with nonresponder patients before administration of chemotherapy (fold change \ensuremath{>}2.5). In addition, post-docetaxel treatment significantly increased transcript levels of these defensin genes in responders (fold change \ensuremath{>}2.8). Our results reveal that patients with higher defensin RNA transcripts in blood respond well to docetaxel therapy. We suggest that monitoring DEFA1, DEFA1B, and DEFA3 RNA transcripts in blood prior to treatment will be helpful to determine which patients are better candidates to receive docetaxel chemotherapy.},
  timestamp = {2015-08-17T21:00:49Z},
  urldate = {2015-08-17},
  journal = {OncoTargets and therapy},
  author = {Kohli, Manish and Young, Charles YF and Tindall, Donald J and Nandy, Debashis and McKenzie, Kyle M and Bevan, Graham H and Donkena, Krishna Vanaja},
  month = jul,
  year = {2015},
  pages = {1915--1922},
  pmid = {26261420},
  pmcid = {PMC4527520}
}

@article{duke_medial_2007,
  title = {The medial and lateral substantia nigra in {{Parkinson}}'s disease: {{mRNA}} profiles associated with higher brain tissue vulnerability},
  volume = {8},
  issn = {1364-6745, 1364-6753},
  shorttitle = {The medial and lateral substantia nigra in {{Parkinson}}'s disease},
  doi = {10.1007/s10048-006-0077-6},
  abstract = {Sporadic Parkinson's disease (PD) is characterized by progressive death of dopaminergic neurons within the substantia nigra. However, pathological cell death within this nucleus is not uniform. In PD, the lateral tier of the substantia nigra (SNl) degenerates earlier and more severely than the more medial nigral component (SNm). The cause of this brain regional vulnerability remains unknown. We have used DNA oligonucleotide microarrays to compare gene expression profiles from the SNl to those of the SNm in both PD and control cases. Genes expressed more highly in the PD SNl included the cell death gene, p53 effector related to PMP22, the tumour necrosis factor (TNF) receptor gene, TNF receptor superfamily, member 21, and the mitochondrial complex I gene, NADH dehydrogenase (ubiquinone) 1\ensuremath{\beta} subcomplex, 3, 12 kDa (NDUF\ensuremath{\beta}3). Genes that were more highly expressed in PD SNm included the dopamine cell signalling gene, cyclic adenosine monophosphate-regulated phosphoprotein, 21 kDa, the activated macrophage gene, stabilin 1, and two glutathione peroxidase (GPX) genes, GPX1 and GPX3. Thus, there is increased expression of genes encoding pro-inflammatory cytokines and subunits of the mitochondrial electron transport chain, and there is a decreased expression of several glutathione-related genes in the SNl suggesting a molecular basis for pathoclisis. Importantly, some of the genes that are differentially regulated in the SNl are known to be expressed highly or predominately in glial cells. These findings support the view that glial cells can be primarily affected in PD emphasizing the importance of using a whole tissue approach when investigating degenerative CNS disease.},
  language = {en},
  timestamp = {2016-06-05T07:57:51Z},
  number = {2},
  urldate = {2016-06-05},
  journal = {Neurogenetics},
  author = {Duke, D. C. and Moran, L. B. and Pearce, R. K. B. and Graeber, M. B.},
  month = jan,
  year = {2007},
  keywords = {gene expression,glia,Human Genetics,microarray,Mitochondria,Molecular Medicine,Neurosciences,Tumour necrosis factor},
  pages = {83--94}
}

@article{naef_solving_2003,
  title = {Solving the riddle of the bright mismatches: labeling and effective binding in oligonucleotide arrays},
  volume = {68},
  issn = {1539-3755},
  shorttitle = {Solving the riddle of the bright mismatches},
  abstract = {RNA binding to high-density oligonucleotide arrays has shown tantalizing differences with solution experiments. We analyze here its sequence specificity, fitting binding affinities to sequence composition in large datasets. Our results suggest that the fluorescent labels interfere with binding, causing a catch-22. To be detected, the RNA must both glow and bind: without labels it cannot be seen even if bound, while with too many it will not bind. A simple model for the binding of labeled oligonucleotides sheds light on the interplay between binding energies and labeling probability.},
  language = {eng},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1 Pt 1},
  journal = {Physical Review. E, Statistical, Nonlinear, and Soft Matter Physics},
  author = {Naef, Felix and Magnasco, Marcelo O.},
  month = jul,
  year = {2003},
  keywords = {Base Sequence,Biophysical Phenomena,Biophysics,Biotinylation,Humans,Models; Statistical,Molecular Sequence Data,Oligonucleotide Array Sequence Analysis,RNA,RNA; Messenger,unread},
  pages = {011906},
  pmid = {12935175}
}

@article{mcclintick_stress-response_2013,
  title = {Stress-response pathways are altered in the hippocampus of chronic alcoholics},
  volume = {47},
  issn = {1873-6823},
  doi = {10.1016/j.alcohol.2013.07.002},
  abstract = {The chronic high-level alcohol consumption seen in alcoholism leads to dramatic effects on the hippocampus, including decreased white matter, loss of oligodendrocytes and other glial cells, and inhibition of neurogenesis. Examining gene expression in post mortem hippocampal tissue from 20 alcoholics and 19 controls allowed us to detect differentially expressed genes that may play a role in the risk for alcoholism or whose expression is modified by chronic consumption of alcohol. We identified 639 named genes whose expression significantly differed between alcoholics and controls at a False Discovery Rate (FDR) \ensuremath{\leq} 0.20; 52\% of these genes differed by at least 1.2-fold. Differentially expressed genes included the glucocorticoid receptor and the related gene FK506 binding protein 5 (FKBP5), UDP glycosyltransferase 8 (UGT8), urea transporter (SLC14A1), zinc transporter (SLC39A10), Interleukin 1 receptor type 1 (IL1R1), thioredoxin interacting protein (TXNIP), and many metallothioneins. Pathways related to inflammation, hypoxia, and stress showed activation, and pathways that play roles in neurogenesis and myelination showed decreases. The cortisol pathway dysregulation and increased inflammation identified here are seen in other stress-related conditions such as depression and post-traumatic stress disorder and most likely play a role in addiction. Many of the detrimental effects on the hippocampus appear to be mediated through NF-\ensuremath{\kappa}B signaling. Twenty-four of the differentially regulated genes were previously identified by genome-wide association studies of alcohol use disorders; this raises the potential interest of genes not normally associated with alcoholism, such as suppression of tumorigenicity 18 (ST18), BCL2-associated athanogene 3 (BAG3), and von Willebrand factor (VWF).},
  language = {eng},
  timestamp = {2015-08-13T22:18:44Z},
  number = {7},
  journal = {Alcohol (Fayetteville, N.Y.)},
  author = {McClintick, Jeanette N. and Xuei, Xiaoling and Tischfield, Jay A. and Goate, Alison and Foroud, Tatiana and Wetherill, Leah and Ehringer, Marissa A. and Edenberg, Howard J.},
  month = nov,
  year = {2013},
  keywords = {Adult,Aged,Alcoholics,Alcoholism,Anoxia,Female,Gene Ontology,Hippocampus,Humans,Inflammation,Male,Middle Aged,Neurogenesis,NF-kappa B,transcriptome},
  pages = {505--515},
  pmid = {23981442},
  pmcid = {PMC3836826}
}

@article{chung_cell_2005,
  title = {Cell type-specific gene expression of midbrain dopaminergic neurons reveals molecules involved in their vulnerability and protection},
  volume = {14},
  issn = {0964-6906, 1460-2083},
  doi = {10.1093/hmg/ddi178},
  abstract = {Molecular differences between dopamine (DA) neurons may explain why the mesostriatal DA neurons in the A9 region preferentially degenerate in Parkinson's disease (PD) and toxic models, whereas the adjacent A10 region mesolimbic and mesocortical DA neurons are relatively spared. To characterize innate physiological differences between A9 and A10 DA neurons, we determined gene expression profiles in these neurons in the adult mouse by laser capture microdissection, microarray analysis and real-time PCR. We found 42 genes relatively elevated in A9 DA neurons, whereas 61 genes were elevated in A10 DA neurons [\ensuremath{>}2-fold; false discovery rate (FDR) \ensuremath{<}1\%]. Genes of interest for further functional analysis were selected by criteria of (i) fold differences in gene expression, (ii) real-time PCR validation and (iii) potential roles in neurotoxic or protective biochemical pathways. Three A9-elevated molecules [G-protein coupled inwardly rectifying K channel 2 (GIRK2), adenine nucleotide translocator 2 (ANT-2) and the growth factor IGF-1] and three A10-elevated peptides (GRP, CGRP and PACAP) were further examined in both \ensuremath{\alpha}-synuclein overexpressing PC12 (PC12-\ensuremath{\alpha}Syn) cells and rat primary ventral mesencephalic (VM) cultures exposed to MPP+ neurotoxicity. GIRK2-positive DA neurons were more vulnerable to MPP+ toxicity and overexpression of GIRK2 increased the vulnerability of PC12-\ensuremath{\alpha}Syn cells to the toxin. Blocking of ANT decreased vulnerability to MPP+ in both cell culture systems. Exposing cells to IGF-1, GRP and PACAP decreased vulnerability of both cell types to MPP+, whereas CGRP protected PC12-\ensuremath{\alpha}Syn cells but not primary VM DA neurons. These results indicate that certain differentially expressed molecules in A9 and A10 DA neurons may play key roles in their relative vulnerability to toxins and PD.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {13},
  urldate = {2014-11-04},
  journal = {Human Molecular Genetics},
  author = {Chung, Chee Yeun and Seo, Hyemyung and Sonntag, Kai Christian and Brooks, Andrew and Lin, Ling and Isacson, Ole},
  month = jan,
  year = {2005},
  pages = {1709--1725},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/RTFHRN2Q/1709.html:},
  pmid = {15888489}
}

@article{irizarry_exploration_2003,
  title = {Exploration, normalization, and summaries of high density oligonucleotide array probe level data},
  volume = {4},
  issn = {1465-4644},
  doi = {10.1093/biostatistics/4.2.249},
  abstract = {In this paper we report exploratory analyses of high-density oligonucleotide array data from the Affymetrix GeneChip system with the objective of improving upon currently used measures of gene expression. Our analyses make use of three data sets: a small experimental study consisting of five MGU74A mouse GeneChip arrays, part of the data from an extensive spike-in study conducted by Gene Logic and Wyeth's Genetics Institute involving 95 HG-U95A human GeneChip arrays; and part of a dilution study conducted by Gene Logic involving 75 HG-U95A GeneChip arrays. We display some familiar features of the perfect match and mismatch probe (PM and MM) values of these data, and examine the variance-mean relationship with probe-level data from probes believed to be defective, and so delivering noise only. We explain why we need to normalize the arrays to one another using probe level intensities. We then examine the behavior of the PM and MM using spike-in data and assess three commonly used summary measures: Affymetrix's (i) average difference (AvDiff) and (ii) MAS 5.0 signal, and (iii) the Li and Wong multiplicative model-based expression index (MBEI). The exploratory data analyses of the probe level data motivate a new summary measure that is a robust multi-array average (RMA) of background-adjusted, normalized, and log-transformed PM values. We evaluate the four expression summary measures using the dilution study data, assessing their behavior in terms of bias, variance and (for MBEI and RMA) model fit. Finally, we evaluate the algorithms in terms of their ability to detect known levels of differential expression using the spike-in data. We conclude that there is no obvious downside to using RMA and attaching a standard error (SE) to this quantity using a linear model which removes probe-specific affinities.},
  language = {eng},
  timestamp = {2016-02-23T06:23:56Z},
  number = {2},
  journal = {Biostatistics (Oxford, England)},
  author = {Irizarry, Rafael A. and Hobbs, Bridget and Collin, Francois and Beazer-Barclay, Yasmin D. and Antonellis, Kristen J. and Scherf, Uwe and Speed, Terence P.},
  month = apr,
  year = {2003},
  keywords = {Algorithms,Animals,Data Interpretation; Statistical,DNA Probes,Gene Expression Profiling,Humans,Linear Models,Mice,Normal Distribution,Oligonucleotide Array Sequence Analysis,Reproducibility of Results,Statistics; Nonparametric},
  pages = {249--264},
  pmid = {12925520}
}

@article{pham-dinh_structure_1995,
  title = {Structure of the {{Human Myelin}}/{{Oligodendrocyte Glycoprotein Gene}} and {{Multiple Alternative Spliced Isoforms}}},
  volume = {29},
  issn = {0888-7543},
  doi = {10.1006/geno.1995.9995},
  abstract = {Myelin/oligodendrocyte glycoprotein (MOG), a specific component of the central nervous system localized on the outermost lamellae of mature myelin, is a member of the immunoglobulin superfamily. We report here the organization of the humanMOGgene, which spans approximately 17 kb, and the characterization of six MOG mRNA splicing variants. The intron/exon structure of the humanMOGgene confirmed the splicing pattern, supporting the hypothesis that mRNA isoforms could arise by alternative splicing of a single gene. In addition to the eight exons coding for the major MOG isoform, the humanMOGgene also contains, in the 3\ensuremath{'} region, a previously unknown alternatively spliced coding exon, VIA. Alternative utilization of two acceptor splicing sites for exon VIII could produce two different C-termini. The nucleotide sequences presented here may be a useful tool to study further possible involvement of theMOGgene in hereditary neurological disorders.},
  timestamp = {2016-05-29T10:15:40Z},
  number = {2},
  urldate = {2016-05-29},
  journal = {Genomics},
  author = {Pham-Dinh, Danielle and DELLAGASPERA, BRUNO and KERLERODEROSBO, NICOLE and DAUTIGNY, ANDR{\'E}},
  month = sep,
  year = {1995},
  pages = {345--352}
}

@article{dougherty_disruption_2013,
  title = {The {{Disruption}} of {{Celf6}}, a {{Gene Identified}} by {{Translational Profiling}} of {{Serotonergic Neurons}}, {{Results}} in {{Autism-Related Behaviors}}},
  volume = {33},
  issn = {0270-6474, 1529-2401},
  doi = {10.1523/JNEUROSCI.4762-12.2013},
  abstract = {The immense molecular diversity of neurons challenges our ability to understand the genetic and cellular etiology of neuropsychiatric disorders. Leveraging knowledge from neurobiology may help parse the genetic complexity: identifying genes important for a circuit that mediates a particular symptom of a disease may help identify polymorphisms that contribute to risk for the disease as a whole. The serotonergic system has long been suspected in disorders that have symptoms of repetitive behaviors and resistance to change, including autism. We generated a bacTRAP mouse line to permit translational profiling of serotonergic neurons. From this, we identified several thousand serotonergic-cell expressed transcripts, of which 174 were highly enriched, including all known markers of these cells. Analysis of common variants near the corresponding genes in the AGRE collection implicated the RNA binding protein CELF6 in autism risk. Screening for rare variants in CELF6 identified an inherited premature stop codon in one of the probands. Subsequent disruption of Celf6 in mice resulted in animals exhibiting resistance to change and decreased ultrasonic vocalization as well as abnormal levels of serotonin in the brain. This work provides a reproducible and accurate method to profile serotonergic neurons under a variety of conditions and suggests a novel paradigm for gaining information on the etiology of psychiatric disorders.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {7},
  urldate = {2014-10-21},
  journal = {The Journal of Neuroscience},
  author = {Dougherty, Joseph D. and Maloney, Susan E. and Wozniak, David F. and Rieger, Michael A. and Sonnenblick, Lisa and Coppola, Giovanni and Mahieu, Nathaniel G. and Zhang, Juliet and Cai, Jinlu and Patti, Gary J. and Abrahams, Brett S. and Geschwind, Daniel H. and Heintz, Nathaniel},
  month = feb,
  year = {2013},
  pages = {2732--2753},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/4Q9UQE45/2732.html:},
  pmid = {23407934}
}

@article{beura_normalizing_2016,
  title = {Normalizing the environment recapitulates adult human immune traits in laboratory mice},
  volume = {advance online publication},
  copyright = {\textcopyright{} 2016 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {0028-0836},
  doi = {10.1038/nature17655},
  abstract = {Our current understanding of immunology was largely defined in laboratory mice, partly because they are inbred and genetically homogeneous, can be genetically manipulated, allow kinetic tissue analyses to be carried out from the onset of disease, and permit the use of tractable disease models. Comparably reductionist experiments are neither technically nor ethically possible in humans. However, there is growing concern that laboratory mice do not reflect relevant aspects of the human immune system, which may account for failures to translate disease treatments from bench to bedside. Laboratory mice live in abnormally hygienic specific pathogen free (SPF) barrier facilities. Here we show that standard laboratory mouse husbandry has profound effects on the immune system and that environmental changes produce mice with immune systems closer to those of adult humans. Laboratory mice\textemdash{}like newborn, but not adult, humans\textemdash{}lack effector-differentiated and mucosally distributed memory T cells. These cell populations were present in free-living barn populations of feral mice and pet store mice with diverse microbial experience, and were induced in laboratory mice after co-housing with pet store mice, suggesting that the environment is involved in the induction of these cells. Altering the living conditions of mice profoundly affected the cellular composition of the innate and adaptive immune systems, resulted in global changes in blood cell gene expression to patterns that more closely reflected the immune signatures of adult humans rather than neonates, altered resistance to infection, and influenced T-cell differentiation in response to a de novo viral infection. These data highlight the effects of environment on the basal immune state and response to infection and suggest that restoring physiological microbial exposure in laboratory mice could provide a relevant tool for modelling immunological events in free-living organisms, including humans.},
  language = {en},
  timestamp = {2016-04-20T20:54:23Z},
  urldate = {2016-04-20},
  journal = {Nature},
  author = {Beura, Lalit K. and Hamilton, Sara E. and Bi, Kevin and Schenkel, Jason M. and Odumade, Oludare A. and Casey, Kerry A. and Thompson, Emily A. and Fraser, Kathryn A. and Rosato, Pamela C. and Filali-Mouhim, Ali and Sekaly, Rafick P. and Jenkins, Marc K. and Vezys, Vaiva and Haining, W. Nicholas and Jameson, Stephen C. and Masopust, David},
  month = apr,
  year = {2016}
}

@article{aumann_environmental_2013,
  title = {Environmental and behavioral modulation of the number of substantia nigra dopamine neurons in adult mice},
  volume = {3},
  issn = {2162-3279},
  doi = {10.1002/brb3.163},
  abstract = {Background
Recent evidence indicates that hypothalamic neurons acquire or lose the capacity to synthesize and release dopamine (DA) in response to environmental stimuli, and this has functional and behavioral consequences for adult rats. We have evidence that neuronal activity, including that driven by afferent input, regulates acquisition and loss of the DA phenotype by substantia nigra pars compacta (SNc) neurons in adult mice., Hypotheses The aims of the present study were to determine whether the environment or behavior regulates the number of SNc DA neurons in adult mice, and whether this is mediated by afferent input.

Methods
Adult mice were subject to two different environments/behaviors: ``mating'' for 1 week or ``environment enrichment'' (EE) for 2 weeks; then the numbers of tyrosine hydroxylase (TH, the rate limiting enzyme in DA synthesis) immunopositive (TH+) and immunonegative (TH-) SNc neurons were counted.

Results
More TH+ neurons were present in mated males whereas less TH+ neurons were present in mated females. Also, more TH+ neurons were present in EE males, and this increase was completely abolished by concurrent local infusion of GABAA receptor antagonists.

Conclusions
The number of DA neurons in the adult SNc is not fixed, but readily increases and decreases in response to environmental stimuli and/or behaviors. These changes are mediated by afferent input relaying information about the environment or behavior to SNc neurons.},
  timestamp = {2015-10-27T00:44:11Z},
  number = {6},
  urldate = {2015-10-27},
  journal = {Brain and Behavior},
  author = {Aumann, Tim D and Tomas, Doris and Horne, Malcolm K},
  month = nov,
  year = {2013},
  pages = {617--625},
  pmid = {24363965},
  pmcid = {PMC3868167}
}

@article{kang_spatio-temporal_2011,
  title = {Spatio-temporal transcriptome of the human brain},
  volume = {478},
  copyright = {\textcopyright{} 2011 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {0028-0836},
  doi = {10.1038/nature10523},
  abstract = {Brain development and function depend on the precise regulation of gene expression. However, our understanding of the complexity and dynamics of the transcriptome of the human brain is incomplete. Here we report the generation and analysis of exon-level transcriptome and associated genotyping data, representing males and females of different ethnicities, from multiple brain regions and neocortical areas of developing and adult post-mortem human brains. We found that 86 per cent of the genes analysed were expressed, and that 90 per cent of these were differentially regulated at the whole-transcript or exon level across brain regions and/or time. The majority of these spatio-temporal differences were detected before birth, with subsequent increases in the similarity among regional transcriptomes. The transcriptome is organized into distinct co-expression networks, and shows sex-biased gene expression and exon usage. We also profiled trajectories of genes associated with neurobiological categories and diseases, and identified associations between single nucleotide polymorphisms and gene expression. This study provides a comprehensive data set on the human brain transcriptome and insights into the transcriptional foundations of human neurodevelopment.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {7370},
  urldate = {2015-08-06},
  journal = {Nature},
  author = {Kang, Hyo Jung and Kawasawa, Yuka Imamura and Cheng, Feng and Zhu, Ying and Xu, Xuming and Li, Mingfeng and Sousa, Andr{\'e} M. M. and Pletikos, Mihovil and Meyer, Kyle A. and Sedmak, Goran and Guennel, Tobias and Shin, Yurae and Johnson, Matthew B. and Krsnik, {\v Z}eljka and Mayer, Simone and Fertuzinhos, Sofia and Umlauf, Sheila and Lisgo, Steven N. and Vortmeyer, Alexander and Weinberger, Daniel R. and Mane, Shrikant and Hyde, Thomas M. and Huttner, Anita and Reimers, Mark and Kleinman, Joel E. and {\v S}estan, Nenad},
  month = oct,
  year = {2011},
  keywords = {neuroscience},
  pages = {483--489}
}

@article{ye_fgf_1998,
  title = {{{FGF}} and {{Shh Signals Control Dopaminergic}} and {{Serotonergic Cell Fate}} in the {{Anterior Neural Plate}}},
  volume = {93},
  issn = {0092-8674},
  doi = {10.1016/S0092-8674(00)81437-3},
  abstract = {During development, distinct classes of neurons are specified in precise locations along the dorso\textendash{}ventral and anterior\textendash{}posterior axes of the neural tube. We provide evidence that intersections of Shh, which is expressed along the ventral neural tube, and FGF8, which is locally produced at the mid/hindbrain boundary and in the rostral forebrain, create induction sites for dopaminergic neurons in the midbrain and forebrain. The same intersection, when preceded by a third signal, FGF4, which is expressed in the primitive streak, defines an inductive center for hindbrain 5-HT neurons. These findings illustrate that cell patterning in the neural plate is a multistep process in which early inducers, which initially divide the neural plate into crude compartments, are replaced by multiple local organizing centers, which specify distinct neuronal cell types within these compartments.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {5},
  urldate = {2014-11-19},
  journal = {Cell},
  author = {Ye, Weilan and Shimamura, Kenji and Rubenstein, John L. R and Hynes, Mary A and Rosenthal, Arnon},
  month = may,
  year = {1998},
  keywords = {Htr1a},
  pages = {755--766},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/QPC8U4KT/S0092867400814373.html:}
}

@article{shen-orr_cell_2010-1,
  title = {Cell type\textendash{}specific gene expression differences in complex tissues},
  volume = {7},
  copyright = {\textcopyright{} 2010 Nature Publishing Group},
  issn = {1548-7091},
  doi = {10.1038/nmeth.1439},
  abstract = {We describe cell type\textendash{}specific significance analysis of microarrays (csSAM) for analyzing differential gene expression for each cell type in a biological sample from microarray data and relative cell-type frequencies. First, we validated csSAM with predesigned mixtures and then applied it to whole-blood gene expression datasets from stable post-transplant kidney transplant recipients and those experiencing acute transplant rejection, which revealed hundreds of differentially expressed genes that were otherwise undetectable.},
  language = {en},
  timestamp = {2015-08-18T01:45:53Z},
  number = {4},
  urldate = {2015-08-18},
  journal = {Nature Methods},
  author = {Shen-Orr, Shai S. and Tibshirani, Robert and Khatri, Purvesh and Bodian, Dale L. and Staedtler, Frank and Perry, Nicholas M. and Hastie, Trevor and Sarwal, Minnie M. and Davis, Mark M. and Butte, Atul J.},
  month = apr,
  year = {2010},
  pages = {287--289}
}

@article{kang_embryonic_2011,
  title = {Embryonic and induced pluripotent stem cell staining and sorting with the live-cell fluorescence imaging probe {{CDy1}}},
  volume = {6},
  copyright = {\textcopyright{} 2011 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1754-2189},
  doi = {10.1038/nprot.2011.350},
  abstract = {Detecting and isolating specific types of cells is crucial to understanding a variety of biological processes, including development, aging, regeneration and pathogenesis; this understanding, in turn, allows the use of cells for therapeutic purposes, for which stem cells have emerged recently as invaluable materials. The current methods of isolation and characterization of stem cells depend on cell morphology in culture or on immunostaining of specific markers. These methods are, however, time consuming and involve the use of antibodies that may often make the cells unsuitable for further study. We recently developed a fluorescent small molecule named CDy1 (compound of designation yellow 1) that selectively stains live embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs). This protocol describes detailed procedures for staining ESC and iPSC in live conditions and for fluorescence-activated cell sorting (FACS) of ESC using CDy1. Cell staining, image acquisition and FACS can be done within 6 h.},
  language = {en},
  timestamp = {2016-03-16T06:27:31Z},
  number = {7},
  urldate = {2016-03-16},
  journal = {Nature Protocols},
  author = {Kang, Nam-Young and Yun, Seong-Wook and Ha, Hyung-Ho and Park, Sung-Jin and Chang, Young-Tae},
  month = jun,
  year = {2011},
  keywords = {Flow Cytometry,Fluorescence imaging,Pluripotent stem cells},
  pages = {1044--1052}
}

@article{hegde_concise_2000,
  title = {A concise guide to {{cDNA}} microarray analysis},
  volume = {29},
  issn = {0736-6205},
  abstract = {Microarray expression analysis has become one of the most widely used functional genomics tools. Efficient application of this technique requires the development of robust and reproducible protocols. We have optimized all aspects of the process, including PCR amplification of target cDNA clones, microarray printing, probe labeling and hybridization, and have developed strategies for data normalization and analysis.},
  language = {eng},
  timestamp = {2016-02-13T03:49:59Z},
  number = {3},
  journal = {BioTechniques},
  author = {Hegde, P. and Qi, R. and Abernathy, K. and Gay, C. and Dharap, S. and Gaspard, R. and Hughes, J. E. and Snesrud, E. and Lee, N. and Quackenbush, J.},
  month = sep,
  year = {2000},
  keywords = {DNA; Complementary,Humans,Nucleic Acid Hybridization,Oligonucleotide Array Sequence Analysis,Polymerase Chain Reaction,RNA Probes},
  pages = {548--550, 552--554, 556 passim},
  pmid = {10997270}
}

@article{novikova_early_2006,
  title = {Early signs of neuronal apoptosis in the substantia nigra pars compacta of the progressive neurodegenerative mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid model of {{Parkinson}}'s disease},
  volume = {140},
  issn = {0306-4522},
  doi = {10.1016/j.neuroscience.2006.02.007},
  abstract = {Parkinson's disease is associated with a progressive loss of substantia nigra pars compacta dopaminergic neurons. The cellular and molecular mechanisms underlying Parkinson's disease neurodegeneration have not been fully determined. Clinical investigations and subacute in vivo studies using the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine have generated some observations suggesting that apoptosis is involved in neurodegeneration; however, this view remains equivocal. In this study, the substantia nigra pars compacta neurodegenerative process was examined in the chronic mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid model of Parkinson's disease treated with 10 doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (25 mg/kg) and probenecid (250 mg/kg) over five weeks. One day after chronic treatment, numerous terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling-positive cells were detected specifically in the substantia nigra pars compacta displaying shrunken volume, chromatin condensation, and DNA fragmentation. The number of apoptotic cells declined over time. No terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling-positive cells were found in untreated or probenecid-treated control animals. Cytomorphometric analysis of substantia nigra pars compacta nuclear loci revealed eccentric nucleoli dislocation and vesicular degranulation in all of the apoptotic neurons for the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid model for Parkinson's disease. The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling-positive cells phenotypically showed neuronal origin (NeuN-positive) with a loss of tyrosine hydroxylase immunoreactivity. While the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling-positive cells were not co-localized with astroglial (GFAP-positive) cells, some apoptotic cells were clearly associated with the activated microglial (macrophage antigen complex-1 and isolectin B4-positive) cells suggesting an active process of dead cell removal. In the one-day and seven-day post-treated mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid model for Parkinson's disease, marked depression of tyrosine hydroxylase immunoreactivity in the substantia nigra pars compacta and striatum was observed, which was correlated with significant reductions of striatal dopamine content and uptake. These results suggest that initial neuronal apoptosis and morphological changes are involved, at least in part, in the chronic neurodegeneration of mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid model for Parkinson's disease.},
  timestamp = {2015-08-27T18:55:09Z},
  number = {1},
  urldate = {2015-08-26},
  journal = {Neuroscience},
  author = {Novikova, L. and Garris, B. L. and Garris, D. R. and Lau, Y. -S.},
  year = {2006},
  keywords = {chronic parkinsonian mouse,dopaminergic neurodegeneration,microglial activation,neuroapoptosis,TUNEL,Tyrosine hydroxylase},
  pages = {67--76}
}

@article{schmitt_is_2008,
  title = {Is {{Brain Banking}} of {{Psychiatric Cases Valuable}} for {{Neurobiological Research}}?},
  volume = {63},
  issn = {1807-5932},
  abstract = {It is widely accepted that neurobiological abnormalities underlie the symptoms of psychiatric disorders such as schizophrenia and unipolar or bipolar affective disorders. New molecular methods, computer-assisted quantification techniques and neurobiological investigation methods that can be applied to the human brain are all used in post-mortem investigations of psychiatric disorders. The following article describes modern quantitative methods and recent post-mortem findings in schizophrenia and affective disorders. Using our brain bank as an example, necessary considerations of modern brain banking are addressed such as ethical considerations, clinical work-up, preparation techniques and the organization of a brain bank, the value of modern brain banking for investigations of psychiatric disorders is summarized.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2015-08-06},
  journal = {Clinics (Sao Paulo, Brazil)},
  author = {Schmitt, Andrea and Parlapani, Eleni and Bauer, Manfred and Heinsen, Helmut and Falkai, Peter},
  month = apr,
  year = {2008},
  pages = {255--266},
  pmid = {18438581},
  pmcid = {PMC2664212}
}

@article{melchitzky_tyrosine_2000,
  title = {Tyrosine {{Hydroxylase}}- and {{Dopamine Transporter-Immunoreactive Axons}} in the {{Primate Cerebellum}}},
  volume = {22},
  copyright = {\textcopyright{} 2000 Nature Publishing Group},
  issn = {0893-133X},
  doi = {10.1016/S0893-133X(99)00139-6},
  abstract = {The cerebellum seems to play a critical role in many motor and cognitive functions, including those that are disturbed in schizophrenia. Although dopamine is known to influence the motor or cognitive functions mediated by other brain regions and to play a role in the pathophysiology of schizophrenia, the cerebellum has not been thought to be a target of dopamine-containing axons. However, given recent reports of dopamine receptors in the cerebellum, we sought to determine whether axons immunoreactive for the proteins involved in dopamine synthesis and reuptake are present in the cerebellum of macaque monkeys. We found that axons immunoreactive for the dopamine membrane transporter, a specific marker of dopamine axons, were present in high density, but only in certain lobules of the cerebellar vermis. In addition, these axons were found principally in the granule cell layer, where they densely arborized immediately subjacent to the Purkinje cells. Similarly, axons labeled for tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis, were also present in high density in the granule cell layer of the same lobules of the vermis. In contrast, axons immunoreactive for dopamine beta-hydroxylase, a marker of noradrenergic axons, exhibited a different and more widespread pattern of innervation. These findings are consistent with a dopamine innervation of the primate cerebellum that is both lobular- and laminar-specific, and they suggest that dopamine may play a role in certain cerebellar functions.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {5},
  urldate = {2014-11-04},
  journal = {Neuropsychopharmacology},
  author = {Melchitzky, Darlene S. and Lewis, David A.},
  month = may,
  year = {2000},
  keywords = {Cerebellar vermis,Dopamine-beta-hydroxylase,Monkey,Purkinje cells,Schizophrenia},
  pages = {466--472},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/BBE8X79G/1395463a.html:}
}

@article{tan_neuron-enriched_2013-2,
  title = {Neuron-enriched gene expression patterns are regionally anti-correlated with oligodendrocyte-enriched patterns in the adult mouse and human brain},
  volume = {7},
  doi = {10.3389/fnins.2013.00005},
  abstract = {An important goal in neuroscience is to understand gene expression patterns in the brain. The recent availability of comprehensive and detailed expression atlases for mouse and human creates opportunities to discover global patterns and perform cross-species comparisons. Recently we reported that the major source of variation in gene transcript expression in the adult normal mouse brain can be parsimoniously explained as reflecting regional variation in glia to neuron ratios, and is correlated with degree of connectivity and location in the brain along the anterior-posterior axis. Here we extend this investigation to two gene expression assays of adult normal human brains that consisted of over 300 brain region samples, and perform comparative analyses of brain-wide expression patterns to the mouse. We performed principal components analysis (PCA) on the regional gene expression of the adult human brain to identify the expression pattern that has the largest variance. As in the mouse, we observed that the first principal component is composed of two anti-correlated patterns enriched in oligodendrocyte and neuron markers respectively. However, we also observed interesting discordant patterns between the two species. For example, a few mouse neuron markers show expression patterns that are more correlated with the human oligodendrocyte-enriched pattern and vice-versa. In conclusion, our work provides insights into human brain function and evolution by probing global relationships between regional cell type marker expression patterns in the human and mouse brain.},
  timestamp = {2016-05-09T23:52:03Z},
  urldate = {2016-05-09},
  journal = {Neurogenomics},
  author = {Tan, Powell Patrick Cheng and French, Leon and Pavlidis, Paul},
  year = {2013},
  keywords = {cell type,evolution,gene expression pattern,glia,neuron,transcriptome},
  pages = {5}
}

@article{hendricks_ets_1999,
  title = {The {{ETS Domain Factor Pet}}-1 {{Is}} an {{Early}} and {{Precise Marker}} of {{Central Serotonin Neurons}} and {{Interacts}} with a {{Conserved Element}} in {{Serotonergic Genes}}},
  volume = {19},
  issn = {0270-6474, 1529-2401},
  abstract = {Serotonin (5-HT) plays a crucial neuromodulatory role in numerous physiological and behavioral functions, and dysfunction of the serotonergic system has been implicated in several psychiatric disorders. Despite the widespread importance of the central serotonergic neurotransmitter system, little is known about the molecular mechanisms controlling the development of 5-HT neurons. We previously identified an ETS domain transcription factor, Pet-1, that is expressed in a small number of tissues, including the brain. Here, we show that expression of Pet-1 RNA in the brain is restricted to, and marks, the entire rostrocaudal extent of rat serotonergic hindbrain raphe nuclei. Remarkably, Pet-1 RNA colocalizes with tryptophan hydroxylase-positive neurons in raphe nuclei but not with their nonserotonergic neuron or non-neuronal neighbors. Pet-1 RNA is limited to two domains in the developing hindbrain, which precedes the appearance of 5-HT in each domain by approximately a half day. Conserved Pet-1 binding sites are present in or near the promoter regions of the human and mouse 5-HT1a receptor, serotonin transporter, tryptophan hydroxylase, and aromatic l-amino acid decarboxylase genes whose expression is characteristic of the serotonergic neuron phenotype. These sites are capable of supporting transcriptional activation through interactions with the Pet-1 ETS domain and can function as enhancers. Together, our findings establish Pet-1 as an early and precise marker of 5-HT neurons and suggest that it functions specifically in the differentiation and maintenance of these neurons.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {23},
  urldate = {2014-11-18},
  journal = {The Journal of Neuroscience},
  author = {Hendricks, Timothy and Francis, Nicole and Fyodorov, Dmitry and Deneris, Evan S.},
  month = jan,
  year = {1999},
  keywords = {binding site,ETS factor,Fev,neurotransmitter phenotype,Pet-1,raphe nuclei,serotonin,transcription},
  pages = {10348--10356},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/9XRBHHZR/10348.html:},
  pmid = {10575032}
}

@article{zoubarev_gemma_2012,
  title = {Gemma: a resource for the reuse, sharing and meta-analysis of expression profiling data},
  volume = {28},
  issn = {1367-4811},
  shorttitle = {Gemma},
  doi = {10.1093/bioinformatics/bts430},
  abstract = {Gemma is a database, analysis software system and web site for genomics data re-use and meta-analysis. Currently, Gemma contains analyzed data from over 3300 expression profiling studies, yielding hundreds of millions of differential expression results and coexpression patterns (correlated expression) for retrieval and visualization. With optional registration users can save their own data and securely share it with other users. Web services and integration with third-party resources further increase the scope of the tools, which include a Cytoscape plugin.
AVAILABILITY: http://chibi.ubc.ca/Gemma, Apache 2.0 license.},
  language = {eng},
  timestamp = {2016-02-16T00:49:46Z},
  number = {17},
  journal = {Bioinformatics (Oxford, England)},
  author = {Zoubarev, Anton and Hamer, Kelsey M. and Keshav, Kiran D. and McCarthy, E. Luke and Santos, Joseph Roy C. and {Van Rossum}, Thea and McDonald, Cameron and Hall, Adam and Wan, Xiang and Lim, Raymond and Gillis, Jesse and Pavlidis, Paul},
  month = sep,
  year = {2012},
  keywords = {Database Management Systems,Databases; Genetic,Gene Expression Profiling,Genomics,Meta-Analysis as Topic,Software},
  pages = {2272--2273},
  pmid = {22782548},
  pmcid = {PMC3426847}
}

@article{torrey_stanley_2000,
  title = {The {{Stanley Foundation}} brain collection and {{Neuropathology Consortium}}},
  volume = {44},
  issn = {0920-9964},
  doi = {10.1016/S0920-9964(99)00192-9},
  abstract = {The Stanley Foundation brain collection is an attempt to supplement existing brain collections for the purpose of promoting research on schizophrenia and bipolar disorder. Specimens are collected with the permission of the families in a standardized manner, with half of each specimen being frozen and half fixed in formalin. The Neuropathology Consortium is a subset of 60 specimens from the collection, well-matched groups of 15 each with diagnoses of schizophrenia, bipolar disorder, major depressive disorder without psychotic features, and normal controls. More than 75 000 sections and blocks from the Consortium have been sent to over 50 research groups worldwide to carry out a wide variety of assessments. These data will be integrated to provide a more complete picture of the neuropathology of these disorders.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2015-08-06},
  journal = {Schizophrenia Research},
  author = {Torrey, E. Fuller and Webster, Maree and Knable, Michael and Johnston, Nancy and Yolken, Robert H.},
  month = aug,
  year = {2000},
  keywords = {bipolar disorder,Brain bank,depression,Neuropathology,Schizophrenia},
  pages = {151--155}
}

@article{eisen_cluster_1998,
  title = {Cluster {{Analysis}} and {{Display}} of {{Genome-Wide Expression Patterns}}},
  volume = {95},
  issn = {0027-8424},
  abstract = {A system of cluster analysis for genome-wide expression data from DNA microarray hybridization is described that uses standard statistical algorithms to arrange genes according to similarity in pattern of gene expression. The output is displayed graphically, conveying the clustering and the underlying expression data simultaneously in a form intuitive for biologists. We have found in the budding yeast Saccharomyces cerevisiae that clustering gene expression data groups together efficiently genes of known similar function, and we find a similar tendency in human data. Thus patterns seen in genome-wide expression experiments can be interpreted as indications of the status of cellular processes. Also, coexpression of genes of known function with poorly characterized or novel genes may provide a simple means of gaining leads to the functions of many genes for which information is not available currently.},
  timestamp = {2016-03-16T01:54:40Z},
  number = {25},
  urldate = {2016-03-16},
  journal = {Proceedings of the National Academy of Sciences of the United States of America},
  author = {Eisen, Michael B. and Spellman, Paul T. and Brown, Patrick O. and Botstein, David},
  year = {1998},
  pages = {14863--14868}
}

@misc{_filevon_????,
  title = {File:{{Von Miller}} ({{Broncos}}).{{JPG}}},
  copyright = {Creative Commons Attribution-ShareAlike License},
  shorttitle = {File},
  language = {en},
  timestamp = {2016-02-10T06:47:31Z},
  urldate = {2016-02-10},
  journal = {Wikipedia, the free encyclopedia},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/6EG3NZJW/FileVon_Miller_(Broncos).html:}
}

@article{kaplan_neuronal_2014,
  title = {Neuronal {{Matrix Metalloproteinase}}-9 {{Is}} a {{Determinant}} of {{Selective Neurodegeneration}}},
  volume = {81},
  issn = {0896-6273},
  doi = {10.1016/j.neuron.2013.12.009},
  abstract = {Summary
Selective neuronal loss is the hallmark of neurodegenerative diseases. In patients with amyotrophic lateral sclerosis (ALS), most motor neurons die but those innervating extraocular, pelvic sphincter, and slow limb muscles exhibit selective resistance. We identified 18 genes that show \&gt;10-fold differential expression between resistant and vulnerable motor neurons. One of these, matrix metalloproteinase-9 (MMP-9), is expressed only by fast motor neurons, which are selectively vulnerable. In ALS model mice expressing mutant superoxide dismutase (SOD1), reduction of MMP-9 function using gene ablation, viral gene therapy, or pharmacological inhibition significantly delayed muscle denervation. In the presence of mutant SOD1, MMP-9 expressed by fast motor neurons themselves enhances activation of ER stress and is sufficient to trigger axonal die-back. These findings define MMP-9 as a candidate therapeutic target for ALS. The molecular basis of neuronal diversity thus provides significant insights into mechanisms of selective vulnerability to neurodegeneration.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-10-21},
  journal = {Neuron},
  author = {Kaplan, Artem and Spiller, Krista~J. and Towne, Christopher and Kanning, Kevin~C. and Choe, Ginn~T. and Geber, Adam and Akay, Turgay and Aebischer, Patrick and Henderson, Christopher~E.},
  month = jan,
  year = {2014},
  pages = {333--348},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/I73EP8JW/S0896627313011392.html:}
}

