Transcriptomic analysis of purified human cortical microglia reveals age-associated changes

In the paper

“IFI16 is also involved in overcoming inhibitor of differentiation proteins (IDs) blocking of terminal cell differentiation 45 ,”

What the sources say

• Disputed

  Section 3.2 attributes the ability to overcome Id-protein inhibition of differentiation to p204, not IFI16. The Summary and perspectives identifies IFI16 as a human protein structurally similar to p204, but does not assign p204’s Id-blocking activity to IFI16. The indexed passages provide no page numbers. (LLM, conf=0.88)

  Checked by a reasoning model — may be wrong.

  cites [45] Luan, Y., Lengyel, P. & Liu, C.-J. p204, a p200 family protein, as a multifunctional regulator of cell proliferation and differentiation. Cytokine Growth Factor Rev. 19, 357–369 (2008). sourceExperimental — accuracy not yet measured

In the paper

“While CIITA expression is restricted to antigen-presenting cells, NLRC5 is constitutively expressed in various tissues, most highly in cells from the hematopoietic lineage (CD4 + T cells, CD8 + T cells, CD19 + B cells, natural killer cells and natural killer T cells).”

What the sources say

• ?Could not verify

  The Results describe experiments in Jurkat T cells and an epithelial cell line, but do not compare constitutive NLRC5 expression across tissues or hematopoietic cell types. Searches for CD19, hematopoietic expression, and tissue distribution found no passage establishing the claimed ranking or the listed cell types. (LLM, conf=0.76)

  cites [39] Meissner, T.B. et al. NLR family member NLRC5 is a transcriptional regulator of MHC class I genes. Proc. Natl. Acad. Sci. USA 107, 13794–13799 (2010). sourceExperimental — accuracy not yet measured

In the paper

“Overall, we observed an extensive overlap in gene expression between these data sets: the median ∆ percentile was 10.1, indicating most genes were similarly expressed in both data sets ( Fig. 2b ).”

What the sources say

• ?Could not verify

  The Results section on acutely purified human brain cells reports microglial gene-expression markers, but not a comparison between a human microglial core and a published CD45+ population. The reported gene-expression overlap in the Results section on human and mouse astrocytes concerns different cell populations. Searches for CD45+ microglia and a median Δ percentile of 10.1 found no passage addressing the claim. (LLM, conf=0.73)

  cites [15] Zhang, Y. et al. Purification and characterization of progenitor and mature human astrocytes reveals transcriptional and functional differences with mouse. Neuron 89, 37–53 (2016). sourceExperimental — accuracy not yet measured

In the paper

“Little is known about microglial gender differences, but a few studies have identified a gender-specific role for microglia in the rat brain 49 .”

What the sources say

• Supported

  The “Sexual Dimorphism in Stroke and Poststroke Inflammation” section reports sex differences in microglial activation after stroke and discusses rat ischemia models. The “Sexual Dimorphism in Response to Antiinflammatory Treatments” section says the few studies in this area point to large male–female differences; the References list a study of microglial activation in male but not female rats. The evidence concerns ischemia and its treatment, rather than every role of microglia in the rat brain. (LLM, conf=0.88)

  cites [49] Chen, Y., Won, S.J., Xu, Y. & Swanson, R.A. Targeting microglial activation in stroke therapy: pharmacological tools and gender effects. Curr. Med. Chem. 21, 2146–2155 (2014). source

In the paper

“recent reports on the induction of human pluripotent stem cell-derived microglia-like cells demonstrated high levels of this transcription factor in such cells 40 .”

What the sources say

• Supported

  The Results section (‘pMGLs resemble primary human microglia, and differ from peripheral macrophages’) states that the derived microglia-like cells display high IRF8 expression. The Introduction identifies these cells as derived from human ES and iPS cells. (LLM, conf=0.94)

  cites [40] Muffat, J. et al. Efficient derivation of microglia-like cells from human pluripotent stem cells. Nat. Med. 22, 1358–1367 (2016). source

In the paper

“SIGLECs regulate the effects of activation, phagocytosis and inflammasome formation via their immunoreceptor tyrosine-based inhibition motif (ITIM) 37 .”

