Transcriptome analysis reveals that in pancreatic beta cells weaning increases the expression of genes involved in replication licensing, suggesting a mechanism to increased responsiveness to the mitogenic activity of high glucose.
No associated publication
Specimen part
View SamplesMononuclear phagocytes (MPs), including monocytes and macrophages, play complex roles in the pathogenesis of age-related macular degeneration (AMD). We aimed to perform global transcriptome analysis on monocytes from AMD patients to obtain additional insight to the role of MPs in AMD. Peripheral blood was taken from treatment-nave neovascular AMD (nvAMD) patients (n=14), and age-matched controls (n=15). Peripheral blood mononuclear cells (PBMCs) were separated and monocytes were isolated via negative selection. Gene expression was evaluated with Affymetrix Gene1.0 ST microarrays. Statistical/bioinformatics analysis was performed using open sourceware programs.
Transcriptome Analysis on Monocytes from Patients with Neovascular Age-Related Macular Degeneration.
Specimen part, Disease, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Sex, Age, Specimen part
View SamplesChronic inflammation is a common underlying condition associated with tumor development, accounting for approximately 20% of human cancers. This association is especially apparent in Hepatocellular carcinoma (HCC), which often develops on the background of chronic hepatitis and hepatic fibrosis, slowly unfolding on a background of chronic inflammation. HCC is one of the most common tumors worldwide, exhibiting a very poor prognosis and high mortality rate with limited available therapeutic tools. The etiology of liver cancer is well known, however there is still a lack of precise knowledge about pathogenesis of HCC. IL-6 have been shown to be of importance for liver protection and prevention of liver injury in animal models of acute sclerosing cholangitis and correlate with increased HCC in human patients. Using a murine model of chronic cholangitis based on the ablation of the Mdr2 gene, this study has examined the role of IL-6 signaling in chronic hepatitis and in the subsequent development of liver cancer. The main observations of this study are that IL-6 signaling in female Mdr2-KO mice protects from the development of liver injury and fibrosis, but simultaneously rduced tumor initiation.
No associated publication
Sex, Age
View SamplesChronic inflammation is a common underlying condition associated with tumor development, accounting for approximately 20% of human cancers. This association is especially apparent in Hepatocellular carcinoma (HCC), which often develops on the background of chronic hepatitis and hepatic fibrosis, slowly unfolding on a background of chronic inflammation. HCC is one of the most common tumors worldwide, exhibiting a very poor prognosis and high mortality rate with limited available therapeutic tools. The etiology of liver cancer is well known, however there is still a lack of precise knowledge about pathogenesis of HCC. IL-6 have been shown to be of importance for liver protection and prevention of liver injury in animal models of acute sclerosing cholangitis and correlate with increased HCC in human patients. Using a murine model of chronic cholangitis based on the ablation of the Mdr2 gene, this study has examined the role of IL-6 signaling in chronic hepatitis and in the subsequent development of liver cancer. The main observations of this study are that IL-6 signaling in male Mdr2-KO mice protects from the development of liver injury and fibrosis, but simultaneously promotes tumor initiation. Thus, IL-6 deficiency in male Mdr2-KO mice dissociates the tight correlation between liver fibrosis and the development of inflammation-associated HCC.
No associated publication
Sex, Age, Specimen part
View SamplesHow organ size and form are controlled during development is a major question of biology. Blood vessels have been shown to be essential for early development of the liver and pancreas, and are fundamental to normal and pathological tissue growth. Here we report that non-nutritional signals from blood vessels surprisingly act to restrain pancreas growth. Elimination of endothelial cells increases the size of embryonic pancreatic buds. Conversely, VEGF-induced hypervascularization decreases pancreas size. The growth phenotype results from vascular restriction of pancreatic tip cell formation, lateral branching and differentiation of the pancreatic epithelium into endocrine and acinar cells. The effects are seen both in vivo and ex vivo, indicating a perfusion-independent mechanism. Thus the vasculature controls pancreas morphogenesis and growth by reducing branching and differentiation of primitive epithelial cells.
Blood vessels restrain pancreas branching, differentiation and growth.
Specimen part
View SamplesHaving found that LexA degradation was significantly higher under apoptotic like death (ALD) than under SOS conditions, we hypothesized that additional genes tightly regulated by LexA would be transcribed under ALD conditions.
Apoptosis-like death, an extreme SOS response in Escherichia coli.
Disease, Treatment
View SamplesHIBM is a neuromuscular disorder characterized by adult-onset, slowly progressive distal and proximal muscle weakness. Here, gene expression was measured in muscle specimens from 10 HIBM patients carrying the M712T Persian Jewish founder mutation in GNE and presenting with mild histological changes, and from 10 healthy matched control individuals.
Mitochondrial processes are impaired in hereditary inclusion body myopathy.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
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Specimen part
View SamplesWe used microarrays to identify the gene expression changes after SET knockdown in ESCs and 4 day RA differentiated ESCs
Alternative SET/TAFI Promoters Regulate Embryonic Stem Cell Differentiation.
Specimen part
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