@incollection{oberdick_analysis_2013,
  title = {Analysis of {{Gene Networks}} in {{Cerebellar Development}}},
  copyright = {\textcopyright{}2013 Springer Science+Business Media Dordrecht},
  isbn = {978-94-007-1332-1 978-94-007-1333-8},
  abstract = {The purpose of this chapter is to provide a brief overview of the major gene networks that control cerebellum development. To simplify this task, all developmental control genes relevant to the cerebellum have been grouped into four categories based on 13 spontaneous mouse mutations with cerebellar developmental defects and for which the aberrant gene has been identified. These categories include genetic switch genes and genes for morphogenesis, physiology, and metabolism. Three distinct gene targetome studies are discussed in order to introduce some signature networks of major importance to cerebellum development based on the genetic switches En2, Atoh1 (Math1), and Rora (ROR\ensuremath{\alpha}). Similarly, array approaches have begun to reveal gene expression changes due to mutations in physiology and metabolism genes, such as Kcnj6 (Girk2) and Agtpbp1 (Nna1), respectively. These studies are revealing the interplay between transcription, morphogenetic factors, physiology, and metabolism during development. Lastly, genomics and informatics approaches are uncovering new markers of all cerebellar cell types at all stages that will be useful in the future for further clarifying the complex and often reciprocal nature of developmental mechanisms in the nervous system.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2014-11-08},
  booktitle = {Handbook of the {{Cerebellum}} and {{Cerebellar Disorders}}},
  publisher = {{Springer Netherlands}},
  author = {Oberdick, Dr John},
  editor = {Manto, Mario and Schmahmann, Jeremy D. and Rossi, Ferdinando and Gruol, Donna L. and Koibuchi, Noriyuki},
  month = jan,
  year = {2013},
  keywords = {Human Physiology,Neurobiology,Neurochemistry,Neurology,Neurosciences,Neurosurgery},
  pages = {127--145},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/3MVKE68P/10.html:}
}

@article{stolt_sox9_2003,
  title = {The {{Sox9}} transcription factor determines glial fate choice in the developing spinal cord},
  volume = {17},
  issn = {0890-9369, 1549-5477},
  doi = {10.1101/gad.259003},
  abstract = {The mechanism that causes neural stem cells in the central nervous system to switch from neurogenesis to gliogenesis is poorly understood. Here we analyzed spinal cord development of mice in which the transcription factor Sox9 was specifically ablated from neural stem cells by the CRE/loxP recombination system. These mice exhibit defects in the specification of oligodendrocytes and astrocytes, the two main types of glial cells in the central nervous system. Accompanying an early dramatic reduction in progenitors of the myelin-forming oligodendrocytes, there was a transient increase in motoneurons. Oligodendrocyte progenitor numbers recovered at later stages of development, probably owing to compensatory actions of the related Sox10 and Sox8, both of which overlap with Sox9 in the oligodendrocyte lineage. In agreement, compound loss of Sox9 and Sox10 led to a further decrease in oligodendrocyte progenitors. Astrocyte numbers were also severely reduced in the absence of Sox9 and did not recover at later stages of spinal cord development. Taking the common origin of motoneurons and oligodendrocytes as well as V2 interneurons and some astrocytes into account, stem cells apparently fail to switch from neurogenesis to gliogenesis in at least two domains of the ventricular zone, indicating that Sox9 is a major molecular component of the neuron\textendash{}glia switch in the developing spinal cord.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {13},
  urldate = {2014-11-18},
  journal = {Genes \& Development},
  author = {Stolt, C. Claus and Lommes, Petra and Sock, Elisabeth and Chaboissier, Marie-Christine and Schedl, Andreas and Wegner, Michael},
  month = jan,
  year = {2003},
  keywords = {astrocyte,HMG-box,neural stem cell,oligodendrocyte,Sox10,Sry},
  pages = {1677--1689},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/DZIFDMFW/1677.html:},
  pmid = {12842915}
}

@article{redwine_markers_2002,
  title = {Markers of central nervous system glia and neurons in vivo during normal and pathological conditions},
  volume = {265},
  issn = {0070-217X},
  language = {eng},
  timestamp = {2015-08-13T22:18:44Z},
  journal = {Current Topics in Microbiology and Immunology},
  author = {Redwine, J. M. and Evans, C. F.},
  year = {2002},
  keywords = {Animals,Biological Markers,Central Nervous System,Humans,Neuroglia,Neurons},
  pages = {119--140},
  pmid = {12014186}
}

@article{sofroniew_astrocytes_2010,
  title = {Astrocytes: biology and pathology},
  volume = {119},
  issn = {0001-6322},
  shorttitle = {Astrocytes},
  doi = {10.1007/s00401-009-0619-8},
  abstract = {Astrocytes are specialized glial cells that outnumber neurons by over fivefold. They contiguously tile the entire central nervous system (CNS) and exert many essential complex functions in the healthy CNS. Astrocytes respond to all forms of CNS insults through a process referred to as reactive astrogliosis, which has become a pathological hallmark of CNS structural lesions. Substantial progress has been made recently in determining functions and mechanisms of reactive astrogliosis and in identifying roles of astrocytes in CNS disorders and pathologies. A vast molecular arsenal at the disposal of reactive astrocytes is being defined. Transgenic mouse models are dissecting specific aspects of reactive astrocytosis and glial scar formation in vivo. Astrocyte involvement in specific clinicopathological entities is being defined. It is now clear that reactive astrogliosis is not a simple all-or-none phenomenon but is a finely gradated continuum of changes that occur in context-dependent manners regulated by specific signaling events. These changes range from reversible alterations in gene expression and cell hypertrophy with preservation of cellular domains and tissue structure, to long-lasting scar formation with rearrangement of tissue structure. Increasing evidence points towards the potential of reactive astrogliosis to play either primary or contributing roles in CNS disorders via loss of normal astrocyte functions or gain of abnormal effects. This article reviews (1) astrocyte functions in healthy CNS, (2) mechanisms and functions of reactive astrogliosis and glial scar formation, and (3) ways in which reactive astrocytes may cause or contribute to specific CNS disorders and lesions.},
  timestamp = {2016-03-15T00:15:47Z},
  number = {1},
  urldate = {2016-03-15},
  journal = {Acta Neuropathologica},
  author = {Sofroniew, Michael V. and Vinters, Harry V.},
  month = jan,
  year = {2010},
  pages = {7--35},
  pmid = {20012068},
  pmcid = {PMC2799634}
}

@article{biagioli_unexpected_2009,
  title = {Unexpected expression of \ensuremath{\alpha}- and \ensuremath{\beta}-globin in mesencephalic dopaminergic neurons and glial cells},
  volume = {106},
  issn = {0027-8424, 1091-6490},
  doi = {10.1073/pnas.0813216106},
  abstract = {The mesencephalic dopaminergic (mDA) cell system is composed of two major groups of projecting cells in the substantia nigra (SN) (A9 neurons) and the ventral tegmental area (VTA) (A10 cells). A9 neurons form the nigrostriatal pathway and are involved in regulating voluntary movements and postural reflexes. Their selective degeneration leads to Parkinson's disease. Here, we report that gene expression analysis of A9 dopaminergic neurons (DA) identifies transcripts for \ensuremath{\alpha}- and \ensuremath{\beta}-chains of hemoglobin (Hb). Globin immunoreactivity decorates the majority of A9 DA, a subpopulation of cortical and hippocampal astrocytes and mature oligodendrocytes. This pattern of expression was confirmed in different mouse strains and in rat and human. We show that Hb is expressed in the SN of human postmortem brain. By microarray analysis of dopaminergic cell lines overexpressing \ensuremath{\alpha}- and \ensuremath{\beta}-globin chains, changes in genes involved in O2 homeostasis and oxidative phopshorylation were observed, linking Hb expression to mitochondrial function. Our data suggest that the most famed oxygen-carrying globin is not exclusively restricted to the blood, but it may play a role in the normal physiology of the brain and neurodegenerative diseases.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {36},
  urldate = {2014-11-14},
  journal = {Proceedings of the National Academy of Sciences},
  author = {Biagioli, Marta and Pinto, Milena and Cesselli, Daniela and Zaninello, Marta and Lazarevic, Dejan and Roncaglia, Paola and Simone, Roberto and Vlachouli, Christina and Plessy, Charles and Bertin, Nicolas and Beltrami, Antonio and Kobayashi, Kazuto and Gallo, Vittorio and Santoro, Claudio and Ferrer, Isidro and Rivella, Stefano and Beltrami, Carlo Alberto and Carninci, Piero and Raviola, Elio and Gustincich, Stefano},
  month = aug,
  year = {2009},
  keywords = {astrocytes,hemoglobin,oligodendrocytes,oxidative phosphorylation,Parkinson},
  pages = {15454--15459},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/35FJJDTX/15454.html:},
  pmid = {19717439}
}

@article{krey_knockout_2015,
  title = {Knockout of silent information regulator 2 ({{SIRT2}}) preserves neurological function after experimental stroke in mice},
  copyright = {\textcopyright{} 2015 Nature Publishing Group},
  issn = {0271-678X},
  doi = {10.1038/jcbfm.2015.178},
  abstract = {Sirtuin-2 (Sirt2) is a member of the NAD+-dependent protein deacetylase family. Various members of the sirtuin class have been found to be involved in processes related to longevity, regulation of inflammation, and neuroprotection. Induction of Sirt2 mRNA was found in the whole hemisphere after experimental stroke in a recent screening approach. Moreover, Sirt2 protein is highly expressed in myelin-rich brain regions after stroke. To examine the effects of Sirt2 on ischemic stroke, we induced transient focal cerebral ischemia in adult male Sirt2-knockout and wild-type mice. Two stroke models with different occlusion times were applied: a severe ischemia (45 minutes of middle cerebral artery occlusion (MCAO)) and a mild one (15 minutes of MCAO), which was used to focus on subcortical infarcts. Neurological deficit was determined at 48 hours after 45 minutes of MCAO, and up to 7 days after induction of 15 minutes of cerebral ischemia. In contrast to recent data on Sirt1, Sirt2-/- mice showed less neurological deficits in both models of experimental stroke, with the strongest manifestation after 48 hours of reperfusion. However, we did not observe a significant difference of stroke volumes or inflammatory cell count between Sirt2-deficient and wild-type mice. Thus we postulate that Sirt2 mediates myelin-dependent neuronal dysfunction during the early phase after ischemic stroke.},
  language = {en},
  timestamp = {2015-08-17T19:08:31Z},
  urldate = {2015-08-17},
  journal = {Journal of Cerebral Blood Flow \& Metabolism},
  author = {Krey, Lea and L{\"u}hder, Fred and Kusch, Kathrin and Czech-Zechmeister, Bozena and K{\"o}nnecke, Birte and Outeiro, Tiago Fleming and Trendelenburg, George},
  month = jul,
  year = {2015},
  keywords = {cerebral ischemia,inflammasome,Inflammation,sirtuin,stroke}
}

@article{handley_designing_2015,
  title = {Designing {{Cell-Type-Specific Genome}}-wide {{Experiments}}},
  volume = {58},
  issn = {1097-2765},
  doi = {10.1016/j.molcel.2015.04.024},
  abstract = {Multicellular organisms depend on cell-type-specific division of labor for survival. Specific cell types have their unique developmental program and respond differently to environmental challenges, yet are orchestrated by the same genetic blueprint. A key challenge in biology is thus to understand how genes are expressed in the right place, at the right time, and to the right level. Further, this exquisite control of gene expression is perturbed in many diseases. As a consequence, coordinated physiological responses to the environment are compromised. Recently, innovative tools have been developed that are able to capture genome-wide gene expression using cell-type-specific approaches. These novel techniques allow us to understand gene regulation in~vivo with unprecedented resolution and give us mechanistic insights into how multicellular organisms adapt to changing environments. In this article, we discuss the considerations needed when designing your own cell-type-specific experiment from the isolation of your starting material through selecting the appropriate controls and validating the data.},
  timestamp = {2016-05-09T22:36:06Z},
  number = {4},
  urldate = {2016-05-09},
  journal = {Molecular Cell},
  author = {Handley, Ava and Schauer, Tam{\'a}s and Ladurner, Andreas~G. and Margulies, Carla~E.},
  month = may,
  year = {2015},
  pages = {621--631}
}

@article{whitney_individuality_2003,
  title = {Individuality and variation in gene expression patterns in human blood},
  volume = {100},
  issn = {0027-8424, 1091-6490},
  doi = {10.1073/pnas.252784499},
  abstract = {The nature and extent of interindividual and temporal variation in gene expression patterns in specific cells and tissues is an important and relatively unexplored issue in human biology. We surveyed variation in gene expression patterns in peripheral blood from 75 healthy volunteers by using cDNA microarrays. Characterization of the variation in gene expression in healthy tissue is an essential foundation for the recognition and interpretation of the changes in these patterns associated with infections and other diseases, and peripheral blood was selected because it is a uniquely accessible tissue in which to examine this variation in patients or healthy volunteers in a clinical setting. Specific features of interindividual variation in gene expression patterns in peripheral blood could be traced to variation in the relative proportions of specific blood cell subsets; other features were correlated with gender, age, and the time of day at which the sample was taken. An analysis of multiple sequential samples from the same individuals allowed us to discern donor-specific patterns of gene expression. These data help to define human individuality and provide a database with which disease-associated gene expression patterns can be compared.},
  language = {en},
  timestamp = {2015-08-18T01:02:10Z},
  number = {4},
  urldate = {2015-08-18},
  journal = {Proceedings of the National Academy of Sciences},
  author = {Whitney, Adeline R. and Diehn, Maximilian and Popper, Stephen J. and Alizadeh, Ash A. and Boldrick, Jennifer C. and Relman, David A. and Brown, Patrick O.},
  month = feb,
  year = {2003},
  pages = {1896--1901},
  pmid = {12578971}
}

@article{chikina_cellcode_2015,
  title = {{{CellCODE}}: {{A}} robust latent variable approach to differential expression analysis for heterogeneous cell populations},
  issn = {1367-4803, 1460-2059},
  shorttitle = {{{CellCODE}}},
  doi = {10.1093/bioinformatics/btv015},
  abstract = {Motivation: Identifying alterations in gene expression associated with different clinical states is important for the study of human biology. However, clinical samples used in gene expression studies are often derived from heterogeneous mixtures with variable cell-type composition, complicating statistical analysis. Considerable effort has been devoted to modeling sample heterogeneity, and presently there are many methods that can estimate cell proportions or pure cell- type expression from mixture data. However, there is no method that comprehensively addresses mixture analysis in the context of differential expression without relying on additional proportion information, which can be inaccurate and is frequently unavailable.
Results: In this study we consider a clinically relevant situation where neither accurate proportion estimates nor pure cell expression is of direct interest, but where we are rather interested in detecting and interpreting relevant differential expression in mixture samples. We develop a method, cell-type COmputational Differential Estimation (CellCODE), that addresses the specific statistical question directly, without requiring a physical model for mixture components. Our approach is based on latent variable analysis and is computationally transparent, requires no additional experimental data, yet outperforms existing methods that use independent proportion measurements. CellCODE has few parameters that are robust and easy to interpret. The method can be used to track changes in proportion, improve power to detect differential expression and assign the differentially expressed genes to the correct cell-type.
Availability: The CellCODE R package can be downloaded at http://www.pitt.edu/\textasciitilde{}mchikina/CellCODE/ or installed from the GitHub repository ``mchikina/CellCODE''
Contact: mchikina@pitt.edu},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2015-02-05},
  journal = {Bioinformatics},
  author = {Chikina, Maria and Zaslavsky, Elena and Sealfon, Stuart C.},
  month = jan,
  year = {2015},
  pages = {btv015},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/9NB6FED4/bioinformatics.html:},
  pmid = {25583121}
}

@article{metidji_ifn-/_2015,
  title = {{{IFN}}-\ensuremath{\alpha}/\ensuremath{\beta} {{Receptor Signaling Promotes Regulatory T Cell Development}} and {{Function}} under {{Stress Conditions}}},
  volume = {194},
  issn = {0022-1767, 1550-6606},
  doi = {10.4049/jimmunol.1500036},
  abstract = {Type I IFNs are a family of cytokines with antiviral and immunomodulatory properties. Although the antiviral effects of IFNs are well characterized, their immunomodulatory properties are less clear. To specifically address the effects of type I IFNs on T regulatory cells (Tregs), we studied mixed bone marrow chimeras between wild-type and IFN-\ensuremath{\alpha}/\ensuremath{\beta} receptor (IFNAR) knockout (KO) mice, and heterozygous female mice expressing a Treg-specific deletion of the IFNAR. In these two models, IFNAR signaling promotes the development of the Treg lineage in the thymus and their survival in the periphery. IFNAR KO Tregs had a higher expression of the proapoptotic gene Bim and higher frequency of active caspase-positive cells. IFNAR KO Tregs from chimeric mice displayed a more naive phenotype, accompanied by lower levels of CD25 and phosphorylated STAT5. Therefore, in Tregs, IFNAR signaling may directly or indirectly affect phosphorylation of STAT5. In mixed chimeras with Scurfy fetal liver, Tregs derived from IFNAR KO bone marrow were unable to control T effector cell activation and tissue inflammation. Under stress conditions or in a competitive environment, IFNAR signaling may be required to maintain Treg homeostasis and function.},
  language = {en},
  timestamp = {2015-08-17T19:31:06Z},
  number = {9},
  urldate = {2015-08-17},
  journal = {The Journal of Immunology},
  author = {Metidji, Amina and Rieder, Sadiye Amcaoglu and Glass, Deborah Dacek and Cremer, Isabelle and Punkosdy, George A. and Shevach, Ethan M.},
  month = jan,
  year = {2015},
  pages = {4265--4276},
  pmid = {25795758}
}

@article{sugino_cell-type-specific_2014,
  title = {Cell-{{Type-Specific Repression}} by {{Methyl-CpG-Binding Protein}} 2 {{Is Biased}} toward {{Long Genes}}},
  volume = {34},
  issn = {0270-6474, 1529-2401},
  doi = {10.1523/JNEUROSCI.2674-14.2014},
  abstract = {Mutations in methyl-CpG-binding protein 2 (MeCP2) cause Rett syndrome and related autism spectrum disorders (Amir et al., 1999). MeCP2 is believed to be required for proper regulation of brain gene expression, but prior microarray studies in Mecp2 knock-out mice using brain tissue homogenates have revealed only subtle changes in gene expression (Tudor et al., 2002; Nuber et al., 2005; Jordan et al., 2007; Chahrour et al., 2008). Here, by profiling discrete subtypes of neurons we uncovered more dramatic effects of MeCP2 on gene expression, overcoming the ``dilution problem'' associated with assaying homogenates of complex tissues. The results reveal misregulation of genes involved in neuronal connectivity and communication. Importantly, genes upregulated following loss of MeCP2 are biased toward longer genes but this is not true for downregulated genes, suggesting MeCP2 may selectively repress long genes. Because genes involved in neuronal connectivity and communication, such as cell adhesion and cell\textendash{}cell signaling genes, are enriched among longer genes, their misregulation following loss of MeCP2 suggests a possible etiology for altered circuit function in Rett syndrome.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {38},
  urldate = {2014-11-05},
  journal = {The Journal of Neuroscience},
  author = {Sugino, Ken and Hempel, Chris M. and Okaty, Benjamin W. and Arnson, Hannah A. and Kato, Saori and Dani, Vardhan S. and Nelson, Sacha B.},
  month = sep,
  year = {2014},
  keywords = {cell adhesion,MeCP2,microarray,Rett syndrome},
  pages = {12877--12883},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/4UWSARIX/12877.html:},
  pmid = {25232122}
}

@article{dopico_widespread_2015,
  title = {Widespread seasonal gene expression reveals annual differences in human immunity and physiology},
  volume = {6},
  copyright = {\textcopyright{} 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  doi = {10.1038/ncomms8000},
  abstract = {Seasonal variations are rarely considered a contributing component to human tissue function or health, although many diseases and physiological process display annual periodicities. Here we find more than 4,000 protein-coding mRNAs in white blood cells and adipose tissue to have seasonal expression profiles, with inverted patterns observed between Europe and Oceania. We also find the cellular composition of blood to vary by season, and these changes, which differ between the United Kingdom and The Gambia, could explain the gene expression periodicity. With regards to tissue function, the immune system has a profound pro-inflammatory transcriptomic profile during European winter, with increased levels of soluble IL-6 receptor and C-reactive protein, risk biomarkers for cardiovascular, psychiatric and autoimmune diseases that have peak incidences in winter. Circannual rhythms thus require further exploration as contributors to various aspects of human physiology and disease.},
  language = {en},
  timestamp = {2015-08-17T18:18:55Z},
  urldate = {2015-08-17},
  journal = {Nature Communications},
  author = {Dopico, Xaquin Castro and Evangelou, Marina and Ferreira, Ricardo C. and Guo, Hui and Pekalski, Marcin L. and Smyth, Deborah J. and Cooper, Nicholas and Burren, Oliver S. and Fulford, Anthony J. and Hennig, Branwen J. and Prentice, Andrew M. and Ziegler, Anette-G. and Bonifacio, Ezio and Wallace, Chris and Todd, John A.},
  month = may,
  year = {2015},
  keywords = {Biological sciences,Genetics,Medical research}
}

@article{paul_developmental_2012,
  title = {Developmental coordination of gene expression between synaptic partners during {{GABAergic}} circuit assembly in cerebellar cortex},
  volume = {6},
  doi = {10.3389/fncir.2012.00037},
  abstract = {The assembly of neural circuits involves multiple sequential steps such as the specification of cell-types, their migration to proper brain locations, morphological and physiological differentiation, and the formation and maturation of synaptic connections. This intricate and often prolonged process is guided by elaborate genetic mechanisms that regulate each step. Evidence from numerous systems suggests that each cell-type, once specified, is endowed with a genetic program that unfolds in response to, and is regulated by, extrinsic signals, including cell\textendash{}cell and synaptic interactions. To a large extent, the execution of this intrinsic program is achieved by the expression of specific sets of genes that support distinct developmental processes. Therefore, a comprehensive analysis of the developmental progression of gene expression in synaptic partners of neurons may provide a basis for exploring the genetic mechanisms regulating circuit assembly. Here we examined the developmental gene expression profiles of well-defined cell-types in a stereotyped microcircuit of the cerebellar cortex. We found that the transcriptomes of Purkinje cell and stellate/basket cells are highly dynamic throughout postnatal development. We revealed ``phasic expression'' of transcription factors, ion channels, receptors, cell adhesion molecules, gap junction proteins, and identified distinct molecular pathways that might contribute to sequential steps of cerebellar inhibitory circuit formation. We further revealed a correlation between genomic clustering and developmental co-expression of hundreds of transcripts, suggesting the involvement of chromatin level gene regulation during circuit formation.},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2014-10-21},
  journal = {Frontiers in Neural Circuits},
  author = {Paul, Anirban and Cai, Ying and Atwal, Gurinder Singh and Huang, Z. Josh},
  year = {2012},
  keywords = {cerebellum,circuit assembly,development,GABAergic,gene expression,microcircuit,Purkinje cell,stellate basket cell},
  pages = {37}
}

@article{lyons_novel_2010,
  title = {Novel expression signatures identified by transcriptional analysis of separated leucocyte subsets in systemic lupus erythematosus and vasculitis},
  volume = {69},
  issn = {1468-2060},
  doi = {10.1136/ard.2009.108043},
  abstract = {OBJECTIVE: To optimise a strategy for identifying gene expression signatures differentiating systemic lupus erythematosus (SLE) and antineutrophil cytoplasmic antibody-associated vasculitis that provide insight into disease pathogenesis and identify biomarkers.
METHODS: 44 vasculitis patients, 13 SLE patients and 25 age and sex-matched controls were enrolled. CD4 and CD8 T cells, B cells, monocytes and neutrophils were isolated from each patient and, together with unseparated peripheral blood mononuclear cells (PBMC), were hybridised to spotted oligonucleotide microarrays.
RESULTS: Using expression data obtained from purified cells a substantial number of differentially expressed genes were identified that were not detectable in the analysis of PBMC. Analysis of purified T cells identified a SLE-associated, CD4 T-cell signature consistent with type 1 interferon signalling driving the generation and survival of tissue homing T cells and thereby contributing to disease pathogenesis. Moreover, hierarchical clustering using expression data from purified monocytes provided significantly improved discrimination between the patient groups than that obtained using PBMC data, presumably because the differentially expressed genes reflect genuine differences in processes underlying disease pathogenesis.
CONCLUSION: Analysis of leucocyte subsets enabled the identification of gene signatures of both pathogenic relevance and with better disease discrimination than those identified in PBMC. This approach thus provides substantial advantages in the search for diagnostic and prognostic biomarkers in autoimmune disease.},
  language = {eng},
  timestamp = {2015-08-13T22:58:44Z},
  number = {6},
  journal = {Annals of the Rheumatic Diseases},
  author = {Lyons, Paul A. and McKinney, Eoin F. and Rayner, Tim F. and Hatton, Alexander and Woffendin, Hayley B. and Koukoulaki, Maria and Freeman, Thomas C. and Jayne, David R. W. and Chaudhry, Afzal N. and Smith, Kenneth G. C.},
  month = jun,
  year = {2010},
  keywords = {Adult,Aged,Aged; 80 and over,Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis,CD4-Positive T-Lymphocytes,Diagnosis; Differential,Female,gene expression,Gene Expression Profiling,Humans,Leukocytes,Lupus Erythematosus; Systemic,Lymphocyte Activation,Male,Middle Aged,Monocytes,Oligonucleotide Array Sequence Analysis,Prognosis,Severity of Illness Index,T-Lymphocyte Subsets,Transcription; Genetic,Young Adult},
  pages = {1208--1213},
  pmid = {19815495},
  pmcid = {PMC2935323}
}

@article{prieto_human_2008,
  title = {Human {{Gene Coexpression Landscape}}: {{Confident Network Derived}} from {{Tissue Transcriptomic Profiles}}},
  volume = {3},
  shorttitle = {Human {{Gene Coexpression Landscape}}},
  doi = {10.1371/journal.pone.0003911},
  abstract = {Background
Analysis of gene expression data using genome-wide microarrays is a technique often used in genomic studies to find coexpression patterns and locate groups of co-transcribed genes. However, most studies done at global ``omic'' scale are not focused on human samples and when they correspond to human very often include heterogeneous datasets, mixing normal with disease-altered samples. Moreover, the technical noise present in genome-wide expression microarrays is another well reported problem that many times is not addressed with robust statistical methods, and the estimation of errors in the data is not provided.

Methodology/Principal Findings
Human genome-wide expression data from a controlled set of normal-healthy tissues is used to build a confident human gene coexpression network avoiding both pathological and technical noise. To achieve this we describe a new method that combines several statistical and computational strategies: robust normalization and expression signal calculation; correlation coefficients obtained by parametric and non-parametric methods; random cross-validations; and estimation of the statistical accuracy and coverage of the data. All these methods provide a series of coexpression datasets where the level of error is measured and can be tuned. To define the errors, the rates of true positives are calculated by assignment to biological pathways. The results provide a confident human gene coexpression network that includes 3327 gene-nodes and 15841 coexpression-links and a comparative analysis shows good improvement over previously published datasets. Further functional analysis of a subset core network, validated by two independent methods, shows coherent biological modules that share common transcription factors. The network reveals a map of coexpression clusters organized in well defined functional constellations. Two major regions in this network correspond to genes involved in nuclear and mitochondrial metabolism and investigations on their functional assignment indicate that more than 60\% are house-keeping and essential genes. The network displays new non-described gene associations and it allows the placement in a functional context of some unknown non-assigned genes based on their interactions with known gene families.

Conclusions/Significance
The identification of stable and reliable human gene to gene coexpression networks is essential to unravel the interactions and functional correlations between human genes at an omic scale. This work contributes to this aim, and we are making available for the scientific community the validated human gene coexpression networks obtained, to allow further analyses on the network or on some specific gene associations.
The data are available free online at http://bioinfow.dep.usal.es/coexpression/.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {12},
  urldate = {2014-10-28},
  journal = {PLoS ONE},
  author = {Prieto, Carlos and Risue{\~n}o, Alberto and Fontanillo, Celia and {De Las Rivas}, Javier},
  month = dec,
  year = {2008},
  pages = {e3911},
  file = {PLoS Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/36QH2DRW/infodoi10.1371journal.pone.html:}
}

@article{capurro_computational_2015,
  title = {Computational deconvolution of genome wide expression data from {{Parkinson}}'s and {{Huntington}}'s disease brain tissues using population-specific expression analysis},
  volume = {8},
  doi = {10.3389/fnins.2014.00441},
  abstract = {The characterization of molecular changes in diseased tissues gives insight into pathophysiological mechanisms and is important for therapeutic development. Genome-wide gene expression analysis has proven valuable for identifying biological processes in neurodegenerative diseases using post mortem human brain tissue and numerous datasets are publically available. However, many studies utilize heterogeneous tissue samples consisting of multiple cell types, all of which contribute to global gene expression values, confounding biological interpretation of the data. In particular, changes in numbers of neuronal and glial cells occurring in neurodegeneration confound transcriptomic analyses, particularly in human brain tissues where sample availability and controls are limited. To identify cell specific gene expression changes in neurodegenerative disease, we have applied our recently published computational deconvolution method, population specific expression analysis (PSEA). PSEA estimates cell-type-specific expression values using reference expression measures, which in the case of brain tissue comprises mRNAs with cell-type-specific expression in neurons, astrocytes, oligodendrocytes and microglia. As an exercise in PSEA implementation and hypothesis development regarding neurodegenerative diseases, we applied PSEA to Parkinson's and Huntington's disease (PD, HD) datasets. Genes identified as differentially expressed in substantia nigra pars compacta neurons by PSEA were validated using external laser capture microdissection data. Network analysis and Annotation Clustering (DAVID) identified molecular processes implicated by differential gene expression in specific cell types. The results of these analyses provided new insights into the implementation of PSEA in brain tissues and additional refinement of molecular signatures in human HD and PD.},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2015-01-14},
  journal = {Neurogenomics},
  author = {Capurro, Alberto and Bodea, Liviu-Gabriel and Schaefer, Patrick and Luthi-Carter, Ruth and Perreau, Victoria M.},
  year = {2015},
  keywords = {autophagy,computational deconvolution,Huntington's disease,microarray,Parkinson's disease,transcriptomic analysis},
  pages = {441}
}

@article{grange_cell-typebased_2014,
  title = {Cell-type\textendash{}based model explaining coexpression patterns of genes in the brain},
  volume = {111},
  issn = {0027-8424, 1091-6490},
  doi = {10.1073/pnas.1312098111},
  abstract = {Spatial patterns of gene expression in the vertebrate brain are not independent, as pairs of genes can exhibit complex patterns of coexpression. Two genes may be similarly expressed in one region, but differentially expressed in other regions. These correlations have been studied quantitatively, particularly for the Allen Atlas of the adult mouse brain, but their biological meaning remains obscure. We propose a simple model of the coexpression patterns in terms of spatial distributions of underlying cell types and establish its plausibility using independently measured cell-type\textendash{}specific transcriptomes. The model allows us to predict the spatial distribution of cell types in the mouse brain.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {14},
  urldate = {2014-10-15},
  journal = {Proceedings of the National Academy of Sciences},
  author = {Grange, Pascal and Bohland, Jason W. and Okaty, Benjamin W. and Sugino, Ken and Bokil, Hemant and Nelson, Sacha B. and Ng, Lydia and Hawrylycz, Michael and Mitra, Partha P.},
  month = aug,
  year = {2014},
  keywords = {bioinformatics,neuroanatomy,neuroscience},
  pages = {5397--5402},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/MNV8SN9C/5397.html:},
  pmid = {24706869}
}

@article{okaty_transcriptional_2009,
  title = {Transcriptional and electrophysiological maturation of neocortical fastspiking {{GABAergic}} interneurons},
  volume = {29},
  issn = {0270-6474},
  doi = {10.1523/JNEUROSCI.0105-09.2009},
  abstract = {Fast-spiking (FS) interneurons are important elements of neocortical circuitry that constitute the primary source of synaptic inhibition in adult cortex and impart temporal organization on ongoing cortical activity. The highly specialized intrinsic membrane and firing properties that allow cortical FS interneurons to perform these functions are due to equally specialized gene expression, which is ultimately coordinated by cell-type-specific transcriptional regulation. While embryonic transcriptional events govern the initial steps of cell-type specification in most cortical interneurons, including FS cells, the electrophysiological properties that distinguish adult cortical cell types emerge relatively late in postnatal development, and the transcriptional events that drive this maturational process are not known. To address this, we used mouse whole-genome microarrays and whole-cell patch clamp to characterize the transcriptional and electrophysiological maturation of cortical FS interneurons between postnatal day 7 (P7) and P40. We found that the intrinsic and synaptic physiology of FS cells undergoes profound regulation over the first four postnatal weeks, and that these changes are correlated with largely monotonic but bidirectional transcriptional regulation of thousands of genes belonging to multiple functional classes. Using our microarray screen as a guide, we discovered that upregulation of 2-pore K+ leak channels between P10 and P25 contributes to one of the major differences between the intrinsic membrane properties of immature and adult FS cells, and found a number of other candidate genes that likely confer cell-type specificity on mature FS cells.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {21},
  urldate = {2014-10-21},
  journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
  author = {Okaty, Benjamin W and Miller, Mark N and Sugino, Ken and Hempel, Chris M and Nelson, Sacha B},
  month = may,
  year = {2009},
  pages = {7040--7052},
  pmid = {19474331},
  pmcid = {PMC2749660}
}

@article{solga_rna-sequencing_2014,
  title = {{{RNA}}-sequencing reveals oligodendrocyte and neuronal transcripts in microglia relevant to central nervous system disease},
  issn = {1098-1136},
  doi = {10.1002/glia.22754},
  abstract = {Expression profiling of distinct central nervous system (CNS) cell populations has been employed to facilitate disease classification and to provide insights into the molecular basis of brain pathology. One important cell type implicated in a wide variety of CNS disease states is the resident brain macrophage (microglia). In these studies, microglia are often isolated from dissociated brain tissue by flow sorting procedures [fluorescence-activated cell sorting (FACS)] or from postnatal glial cultures by mechanic isolation. Given the highly dynamic and state-dependent functions of these cells, the use of FACS or short-term culture methods may not accurately capture the biology of brain microglia. In the current study, we performed RNA-sequencing using Cx3cr1(+/GFP) labeled microglia isolated from the brainstem of 6-week-old mice to compare the transcriptomes of FACS-sorted versus laser capture microdissection (LCM). While both isolation techniques resulted in a large number of shared (common) transcripts, we identified transcripts unique to FACS-isolated and LCM-captured microglia. In particular, \ensuremath{\sim}50\% of these LCM-isolated microglial transcripts represented genes typically associated with neurons and glia. While these transcripts clearly localized to microglia using complementary methods, they were not translated into protein. Following the induction of murine experimental autoimmune encephalomyelitis, increased oligodendrocyte and neuronal transcripts were detected in microglia, while only the myelin basic protein oligodendrocyte transcript was increased in microglia after traumatic brain injury. Collectively, these findings have implications for the design and interpretation of microglia transcriptome-based investigations. GLIA 2014.},
  language = {ENG},
  timestamp = {2015-08-13T22:18:44Z},
  journal = {Glia},
  author = {Solga, Anne C. and Pong, Winnie W. and Walker, Jason and Wylie, Todd and Magrini, Vincent and Apicelli, Anthony J. and Griffith, Malachi and Griffith, Obi L. and Kohsaka, Shinichi and Wu, Gregory F. and Brody, David L. and Mardis, Elaine R. and Gutmann, David H.},
  month = sep,
  year = {2014},
  pmid = {25258010}
}

@article{anderson_bipolar_2012,
  title = {Bipolar disorder},
  volume = {345},
  issn = {1756-1833},
  doi = {10.1136/bmj.e8508},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {dec27 3},
  urldate = {2014-12-16},
  journal = {BMJ},
  author = {Anderson, I. M. and Haddad, P. M. and Scott, J.},
  month = apr,
  year = {2012},
  pages = {e8508--e8508},
  file = {Bipolar disorder | The BMJ:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/6C44HSFV/bmj.e8508.html:}
}

@article{shay_conservation_2013-1,
  title = {Conservation and divergence in the transcriptional programs of the human and mouse immune systems},
  volume = {110},
  issn = {0027-8424},
  doi = {10.1073/pnas.1222738110},
  abstract = {Much of the knowledge about cell differentiation and function in the immune system has come from studies in mice, but the relevance to human immunology, diseases, and therapy has been challenged, perhaps more from anecdotal than comprehensive evidence. To this end, we compare two large compendia of transcriptional profiles of human and mouse immune cell types. Global transcription profiles are conserved between corresponding cell lineages. The expression patterns of most orthologous genes are conserved, particularly for lineage-specific genes. However, several hundred genes show clearly divergent expression across the examined cell lineages, and among them, 169 genes did so even with highly stringent criteria. Finally, regulatory mechanisms\textemdash{}reflected by regulators' differential expression or enriched cis-elements\textemdash{}are conserved between the species but to a lower degree, suggesting that distinct regulation may underlie some of the conserved transcriptional responses.},
  timestamp = {2016-03-27T09:12:05Z},
  number = {8},
  urldate = {2016-03-27},
  journal = {Proceedings of the National Academy of Sciences of the United States of America},
  author = {Shay, Tal and Jojic, Vladimir and Zuk, Or and Rothamel, Katherine and Puyraimond-Zemmour, David and Feng, Ting and Wakamatsu, Ei and Benoist, Christophe and Koller, Daphne and Regev, Aviv},
  month = feb,
  year = {2013},
  pages = {2946--2951},
  pmid = {23382184},
  pmcid = {PMC3581886}
}

@article{corral_markers_2001,
  title = {Markers in vertebrate neurogenesis},
  volume = {2},
  copyright = {\textcopyright{} 2001 Nature Publishing Group},
  issn = {1471-003X},
  doi = {10.1038/35097587},
  abstract = {Embryologists have long used morphological characteristics, and more recently marker genes, to identify neural tissue and to test the neural-inducing activity of specific cell populations and signalling molecules. These markers are also used to assess the function(s) of neural genes themselves. Progression from neural induction to terminal differentiation of neurons is a multistep process, and each step involves the activation and/or repression of genes that can be used as molecular markers for these different events. Here we briefly review these key steps in neurogenesis within the vertebrate central nervous system, and evaluate the markers used to define them. We emphasize the importance of cellular context and an understanding of gene function for interpreting the significance of marker genes.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {11},
  urldate = {2014-10-31},
  journal = {Nature Reviews Neuroscience},
  author = {{del Corral}, Ruth Diez and Storey, Kate G.},
  month = nov,
  year = {2001},
  pages = {835--839},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/2GI57FME/nrn1101-835a.html:}
}

@article{maycox_analysis_2009,
  title = {Analysis of gene expression in two large schizophrenia cohorts identifies multiple changes associated with nerve terminal function},
  volume = {14},
  issn = {1476-5578},
  doi = {10.1038/mp.2009.18},
  abstract = {Schizophrenia is a severe psychiatric disorder with a world-wide prevalence of 1\%. The pathophysiology of the illness is not understood, but is thought to have a strong genetic component with some environmental influences on aetiology. To gain further insight into disease mechanism, we used microarray technology to determine the expression of over 30 000 mRNA transcripts in post-mortem tissue from a brain region associated with the pathophysiology of the disease (Brodmann area 10: anterior prefrontal cortex) in 28 schizophrenic and 23 control patients. We then compared our study (Charing Cross Hospital prospective collection) with that of an independent prefrontal cortex dataset from the Harvard Brain Bank. We report the first direct comparison between two independent studies. A total of 51 gene expression changes have been identified that are common between the schizophrenia cohorts, and 49 show the same direction of disease-associated regulation. In particular, changes were observed in gene sets associated with synaptic vesicle recycling, transmitter release and cytoskeletal dynamics. This strongly suggests multiple, small but synergistic changes in gene expression that affect nerve terminal function.},
  language = {eng},
  timestamp = {2015-08-13T22:18:44Z},
  number = {12},
  journal = {Molecular Psychiatry},
  author = {Maycox, P. R. and Kelly, F. and Taylor, A. and Bates, S. and Reid, J. and Logendra, R. and Barnes, M. R. and Larminie, C. and Jones, N. and Lennon, M. and Davies, C. and Hagan, J. J. and Scorer, C. A. and Angelinetta, C. and Akbar, M. T. and Akbar, T. and Hirsch, S. and Mortimer, A. M. and Barnes, T. R. E. and {de Belleroche}, J.},
  month = dec,
  year = {2009},
  keywords = {Adult,Aged,Aged; 80 and over,Cohort Studies,Computational Biology,Confidence Intervals,Female,Gene Expression Profiling,Gene Expression Regulation,Humans,Male,Middle Aged,Nerve Endings,Oligonucleotide Array Sequence Analysis,Prefrontal Cortex,RNA; Messenger,Schizophrenia,Synapses},
  pages = {1083--1094},
  pmid = {19255580}
}

@incollection{ugrumov_chapter_2013,
  series = {A New Era of Catecholamines in the Laboratory and Clinic},
  title = {Chapter {{Four}} - {{Brain Neurons Partly Expressing Dopaminergic Phenotype}}: {{Location}}, {{Development}}, {{Functional Significance}}, and {{Regulation}}},
  volume = {68},
  shorttitle = {Chapter {{Four}} - {{Brain Neurons Partly Expressing Dopaminergic Phenotype}}},
  abstract = {In addition to catecholaminergic neurons possessing all the enzymes of catecholamine synthesis and the specific membrane transporters, neurons partly expressing the catecholaminergic phenotype have been found a quarter of a century ago. Most of them express individual enzymes of dopamine (DA) synthesis, tyrosine hydroxylase (TH), or aromatic l-amino acid decarboxylase (AADC), lacking the DA membrane transporter and the vesicular monoamine transporter, type 2. These so-called monoenzymatic neurons are widely distributed throughout the brain in ontogenesis and adulthood being in some brain regions even more numerous than dopaminergic (DA-ergic) neurons. Individual enzymes of DA synthesis are expressed in these neurons continuously or transiently in norm and pathology. It has been proven that monoenzymatic TH neurons and AADC neurons are capable of producing DA in cooperation. It means that l-3,4-dihydroxyphenylalanine (l-DOPA) synthesized from l-tyrosine in monoenzymatic TH neurons is transported to monoenzymatic AADC neurons for DA synthesis. Such cooperative synthesis of DA is considered as a compensatory reaction under a failure of DA-ergic neurons, for example, in neurodegenerative diseases like hyperprolactinemia and Parkinson's disease. Moreover, l-DOPA, produced in monoenzymatic TH neurons, is assumed to play a role of a neurotransmitter or neuromodulator affecting the target neurons via catecholamine receptors.