What the sources say

• Partly supported

  The introductory passage labelled Abstract says most Siglecs contain ITIMs and signal negatively, supporting a role in regulating activation. The 'Interactions of Siglecs with bacteria' section describes macrophage phagocytosis promoted by sialoadhesin, but explicitly says that receptor lacks intrinsic signaling motifs. No passage found supports regulation of inflammasome formation via ITIMs. (LLM, conf=0.87)

  cites [37] Macauley, M.S., Crocker, P.R. & Paulson, J.C. Siglec-mediated regulation of immune cell function in disease. Nat. Rev. Immunol. 14, 653–666 (2014). sourceExperimental — accuracy not yet measured

In the paper

“A quality check of aligned data was done with RNA-SEQC 55 and showed high quality alignment and data.”

What the sources say

• Supported

  The Abstract identifies RNA-SeQC as a program that provides data-quality measures, including alignment rates. The Metrics section says it accepts aligned BAM files and reports quality-control metrics. The statement that the citing authors' data were high quality is their own result, not a finding attributed to this source. (LLM, conf=0.91)

  cites [55] DeLuca, D.S. et al. RNA-SeQC: RNA-seq metrics for quality control and process optimization. Bioinformatics 28, 1530–1532 (2012). source

In the paper

“These receptors and their downstream signaling are implicated in chemotaxis and are part of the microglial sensome 4 .”

What the sources say

• Partly supported

  The Results section (Identification of the microglial Sensome by DRS; page unavailable) defines the sensome to include receptors and describes DAP12 as an adaptor that regulates signaling via TREM2. The Results section (Microglia vs. Macrophages; page unavailable) also identifies chemokine receptors among sensome genes. The copy does not link these receptors or their downstream signaling to chemotaxis. (LLM, conf=0.83)

  cites [4] Hickman, S.E. et al. The microglial sensome revealed by direct RNA sequencing. Nat. Neurosci. 16, 1896–1905 (2013). sourceExperimental — accuracy not yet measured

In the paper

“P2RY12, an established microglial marker 3,4 ,”

What the sources say

• Supported

  The Results section, “Identification of unique microglial surface molecules,” identifies P2ry12 as a unique microglial gene and reports that anti-P2ry12 stained resident microglia but not recruited monocytes, astrocytes, or neurons. This supports its use as a microglial marker. (LLM, conf=0.93)

  cites [3] Butovsky, O. et al. Identification of a unique TGF-β-dependent molecular and functional signature in microglia. Nat. Neurosci. 17, 131–143 (2014). source
• Supported

  The Results section on dual fluorescent in situ hybridization reports that P2ry12 mRNA co-localized with the microglial marker CD11b in young mouse brain: 98% of CD11b-expressing cells also expressed P2ry12, while CD11b-negative cells did not. The paper also identifies P2ry12 as a microglia-enriched sensome gene, supporting its use as a microglial marker. (LLM, conf=0.93)

  cites [4] Hickman, S.E. et al. The microglial sensome revealed by direct RNA sequencing. Nat. Neurosci. 16, 1896–1905 (2013). source

In the paper

“While CIITA expression is restricted to antigen-presenting cells, NLRC5 is constitutively expressed in various tissues, most highly in cells from the hematopoietic lineage (CD4 + T cells, CD8 + T cells, CD19 + B cells, natural killer cells and natural killer T cells).”

What the sources say

• Partly supported

  The paper’s opening section says CIITA expression is generally restricted to lymphocytes and professional antigen-presenting cells. The claim omits lymphocytes as a separate group and makes the restriction to antigen-presenting cells more absolute than the source does. (LLM, conf=0.88)

  cites [39] Meissner, T.B. et al. NLR family member NLRC5 is a transcriptional regulator of MHC class I genes. Proc. Natl. Acad. Sci. USA 107, 13794–13799 (2010). sourceExperimental — accuracy not yet measured

In the paper

“This is supported by observations in mice, where host microbiota control the maturation and function of microglia 33 .”

What the sources say

• Supported

  In “Defective microglia can be restored by a complex microbiota,” the paper states that microglia maturation and function are tightly controlled by the microbiota. The Introduction identifies germ-free and antibiotic-treated mice as the relevant observations, matching the citing sentence’s qualifier. (LLM, conf=0.95)

  cites [33] Erny, D. et al. Host microbiota constantly control maturation and function of microglia in the CNS. Nat. Neurosci. 18, 965–977 (2015). source

In the paper

“NLRC5 expression levels are intermediate in monocytic CD14 + cells and CD11B + splenic myeloid cells.”

