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DNA methylation of gene promoter regions represses transcription and is a mechanism via which environmental risk factors could affect cells during development in individuals at risk for schizophrenia. We investigated DNA methylation in patient-derived cells that might shed light on early development in schizophrenia. Induced pluripotent stem cells (iPS cells) may reflect a “ground state” upon which developmental and environmental influences would be minimal. Olfactory neurosphere-derived cells (ONS cells) are an adult-derived neuro-ectodermal stem cell modified by developmental and environmental influences. Fibroblasts provide a non-neural control for life-long developmental and environmental influences. Genome-wide profiling of DNA methylation and gene expression was done in these three cell types from the same individuals. All cell types had distinct, statistically significant schizophrenia-associated differences in DNA methylation and linked gene expression, with Gene Ontology analysis showing that the differentially affected genes clustered in networks associated with cell growth, proliferation and movement, functions known to be affected in schizophrenia patient-derived cells. Only 5 gene loci were differentially methylated in all three cell types. These findings suggest that schizophrenia-associated DNA methylation may be a response to the homeostatic demands of different cell types in their local environments. Understanding the role of epigenetics in cell function in the brain in schizophrenia is likely to be complicated by similar cell type differences in intrinsic and environmentally-induced epigenetic regulation. This dataset represents the gene expression part of the study. The DNA methylation data is deposited under accession E-MTAB-2154.
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The study aims to show that Sox9+ Chd1+ mouse embryonic lung progenitors can be isolated and expanded long-term in 3D culture while maintaining their multipotency. in vitro cultured Sox9+ Chd1+ lung progenitors transcriptionally resemble their in vivo counterparts and show significant difference from adult lung epithelial (Cdh1+ and EpCAM+) and non-epithelial (Cdh1- and EpCAM-) cells
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Infectious bursal disease virus (IBDV) belongs to the family Birnaviridae and is economically important to the poultry industry worldwide. IBDV infects B cells in the bursa of Fabricius (BF), which can cause severe immunosuppression and mortality in young chickens. Earlier studies have shown that strains of IBDV lose their virulence potential after serial passage in non-B lymphoid cells, for reasons that are poorly understood. This study aimed to investigate the gene expression profiles of one cell-culture adapted attenuated IBDV strain (D78) and one very virulent IBDV strain (UK661) in chicken primary B cells cultured ex vivo from the bursa of Fabricius. The viruses were studied in B cells over 48h and their gene expression was initially evaluated with qPCR. The mRNA was isolated from the cells at 18 hours post-infection and screened with Affymetrix microarrays in triplicate. The study included mock controls which were conducted in triplicate.
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BldC is a transcriptional regulator essential for morphological development Streptomyces venezuelae. Although bldC deletion strain is unable to produce aerial hyphae, electron microscopy reveals that almost all of the colony biomass is in the form of spores rather than undifferentiated vegetative hyphae. This ChIP-chip experiment was carried out to determine the binding sites, and thence the regulon, of BldC in Streptomyces venezuelae. Cy3(IP):Cy5(Total) signal ratios in the wild type were compared to those in a bldC knockout strain.
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Gene expression profiling of EHEC and its luxS-deficient mutant strain which cannot produce autoinducer-2 molecule at the late log-phase in 0.6M NaCl LB broth (osmotic stress condition) against controls grown under normal osmotic condition (LB broth)
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Analysis of gene expression patterns of B-1 cells from C57BL6 wild type mice versus B-1 cells fromIL-10 Knockout mice. This study will help in the identification of factors in B-1 cells involved in changing of metastatic behavior of B16 melanoma after contacting with B-1 lymphocytes.
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Along the trachea-bronchial tree, including the small airway region, cigarette smoke exposure induces inflammation, which can exacerbate the development of chronic obstructive pulmonary disease (COPD). The small airway region is known as the primary location of airway blockage in COPD and asthma. Therefore, evaluating exposure impact on the small airway is relevant for risk assessment. Using an in vitro human small airway culture model and a Systems Toxicology approach, this present study reports an assessment of the biological impact of an aerosol from a candidate modified-risk tobacco product, tobacco heating system (THS) 2.2, as compared with 3R4F smoke, at similar nicotine concentrating other functional measures (e.g., cytotoxicity, ciliary beating function, secretion of pro-inflammatory mediators) and histological assessment. The NPA methodology provides not only a qualitative measure of the exposure impact, but also a quantification of the exposure effect: the highest biological impact was observed in cultures 4 h post-exposure to 3R4F smoke at 0.15 mg nicotine/L (100% impact). In contrast, THS2.2 aerosol at similar nicotine concentration, only elicited 15% relative biological impact at 4 h post-exposure in the context of various biological processes modeled in the networks: Cell Fate, Cell Proliferation, Cell Stress, and Inflammatory Process Networks. Consistently, ciliary beating function and culture morphology were not remarkably altered in samples exposed to THS2.2 aerosol, even at nicotine concentration three times that of 3R4F smoke.
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We measured global mRNA expression in unstimulated and Bone Marrow Derived Murine Dendritic Cells (BMDCs) stimulated with CD40L in presence or absence of Neuronal precursor cell (NPC) condition medium at 6h and 18h.
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Background: Aspergillus colonization after lung transplant is associated with an increased risk of chronic lung allograft dysfunction (CLAD). We hypothesized that gene expression during Aspergillus colonization could provide clues to CLAD pathogenesis. Methods: We examined transcriptional profiles in 3 or 6-month surveillance bronchoalveolar lavage fluid cell pellets from recipients with A. fumigatus colonization (n=12) and without colonization (n=10). Among the Aspergillus colonized, we also explored profiles in those who developed CLAD (n=6) or remained CLAD free (n=6). Transcription profiles were assayed with the HG-U133 Plus 2.0 microarray (Affymetrix). Statistical Analysis: Differential gene expression analyses were performed to select candidate lists of genes. Functional analyses on these selected genes were explored.
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Benzene, a natural component of petroleum products, is a known hematotoxic and leukemogenic agent. The haematotoxic effect and excess leukemia has been reported below 1 ppm, an exposure level previously considered not to cause any health effects. Gene expression studies suggest that benzene affects genes involved in AML and immune response pathways in a supra-linear manner, and at exposure levels as low as 0.1 ppm benzene. An increased risk of haematopoietic malignancies and altered gene expression also at exposure below 1 ppm is compatible with the emerging knowledge of a non-linear metabolism of benzene, favouring production of a greater proportion of toxic metabolites in subjects exposed to benzene concentrations below 1 ppm than in heavily exposed workers. In the present study, we investigated whether workers found to have a dose-dependent decline in relevant immune cells after benzene-exposure deviated from the unexposed referents in global gene expression changes in whole blood samples, and whether any pathways or genes previously reported in similar low-dose gene expression studies were differentially affected. The study population comprised eight benzene-exposed petroleum workers and five referents deemed unexposed to benzene recruited from the catering section on the same offshore installation (for sampling strategy, see sampling protocol). The two groups significantly differed in age. The dataset was therefore balanced for age by excluding workers at age 55 in the data modelling to identify significant genes.
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