Thus, numerous widespread neurons expressing individual complementary enzymes of DA synthesis serve to produce DA in cooperation that is a compensatory reaction at failure of DA-ergic neurons.},
  timestamp = {2016-06-03T05:42:49Z},
  urldate = {2016-06-03},
  booktitle = {Advances in {{Pharmacology}}},
  publisher = {{Academic Press}},
  author = {Ugrumov, Michael V.},
  editor = {Eiden, Lee E.},
  year = {2013},
  keywords = {Adulthood,aromatic l-amino acid decarboxylase,Brain,development,Dopamine,hypothalamus,l-DOPA,Mammals,Striatum,Tyrosine hydroxylase},
  pages = {37--91},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/5IKEHQM5/B978012411512500004X.html:}
}

@article{januszyk_evaluating_2015,
  title = {Evaluating the {{Effect}} of {{Cell Culture}} on {{Gene Expression}} in {{Primary Tissue Samples Using Microfluidic-Based Single Cell Transcriptional Analysis}}},
  volume = {4},
  copyright = {http://creativecommons.org/licenses/by/3.0/},
  doi = {10.3390/microarrays4040540},
  abstract = {Significant transcriptional heterogeneity is an inherent property of complex tissues such as tumors and healing wounds. Traditional methods of high-throughput analysis rely on pooling gene expression data from hundreds of thousands of cells and reporting  a population-wide average that is unable to capture differences within distinct cell subsets. Recent advances in microfluidic technology have permitted the development of large-scale single cell analytic methods that overcome this limitation. The increased granularity afforded by such approaches allows us to answer the critical question of whether expansion in cell culture significantly alters the transcriptional characteristics of cells isolated from primary tissue. Here we examine an established population of human adipose-derived stem cells (ASCs) using a novel, microfluidic-based method for high-throughput transcriptional interrogation, coupled with advanced bioinformatic analysis, to evaluate the dynamics of single cell gene expression among primary, passage 0, and passage 1 stem cells. We find significant differences in the transcriptional profiles of cells from each group, as well as  a considerable shift in subpopulation dynamics as those subgroups better able to adhere and proliferate under these culture conditions gradually emerge as dominant. Taken together, these findings reinforce the importance of using primary or very early passage cells in future studies.},
  language = {en},
  timestamp = {2016-04-20T00:55:13Z},
  number = {4},
  urldate = {2016-04-20},
  journal = {Microarrays},
  author = {Januszyk, Michael and Rennert, Robert C. and Sorkin, Michael and Maan, Zeshaan N. and Wong, Lisa K. and Whittam, Alexander J. and Whitmore, Arnetha and Duscher, Dominik and Gurtner, Geoffrey C.},
  month = nov,
  year = {2015},
  keywords = {bioinformatics,Cell culture,gene expression,microfluidics,singe-cell,subpopulations,transcriptional analysis},
  pages = {540--550}
}

@article{fauser_disorganization_2013,
  title = {Disorganization of neocortical lamination in focal cortical dysplasia is brain-region dependent: evidence from layer-specific marker expression},
  volume = {1},
  issn = {2051-5960},
  shorttitle = {Disorganization of neocortical lamination in focal cortical dysplasia is brain-region dependent},
  doi = {10.1186/2051-5960-1-47},
  abstract = {Background
Focal cortical dysplasias (FCD) are local disturbances of neocortical architecture and a common cause of pharmaco-resistant focal epilepsy. Little is known about the pathomechanisms leading to architectural abnormalities associated with FCD.

Results
In the present study we compared 52 FCD cases originating from the frontal or temporal lobe with or without Ammon's horn sclerosis (AHS) with regard to structural and molecular differences. We applied layer-specific (ER81, ROR\ss{}, SMI32, TLE4) and interneuron (calbindin, parvalbumin) markers by means of immunohistochemistry, in situ hybridization (ISH), and real time RT-PCR and correlated our findings with clinical parameters. We found that: (1) Structural abnormalities were most prominent in layers III-VI including changed morphology of individual neurons or dispersion, blurring and thinning of layers. These alterations were most pronounced in isolated frontal FCD, whereas the most homogeneous group was FCD IIIa. (2) Numbers of calbindin- and parvalbumin-positive interneurons varied considerably within the different FCD groups, but were not generally reduced. A significant decrease was only found for calbindin-positive interneurons in frontal FCD, and for parvalbumin-positive interneurons in FCD IIIa. (3) Interestingly, FCD IIIa presented with significant changes in the numbers of calbindin- or TLE4-positive neurons when compared to isolated FCD or controls. (4) Correlations between clinical and cellular parameters strongly depended on FCD localisation and age of the patients.

Conclusions
In summary, our data suggest that late cortical development is disturbed in FCD, yet most likely by different causes depending on brain region, FCD type and FCD severity.},
  timestamp = {2015-12-21T20:19:41Z},
  urldate = {2015-12-21},
  journal = {Acta Neuropathologica Communications},
  author = {Fauser, Susanne and H{\"a}ussler, Ute and Donkels, Catharina and Huber, Susanne and Nakagawa, Julia and Prinz, Marco and Schulze-Bonhage, Andreas and Zentner, Josef and Haas, Carola A},
  month = aug,
  year = {2013},
  pages = {47},
  pmid = {24252438},
  pmcid = {PMC3893528}
}

@article{bellesi_effects_2013,
  title = {Effects of {{Sleep}} and {{Wake}} on {{Oligodendrocytes}} and {{Their Precursors}}},
  volume = {33},
  issn = {0270-6474, 1529-2401},
  doi = {10.1523/JNEUROSCI.5102-12.2013},
  abstract = {Previous studies of differential gene expression in sleep and wake pooled transcripts from all brain cells and showed that several genes expressed at higher levels during sleep are involved in the synthesis/maintenance of membranes in general and of myelin in particular, a surprising finding given the reported slow turnover of many myelin components. Other studies showed that oligodendrocyte precursor cells (OPCs) are responsible for the formation of new myelin in both the injured and the normal adult brain, and that glutamate released from neurons, via neuron\textendash{}OPC synapses, can inhibit OPC proliferation and affect their differentiation into myelin-forming oligodendrocytes. Because glutamatergic transmission is higher in wake than in sleep, we asked whether sleep and wake can affect oligodendrocytes and OPCs. Using the translating ribosome affinity purification technology combined with microarray analysis in mice, we obtained a genome-wide profiling of oligodendrocytes after sleep, spontaneous wake, and forced wake (acute sleep deprivation). We found that hundreds of transcripts being translated in oligodendrocytes are differentially expressed in sleep and wake: genes involved in phospholipid synthesis and myelination or promoting OPC proliferation are transcribed preferentially during sleep, while genes implicated in apoptosis, cellular stress response, and OPC differentiation are enriched in wake. We then confirmed through BrdU and other experiments that OPC proliferation doubles during sleep and positively correlates with time spent in REM sleep, whereas OPC differentiation is higher during wake. Thus, OPC proliferation and differentiation are not perfectly matched at any given circadian time but preferentially occur during sleep and wake, respectively.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {36},
  urldate = {2014-10-21},
  journal = {The Journal of Neuroscience},
  author = {Bellesi, Michele and Pfister-Genskow, Martha and Maret, Stephanie and Keles, Sunduz and Tononi, Giulio and Cirelli, Chiara},
  month = apr,
  year = {2013},
  pages = {14288--14300},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/F3ZG5WXR/14288.html:},
  pmid = {24005282}
}

@article{arlotta_neuronal_2005,
  title = {Neuronal {{Subtype-Specific Genes}} that {{Control Corticospinal Motor Neuron Development In Vivo}}},
  volume = {45},
  issn = {0896-6273},
  doi = {10.1016/j.neuron.2004.12.036},
  abstract = {Within the vertebrate nervous system, the presence of many different lineages of neurons and glia complicates the molecular characterization of single neuronal populations. In order to elucidate molecular mechanisms underlying the specification and development of corticospinal motor neurons (CSMN), we purified CSMN at distinct stages of development in vivo and compared their gene expression to two other pure populations of cortical projection neurons: callosal projection neurons and corticotectal projection neurons. We found genes that are potentially instructive for CSMN development, as well as genes that are excluded from CSMN and are restricted to other populations of neurons, even within the same cortical layer. Loss-of-function experiments in null mutant mice for Ctip2 (also known as Bcl11b), one of the newly characterized genes, demonstrate that it plays a critical role in the development of CSMN axonal projections to the spinal cord in vivo, confirming that we identified central genetic determinants of the CSMN population.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-10-21},
  journal = {Neuron},
  author = {Arlotta, Paola and Molyneaux, Bradley J. and Chen, Jinhui and Inoue, Jun and Kominami, Ryo and Macklis, Jeffrey D.},
  month = jan,
  year = {2005},
  pages = {207--221}
}

@article{parikshak_systems_2015,
  title = {Systems biology and gene networks in neurodevelopmental and neurodegenerative disorders},
  volume = {16},
  copyright = {\textcopyright{} 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1471-0056},
  doi = {10.1038/nrg3934},
  abstract = {Genetic and genomic approaches have implicated hundreds of genetic loci in neurodevelopmental disorders and neurodegeneration, but mechanistic understanding continues to lag behind the pace of gene discovery. Understanding the role of specific genetic variants in the brain involves dissecting a functional hierarchy that encompasses molecular pathways, diverse cell types, neural circuits and, ultimately, cognition and behaviour. With a focus on transcriptomics, this Review discusses how high-throughput molecular, integrative and network approaches inform disease biology by placing human genetics in a molecular systems and neurobiological context. We provide a framework for interpreting network biology studies and leveraging big genomics data sets in neurobiology.},
  language = {en},
  timestamp = {2016-02-01T07:52:47Z},
  number = {8},
  urldate = {2016-02-01},
  journal = {Nature Reviews Genetics},
  author = {Parikshak, Neelroop N. and Gandal, Michael J. and Geschwind, Daniel H.},
  month = aug,
  year = {2015},
  keywords = {Disease genetics,Diseases of the nervous system,Gene regulatory networks,Genetics of the nervous system,Neurodevelopmental disorders},
  pages = {441--458},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/ZH9VDATE/nrg3934.html:}
}

@article{annese_evidence_2013,
  title = {Evidence of oligodendrogliosis in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine ({{MPTP}})-induced {{Parkinsonism}}},
  volume = {39},
  copyright = {\textcopyright{} 2012 The Authors. Neuropathology and Applied Neurobiology \textcopyright{} 2012 British Neuropathological Society},
  issn = {1365-2990},
  doi = {10.1111/j.1365-2990.2012.01271.x},
  abstract = {V. Annese, C. Barcia, F. Ros-Bernal, A. G{\'o}mez, C. M. Ros, V. De Pablos, E. Fern{\'a}ndez-Villalba, M.-E. De Stefano and M. T. Herrero (2013) Neuropathology and Applied Neurobiology39, 132\textendash{}143 Evidence of oligodendrogliosis in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism Aims: Mice and nonhuman primates administered with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) represent elective experimental models of Parkinsonism, in which degeneration of the nigrostriatal dopaminergic pathway is associated with prominent neuroinflammation, characterized by activated microglia and astrocytes in both substantia nigra (SN) and striatum. To date, it is unknown whether oligodendrocytes play a role in these events. Methods: We performed a detailed qualitative and quantitative analysis of oligodendrocyte-associated changes induced by acute and chronic MPTP treatment, in the SN and striatum of mice and macaques respectively. Oligodendrocytes were immunolabelled by cell-specific markers and analysed by confocal microscopy. Results: In both experimental models, MPTP treatment induces an increase in oligodendrocyte cell number and average size, as well as in the total area occupied by this cell type per tissue section, accompanied by evident morphological changes. This multifaceted array of changes, herein referred to as oligodendrogliosis, significantly correlates with the reduction in the level of dopaminergic innervation to the striatum. Conclusions: This event, associated with early damage of the dopaminergic neurone axons and of the complex striatal circuits of which they are part, may result in an important, although neglected, aspect in the onset and progression of Parkinsonism.},
  language = {en},
  timestamp = {2016-06-03T05:45:39Z},
  number = {2},
  urldate = {2016-06-03},
  journal = {Neuropathology and Applied Neurobiology},
  author = {Annese, V. and Barcia, C. and Ros-Bernal, F. and G{\'o}mez, A. and Ros, C. M. and {De Pablos}, V. and Fern{\'a}ndez-Villalba, E. and {De Stefano}, M. E. and Herrero, M.-T.},
  month = feb,
  year = {2013},
  keywords = {glial response,MPTP,neurodegeneration,oligodendrocytes,Parkinson's disease},
  pages = {132--143},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/2WMW35AC/full.html:}
}

@article{tjaden_identifying_2002,
  title = {Identifying operons and untranslated regions of transcripts using {{Escherichia}} coli {{RNA}} expression analysis},
  volume = {18},
  issn = {1367-4803, 1460-2059},
  doi = {10.1093/bioinformatics/18.suppl_1.S337},
  abstract = {Microarrays traditionally have been used to assay the transcript expression of coding regions of genes. Here, we use Escherichia coli oligonucleotide microarrays to assay transcript expression of both open reading frames (ORFs) and intergenic regions. We then use hidden Markov models to analyse this expression data and estimate transcription boundaries of genes. This approach allows us to identify 5\ensuremath{'} untranslated regions (5\ensuremath{'} UTRs) of transcripts as well as genes that are likely to be operon members. The operon elements we identify correspond to documented operons with 99\% specificity and 63\% sensitivity. Similarly we find that our 5\ensuremath{'} UTR results accurately coincide with experimentally verified promoter regions for most genes.
Contact: tjaden@cs.washington.edu
Keywords: untranslated regions; operons; intergenic; microarrays; Escherichia coli.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {suppl 1},
  urldate = {2014-11-28},
  journal = {Bioinformatics},
  author = {Tjaden, Brian and Haynor, David R. and Stolyar, Sergey and Rosenow, Carsten and Kolker, Eugene},
  month = jan,
  year = {2002},
  pages = {S337--S344},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/W45H2B7D/S337.html:},
  pmid = {12169564}
}

@article{chan_emx1_2001,
  title = {Emx1 is a {{Marker}} for {{Pyramidal Neurons}} of the},
  volume = {11},
  issn = {1047-3211, 1460-2199},
  doi = {10.1093/cercor/11.12.1191},
  abstract = {The homeobox-containing gene, Emx1, a mouse homologue of Drosophila empty spiracles, is specifically expressed in the developing telencephalic cortex. It has been reported that Emx1 transcripts and the protein product are localized in most cells of the cerebral cortex during the process of proliferation, migration, differentiation and maturation. We provide evidence here, based on a multitude of experimental approaches in developing rats, in support of the hypothesis that the expression of this gene is restricted to pyramidal neurons. Specifically, we found that, similar to pyramidal neurons, cells expressing Emx1 are distributed in all cortical layers, except layer I. Using in situ hybridization and immunocytochemistry at the light and electron microscope levels, we have shown that the density, distribution, soma shape and ultrastructural features of these cells were identical to those of pyramidal neurons. Double-labelling experiments confirmed that the vast majority of Emx1-expressing cells also contained glutamate, a marker of pyramidal neurons. We also found that this gene is expressed by most glutamate-containing neurons in dissociated cortical cell cultures and the vast majority of cells in radially arranged clones of pyramidal cells in the cortices of chimeric mice. Thus, the homeobox gene Emx1 can be reliably used as a marker of the pyramidal cell lineage.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {12},
  urldate = {2014-11-05},
  journal = {Cerebral Cortex},
  author = {Chan, C.-H. and Godinho, L. N. and Thomaidou, D. and Tan, S.-S. and Gulisano, M. and Parnavelas, J. G.},
  month = jan,
  year = {2001},
  pages = {1191--1198},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/DQKCWHRG/1191.html:},
  pmid = {11709490}
}

@article{roost_keygenes_????,
  title = {{{KeyGenes}}, a {{Tool}} to {{Probe Tissue Differentiation Using}} a {{Human Fetal Transcriptional Atlas}}},
  issn = {2213-6711},
  doi = {10.1016/j.stemcr.2015.05.002},
  abstract = {Summary
Differentiated derivatives of human pluripotent stem cells in culture are generally phenotypically immature compared to their adult counterparts. Their identity is often difficult to determine with certainty because little is known about their human fetal equivalents in~vivo. Cellular identity and signaling pathways directing differentiation are usually determined by extrapolating information from either human adult tissue or model organisms, assuming conservation with humans. To resolve this, we generated a collection of human fetal transcriptional profiles at different developmental stages. Moreover, we developed an algorithm, KeyGenes, which uses this dataset to quantify the extent to which next-generation sequencing or microarray data resemble specific cell or tissue types in the human fetus. Using KeyGenes combined with the human fetal atlas, we identified multiple cell and tissue samples unambiguously on a limited set of features. We thus provide a flexible and expandable platform to monitor and evaluate the efficiency of differentiation in~vitro.},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2015-06-06},
  journal = {Stem Cell Reports},
  author = {Roost, Matthias~S. and van~Iperen, Liesbeth and Ariyurek, Yavuz and Buermans, Henk~P. and Arindrarto, Wibowo and Devalla, Harsha~D. and Passier, Robert and Mummery, Christine~L. and Carlotti, Fran{\c c}oise and de~Koning, Eelco~J. P. and van~Zwet, Erik~W. and Goeman, Jelle~J. and Chuva~de~Sousa~Lopes, Susana~M.},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/S3STGPER/S2213671115001319.html:}
}

@article{hoegg-beiler_disrupting_2014,
  title = {Disrupting {{MLC1}} and {{GlialCAM}} and {{ClC}}-2 interactions in leukodystrophy entails glial chloride channel dysfunction},
  volume = {5},
  copyright = {\textcopyright{} 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights                 Reserved.},
  doi = {10.1038/ncomms4475},
  abstract = {Defects in the astrocytic membrane protein MLC1, the adhesion molecule GlialCAM or the chloride channel ClC-2 underlie human leukoencephalopathies. Whereas GlialCAM binds ClC-2 and MLC1, and modifies ClC-2 currents in vitro, no functional connections between MLC1 and ClC-2 are known. Here we investigate this by generating loss-of-function Glialcam and Mlc1 mouse models manifesting myelin vacuolization. We find that ClC-2 is unnecessary for MLC1 and GlialCAM localization in brain, whereas GlialCAM is important for targeting MLC1 and ClC-2 to specialized glial domains in vivo and for modifying ClC-2's biophysical properties specifically in oligodendrocytes (OLs), the cells chiefly affected by vacuolization. Unexpectedly, MLC1 is crucial for proper localization of GlialCAM and ClC-2, and for changing ClC-2 currents. Our data unmask an unforeseen functional relationship between MLC1 and ClC-2 in vivo, which is probably mediated by GlialCAM, and suggest that ClC-2 participates in the pathogenesis of megalencephalic leukoencephalopathy with subcortical cysts.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2014-11-20},
  journal = {Nature Communications},
  author = {Hoegg-Beiler, Maja B. and Sirisi, S{\`o}nia and Orozco, Ian J. and Ferrer, Isidre and Hohensee, Svea and Auberson, Muriel and G{\"o}dde, Kathrin and Vilches, Clara and {de Heredia}, Miguel L{\'o}pez and Nunes, Virginia and Est{\'e}vez, Ra{\'u}l and Jentsch, Thomas J.},
  month = mar,
  year = {2014},
  keywords = {Biological sciences,neuroscience},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/VN832RJI/ncomms4475.html:}
}

@article{mardinly_sensory_2016,
  title = {Sensory experience regulates cortical inhibition by inducing {{IGF1}} in {{VIP}} neurons},
  volume = {531},
  copyright = {\textcopyright{} 2016 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {0028-0836},
  doi = {10.1038/nature17187},
  abstract = {Inhibitory neurons regulate the adaptation of neural circuits to sensory experience, but the molecular mechanisms by which experience controls the connectivity between different types of inhibitory neuron to regulate cortical plasticity are largely unknown. Here we show that exposure of dark-housed mice to light induces a gene program in cortical vasoactive intestinal peptide (VIP)-expressing neurons that is markedly distinct from that induced in excitatory neurons and other subtypes of inhibitory neuron. We identify Igf1 as one of several activity-regulated genes that are specific to VIP neurons, and demonstrate that IGF1 functions cell-autonomously in VIP neurons to increase inhibitory synaptic input onto these neurons. Our findings further suggest that in cortical VIP neurons, experience-dependent gene transcription regulates visual acuity by activating the expression of IGF1, thus promoting the inhibition of disinhibitory neurons and affecting inhibition onto cortical pyramidal neurons.},
  language = {en},
  timestamp = {2016-04-08T18:45:43Z},
  number = {7594},
  urldate = {2016-04-08},
  journal = {Nature},
  author = {Mardinly, A. R. and Spiegel, I. and Patrizi, A. and Centofante, E. and Bazinet, J. E. and Tzeng, C. P. and Mandel-Brehm, C. and Harmin, D. A. and Adesnik, H. and Fagiolini, M. and Greenberg, M. E.},
  month = mar,
  year = {2016},
  keywords = {Neural circuits,Neurotrophic factors,synaptic plasticity,Visual system},
  pages = {371--375}
}

@article{zhang_purification_2016,
  title = {Purification and {{Characterization}} of {{Progenitor}} and {{Mature Human Astrocytes Reveals Transcriptional}} and {{Functional Differences}} with {{Mouse}}},
  volume = {89},
  issn = {0896-6273},
  doi = {10.1016/j.neuron.2015.11.013},
  language = {English},
  timestamp = {2016-05-09T23:50:18Z},
  number = {1},
  urldate = {2016-05-09},
  journal = {Neuron},
  author = {Zhang, Ye and Sloan, Steven A. and Clarke, Laura E. and Caneda, Christine and Plaza, Colton A. and Blumenthal, Paul D. and Vogel, Hannes and Steinberg, Gary K. and Edwards, Michael S. B. and Li, Gordon and Duncan, John A. and Cheshier, Samuel H. and Shuer, Lawrence M. and Chang, Edward F. and Grant, Gerald A. and Gephart, Melanie G. Hayden and Barres, Ben A.},
  month = jan,
  year = {2016},
  pages = {37--53},
  pmid = {26687838, 26687838}
}

@article{sauvageot_molecular_2002,
  title = {Molecular mechanisms controlling cortical gliogenesis},
  volume = {12},
  issn = {0959-4388},
  doi = {10.1016/S0959-4388(02)00322-7},
  abstract = {The sequential appearance of neurons and glia in the vertebrate central nervous system may be governed by competition between growth factor signaling pathways and downstream transcription factors. In cortical progenitor cell cultures, the proneural basic helix\textendash{}loop\textendash{}helix transcription factor Ngn1 suppresses formation of astrocytes by sequestering coactivator proteins that are required by signal transducers and activators of transcription for the expression of astrocyte-specific genes. In the developing neural tube, combinatorial interactions between the proneural transcription factor Ngn2 and the basic helix\textendash{}loop\textendash{}helix transcription factor Olig2 specify the formation of motor neurons or oligodendrocytes.},
  timestamp = {2016-06-07T05:11:00Z},
  number = {3},
  urldate = {2016-06-07},
  journal = {Current Opinion in Neurobiology},
  author = {Sauvageot, Claire M and Stiles, Charles D},
  month = jun,
  year = {2002},
  keywords = {astrocytes,CBP/p300,Gliogenesis,growth factors,Ngn1,Olig,oligodendrocytes,STAT,Transcription Factors},
  pages = {244--249}
}

@article{spruston_pyramidal_2008,
  title = {Pyramidal neurons: dendritic structure and synaptic integration},
  volume = {9},
  copyright = {\textcopyright{} 2008 Nature Publishing Group},
  issn = {1471-003X},
  shorttitle = {Pyramidal neurons},
  doi = {10.1038/nrn2286},
  abstract = {Pyramidal neurons are characterized by their distinct apical and basal dendritic trees and the pyramidal shape of their soma. They are found in several regions of the CNS and, although the reasons for their abundance remain unclear, functional studies \textemdash{} especially of CA1 hippocampal and layer V neocortical pyramidal neurons \textemdash{} have offered insights into the functions of their unique cellular architecture. Pyramidal neurons are not all identical, but some shared functional principles can be identified. In particular, the existence of dendritic domains with distinct synaptic inputs, excitability, modulation and plasticity appears to be a common feature that allows synapses throughout the dendritic tree to contribute to action-potential generation. These properties support a variety of coincidence-detection mechanisms, which are likely to be crucial for synaptic integration and plasticity.},
  language = {en},
  timestamp = {2016-03-15T03:04:46Z},
  number = {3},
  urldate = {2016-03-15},
  journal = {Nature Reviews Neuroscience},
  author = {Spruston, Nelson},
  month = mar,
  year = {2008},
  pages = {206--221}
}

@article{reddy_role_????,
  title = {Role of differential phosphorylation of c-{{Jun N}}-terminal domain in degenerative and inflammatory pathways of {{CNS}}, {{Die Rolle}} der unterschiedlichen {{Phosphorylierung}} von c-{{Jun N}}-terminale {{Dom{\~A}}}\textcurrency{}ne bei degenerativen und {{entz{\~A}}}\textonequarter{}ndlichen {{Wirkungen}} im {{Nervengewebe}}},
  abstract = {In this study we have investigated the possible role of c-Jun and it{\^a}{\mbox{\texteuro}}\texttrademark{}s activation by the JNK pathway in neuronal cell death and in the inflammatory response of activated astrocytes. The first part of this thesis focuses on the role of site specific phosphorylation of c-Jun in neuronal cell death. The second part focuses on the function of c-Jun in LPS-mediated activation of Bergmann glia cells. In the nervous system, activation of c-Jun transcription factor by different isoforms of c-Jun N-terminal kinase (JNK) functions in various cellular programs, including neurite outgrowth, repair and apoptosis. Yet, the regulatory mechanism underlying the functional dichotomy of c-Jun remains to be elucidated. Serine (S) 63/73 and threonine (T) 91/93 of c-Jun are the target phosphorylation sites for JNKs in response to various stimuli. Yet, these two groups of phosphorylation sites are differentially regulated in vivo, as the S63/73 sites are promptly phosphorylated upon JNK activation, whereas T91/93 phosphorylation requires a priming event at the adjacent T95 site. In our study, we used cerebellar granule cell (CGC) apoptosis by trophic/potassium (TK) deprivation as a model system to investigate the regulation and function of site-specific c-Jun phosphorylation at the S63 and T91/T93 JNK-sites in neuronal cell death. In this model system, JNK induces pro-apoptotic genes through the c-Jun/Ap-1 transcription factor. On the other side, a survival pathway initiated by lithium leads to repression of pro-apoptotic c-Jun/Ap-1 target genes without interfering with JNK activity. Yet, the mechanism by which lithium inhibits c-Jun activity remains to be elucidated. We found that TK-deprivation led to c-Jun phosphorylation at all three JNK sites. However, immunofluorescence analysis of c-Jun phosphorylation at single cell level revealed that the S63 site was phosphorylated in all c-Jun-expressing cells, whereas the response of T91/T93 phosphorylation was more sensitive, mirroring the switch-like apoptotic response of cerebellar granular cells (CGCs). Furthermore, we observed that lithium impaired c-Jun phosphorylation at T91/93, without interfering with S63/73 phosphorylation or JNK activation, suggesting that T91/T93 phosphorylation triggers c-Jun pro-apoptotic activity. Notably, expression of a c-Jun mutant lacking the T95-priming site for T91/93 phosphorylation (c-Jun A95) mimicked the effect of lithium on both cell death and c-Jun site-specific phosphorylation, whereas it was fully able to induce neurite outgrowth in na{\~A}\textasciimacron{}ve PC12 cells. Vice-versa, a c-Jun mutant bearing aspartate-substitution of T95 overwhelmed lithium-mediate protection of CGCs from TK-deprivation, validating that inhibition of T91/T93/T95 phosphorylation underlies the effect of lithium on cell death. Mass-spectrometry analysis confirmed that c-Jun is phosphorylation at T91/T93/T95 in cells. Moreover, recombinant-JNK phosphorylated c-Jun at T91/T93 in a T95-dependent manner. Based on our results, we propose that T91/T93/T95 phosphorylation of c-Jun functions as a sensitivity amplifier of the JNK cascade, setting the threshold for c-Jun pro-apoptotic activity in neuronal cells. In the central nervous system (CNS), the c-Jun transcription factor has been mainly studied in neuronal cells and coupled to apoptotic and regenerative pathways following brain injury. Besides, several studies have shown a transcriptional role of c-Jun in activated cortical and spinal astrocytes. In contrast, little is known about c-Jun expression and activation in Bergmann glial (BG) cells, the radial cerebellar astrocytes playing crucial roles in cerebellar development and physiology. In this study, we used neuronal/glial cerebellar cultures from neonatal mice to assess putative functions of c-Jun in BG cells. By performing double immunocytochemical staining of c-Jun and two BG specific markers, S100 and GLAST, we observed that c-Jun was highly expressed in radial glial cells derived from Bergmann glia. Bergmann glia-derived cells expressed toll-like receptor (TLR 4) and treatment with bacterial lipopolysaccharide (Le et al.) induced c-Jun phosphorylation at S63, exclusively in BG cells. Moreover, LPS induced IL-1{\^I}\ensuremath{^2} expression and inhibition of JNK activity abolished both c-Jun phosphorylation and the increase of IL-1{\^I}\ensuremath{^2} mRNA. Notably, we also observed that LPS failed to induce IL-1{\^I}\ensuremath{^2} mRNA in neuronal/glial cerebellar cultures generated from conditional knockout mice lacking c-Jun expression in the CNS. These results indicate that c-Jun plays a central role in c-Jun in astroglial-specific induction of IL-1{\^I}\ensuremath{^2}. Furthermore, we confirmed in vivo that c-Jun is expressed in BG cells, during the formation of the BG monolayer. Altogether, our finding underlines a putative role of c-Jun in astroglia-mediated neuroinflammatory dysfunctions of the cerebellum., In dieser Studie wurde die Rolle des Transkriptionsfaktors c-Jun sowie seine Aktivierung durch den JNK Signalweg beim neuronalen Zelltod und bei der entz{\"u}ndlichen Reaktion von aktivierten Astrozyten untersucht. Der erste Teil dieser Arbeit besch{\"a}ftigt sich mit der Rolle von mehrfacher c-Jun Phosphorylierung an den Aminos{\"a}uren Threonin 91/93/95 beim neuronalen Zelltod. Der zweite Teil konzentriert sich auf die Rolle von c-Jun und seine Transaktivierung in LPS-vermittelter Aktivierung von Bergmann Gliazellen. Als Modellsystem f{\"u}r den neuronalen Zelltod wurde die Apoptose von cerebell{\"a}ren Granularzellen (CGC) durch trophische Granulazellen Kaliumkonzentration-Erniedrigung (TK) verwendet, da es ein Modell der Um das ist, das Zusammenspiel von pro-apoptotischen und pro-{\"U}berleben Signalwegen beim neuronalen Zelltod zu studieren. In diesem Modell induziert die c-Jun N-terminale Kinase (JNK) pro-apoptotische Gene durch den c-Jun/Ap-1 Transkriptionsfaktor. Auf der anderen Seite, f{\"u}hrt ein Lithium-induzierter {\"U}berleben-Signalweg zur Unterdr{\"u}ckung der pro-apoptotischen c-Jun/Ap-1 Zielgene, ohne Interferenz mit JNK Aktivit{\"a}t. Es blieb jedoch der Mechanismus zu kl{\"a}ren, durch den Lithium c-Jun-Aktivit{\"a}t hemmt. In der Arbeit wurde dieses Modellsystem benutzt, um die Regulation und Funktion der c-Jun-Phosphorylierung durch JNK an den Stellen S63 und T91/T93 beim neuronalen Zelltod zu studieren. Es wurde gefunden, dass TK-Kaliumerniedrigung zu c-Jun phosphorylierung f{\"u}hrte und zwar an allen drei durch JNK phosphorylierbaren Ser/Thr (JNK-Stellen). Immunfluoreszenzanalyse von c-Jun Phosphorylierung auf Einzel-Zell-Ebene ergab jedoch, dass die S63-Stelle in allen c-Jun-exprimierenden Zellen phosphoryliert wurde, w{\"a}hrend T91/T93 Phosphorylierung empfindlicher war, analog zur Schalter-{\"a}hnlichen apoptotischen Antwort von CGCs. Umgekehrt verhinderte Lithium T91 und T93 Phosphorylierung und Zelltod ohne Wirkung auf die S63-Seite, was darauf hindeutet, dass T91/T93 Phosphorylierung durch c-Jun eine pro-apoptotische Aktivit{\"a}t ausl{\"o}st. Dementsprechend sch{\"u}tzte eine c-Jun-Mutation, der die T95 Priming-Stelle f{\"u}r T91/93 Phosphorylierung fehlt (T95A), CGCs vor Apoptose, wohingegen T95A Neuriten-wachstum in PC12-Zellen induzieren konnte. Umgekehrt f{\"u}hrte eine c-Jun Mutante mit Aspartat-Substitution von T95 (T95D ) zur Aufhebung der sch{\"u}tzenden Wirkung von Lithium auf CGC Apoptose, wodurch best{\"a}tigt wurde, dass die Inhibierung der T91/T93/T95 Phosphorylierung der Wirkung von Lithium auf den Zelltod zugrundeliegt. Massenspektrometrie-Analyse best{\"a}tigte multiple Phosphorylierung von c-Jun an T91/T93/T95 in den Zellen. Au\ss{}erdem wurde rekombinantes c-Jun durch JNK an T91/T93 in einer T95-abh{\"a}ngigen Weise phosphoryliert. Basierend auf diesen Ergebnissen wird vorgeschlagen, dass T91/T93/T95 phosphorylierung von c-Jun als Empfindlichkeit-Verst{\"a}rker der JNK-Kaskade fungiert, der die Schwelle f{\"u}r die pro-apoptotische Aktivit{\"a}t von c-Jun in neuronalen Zellen einstellt. Im zentralen Nervensystem (ZNS) wurde die Rolle des c-Jun Transkriptionsfaktors haupts{\"a}chlich bei neuronalem Zelltod und bei neuronaler Regeneration nach Hirnsch{\"a}digung untersucht. Au\ss{}erdem wurde auch eine Rolle f{\"u}r c-Jun bei der Transkription in aktivierten kortikalen und spinalen Astrozyten beschrieben. Im Gegensatz dazu ist wenig bekannt {\"u}ber die Expression von c-Jun und dessen Transaktivierung in Bergmann Gliazellen (BG)-Zellen, die eine entscheidende Rolle bei der Entwicklung des Kleinhirns und dessen Physiologie spielen. In dieser Arbeit wurde die putative Rolle von c-Jun bei kultivierten neuronalen/BG-Zellen aus dem Maus-Kleinhirn untersucht. Immunfluoreszenzanalyse von c-Jun und zwei f{\"u}r BG-Zellen spezifische Marker, S100 und GLAST, ergab, dass c-Jun in BG-Zellen hoch exprimiert wurde. Au\ss{}erdem wurde gefunden, dass der Toll-like Rezeptor TLR4 in BG-Zellen exprimiert ist und dass die Behandlung mit bakteriellem Lipopolysaccharid (Le et al.) die c-Jun- Phosphorylierung an S63 induziert. Zus{\"a}tzlich wurde gefunden, dass LPS IL-1b Expression induziert und die Inhibierung von JNK Aktivit{\"a}t verhinderte sowohl c-Jun-Phosphorylierung, als auch die Zunahme von IL-1 b mRNA. Insbesondere konnte LPS die IL-1b mRNA-Produktion in neuronalen / BG-Kulturen aus konditionellen Knockout M{\"a}usen, denen c-Jun im ZNS fehlte, nicht induzieren, womit gezeigt wurde, dass c-Jun bei der Astroglia-spezifischen Induktion von IL-1 b essentiell ist. Immunohistochemische Analyse von c-Jun-exprimierenden Zellen im postnatalen Kleinhirn best{\"a}tigte in-vivo die Expression von c-Jun in BG Zellen und f{\"o}rderte eine dynamische Expression von c-Jun w{\"a}hrend der Entwicklung der BG Monolayer zutage. Insgesamt unterstreichen die Befunde dieser Arbeit eine wahrscheinliche Rolle von c-Jun bei Astroglia-vermittelten neuroinflammatorischen Funktionsst{\"o}rungen des Kleinhirns.},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2014-11-20},
  author = {Reddy, Edamakanti Chandrakanth},
  note = {In this study we have investigated the possible role of c-Jun and it{\^a}{\mbox{\texteuro}}\texttrademark{}s activation by the JNK pathway in neuronal cell death and in the inflammatory response of activated astrocytes. The first part of this thesis focuses on the role of site specific phosphorylation of c-Jun in neuronal cell death. The second part focuses on the function of c-Jun in LPS-mediated activation of Bergmann glia cells.
In the nervous system, activation of c-Jun transcription factor by different isoforms of c-Jun N-terminal kinase (JNK) functions in various cellular programs, including neurite outgrowth, repair and apoptosis. Yet, the regulatory mechanism underlying the functional dichotomy of c-Jun remains to be elucidated. Serine (S) 63/73 and threonine (T) 91/93 of c-Jun are the target phosphorylation sites for JNKs in response to various stimuli. Yet, these two groups of phosphorylation sites are differentially regulated in vivo, as the S63/73 sites are promptly phosphorylated upon JNK activation, whereas T91/93 phosphorylation requires a priming event at the adjacent T95 site. In our study, we used cerebellar granule cell (CGC) apoptosis by trophic/potassium (TK) deprivation as a model system to investigate the regulation and function of site-specific c-Jun phosphorylation at the S63 and T91/T93 JNK-sites in neuronal cell death. In this model system, JNK induces pro-apoptotic genes through the c-Jun/Ap-1 transcription factor. On the other side, a survival pathway initiated by lithium leads to repression of pro-apoptotic c-Jun/Ap-1 target genes without interfering with JNK activity. Yet, the mechanism by which lithium inhibits c-Jun activity remains to be elucidated. We found that TK-deprivation led to c-Jun phosphorylation at all three JNK sites. However, immunofluorescence analysis of c-Jun phosphorylation at single cell level revealed that the S63 site was phosphorylated in all c-Jun-expressing cells, whereas the response of T91/T93 phosphorylation was more sensitive, mirroring the switch-like apoptotic response of cerebellar granular cells (CGCs). Furthermore, we observed that lithium impaired c-Jun phosphorylation at T91/93, without interfering with S63/73 phosphorylation or JNK activation, suggesting that T91/T93 phosphorylation triggers c-Jun pro-apoptotic activity. Notably, expression of a c-Jun mutant lacking the T95-priming site for T91/93 phosphorylation (c-Jun A95) mimicked the effect of lithium on both cell death and c-Jun site-specific phosphorylation, whereas it was fully able to induce neurite outgrowth in na{\~A}\textasciimacron{}ve PC12 cells. Vice-versa, a c-Jun mutant bearing aspartate-substitution of T95 overwhelmed lithium-mediate protection of CGCs from TK-deprivation, validating that inhibition of T91/T93/T95 phosphorylation underlies the effect of lithium on cell death. Mass-spectrometry analysis confirmed that c-Jun is phosphorylation at T91/T93/T95 in cells. Moreover, recombinant-JNK phosphorylated c-Jun at T91/T93 in a T95-dependent manner. Based on our results, we propose that T91/T93/T95 phosphorylation of c-Jun functions as a sensitivity amplifier of the JNK cascade, setting the threshold for c-Jun pro-apoptotic activity in neuronal cells.
In the central nervous system (CNS), the c-Jun transcription factor has been mainly studied in neuronal cells and coupled to apoptotic and regenerative pathways following brain injury. Besides, several studies have shown a transcriptional role of c-Jun in activated cortical and spinal astrocytes. In contrast, little is known about c-Jun expression and activation in Bergmann glial (BG) cells, the radial cerebellar astrocytes playing crucial roles in cerebellar development and physiology. In this study, we used neuronal/glial cerebellar cultures from neonatal mice to assess putative functions of c-Jun in BG cells. By performing double immunocytochemical staining of c-Jun and two BG specific markers, S100 and GLAST, we observed that c-Jun was highly expressed in radial glial cells derived from Bergmann glia. Bergmann glia-derived cells expressed toll-like receptor (TLR 4) and treatment with bacterial lipopolysaccharide (Le et al.) induced c-Jun phosphorylation at S63, exclusively in BG cells. Moreover, LPS induced IL-1{\^I}\ensuremath{^2} expression and inhibition of JNK activity abolished both c-Jun phosphorylation and the increase of IL-1{\^I}\ensuremath{^2} mRNA. Notably, we also observed that LPS failed to induce IL-1{\^I}\ensuremath{^2} mRNA in neuronal/glial cerebellar cultures generated from conditional knockout mice lacking c-Jun expression in the CNS. These results indicate that c-Jun plays a central role in c-Jun in astroglial-specific induction of IL-1{\^I}\ensuremath{^2}. Furthermore, we confirmed in vivo that c-Jun is expressed in BG cells, during the formation of the BG monolayer. Altogether, our finding underlines a putative role of c-Jun in astroglia-mediated neuroinflammatory dysfunctions of the cerebellum.},
  keywords = {S100b,Slc1a3}
}

@article{imai_novel_1996,
  title = {A novel gene iba1 in the major histocompatibility complex class {{III}} region encoding an {{EF}} hand protein expressed in a monocytic lineage},
  volume = {224},
  issn = {0006-291X},
  doi = {10.1006/bbrc.1996.1112},
  abstract = {We successfully isolated a rat cDNA clone encoding a novel EF hand protein with a molecular weight of about 17 kDa and designated this gene iba1 (ionized calcium binding adapter molecule 1). The genomic copy of the iba1 gene was located within a segment of the major histocompatibility complex class III region between the Bat2 and TNF alpha genes. The iba1 gene was shown to be highly expressed in testis and spleen, but weakly expressed in brain, lung, and kidney. Among brain cells, the iba1 gene was specifically expressed in microglia. A screening of hemopoietic cell lines showed that the Iba1 protein was clearly expressed in monoblastic cell lines but only very weakly expressed in myeloid cell lines. Iba1 protein is therefore suggested to act as an adapter molecule, mediating calcium signals that may function in a monocytic lineage including microglia.},
  language = {eng},
  timestamp = {2016-03-23T09:00:49Z},
  number = {3},
  journal = {Biochemical and Biophysical Research Communications},
  author = {Imai, Y. and Ibata, I. and Ito, D. and Ohsawa, K. and Kohsaka, S.},
  month = jul,
  year = {1996},
  keywords = {Amino Acid Sequence,Animals,Base Sequence,Calcium-Binding Proteins,Cell Line,Cloning; Molecular,DNA; Complementary,Major Histocompatibility Complex,Microfilament Proteins,Molecular Sequence Data,Monocytes,Rats,RNA,Sequence Homology; Amino Acid},
  pages = {855--862},
  pmid = {8713135}
}