What the sources say

• ?Could not verify

  The Results describe NLRC5 experiments in Jurkat T cells, HeLa cells, and HEK293T cells, but do not report its relative expression in CD14+ monocytes or CD11B+ splenic myeloid cells. Searches for CD14, CD11B, and intermediate expression in those cell types found no passage addressing the claim; page numbers were unavailable in our copy. (LLM, conf=0.72)

  cites [39] Meissner, T.B. et al. NLR family member NLRC5 is a transcriptional regulator of MHC class I genes. Proc. Natl. Acad. Sci. USA 107, 13794–13799 (2010). sourceExperimental — accuracy not yet measured

In the paper

“PCA of our human microglial and published monocyte and macrophage data 30 indicated that these three data sets segregated and that microglia were the most distinct ( Supplementary Figure 1a ).”

What the sources say

• Supported

  The citation identifies the published monocyte and macrophage data used in the citing authors’ PCA, not the PCA result itself. The source paper’s Methodology (Genome-wide epigenetic profiling) describes profiles for human monocytes and macrophages and gives their data accession, GSE58310. (LLM, conf=0.92)

  cites [30] Saeed, S. et al. Epigenetic programming of monocyte-to-macrophage differentiation and trained innate immunity. Science 345, 1251086 (2014). source

In the paper

“An extensive overlap was observed between human and these three independent mouse microglial gene expression data sets ( Fig. 2c ). The median ∆ percentiles were 14.3, 20.4 and 9.3 for our own expression data set, that of Grabert et al. 23 and that of Matcovich-Natan et al. 24 , respectively.”

What the sources say

• Supported

  The citation identifies Grabert et al. as one of the mouse microglial gene-expression datasets used in the citing authors’ comparison. Grabert et al.’s Methods (Transcriptional profiling using gene expression microarrays; page unavailable) describe profiling RNA on whole-mouse-genome arrays. The overlap and median Δ percentiles are results reported by the citing authors, not attributed to Grabert et al. as findings of that paper. (LLM, conf=0.91)

  cites [23] Grabert, K. et al. Microglial brain region-dependent diversity and selective regional sensitivities to aging. Nat. Neurosci. 19, 504–516 (2016). source
• ?Not checked — no full text of the sourcecites [24] Matcovitch-Natan, O. et al. Microglia development follows a stepwise program to regulate brain homeostasis. Science 353, aad8670 (2016). source

In the paper

“IFI16 (p204) is associated with viral infection and the response to cytosolic double-stranded DNA 44 .”

What the sources say

• Supported

  The ‘Role of PYHIN proteins in DNA sensing’ section identifies IFI16 and its apparent mouse functional ortholog p204 as DNA sensors. It reports that p204 knockdown inhibited responses to DNA and HSV-1 infection, and that IFI16 bound viral double-stranded DNA used to study cytosolic sensing. (LLM, conf=0.94)

  cites [44] Gürtler, C. & Bowie, A.G. Innate immune detection of microbial nucleic acids. Trends Microbiol. 21, 413–420 (2013). source

In the paper

“CD33 (SIGLEC3), a known microglial marker, is associated with the accumulation of amyloidβ plaques in mouse Alzheimer's disease models due to the diminished phagocytic capacity of microglial cells upregulating this gene 38 .”

What the sources say

• Partly supported

  The Results section, “CD33 Activity Promotes Amyloid Beta Pathology In Vivo” (page not provided), reports reduced plaque burden in APP/PS1 mice lacking CD33 and suggests that CD33-deficient microglia have greater Aβ clearance capacity. The paper also shows that higher CD33 levels impair microglial Aβ uptake in culture. It reports increased microglial CD33 expression in human AD brains, but does not show that microglia upregulate CD33 in the mouse models. (LLM, conf=0.85)

  cites [38] Griciuc, A. et al. Alzheimer's disease risk gene CD33 inhibits microglial uptake of amyloid beta. Neuron 78, 631–643 (2013). sourceExperimental — accuracy not yet measured

In the paper

“In monocytes, heterodimers between CXCR2 and CD74 or between CXCR4 and CD74 induce PI3K-AKT signaling and p53 inhibition, leading to increased survival, proliferation and apoptosis evasion 22 .”

What the sources say

• Partly supported

  The Results and Discussion (page not provided) support MIF-mediated p53 inhibition and reduced apoptosis in mouse macrophages. They describe a Cox-2/PGE2 mechanism, not CXCR2–CD74 or CXCR4–CD74 heterodimers or PI3K–AKT signaling; they also do not establish increased monocyte proliferation. (LLM, conf=0.88)

  cites [22] Mitchell, R.A. et al. Macrophage migration inhibitory factor (MIF) sustains macrophage proinflammatory function by inhibiting p53: regulatory role in the innate immune response. Proc. Natl. Acad. Sci. USA 99, 345–350 (2002). sourceExperimental — accuracy not yet measured

In the paper

“It regulates cell proliferation and transcription through different interactions with p53 and STAT3.”

