Adropin is a multifunctional peptide hormone encoded by the ENHO (energy homeostasis associated) gene. It plays a role in mechanisms related to increased adiposity, insulin resistance, as well as glucose and lipid metabolism. The low adropin levels are strongly associated with obesity independent insulin resistance. On the other hand, overexpression or exogenous administration of adropin improves glucose homeostasis. The multidirectional, adropin-related effects associated with the regulation of metabolism in humans also appear to be attributable to the effects of this peptide on the activity of various elements of the endocrine system including adrenal cortex. Therefore, the main purpose of the present study was to investigate the effect of adropin on proliferation and secretory activity in the human HAC15 adrenal carcinoma cell line.
Adropin Stimulates Proliferation and Inhibits Adrenocortical Steroidogenesis in the Human Adrenal Carcinoma (HAC15) Cell Line.
Specimen part, Cell line
View SamplesThe character of the earliest cardiac precursor cells remains largely unknown. To elucidate this further, we constructed single cell cDNAs from the mouse embryonic cardiac precurcsor cells of the early allantoic bud stage and the early headfold stage, and subjected them to deep sequencing. Overall design: The most anterior part of the embryos where cardiac precursor cells exist was digested by trypsin to separate into single cells. After a cell was transferred into a reaction tube, single cell cDNAs were constructed as PCR amplicons. cDNAs of cardiac precursor cells were identified by PCR of marker genes.
Single-Cell Expression Profiling Reveals a Dynamic State of Cardiac Precursor Cells in the Early Mouse Embryo.
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View SamplesAsthma is a complex, chronic respiratory disease with marked clinical and pathophysiological heterogeneity. Distinct inflammatory phenotypes of eosinophilic, mixed, neutrophilic and paucigranulocytic asthma are identified in patients, but most in vivo mouse models, studying asthma mechanisms, mimic only eosinophilic phenotype in humans. The detailed unbiased in vivo studies on molecular responses among different kinds of inflammation in asthma models are lacking. Therefore, we developed mouse models representing three different inflammatory phenotypes of airway inflammation, namely eosinophilic, mixed, and neutrophilic asthma via different methods of house dust mite sensitisation.
Tight junction, mucin, and inflammasome-related molecules are differentially expressed in eosinophilic, mixed, and neutrophilic experimental asthma in mice.
Specimen part
View SamplesWe are investigating the transcriptional response of newborns in response to prenatal arsenic exposure
Activation of inflammation/NF-kappaB signaling in infants born to arsenic-exposed mothers.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Systems scale interactive exploration reveals quantitative and qualitative differences in response to influenza and pneumococcal vaccines.
Sex, Age, Race, Subject
View SamplesThe objective of this study is to: 1) Characterize the immune responsiveness to administration of non-live vaccines in three cohorts of healthy adult subjects through the analysis of blood leukocytes transcriptional profiles. 2) Validate whole blood transcriptional profiles generated from standard 3mL blood draws versus 200uL blood draws obtained by finger stick. 3) Discover potential biomarkers for immune-responsiveness to non-live vaccines.
Systems scale interactive exploration reveals quantitative and qualitative differences in response to influenza and pneumococcal vaccines.
Sex, Age, Race, Subject
View SamplesThe objective of this study is to: 1) Characterize the cellular origin of transciptional signatures observed on day 1 after vaccination with 2009/10 seasonal influenza and pneumococcal vaccine discovered by transcriptional profiling of whole blood samples in data set WholeBlood_SysVax. 2) Discover potential biomarkers for immune-responsiveness to non-live vaccines.
Systems scale interactive exploration reveals quantitative and qualitative differences in response to influenza and pneumococcal vaccines.
Sex, Age, Race, Subject
View SamplesThe development of cytostatic-drug resistance renders chemotherapy ineffective in treating ovarian cancer, the most lethal gynaecological malignancy. In many cases, it is difficult to explain the development of drug resistance based on the expression patterns of genes known to be involved in this process. Microarray-based assays can provide information about new genes that are involved in the resistance to cytostatic drugs. This report describes alterations in the level of expression of genes in cisplatin- (CisPt), doxorubicin- (Dox), topotecan- (Top), and paclitaxel- (Pac) resistant variants of W1 and A2780 ovarian cancer cell lines. These drug-resistant variants of the W1 and A2780 cell lines were generated through the stepwise selection of cells tolerant of exposure to the indicated drugs at incrementally increased concentrations. Affymetrix GeneChip Human Genome Array Strips were used for hybridization assays. The genes with significantly altered expression levels (upregulated by more than fivefold or downregulated by less than fivefold relative to the level in the parental line) in the drug-resistant sublines were selected and were filtered using volcano plotting.
Microarray-based detection and expression analysis of extracellular matrix proteins in drug‑resistant ovarian cancer cell lines.
Cell line
View SamplesPlastids emit signals that broadly affect cellular processes. Based on previous genetic analyses, we propose that plastid signaling regulates the downstream components of a light signaling network and that these interactions coordinate chloroplast biogenesis with both the light environment and development by regulating gene expression. We tested these ideas by analyzing light-regulated and plastid-regulated transcriptomes. We found that the plastid is a major regulator of light signaling, attenuating the expression of more than half of all light-regulated genes in our dataset and changing the nature of light regulation for a smaller fraction of these light-regulated genes.
Plastids are major regulators of light signaling in Arabidopsis.
Age, Specimen part
View SamplesThe present study aimed to delineate the central mechanisms by which androgens delay wound repair. Blocking the conversion of testosterone to 5alpha-dihydrotestosterone (DHT) by 5alpha-reductase limits its ability to impair skin wound healing, suggesting that DHT is a more potent inhibitor of repair than is testosterone. This study aims to identify, through transcription profiling, potential mechanisms by which the 5alpha-reductase inhibitor MK-434 modulates repair. Microarray analysis of wound RNA samples from rats in which the transformation of testosterone to DHT is prevented has identified biological processes and key individual genes through which DHT may contribute to the altered healing profile in such animals. These include genes with putative roles in wound contraction and re-epithelialization.
5alpha-dihydrotestosterone (DHT) retards wound closure by inhibiting re-epithelialization.
Sex, Age, Specimen part, Compound
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