@article{rudy_three_2011,
  title = {Three groups of interneurons account for nearly 100\% of neocortical {{GABAergic}} neurons},
  volume = {71},
  issn = {1932-846X},
  doi = {10.1002/dneu.20853},
  abstract = {An understanding of the diversity of cortical GABAergic interneurons is critical to understand the function of the cerebral cortex. Recent data suggest that neurons expressing three markers, the Ca2+-binding protein parvalbumin (PV), the neuropeptide somatostatin (SST), and the ionotropic serotonin receptor 5HT3a (5HT3aR) account for nearly 100\% of neocortical interneurons. Interneurons expressing each of these markers have a different embryological origin. Each group includes several types of interneurons that differ in morphological and electrophysiological properties and likely have different functions in the cortical circuit. The PV group accounts for \ensuremath{\sim}40\% of GABAergic neurons and includes fast spiking basket cells and chandelier cells. The SST group, which represents \ensuremath{\sim}30\% of GABAergic neurons, includes the Martinotti cells and a set of neurons that specifically target layerIV. The 5HT3aR group, which also accounts for \ensuremath{\sim}30\% of the total interneuronal population, is heterogeneous and includes all of the neurons that express the neuropeptide VIP, as well as an equally numerous subgroup of neurons that do not express VIP and includes neurogliaform cells. The universal modulation of these neurons by serotonin and acetylcholine via ionotropic receptors suggests that they might be involved in shaping cortical circuits during specific brain states and behavioral contexts.},
  language = {eng},
  timestamp = {2016-02-23T00:11:38Z},
  number = {1},
  journal = {Developmental Neurobiology},
  author = {Rudy, Bernardo and Fishell, Gordon and Lee, SooHyun and Hjerling-Leffler, Jens},
  month = jan,
  year = {2011},
  keywords = {Animals,Cell Count,gamma-Aminobutyric Acid,Humans,interneurons,Neocortex,Nerve Net,Neural Pathways},
  pages = {45--61},
  pmid = {21154909},
  pmcid = {PMC3556905}
}

@article{pickel_monoamine-synthesizing_1976,
  title = {Monoamine-synthesizing enzymes in central dopaminergic, noradrenergic and serotonergic neurons. {{Immunocytochemical}} localization by light and electron microscopy.},
  volume = {24},
  issn = {0022-1554, 1551-5044},
  doi = {10.1177/24.7.8567},
  abstract = {The monoamine-synthesizing enzymes tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH) and tryptophan hydroxylase (TrH) were immunocytochemical localized in dopaminergic, noradrenergic and serotonergic neurons of rat brain by light and electron microscopy. In dopaminergic and serotonergic neurons, the respective synthesizing enzymes. TH and TrH, were distributed throughout the cytoplasm of the neuronal perikarya, dendrites, axons and terminals. The most selective accumulation of reaction product for the specific enzyme was associated: (a) in perikarya with endoplasmic reticulum, Golgi apparatus and microtubules, (b) in processes with microtubules, and (c) in terminals with dense granules or clear vesicles. The labeled terminals were characterized by their content of labeled organelles and the absence of synaptic junctions. In noradrenergic neurons, both TH and DBH were localized in the perikarya, similar to TH in dopamine neurons. TH and DBH differed in their localization within proximal axons and dendrites in that TH was associated with microtubules but DBH was not. These results provide ultrastructural evidence to suggest that monoamines may be: (a) synthesized by enzymes which are associated with different organelles depending on the portion of the neuron and the type of enzyme; (b) synthesized in both axons and dendrites and (c) released from terminals without postsynaptic membrane specializations.},
  language = {en},
  timestamp = {2016-05-14T17:15:22Z},
  number = {7},
  urldate = {2016-05-14},
  journal = {Journal of Histochemistry \& Cytochemistry},
  author = {Pickel, V. M. and Joh, T. H. and Reis, D. J.},
  month = jan,
  year = {1976},
  pages = {792--792},
  pmid = {8567}
}

@article{ernsberger_expression_2000,
  title = {The expression of dopamine \ensuremath{\beta}-hydroxylase, tyrosine hydroxylase, and {{Phox2}} transcription factors in sympathetic neurons: evidence for common regulation during noradrenergic induction and diverging regulation later in development},
  volume = {92},
  issn = {0925-4773},
  shorttitle = {The expression of dopamine \ensuremath{\beta}-hydroxylase, tyrosine hydroxylase, and {{Phox2}} transcription factors in sympathetic neurons},
  doi = {10.1016/S0925-4773(99)00336-6},
  abstract = {During differentiation of sympathetic neurons in chick embryos, tyrosine hydroxylase (TH) and dopamine \ensuremath{\beta}-hydroxylase (DBH) mRNAs become detectable during the same developmental period and are both induced by BMP 4. Later during sympathetic ganglion development, DBH is detectable in TH-positive and -negative cells. Moreover, BMPs reduce DBH mRNA in cultures of sympathetic neurons while leaving TH unaffected. The data provide evidence for a common regulation of TH and DBH early during sympathetic neuron differentiation and indicate that BMPs promote their initial expression but not the maintenance during later development. The time course of Phox2a and 2b expression suggests an evolutionary conserved role in noradrenergic induction. In addition, Phox2a, Phox2b, and c-ret may be involved in the differentiation of cholinergic sympathetic neurons.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-12-04},
  journal = {Mechanisms of Development},
  author = {Ernsberger, Uwe and Reissmann, Eva and Mason, Ivor and Rohrer, Hermann},
  month = apr,
  year = {2000},
  keywords = {Bone morphogenetic proteins,c-ret,Differentiation,Dopamine β-hydroxylase,Noradrenergic,Phox2a,Phox2b,Sympathetic,Tyrosine hydroxylase,unread},
  pages = {169--177},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/3AAC4X7D/S0925477399003366.html:}
}

@incollection{valenzuela_review_2010,
  series = {Functional Plasticity and Genetic Variation: Insights into the Neurobiology of Alcoholism},
  title = {A {{Review}} of {{Synaptic Plasticity}} at {{Purkinje Neurons}} with a {{Focus}} on {{Ethanol-Induced Cerebellar Dysfunction}}},
  volume = {91},
  abstract = {The cerebellum controls balance, posture, motor coordination, and cognition, and studies suggest that ethanol impairs these cerebellar functions. However, the mechanisms through which ethanol produces these effects are not fully understood. Here, we review evidence suggesting that ethanol acts, in part, by impairing synaptic plasticity mechanisms at cerebellar Purkinje neurons. We will primarily focus on recent experiments indicating that long-term depression at both parallel fiber\textendash{} and climbing fiber\textendash{}Purkinje cell synapses is inhibited by acute ethanol exposure. We will also discuss experimental evidence showing that chronic prenatal ethanol exposure converts long-term depression into long-term potentiation at parallel fiber\textendash{}Purkinje cell synapses.},
  timestamp = {2016-03-24T09:07:22Z},
  urldate = {2016-03-24},
  booktitle = {International {{Review}} of {{Neurobiology}}},
  publisher = {{Academic Press}},
  author = {Valenzuela, C. Fernando and Lindquist, Britta and Zamudio-Bulcock, Paula A.},
  editor = {Lovinger, Matthew T. Reilly and David M.},
  year = {2010},
  keywords = {Alcohol,cerebellum,development,Electrophysiology,Neurotransmitter,Plasticity,Synapse},
  pages = {339--372}
}

@article{yang_participation_2014,
  title = {Participation of {{Central P2X7 Receptors}} in {{CFA}}-induced {{Inflammatory Pain}} in the {{Orofacial Area}} of {{Rats}}},
  volume = {39},
  issn = {1226-7155},
  language = {Korean},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-11-20},
  journal = {International Journal of Oral Biology},
  author = {Yang, Kui Ye and Kim, Myung Dong and Ju, Jin Sook and Kim, Min Ji and Ahn, Dong Kuk},
  month = mar,
  year = {2014},
  pages = {49--56},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/77R8IZRH/SearchBasic.html:}
}

@article{ingersoll_comparison_2010,
  title = {Comparison of gene expression profiles between human and mouse monocyte subsets},
  volume = {115},
  issn = {1528-0020},
  doi = {10.1182/blood-2009-07-235028},
  abstract = {Blood of both humans and mice contains 2 main monocyte subsets. Here, we investigated the extent of their similarity using a microarray approach. Approximately 270 genes in humans and 550 genes in mice were differentially expressed between subsets by 2-fold or more. More than 130 of these gene expression differences were conserved between mouse and human monocyte subsets. We confirmed numerous of these differences at the cell surface protein level. Despite overall conservation, some molecules were conversely expressed between the 2 species' subsets, including CD36, CD9, and TREM-1. Other differences included a prominent peroxisome proliferator-activated receptor gamma (PPARgamma) signature in mouse monocytes, which is absent in humans, and strikingly opposed patterns of receptors involved in uptake of apoptotic cells and other phagocytic cargo between human and mouse monocyte subsets. Thus, whereas human and mouse monocyte subsets are far more broadly conserved than currently recognized, important differences between the species deserve consideration when models of human disease are studied in mice.},
  language = {eng},
  timestamp = {2015-09-03T21:49:37Z},
  number = {3},
  journal = {Blood},
  author = {Ingersoll, Molly A. and Spanbroek, Rainer and Lottaz, Claudio and Gautier, Emmanuel L. and Frankenberger, Marion and Hoffmann, Reinhard and Lang, Roland and Haniffa, Muzlifah and Collin, Matthew and Tacke, Frank and Habenicht, Andreas J. R. and Ziegler-Heitbrock, Loems and Randolph, Gwendalyn J.},
  month = jan,
  year = {2010},
  keywords = {Animals,Cells; Cultured,Gene Expression Profiling,Humans,Male,Mice,Mice; Inbred C57BL,Monocytes,Oligonucleotide Array Sequence Analysis},
  pages = {e10--19},
  pmid = {19965649},
  pmcid = {PMC2810986}
}

@article{wang_functional_2012,
  title = {Functional classification of skeletal muscle networks. {{II}}. {{Applications}} to pathophysiology},
  volume = {113},
  issn = {1522-1601},
  doi = {10.1152/japplphysiol.01515.2011},
  abstract = {In our preceding companion paper (Wang Y, Winters J, Subramaniam S. J Appl Physiol. doi: 10.1152/japplphysiol.01514.2011), we used extensive expression profile data on normal human subjects, in combination with legacy knowledge to classify skeletal muscle function into four models, namely excitation-activation, mechanical, metabolic, and signaling-production model families. In this paper, we demonstrate how this classification can be applied to study two well-characterized myopathies: amyotrophic lateral sclerosis (ALS) and Duchenne muscular dystrophy (DMD). Using skeletal muscle profile data from ALS and DMD patients compared with that from normal subjects, normal young in the case of DMD, we delineate molecular mechanisms that are causative and consequential to skeletal muscle dysfunction. In ALS, our analysis establishes the metabolic role and specifically identifies the mechanisms of calcium dysregulation and defects in mitochondrial transport of materials as important for muscle dysfunction. In DMD, we illustrate how impaired mechanical function is strongly coordinated with other three functional networks, resulting in transformation of the skeletal muscle into hybrid forms as a compensatory mechanism. Our functional models also provide, in exquisite detail, the mechanistic role of myriad proteins in these four families in normal and disease function.},
  language = {eng},
  timestamp = {2016-02-22T19:37:30Z},
  number = {12},
  journal = {Journal of Applied Physiology (Bethesda, Md.: 1985)},
  author = {Wang, Yu and Winters, Jack and Subramaniam, Shankar},
  month = dec,
  year = {2012},
  note = {00000 PMID: 23085957},
  keywords = {Animals,Calcium Signaling,Computer Simulation,Humans,Ion Channels,Models; Biological,Muscle Contraction,Muscle Proteins,Muscle; Skeletal,Muscular Diseases,Reference Values},
  pages = {1902--1920},
  pmcid = {PMC3544493}
}

@article{chen_removing_2011,
  title = {Removing {{Batch Effects}} in {{Analysis}} of {{Expression Microarray Data}}: {{An Evaluation}} of {{Six Batch Adjustment Methods}}},
  volume = {6},
  shorttitle = {Removing {{Batch Effects}} in {{Analysis}} of {{Expression Microarray Data}}},
  doi = {10.1371/journal.pone.0017238},
  abstract = {The expression microarray is a frequently used approach to study gene expression on a genome-wide scale. However, the data produced by the thousands of microarray studies published annually are confounded by ``batch effects,'' the systematic error introduced when samples are processed in multiple batches. Although batch effects can be reduced by careful experimental design, they cannot be eliminated unless the whole study is done in a single batch. A number of programs are now available to adjust microarray data for batch effects prior to analysis. We systematically evaluated six of these programs using multiple measures of precision, accuracy and overall performance. ComBat, an Empirical Bayes method, outperformed the other five programs by most metrics. We also showed that it is essential to standardize expression data at the probe level when testing for correlation of expression profiles, due to a sizeable probe effect in microarray data that can inflate the correlation among replicates and unrelated samples.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-10-16},
  journal = {PLoS ONE},
  author = {Chen, Chao and Grennan, Kay and Badner, Judith and Zhang, Dandan and Gershon, Elliot and Jin, Li and Liu, Chunyu},
  month = feb,
  year = {2011},
  pages = {e17238},
  file = {Chen et al_2011_Removing Batch Effects in Analysis of Expression Microarray Data.pdf:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/P2GEF5F2/Chen et al_2011_Removing Batch Effects in Analysis of Expression Microarray Data.pdf:application/pdf;PLoS Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/TF7T2JUC/infodoi10.1371journal.pone.html:}
}

@article{friedman_situ_1989,
  title = {In situ demonstration of mature oligodendrocytes and their processes: {{An}} immunocytochemical study with a new monoclonal antibody, {{Rip}}},
  volume = {2},
  copyright = {Copyright \textcopyright{} 1989 Alan R. Liss, Inc.},
  issn = {1098-1136},
  shorttitle = {In situ demonstration of mature oligodendrocytes and their processes},
  doi = {10.1002/glia.440020510},
  abstract = {This paper introduces ``Rip'' a monoclonal antibody that produces relatively complete staining of oligodendrocytes and their processes in the adult central nervous system (CNS). The distribution of Rip immunoreactivity coincides with that of myelinated axons in both the spinal cord and the cerebellum. In addition, doubleimmunolabeling experiments demonstrate that Rip stains processes containing myelin basic protein but does not stain processes that express glial fibrillary acidic protein. These results indicate that Rip selectively stains oligodendrocytes but not astrocytes. Moreover, individual Rip-stained oligodendroglial somata and their cytoplasmic processes were observable at both the light microscopic and electron microscopic level when the staining of myelin was reduced. This was accomplished by omitting detergents from antibody incubation steps. Rip-stained oligodendrocytes have multiple processes of varying thickness, some of which end in close proximity to myelin sheaths. These immunostained profiles, reminiscent of those observed in oligodendrocytes stained by Golgi methods, are unique to Rip and indicate that its immunoreactivity is distinct from that of existing serological markers for oligodendrocytes.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {5},
  urldate = {2014-11-26},
  journal = {Glia},
  author = {Friedman, B. and Hockfield, S. and Black, J.a. and Woodruff, K.a. and Waxman, S.g.},
  month = jan,
  year = {1989},
  keywords = {cerebellum,Immunocytochemistry,Myelin,oligodendrocytes,Spinal cord},
  pages = {380--390},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/IB9K9KDE/abstract.html:}
}

@article{xu_cell_2013,
  title = {Cell type-specific analysis of human brain transcriptome data to predict alterations in cellular composition},
  volume = {1},
  issn = {2162-8130, 2162-8149},
  doi = {10.4161/sysb.25630},
  abstract = {The central nervous system (CNS) is composed of hundreds of distinct cell types, each expressing different subsets of genes from the genome. High throughput gene expression analysis of the CNS from patients and controls is a common method to screen for potentially pathological molecular mechanisms of psychiatric disease. One mechanism by which gene expression might be seen to vary across samples would be alterations in the cellular composition of the tissue. While the expressions of gene ``markers'' for each cell type can provide certain information of cellularity, for many rare cell types markers are not well characterized. Moreover, if only small sets of markers are known, any substantial variation of a marker's expression pattern due to experiment conditions would result in poor sensitivity and specificity. Here, our proposed method combines prior information from mice cell-specific transcriptome profiling experiments with co-expression network analysis, to select large sets of potential cell type-specific gene markers in a systematic and unbiased manner. The method is efficient and robust, and identifies sufficient markers for further cellularity analysis. We then employ the markers to analytically detect changing cellular composition in human brain. Application of our method to temporal human brain microarray data successfully detects changes in cellularity over time that roughly correspond to known epochs of human brain development. Furthermore, application of our method to human brain samples with the neurodevelopmental disorder of autism supports the interpretation that the changes in astrocytes and neurons might contribute to the disorder.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {3},
  urldate = {2014-10-15},
  journal = {Systems Biomedicine},
  author = {Xu, Xiaoxiao and Nehorai, Arye and Dougherty, Joseph D.},
  month = sep,
  year = {2013},
  pages = {151--160},
  file = {Xu et al_2013_Cell type-specific analysis of human brain transcriptome data to predict.pdf:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/7FDG3GJV/Xu et al_2013_Cell type-specific analysis of human brain transcriptome data to predict.pdf:application/pdf;Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/WWCMSKH2/Xu et al. - 2013 - Cell type-specific analysis of human brain transcr.html:}
}

@article{hawrylycz_anatomically_2012,
  title = {An anatomically comprehensive atlas of the adult human brain transcriptome},
  volume = {489},
  copyright = {\textcopyright{} 2012 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {0028-0836},
  doi = {10.1038/nature11405},
  abstract = {Neuroanatomically precise, genome-wide maps of transcript distributions are critical resources to complement genomic sequence data and to correlate functional and genetic brain architecture. Here we describe the generation and analysis of a transcriptional atlas of the adult human brain, comprising extensive histological analysis and comprehensive microarray profiling of \textasciitilde{}900 neuroanatomically precise subdivisions in two individuals. Transcriptional regulation varies enormously by anatomical location, with different regions and their constituent cell types displaying robust molecular signatures that are highly conserved between individuals. Analysis of differential gene expression and gene co-expression relationships demonstrates that brain-wide variation strongly reflects the distributions of major cell classes such as neurons, oligodendrocytes, astrocytes and microglia. Local neighbourhood relationships between fine anatomical subdivisions are associated with discrete neuronal subtypes and genes involved with synaptic transmission. The neocortex displays a relatively homogeneous transcriptional pattern, but with distinct features associated selectively with primary sensorimotor cortices and with enriched frontal lobe expression. Notably, the spatial topography of the neocortex is strongly reflected in its molecular topography\textemdash{}the closer two cortical regions, the more similar their transcriptomes. This freely accessible online data resource forms a high-resolution transcriptional baseline for neurogenetic studies of normal and abnormal human brain function.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {7416},
  urldate = {2014-12-23},
  journal = {Nature},
  author = {Hawrylycz, Michael J. and Lein, Ed S. and Guillozet-Bongaarts, Angela L. and Shen, Elaine H. and Ng, Lydia and Miller, Jeremy A. and {van de Lagemaat}, Louie N. and Smith, Kimberly A. and Ebbert, Amanda and Riley, Zackery L. and Abajian, Chris and Beckmann, Christian F. and Bernard, Amy and Bertagnolli, Darren and Boe, Andrew F. and Cartagena, Preston M. and Chakravarty, M. Mallar and Chapin, Mike and Chong, Jimmy and Dalley, Rachel A. and Daly, Barry David and Dang, Chinh and Datta, Suvro and Dee, Nick and Dolbeare, Tim A. and Faber, Vance and Feng, David and Fowler, David R. and Goldy, Jeff and Gregor, Benjamin W. and Haradon, Zeb and Haynor, David R. and Hohmann, John G. and Horvath, Steve and Howard, Robert E. and Jeromin, Andreas and Jochim, Jayson M. and Kinnunen, Marty and Lau, Christopher and Lazarz, Evan T. and Lee, Changkyu and Lemon, Tracy A. and Li, Ling and Li, Yang and Morris, John A. and Overly, Caroline C. and Parker, Patrick D. and Parry, Sheana E. and Reding, Melissa and Royall, Joshua J. and Schulkin, Jay and Sequeira, Pedro Adolfo and Slaughterbeck, Clifford R. and Smith, Simon C. and Sodt, Andy J. and Sunkin, Susan M. and Swanson, Beryl E. and Vawter, Marquis P. and Williams, Derric and Wohnoutka, Paul and Zielke, H. Ronald and Geschwind, Daniel H. and Hof, Patrick R. and Smith, Stephen M. and Koch, Christof and Grant, Seth G. N. and Jones, Allan R.},
  month = sep,
  year = {2012},
  keywords = {Databases,Genetics,Genomics,neuroscience},
  pages = {391--399},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/IK4UZP7N/nature11405.html:;Hawrylycz et al_2012_An anatomically comprehensive atlas of the adult human brain transcriptome.pdf:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/XXJN6GR3/Hawrylycz et al_2012_An anatomically comprehensive atlas of the adult human brain transcriptome.pdf:application/pdf}
}

@article{mirnics_analysis_2001,
  title = {Analysis of complex brain disorders with gene expression microarrays: schizophrenia as a disease of the synapse},
  volume = {24},
  issn = {0166-2236},
  shorttitle = {Analysis of complex brain disorders with gene expression microarrays},
  doi = {10.1016/S0166-2236(00)01862-2},
  abstract = {The level of cellular and molecular complexity of the nervous system creates unique problems for the neuroscientist in the design and implementation of functional genomic studies. Microarray technologies can be powerful, with limitations, when applied to the analysis of human brain disorders. Recently, using cDNA microarrays, altered gene expression patterns between subjects with schizophrenia and controls were shown. Functional data mining led to two novel discoveries: a consistent decrease in the group of transcripts encoding proteins that regulate presynaptic function; and the most changed gene, which has never been previously associated with schizophrenia, regulator of G-protein signaling 4. From these and other findings, a hypothesis has been formulated to suggest that schizophrenia is a disease of the synapse. In the context of a neurodevelopmental model, it is proposed that impaired mechanics of synaptic transmission in specific neural circuits during childhood and adolescence ultimately results in altered synapse formation or pruning, or both, which manifest in the clinical onset of the disease.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {8},
  urldate = {2014-12-16},
  journal = {Trends in Neurosciences},
  author = {Mirnics, K{\'a}roly and Middleton, Frank A. and Lewis, David A. and Levitt, Pat},
  month = aug,
  year = {2001},
  keywords = {cDNA,PSYN,RGS4,synaptic transmission},
  pages = {479--486},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/JZESEFDT/S0166223600018622.html:}
}

@article{moore_biospecimen_2011,
  title = {Biospecimen reporting for improved study quality ({{BRISQ}})},
  volume = {119},
  issn = {1934662X},
  doi = {10.1002/cncy.20147},
  language = {en},
  timestamp = {2015-08-13T22:14:48Z},
  number = {2},
  urldate = {2014-12-23},
  journal = {Cancer Cytopathology},
  author = {Moore, Helen M. and Kelly, Andrea B. and Jewell, Scott D. and McShane, Lisa M. and Clark, Douglas P. and Greenspan, Renata and Hayes, Daniel F. and Hainaut, Pierre and Kim, Paula and Mansfield, Elizabeth A. and Potapova, Olga and Riegman, Peter and Rubinstein, Yaffa and Seijo, Edward and Somiari, Stella and Watson, Peter and Weier, Heinz-Ulrich and Zhu, Claire and Vaught, Jim},
  month = apr,
  year = {2011},
  pages = {92--102},
  file = {Availability of data & materials \: authors & referees @ npg:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/82VW6RQN/availability.html:}
}

@article{chen_effects_2016,
  title = {Effects of aging on circadian patterns of gene expression in the human prefrontal cortex},
  volume = {113},
  issn = {1091-6490},
  doi = {10.1073/pnas.1508249112},
  abstract = {With aging, significant changes in circadian rhythms occur, including a shift in phase toward a "morning" chronotype and a loss of rhythmicity in circulating hormones. However, the effects of aging on molecular rhythms in the human brain have remained elusive. Here, we used a previously described time-of-death analysis to identify transcripts throughout the genome that have a significant circadian rhythm in expression in the human prefrontal cortex [Brodmann's area 11 (BA11) and BA47]. Expression levels were determined by microarray analysis in 146 individuals. Rhythmicity in expression was found in \ensuremath{\sim} 10\% of detected transcripts (P \ensuremath{<} 0.05). Using a metaanalysis across the two brain areas, we identified a core set of 235 genes (q \ensuremath{<} 0.05) with significant circadian rhythms of expression. These 235 genes showed 92\% concordance in the phase of expression between the two areas. In addition to the canonical core circadian genes, a number of other genes were found to exhibit rhythmic expression in the brain. Notably, we identified more than 1,000 genes (1,186 in BA11; 1,591 in BA47) that exhibited age-dependent rhythmicity or alterations in rhythmicity patterns with aging. Interestingly, a set of transcripts gained rhythmicity in older individuals, which may represent a compensatory mechanism due to a loss of canonical clock function. Thus, we confirm that rhythmic gene expression can be reliably measured in human brain and identified for the first time (to our knowledge) significant changes in molecular rhythms with aging that may contribute to altered cognition, sleep, and mood in later life.},
  language = {eng},
  timestamp = {2016-06-03T01:49:02Z},
  number = {1},
  journal = {Proceedings of the National Academy of Sciences of the United States of America},
  author = {Chen, Cho-Yi and Logan, Ryan W. and Ma, Tianzhou and Lewis, David A. and Tseng, George C. and Sibille, Etienne and McClung, Colleen A.},
  month = jan,
  year = {2016},
  keywords = {Adolescent,Adult,Aged,Aged; 80 and over,Aging,Circadian Rhythm,circadian rhythms,gene expression,Gene Expression Regulation,Genome; Human,Humans,Male,Middle Aged,Oligonucleotide Array Sequence Analysis,postmortem,Prefrontal Cortex,Sleep,Transcription; Genetic,Young Adult},
  pages = {206--211},
  pmid = {26699485},
  pmcid = {PMC4711850}
}

@article{phani_vta_2010,
  title = {{{VTA}} neurons show a potentially protective transcriptional response to {{MPTP}}},
  volume = {1343},
  issn = {0006-8993},
  doi = {10.1016/j.brainres.2010.04.061},
  abstract = {Parkinson's disease and its characteristic symptoms are thought to arise from the progressive degeneration of specific midbrain dopamine (DA) neurons. In humans, DA neurons of the substantia nigra (SN) and their projections to the striatum show selective vulnerability, while neighboring DA neurons of the ventral tegmental area (VTA) are relatively spared from degeneration. This pattern of cell loss is mimicked in humans, primates, and certain rodents by the neurotoxin MPTP. In this study, we aimed to test the hypothesis that there are factors in the VTA that are potentially neuroprotective against MPTP and that these factors change over time. We have found a dynamic transcriptional response within the cells of the VTA to sustained exposure to a low dose of MPTP. Specifically, the VTA has increased expression of 148 genes as an early response to MPTP and 113 genes as a late response to MPTP toxicity. This response encompasses many areas of cellular function, including protein regulation (Phf6) and ion/metal regulation (PANK2 and Car4). Notably, these responses were largely absent from the cells of the SN. Our data show a clear dynamic response in maintaining the homeostasis and viability of the neurons in the VTA that is lacking in the SN after neurotoxin challenge.},
  timestamp = {2015-12-07T21:58:10Z},
  urldate = {2015-12-07},
  journal = {Brain Research},
  author = {Phani, Sudarshan and Gonye, Gregory and Iacovitti, Lorraine},
  month = jul,
  year = {2010},
  keywords = {microarray,Substantia nigra,Ventral tegmental area},
  pages = {1--13}
}

@article{jahn_genetic_2015,
  title = {Genetic control of astrocyte function in neural circuits},
  volume = {9},
  issn = {1662-5102},
  doi = {10.3389/fncel.2015.00310},
  abstract = {During the last two decades numerous genetic approaches affecting cell function in vivo have been developed. Current state-of-the-art technology permits the selective switching of gene function in distinct cell populations within the complex organization of a given tissue parenchyma. The tamoxifen-inducible Cre/loxP gene recombination and the doxycycline-dependent modulation of gene expression are probably the most popular genetic paradigms. Here, we will review applications of these two strategies while focusing on the interactions of astrocytes and neurons in the central nervous system (CNS) and their impact for the whole organism. Abolishing glial sensing of neuronal activity by selective deletion of glial transmitter receptors demonstrated the impact of astrocytes for higher cognitive functions such as learning and memory, or the more basic body control of muscle coordination. Interestingly, also interfering with glial output, i.e., the release of gliotransmitters can drastically change animal's physiology like sleeping behavior. Furthermore, such genetic approaches have also been used to restore astrocyte function. In these studies two alternatives were employed to achieve proper genetic targeting of astrocytes: transgenes using the promoter of the human glial fibrillary acidic protein (GFAP) or homologous recombination into the glutamate-aspartate transporter (GLAST) locus. We will highlight their specific properties that could be relevant for their use.},
  timestamp = {2016-03-24T08:39:48Z},
  urldate = {2016-03-24},
  journal = {Frontiers in Cellular Neuroscience},
  author = {Jahn, Hannah M. and Scheller, Anja and Kirchhoff, Frank},
  month = aug,
  year = {2015},
  pmid = {26347607},
  pmcid = {PMC4538289}
}

@article{bushel_blood_2007-1,
  title = {Blood gene expression signatures predict exposure levels},
  volume = {104},
  issn = {0027-8424, 1091-6490},
  doi = {10.1073/pnas.0706987104},
  abstract = {To respond to potential adverse exposures properly, health care providers need accurate indicators of exposure levels. The indicators are particularly important in the case of acetaminophen (APAP) intoxication, the leading cause of liver failure in the U.S. We hypothesized that gene expression patterns derived from blood cells would provide useful indicators of acute exposure levels. To test this hypothesis, we used a blood gene expression data set from rats exposed to APAP to train classifiers in two prediction algorithms and to extract patterns for prediction using a profiling algorithm. Prediction accuracy was tested on a blinded, independent rat blood test data set and ranged from 88.9\% to 95.8\%. Genomic markers outperformed predictions based on traditional clinical parameters. The expression profiles of the predictor genes from the patterns extracted from the blood exhibited remarkable (97\% accuracy) transtissue APAP exposure prediction when liver gene expression data were used as a test set. Analysis of human samples revealed separation of APAP-intoxicated patients from control individuals based on blood expression levels of human orthologs of the rat discriminatory genes. The major biological signal in the discriminating genes was activation of an inflammatory response after exposure to toxic doses of APAP. These results support the hypothesis that gene expression data from peripheral blood cells can provide valuable information about exposure levels, well before liver damage is detected by classical parameters. It also supports the potential use of genomic markers in the blood as surrogates for clinical markers of potential acute liver damage.},
  language = {en},
  timestamp = {2015-08-18T01:55:06Z},
  number = {46},
  urldate = {2015-08-18},
  journal = {Proceedings of the National Academy of Sciences},
  author = {Bushel, P. R. and Heinloth, A. N. and Li, J. and Huang, L. and Chou, J. W. and Boorman, G. A. and Malarkey, D. E. and Houle, C. D. and Ward, S. M. and Wilson, R. E. and Fannin, R. D. and Russo, M. W. and Watkins, P. B. and Tennant, R. W. and Paules, R. S.},
  month = nov,
  year = {2007},
  keywords = {acetaminophen,Genomics,hepatotoxicity,microarray,prediction},
  pages = {18211--18216},
  pmid = {17984051}
}

@article{heiman_cell_2014,
  title = {Cell type\textendash{}specific {{mRNA}} purification by translating ribosome affinity purification ({{TRAP}})},
  volume = {9},
  copyright = {\textcopyright{} 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1754-2189},
  doi = {10.1038/nprot.2014.085},
  abstract = {Cellular diversity and architectural complexity create barriers to understanding the function of the mammalian CNS at a molecular level. To address this problem, we have recently developed a methodology that provides the ability to profile the entire translated mRNA complement of any genetically defined cell population. This methodology, which we termed translating ribosome affinity purification, or TRAP, combines cell type\textendash{}specific transgene expression with affinity purification of translating ribosomes. TRAP can be used to study the cell type\textendash{}specific mRNA profiles of any genetically defined cell type, and it has been used in organisms ranging from Drosophila melanogaster to mice and human cultured cells. Unlike other methodologies that rely on microdissection, cell panning or cell sorting, the TRAP methodology bypasses the need for tissue fixation or single-cell suspensions (and the potential artifacts that these treatments introduce) and reports on mRNAs in the entire cell body. This protocol provides a step-by-step guide to implement the TRAP methodology, which takes 2 d to complete once all materials are in hand.},
  language = {en},
  timestamp = {2016-02-16T01:28:55Z},
  number = {6},
  urldate = {2016-02-16},
  journal = {Nature Protocols},
  author = {Heiman, Myriam and Kulicke, Ruth and Fenster, Robert J. and Greengard, Paul and Heintz, Nathaniel},
  month = jun,
  year = {2014},
  keywords = {Gene Expression Profiling,immunoprecipitation,Isolation,Molecular neuroscience,separation and purification},
  pages = {1282--1291}
}

@article{liotta_molecular_2000,
  title = {Molecular profiling of human cancer},
  volume = {1},
  copyright = {\textcopyright{} 2000 Nature Publishing Group},
  issn = {1471-0056},
  doi = {10.1038/35049567},
  abstract = {The completion of the human genome sequence will soon provide the foundation of knowledge to tackle the next (and greatest) challenge of biology and medicine \textemdash{} the comprehensive understanding of the `software and the hardware' of the cell and the organism in diseased as well as healthy states. Owing to the layered complexity and interdependence of biological systems, this goal cannot be realistically approached by studying one gene or one protein at a time.},
  language = {en},
  timestamp = {2016-03-16T06:44:11Z},
  number = {1},
  urldate = {2016-03-16},
  journal = {Nature Reviews Genetics},
  author = {Liotta, Lance and Petricoin, Emanuel},
  month = oct,
  year = {2000},
  pages = {48--56}
}

@article{fornuskova_novel_2010,
  title = {Novel insights into the assembly and function of human nuclear-encoded cytochrome {\emph{c}} oxidase subunits 4, 5a, 6a, 7a and 7b},
  volume = {428},
  issn = {0264-6021, 1470-8728},
  doi = {10.1042/BJ20091714},
  language = {en},
  timestamp = {2016-02-22T19:37:30Z},
  number = {3},
  urldate = {2014-09-19},
  journal = {Biochemical Journal},
  author = {Fornuskova, Daniela and Stiburek, Lukas and Wenchich, Laszlo and Vinsova, Kamila and Hansikova, Hana and Zeman, Jiri},
  month = jun,
  year = {2010},
  note = {00000},
  pages = {363--374}
}

@article{zeisel_cell_2015,
  title = {Cell types in the mouse cortex and hippocampus revealed by single-cell {{RNA}}-seq},
  volume = {347},
  issn = {0036-8075, 1095-9203},
  doi = {10.1126/science.aaa1934},
  abstract = {The mammalian cerebral cortex supports cognitive functions such as sensorimotor integration, memory, and social behaviors. Normal brain function relies on a diverse set of differentiated cell types, including neurons, glia, and vasculature. Here, we have used large-scale single-cell RNA sequencing (RNA-seq) to classify cells in the mouse somatosensory cortex and hippocampal CA1 region. We found 47 molecularly distinct subclasses, comprising all known major cell types in the cortex. We identified numerous marker genes, which allowed alignment with known cell types, morphology, and location. We found a layer I interneuron expressing Pax6 and a distinct postmitotic oligodendrocyte subclass marked by Itpr2. Across the diversity of cortical cell types, transcription factors formed a complex, layered regulatory code, suggesting a mechanism for the maintenance of adult cell type identity.
Cellular diversity in the brain revealed
The mammalian brain has an extraordinarily large number of cells. Although there are quite a few different cell types, many cells in any one category tend to look alike. Zeisel et al. analyzed the transcriptomes of mouse brain cells to reveal more than meets the eye. Interneurons of similar type were found in dissimilar regions of the brain. Oligodendrocytes that seemed to be all of one class were differentiated by their molecular signatures into a half-dozen classes. Microglia associated with blood vessels were distinguished from look-alike perivascular macrophages. Thus, the complex microanatomy of the brain can be revealed by the RNAs expressed in its cells.
Science, this issue p. 1138},
  language = {en},
  timestamp = {2015-08-27T18:55:09Z},
  number = {6226},
  urldate = {2015-08-27},
  journal = {Science},
  author = {Zeisel, Amit and Mu{\~n}oz-Manchado, Ana B. and Codeluppi, Simone and L{\"o}nnerberg, Peter and Manno, Gioele La and Jur{\'e}us, Anna and Marques, Sueli and Munguba, Hermany and He, Liqun and Betsholtz, Christer and Rolny, Charlotte and Castelo-Branco, Gon{\c c}alo and Hjerling-Leffler, Jens and Linnarsson, Sten},
  month = jun,
  year = {2015},
  pages = {1138--1142},
  pmid = {25700174}
}

@article{ziegler-heitbrock_nomenclature_2010,
  title = {Nomenclature of monocytes and dendritic cells in blood},
  volume = {116},
  issn = {1528-0020},
  doi = {10.1182/blood-2010-02-258558},
  abstract = {Monocytes and cells of the dendritic cell lineage circulate in blood and eventually migrate into tissue where they further mature and serve various functions, most notably in immune defense. Over recent years these cells have been characterized in detail with the use of cell surface markers and flow cytometry, and subpopulations have been described. The present document proposes a nomenclature for these cells and defines 3 types of monocytes (classical, intermediate, and nonclassical monocytes) and 3 types of dendritic cells (plasmacytoid and 2 types of myeloid dendritic cells) in human and in mouse blood. This classification has been approved by the Nomenclature Committee of the International Union of Immunological Societies, and we are convinced that it will facilitate communication among experts and in the wider scientific community.},
  language = {eng},
  timestamp = {2015-08-21T01:21:39Z},
  number = {16},
  journal = {Blood},
  author = {Ziegler-Heitbrock, Loems and Ancuta, Petronela and Crowe, Suzanne and Dalod, Marc and Grau, Veronika and Hart, Derek N. and Leenen, Pieter J. M. and Liu, Yong-Jun and MacPherson, Gordon and Randolph, Gwendalyn J. and Scherberich, Juergen and Schmitz, Juergen and Shortman, Ken and Sozzani, Silvano and Strobl, Herbert and Zembala, Marek and Austyn, Jonathan M. and Lutz, Manfred B.},
  month = oct,
  year = {2010},
  keywords = {Animals,Blood Cells,Dendritic Cells,Humans,Mice,Monocytes,Terminology as Topic},
  pages = {e74--80},
  pmid = {20628149}
}

@article{sugino_molecular_2006,
  title = {Molecular taxonomy of major neuronal classes in the adult mouse forebrain},
  volume = {9},
  copyright = {\textcopyright{} 2005 Nature Publishing Group},
  issn = {1097-6256},
  doi = {10.1038/nn1618},
  abstract = {Identifying the neuronal cell types that comprise the mammalian forebrain is a central unsolved problem in neuroscience. Global gene expression profiles offer a potentially unbiased way to assess functional relationships between neurons. Here, we carried out microarray analysis of 12 populations of neurons in the adult mouse forebrain. Five of these populations were chosen from cingulate cortex and included several subtypes of GABAergic interneurons and pyramidal neurons. The remaining seven were derived from the somatosensory cortex, hippocampus, amygdala and thalamus. Using these expression profiles, we were able to construct a taxonomic tree that reflected the expected major relationships between these populations, such as the distinction between cortical interneurons and projection neurons. The taxonomic tree indicated highly heterogeneous gene expression even within a single region. This dataset should be useful for the classification of unknown neuronal subtypes, the investigation of specifically expressed genes and the genetic manipulation of specific neuronal circuit elements.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-10-21},
  journal = {Nature Neuroscience},
  author = {Sugino, Ken and Hempel, Chris M. and Miller, Mark N. and Hattox, Alexis M. and Shapiro, Peter and Wu, Caizi and Huang, Z. Josh and Nelson, Sacha B.},
  month = jan,
  year = {2006},
  pages = {99--107},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/H83VFRPV/nn1618.html:}
}

@article{koirala_identification_2010,
  title = {Identification of {{Novel Glial Genes}} by {{Single-Cell Transcriptional Profiling}} of {{Bergmann Glial Cells}} from {{Mouse Cerebellum}}},
  volume = {5},
  doi = {10.1371/journal.pone.0009198},
  abstract = {Bergmann glial cells play critical roles in the structure and function of the cerebellum. During development, their radial processes serve as guides for migrating granule neurons and their terminal endfeet tile to form the glia limitans. As the cerebellum matures, Bergmann glia perform important roles in synaptic transmission and synapse maintenance, while continuing to serve as essential structural elements. Despite growing evidence of the diverse functions of Bergmann glia, the molecular mechanisms that mediate these functions have remained largely unknown. As a step toward identifying the molecular repertoire underlying Bergmann glial function, here we examine global gene expression in individual Bergmann glia from developing (P6) and mature (P30) mouse cerebellum. When we select for developmentally regulated genes, we find that transcription factors and ribosomal genes are particularly enriched at P6 relative to P30; whereas synapse associated molecules are enriched at P30 relative to P6. We also analyze genes expressed at high levels at both ages. In all these categories, we find genes that were not previously known to be expressed in glial cells, and discuss novel functions some of these genes may potentially play in Bergmann glia. We also show that Bergmann glia, even in the adult, express a large set of genes thought to be specific to stem cells, suggesting that Bergmann glia may retain neural precursor potential as has been proposed. Finally, we highlight several genes that in the cerebellum are expressed in Bergmann glia but not astrocytes, and may therefore serve as new, specific markers for Bergmann glia.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-11-11},
  journal = {PLoS ONE},
  author = {Koirala, Samir and Corfas, Gabriel},
  month = feb,
  year = {2010},
  keywords = {unread},
  pages = {e9198},
  file = {PLoS Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/5GNXD46F/infodoi10.1371journal.pone.html:}
}