What the sources say

• ?Could not verify

  The section “Role of PYHIN proteins in DNA sensing” (page unavailable) describes IFI16 as a DNA sensor involved in immune signaling and gene induction. Neither that section nor the additional passages retrieved for p53 and STAT3 address IFI16 regulating cell proliferation or transcription through interactions with those proteins. (LLM, conf=0.72)

  cites [44] Gürtler, C. & Bowie, A.G. Innate immune detection of microbial nucleic acids. Trends Microbiol. 21, 413–420 (2013). sourceExperimental — accuracy not yet measured

In the paper

“For instance, talin-1 (TLN1), a protein involved in actin remodeling and cell motility; profilin (PFN1), a protein directly involved in actin binding and polymerization; and VASP, a protein involved in actin filaments elongation, are less abundant in microglia isolated from older donors 47 .”

What the sources say

• ?Could not verify

  The Methods (Cells; page unavailable) describe microglia cultured from 1- to 2-day-old rat pups, not older donors. The Results identify talin in microglial podosomes, but the passages found when searching for PFN1, VASP, and age-related abundance do not report a comparison between younger and older donors. (LLM, conf=0.76)

  cites [47] Vincent, C., Siddiqui, T.A. & Schlichter, L.C. Podosomes in migrating microglia: components and matrix degradation. J. Neuroinflammation 9, 190 (2012). sourceExperimental — accuracy not yet measured

In the paper

“Chromatin immunoprecipitation and sequencing analysis previously indicated that TAL1 forms a complex with RUNX1 and LYL1 (ref. 42),”

What the sources say

• Partly supported

  The Results report ChIP-seq evidence that SCL/TAL1, LYL1, and RUNX1 bind in close proximity, suggesting cooperative binding. They also report coimmunoprecipitation evidence for a SCL–RUNX1 protein complex, but do not establish that LYL1 is part of that same complex. (LLM, conf=0.86)

  cites [42] Wilson, N.K. et al. Combinatorial transcriptional control in blood stem/progenitor cells: genome-wide analysis of ten major transcriptional regulators. Cell Stem Cell 7, 532–544 (2010). sourceExperimental — accuracy not yet measured

In the paper

“Sex differences in microglial function in the developing brain are associated with neurodevelopmental and psychiatric conditions 50 .”

What the sources say

• Supported

  The Abstract says sex differences in microglia and neuroimmune signaling may contribute to sex differences in the incidence of neuropsychiatric and neurological disorders. In “Sex Differences in Neurodevelopmental Disorders” (page unavailable), the authors hypothesize that microglia and inflammatory molecules involved in normal brain sexual differentiation contribute to male vulnerability to disorders including autism. (LLM, conf=0.90)

  cites [50] Lenz, K.M. & McCarthy, M.M. A starring role for microglia in brain sex differences. Neuroscientist 21, 306–321 (2015). source

In the paper

“NLRC5 and CIITA are the respective master regulators of MHC class I and II gene expression 39 .”

What the sources say

• Partly supported

  The Discussion calls CIITA a master regulator of MHC class II expression. It finds NLRC5 necessary and sufficient for MHC class I induction in the experiments reported, but says only that NLRC5 may play a dominant role and may act as CIITA’s counterpart; its status as a master regulator is therefore overstated. Page numbers are not provided in the supplied passages. (LLM, conf=0.86)

  cites [39] Meissner, T.B. et al. NLR family member NLRC5 is a transcriptional regulator of MHC class I genes. Proc. Natl. Acad. Sci. USA 107, 13794–13799 (2010). sourceExperimental — accuracy not yet measured

In the paper

“Notably, microglial process motility directed toward site of damage was significantly impaired in mice with A β plaques 48 .”

What the sources say

• Supported

  The Results section, “Directed Microglial Process Motility Towards Acute Tissue Lesion is Impaired in Transgenic AD Mice,” reports a markedly reduced response to laser-induced injury in Aβ plaque-bearing APPPS1 mice compared with controls. Figure 1 reports the lesion-directed movement difference as significant (p<0.05). (LLM, conf=0.94)

  cites [48] Krabbe, G. et al. Functional impairment of microglia coincides with Beta-amyloid deposition in mice with Alzheimer-like pathology. PLoS One 8, e60921 (2013). source

In the paper

“To minimize the reported effect of brain region on microglial gene expression 6,23,24 , only cortical microglia were included in our comparisons.”