@article{jaffe_postmortem_2015,
  title = {Postmortem human brain genomics in neuropsychiatric disorders-how far can we go?},
  volume = {36},
  issn = {1873-6882},
  doi = {10.1016/j.conb.2015.11.002},
  abstract = {Large-scale collection of postmortem human brain tissue and subsequent genomic data generation has become a useful approach for better identifying etiological factors contributing to neuropsychiatric disorders. In particular, studying genetic risk variants in non-psychiatric controls can identify biological mechanisms of risk free from confounding factors related to epiphenomena of illness. While the field has begun moving towards cell type-specific analyses, homogenate brain tissue with accompanying cellular profiles, can still identify useful hypotheses for more focused experiments, particularly when the dysregulated cell types are unknown. Technological advances, larger sample sizes, and focused research questions can continue to further leverage postmortem human brain research to better identify and understand the molecular etiology of neuropsychiatric disorders.},
  language = {ENG},
  timestamp = {2016-02-02T04:39:16Z},
  journal = {Current Opinion in Neurobiology},
  author = {Jaffe, Andrew E.},
  month = dec,
  year = {2015},
  pages = {107--111},
  pmid = {26685806}
}

@article{wu_quantitative_2014,
  title = {Quantitative assessment of single-cell {{RNA}}-sequencing methods},
  volume = {11},
  copyright = {\textcopyright{} 2013 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1548-7091},
  doi = {10.1038/nmeth.2694},
  abstract = {Interest in single-cell whole-transcriptome analysis is growing rapidly, especially for profiling rare or heterogeneous populations of cells. We compared commercially available single-cell RNA amplification methods with both microliter and nanoliter volumes, using sequence from bulk total RNA and multiplexed quantitative PCR as benchmarks to systematically evaluate the sensitivity and accuracy of various single-cell RNA-seq approaches. We show that single-cell RNA-seq can be used to perform accurate quantitative transcriptome measurement in individual cells with a relatively small number of sequencing reads and that sequencing large numbers of single cells can recapitulate bulk transcriptome complexity.},
  language = {en},
  timestamp = {2016-02-13T05:12:01Z},
  number = {1},
  urldate = {2016-02-13},
  journal = {Nature Methods},
  author = {Wu, Angela R. and Neff, Norma F. and Kalisky, Tomer and Dalerba, Piero and Treutlein, Barbara and Rothenberg, Michael E. and Mburu, Francis M. and Mantalas, Gary L. and Sim, Sopheak and Clarke, Michael F. and Quake, Stephen R.},
  month = jan,
  year = {2014},
  keywords = {Gene expression analysis,Genome-wide analysis of gene expression,Transcriptomics},
  pages = {41--46}
}

@article{pongrac_gene_2002,
  title = {Gene expression profiling with {{DNA}} microarrays: advancing our understanding of psychiatric disorders},
  volume = {27},
  issn = {0364-3190},
  shorttitle = {Gene expression profiling with {{DNA}} microarrays},
  abstract = {DNA microarray transcriptome profiling of the postmortem brain opens novel horizons in understanding molecular changes associated with complex psychiatric disorders. With careful analysis and interpretation of microarray data we are uncovering previously unknown, expression patterns that maybe subject-specific and pivotal in understanding the disease process. In our recent studies, analyses of the prefrontal cortex of subjects with schizophrenia and matched controls uncovered complex changes in the expression of genes related to presynaptic secretory release, GABAergic and glutamatergic transmission, metabolic pathways, myelination, as well as cAMP and phosphoinositol second messenger systems. Our goal will be to integrate this expression data within the context of the relevant anatomical, biochemical, molecular, imaging and clinical findings.},
  language = {eng},
  timestamp = {2015-08-13T22:18:44Z},
  number = {10},
  journal = {Neurochemical Research},
  author = {Pongrac, Julie and Middleton, Frank A. and Lewis, David A. and Levitt, Pat and Mirnics, K{\'a}roly},
  month = oct,
  year = {2002},
  keywords = {Brain,Gene Expression Profiling,Humans,Mental Disorders,Oligonucleotide Array Sequence Analysis,Schizophrenia,Synapses,unread},
  pages = {1049--1063},
  pmid = {12462404}
}

@article{boesmans_astrocyte_2014,
  title = {The astrocyte marker {{Aldh1L1}} does not reliably label enteric glial cells},
  volume = {566},
  issn = {0304-3940},
  doi = {10.1016/j.neulet.2014.02.042},
  abstract = {Enteric glial cells are increasingly acknowledged as important partners of enteric neurons in the control of gastrointestinal function. They share morphological features and expression of antigenic markers with astrocytes of the central nervous system. Recently, aldehyde dehydrogenase 1 family member L1 (Aldh1L1) has been proposed as a novel and specific marker for astrocytes. Taking the known similarities between astrocytes and enteric glia into account, we sought to investigate whether enteric glial cells also express Aldh1L1. To this end, we performed immunostaining on preparations of myenteric plexus obtained from adult Aldh1L1-eGFP bacterial artificial chromosome (BAC) transgenic mice and found that the Aldh1L1 promoter is indeed active in enteric glia, albeit mainly in cells residing outside the myenteric ganglia. Apart from enteric glia, we also observed eGFP expression in interstitial cells of Cajal. Furthermore, myenteric ganglia of the large intestine contained eGFP positive neurons. Taken together, our data indicate that Aldh1L1 is not a suitable marker for enteric glial cells.},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2014-11-20},
  journal = {Neuroscience Letters},
  author = {Boesmans, Werend and Rocha, Nat{\'a}lia Pessoa and Reis, Helton Jos{\'e} and Holt, Matthew and {Vanden Berghe}, Pieter},
  month = apr,
  year = {2014},
  keywords = {Aldh1L1,Aldh1l1,astrocyte,Enteric glial cell,Enteric nervous system,Enteric neuron},
  pages = {102--105},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/6GMN6MNX/S0304394014001463.html:}
}

@article{okaty_quantitative_2011,
  title = {A {{Quantitative Comparison}} of {{Cell-Type-Specific Microarray Gene Expression Profiling Methods}} in the {{Mouse Brain}}},
  volume = {6},
  doi = {10.1371/journal.pone.0016493},
  abstract = {Expression profiling of restricted neural populations using microarrays can facilitate neuronal classification and provide insight into the molecular bases of cellular phenotypes. Due to the formidable heterogeneity of intermixed cell types that make up the brain, isolating cell types prior to microarray processing poses steep technical challenges that have been met in various ways. These methodological differences have the potential to distort cell-type-specific gene expression profiles insofar as they may insufficiently filter out contaminating mRNAs or induce aberrant cellular responses not normally present in vivo. Thus we have compared the repeatability, susceptibility to contamination from off-target cell-types, and evidence for stress-responsive gene expression of five different purification methods - Laser Capture Microdissection (LCM), Translating Ribosome Affinity Purification (TRAP), Immunopanning (PAN), Fluorescence Activated Cell Sorting (FACS), and manual sorting of fluorescently labeled cells (Manual). We found that all methods obtained comparably high levels of repeatability, however, data from LCM and TRAP showed significantly higher levels of contamination than the other methods. While PAN samples showed higher activation of apoptosis-related, stress-related and immediate early genes, samples from FACS and Manual studies, which also require dissociated cells, did not. Given that TRAP targets actively translated mRNAs, whereas other methods target all transcribed mRNAs, observed differences may also reflect translational regulation.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2015-02-12},
  journal = {PLoS ONE},
  author = {Okaty, Benjamin W. and Sugino, Ken and Nelson, Sacha B.},
  month = jan,
  year = {2011},
  keywords = {Animals,Brain,Gene Expression Profiling,Mice,Microarray Analysis,Neurons,Protein Biosynthesis,Reproducibility of Results,RNA; Messenger,Tissue Distribution,Transcription; Genetic},
  pages = {e16493}
}

@article{alberts_expression_2011,
  title = {Expression {{QTL}} mapping in regulatory and helper {{T}} cells from the {{BXD}} family of strains reveals novel cell-specific genes, gene-gene interactions and candidate genes for auto-immune disease},
  volume = {12},
  issn = {1471-2164},
  doi = {10.1186/1471-2164-12-610},
  abstract = {BACKGROUND: Regulatory T cells (Tregs) play an essential role in the control of the immune response. Treg cells represent important targets for therapeutic interventions of the immune system. Therefore, it will be very important to understand in more detail which genes are specifically activated in Treg cells versus T helper (Th) cells, and which gene regulatory circuits may be involved in specifying and maintaining Treg cell homeostasis.
RESULTS: We isolated Treg and Th cells from a genetically diverse family of 31 BXD type recombinant inbred strains and the fully inbred parental strains of this family--C57BL/6J and DBA/2J. Subsequently genome-wide gene expression studies were performed from the isolated Treg and Th cells. A comparative analysis of the transcriptomes of these cell populations allowed us to identify many novel differentially expressed genes. Analysis of cis- and trans-expression Quantitative Trait Loci (eQTLs) highlighted common and unique regulatory mechanisms that are active in the two cell types. Trans-eQTL regions were found for the Treg functional genes Nrp1, Stat3 and Ikzf4. Analyses of the respective QTL intervals suggested several candidate genes that may be involved in regulating these genes in Treg cells. Similarly, possible candidate genes were found which may regulate the expression of F2rl1, Ctla4, Klrb1f. In addition, we identified a focused group of candidate genes that may be important for the maintenance of self-tolerance and the prevention of allergy.
CONCLUSIONS: Variation of expression across the strains allowed us to find many novel gene-interaction networks in both T cell subsets. In addition, these two data sets enabled us to identify many differentially expressed genes and to nominate candidate genes that may have important functions for the maintenance of self-tolerance and the prevention of allergy.},
  language = {eng},
  timestamp = {2015-08-21T21:41:16Z},
  journal = {BMC genomics},
  author = {Alberts, Rudi and Chen, Hairong and Pommerenke, Claudia and Smit, August B. and Spijker, Sabine and Williams, Robert W. and Geffers, Robert and Bruder, Dunja and Schughart, Klaus},
  year = {2011},
  keywords = {Animals,Autoimmune Diseases,Mice,Mice; Inbred C57BL,Mice; Inbred DBA,Quantitative Trait Loci,T-Lymphocytes; Helper-Inducer,T-Lymphocytes; Regulatory},
  pages = {610},
  pmid = {22182475},
  pmcid = {PMC3277499}
}

@article{bearden_neuropsychology_2001,
  title = {The neuropsychology and neuroanatomy of bipolar affective disorder: a critical review},
  volume = {3},
  issn = {1399-5618},
  shorttitle = {The neuropsychology and neuroanatomy of bipolar affective disorder},
  doi = {10.1034/j.1399-5618.2001.030302.x},
  abstract = {Objectives: To present a comprehensive review of the existing neuropsychological and neuroimaging literature on bipolar affective disorder. This review critically evaluates two common conceptions regarding the neuropsychology of bipolar disorder: 1) that, in contrast to schizophrenia, bipolar affective disorder is not associated with general cognitive impairment independent of illness episodes, and 2) relative right hemisphere (RH) dysfunction is implicated in bipolar illness patients, supported by reports of relatively greater impairment in visuospatial functioning, lateralization abnormalities, and mania secondary to RH lesions.  Methods: The major computerized databases (Medline and PSYCInfo) were consulted in order to conduct a comprehensive, integrated review of the literature on the neuropsychology and neuroanatomy of bipolar disorder. Articles meeting specified criteria were included in this review.  Results: In a critical evaluation of the above notions, this paper determines that: 1) while there is little evidence for selective RH dysfunction, significant cognitive impairment may be present in bipolar illness, particularly in a subgroup of chronic, elderly or multiple-episode patients, suggesting a possible toxic disease process, and 2) the underlying functional correlate of these cognitive deficits may be white matter lesions (`signal hyperintensities') in the frontal lobes and basal ganglia, regions critical for executive function, attention, speeded information processing, learning and memory, and affect regulation. While this hypothesized neural correlate of cognitive impairment in bipolar disorder is speculative, preliminary functional neuroimaging evidence supports the notion of frontal and subcortical hypometabolism in bipolar illness.  Conclusions: The etiology of the structural brain abnormalities commonly seen in bipolar illness, and their corresponding functional deficits, remains unknown. It is possible that neurodevelopmental anomalies may play a role, and it remains to be determined whether there is also some pathophysiological progression that occurs with repeated illness episodes. More research is needed on first-episode patients, relatives of bipolar probands, and within prospective longitudinal paradigms in order to isolate disease-specific impairments and genetic markers of neurocognitive function in bipolar disorder.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {3},
  urldate = {2014-12-17},
  journal = {Bipolar Disorders},
  author = {Bearden, Carrie E and Hoffman, Kathleen M and Cannon, Tyrone D},
  year = {2001},
  keywords = {affective disorders,bipolar disorder,cognition,depression,mania,neuroanatomy,neuroimaging,neuropsychology},
  pages = {106--150},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/R6SQ6KBG/full.html:}
}

@article{mieczkowski_probe_2010,
  title = {Probe set filtering increases correlation between {{Affymetrix GeneChip}} and {{qRT-PCR}} expression measurements},
  volume = {11},
  copyright = {2010 Mieczkowski et al; licensee BioMed Central Ltd.},
  issn = {1471-2105},
  doi = {10.1186/1471-2105-11-104},
  abstract = {Affymetrix GeneChip microarrays are popular platforms for expression profiling in two types of studies: detection of differential expression computed by p-values of t-test and estimation of fold change between analyzed groups. There are many different preprocessing algorithms for summarizing Affymetrix data. The main goal of these methods is to remove effects of non-specific hybridization, and to optimally combine information from multiple probes annotated to the same transcript. The methods are benchmarked by comparison with reference methods, such as quantitative reverse-transcription PCR (qRT-PCR).
PMID: 20181266},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2015-01-14},
  journal = {BMC Bioinformatics},
  author = {Mieczkowski, Jakub and Tyburczy, Magdalena E. and Dabrowski, Michal and Pokarowski, Piotr},
  month = feb,
  year = {2010},
  pages = {104},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/WKVHIAUJ/104.html:},
  pmid = {20181266}
}

@article{labaj_characterization_2011,
  title = {Characterization and improvement of {{RNA-Seq}} precision in quantitative transcript expression profiling},
  volume = {27},
  issn = {1367-4803, 1460-2059},
  doi = {10.1093/bioinformatics/btr247},
  abstract = {Motivation: Measurement precision determines the power of any analysis to reliably identify significant signals, such as in screens for differential expression, independent of whether the experimental design incorporates replicates or not. With the compilation of large-scale RNA-Seq datasets with technical replicate samples, however, we can now, for the first time, perform a systematic analysis of the precision of expression level estimates from massively parallel sequencing technology. This then allows considerations for its improvement by computational or experimental means.
Results: We report on a comprehensive study of target identification and measurement precision, including their dependence on transcript expression levels, read depth and other parameters. In particular, an impressive recall of 84\% of the estimated true transcript population could be achieved with 331 million 50 bp reads, with diminishing returns from longer read lengths and even less gains from increased sequencing depths. Most of the measurement power (75\%) is spent on only 7\% of the known transcriptome, however, making less strongly expressed transcripts harder to measure. Consequently, \ensuremath{<}30\% of all transcripts could be quantified reliably with a relative error \ensuremath{<}20\%. Based on established tools, we then introduce a new approach for mapping and analysing sequencing reads that yields substantially improved performance in gene expression profiling, increasing the number of transcripts that can reliably be quantified to over 40\%. Extrapolations to higher sequencing depths highlight the need for efficient complementary steps. In discussion we outline possible experimental and computational strategies for further improvements in quantification precision.
Contact: rnaseq10@boku.ac.at
Supplementary information: Supplementary data are available at Bioinformatics online.},
  language = {en},
  timestamp = {2016-02-15T19:39:04Z},
  number = {13},
  urldate = {2016-02-15},
  journal = {Bioinformatics},
  author = {\L{}abaj, Pawe\l{} P. and Leparc, Germ{\'a}n G. and Linggi, Bryan E. and Markillie, Lye Meng and Wiley, H. Steven and Kreil, David P.},
  month = jan,
  year = {2011},
  pages = {i383--i391},
  pmid = {21685096}
}

@article{watanabe_monoclonal_2006,
  title = {Monoclonal antibody {{Rip}} specifically recognizes 2\ensuremath{'},3\ensuremath{'}-cyclic nucleotide 3\ensuremath{'}-phosphodiesterase in oligodendrocytes},
  volume = {84},
  copyright = {Copyright \textcopyright{} 2006 Wiley-Liss, Inc.},
  issn = {1097-4547},
  doi = {10.1002/jnr.20950},
  abstract = {The antigen recognized with monoclonal antibody (mAb) Rip (Rip-antigen) has been long used as a marker of oligodendrocytes and myelin sheaths. However, the identity of Rip-antigen has yet to be elucidated. We herein identified the Rip-antigen. No signal recognized by mAb-Rip was detected by immunoblot analyses in the rat brain, cultured rat oligodendrocytes, or the oligodendrocyte cell line CG-4. As this antibody worked very well on immunocytochemistry and immunohistochemistry, Rip-antigen was immunopurified with mAb-Rip from the differentiated CG-4 cells. Eight strong-intensity bands thus appeared on 5\textendash{}20\% SDS-PAGE with SYPRO ruby fluorescence staining. To identify these molecules, each band extracted from the gel was analyzed by MALDI-QIT/TOF mass spectrometry. We found an interesting molecule in the oligodendrocytes from an approximately 44-kDa band as 2\ensuremath{'},3\ensuremath{'}-cyclic nucleotide 3\ensuremath{'}-phosphodiesterase (CNP). To test whether CNP was recognized by mAb-Rip, double-immunofluorescence staining was performed by using Alexa Fluor 488-conjugated mAb-Rip and Alexa Fluor 568-conjugated mAb-CNP in the rat cerebellum, mouse cerebellum, cultured rat oligodendrocytes, and CG-4 cells. The Rip-antigen was colocalized with CNP in these cells and tissues. To provide direct evidence that CNP was recognized by mAb-Rip, rat Cnp1-transfected HEK293T cells were used for double-immunofluorescence staining with mAb-Rip and mAb-CNP. The Rip-antigen was colocalized with CNP in rat Cnp1-transfected HEK293T cells, but the antigen was not detected by mAb-Rip and mAb-CNP in mock-transfected HEK293T cells. Overall, we have demonstrated that the antigen labeled with mAb-Rip is CNP in the oligodendrocytes. \textcopyright{} 2006 Wiley-Liss, Inc.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {3},
  urldate = {2014-11-26},
  journal = {Journal of Neuroscience Research},
  author = {Watanabe, Masatomo and Sakurai, Yoko and Ichinose, Tatsuya and Aikawa, Yoshikatsu and Kotani, Masaharu and Itoh, Kouichi},
  month = aug,
  year = {2006},
  keywords = {CG-4,immunoprecipitation,mass spectrometry,oligodendrocytes},
  pages = {525--533},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/9XBV2IWB/abstract.html:}
}

@article{ortutay_proprotein_2015,
  title = {Proprotein convertase {{FURIN}} regulates {{T}} cell receptor-induced transactivation},
  volume = {98},
  issn = {1938-3673},
  doi = {10.1189/jlb.2A0514-257RR},
  abstract = {Antigen emergence rapidly stimulates T cells, which leads to changes in cytokine production, cell proliferation, and differentiation. Some of the key molecules involved in these events, such as TGF-\ensuremath{\beta}1 and NOTCH1, are synthesized initially as inactive precursors and are proteolytically activated during T cell activation. PCSKs regulate proprotein maturation by catalyzing the proteolytic cleavage of their substrates. The prototype PCSK FURIN is induced upon TCR activation, and its expression in T cells is critical for the maintenance of peripheral immune tolerance. In this study, we tested the hypothesis that FURIN regulates T cell activation. Our data demonstrate that IL-2 is increased initially in FURIN-deficient mouse CD4(+) T cells, but the TCR-induced IL-2 mRNA expression is not sustained in the absence of FURIN. Accordingly, the inhibition of FURIN in human Jurkat T cell lines also results in a decrease in IL-2 production, whereas the overexpression of WT FURIN is associated with elevated IL-2 levels. In Jurkat cells, FURIN is dispensable for immediate TCR signaling steps, such as ERK, ZAP70, or LAT phosphorylation. However, with the use of gene reporter assays, we demonstrate that FURIN regulates the AP-1, NFAT, and NF-\ensuremath{\kappa}B transcription factors. Finally, by performing a transcription factor-binding site enrichment analysis on FURIN-dependent transcriptomes, we identify the FURIN-regulated transcription factors in mouse CD4(+) T cell subsets. Collectively, our work confirms the hypothesis that the TCR-regulated protease FURIN plays an important role in T cell activation and that it can specifically modulate TCR-activated transactivation.},
  language = {eng},
  timestamp = {2015-08-20T22:56:56Z},
  number = {1},
  journal = {Journal of Leukocyte Biology},
  author = {Ortutay, Zsuzsanna and Oksanen, Anna and Aittom{\"a}ki, Saara and Ortutay, Csaba and Pesu, Marko},
  month = jul,
  year = {2015},
  pages = {73--83},
  pmid = {25926688}
}

@article{tasic_adult_2016,
  title = {Adult mouse cortical cell taxonomy revealed by single cell transcriptomics},
  volume = {19},
  issn = {1546-1726},
  doi = {10.1038/nn.4216},
  abstract = {Nervous systems are composed of various cell types, but the extent of cell type diversity is poorly understood. We constructed a cellular taxonomy of one cortical region, primary visual cortex, in adult mice on the basis of single-cell RNA sequencing. We identified 49 transcriptomic cell types, including 23 GABAergic, 19 glutamatergic and 7 non-neuronal types. We also analyzed cell type-specific mRNA processing and characterized genetic access to these transcriptomic types by many transgenic Cre lines. Finally, we found that some of our transcriptomic cell types displayed specific and differential electrophysiological and axon projection properties, thereby confirming that the single-cell transcriptomic signatures can be associated with specific cellular properties.},
  language = {eng},
  timestamp = {2016-02-01T04:42:44Z},
  number = {2},
  journal = {Nature Neuroscience},
  author = {Tasic, Bosiljka and Menon, Vilas and Nguyen, Thuc Nghi and Kim, Tae Kyung and Jarsky, Tim and Yao, Zizhen and Levi, Boaz and Gray, Lucas T. and Sorensen, Staci A. and Dolbeare, Tim and Bertagnolli, Darren and Goldy, Jeff and Shapovalova, Nadiya and Parry, Sheana and Lee, Changkyu and Smith, Kimberly and Bernard, Amy and Madisen, Linda and Sunkin, Susan M. and Hawrylycz, Michael and Koch, Christof and Zeng, Hongkui},
  month = feb,
  year = {2016},
  pages = {335--346},
  pmid = {26727548}
}

@article{kangelaris_increased_2015,
  title = {Increased expression of neutrophil-related genes in patients with early sepsis-induced {{ARDS}}},
  volume = {308},
  copyright = {Copyright \textcopyright{} 2015 the American Physiological Society},
  issn = {1040-0605, 1522-1504},
  doi = {10.1152/ajplung.00380.2014},
  abstract = {The early sequence of events leading to the development of the acute respiratory distress syndrome (ARDS) in patients with sepsis remains inadequately understood. The purpose of this study was to identify changes in gene expression early in the course of illness, when mechanisms of injury may provide the most relevant treatment and prognostic targets. We collected whole blood RNA in critically ill patients admitted from the Emergency Department to the intensive care unit within 24 h of admission at a tertiary care center. Whole genome expression was compared in patients with sepsis and ARDS to patients with sepsis alone. We selected genes with \ensuremath{>}1 log2 fold change and false discovery rate \ensuremath{<}0.25, determined their significance in the literature, and performed pathway analysis. Several genes were upregulated in 29 patients with sepsis with ARDS compared with 28 patients with sepsis alone. The most differentially expressed genes included key mediators of the initial neutrophil response to infection: olfactomedin 4, lipocalin 2, CD24, and bactericidal/permeability-increasing protein. These gene expression differences withstood adjustment for age, sex, study batch, white blood cell count, and presence of pneumonia or aspiration. Pathway analysis demonstrated overrepresentation of genes involved in known respiratory and infection pathways. These data indicate that several neutrophil-related pathways may be involved in the early pathogenesis of sepsis-related ARDS. In addition, identifiable gene expression differences occurring early in the course of sepsis-related ARDS may further elucidate understanding of the neutrophil-related mechanisms in progression to ARDS.},
  language = {en},
  timestamp = {2015-08-17T19:25:17Z},
  number = {11},
  urldate = {2015-08-17},
  journal = {American Journal of Physiology - Lung Cellular and Molecular Physiology},
  author = {Kangelaris, Kirsten Neudoerffer and Prakash, Arun and Liu, Kathleen D. and Aouizerat, Bradley and Woodruff, Prescott G. and Erle, David J. and Rogers, Angela and Seeley, Eric J. and Chu, Jeffrey and Liu, Tom and Osterberg-Deiss, Thomas and Zhuo, Hanjing and Matthay, Michael A. and Calfee, Carolyn S.},
  month = jun,
  year = {2015},
  pages = {L1102--L1113},
  pmid = {25795726}
}

@incollection{fuxe_morphological_1970,
  title = {Morphological and {{Functional Aspects}} of {{Central Monoamine Neurons}}},
  volume = {13},
  abstract = {This chapter provides an overview of the morphology of central monoamine neurons and the function of central monoamine neurons. The Nigro\textendash{}Neostriatal neurons perform both the motor and mental functions. Their degeneration causes hypokinesia and rigidity while overstimulation of neostriatal dopamine (DA) receptors causes stereotyped behavior. The tubro-infundibular DA neurons probably act by way of inhibiting the release of luteinizing hormone releasing factor (LHRF) from the median eminence. The central noradrenaline (NA) neurons perform various functions, such as function in wakefulness, emotion, behavior, neuroendocrine function, and function in reflex activity. The central 5-hydroxytryptamine (5-HT) neurons contribute to the function in mood, wakefulness, thought process, behavior, neuroendocrine function, and function in reflex activity. The NA neurons probably are essential for conditioned processes as are the DA neurons while a destruction of the 5-HT neurons results in insomnia. Increased NA receptor activity results in aggression. The descending bulbospinal 5-HT neurons participate in the control of autonomic and somatic reflex activity, especially in the lumbosacral part.},
  timestamp = {2016-03-27T05:08:29Z},
  urldate = {2016-03-27},
  booktitle = {International {{Review}} of {{Neurobiology}}},
  publisher = {{Academic Press}},
  author = {Fuxe, Kjell and H{\"o}kfelt, Tomas and Ungerstedt, Urban},
  editor = {Smythies, Carl C. Pfeiffer and John R.},
  year = {1970},
  pages = {93--126}
}

@article{saunders_corelease_2015,
  title = {Corelease of acetylcholine and {{GABA}} from cholinergic forebrain neurons},
  volume = {4},
  issn = {2050-084X},
  doi = {10.7554/eLife.06412},
  abstract = {Neurotransmitter corelease is emerging as a common theme of central neuromodulatory systems. Though corelease of glutamate or GABA with acetylcholine has been reported within the cholinergic system, the full extent is unknown. To explore synaptic signaling of cholinergic forebrain neurons, we activated choline acetyltransferase expressing neurons using channelrhodopsin while recording post-synaptic currents (PSCs) in layer 1 interneurons. Surprisingly, we observed PSCs mediated by GABAA receptors in addition to nicotinic acetylcholine receptors. Based on PSC latency and pharmacological sensitivity, our results suggest monosynaptic release of both GABA and ACh. Anatomical analysis showed that forebrain cholinergic neurons express the GABA synthetic enzyme Gad2 and the vesicular GABA transporter (Slc32a1). We confirmed the direct release of GABA by knocking out Slc32a1 from cholinergic neurons. Our results identify GABA as an overlooked fast neurotransmitter utilized throughout the forebrain cholinergic system. GABA/ACh corelease may have major implications for modulation of cortical function by cholinergic neurons.},
  language = {eng},
  timestamp = {2015-08-21T02:15:26Z},
  journal = {eLife},
  author = {Saunders, Arpiar and Granger, Adam J. and Sabatini, Bernardo L.},
  year = {2015},
  keywords = {gad2},
  pmid = {25723967},
  pmcid = {PMC4371381}
}

@article{bader_automated_2003,
  title = {An automated method for finding molecular complexes in large protein interaction networks},
  volume = {4},
  copyright = {2003 Bader and Hogue; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.},
  issn = {1471-2105},
  doi = {10.1186/1471-2105-4-2},
  abstract = {Recent advances in proteomics technologies such as two-hybrid, phage display and mass spectrometry have enabled us to create a detailed map of biomolecular interaction networks. Initial mapping efforts have already produced a wealth of data. As the size of the interaction set increases, databases and computational methods will be required to store, visualize and analyze the information in order to effectively aid in knowledge discovery.
PMID: 12525261},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-10-29},
  journal = {BMC Bioinformatics},
  author = {Bader, Gary D. and Hogue, Christopher WV},
  month = jan,
  year = {2003},
  pages = {2},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/NRCMQTGK/2.html:},
  pmid = {12525261}
}

@article{goldstein_inflammation_2009,
  title = {Inflammation and the {{Phenomenology}}, {{Pathophysiology}}, {{Comorbidity}}, and {{Treatment}} of {{Bipolar Disorder}}: {{A Systematic Review}} of the {{Literature}}},
  volume = {70},
  issn = {0160-6689},
  shorttitle = {Inflammation and the {{Phenomenology}}, {{Pathophysiology}}, {{Comorbidity}}, and {{Treatment}} of {{Bipolar Disorder}}},
  doi = {10.4088/JCP.08r04505},
  timestamp = {2015-08-13T22:18:44Z},
  number = {8},
  urldate = {2014-12-17},
  journal = {The Journal of Clinical Psychiatry},
  author = {Goldstein, Benjamin I. and Kemp, David E. and Soczynska, Joanna K. and McIntyre, Roger S.},
  month = aug,
  year = {2009},
  pages = {1078--1090},
  file = {Inflammation and the phenomenology, pathophysiology, comorbidity, and treatment of bipolar... - Abstract - Europe PubMed Central:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/869NIB2T/19497250.html:}
}

@article{ren_production_2016,
  title = {Production of dopamine by aromatic {{L}}-amino acid decarboxylase cells after spinal cord injury},
  issn = {0897-7151},
  doi = {10.1089/neu.2015.4037},
  abstract = {Aromatic L-amino acid decarboxylase (AADC) cells are widely distributed in the spinal cord and their functions are largely unknown. We have previously found that AADC cells in the spinal cord could increase their ability to produce serotonin from 5-hydroxytryptophan after spinal cord injury (SCI). Since AADC is a common enzyme catalyzing 5-hydroxytryptophan to serotonin and L-dopa to dopamine (DA), it seems likely that the ability of AADC cells using L-dopa to synthesize DA is also increased. To prove whether this is the case a same rat sacral SCI model and a similar experimental paradigm were adopted as we used previously (Wienecke et al., J. Neurosci. 34, 11984, 2014). In the chronic SCI rats (\ensuremath{>} 45d), no AADC cells expressed DA if there was no exogenous L-dopa application. However, following administration of a peripheral AADC inhibitor (carbidopa) with or without a monoamine oxidase inhibitor (pargyline) co-application, systemic administration of L-dopa resulted in \textasciitilde{} 94\% of AADC cells to become DA-immunopositive in the spinal cord below the lesion, whereas in normal or sham-operated rats none or very few of AADC cells became DA-immunopositive with the same treatment. Using tail electromyography, spontaneous tail muscle activity was increased nearly 5-fold over the baseline level. When pretreated with a central AADC inhibitor (NSD1015), further application of L-dopa failed to increase the motoneuron activity although the expression of DA in the AADC cells was not completely inhibited. These findings demonstrate that AADC cells in the spinal cord below the lesion gain the ability to produce DA from its precursor in response to SCI. This ability also enables the AADC cells to produce 5-HT and trace-amines, and likely contributes to the development of hyperexcitability. These results might also be implicated for revealing the pathological mechanisms underlying L-dopa-induced dyskinesia in Parkinson's disease.},
  timestamp = {2016-03-22T23:30:52Z},
  urldate = {2016-03-22},
  journal = {Journal of Neurotrauma},
  author = {Ren, Liqun and Wienecke, Jacob and Hultborn, Hans and Zhang, Mengliang},
  month = feb,
  year = {2016},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/EFZ46VG2/neu.2015.html:}
}

@article{bennett_new_2016,
  title = {New tools for studying microglia in the mouse and human {{CNS}}},
  volume = {113},
  issn = {1091-6490},
  doi = {10.1073/pnas.1525528113},
  abstract = {The specific function of microglia, the tissue resident macrophages of the brain and spinal cord, has been difficult to ascertain because of a lack of tools to distinguish microglia from other immune cells, thereby limiting specific immunostaining, purification, and manipulation. Because of their unique developmental origins and predicted functions, the distinction of microglia from other myeloid cells is critically important for understanding brain development and disease; better tools would greatly facilitate studies of microglia function in the developing, adult, and injured CNS. Here, we identify transmembrane protein 119 (Tmem119), a cell-surface protein of unknown function, as a highly expressed microglia-specific marker in both mouse and human. We developed monoclonal antibodies to its intracellular and extracellular domains that enable the immunostaining of microglia in histological sections in healthy and diseased brains, as well as isolation of pure nonactivated microglia by FACS. Using our antibodies, we provide, to our knowledge, the first RNAseq profiles of highly pure mouse microglia during development and after an immune challenge. We used these to demonstrate that mouse microglia mature by the second postnatal week and to predict novel microglial functions. Together, we anticipate these resources will be valuable for the future study and understanding of microglia in health and disease.},
  language = {eng},
  timestamp = {2016-05-10T23:15:59Z},
  number = {12},
  journal = {Proceedings of the National Academy of Sciences of the United States of America},
  author = {Bennett, Mariko L. and Bennett, F. Chris and Liddelow, Shane A. and Ajami, Bahareh and Zamanian, Jennifer L. and Fernhoff, Nathaniel B. and Mulinyawe, Sara B. and Bohlen, Christopher J. and Adil, Aykezar and Tucker, Andrew and Weissman, Irving L. and Chang, Edward F. and Li, Gordon and Grant, Gerald A. and {Hayden Gephart}, Melanie G. and Barres, Ben A.},
  month = mar,
  year = {2016},
  keywords = {developmental neuroscience,glia,macrophage,microglia,RNAseq},
  pages = {E1738--1746},
  pmid = {26884166},
  pmcid = {PMC4812770}
}

@article{seringhaus_mismatch_2008,
  title = {Mismatch oligonucleotides in human and yeast: guidelines for probe design on tiling microarrays},
  volume = {9},
  copyright = {2008 Seringhaus et al; licensee BioMed Central Ltd.},
  issn = {1471-2164},
  shorttitle = {Mismatch oligonucleotides in human and yeast},
  doi = {10.1186/1471-2164-9-635},
  abstract = {Mismatched oligonucleotides are widely used on microarrays to differentiate specific from nonspecific hybridization. While many experiments rely on such oligos, the hybridization behavior of various degrees of mismatch (MM) structure has not been extensively studied. Here, we present the results of two large-scale microarray experiments on S. cerevisiae and H. sapiens genomic DNA, to explore MM oligonucleotide behavior with real sample mixtures under tiling-array conditions.
PMID: 19117516},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-11-28},
  journal = {BMC Genomics},
  author = {Seringhaus, Michael and Rozowsky, Joel and Royce, Thomas and Nagalakshmi, Ugrappa and Jee, Justin and Snyder, Michael and Gerstein, Mark},
  month = dec,
  year = {2008},
  pages = {635},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/AKX673VU/635.html:},
  pmid = {19117516}
}

@article{sanz_cell-type-specific_2009,
  title = {Cell-type-specific isolation of ribosome-associated {{mRNA}} from complex tissues},
  volume = {106},
  issn = {0027-8424, 1091-6490},
  doi = {10.1073/pnas.0907143106},
  abstract = {Gene profiling techniques allow the assay of transcripts from organs, tissues, and cells with an unprecedented level of coverage. However, most of these approaches are still limited by the fact that organs and tissues are composed of multiple cell types that are each unique in their patterns of gene expression. To identify the transcriptome from a single cell type in a complex tissue, investigators have relied upon physical methods to separate cell types or in situ hybridization and immunohistochemistry. Here, we describe a strategy to rapidly and efficiently isolate ribosome-associated mRNA transcripts from any cell type in vivo. We have created a mouse line, called RiboTag, which carries an Rpl22 allele with a floxed wild-type C-terminal exon followed by an identical C-terminal exon that has three copies of the hemagglutinin (HA) epitope inserted before the stop codon. When the RiboTag mouse is crossed to a cell-type-specific Cre recombinase-expressing mouse, Cre recombinase activates the expression of epitope-tagged ribosomal protein RPL22ha, which is incorporated into actively translating polyribosomes. Immunoprecipitation of polysomes with a monoclonal antibody against HA yields ribosome-associated mRNA transcripts from specific cell types. We demonstrate the application of this technique in brain using neuron-specific Cre recombinase-expressing mice and in testis using a Sertoli cell Cre recombinase-expressing mouse.},
  language = {en},
  timestamp = {2016-03-16T07:10:20Z},
  number = {33},
  urldate = {2016-03-16},
  journal = {Proceedings of the National Academy of Sciences},
  author = {Sanz, Elisenda and Yang, Linghai and Su, Thomas and Morris, David R. and McKnight, G. Stanley and Amieux, Paul S.},
  month = aug,
  year = {2009},
  keywords = {gene profiling,immunopreciptation,mouse genetics},
  pages = {13939--13944},
  pmid = {19666516}
}

@article{irizarry_comparison_2006,
  title = {Comparison of {{Affymetrix GeneChip}} expression measures},
  volume = {22},
  issn = {1367-4803, 1460-2059},
  doi = {10.1093/bioinformatics/btk046},
  abstract = {Motivation: In the Affymetrix GeneChip system, preprocessing occurs before one obtains expression level measurements. Because the number of competing preprocessing methods was large and growing we developed a benchmark to help users identify the best method for their application. A webtool was made available for developers to benchmark their procedures. At the time of writing over 50 methods had been submitted.
Results: We benchmarked 31 probe set algorithms using a U95A dataset of spike in controls. Using this dataset, we found that background correction, one of the main steps in preprocessing, has the largest effect on performance. In particular, background correction appears to improve accuracy but, in general, worsen precision. The benchmark results put this balance in perspective. Furthermore, we have improved some of the original benchmark metrics to provide more detailed information regarding precision and accuracy. A handful of methods stand out as providing the best balance using spike-in data with the older U95A array, although different experiments on more current arrays may benchmark differently.
Availability: The affycomp package, now version 1.5.2, continues to be available as part of the Bioconductor project (http://www.bioconductor.org). The webtool continues to be available at http://affycomp.biostat.jhsph.edu
Contact:rafa@jhu.edu
Supplementary information: Supplementary data are available at Bioinformatics online.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {7},
  urldate = {2014-10-17},
  journal = {Bioinformatics},
  author = {Irizarry, Rafael A. and Wu, Zhijin and Jaffee, Harris A.},
  month = jan,
  year = {2006},
  pages = {789--794},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/BGEGEZDH/789.html:},
  pmid = {16410320}
}

@article{quintens_mice_2013,
  title = {Mice {{Deficient}} in the {{Respiratory Chain Gene Cox6a2 Are Protected}} against {{High-Fat Diet-Induced Obesity}} and {{Insulin Resistance}}},
  volume = {8},
  doi = {10.1371/journal.pone.0056719},
  abstract = {Oxidative phosphorylation in mitochondria is responsible for 90\% of ATP synthesis in most cells. This essential housekeeping function is mediated by nuclear and mitochondrial genes encoding subunits of complex I to V of the respiratory chain. Although complex IV is the best studied of these complexes, the exact function of the striated muscle-specific subunit COX6A2 is still poorly understood. In this study, we show that Cox6a2-deficient mice are protected against high-fat diet-induced obesity, insulin resistance and glucose intolerance. This phenotype results from elevated energy expenditure and a skeletal muscle fiber type switch towards more oxidative fibers. At the molecular level we observe increased formation of reactive oxygen species, constitutive activation of AMP-activated protein kinase, and enhanced expression of uncoupling proteins. Our data indicate that COX6A2 is a regulator of respiratory uncoupling in muscle and we demonstrate that a novel and direct link exists between muscle respiratory chain activity and diet-induced obesity/insulin resistance.},
  timestamp = {2016-02-22T19:37:30Z},
  number = {2},
  urldate = {2014-09-08},
  journal = {PLoS ONE},
  author = {Quintens, Roel and Singh, Sarvjeet and Lemaire, Katleen and {De Bock}, Katrien and Granvik, Mikaela and Schraenen, Anica and Vroegrijk, Irene Olga Cornelia Maria and Costa, Veronica and {Van Noten}, Pieter and Lambrechts, Dennis and Lehnert, Stefan and {Van Lommel}, Leentje and Thorrez, Lieven and {De Faudeur}, Geoffroy and Romijn, Johannes Anthonius and Shelton, John Michael and Scorrano, Luca and Lijnen, Henri Roger and Voshol, Peter Jacobus and Carmeliet, Peter and Mammen, Pradeep Puthenveetil Abraham and Schuit, Frans},
  month = feb,
  year = {2013},
  note = {00005},
  pages = {e56719}
}

@article{halliwell_oxidative_2003,
  title = {Oxidative stress in cell culture: an under-appreciated problem?},
  volume = {540},
  issn = {1873-3468},
  shorttitle = {Oxidative stress in cell culture},
  doi = {10.1016/S0014-5793(03)00235-7},
  abstract = {Cell culture studies have given much valuable information about mechanisms of metabolism and signal transduction and of regulation of gene expression, proliferation, senescence, and death. However, cells in culture may behave differently from cells in vivo in many ways. One of these is that cell culture imposes a state of oxidative stress on cells. I argue that cells that survive and grow in culture might use ROS-dependent signal transduction pathways that rarely or never operate in vivo. A further problem is that cell culture media can catalyse the oxidation of compounds added to them, resulting in apparent cellular effects that are in fact due to oxidation products such as ROS. Such artefacts may have affected many studies on the effects of ascorbate, thiols, flavonoids and other polyphenolic compounds on cells in culture.},
  language = {en},
  timestamp = {2016-04-20T00:49:05Z},
  number = {1-3},
  urldate = {2016-04-20},
  journal = {FEBS Letters},
  author = {Halliwell, Barry},
  month = apr,
  year = {2003},
  keywords = {Antioxidant,Cell culture,Free radical,Oxidative stress,ROS; reactive oxygen species,Signal transduction},
  pages = {3--6}
}

@article{tan_neuron-enriched_2013,
  title = {Neuron-enriched gene expression patterns are regionally anti-correlated with oligodendrocyte-enriched patterns in the adult mouse and human brain},
  volume = {7},
  doi = {10.3389/fnins.2013.00005},
  abstract = {An important goal in neuroscience is to understand gene expression patterns in the brain. The recent availability of comprehensive and detailed expression atlases for mouse and human creates opportunities to discover global patterns and perform cross-species comparisons. Recently we reported that the major source of variation in gene transcript expression in the adult normal mouse brain can be parsimoniously explained as reflecting regional variation in glia to neuron ratios, and is correlated with degree of connectivity and location in the brain along the anterior-posterior axis. Here we extend this investigation to two gene expression assays of adult normal human brains that consisted of over 300 brain region samples, and perform comparative analyses of brain-wide expression patterns to the mouse. We performed principal components analysis (PCA) on the regional gene expression of the adult human brain to identify the expression pattern that has the largest variance. As in the mouse, we observed that the first principal component is composed of two anti-correlated patterns enriched in oligodendrocyte and neuron markers respectively. However, we also observed interesting discordant patterns between the two species. For example, a few mouse neuron markers show expression patterns that are more correlated with the human oligodendrocyte-enriched pattern and vice-versa. In conclusion, our work provides insights into human brain function and evolution by probing global relationships between regional cell type marker expression patterns in the human and mouse brain.},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2015-05-12},
  journal = {Neurogenomics},
  author = {Tan, Powell Patrick Cheng and French, Leon and Pavlidis, Paul},
  year = {2013},
  keywords = {cell type,evolution,gene expression pattern,glia,neuron,transcriptome},
  pages = {5}
}

@article{manji_underlying_2003,
  title = {The underlying neurobiology of bipolar disorder},
  volume = {2},
  issn = {1723-8617},
  abstract = {Clinical studies over the past decades have attempted to uncover the biological
factors mediating the pathophysiology of bipolar disorder (BD) utilizing a
variety of biochemical and neuroendocrine strategies. Indeed, assessments
of cerebrospinal fluid chemistry, neuroendocrine responses to pharmacological
challenge, and neuroreceptor and transporter binding have demonstrated a number
of abnormalities in the amine neurotransmitter systems in this disorder. However,
recent studies have also implicated critical signal transduction pathways
as being integral to the pathophysiology and treatment of BD, in addition
to a growing body of data suggesting that impairments of neuroplasticity and
cellular resilience may also underlie the pathophysiology of the disorder.
It is thus noteworthy that mood stabilizers and antidepressants indirectly
regulate a number of factors involved in cell survival pathways - including
MAP kinases, CREB, BDNF and bcl-2 protein - and may thus bring about some
of their delayed long-term beneficial effects via underappreciated neurotrophic
effects.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {3},
  urldate = {2014-12-16},
  journal = {World Psychiatry},
  author = {MANJI, HUSSEINI K and QUIROZ, JORGE A and PAYNE, JENNIFER L and SINGH, JASKARAN and LOPES, BARBARA P and VIEGAS, JENILEE S and ZARATE, CARLOS A},
  month = oct,
  year = {2003},
  pages = {136--146},
  pmid = {16946919},
  pmcid = {PMC1525098}
}

@article{bolstad_comparison_2003,
  title = {A comparison of normalization methods for high density oligonucleotide array data based on variance and bias},
  volume = {19},
  issn = {1367-4803},
  abstract = {MOTIVATION: When running experiments that involve multiple high density oligonucleotide arrays, it is important to remove sources of variation between arrays of non-biological origin. Normalization is a process for reducing this variation. It is common to see non-linear relations between arrays and the standard normalization provided by Affymetrix does not perform well in these situations.
RESULTS: We present three methods of performing normalization at the probe intensity level. These methods are called complete data methods because they make use of data from all arrays in an experiment to form the normalizing relation. These algorithms are compared to two methods that make use of a baseline array: a one number scaling based algorithm and a method that uses a non-linear normalizing relation by comparing the variability and bias of an expression measure. Two publicly available datasets are used to carry out the comparisons. The simplest and quickest complete data method is found to perform favorably.
AVAILABILITY: Software implementing all three of the complete data normalization methods is available as part of the R package Affy, which is a part of the Bioconductor project http://www.bioconductor.org.
SUPPLEMENTARY INFORMATION: Additional figures may be found at http://www.stat.berkeley.edu/\textasciitilde{}bolstad/normalize/index.html},
  language = {eng},
  timestamp = {2016-02-23T06:26:06Z},
  number = {2},
  journal = {Bioinformatics (Oxford, England)},
  author = {Bolstad, B. M. and Irizarry, R. A. and Astrand, M. and Speed, T. P.},
  month = jan,
  year = {2003},
  keywords = {Algorithms,Calibration,Models; Genetic,Molecular Probes,Nonlinear Dynamics,Oligonucleotide Array Sequence Analysis,Quality Control,Sequence Analysis; DNA,Stochastic Processes},
  pages = {185--193},
  pmid = {12538238}
}

@article{mccarthy_whole_2014,
  title = {Whole {{Brain Expression}} of {{Bipolar Disorder Associated Genes}}: {{Structural}} and {{Genetic Analyses}}},
  volume = {9},
  shorttitle = {Whole {{Brain Expression}} of {{Bipolar Disorder Associated Genes}}},
  doi = {10.1371/journal.pone.0100204},
  abstract = {Studies of bipolar disorder (BD) suggest a genetic basis of the illness that alters brain function and morphology. In recent years, a number of genetic variants associated with BD have been identified. However, little is known about the associated genes, or brain circuits that rely upon their function. Using an anatomically comprehensive survey of the human transcriptome (The Allen Brain Atlas), we mapped the expression of 58 genes with suspected involvement in BD based upon their relationship to SNPs identified in genome wide association studies (GWAS). We then conducted a meta-analysis of structural MRI studies to identify brain regions that are abnormal in BD. Of 58 BD associated genes, 22 had anatomically distinct expression patterns that could be categorized into one of three clusters (C1\textendash{}C3). Brain regions with the highest and lowest expression of these genes did not overlap strongly with anatomical sites identified as abnormal by structural MRI except in the parahippocampal gyrus, the inferior/superior temporal gyrus and the cerebellar vermis, regions where overlap was significant. Using the 22 genes in C1\textendash{}C3 as reference points, additional genes with correlated expression patterns were identified and organized into sets based on similarity. Further analysis revealed that five of these gene sets were significantly associated with BD, suggesting that anatomical expression profile is correlated with genetic susceptibility to BD, particularly for genes in C2. Our data suggest that expression profiles of BD-associated genes do not explain the majority of structural abnormalities observed in BD, but may be useful in identifying new candidate genes. Our results highlight the complex neuroanatomical basis of BD, and reinforce illness models that emphasize impaired brain connectivity.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {6},
  urldate = {2014-12-09},
  journal = {PLoS ONE},
  author = {McCarthy, Michael J. and Liang, Sherri and Spadoni, Andrea D. and Kelsoe, John R. and Simmons, Alan N.},
  month = jun,
  year = {2014},
  pages = {e100204},
  file = {PLoS Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/MSFW88AX/infodoi10.1371journal.pone.html:}
}

@article{maze_g9a_2014,
  title = {G9a influences neuronal subtype specification in striatum},
  volume = {17},
  copyright = {\textcopyright{} 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1097-6256},
  doi = {10.1038/nn.3670},
  abstract = {Cocaine-mediated repression of the histone methyltransferase (HMT) G9a has recently been implicated in transcriptional, morphological and behavioral responses to chronic cocaine administration. Here, using a ribosomal affinity purification approach, we found that G9a repression by cocaine occurred in both Drd1-expressing (striatonigral) and Drd2-expressing (striatopallidal) medium spiny neurons. Conditional knockout and overexpression of G9a within these distinct cell types, however, revealed divergent behavioral phenotypes in response to repeated cocaine treatment. Our studies further indicated that such developmental deletion of G9a selectively in Drd2 neurons resulted in the unsilencing of transcriptional programs normally specific to striatonigral neurons and in the acquisition of Drd1-associated projection and electrophysiological properties. This partial striatopallidal to striatonigral 'switching' phenotype in mice indicates a new role for G9a in contributing to neuronal subtype identity and suggests a critical function for cell type\textendash{}specific histone methylation patterns in the regulation of behavioral responses to environmental stimuli.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {4},
  urldate = {2014-10-21},
  journal = {Nature Neuroscience},
  author = {Maze, Ian and Chaudhury, Dipesh and Dietz, David M. and {Von Schimmelmann}, Melanie and Kennedy, Pamela J. and Lobo, Mary Kay and Sillivan, Stephanie E. and Miller, Michael L. and Bagot, Rosemary C. and Sun, HaoSheng and Turecki, Gustavo and Neve, Rachael L. and Hurd, Yasmin L. and Shen, Li and Han, Ming-Hu and Schaefer, Anne and Nestler, Eric J.},
  month = apr,
  year = {2014},
  pages = {533--539},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/NIRB6CQW/nn.3670.html:}
}

@article{wang_rna-seq_2009,
  title = {{{RNA-Seq}}: a revolutionary tool for transcriptomics},
  volume = {10},
  copyright = {\textcopyright{} 2009 Nature Publishing Group},
  issn = {1471-0056},
  shorttitle = {{{RNA-Seq}}},
  doi = {10.1038/nrg2484},
  abstract = {RNA-Seq is a recently developed approach to transcriptome profiling that uses deep-sequencing technologies. Studies using this method have already altered our view of the extent and complexity of eukaryotic transcriptomes. RNA-Seq also provides a far more precise measurement of levels of transcripts and their isoforms than other methods. This article describes the RNA-Seq approach, the challenges associated with its application, and the advances made so far in characterizing several eukaryote transcriptomes.},
  language = {en},
  timestamp = {2016-02-13T05:02:00Z},
  number = {1},
  urldate = {2016-02-13},
  journal = {Nature Reviews Genetics},
  author = {Wang, Zhong and Gerstein, Mark and Snyder, Michael},
  month = jan,
  year = {2009},
  pages = {57--63}
}

@article{Qin2006,
  title = {Evaluation of methods for oligonucleotide array data via quantitative real-time {{PCR}}},
  volume = {7},
  copyright = {2006 Qin et al; licensee BioMed Central Ltd.},
  issn = {1471-2105},
  doi = {10.1186/1471-2105-7-23},
  abstract = {There are currently many different methods for processing and summarizing probe-level data from Affymetrix oligonucleotide arrays. It is of great interest to validate these methods and identify those that are most effective. There is no single best way to do this validation, and a variety of approaches is needed. Moreover, gene expression data are collected to answer a variety of scientific questions, and the same method may not be best for all questions. Only a handful of validation studies have been done so far, most of which rely on spike-in datasets and focus on the question of detecting differential expression. Here we seek methods that excel at estimating relative expression. We evaluate methods by identifying those that give the strongest linear association between expression measurements by array and the "gold-standard" assay.
PMID: 16417622},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-10-17},
  journal = {BMC Bioinformatics},
  author = {Qin, Li-Xuan and Beyer, Richard P. and Hudson, Francesca N. and Linford, Nancy J. and Morris, Daryl E. and Kerr, Kathleen F.},
  month = jan,
  year = {2006},
  pages = {23},
  file = {Qin et al_2006_Evaluation of methods for oligonucleotide array data via quantitative real-time.pdf:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/693FJMCU/Qin et al_2006_Evaluation of methods for oligonucleotide array data via quantitative real-time.pdf:application/pdf;Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/WSKB5PIF/23.html:},
  pmid = {16417622}
}

@article{takahashi_linking_2011,
  title = {Linking oligodendrocyte and myelin dysfunction to neurocircuitry abnormalities in schizophrenia},
  volume = {93},
  issn = {0301-0082},
  doi = {10.1016/j.pneurobio.2010.09.004},
  abstract = {Multiple lines of evidence in schizophrenia, from brain imaging, studies in postmortem brains, and genetic association studies, have implicated oligodendrocyte and myelin dysfunction in this disease. Recent studies suggest that oligodendrocyte and myelin dysfunction leads to changes in synaptic formation and function, which could lead to cognitive dysfunction, a core symptom of schizophrenia. Furthermore, there is accumulating data linking oligodendrocyte and myelin dysfunction with dopamine and glutamate abnormalities, both of which are found in schizophrenia. These findings implicate oligodendrocyte and myelin dysfunction as a primary change in schizophrenia, not only as secondary consequences of the illness or treatment. Strategies targeting oligodendrocyte and myelin abnormalities could therefore provide therapeutic opportunities for patients suffering from schizophrenia.},
  timestamp = {2016-03-24T16:30:26Z},
  number = {1},
  urldate = {2016-03-24},
  journal = {Progress in Neurobiology},
  author = {Takahashi, Nagahide and Sakurai, Takeshi and Davis, Kenneth L. and Buxbaum, Joseph D.},
  month = jan,
  year = {2011},
  keywords = {Brain imaging,Dopamine,gene expression,Genetic association,Glutamate,Myelin,oligodendrocyte,synaptic plasticity},
  pages = {13--24},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/BTA4N2GW/S0301008210001693.html:}
}

@article{islam_quantitative_2014,
  title = {Quantitative single-cell {{RNA}}-seq with unique molecular identifiers},
  volume = {11},
  copyright = {\textcopyright{} 2013 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1548-7091},
  doi = {10.1038/nmeth.2772},
  abstract = {Single-cell RNA sequencing (RNA-seq) is a powerful tool to reveal cellular heterogeneity, discover new cell types and characterize tumor microevolution. However, losses in cDNA synthesis and bias in cDNA amplification lead to severe quantitative errors. We show that molecular labels\textemdash{}random sequences that label individual molecules\textemdash{}can nearly eliminate amplification noise, and that microfluidic sample preparation and optimized reagents produce a fivefold improvement in mRNA capture efficiency.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2015-03-18},
  journal = {Nature Methods},
  author = {Islam, Saiful and Zeisel, Amit and Joost, Simon and {La Manno}, Gioele and Zajac, Pawel and Kasper, Maria and L{\"o}nnerberg, Peter and Linnarsson, Sten},
  month = feb,
  year = {2014},
  pages = {163--166}
}

@article{lein_genome-wide_2007,
  title = {Genome-wide atlas of gene expression in the adult mouse brain},
  volume = {445},
  copyright = {\textcopyright{} 2006 Nature Publishing Group},
  issn = {0028-0836},
  doi = {10.1038/nature05453},
  abstract = {Molecular approaches to understanding the functional circuitry of the nervous system promise new insights into the relationship between genes, brain and behaviour. The cellular diversity of the brain necessitates a cellular resolution approach towards understanding the functional genomics of the nervous system. We describe here an anatomically comprehensive digital atlas containing the expression patterns of 20,000 genes in the adult mouse brain. Data were generated using automated high-throughput procedures for in situ hybridization and data acquisition, and are publicly accessible online. Newly developed image-based informatics tools allow global genome-scale structural analysis and cross-correlation, as well as identification of regionally enriched genes. Unbiased fine-resolution analysis has identified highly specific cellular markers as well as extensive evidence of cellular heterogeneity not evident in classical neuroanatomical atlases. This highly standardized atlas provides an open, primary data resource for a wide variety of further studies concerning brain organization and function.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {7124},
  urldate = {2014-12-22},
  journal = {Nature},
  author = {Lein, Ed S. and Hawrylycz, Michael J. and Ao, Nancy and Ayres, Mikael and Bensinger, Amy and Bernard, Amy and Boe, Andrew F. and Boguski, Mark S. and Brockway, Kevin S. and Byrnes, Emi J. and Chen, Lin and Chen, Li and Chen, Tsuey-Ming and {Chi Chin}, Mei and Chong, Jimmy and Crook, Brian E. and Czaplinska, Aneta and Dang, Chinh N. and Datta, Suvro and Dee, Nick R. and Desaki, Aimee L. and Desta, Tsega and Diep, Ellen and Dolbeare, Tim A. and Donelan, Matthew J. and Dong, Hong-Wei and Dougherty, Jennifer G. and Duncan, Ben J. and Ebbert, Amanda J. and Eichele, Gregor and Estin, Lili K. and Faber, Casey and Facer, Benjamin A. and Fields, Rick and Fischer, Shanna R. and Fliss, Tim P. and Frensley, Cliff and Gates, Sabrina N. and Glattfelder, Katie J. and Halverson, Kevin R. and Hart, Matthew R. and Hohmann, John G. and Howell, Maureen P. and Jeung, Darren P. and Johnson, Rebecca A. and Karr, Patrick T. and Kawal, Reena and Kidney, Jolene M. and Knapik, Rachel H. and Kuan, Chihchau L. and Lake, James H. and Laramee, Annabel R. and Larsen, Kirk D. and Lau, Christopher and Lemon, Tracy A. and Liang, Agnes J. and Liu, Ying and Luong, Lon T. and Michaels, Jesse and Morgan, Judith J. and Morgan, Rebecca J. and Mortrud, Marty T. and Mosqueda, Nerick F. and Ng, Lydia L. and Ng, Randy and Orta, Geralyn J. and Overly, Caroline C. and Pak, Tu H. and Parry, Sheana E. and Pathak, Sayan D. and Pearson, Owen C. and Puchalski, Ralph B. and Riley, Zackery L. and Rockett, Hannah R. and Rowland, Stephen A. and Royall, Joshua J. and Ruiz, Marcos J. and Sarno, Nadia R. and Schaffnit, Katherine and Shapovalova, Nadiya V. and Sivisay, Taz and Slaughterbeck, Clifford R. and Smith, Simon C. and Smith, Kimberly A. and Smith, Bryan I. and Sodt, Andy J. and Stewart, Nick N. and Stumpf, Kenda-Ruth and Sunkin, Susan M. and Sutram, Madhavi and Tam, Angelene and Teemer, Carey D. and Thaller, Christina and Thompson, Carol L. and Varnam, Lee R. and Visel, Axel and Whitlock, Ray M. and Wohnoutka, Paul E. and Wolkey, Crissa K. and Wong, Victoria Y. and Wood, Matthew and Yaylaoglu, Murat B. and Young, Rob C. and Youngstrom, Brian L. and {Feng Yuan}, Xu and Zhang, Bin and Zwingman, Theresa A. and Jones, Allan R.},
  month = jan,
  year = {2007},
  pages = {168--176},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/4IDXA4G2/nature05453.html:}
}

@article{_kick_2014,
  title = {Kick the bar chart habit},
  volume = {11},
  copyright = {\textcopyright{} 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1548-7091},
  doi = {10.1038/nmeth.2837},
  abstract = {Bar charts are too frequently used to communicate data that they cannot represent well. We strongly encourage the use of more appropriate plots to display statistical samples.},
  language = {en},
  timestamp = {2015-08-13T22:14:48Z},
  number = {2},
  urldate = {2014-12-23},
  journal = {Nature Methods},
  month = feb,
  year = {2014},
  pages = {113--113},
  file = {2014_Kick the bar chart habit.pdf:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/7E6Q2N4I/2014_Kick the bar chart habit.pdf:application/pdf;Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/MVGAF26Q/nmeth.2837.html:}
}

@article{sullivan_evaluating_2006,
  title = {Evaluating the comparability of gene expression in blood and brain},
  volume = {141B},
  copyright = {Copyright \textcopyright{} 2006 Wiley-Liss, Inc.},
  issn = {1552-485X},
  doi = {10.1002/ajmg.b.30272},
  abstract = {The availability of an accessible tissue whose gene expression profile is similar to more inaccessible CNS tissues has the potential to advance research in neuropsychiatric disorders. We conducted secondary data analysis of transcriptional profiling of 79 human tissues for 33,698 genes using the Affymetrix U133A microarray augmented with a custom microarray (Affymetrix GNF1H), which were produced by the Genomics Institute of the Novartis Research Foundation (http://symatlas.gnf.org). Our analyses suggested that: (a) on a transcriptome level, whole blood shares significant gene expression similarities with multiple CNS tissues; (b) the median non-parametric correlation between transcripts present in both whole blood and CNS was around 0.5; (c) this correlation of 0.5 was intermediate relative to all tissues in the Novartis data set\textemdash{}less than for the maximum achievable value of 0.85, less than a set of immune tissues (0.64), comparable to a heterogeneous set of somatic tissues (0.57) but greater than muscle (0.48) and peripheral nervous system tissues (0.36); (d) about half of a set of candidate genes relevant to schizophrenia were expressed in both whole blood and prefrontal cortex; and (e) the expression levels of many classes of biologically relevant processes were not significantly different between whole blood and prefrontal cortex. These analyses suggest that gene expression in whole blood is neither perfectly correlated and useful nor perfectly uncorrelated and useless with gene expression in multiple brain tissues. This suggests that the cautious and thoughtful use of peripheral gene expression may be a useful surrogate for gene expression in the CNS when it has been determined that the relevant gene is expressed in both. \textcopyright{} 2006 Wiley-Liss, Inc.},
  language = {en},
  timestamp = {2015-08-18T01:30:38Z},
  number = {3},
  urldate = {2015-08-18},
  journal = {American Journal of Medical Genetics Part B: Neuropsychiatric Genetics},
  author = {Sullivan, Patrick F. and Fan, Cheng and Perou, Charles M.},
  month = apr,
  year = {2006},
  keywords = {Brain,CNS,gene expression,microarray,peripheral blood},
  pages = {261--268}
}

@article{darmanis_survey_2015,
  title = {A survey of human brain transcriptome diversity at the single cell level},
  volume = {112},
  issn = {0027-8424, 1091-6490},
  doi = {10.1073/pnas.1507125112},
  abstract = {The human brain is a tissue of vast complexity in terms of the cell types it comprises. Conventional approaches to classifying cell types in the human brain at single cell resolution have been limited to exploring relatively few markers and therefore have provided a limited molecular characterization of any given cell type. We used single cell RNA sequencing on 466 cells to capture the cellular complexity of the adult and fetal human brain at a whole transcriptome level. Healthy adult temporal lobe tissue was obtained during surgical procedures where otherwise normal tissue was removed to gain access to deeper hippocampal pathology in patients with medical refractory seizures. We were able to classify individual cells into all of the major neuronal, glial, and vascular cell types in the brain. We were able to divide neurons into individual communities and show that these communities preserve the categorization of interneuron subtypes that is typically observed with the use of classic interneuron markers. We then used single cell RNA sequencing on fetal human cortical neurons to identify genes that are differentially expressed between fetal and adult neurons and those genes that display an expression gradient that reflects the transition between replicating and quiescent fetal neuronal populations. Finally, we observed the expression of major histocompatibility complex type I genes in a subset of adult neurons, but not fetal neurons. The work presented here demonstrates the applicability of single cell RNA sequencing on the study of the adult human brain and constitutes a first step toward a comprehensive cellular atlas of the human brain.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {23},
  urldate = {2015-06-15},
  journal = {Proceedings of the National Academy of Sciences},
  author = {Darmanis, Spyros and Sloan, Steven A. and Zhang, Ye and Enge, Martin and Caneda, Christine and Shuer, Lawrence M. and Gephart, Melanie G. Hayden and Barres, Ben A. and Quake, Stephen R.},
  month = sep,
  year = {2015},
  keywords = {human brain,interneurons,Neurons,RNAseq,single cells},
  pages = {7285--7290},
  pmid = {26060301}
}

@article{dalal_translational_2013,
  title = {Translational profiling of hypocretin neurons identifies candidate molecules for sleep regulation},
  volume = {27},
  issn = {0890-9369, 1549-5477},
  doi = {10.1101/gad.207654.112},
  abstract = {Hypocretin (orexin; Hcrt)-containing neurons of the hypothalamus are essential for the normal regulation of sleep and wake behaviors and have been implicated in feeding, anxiety, depression, and reward. The absence of these neurons causes narcolepsy in humans and model organisms. However, little is known about the molecular phenotype of these cells; previous attempts at comprehensive profiling had only limited sensitivity or were inaccurate. We generated a Hcrt translating ribosome affinity purification (bacTRAP) line for comprehensive translational profiling of all ribosome-bound transcripts in these neurons in vivo. From this profile, we identified \ensuremath{>}6000 transcripts detectably expressed above background and 188 transcripts that are highly enriched in these neurons, including all known markers of the cells. Blinded analysis of in situ hybridization databases suggests that \ensuremath{\sim}60\% of these are expressed in a Hcrt marker-like pattern. Fifteen of these were confirmed with double labeling and microscopy, including the transcription factor Lhx9. Ablation of this gene results in a \ensuremath{>}30\% loss specifically of Hcrt neurons, without a general disruption of hypothalamic development. Polysomnography and activity monitoring revealed a profound hypersomnolence in these mice. These data provide an in-depth and accurate profile of Hcrt neuron gene expression and suggest that Lhx9 may be important for specification or survival of a subset of these cells.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {5},
  urldate = {2014-10-21},
  journal = {Genes \& Development},
  author = {Dalal, Jasbir and Roh, Jee Hoon and Maloney, Susan E. and Akuffo, Afua and Shah, Samir and Yuan, Han and Wamsley, Brie and Jones, Wendell B. and Strong, Cristina de Guzman and Gray, Paul A. and Holtzman, David M. and Heintz, Nathaniel and Dougherty, Joseph D.},
  month = jan,
  year = {2013},
  keywords = {bacTRAP,hypocretin,Lhx9,narcolepsy,orexin,translational profiling},
  pages = {565--578},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/ENXPDJ2H/565.html:},
  pmid = {23431030}
}

@article{petrides_dorsolateral_1999,
  title = {Dorsolateral prefrontal cortex: comparative cytoarchitectonic analysis in the human and the macaque brain and corticocortical connection patterns},
  volume = {11},
  issn = {0953-816X},
  shorttitle = {Dorsolateral prefrontal cortex},
  abstract = {The cytoarchitecture of the human and the macaque monkey dorsolateral prefrontal cortex has been examined in a strictly comparative manner in order to resolve major discrepancies between the available segmentations of this cortical region in the human and the monkey brain. In addition, the connections of the dorsolateral prefrontal cortical areas were re-examined in the monkey. The present analysis showed that only a restricted portion of what had previously been labelled as area 46 in the monkey has the same characteristics as area 46 of the human brain; the remaining part of this monkey region has the characteristics of a portion of the middle frontal gyrus in the human brain that had previously been included as part of area 9. We have labelled this cortical area as 9/46 in both species. These two areas (i.e. 46 and 9/46), which constitute the lower half of the mid-dorsolateral frontal cortex, have a well-developed granular layer IV, and can easily be distinguished from area 9, on the upper part of the mid-dorsolateral region, which does not have a well-developed granular layer IV. Area 9 has the same basic pattern of connections as areas 46 and 9/46, but, unlike the latter areas, it does not receive input from the lateral parietal cortex. Caudal to area 9, on the dorsomedial portion of the frontal cortex, there is a distinct strip of cortex (area 8B) which, unlike area 9, receives significant input from the prestriate cortex and the medial parietal cortex. The present results provide a basis for a closer integration of findings from functional neuroimaging studies in human subjects with experimental work in the monkey.},
  language = {eng},
  timestamp = {2015-12-21T20:19:41Z},
  number = {3},
  journal = {The European Journal of Neuroscience},
  author = {Petrides, M. and Pandya, D. N.},
  month = mar,
  year = {1999},
  keywords = {Animals,Brain Mapping,Humans,interneurons,Macaca mulatta,Neural Pathways,Prefrontal Cortex},
  pages = {1011--1036},
  pmid = {10103094}
}

@article{ekdahl_brain_2009,
  series = {Brain - Immune Interactions in Acute and Chronic Brain Disorders},
  title = {Brain inflammation and adult neurogenesis: {{The}} dual role of microglia},
  volume = {158},
  issn = {0306-4522},
  shorttitle = {Brain inflammation and adult neurogenesis},
  doi = {10.1016/j.neuroscience.2008.06.052},
  abstract = {In the adult mammalian brain, neurogenesis from neural stem/progenitor cells continues in two regions: the subgranular zone in the dentate gyrus and the subventricular zone lining the lateral ventricles. The generated neuroblasts migrate to their appropriate location and differentiate to mature granule cells and olfactory bulb interneurons, respectively. Following injury such as stroke, neuroblasts generated in the subventricular zone migrate also into areas which are not normally neurogenic, e.g. striatum and cerebral cortex. In the initial studies in rodents, brain inflammation and microglia activation were found to be detrimental for the survival of the new hippocampal neurons early after they had been born. The role of inflammation for adult neurogenesis has, however, turned out to be much more complex. Recent experimental evidence indicates that microglia under certain circumstances can be beneficial and support the different steps in neurogenesis, progenitor proliferation, survival, migration, and differentiation. Here we summarize the current knowledge on the role of inflammation and in particular of microglia in adult neurogenesis in the intact and injured mammalian brain. We conclude that microglia activation, as an indicator of inflammation, is not pro- or antineurogenic per se but the net outcome is dependent on the balance between secreted molecules with pro- and antiinflammatory action.},
  timestamp = {2016-06-07T05:57:53Z},
  number = {3},
  urldate = {2016-06-07},
  journal = {Neuroscience},
  author = {Ekdahl, C. T. and Kokaia, Z. and Lindvall, O.},
  month = feb,
  year = {2009},
  keywords = {cytokines,Inflammation,microglia,Neurogenesis,status epilepticus,stroke},
  pages = {1021--1029}
}

@article{dougherty_analytical_2010,
  title = {Analytical approaches to {{RNA}} profiling data for the identification of genes enriched in specific cells},
  volume = {38},
  issn = {0305-1048, 1362-4962},
  doi = {10.1093/nar/gkq130},
  abstract = {We have recently developed a novel method for the affinity purification of the complete suite of translating mRNA from genetically labeled cell populations. This method permits comprehensive quantitative comparisons of the genes employed by each specific cell type. We provide a detailed description of tools for analysis of data generated with this and related methodologies. An essential question that arises from these data is how to identify those genes that are enriched in each cell type relative to all others. Genes relatively specifically employed by a cell type may contribute to the unique functions of that cell, and thus may become useful targets for development of pharmacological tools for cell-specific manipulations. We describe here a novel statistic, the specificity index, which can be used for comparative quantitative analysis to identify genes enriched in specific cell populations across a large number of profiles. This measure correctly predicts in situ hybridization patterns for many cell types. We apply this measure to a large survey of CNS cell-specific microarray data to identify those genes that are significantly enriched in each population Data and algorithms are available online (www.bactrap.org).},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {13},
  urldate = {2014-11-03},
  journal = {Nucleic Acids Research},
  author = {Dougherty, Joseph D. and Schmidt, Eric F. and Nakajima, Miho and Heintz, Nathaniel},
  month = jan,
  year = {2010},
  pages = {4218--4230},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/C9INU9BW/4218.html:},
  pmid = {20308160}
}

@article{mcarthur_size_2006,
  title = {The {{Size}} and {{Distribution}} of {{Midbrain Dopaminergic Populations}} are {{Permanently Altered}} by {{Perinatal Glucocorticoid Exposure}} in a {{Sex}}- {{Region}}- and {{Time-Specific Manner}}},
  volume = {32},
  copyright = {\textcopyright{} 2006 Nature Publishing Group},
  issn = {0893-133X},
  doi = {10.1038/sj.npp.1301277},
  abstract = {Central dopaminergic (DA) systems appear to be particularly vulnerable to disruption by exposure to stressors in early life, but the underlying mechanisms are poorly understood. As endogenous glucocorticoids (GCs) are implicated in other aspects of neurobiological programming, this study aimed to characterize the effects of perinatal GC exposure on the cytoarchitecture of DA populations in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA). Dexamethasone was administered non-invasively to rat pups via the mothers' drinking water during embryonic days 16\textendash{}19 or postnatal days 1\textendash{}7, with a total oral intake circa 0.075 or 0.15 mg/kg/day, respectively; controls received normal drinking water. Analysis of tyrosine hydroxylase-immunoreactive cell counts and regional volumes in adult offspring identified notable sex differences in the shape and volume of the SNc and VTA, as well as the topographical organization and size of the DA populations. Perinatal GC treatments increased the DA population size and altered the shape of the SNc and VTA as well as the organization of the DA neurons by expanding and/or shifting them in a caudal direction. This response was sexually dimorphic and included a feminization or demasculinization of the three-dimensional cytoarchitecture in males, and subtle differences that were dependent on the window of exposure. These findings demonstrate that inappropriate perinatal exposure to GCs have enduring effects on the organization of midbrain DA systems that are critically important for normal brain function throughout life.},
  language = {en},
  timestamp = {2015-10-27T00:44:03Z},
  number = {7},
  urldate = {2015-10-27},
  journal = {Neuropsychopharmacology},
  author = {McArthur, Simon and McHale, Emily and Gillies, Glenda E.},
  month = dec,
  year = {2006},
  keywords = {dopaminergic neurons,midbrain,perinatal glucocorticoid treatment,population size,regional volume,sex dimorphism},
  pages = {1462--1476},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/8QJ4XTWB/1301277a.html:}
}

@article{hokama_altered_2014,
  title = {Altered expression of diabetes-related genes in {{Alzheimer}}'s disease brains: the {{Hisayama}} study},
  volume = {24},
  issn = {1460-2199},
  shorttitle = {Altered expression of diabetes-related genes in {{Alzheimer}}'s disease brains},
  doi = {10.1093/cercor/bht101},
  abstract = {Diabetes mellitus (DM) is considered to be a risk factor for dementia including Alzheimer's disease (AD). However, the molecular mechanism underlying this risk is not well understood. We examined gene expression profiles in postmortem human brains donated for the Hisayama study. Three-way analysis of variance of microarray data from frontal cortex, temporal cortex, and hippocampus was performed with the presence/absence of AD and vascular dementia, and sex, as factors. Comparative analyses of expression changes in the brains of AD patients and a mouse model of AD were also performed. Relevant changes in gene expression identified by microarray analysis were validated by quantitative real-time reverse-transcription polymerase chain reaction and western blotting. The hippocampi of AD brains showed the most significant alteration in gene expression profile. Genes involved in noninsulin-dependent DM and obesity were significantly altered in both AD brains and the AD mouse model, as were genes related to psychiatric disorders and AD. The alterations in the expression profiles of DM-related genes in AD brains were independent of peripheral DM-related abnormalities. These results indicate that altered expression of genes related to DM in AD brains is a result of AD pathology, which may thereby be exacerbated by peripheral insulin resistance or DM.},
  language = {eng},
  timestamp = {2015-08-13T22:18:44Z},
  number = {9},
  journal = {Cerebral Cortex (New York, N.Y.: 1991)},
  author = {Hokama, Masaaki and Oka, Sugako and Leon, Julio and Ninomiya, Toshiharu and Honda, Hiroyuki and Sasaki, Kensuke and Iwaki, Toru and Ohara, Tomoyuki and Sasaki, Tomio and LaFerla, Frank M. and Kiyohara, Yutaka and Nakabeppu, Yusaku},
  month = sep,
  year = {2014},
  keywords = {Alzheimer Disease,Animals,Dementia; Vascular,Diabetes Mellitus,Disease Models; Animal,Female,Frontal Lobe,gene expression,Hippocampus,Humans,Male,Mice; Transgenic,Temporal Lobe},
  pages = {2476--2488},
  pmid = {23595620},
  pmcid = {PMC4128707}
}

@article{galloway_cgg_2014,
  title = {{{CGG}} repeats in {{RNA}} modulate expression of {{TDP}}-43 in mouse and fly models of fragile {{X}} tremor ataxia syndrome},
  issn = {0964-6906, 1460-2083},
  doi = {10.1093/hmg/ddu314},
  abstract = {Determining the molecular mechanism(s) leading to Purkinje neuron loss in the neurodegenerative disorder fragile X-associated tremor/ataxia syndrome (FXTAS) is limited by the complex morphology of this cell type. Purkinje neurons are notoriously difficult to isolate and maintain in culture presenting considerable difficultly to identify molecular changes in response to expanded CGG repeat (rCGG)-containing mRNA that induces neurotoxicity in FXTAS. Several studies have uncovered a number of RNA-binding proteins involved in translation that aberrantly interact with the CGG-containing RNA; however, whether these interactions alter the translational profile of cells has not been investigated. Here we employ bacTRAP translational profiling to demonstrate that Purkinje neurons ectopically expressing 90 CGG repeats exhibit a dramatic change in their translational profile even prior to the onset of rCGG-induced phenotypes. This approach identified \ensuremath{\sim}500 transcripts that are differentially associated with ribosomes in r(CGG)90-expressing mice. Functional annotation cluster analysis revealed broad ontologies enriched in the r(CGG)90 list, including RNA binding and response to stress. Intriguingly, a transcript for the Tardbp gene, implicated in a number of other neurodegenerative disorders, exhibits altered association with ribosomes in the presence of r(CGG)90 repeats. We therefore tested and showed that reduced association of Tardbp mRNA with the ribosomes results in a loss of TDP-43 protein expression in r(CGG)90-expressing Purkinje neurons. Furthermore, we showed that TDP-43 could modulate the rCGG repeat-mediated toxicity in a Drosophila model that we developed previously. These findings together suggest that translational dysregulation may be an underlying mechanism of rCGG-induced neurotoxicity in FXTAS.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2014-10-21},
  journal = {Human Molecular Genetics},
  author = {Galloway, Jocelyn N. and Shaw, Chad and Yu, Peng and Parghi, Deena and Poidevin, Mickael and Jin, Peng and Nelson, David L.},
  month = jun,
  year = {2014},
  pages = {ddu314},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/D46BZF7S/hmg.ddu314.html:},
  pmid = {24986919}
}

@article{wang_[analysis_2015,
  title = {[{{Analysis}} of {{TERT}} and {{TIN2 Gene Expression}} in {{Patients}} with {{Acquired Aplastic Anemia}} and {{Their Correlation}} with {{Pathogenesis}}]},
  volume = {23},
  issn = {1009-2137},
  abstract = {OBJECTIVE: To detect the mRNA expression levels of TERT and TIN2 in peripheral blood mononuclear cells of acquired aplastic anemia(AAA) patients, and to explore their correlation with pathogenesis of acquired aplastic anemia.
METHODS: Peripheral blood mononuclear cells of 40 cases of AAA including 33 cases of non-severe aplastic anemia(NSAA), 7 cases of severe aplastic anemia (SAA) and 20 subjects as control group were collected to detect mRNA expression of TERT and TIN2 by using real-time quantitative polymerase chain reaction(RT-qPCR), the correlation of TERT and TIN2 mRNA expression levels with classification of peripheral blood cells were analyzed.
RESULTS: The expression levels of TERT and TIN2 mRNA in patients with AAA were lower significantly than those in control group (P \ensuremath{<} 0.05), and the SAA (P \ensuremath{<} 0.01). The expression levels of TERT and TIN2 mRNA in patients with SAA were all lower significantly than those in patients with NSAA (P \ensuremath{<} 0.05). The expression levels of TIN2 mRNA in patients with NSAA were lower significantly than those in control group (P \ensuremath{<} 0.01). There were no significant difference in the expression level of TERT mRNA between patients with NSAA and control group (P = 0.082). There was significant correlation between the expression level of TERT mRNA and red blood cells count (r = 0.437, P = 0.029), and hemoglobin level (r = 0.522, P = 0.007). There was significant correlation between the expression levels of TIN2 mRNA and the lymphocyte percentage (r = -0.404, P = 0.045).
CONCLUSION: The expression level of TERT mRNA may be associated with the red blood cells and hemoglobin level. The expression level of TIN2 mRNA may be associated with the lymphocyte percentage.},
  language = {chi},
  timestamp = {2015-08-17T19:11:29Z},
  number = {3},
  journal = {Zhongguo Shi Yan Xue Ye Xue Za Zhi / Zhongguo Bing Li Sheng Li Xue Hui = Journal of Experimental Hematology / Chinese Association of Pathophysiology},
  author = {Wang, Yan and Xu, Rui-Rong and Zhou, Yan-Feng and Liu, Zhao-Xia and Luo, Ya-Qin},
  month = jun,
  year = {2015},
  pages = {785--789},
  pmid = {26117037}
}

@article{ito_historical_2002,
  title = {Historical {{Review}} of the {{Significance}} of the {{Cerebellum}} and the {{Role}} of {{Purkinje Cells}} in {{Motor Learning}}},
  volume = {978},
  issn = {1749-6632},
  doi = {10.1111/j.1749-6632.2002.tb07574.x},
  abstract = {Abstract:  Classic studies of the cerebellum before the middle of the twentieth century established the structural entity of the cerebellum and characterized its function as enabling animals and humans to carry out smooth and accurate movements, even at a high speed and without visual feedback. In the 1960s, neuronal circuit structures of the cerebellum were analyzed in detail, which promoted computational approaches toward the study of neuronal network principles of the cerebellum. In the 1970s and 1980s, vestibulo-ocular reflex adaptation, adaptive locomotion, eye blink conditioning, and learning in hand/arm movement were established as effective experimental paradigms for investigating neural mechanisms of cerebellar functions. In the 1980s, long-term depression (LTD) was discovered and considered as a memory process in the cerebellum; in the 1990s, complex signal transduction processes underlying LTD were revealed. It was also in the 1980s that computational approaches were advanced for modeling control system functions of the cerebellum. Currently, there are two alternative models proposed for VOR adaptation. In this decade, we envisage new developments toward the fusion of knowledge of the cerebellum at molecular and cellular levels and those in systems and computation. Studies of LTD will play a key role in pursuing this direction.},
  language = {en},
  timestamp = {2016-03-15T05:10:43Z},
  number = {1},
  urldate = {2016-03-15},
  journal = {Annals of the New York Academy of Sciences},
  author = {Ito, Masao},
  month = dec,
  year = {2002},
  keywords = {internal model,long-term depression,neuronal circuit,vestibulo-ocular reflex},
  pages = {273--288}
}

@article{goldinger_seasonal_2015,
  title = {Seasonal {{Effects}} on {{Gene Expression}}},
  volume = {10},
  doi = {10.1371/journal.pone.0126995},
  abstract = {Many health conditions, ranging from psychiatric disorders to cardiovascular disease, display notable seasonal variation in severity and onset. In order to understand the molecular processes underlying this phenomenon, we have examined seasonal variation in the transcriptome of 606 healthy individuals. We show that 74 transcripts associated with a 12-month seasonal cycle were enriched for processes involved in DNA repair and binding. An additional 94 transcripts demonstrated significant seasonal variability that was largely influenced by blood cell count levels. These transcripts were enriched for immune function, protein production, and specific cellular markers for lymphocytes. Accordingly, cell counts for erythrocytes, platelets, neutrophils, monocytes, and CD19 cells demonstrated significant association with a 12-month seasonal cycle. These results demonstrate that seasonal variation is an important environmental regulator of gene expression and blood cell composition. Notable changes in leukocyte counts and genes involved in immune function indicate that immune cell physiology varies throughout the year in healthy individuals.},
  timestamp = {2015-08-17T19:16:44Z},
  number = {5},
  urldate = {2015-08-17},
  journal = {PLoS ONE},
  author = {Goldinger, Anita and Shakhbazov, Konstantin and Henders, Anjali K. and McRae, Allan F. and Montgomery, Grant W. and Powell, Joseph E.},
  month = may,
  year = {2015},
  pages = {e0126995}
}

@article{satoh_tmem119_2016,
  title = {{{TMEM119}} marks a subset of microglia in the human brain},
  volume = {36},
  issn = {1440-1789},
  doi = {10.1111/neup.12235},
  abstract = {Microglia are resident myeloid cells of the central nervous system (CNS), activated in the brains of various neurological diseases. Microglia are ontogenetically and functionally distinct from monocyte-derived macrophages that infiltrate the CNS under pathological conditions. However, a lack of specific markers that distinguish resident microglia from circulating blood-derived macrophages in human brain tissues hampers accurate evaluation of microglial contributions to the human brain pathology. By comparative analysis of five comprehensive microglial transcriptome datasets, we identified an evolutionarily conserved protein TMEM119 as the most promising candidate for human microglial markers. TMEM119 was expressed on immortalized human microglia, in which the expression levels were not elevated by exposure to lipopolysaccharide, IFN\ensuremath{\gamma}, IL-4, IL-13 or TGF\ensuremath{\beta}1. Notably, TMEM119 immunoreactivity was expressed exclusively on a subset of Iba1(+) CD68(+) microglia with ramified and amoeboid morphologies in the brains of neurodegenerative diseases, such as Alzheimer's disease (AD), whereas Iba1(+) CD68(+) infiltrating macrophages do not express TMEM119 in demyelinating lesions of multiple sclerosis and necrotic lesions of cerebral infarction. TMEM119 mRNA levels were elevated in AD brains, although the protein levels were not significantly different between AD and non-AD cases by western blot and morphometric analyses. TMEM119-positive microglia did not consistently express polarized markers for M1 (CD80) or M2 (CD163, CD209) in AD brains. These results suggest that TMEM119 serves as a reliable microglial marker that discriminates resident microglia from blood-derived macrophages in the human brain.},
  language = {eng},
  timestamp = {2016-03-15T18:41:20Z},
  number = {1},
  journal = {Neuropathology: Official Journal of the Japanese Society of Neuropathology},
  author = {Satoh, Jun-Ichi and Kino, Yoshihiro and Asahina, Naohiro and Takitani, Mika and Miyoshi, Junko and Ishida, Tsuyoshi and Saito, Yuko},
  month = feb,
  year = {2016},
  keywords = {Alzheimer's disease,Brain RNA-Seq,Iba1,microglia,TMEM119},
  pages = {39--49},
  pmid = {26250788}
}

@article{stegle_computational_2015,
  title = {Computational and analytical challenges in single-cell transcriptomics},
  volume = {16},
  issn = {1471-0064},
  doi = {10.1038/nrg3833},
  abstract = {The development of high-throughput RNA sequencing (RNA-seq) at the single-cell level has already led to profound new discoveries in biology, ranging from the identification of novel cell types to the study of global patterns of stochastic gene expression. Alongside the technological breakthroughs that have facilitated the large-scale generation of single-cell transcriptomic data, it is important to consider the specific computational and analytical challenges that still have to be overcome. Although some tools for analysing RNA-seq data from bulk cell populations can be readily applied to single-cell RNA-seq data, many new computational strategies are required to fully exploit this data type and to enable a comprehensive yet detailed study of gene expression at the single-cell level.},
  language = {eng},
  timestamp = {2016-02-04T09:02:13Z},
  number = {3},
  journal = {Nature Reviews. Genetics},
  author = {Stegle, Oliver and Teichmann, Sarah A. and Marioni, John C.},
  month = mar,
  year = {2015},
  keywords = {Animals,Cell Differentiation,Eukaryotic Cells,Gene Expression Profiling,Gene regulatory networks,High-Throughput Nucleotide Sequencing,Humans,Quality Control,RNA; Messenger,Single-Cell Analysis,Software,transcriptome},
  pages = {133--145},
  pmid = {25628217}
}

@article{dougherty_progress_2005,
  title = {Progress in {{Realizing}} the {{Promise}} of {{Microarrays}} in {{Systems Neurobiology}}},
  volume = {45},
  issn = {0896-6273},
  doi = {10.1016/j.neuron.2005.01.007},
  abstract = {The power of microarrays in neuroscience has been challenged by the cellular heterogeneity and complexity of the central nervous system. In this issue of Neuron, Arlotta, Molyneaux, and colleagues have developed a technique combining retrograde labeling, flow cytometry, and microarrays to purify and molecularly characterize a specific population of neurons from the brain, focusing here on cortical projection neurons. We discuss these findings and the implications of this development for both systems and molecular neuroscience.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2015-08-07},
  journal = {Neuron},
  author = {Dougherty, Joseph D. and Geschwind, Daniel H.},
  month = jan,
  year = {2005},
  pages = {183--185}
}

@article{kouadjo_housekeeping_2007,
  title = {Housekeeping and tissue-specific genes in mouse tissues},
  volume = {8},
  issn = {1471-2164},
  doi = {10.1186/1471-2164-8-127},
  abstract = {Background
This study aims to characterize the housekeeping and tissue-specific genes in 15 mouse tissues by using the serial analysis of gene expression (SAGE) strategy which indicates the relative level of expression for each transcript matched to the tag.