What the sources say

• ?Could not verify

  The citation is attached to the reported effect of brain region on microglial gene expression, not to the citing authors’ decision to include only cortical microglia. The Introduction and ‘Creation of an RNA-Seq transcriptome library’ describe profiling cells from mouse cortex, but do not report a comparison of microglial expression across brain regions. Searches for regional differences in microglial expression found no passage addressing that effect. (LLM, conf=0.76)

  cites [6] Zhang, Y. et al. An RNA-sequencing transcriptome and splicing database of glia, neurons, and vascular cells of the cerebral cortex. J. Neurosci. 34, 11929–11947 (2014). sourceExperimental — accuracy not yet measured
• Supported

  The Results section, “The microglial transcriptome is regionally heterogeneous” (page not supplied), reports that expression of 2,527 genes differed by brain region. This supports the attributed regional effect; including only cortical microglia was the citing authors’ own comparison choice, not a choice attributed to this source. (LLM, conf=0.93)

  cites [23] Grabert, K. et al. Microglial brain region-dependent diversity and selective regional sensitivities to aging. Nat. Neurosci. 19, 504–516 (2016). source
• ?Not checked — no full text of the sourcecites [24] Matcovitch-Natan, O. et al. Microglia development follows a stepwise program to regulate brain homeostasis. Science 353, aad8670 (2016). source

In the paper

“Unwanted or hidden sources of variation, such as the use of different library preps (Illumina and Takara) and different batches, were removed using the sva package 60 .”

What the sources say

• Supported

  The Introduction identifies sva as a package for removing batch effects and other unwanted variation in high-throughput experiments. Section 2.2 describes its method for adjusting for hidden variation. The citation identifies the tool used; the library preparations and batches describe the citing study, not a finding attributed to this source. (LLM, conf=0.91)

  cites [60] Leek, J.T., Johnson, W.E., Parker, H.S., Jaffe, A.E. & Storey, J.D. The sva package for removing batch effects and other unwanted variation in high-throughput experiments. Bioinformatics 28, 882–883 (2012). source

In the paper

“Genes with higher expression during aging included integrin modulators DOCK1 and DOCK5 , receptors CXCR4 , CD163 and IGF2R , growth factor VEGFA and transcription factor RUNX3 .”

In the paper

“Noteworthy genes with reduced expression during aging included many actin cytoskeleton-associated genes such as TLN1 , PFN1 , EVL , ARPC1A , ARPC1B , CORO1A , CAP1 , CTNNA2 and VASP , sensome cell surface receptors P2RY12 , IL6R and TLR10 , and cell adhesion molecules and cell surface receptors ICAM3 , ROBO2 , SEMA3C and SEMA7A .”

In the paper

“Of the small number of genes that were shared between human and microglia during aging, about half displayed opposite directionalities in expression during aging-for example, upregulated in mouse and downregulated in human or vice versa.”

In the paper

“while genes involved in cell cycle are also highly expressed.”

In the paper

“Notably, several human microglial genes were much less abundantly expressed in mouse microglia. Examples of human microgliaenriched genes are CD58, an adhesion molecule with a central role in the clustering of mature dendritic cells and T lymphocyte activation 25 .”

In the paper

“as exemplified by the downregulation of ID4 in microglia.”

In the paper

“Microglial and cortical samples segregated cleanly and were highly similar within each tissue group, indicating that microglial expression profiles are very different from unsorted parietal cortex expression data ( Fig. 1b ).”

In the paper

“Notably, although human microglia seem to possess a highly activated pathway for proliferation (the aforementioned CXCR-CD74 axis),”

In the paper

“Cells with highly ramified microglial morphology were detected with the indicated antibodies. Using double immunofluorescence staining, we observed extensive colocalization with established microglial markers IBA1 and HLA-DR.”

In the paper

“Considerable overlap between human and mouse microglial gene expression was observed, but noteworthy dissimilarities were also present.”

In the paper

“Written informed consent for research purposes was obtained and ethics committees from the School of Medicine of the University of São Paulo, Brazil, the Netherlands Brain Bank and the University Medical Center Groningen, the Netherlands approved the procedure.”