Results
Here, we identified constantly expressed housekeeping genes, such as eukaryotic translation elongation factor 2, which is expressed in all tissues without significant difference in expression levels. Moreover, most of these genes were not regulated by experimental conditions such as steroid hormones, adrenalectomy and gonadectomy. In addition, we report previously postulated housekeeping genes such as peptidyl-prolyl cis-trans isomerase A, glyceraldehyde-3-phosphate dehydrogenase and beta-actin, which are expressed in all the tissues, but with significant difference in their expression levels. We have also identified genes uniquely detected in each of the 15 tissues and other tissues from public databases.

Conclusion
These identified housekeeping genes could represent appropriate controls for RT-PCR and northern blot when comparing the expression levels of genes in several tissues. The results reveal several tissue-specific genes highly expressed in testis and pituitary gland. Furthermore, the main function of tissue-specific genes expressed in liver, lung and bone is the cell defence, whereas several keratins involved in cell structure function are exclusively detected in skin and vagina. The results from this study can be used for example to target a tissue for agent delivering by using the promoter of tissue-specific genes. Moreover, this study could be used as basis for further researches on physiology and pathology of these tissues.},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2015-03-23},
  journal = {BMC Genomics},
  author = {Kouadjo, Kouame E and Nishida, Yuichiro and Cadrin-Girard, Jean F and Yoshioka, Mayumi and St-Amand, Jonny},
  month = may,
  year = {2007},
  keywords = {housekeeping},
  pages = {127},
  pmid = {17519037},
  pmcid = {PMC1888706}
}

@article{newman_robust_2015,
  title = {Robust enumeration of cell subsets from tissue expression profiles},
  volume = {12},
  copyright = {\textcopyright{} 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1548-7091},
  doi = {10.1038/nmeth.3337},
  abstract = {We introduce CIBERSORT, a method for characterizing cell composition of complex tissues from their gene expression profiles. When applied to enumeration of hematopoietic subsets in RNA mixtures from fresh, frozen and fixed tissues, including solid tumors, CIBERSORT outperformed other methods with respect to noise, unknown mixture content and closely related cell types. CIBERSORT should enable large-scale analysis of RNA mixtures for cellular biomarkers and therapeutic targets (http://cibersort.stanford.edu/).},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {5},
  urldate = {2015-06-08},
  journal = {Nature Methods},
  author = {Newman, Aaron M. and Liu, Chih Long and Green, Michael R. and Gentles, Andrew J. and Feng, Weiguo and Xu, Yue and Hoang, Chuong D. and Diehn, Maximilian and Alizadeh, Ash A.},
  month = may,
  year = {2015},
  pages = {453--457}
}

@article{zeng_concise_2014,
  title = {Concise {{Review}}: {{Modeling Central Nervous System Diseases Using Induced Pluripotent Stem Cells}}},
  issn = {2157-6564, 2157-6580},
  shorttitle = {Concise {{Review}}},
  doi = {10.5966/sctm.2014-0102},
  abstract = {Induced pluripotent stem cells (iPSCs) offer an opportunity to delve into the mechanisms underlying development while also affording the potential to take advantage of a number of naturally occurring mutations that contribute to either disease susceptibility or resistance. Just as with any new field, several models of screening are being explored, and innovators are working on the most efficient methods to overcome the inherent limitations of primary cell screens using iPSCs. In the present review, we provide a background regarding why iPSCs represent a paradigm shift for central nervous system (CNS) disease modeling. We describe the efforts in the field to develop more biologically relevant CNS disease models, which should provide screening assays useful for the pharmaceutical industry. We also provide some examples of successful uses for iPSC-based screens and suggest that additional development could revolutionize the field of drug discovery. The development and implementation of these advanced iPSC-based screens will create a more efficient disease-specific process underpinned by the biological mechanism in a patient- and disease-specific manner rather than by trial-and-error. Moreover, with careful and strategic planning, shared resources can be developed that will enable exponential advances in the field. This will undoubtedly lead to more sensitive and accurate screens for early diagnosis and allow the identification of patient-specific therapies, thus, paving the way to personalized medicine.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2014-12-17},
  journal = {Stem Cells Translational Medicine},
  author = {Zeng, Xianmin and Hunsberger, Joshua G. and Simeonov, Anton and Malik, Nasir and Pei, Ying and Rao, Mahendra},
  month = nov,
  year = {2014},
  keywords = {Cell-based screening,Central nervous system disease,Genetic engineering,iPSC},
  pages = {sctm.2014--0102},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/UFKDVHXK/sctm.2014-0102.html:},
  pmid = {25368377}
}

@article{tanapat_neuronal_2013,
  title = {Neuronal {{Cell Markers}}},
  volume = {3},
  issn = {2329-5139},
  doi = {10.13070/mm.en.3.196},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2014-11-19},
  journal = {Materials and Methods},
  author = {Tanapat, Patima},
  month = jun,
  year = {2013},
  file = {Neuronal Cell Markers:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/5XHVRZVH/Neuronal-Cell-Markers.html:}
}

@article{irizarry_summaries_2003,
  title = {Summaries of {{Affymetrix GeneChip}} probe level data},
  volume = {31},
  issn = {1362-4962},
  abstract = {High density oligonucleotide array technology is widely used in many areas of biomedical research for quantitative and highly parallel measurements of gene expression. Affymetrix GeneChip arrays are the most popular. In this technology each gene is typically represented by a set of 11-20 pairs of probes. In order to obtain expression measures it is necessary to summarize the probe level data. Using two extensive spike-in studies and a dilution study, we developed a set of tools for assessing the effectiveness of expression measures. We found that the performance of the current version of the default expression measure provided by Affymetrix Microarray Suite can be significantly improved by the use of probe level summaries derived from empirically motivated statistical models. In particular, improvements in the ability to detect differentially expressed genes are demonstrated.},
  language = {eng},
  timestamp = {2016-02-23T06:26:41Z},
  number = {4},
  journal = {Nucleic Acids Research},
  author = {Irizarry, Rafael A. and Bolstad, Benjamin M. and Collin, Francois and Cope, Leslie M. and Hobbs, Bridget and Speed, Terence P.},
  month = feb,
  year = {2003},
  keywords = {Central Nervous System,DNA Probes,Gene Expression Profiling,Humans,Liver,Oligonucleotide Array Sequence Analysis,Reproducibility of Results,RNA; Messenger,Software},
  pages = {e15},
  pmid = {12582260},
  pmcid = {PMC150247}
}

@article{harr_comparison_2006,
  title = {Comparison of algorithms for the analysis of {{Affymetrix}} microarray data as evaluated by co-expression of genes in known operons},
  volume = {34},
  issn = {0305-1048, 1362-4962},
  doi = {10.1093/nar/gnj010},
  abstract = {Oligonucleotide microarrays are an informative tool to elucidate gene regulatory networks. In order for gene expression levels to be comparable across microarrays, normalization procedures have to be invoked. A large number of methods have been described to correct for systematic biases in microarray experiments. The performance of these methods has been tested only to a limited extend. Here, we evaluate two different types of microarray analyses: (i) the same gene in replicate samples and (ii) different, but co-expressed genes in the same sample. The reliability of the latter analysis needs to be determined for the analysis of regulatory networks and our report is the first attempt to evaluate for the accuracy of different microarray normalization methods in this respect. Consistent with previous results we observed a large effect of the normalization method on the outcome of the expression analyses. Our analyses indicate that different normalization methods should be performed depending on whether a study is aiming to detect differential gene expression between independent samples or whether co-expressed genes should be identified. We make recommendations about the most appropriate method to use.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-10-17},
  journal = {Nucleic Acids Research},
  author = {Harr, Bettina and Schl{\"o}tterer, Christian},
  month = jan,
  year = {2006},
  pages = {e8--e8},
  file = {Harr_Schlötterer_2006_Comparison of algorithms for the analysis of Affymetrix microarray data as.pdf:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/H739H3AK/Harr_Schlötterer_2006_Comparison of algorithms for the analysis of Affymetrix microarray data as.pdf:application/pdf;Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/MP3JTKII/e8.html:},
  pmid = {16432259}
}

@article{batliwalla_peripheral_2005,
  title = {Peripheral blood gene expression profiling in rheumatoid arthritis},
  volume = {6},
  copyright = {\textcopyright{} 2005 Nature Publishing Group},
  issn = {1466-4879},
  doi = {10.1038/sj.gene.6364209},
  abstract = {We carried out gene expression profiling of peripheral blood mononuclear cells (PBMCs) in 29 patients with active rheumatoid arthritis (RA) and 21 control subjects using Affymetrix U95Av2 arrays. Using cluster analysis, we observed a significant alteration in the expression pattern of 81 genes (P\ensuremath{<}0.001) in the PBMCs of RA patients compared with controls. Many of these genes correlated with differences in monocyte counts between the two study populations, and we show that a large fraction of these genes are specifically expressed at high levels in monocytes. In addition, a logistic regression analysis was performed to identify genes that performed best in the categorization of RA and control samples. Glutaminyl cyclase, IL1RA, S100A12 (also known as calgranulin or EN-RAGE) and Grb2-associated binding protein (GAB2) were among the top discriminators. Along with previous data, the overexpression of S100A12 in RA patients emphasizes the likely importance of RAGE pathways in disease pathogenesis. The altered expression of GAB2, an intracellular adaptor molecule involved in regulating phosphatase function, is of particular interest given the recent identification of the intracellular phosphatase PTPN22 as a risk gene for RA. These data suggest that a detailed study of gene expression patterns in peripheral blood can provide insight into disease pathogenesis. However, it is also clear that substantially larger sample sizes will be required in order to evaluate fully gene expression profiling as a means of identifying disease subsets, or defining biomarkers of outcome and response to therapy in RA.},
  language = {en},
  timestamp = {2015-08-18T01:55:48Z},
  number = {5},
  urldate = {2015-08-18},
  journal = {Genes and Immunity},
  author = {Batliwalla, F. M. and Baechler, E. C. and Xiao, X. and Li, W. and Balasubramanian, S. and Khalili, H. and Damle, A. and Ortmann, W. A. and Perrone, A. and Kantor, A. B. and Gulko, P. S. and Kern, M. and Furie, R. and Behrens, T. W. and Gregersen, P. K.},
  month = jun,
  year = {2005},
  keywords = {gene expression,microarray,Monocytes,peripheral blood mononuclear cells,rheumatoid arthritis},
  pages = {388--397}
}

@article{cannon_neun_2009-1,
  title = {{{NeuN}} is not a reliable marker of dopamine neurons in rat substantia nigra},
  volume = {464},
  issn = {0304-3940},
  doi = {10.1016/j.neulet.2009.08.023},
  abstract = {Quantification of neuronal cell number is a key endpoint in the characterization of neurodegenerative disease models and neuroprotective regimens. Immunohistochemistry for phenotypic markers, followed by unbiased stereology is often used to quantify the relevant neuronal population. To control for loss of phenotypic markers in the absence of cell death, or to determine if other types of neurons are lost, a general neuronal marker is often desired. Vertebrate neuron-specific nuclear protein (NeuN) is reportedly expressed in most mammalian neurons. In Parkinson's disease models, NeuN has been widely used to determine if there is actual nigral dopamine neuron loss or simply loss of tyrosine hydroxylase expression, a prominent phenotypic marker. To date, the qualitative value of NeuN expression as such a marker in the substantia nigra has not been assessed. Midbrain tissue sections from control rats were stained for NeuN and tyrosine hydroxylase and assessed by light or confocal microscopy. Here we report that NeuN expression level in the rat substantia nigra was highly variable, with many faintly stained cells that would not be meet stereological scoring criteria. Additionally, dopamine neurons with little or no NeuN expression were readily identified. Subcellular compartmentalization of NeuN expression was also variable, with many cells dorsal and ventral to the nigra exhibiting expression in both the nucleus and cytoplasm. NeuN expression also appeared to be much higher in non-dopamine neurons within the ventral midbrain. This characterization of nigral NeuN expression suggests that it is not useful as a quantitative general neuronal marker in the substantia nigra.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-10-27},
  journal = {Neuroscience Letters},
  author = {Cannon, Jason R. and Greenamyre, J. Timothy},
  month = oct,
  year = {2009},
  keywords = {Dopamine neuron,NeuN,Parkinson's disease,Substantia nigra},
  pages = {14--17},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/97VUGCJ3/S0304394009010891.html:}
}

@article{andiappan_genome-wide_2015,
  title = {Genome-wide analysis of the genetic regulation of gene expression in human neutrophils},
  volume = {6},
  copyright = {\textcopyright{} 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  doi = {10.1038/ncomms8971},
  abstract = {Neutrophils are an abundant immune cell type involved in both antimicrobial defence and autoimmunity. The regulation of their gene expression, however, is still largely unknown. Here we report an eQTL study on isolated neutrophils from 114 healthy individuals of Chinese ethnicity, identifying 21,210 eQTLs on 832 unique genes. Unsupervised clustering analysis of these eQTLs confirms their role in inflammatory responses and immunological diseases but also indicates strong involvement in dermatological pathologies. One of the strongest eQTL identified (rs2058660) is also the tagSNP of a linkage block reported to affect leprosy and Crohn's disease in opposite directions. In a functional study, we can link the C allele with low expression of the \ensuremath{\beta}-chain of IL18-receptor (IL18RAP). In neutrophils, this results in a reduced responsiveness to IL-18, detected both on the RNA and protein level. Thus, the polymorphic regulation of human neutrophils can impact beneficial as well as pathological inflammatory responses.},
  language = {en},
  timestamp = {2015-08-17T19:15:50Z},
  urldate = {2015-08-17},
  journal = {Nature Communications},
  author = {Andiappan, Anand Kumar and Melchiotti, Rossella and Poh, Tuang Yeow and Nah, Michelle and Puan, Kia Joo and Vigano, Elena and Haase, Doreen and Yusof, Nurhashikin and {San Luis}, Boris and Lum, Josephine and Kumar, Dilip and Foo, Shihui and Zhuang, Li and Vasudev, Anusha and Irwanto, Astrid and Lee, Bernett and Nardin, Alessandra and Liu, Hong and Zhang, Furen and Connolly, John and Liu, Jianjun and Mortellaro, Alessandra and Wang, De Yun and Poidinger, Michael and Larbi, Anis and Zolezzi, Francesca and Rotzschke, Olaf},
  month = aug,
  year = {2015},
  keywords = {Biological sciences,Genetics,Molecular biology}
}

@article{mccall_frozen_2010,
  title = {Frozen robust multiarray analysis ({{fRMA}})},
  volume = {11},
  issn = {1465-4644, 1468-4357},
  doi = {10.1093/biostatistics/kxp059},
  abstract = {Robust multiarray analysis (RMA) is the most widely used preprocessing algorithm for Affymetrix and Nimblegen gene expression microarrays. RMA performs background correction, normalization, and summarization in a modular way. The last 2 steps require multiple arrays to be analyzed simultaneously. The ability to borrow information across samples provides RMA various advantages. For example, the summarization step fits a parametric model that accounts for probe effects, assumed to be fixed across arrays, and improves outlier detection. Residuals, obtained from the fitted model, permit the creation of useful quality metrics. However, the dependence on multiple arrays has 2 drawbacks: (1) RMA cannot be used in clinical settings where samples must be processed individually or in small batches and (2) data sets preprocessed separately are not comparable. We propose a preprocessing algorithm, frozen RMA (fRMA), which allows one to analyze microarrays individually or in small batches and then combine the data for analysis. This is accomplished by utilizing information from the large publicly available microarray databases. In particular, estimates of probe-specific effects and variances are precomputed and frozen. Then, with new data sets, these are used in concert with information from the new arrays to normalize and summarize the data. We find that fRMA is comparable to RMA when the data are analyzed as a single batch and outperforms RMA when analyzing multiple batches. The methods described here are implemented in the R package fRMA and are currently available for download from the software section of http://rafalab.jhsph.edu.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-11-24},
  journal = {Biostatistics},
  author = {McCall, Matthew N. and Bolstad, Benjamin M. and Irizarry, Rafael A.},
  month = apr,
  year = {2010},
  keywords = {Affymetrix,ArrayExpress,GEO,microarray,Preprocessing,Single-array},
  pages = {242--253},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/DHHN2K7D/242.html:},
  pmid = {20097884}
}

@article{johnson_adjusting_2007,
  title = {Adjusting batch effects in microarray expression data using empirical {{Bayes}} methods},
  volume = {8},
  issn = {1465-4644, 1468-4357},
  doi = {10.1093/biostatistics/kxj037},
  abstract = {Non-biological experimental variation or ``batch effects" are commonly observed across multiple batches of microarray experiments, often rendering the task of combining data from these batches difficult. The ability to combine microarray data sets is advantageous to researchers to increase statistical power to detect biological phenomena from studies where logistical considerations restrict sample size or in studies that require the sequential hybridization of arrays. In general, it is inappropriate to combine data sets without adjusting for batch effects. Methods have been proposed to filter batch effects from data, but these are often complicated and require large batch sizes () to implement. Because the majority of microarray studies are conducted using much smaller sample sizes, existing methods are not sufficient. We propose parametric and non-parametric empirical Bayes frameworks for adjusting data for batch effects that is robust to outliers in small sample sizes and performs comparable to existing methods for large samples. We illustrate our methods using two example data sets and show that our methods are justifiable, easy to apply, and useful in practice. Software for our method is freely available at: http://biosun1.harvard.edu/complab/batch/.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2015-02-13},
  journal = {Biostatistics},
  author = {Johnson, W. Evan and Li, Cheng and Rabinovic, Ariel},
  month = jan,
  year = {2007},
  keywords = {Batch effects,Empirical Bayes,microarrays,Monte Carlo},
  pages = {118--127},
  pmid = {16632515}
}

@article{beckervordersandforth_vivo_2010,
  title = {In {{Vivo Fate Mapping}} and {{Expression Analysis Reveals Molecular Hallmarks}} of {{Prospectively Isolated Adult Neural Stem Cells}}},
  volume = {7},
  issn = {1934-5909},
  doi = {10.1016/j.stem.2010.11.017},
  abstract = {Summary
Until now, limitations in the ability to enrich adult NSCs (aNSCs) have hampered meaningful analysis of these cells at the transcriptome level. Here we show via a split-Cre technology that coincident activity of the hGFAP and prominin1 promoters is a hallmark of aNSCs in~vivo. Sorting of cells from the adult mouse subependymal zone (SEZ) based on their expression of GFAP and prominin1 isolates all self-renewing, multipotent stem cells at high purity. Comparison of the transcriptome of these purified aNSCs to parenchymal nonneurogenic astrocytes and other SEZ cells reveals aNSC hallmarks, including neuronal lineage priming and the importance of cilia- and Ca-dependent signaling pathways. Inducible deletion of the ciliary protein IFT88 in aNSCs validates the role of ciliary function in aNSCs. Our work reveals candidate molecular regulators for unique features of aNSCs and facilitates future selective analysis of aNSCs in other functional contexts, such as aging and injury.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {6},
  urldate = {2014-10-21},
  journal = {Cell Stem Cell},
  author = {Beckervordersandforth, Ruth and Tripathi, Pratibha and Ninkovic, Jovica and Bayam, Efil and Lepier, Alexandra and Stempfhuber, Barbara and Kirchhoff, Frank and Hirrlinger, Johannes and Haslinger, Anja and Lie, D. Chichung and Beckers, Johannes and Yoder, Bradley and Irmler, Martin and G{\"o}tz, Magdalena},
  month = dec,
  year = {2010},
  pages = {744--758},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/JJAKUQR2/S1934590910006399.html:}
}

@article{novershtern_densely_2011,
  title = {Densely interconnected transcriptional circuits control cell states in human hematopoiesis},
  volume = {144},
  issn = {1097-4172},
  doi = {10.1016/j.cell.2011.01.004},
  abstract = {Though many individual transcription factors are known to regulate hematopoietic differentiation, major aspects of the global architecture of hematopoiesis remain unknown. Here, we profiled gene expression in 38 distinct purified populations of human hematopoietic cells and used probabilistic models of gene expression and analysis of cis-elements in gene promoters to decipher the general organization of their regulatory circuitry. We identified modules of highly coexpressed genes, some of which are restricted to a single lineage but most of which are expressed at variable levels across multiple lineages. We found densely interconnected cis-regulatory circuits and a large number of transcription factors that are differentially expressed across hematopoietic states. These findings suggest a more complex regulatory system for hematopoiesis than previously assumed.},
  language = {eng},
  timestamp = {2016-03-24T04:41:22Z},
  number = {2},
  journal = {Cell},
  author = {Novershtern, Noa and Subramanian, Aravind and Lawton, Lee N. and Mak, Raymond H. and Haining, W. Nicholas and McConkey, Marie E. and Habib, Naomi and Yosef, Nir and Chang, Cindy Y. and Shay, Tal and Frampton, Garrett M. and Drake, Adam C. B. and Leskov, Ilya and Nilsson, Bjorn and Preffer, Fred and Dombkowski, David and Evans, John W. and Liefeld, Ted and Smutko, John S. and Chen, Jianzhu and Friedman, Nir and Young, Richard A. and Golub, Todd R. and Regev, Aviv and Ebert, Benjamin L.},
  month = jan,
  year = {2011},
  keywords = {Gene Expression Profiling,Gene Expression Regulation,Gene regulatory networks,Hematopoiesis,Humans,Transcription Factors},
  pages = {296--309},
  pmid = {21241896},
  pmcid = {PMC3049864}
}

@article{hut_cholinergic_2011,
  series = {The cholinergic system and brain function},
  title = {The cholinergic system, circadian rhythmicity, and time memory},
  volume = {221},
  issn = {0166-4328},
  doi = {10.1016/j.bbr.2010.11.039},
  abstract = {This review provides an overview of the interaction between the mammalian cholinergic system and circadian system, and its possible role in time memory. Several studies made clear that circadian (daily) fluctuations in acetylcholine (ACh) release, cholinergic enzyme activity and cholinergic receptor expression varies remarkably between species and even strains. Apparently, cholinergic features can be flexibly adjusted to the needs of a species or strain. Nevertheless, it can be generalized that circadian rhythmicity in the cholinergic system is characterized by high ACh release during the active phase of an individual. During the active phase, the activity of the ACh synthesizing enzyme Choline Acetyltransferase (ChAT) is enhanced, and the activity of the ACh degrading enzyme Acetylcholinesterase (AChE) is reduced. The number of free, unbound and thus available muscarinic acetylcholine receptors (mAChRs) is highest when ACh release is lowest. The cholinergic innervation of the suprachiasmatic nucleus (SCN), the hypothalamic circadian master clock, arises from the cholinergic forebrain and brain stem nuclei. The density of cholinergic fibers and terminals is modest as compared to other hypothalamic nuclei. This is the case for rat, hamster and mouse, three chronobiological model rodent species studied by us. A new finding is that the rat SCN contains some local cholinergic neurons. Hamster SCN contains less cholinergic neurons, whereas the mouse SCN is devoid of such cells. ACh has an excitatory effect on SCN cells (at least in vivo), and functions in close interaction with other neurotransmitters. Originally it was thought that ACh transferred retinal light information to the SCN. This turned out to be wrong. Thereafter, the phase shifting effects of ACh prompted researches to view ACh as an agent for nocturnal clock resetting. It is still not clear, however, what the function consequence is of SCN cholinergic neurotransmission. Here, we postulate the hypothesis that cholinergic neurotransmission in the SCN provides the brain with a mechanism to support the formation of time memory via `time stamping'. We define time memory as the memory of a specific time of the day, for which an animal made an association with a certain event and/or location (for example in case of time-place association). We use the term `time stamping' to refer to the process underlying the encoding of a specific time of day (the time stamp). Only relatively brief but arousing events seem to be time stamped at SCN level. This time stamping requires the engagement of mAChRs. New data suggests that the SCN uses the neuropeptide vasopressin (AVP) as an output system to transfer the specific time of day information to other brain regions such as hippocampus and neocortex where time memory is supposed to be acquired, consolidated and stored. Since time stamping is a cholinergically mediated function of the circadian system, the early disruption of the cholinergic and circadian systems as seen in Alzheimer's disease (AD) may contribute to the cognitive disruption of temporal organization of memory and behavior in these patients.},
  timestamp = {2016-03-24T10:00:40Z},
  number = {2},
  urldate = {2016-03-24},
  journal = {Behavioural Brain Research},
  author = {Hut, R. A. and {Van der Zee}, E. A.},
  month = aug,
  year = {2011},
  keywords = {Acetylcholine,Aging,Alzheimer's disease,Biological rhythms,Cholinergic system,Circadian system,Muscarinic receptor,Nicotinic receptor,Suprachiasmatic nucleus,Time memory,Time stamping},
  pages = {466--480}
}

@article{straka_cd19+_2002,
  title = {The {{CD19}}+ {{B}}-cell counts at peripheral blood stem cell mobilization determine different levels of tumour contamination and autograft purgability in low-grade lymphoma},
  volume = {116},
  issn = {0007-1048},
  abstract = {The tumour load of peripheral blood stem cell (PBSC) harvests and the outcome of ex vivo immunomagnetic B-cell purging was investigated in 19 patients with low-grade lymphoma. To quantify the tumour load, we combined fluorescence-activated cell sorting measurement of CD19+ B-cells and determination of the B-cell light chain ratio (LCR) with consensus complementarity-determining region III-polymerase chain reaction (CDRIII-PCR) and gene scan analysis. The number of tumour cells was calculated using B-cell extracts from the PBSCs. Two different patterns were distinguished. In eight patients (42\%) with CD19+ B cells \ensuremath{>}1\% in the apheresis product, a high tumour load was found, characterized by a monoclonal LCR, positive PCR in seven out of eight cases, \ensuremath{>}5 x 10(7) extracted lymphoma cells in six out of seven PCR-assessable cases, and the presence of residual lymphoma after purging in six of seven cases. In 11 patients (58\%) with \ensuremath{<}1\% CD19+ B-cells in the product, a low tumour load was indicated by a polyclonal LCR, positive PCR in only 4 out of 11 cases, \ensuremath{>}5 x 10(7) extracted lymphoma cells in zero out of four PCR-assessable cases, and the presence of residual lymphoma after purging in zero out of four of these cases. The level of residual lymphoma following purging largely depended on the level of tumour contamination. CD19+ B-cells \ensuremath{>}50/microl in the peripheral blood at mobilization predicted a high tumour load in the apheresis product.},
  language = {eng},
  timestamp = {2015-08-31T23:51:48Z},
  number = {3},
  journal = {British Journal of Haematology},
  author = {Straka, Christian and Oduncu, Fuat and Drexler, Eva and Mitterer, Manfred and Schnabel, Brigitte and K{\"o}nig, August and Brack, Norbert and Nerl, Christoph and Emmerich, Bertold},
  month = mar,
  year = {2002},
  keywords = {Adult,Antigens; CD19,B-Lymphocyte Subsets,Bone Marrow Purging,Female,Hematopoietic Stem Cell Mobilization,Hematopoietic Stem Cell Transplantation,Humans,Immunomagnetic Separation,Lymphocyte Count,Lymphoma; Non-Hodgkin,Male,Middle Aged,Neoplasm; Residual,Neoplastic Cells; Circulating,Transplantation; Autologous},
  pages = {695--701},
  pmid = {11849235}
}

@article{zenaro_neutrophils_2015,
  title = {Neutrophils promote {{Alzheimer}}'s disease-like pathology and cognitive decline via {{LFA}}-1 integrin},
  volume = {21},
  copyright = {\textcopyright{} 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1078-8956},
  doi = {10.1038/nm.3913},
  abstract = {Inflammation is a pathological hallmark of Alzheimer's disease, and innate immune cells have been shown to contribute to disease pathogenesis. In two transgenic models of Alzheimer's disease (5xFAD and 3xTg-AD mice), neutrophils extravasated and were present in areas with amyloid-\ensuremath{\beta} (A\ensuremath{\beta}) deposits, where they released neutrophil extracellular traps (NETs) and IL-17. A\ensuremath{\beta}42 peptide triggered the LFA-1 integrin high-affinity state and rapid neutrophil adhesion to integrin ligands. In vivo, LFA-1 integrin controlled neutrophil extravasation into the CNS and intraparenchymal motility. In transgenic Alzheimer's disease models, neutrophil depletion or inhibition of neutrophil trafficking via LFA-1 blockade reduced Alzheimer's disease\textendash{}like neuropathology and improved memory in mice already showing cognitive dysfunction. Temporary depletion of neutrophils for 1 month at early stages of disease led to sustained improvements in memory. Transgenic Alzheimer's disease model mice lacking LFA-1 were protected from cognitive decline and had reduced gliosis. In humans with Alzheimer's disease, neutrophils adhered to and spread inside brain venules and were present in the parenchyma, along with NETs. Our results demonstrate that neutrophils contribute to Alzheimer's disease pathogenesis and cognitive impairment and suggest that the inhibition of neutrophil trafficking may be beneficial in Alzheimer's disease.},
  language = {en},
  timestamp = {2015-08-17T19:09:06Z},
  number = {8},
  urldate = {2015-08-17},
  journal = {Nature Medicine},
  author = {Zenaro, Elena and Pietronigro, Enrica and Bianca, Vittorina Della and Piacentino, Gennj and Marongiu, Laura and Budui, Simona and Turano, Ermanna and Rossi, Barbara and Angiari, Stefano and Dusi, Silvia and Montresor, Alessio and Carlucci, Tommaso and Nan{\`\i}, Sara and Tosadori, Gabriele and Calciano, Lucia and Catalucci, Daniele and Berton, Giorgio and Bonetti, Bruno and Constantin, Gabriela},
  month = aug,
  year = {2015},
  pages = {880--886}
}

@article{wylie_distinct_2010,
  title = {Distinct {{Transcriptomes Define Rostral}} and {{Caudal Serotonin Neurons}}},
  volume = {30},
  issn = {0270-6474, 1529-2401},
  doi = {10.1523/JNEUROSCI.4656-09.2010},
  abstract = {The molecular architecture of developing serotonin (5HT) neurons is poorly understood, yet its determination is likely to be essential for elucidating functional heterogeneity of these cells and the contribution of serotonergic dysfunction to disease pathogenesis. Here, we describe the purification of postmitotic embryonic 5HT neurons by flow cytometry for whole-genome microarray expression profiling of this unitary monoaminergic neuron type. Our studies identified significantly enriched expression of hundreds of unique genes in 5HT neurons, thus providing an abundance of new serotonergic markers. Furthermore, we identified several hundred transcripts encoding homeodomain, axon guidance, cell adhesion, intracellular signaling, ion transport, and imprinted genes associated with various neurodevelopmental disorders that were differentially enriched in developing rostral and caudal 5HT neurons. These findings suggested a homeodomain code that distinguishes rostral and caudal 5HT neurons. Indeed, verification studies demonstrated that Hmx homeodomain and Hox gene expression defined an Hmx+ rostral subtype and Hox+ caudal subtype. Expression of engrailed genes in a subset of 5HT neurons in the rostral domain further distinguished two subtypes defined as Hmx+En+ and Hmx+En-. The differential enrichment of gene sets for different canonical pathways and gene ontology categories provided additional evidence for heterogeneity between rostral and caudal 5HT neurons. These findings demonstrate a deep transcriptome and biological pathway duality for neurons that give rise to the ascending and descending serotonergic subsystems. Our databases provide a rich, clinically relevant resource for definition of 5HT neuron subtypes and elucidation of the genetic networks required for serotonergic function.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-10-21},
  journal = {The Journal of Neuroscience},
  author = {Wylie, Christi J. and Hendricks, Timothy J. and Zhang, Bing and Wang, Lily and Lu, Pengcheng and Leahy, Patrick and Fox, Stephanie and Maeno, Hiroshi and Deneris, Evan S.},
  month = jan,
  year = {2010},
  pages = {670--684},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/TXEDBVVX/670.html:},
  pmid = {20071532}
}

@article{anandasabapathy_flt3l_2011,
  title = {{{Flt3L}} controls the development of radiosensitive dendritic cells in the meninges and choroid plexus of the steady-state mouse brain},
  volume = {208},
  issn = {0022-1007, 1540-9538},
  doi = {10.1084/jem.20102657},
  abstract = {Back to TopAbstract
Antigen-presenting cells in the disease-free brain have been identified primarily by expression of antigens such as CD11b, CD11c, and MHC II, which can be shared by dendritic cells (DCs), microglia, and monocytes. In this study, starting with the criterion of Flt3 (FMS-like receptor tyrosine kinase 3)-dependent development, we characterize the features of authentic DCs within the meninges and choroid plexus in healthy mouse brains. Analyses of morphology, gene expression, and antigen-presenting function established a close relationship between meningeal and choroid plexus DCs (m/chDCs) and spleen DCs. DCs in both sites shared an intrinsic requirement for Flt3 ligand. Microarrays revealed differences in expression of transcripts encoding surface molecules, transcription factors, pattern recognition receptors, and other genes in m/chDCs compared with monocytes and microglia. Migrating pre-DC progenitors from bone marrow gave rise to m/chDCs that had a 5\textendash{}7-d half-life. In contrast to microglia, DCs actively present self-antigens and stimulate T cells. Therefore, the meninges and choroid plexus of a steady-state brain contain DCs that derive from local precursors and exhibit a differentiation and antigen-presenting program similar to spleen DCs and distinct from microglia.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {8},
  urldate = {2014-10-21},
  journal = {The Journal of Experimental Medicine},
  author = {Anandasabapathy, Niroshana and Victora, Gabriel D. and Meredith, Matthew and Feder, Rachel and Dong, Baojun and Kluger, Courtney and Yao, Kaihui and Dustin, Michael L. and Nussenzweig, Michel C. and Steinman, Ralph M. and Liu, Kang},
  month = jan,
  year = {2011},
  pages = {1695--1705},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/RDIGZC4C/1695.html:},
  pmid = {21788405}
}

@article{costa_effects_2014,
  title = {The {{Effects}} of {{Aging}} on {{Substantia Nigra Dopamine Neurons}}},
  volume = {34},
  issn = {0270-6474, 1529-2401},
  doi = {10.1523/JNEUROSCI.3739-14.2014},
  language = {en},
  timestamp = {2016-04-28T09:09:14Z},
  number = {46},
  urldate = {2016-04-28},
  journal = {The Journal of Neuroscience},
  author = {Costa, Kau{\^e} M.},
  month = dec,
  year = {2014},
  pages = {15133--15134},
  pmid = {25392480}
}

@article{shankavaram_transcript_2007,
  title = {Transcript and protein expression profiles of the {{NCI}}-60 cancer cell panel: an integromic microarray study},
  volume = {6},
  issn = {1535-7163, 1538-8514},
  shorttitle = {Transcript and protein expression profiles of the {{NCI}}-60 cancer cell panel},
  doi = {10.1158/1535-7163.MCT-06-0650},
  abstract = {To evaluate the utility of transcript profiling for prediction of protein expression levels, we compared profiles across the NCI-60 cancer cell panel, which represents nine tissues of origin. For that analysis, we present here two new NCI-60 transcript profile data sets (A based on Affymetrix HG-U95 and HG-U133A chips; Affymetrix, Santa Clara, CA) and one new protein profile data set (based on reverse-phase protein lysate arrays). The data sets are available online at http://discover.nci.nih.gov in the CellMiner program package. Using the new transcript data in combination with our previously published cDNA array and Affymetrix HU6800 data sets, we first developed a ``consensus set'' of transcript profiles based on the four different microarray platforms. Using that set, we found that 65\% of the genes showed statistically significant transcript-protein correlation, and the correlations were generally higher than those reported previously for panels of mammalian cells. Using the predictive analysis of microarray nearest shrunken centroid algorithm for functional prediction of tissue of origin, we then found that (a) the consensus mRNA set did better than did data from any of the individual mRNA platforms and (b) the protein data seemed to do somewhat better (P = 0.027) on a gene-for-gene basis in this particular study than did the consensus mRNA data, but both did well. Analysis based on the Gene Ontology showed protein levels of structure-related genes to be well predicted by mRNA levels (mean r = 0.71). Because the transcript-based technologies are more mature and are currently able to assess larger numbers of genes at one time, they continue to be useful, even when the ultimate aim is information about proteins. [Mol Cancer Ther 2007;6(3):820\textendash{}32]},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {3},
  urldate = {2014-12-22},
  journal = {Molecular Cancer Therapeutics},
  author = {Shankavaram, Uma T. and Reinhold, William C. and Nishizuka, Satoshi and Major, Sylvia and Morita, Daisaku and Chary, Krishna K. and Reimers, Mark A. and Scherf, Uwe and Kahn, Ari and Dolginow, Douglas and Cossman, Jeffrey and Kaldjian, Eric P. and Scudiero, Dominic A. and Petricoin, Emanuel and Liotta, Lance and Lee, Jae K. and Weinstein, John N.},
  month = jan,
  year = {2007},
  keywords = {cancer cell line,microarray,NCI-60,pharmacogenomics,reverse-phase lysate array},
  pages = {820--832},
  pmid = {17339364}
}

@article{bushel_blood_2007,
  title = {Blood gene expression signatures predict exposure levels},
  volume = {104},
  issn = {0027-8424, 1091-6490},
  doi = {10.1073/pnas.0706987104},
  abstract = {To respond to potential adverse exposures properly, health care providers need accurate indicators of exposure levels. The indicators are particularly important in the case of acetaminophen (APAP) intoxication, the leading cause of liver failure in the U.S. We hypothesized that gene expression patterns derived from blood cells would provide useful indicators of acute exposure levels. To test this hypothesis, we used a blood gene expression data set from rats exposed to APAP to train classifiers in two prediction algorithms and to extract patterns for prediction using a profiling algorithm. Prediction accuracy was tested on a blinded, independent rat blood test data set and ranged from 88.9\% to 95.8\%. Genomic markers outperformed predictions based on traditional clinical parameters. The expression profiles of the predictor genes from the patterns extracted from the blood exhibited remarkable (97\% accuracy) transtissue APAP exposure prediction when liver gene expression data were used as a test set. Analysis of human samples revealed separation of APAP-intoxicated patients from control individuals based on blood expression levels of human orthologs of the rat discriminatory genes. The major biological signal in the discriminating genes was activation of an inflammatory response after exposure to toxic doses of APAP. These results support the hypothesis that gene expression data from peripheral blood cells can provide valuable information about exposure levels, well before liver damage is detected by classical parameters. It also supports the potential use of genomic markers in the blood as surrogates for clinical markers of potential acute liver damage.},
  language = {en},
  timestamp = {2015-08-18T01:54:39Z},
  number = {46},
  urldate = {2015-08-18},
  journal = {Proceedings of the National Academy of Sciences},
  author = {Bushel, P. R. and Heinloth, A. N. and Li, J. and Huang, L. and Chou, J. W. and Boorman, G. A. and Malarkey, D. E. and Houle, C. D. and Ward, S. M. and Wilson, R. E. and Fannin, R. D. and Russo, M. W. and Watkins, P. B. and Tennant, R. W. and Paules, R. S.},
  month = nov,
  year = {2007},
  keywords = {acetaminophen,Genomics,hepatotoxicity,microarray,prediction},
  pages = {18211--18216},
  pmid = {17984051}
}

@article{westra_cell_2015,
  title = {Cell {{Specific eQTL Analysis}} without {{Sorting Cells}}},
  volume = {11},
  doi = {10.1371/journal.pgen.1005223},
  abstract = {Author Summary Many variants in the genome, including variants associated with disease, affect the expression of genes. These so-called expression quantitative trait loci (eQTL) can be used to gain insight in the downstream consequences of disease. While it has been shown that many disease-associated variants alter gene expression in a cell-type dependent manner, eQTL datasets for specific cell types may not always be available and their sample size is often limited. We present a method that is able to detect cell type specific effects within eQTL datasets that have been generated from whole tissues (which may be composed of many cell types), in our case whole blood. By combining numerous whole blood datasets through meta-analysis, we show that we are able to detect eQTL effects that are specific for neutrophils and lymphocytes (two blood cell types). Additionally, we show that the variants associated with some diseases may preferentially alter the gene expression in one of these cell types. We conclude that our method is an alternative method to detect cell type specific eQTL effects, that may complement generating cell type specific eQTL datasets and that may be applied on other cell types and tissues as well.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {5},
  urldate = {2015-05-31},
  journal = {PLoS Genet},
  author = {Westra, Harm-Jan and Arends, Danny and Esko, T{\~o}nu and Peters, Marjolein J. and Schurmann, Claudia and Schramm, Katharina and Kettunen, Johannes and Yaghootkar, Hanieh and Fairfax, Benjamin P. and Andiappan, Anand Kumar and Li, Yang and Fu, Jingyuan and Karjalainen, Juha and Platteel, Mathieu and Visschedijk, Marijn and Weersma, Rinse K. and Kasela, Silva and Milani, Lili and Tserel, Liina and Peterson, P{\"a}rt and Reinmaa, Eva and Hofman, Albert and Uitterlinden, Andr{\'e} G. and Rivadeneira, Fernando and Homuth, Georg and Petersmann, Astrid and Lorbeer, Roberto and Prokisch, Holger and Meitinger, Thomas and Herder, Christian and Roden, Michael and Grallert, Harald and Ripatti, Samuli and Perola, Markus and Wood, Andrew R. and Melzer, David and Ferrucci, Luigi and Singleton, Andrew B. and Hernandez, Dena G. and Knight, Julian C. and Melchiotti, Rossella and Lee, Bernett and Poidinger, Michael and Zolezzi, Francesca and Larbi, Anis and Wang, De Yun and {van den Berg}, Leonard H. and Veldink, Jan H. and Rotzschke, Olaf and Makino, Seiko and Salomaa, Veikko and Strauch, Konstantin and V{\"o}lker, Uwe and {van Meurs}, Joyce B. J. and Metspalu, Andres and Wijmenga, Cisca and Jansen, Ritsert C. and Franke, Lude},
  month = may,
  year = {2015},
  pages = {e1005223}
}

@article{hughes_functional_2000,
  title = {Functional {{Discovery}} via a {{Compendium}} of {{Expression Profiles}}},
  volume = {102},
  issn = {0092-8674},
  doi = {10.1016/S0092-8674(00)00015-5},
  abstract = {Ascertaining the impact of uncharacterized perturbations on the cell is a fundamental problem in biology. Here, we describe how a single assay can be used to monitor hundreds of different cellular functions simultaneously. We constructed a reference database or ``compendium'' of expression profiles corresponding to 300 diverse mutations and chemical treatments in S. cerevisiae, and we show that the cellular pathways affected can be determined by pattern matching, even among very subtle profiles. The utility of this approach is validated by examining profiles caused by deletions of uncharacterized genes: we identify and experimentally confirm that eight uncharacterized open reading frames encode proteins required for sterol metabolism, cell wall function, mitochondrial respiration, or protein synthesis. We also show that the compendium can be used to characterize pharmacological perturbations by identifying a novel target of the commonly used drug dyclonine.},
  timestamp = {2016-03-16T01:55:45Z},
  number = {1},
  urldate = {2016-03-16},
  journal = {Cell},
  author = {Hughes, Timothy R and Marton, Matthew J and Jones, Allan R and Roberts, Christopher J and Stoughton, Roland and Armour, Christopher D and Bennett, Holly A and Coffey, Ernest and Dai, Hongyue and He, Yudong D and Kidd, Matthew J and King, Amy M and Meyer, Michael R and Slade, David and Lum, Pek Y and Stepaniants, Sergey B and Shoemaker, Daniel D and Gachotte, Daniel and Chakraburtty, Kalpana and Simon, Julian and Bard, Martin and Friend, Stephen H},
  month = jul,
  year = {2000},
  pages = {109--126}
}

@article{eisenberg_human_2013,
  series = {Human Genetics},
  title = {Human housekeeping genes, revisited},
  volume = {29},
  issn = {0168-9525},
  doi = {10.1016/j.tig.2013.05.010},
  abstract = {Housekeeping genes are involved in basic cell maintenance and, therefore, are expected to maintain constant expression levels in all cells and conditions. Identification of these genes facilitates exposure of the underlying cellular infrastructure and increases understanding of various structural genomic features. In addition, housekeeping genes are instrumental for calibration in many biotechnological applications and genomic studies. Advances in our ability to measure RNA expression have resulted in a gradual increase in the number of identified housekeeping genes. Here, we describe housekeeping gene detection in the era of massive parallel sequencing and RNA-seq. We emphasize the importance of expression at a constant level and provide a list of 3804 human genes that are expressed uniformly across a panel of tissues. Several exceptionally uniform genes are singled out for future experimental use, such as RT-PCR control genes. Finally, we discuss both ways in which current technology can meet some of past obstacles encountered, and several as yet unmet challenges.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {10},
  urldate = {2015-03-23},
  journal = {Trends in Genetics},
  author = {Eisenberg, Eli and Levanon, Erez Y.},
  month = oct,
  year = {2013},
  keywords = {gene expression patterns,housekeeping genes,internal control,next generation sequencing,RNA-seq},
  pages = {569--574}
}

@article{li_model-based_2001,
  title = {Model-based analysis of oligonucleotide arrays: {{Expression}} index computation and outlier detection},
  volume = {98},
  issn = {0027-8424, 1091-6490},
  shorttitle = {Model-based analysis of oligonucleotide arrays},
  doi = {10.1073/pnas.98.1.31},
  abstract = {Recent advances in cDNA and oligonucleotide DNA arrays have made it possible to measure the abundance of mRNA transcripts for many genes simultaneously. The analysis of such experiments is nontrivial because of large data size and many levels of variation introduced at different stages of the experiments. The analysis is further complicated by the large differences that may exist among different probes used to interrogate the same gene. However, an attractive feature of high-density oligonucleotide arrays such as those produced by photolithography and inkjet technology is the standardization of chip manufacturing and hybridization process. As a result, probe-specific biases, although significant, are highly reproducible and predictable, and their adverse effect can be reduced by proper modeling and analysis methods. Here, we propose a statistical model for the probe-level data, and develop model-based estimates for gene expression indexes. We also present model-based methods for identifying and handling cross-hybridizing probes and contaminating array regions. Applications of these results will be presented elsewhere.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {1},
  urldate = {2014-11-24},
  journal = {Proceedings of the National Academy of Sciences},
  author = {Li, Cheng and Wong, Wing Hung},
  month = feb,
  year = {2001},
  pages = {31--36},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/VRS4F5CB/31.html:}
}

@article{chang_genotype_2014,
  title = {Genotype to phenotype relationships in autism spectrum disorders},
  volume = {advance online publication},
  copyright = {\textcopyright{} 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {1097-6256},
  doi = {10.1038/nn.3907},
  abstract = {Autism spectrum disorders (ASDs) are characterized by phenotypic and genetic heterogeneity. Our analysis of functional networks perturbed in ASD suggests that both truncating and nontruncating de novo mutations contribute to autism, with a bias against truncating mutations in early embryonic development. We find that functional mutations are preferentially observed in genes likely to be haploinsufficient. Multiple cell types and brain areas are affected, but the impact of ASD mutations appears to be strongest in cortical interneurons, pyramidal neurons and the medium spiny neurons of the striatum, implicating cortical and corticostriatal brain circuits. In females, truncating ASD mutations on average affect genes with 50\textendash{}100\% higher brain expression than in males. Our results also suggest that truncating de novo mutations play a smaller role in the etiology of high-functioning ASD cases. Overall, we find that stronger functional insults usually lead to more severe intellectual, social and behavioral ASD phenotypes.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2015-01-14},
  journal = {Nature Neuroscience},
  author = {Chang, Jonathan and Gilman, Sarah R. and Chiang, Andrew H. and Sanders, Stephan J. and Vitkup, Dennis},
  month = dec,
  year = {2014},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/RCVJVZ8A/nn.3907.html:}
}

@article{pissadaki_energy_2013,
  title = {The energy cost of action potential propagation in dopamine neurons: clues to susceptibility in {{Parkinson}}'s disease},
  volume = {7},
  issn = {1662-5188},
  shorttitle = {The energy cost of action potential propagation in dopamine neurons},
  doi = {10.3389/fncom.2013.00013},
  abstract = {Dopamine neurons of the substantia nigra pars compacta (SNc) are uniquely sensitive to degeneration in Parkinson's disease (PD) and its models. Although a variety of molecular characteristics have been proposed to underlie this sensitivity, one possible contributory factor is their massive, unmyelinated axonal arbor that is orders of magnitude larger than other neuronal types. We suggest that this puts them under such a high energy demand that any stressor that perturbs energy production leads to energy demand exceeding supply and subsequent cell death. One prediction of this hypothesis is that those dopamine neurons that are selectively vulnerable in PD will have a higher energy cost than those that are less vulnerable. We show here, through the use of a biology-based computational model of the axons of individual dopamine neurons, that the energy cost of axon potential propagation and recovery of the membrane potential increases with the size and complexity of the axonal arbor according to a power law. Thus SNc dopamine neurons, particularly in humans, whose axons we estimate to give rise to more than 1 million synapses and have a total length exceeding 4 m, are at a distinct disadvantage with respect to energy balance which may be a factor in their selective vulnerability in PD.},
  timestamp = {2015-08-13T22:18:44Z},
  urldate = {2014-11-26},
  journal = {Frontiers in Computational Neuroscience},
  author = {Pissadaki, Eleftheria K. and Bolam, J. Paul},
  month = mar,
  year = {2013},
  keywords = {Dopaminergic,Energy,Myelin,Parkinson},
  pmid = {23515615},
  pmcid = {PMC3600574}
}

@incollection{noble_chapter_2009,
  series = {Guide to Protein Purification, 2nd Edition},
  title = {Chapter 8 {{Quantitation}} of {{Protein}}},
  volume = {463},
  abstract = {The measurement of protein concentration in an aqueous sample is an important assay in biochemistry research and development labs for applications ranging from enzymatic studies to providing data for biopharmaceutical lot release. Spectrophotometric protein quantitation assays are methods that use UV and visible spectroscopy to rapidly determine the concentration of protein, relative to a standard, or using an assigned extinction coefficient. Methods are described to provide information on how to analyze protein concentration using UV protein spectroscopy measurements, traditional dye-based absorbance measurements; BCA, Lowry, and Bradford assays and the fluorescent dye-based assays; amine derivatization and detergent partition assays. The observation that no single assay dominates the market is due to specific limitations of certain methods that investigators need to consider before selecting the most appropriate assay for their sample. Many of the dye-based assays have unique chemical mechanisms that are prone to interference from chemicals prevalent in many biological buffer preparations. A discussion of which assays are prone to interference and the selection of alternative methods is included.},
  timestamp = {2016-02-12T00:56:27Z},
  urldate = {2016-02-12},
  booktitle = {Methods in {{Enzymology}}},
  publisher = {{Academic Press}},
  author = {Noble, James E. and Bailey, Marc J. A.},
  editor = {Deutscher, Richard R. Burgess and Murray P.},
  year = {2009},
  pages = {73--95},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/J9HDPBPR/S0076687909630081.html:;Noble_Bailey_2009_Chapter 8 Quantitation of Protein.pdf:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/RCQFGSVH/Noble_Bailey_2009_Chapter 8 Quantitation of Protein.pdf:application/pdf}
}

@article{duan_novel_2015,
  title = {Novel {{Insights}} into {{NeuN}}: from {{Neuronal Marker}} to {{Splicing Regulator}}},
  issn = {0893-7648, 1559-1182},
  shorttitle = {Novel {{Insights}} into {{NeuN}}},
  doi = {10.1007/s12035-015-9122-5},
  abstract = {Neuronal nuclei (NeuN) is a well-recognized ``marker'' that is detected exclusively in post-mitotic neurons and was initially identified through an immunological screen to produce neuron-specific antibodies. Immunostaining evidence indicates that NeuN is distributed in the nuclei of mature neurons in nearly all parts of the vertebrate nervous system. NeuN is highly conserved among species and is stably expressed during specific stages of development. Therefore, NeuN has been considered to be a reliable marker of mature neurons for the past two decades. However, this role has been challenged by recent studies indicating that NeuN staining is variable and even absent during certain diseases and specific physiological states. More importantly, despite the widespread use of the anti-NeuN antibody, the natural identity of the NeuN protein remained elusive for 17 years. NeuN was recently eventually identified as an epitope of Rbfox3, which is a novel member of the Rbfox1 family of splicing factors. This identification might provide a novel perspective on NeuN expression during both physiological and pathological conditions. This review summarizes the current progress on the biochemical identity and biological significance of NeuN and recommends caution when applying NeuN immunoreactivity as a definitive marker of mature neurons in certain diseases and specific physiological states.},
  language = {en},
  timestamp = {2015-08-27T18:55:09Z},
  urldate = {2015-08-25},
  journal = {Molecular Neurobiology},
  author = {Duan, Wei and Zhang, Yu-Ping and Hou, Zhi and Huang, Chen and Zhu, He and Zhang, Chun-Qing and Yin, Qing},
  month = feb,
  year = {2015},
  keywords = {Cell Biology,Mature neurons,NeuN,Neurobiology,Neurology,Neuronal marker,Neurosciences,Rbfox3,Splicing regulator},
  pages = {1--11}
}

@article{wit_detection_2015,
  title = {The detection of {{EpCAM}}+ and {{EpCAM}}\textendash{} circulating tumor cells},
  volume = {5},
  issn = {2045-2322},
  doi = {10.1038/srep12270},
  timestamp = {2015-08-17T19:08:12Z},
  urldate = {2015-08-17},
  journal = {Scientific Reports},
  author = {{de Wit}, Sanne and {van Dalum}, Guus and Lenferink, Aufried T. M. and Tibbe, Arjan G. J. and Hiltermann, T. Jeroen N. and Groen, Harry J. M. and {van Rijn}, Cees J. M. and Terstappen, Leon W. M. M.},
  month = jul,
  year = {2015},
  pages = {12270}
}

@article{tkachev_oligodendrocyte_2003,
  title = {Oligodendrocyte dysfunction in schizophrenia and bipolar disorder},
  volume = {362},
  issn = {0140-6736},
  doi = {10.1016/S0140-6736(03)14289-4},
  abstract = {SummaryBackground
Results of array studies have suggested abnormalities in expression of lipid and myelin-related genes in schizophrenia. Here, we investigated oligodendrocyte-specific and myelination-associated gene expression in schizophrenia and bipolar affective disorder.
Methods
We used samples from the Stanley brain collection, consisting of 15 schizophrenia, 15 bipolar affective disorder, and 15 control brains. Indexing-based differential display PCR was done to screen for differences in gene expression in schizophrenia patients versus controls. Results were cross-validated with quantitative PCR, which was also used to investigate expression profiles of 16 other oligodendrocyte and myelin genes in schizophrenia and bipolar disorder. These genes were further investigated with an ongoing microarray analysis.
Findings
Results of differential display and quantitative PCR analysis showed a reduction of key oligodendrocyte-related and myelin-related genes in schizophrenia and bipolar patients; expression changes for both disorders showed a high degree of overlap. Microarray results of the same genes investigated by quantitative PCR correlated well overall.
Interpretation
Schizophrenia and bipolar brains showed downregulation of key oligodendrocyte and myelination genes, including transcription factors that regulate these genes, compared with control brains. These results lend support to and extend observations from other microarray investigations. Our study also showed similar expression changes to the schizophrenia group in bipolar brains, which thus lends support to the notion that the disorders share common causative and pathophysiological pathways.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {9386},
  urldate = {2014-12-18},
  journal = {The Lancet},
  author = {Tkachev, Dmitri and Mimmack, Michael L and Ryan, Margaret M and Wayland, Matt and Freeman, Tom and Jones, Peter B and Starkey, Michael and Webster, Maree J and Yolken, Robert H and Bahn, Sabine},
  month = sep,
  year = {2003},
  pages = {798--805},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/SD5SPHUI/S0140673603142894.html:}
}

@article{de_camilli_anatomy_1984,
  title = {Anatomy of cerebellar {{Purkinje}} cells in the rat determined by a specific immunohistochemical marker},
  volume = {11},
  issn = {0306-4522},
  doi = {10.1016/0306-4522(84)90193-3},
  abstract = {In the present study we have used guanosine 3\ensuremath{'}: 5\ensuremath{'}-phosphate-dependent protein kinase antiserum, a specific immunohistochemical marker for cerebellar Purkinje cells, [Lohmann, Walter, Miller, Greengard and De Camilli (1981) Proc. natn. Acad. Sci. U.S.A. 78, 653\textendash{}657], to carry out a detailed analysis of the architecture and projections of Purkinje cells in the adult rat. We have obtained a novel view of aspects of Purkinje cell morphology that were already known and, in addition, we have provided some new information, in particular on the targets of Purkinje cell axons and their pattern of innervation, and on the morphology and course of Purkinje cell axons. Furthermore, we have found a few cells positive for guanosine 3\ensuremath{'}: 5\ensuremath{'} phosphate-dependent protein kinase which are very similar morphologically to Purkinje cells but are located outside of the cerebellar cortex.

A unique feature of Purkinje cells is their peculiar monoplanar shape. Not only do their dendritic arbors lie in planes perpendicular to the major axis of the folia, but their axons, including the collaterals, also travel roughly in the same planes. Thus, Purkinje cells can be imagined as lying in longitudinal sheets radiating from the deep cerebellar nuclei. In these sheets, Purkinje cell axons originating from cells located at different rostrocaudal levels of the cortex converge towards the deep cerebellar nuclei without intersecting each other. It is as a result of this precise organization that Purkinje cell axons reach the deep cerebellar nuclei with a mediolateral and rostrocaudal topology that closely reflects the position of their parent cells in the cerebellar cortex. In the subcortical rays of white matter, Purkinje cell axons are interspersed with other axons, being excluded only from longitudinal strips which correspond to the cerebellar raphes. Upon converging towards the deep cerebellar nuclei they segregate into tracts of white matter that alternate with tracts of white matter from which they are excluded. The great majority of Purkinje cell axons terminate in the deep cerebellar nuclei. Recurrent collaterals terminate in close proximity to the Purkinje cell layer. Dense innervation by these axons is found around large interneurons (Lugaro and Golgi cells) and around the Purkinje cell pinceaux. No direct input of recurrent collaterals to Purkinje cell somata is evident in immunostained material.

A substantial number of Purkinje cell axons continue beyond the cerebellar nuclei to innervate nearby regions in the brain stem. The most prominently innervated extracerebellar target region is the dorsal part of the lateral vestibular nucleus, which is as heavily innervated by Purkinje axons as the deep cerebellar nuclei are. All the other major parts of the vestibular formation and some adjacent nuclei (including the parabrachial nuclei, the prepositus hypoglossal nucleus and the nucleus of the solitary tract) are innervated to various degrees by Purkinje cells. In these regions heavily innervated cells are interspersed with cells which receive only a moderate degree of innervation and with cells which apparently lack Purkinje cell inputs. Upon reaching the deep cerebellar nuclei, axons destined to extracerebellar targets deviate from the planes of dendritic arborization of their parent cells. They converge into tight bundles which follow an irregular course and intersect each other to reach their targets. Axons travelling in the same bundle often appear to terminate on the same cell.

At all target sites Purkinje axons end as varicose terminals which synapse primarily with the perikarya and proximal dendrites of target cells. On the surface of these cells Purkinje cell terminals are often tightly apposed to form a compact mosaic. Both the course of Purkinje cell axons and their pattern of innervation of target cells are consistent with the possibility that contacts between Purkinje cells and their target neurons in the deep cerebellar nuclei and the brain stem are established early in ontogenesis.

Purkinje cell-like cells positive for guanosine 3\ensuremath{'}:5\ensuremath{'}-phosphate-dependent protein kinase not located in the cerebellar cortex were found predominantly at the dorsal surface of the brain stem and, in particular, in the cortex of the dorsal cochlear nucleus. Only on exception were they found in the cerebellar medulla or in nearby noncortical regions of the brain stem. While some of these cells might be ectopies, the significance of Purkinje cell-like cells in the dorsal cochlear nucleus, a region strikingly similar in architecture to the cerebellar cortex, remains to be established.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {4},
  urldate = {2014-12-02},
  journal = {Neuroscience},
  author = {{De Camilli}, P. and Miller, P. E. and Levitt, P. and Walter, U. and Greengard, P.},
  month = apr,
  year = {1984},
  pages = {761--IN2}
}

@article{kolodziejczyk_technology_2015,
  title = {The {{Technology}} and {{Biology}} of {{Single-Cell RNA Sequencing}}},
  volume = {58},
  issn = {1097-2765},
  doi = {10.1016/j.molcel.2015.04.005},
  language = {English},
  timestamp = {2016-03-15T06:20:59Z},
  number = {4},
  urldate = {2016-03-15},
  journal = {Molecular Cell},
  author = {Kolodziejczyk, Aleksandra A. and Kim, Jong Kyoung and Svensson, Valentine and Marioni, John C. and Teichmann, Sarah A.},
  month = may,
  year = {2015},
  pages = {610--620},
  pmid = {26000846}
}

@article{de_wildt_antibody_2000,
  title = {Antibody arrays for high-throughput screening of antibody\textendash{}antigen interactions},
  volume = {18},
  copyright = {\textcopyright{} 2000 Nature Publishing Group},
  issn = {1087-0156},
  doi = {10.1038/79494},
  abstract = {We have developed a novel technique for high-throughput screening of recombinant antibodies, based on the creation of antibody arrays. Our method uses robotic picking and high-density gridding of bacteria containing antibody genes followed by filter-based enzyme-linked immunosorbent assay (ELISA) screening to identify clones that express binding antibody fragments. By eliminating the need for liquid handling, we can thereby screen up to 18,342 different antibody clones at a time and, because the clones are arrayed from master stocks, the same antibodies can be double spotted and screened simultaneously against 15 different antigens. We have used our technique in several different applications, including isolating antibodies against impure proteins and complex antigens, where several rounds of phage display often fail. Our results indicate that antibody arrays can be used to identify differentially expressed proteins.},
  language = {en},
  timestamp = {2016-02-12T21:27:52Z},
  number = {9},
  urldate = {2016-02-12},
  journal = {Nature Biotechnology},
  author = {{de Wildt}, Ruud M. T. and Mundy, Chris R. and Gorick, Barbara D. and Tomlinson, Ian M.},
  month = sep,
  year = {2000},
  pages = {989--994}
}

@article{mckinstry_effector_2014,
  title = {Effector {{CD4 T}}-cell transition to memory requires late cognate interactions that induce autocrine {{IL}}-2},
  volume = {5},
  issn = {2041-1723},
  doi = {10.1038/ncomms6377},
  abstract = {It is unclear how CD4 T-cell memory formation is regulated following pathogen challenge, and when critical mechanisms act to determine effector T-cell fate. Here, we report that following influenza infection most effectors require signals from major histocompatibility complex class II molecules and CD70 during a late window well after initial priming to become memory. During this timeframe, effector cells must produce IL-2 or be exposed to high levels of paracrine or exogenously added IL-2 to survive an otherwise rapid default contraction phase. Late IL-2 promotes survival through acute downregulation of apoptotic pathways in effector T cells and by permanently upregulating their IL-7 receptor expression, enabling IL-7 to sustain them as memory T cells. This new paradigm defines a late checkpoint during the effector phase at which cognate interactions direct CD4 T-cell memory generation.},
  language = {eng},
  timestamp = {2015-08-20T22:37:38Z},
  journal = {Nature Communications},
  author = {McKinstry, K. Kai and Strutt, Tara M. and Bautista, Bianca and Zhang, Wenliang and Kuang, Yi and Cooper, Andrea M. and Swain, Susan L.},
  year = {2014},
  pages = {5377},
  pmid = {25369785},
  pmcid = {PMC4223689}
}

@article{yoo_microrna-mediated_2011,
  title = {{{MicroRNA}}-mediated conversion of human fibroblasts to neurons},
  volume = {476},
  copyright = {\textcopyright{} 2011 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {0028-0836},
  doi = {10.1038/nature10323},
  abstract = {Neurogenic transcription factors and evolutionarily conserved signalling pathways have been found to be instrumental in the formation of neurons. However, the instructive role of microRNAs (miRNAs) in neurogenesis remains unexplored. We recently discovered that miR-9* and miR-124 instruct compositional changes of SWI/SNF-like BAF chromatin-remodelling complexes, a process important for neuronal differentiation and function. Nearing mitotic exit of neural progenitors, miR-9* and miR-124 repress the BAF53a subunit of the neural-progenitor (np)BAF chromatin-remodelling complex. After mitotic exit, BAF53a is replaced by BAF53b, and BAF45a by BAF45b and BAF45c, which are then incorporated into neuron-specific (n)BAF complexes essential for post-mitotic functions. Because miR-9/9* and miR-124 also control multiple genes regulating neuronal differentiation and function, we proposed that these miRNAs might contribute to neuronal fates. Here we show that expression of miR-9/9* and miR-124 (miR-9/9*-124) in human fibroblasts induces their conversion into neurons, a process facilitated by NEUROD2. Further addition of neurogenic transcription factors ASCL1 and MYT1L enhances the rate of conversion and the maturation of the converted neurons, whereas expression of these transcription factors alone without miR-9/9*-124 was ineffective. These studies indicate that the genetic circuitry involving miR-9/9*-124 can have an instructive role in neural fate determination.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {7359},
  urldate = {2014-11-19},
  journal = {Nature},
  author = {Yoo, Andrew S. and Sun, Alfred X. and Li, Li and Shcheglovitov, Aleksandr and Portmann, Thomas and Li, Yulong and Lee-Messer, Chris and Dolmetsch, Ricardo E. and Tsien, Richard W. and Crabtree, Gerald R.},
  month = aug,
  year = {2011},
  keywords = {Developmental biology,Htr2c,Medical research,neuroscience,Serotonergic,Stem cells},
  pages = {228--231},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/QNUFXIXD/nature10323.html:}
}

@article{wilhelm_mass-spectrometry-based_2014,
  title = {Mass-spectrometry-based draft of the human proteome},
  volume = {509},
  copyright = {\textcopyright{} 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
  issn = {0028-0836},
  doi = {10.1038/nature13319},
  abstract = {Proteomes are characterized by large protein-abundance differences, cell-type- and time-dependent expression patterns and post-translational modifications, all of which carry biological information that is not accessible by genomics or transcriptomics. Here we present a mass-spectrometry-based draft of the human proteome and a public, high-performance, in-memory database for real-time analysis of terabytes of big data, called ProteomicsDB. The information assembled from human tissues, cell lines and body fluids enabled estimation of the size of the protein-coding genome, and identified organ-specific proteins and a large number of translated lincRNAs (long intergenic non-coding RNAs). Analysis of messenger RNA and protein-expression profiles of human tissues revealed conserved control of protein abundance, and integration of drug-sensitivity data enabled the identification of proteins predicting resistance or sensitivity. The proteome profiles also hold considerable promise for analysing the composition and stoichiometry of protein complexes. ProteomicsDB thus enables navigation of proteomes, provides biological insight and fosters the development of proteomic technology.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {7502},
  urldate = {2014-12-24},
  journal = {Nature},
  author = {Wilhelm, Mathias and Schlegl, Judith and Hahne, Hannes and Gholami, Amin Moghaddas and Lieberenz, Marcus and Savitski, Mikhail M. and Ziegler, Emanuel and Butzmann, Lars and Gessulat, Siegfried and Marx, Harald and Mathieson, Toby and Lemeer, Simone and Schnatbaum, Karsten and Reimer, Ulf and Wenschuh, Holger and Mollenhauer, Martin and Slotta-Huspenina, Julia and Boese, Joos-Hendrik and Bantscheff, Marcus and Gerstmair, Anja and Faerber, Franz and Kuster, Bernhard},
  month = may,
  year = {2014},
  keywords = {Proteomics},
  pages = {582--587},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/4R3D76HM/nature13319.html:}
}

@article{nakano_complement_2015,
  title = {Complement receptor {{C5aR1}}/{{CD88}} and dipeptidyl peptidase-4/{{CD26}} define distinct hematopoietic lineages of dendritic cells},
  volume = {194},
  issn = {1550-6606},
  doi = {10.4049/jimmunol.1402195},
  abstract = {Differential display of the integrins CD103 and CD11b are widely used to distinguish two major dendritic cell (DC) subsets in nonlymphoid tissues. CD103(+) DCs arise from FLT3-dependent DC precursors (preDCs), whereas CD11b(hi) DCs can arise either from preDCs or FLT3-independent monocytes. Functional characterization of these two lineages of CD11b(hi) DCs has been hindered by the lack of a widely applicable method to distinguish between them. We performed gene expression analysis of fractionated lung DCs from C57BL/6 mice and found that monocyte-derived DCs (moDCs), including CD11b(hi)Ly-6C(lo) tissue-resident and CD11b(hi)Ly-6C(hi) inflammatory moDCs, express the complement 5a receptor 1/CD88, whereas preDC-derived conventional DCs (cDCs), including CD103(+) and CD11b(hi) cDCs, express dipeptidyl peptidase-4/CD26. Flow cytometric analysis of multiple organs, including the kidney, liver, lung, lymph nodes, small intestine, and spleen, confirmed that reciprocal display of CD88 and CD26 can reliably distinguish FLT3-independent moDCs from FLT3-dependent cDCs in C57BL/6 mice. Similar results were obtained when DCs from BALB/c mice were analyzed. Using this novel approach to study DCs in mediastinal lymph nodes, we observed that most blood-derived lymph node-resident DCs, as well as tissue-derived migratory DCs, are cDCs. Furthermore, cDCs, but not moDCs, stimulated naive T cell proliferation. We anticipate that the use of Abs against CD88 and CD26 to distinguish moDCs and cDCs in multiple organs and mouse strains will facilitate studies aimed at assigning specific functions to distinct DC lineages in immune responses.},
  language = {eng},
  timestamp = {2015-08-21T01:21:47Z},
  number = {8},
  journal = {Journal of Immunology (Baltimore, Md.: 1950)},
  author = {Nakano, Hideki and Moran, Timothy P. and Nakano, Keiko and Gerrish, Kevin E. and Bortner, Carl D. and Cook, Donald N.},
  month = apr,
  year = {2015},
  keywords = {Animals,Antigens; CD,Antigens; CD11b,Cell Proliferation,Dendritic Cells,Dipeptidyl Peptidase 4,fms-Like Tyrosine Kinase 3,Gene Expression Regulation,Integrin alpha Chains,Mice,Mice; Inbred BALB C,Mice; Knockout,Monocytes,Organ Specificity,Receptor; Anaphylatoxin C5a},
  pages = {3808--3819},
  pmid = {25769922},
  pmcid = {PMC4390500}
}

@article{zamanian_genomic_2012,
  title = {Genomic {{Analysis}} of {{Reactive Astrogliosis}}},
  volume = {32},
  issn = {0270-6474, 1529-2401},
  doi = {10.1523/JNEUROSCI.6221-11.2012},
  abstract = {Reactive astrogliosis is characterized by a profound change in astrocyte phenotype in response to all CNS injuries and diseases. To better understand the reactive astrocyte state, we used Affymetrix GeneChip arrays to profile gene expression in populations of reactive astrocytes isolated at various time points after induction using two mouse injury models, ischemic stroke and neuroinflammation. We find reactive gliosis consists of a rapid, but quickly attenuated, induction of gene expression after insult and identify induced Lcn2 and Serpina3n as strong markers of reactive astrocytes. Strikingly, reactive astrocyte phenotype strongly depended on the type of inducing injury. Although there is a core set of genes that is upregulated in reactive astrocytes from both injury models, at least 50\% of the altered gene expression is specific to a given injury type. Reactive astrocytes in ischemia exhibited a molecular phenotype that suggests that they may be beneficial or protective, whereas reactive astrocytes induced by LPS exhibited a phenotype that suggests that they may be detrimental. These findings demonstrate that, despite well established commonalities, astrocyte reactive gliosis is a highly heterogeneous state in which astrocyte activities are altered to respond to the specific injury. This raises the question of how many subtypes of reactive astrocytes exist. Our findings provide transcriptome databases for two subtypes of reactive astrocytes that will be highly useful in generating new and testable hypotheses of their function, as well as for providing new markers to detect different types of reactive astrocytes in human neurological diseases.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {18},
  urldate = {2014-10-21},
  journal = {The Journal of Neuroscience},
  author = {Zamanian, Jennifer L. and Xu, Lijun and Foo, Lynette C. and Nouri, Navid and Zhou, Lu and Giffard, Rona G. and Barres, Ben A.},
  month = feb,
  year = {2012},
  pages = {6391--6410},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/RZRA3VMK/6391.html:},
  pmid = {22553043}
}

@article{iwamoto_molecular_2004,
  title = {Molecular characterization of bipolar disorder by comparing gene expression profiles of postmortem brains of major mental disorders},
  volume = {9},
  copyright = {\textcopyright{} 2004 Nature Publishing Group},
  issn = {1359-4184},
  doi = {10.1038/sj.mp.4001437},
  abstract = {We performed the oligonucleotide microarray analysis in bipolar disorder, major depression, schizophrenia, and control subjects using postmortem prefrontal cortices provided by the Stanley Foundation Brain Collection. By comparing the gene expression profiles of similar but distinctive mental disorders, we explored the uniqueness of bipolar disorder and its similarity to other mental disorders at the molecular level. Notably, most of the altered gene expressions in each disease were not shared by one another, suggesting the molecular distinctiveness of these mental disorders. We found a tendency of downregulation of the genes encoding receptor, channels or transporters, and upregulation of the genes encoding stress response proteins or molecular chaperons in bipolar disorder. Altered expressions in bipolar disorder shared by other mental disorders mainly consisted of upregulation of the genes encoding proteins for transcription or translation. The genes identified in this study would be useful for the understanding of the pathophysiology of bipolar disorder, as well as the common pathophysiological background in major mental disorders at the molecular level. In addition, we found the altered expression of LIM and HSPF1 both in the brains and lymphoblastoid cells in bipolar disorder. These genes may have pathophysiological importance and would be novel candidate genes for bipolar disorder.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {4},
  urldate = {2015-08-06},
  journal = {Molecular Psychiatry},
  author = {Iwamoto, K. and Kakiuchi, C. and Bundo, M. and Ikeda, K. and Kato, T.},
  month = jan,
  year = {2004},
  keywords = {depression,lymphoblastoid,microarray,Schizophrenia},
  pages = {406--416}
}

@article{liang_gene_2007,
  title = {Gene expression profiles in anatomically and functionally distinct regions of the normal aged human brain},
  volume = {28},
  copyright = {Copyright \textcopyright{} 2007 the American Physiological Society},
  issn = {1094-8341, 1531-2267},
  doi = {10.1152/physiolgenomics.00208.2006},
  abstract = {In this article, we have characterized and compared gene expression profiles from laser capture microdissected neurons in six functionally and anatomically distinct regions from clinically and histopathologically normal aged human brains. These regions, which are also known to be differentially vulnerable to the histopathological and metabolic features of Alzheimer's disease (AD), include the entorhinal cortex and hippocampus (limbic and paralimbic areas vulnerable to early neurofibrillary tangle pathology in AD), posterior cingulate cortex (a paralimbic area vulnerable to early metabolic abnormalities in AD), temporal and prefrontal cortex (unimodal and heteromodal sensory association areas vulnerable to early neuritic plaque pathology in AD), and primary visual cortex (a primary sensory area relatively spared in early AD). These neuronal profiles will provide valuable reference information for future studies of the brain, in normal aging, AD and other neurological and psychiatric disorders.},
  language = {en},
  timestamp = {2015-08-13T22:18:44Z},
  number = {3},
  urldate = {2014-11-28},
  journal = {Physiological Genomics},
  author = {Liang, Winnie S. and Dunckley, Travis and Beach, Thomas G. and Grover, Andrew and Mastroeni, Diego and Walker, Douglas G. and Caselli, Richard J. and Kukull, Walter A. and McKeel, Daniel and Morris, John C. and Hulette, Christine and Schmechel, Donald and Alexander, Gene E. and Reiman, Eric M. and Rogers, Joseph and Stephan, Dietrich A.},
  month = mar,
  year = {2007},
  note = {In this article, we have characterized and compared gene expression profiles from laser capture microdissected neurons in six functionally and anatomically distinct regions from clinically and histopathologically normal aged human brains. These regions, which are also known to be differentially vulnerable to the histopathological and metabolic features of Alzheimer's disease (AD), include the entorhinal cortex and hippocampus (limbic and paralimbic areas vulnerable to early neurofibrillary tangle pathology in AD), posterior cingulate cortex (a paralimbic area vulnerable to early metabolic abnormalities in AD), temporal and prefrontal cortex (unimodal and heteromodal sensory association areas vulnerable to early neuritic plaque pathology in AD), and primary visual cortex (a primary sensory area relatively spared in early AD). These neuronal profiles will provide valuable reference information for future studies of the brain, in normal aging, AD and other neurological and psychiatric disorders.},
  pages = {311--322},
  file = {Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/8JKRRAT2/311.html:},
  pmid = {17077275}
}

@article{kondo_focal_2014,
  title = {Focal {{Transplantation}} of {{Human iPSC-Derived Glial-Rich Neural Progenitors Improves Lifespan}} of {{ALS Mice}}},
  volume = {3},
  issn = {2213-6711},
  doi = {10.1016/j.stemcr.2014.05.017},
  abstract = {Summary
Transplantation of glial-rich neural progenitors has been demonstrated to attenuate motor neuron degeneration and disease progression in rodent models of mutant superoxide dismutase 1 (SOD1)-mediated amyotrophic lateral sclerosis (ALS). However, translation of these results into a clinical setting requires a renewable human cell source. Here, we derived glial-rich neural progenitors from human iPSCs and transplanted them into the lumbar spinal cord of ALS mouse models. The transplanted cells differentiated into astrocytes, and the treated mouse group showed prolonged lifespan. Our data suggest a potential therapeutic mechanism via activation of AKT signal. The results demonstrated the efficacy of cell therapy for ALS by the use of human iPSCs as cell source.},
  timestamp = {2015-08-13T22:18:44Z},
  number = {2},
  urldate = {2014-11-20},
  journal = {Stem Cell Reports},
  author = {Kondo, Takayuki and Funayama, Misato and Tsukita, Kayoko and Hotta, Akitsu and Yasuda, Akimasa and Nori, Satoshi and Kaneko, Shinjiro and Nakamura, Masaya and Takahashi, Ryosuke and Okano, Hideyuki and Yamanaka, Shinya and Inoue, Haruhisa},
  month = aug,
  year = {2014},
  keywords = {Aldh1a1},
  pages = {242--249},
  file = {ScienceDirect Snapshot:/home/omancarci/.zotero/zotero/465193y4.default/zotero/storage/JXJQSKHT/S2213671114001581.html:}
}

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1 ExplicitGroup:Substantia nigra male vs female\;0\;aumann_environment
al_2013\;mcarthur_size_2006\;bourque_male/female_2011\;;
1 ExplicitGroup:Layer specific expression\;0\;petrides_dorsolateral_19
99\;fauser_disorganization_2013\;;
1 ExplicitGroup:Cox6a2\;0\;tong_gene_2011\;wang_functional_2012\;fornu
skova_novel_2010\;quintens_mice_2013\;adler-wailes_effects_2008\;;
1 ExplicitGroup:parkinson's\;0\;lesnick_genomic_2007\;gillies_sex_2014
\;papapetropoulos_multiregional_2006\;costa_effects_2014\;moran_whole_
2006\;duke_medial_2007\;simunovic_gene_2009\;;
1 ExplicitGroup:Microglia\;0\;satoh_tmem119_2016\;;
}