In the paper

“In adults, TAL1 is expressed in hematopoietic cells but also in specific regions of the midbrain, hindbrain and spinal cord 41 .”

What the sources say

• ?Not checked — no full text of the sourcecites [41] van Eekelen, J.A. et al. Expression pattern of the stem cell leukaemia gene in the CNS of the embryonic and adult mouse. Neuroscience 122, 421–436 (2003). source

In the paper

“FAST-QC (http://www.bioinformatics.babraham.ac.uk/projects/fastqc/) 52 quality checks were done to determine high quality base pairs,”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [52] Babraham Bioinformatics. FastQC: a quality control tool for high throughput sequence data http://www.bioinformatics.babraham.ac.uk/projects/fastqc/ (accessed 5 February 2017).

In the paper

“These data confirm that human microglia are immunocompetent and phagocytic cells of the CNS that express a wide range of immune receptors and ligands, equipped to respond to a wide variety of pathogen- and damage-associated molecules.”

In the paper

“Cells were sorted on the basis of CD11b high CD45 int expression and negative staining for DAPI or the LIVE/DEAD Fixable Red Dead Cell stain (L23102, ThermoFisher Scientific) and collected in RNAlater (Qiagen, Germany).”

In the paper

“The overlap in genes differentially expressed during aging between human and mouse is very limited, suggesting that the microglia of physiologically aged mice do not recapitulate the effect of aging on human microglia.”

In the paper

“The leptomeninges were removed to avoid potential contamination by meningeal macrophages.”

In the paper

“RUNX1 activates the transcription of SPI-1 (ref. 43), a bona fide microglial transcription factor.”

What the sources say

• ?Not checked — no full text of the sourcecites [43] Huang, G. et al. PU.1 is a major downstream target of AML1 (RUNX1) in adult mouse hematopoiesis. Nat. Genet. 40, 51–60 (2008). source

In the paper

“RNA quality was checked with the Experion RNA HighSens Analysis Kit (Bio-Rad, USA) and RNA Screen Tape (Agilent Technologies, USA).”

In the paper

“IRF8 is necessary for microglial genesis, along with SPI-1 (ref. 2),”

What the sources say

• ?Not checked — no full text of the sourcecites [2] Kierdorf, K. et al. Microglia emerge from erythromyeloid precursors via Pu.1- and Irf8-dependent pathways. Nat. Neurosci. 16, 273–280 (2013). source

In the paper

“These data corroborate the notion that human microglia are potent antigen-presenting cells and are able to interact with CD4 and CD8 T-helper cell subsets.”

In the paper

“Integrin-SYK signaling is also responsible for negatively regulating Toll-like receptor (TLR) signaling and the NFκ B pathway by promoting the degradation of MYD88 (ref. 21).”

What the sources say

• ?Not checked — no full text of the sourcecites [21] Kondo, T., Kawai, T. & Akira, S. Dissecting negative regulation of Toll-like receptor signaling. Trends Immunol. 33, 449–458 (2012). source

In the paper

“No statistical methods were used to predetermine samples sizes; as many samples as possible were collected in the available time period.”

In the paper

“Two of these transcription factors are essential for microglial ontogeny: SPI-1 (PU.1) and IRF8 (ref. 2).”

What the sources say

• ?Not checked — no full text of the sourcecites [2] Kierdorf, K. et al. Microglia emerge from erythromyeloid precursors via Pu.1- and Irf8-dependent pathways. Nat. Neurosci. 16, 273–280 (2013). source

In the paper

“IFI16 may support the relative microglial quiescence that is observed under normal conditions.”

In the paper

“Our finding that human microglia express many SIGLECs highlights their importance and the specialization of microglia for the maintenance of a homeostatic microenvironment.”

In the paper

“The expression values were adjusted according to the surrogate variables identified by sva using the function removeBatchEffect from the limma package.”

In the paper

“Per sample, on average 17.6 million uniquely mapped reads were generated, ranging between 6 and 61.1 million.”

In the paper

“The second comparison was performed as a multivariate linear model that included gender as a binary variable, while age, PMD and the surrogate variables calculated with sva were used as quantitative variables.”

In the paper

“Samples were not randomized; all collected samples were RNA-sequenced or used for protein sample preparation.”

In the paper

“Data collection and analysis were not performed blind to the conditions of the experiments and no data points were excluded from the analyses.”

In the paper

“Vimentin was used as in internal standard for membrane normalization.”

In the paper

“The distribution of the RNA-seq data was as expected for sequencing data; no particular testing was performed.”