Consumption of resistant starch (RS) has been associated with various intestinal health benefits, but knowledge on its effects on global gene expression in the colon is limited. The main objective of the current study was to identify genes affected by RS in the proximal colon to infer which biologic pathways were modulated. Ten 17-wk-old male pigs, fitted with a cannula in the proximal colon for repeated collection of tissue biopsy samples and luminal content, were fed a digestible starch (DS) diet or a diet high in RS (34%) for 2 consecutive periods of 14 d in a crossover design. Analysis of the colonic transcriptome profiles revealed that, upon RS feeding, oxidative metabolic pathways, such as the tricarboxylic acid cycle and -oxidation, were induced, whereas many immune response pathways, including adaptive and innate immune system, as well as cell division were suppressed. The nuclear receptor peroxisome proliferator-activated receptor (PPARG) was identified as a potential key upstream regulator. RS significantly (P < 0.05) increased the relative abundance of several butyrate-producing microbial groups, including the butyrate producers Faecalibacterium prausnitzii and Megasphaera elsdenii, and reduced the abundance of potentially pathogenic members of the genus Leptospira and the phylum Proteobacteria. Concentrations in carotid plasma of the 3 main short-chain fatty acids acetate, propionate, and butyrate were significantly higher with RS consumption compared with DS consumption. Overall, this study provides novel insights on effects of RS in proximal colon and contributes to our understanding of a healthy diet.
Resistant starch induces catabolic but suppresses immune and cell division pathways and changes the microbiome in the proximal colon of male pigs.
Sex, Age, Specimen part
View SamplesDespite substantial investments, tuberculosis remains one of the biggest challenges in public health.
Synergy of chemotherapy and immunotherapy revealed by a genome-scale analysis of murine tuberculosis.
Sex, Specimen part
View SamplesMutations in GRIN2B are associated with intellectual disability in humans. We generated iPSC derived mature cortical neurons with mutations in GRIN2B and compared them to isogenic control cells. We found that both loss of function (LOF) and reduced dosage (RD) mutations in GRIN2B lead to reduced expression of NMDAR genes and increased expression of marker of immaturity, including KI67 and MET. Overall design: Examination of transcriptome in iPSC-derved mature neurons with and without the presence of mutations in GRIN2B
Disruption of GRIN2B Impairs Differentiation in Human Neurons.
Subject
View SamplesIdentifying novel candidate biomarker gene differentially expressed in the peripheral blood cells of patients with early stage acute myocardial infarction using microarray as a high throughput screening technology.
Novel genes detected by transcriptional profiling from whole-blood cells in patients with early onset of acute coronary syndrome.
Specimen part, Disease, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Subtype-specific genomic alterations define new targets for soft-tissue sarcoma therapy.
Specimen part, Disease, Cell line
View SamplesSoft tissue sarcomas are aggressive mesenchymal cancers that affect more than 10,600 new patients per year in the US, about 40% of whom will die of their disease. Soft tissue sarcomas exhibit remarkable histologic diversity, with more than 50 recognized subtypes, but our knowledge of their genomic alterations is limited. Here we describe the results of an integrative analysis of DNA sequence, copy number, and mRNA expression in 207 samples encompassing seven major subtypes. Genes mutated in more than 5% of samples within a subtype were KIT (in gastrointestinal stromal cell tumors, or GISTs), TP53 (pleomorphic liposarcomas), PIK3CA (myxoid/round-cell liposarcoma), and NF1 (both myxofibrosarcoma and pleomorphic liposarcoma). We show evidence that PIK3CA mutations, found in 18% of myxoid/round-cell liposarcomas, activate AKT in vivo and are associated with poor outcomes. Point mutations in the tumor suppressor gene NF1 were discovered in both myxofibrosarcomas and pleomorphic liposarcomas, while genomic deletions were observed in all subtypes at varying frequencies. Finally, we found that short hairpin RNA-based knockdown of a subset of genes that are amplified in dedifferentiated liposarcoma, including CDK4 and YEATS4, decreased cell proliferation. Our study yields the most detailed map of molecular alterations across diverse sarcoma subtypes to date and provides potential subtype-specific targets for therapy.
Subtype-specific genomic alterations define new targets for soft-tissue sarcoma therapy.
Specimen part, Disease
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity.
No sample metadata fields
View SamplesThe Cancer Cell Line Encyclopedia (CCLE) project is a collaboration between the Broad Institute, the Novartis Institutes for Biomedical Research and the Genomics Novartis Foundation to conduct a detailed genetic and pharmacologic characterization of a large panel of human cancer models
The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Identification of artifactual microarray probe signals constantly present in multiple sample types.
Specimen part
View SamplesThe correlation of the RNA profiles obtained by microarray analysis was compared with that obtained from RNA-Seq by using reduced complexity sperm datasets. This resolved as a series of discordant probes. The extent of discordancy among other datasets was then determined.
Identification of artifactual microarray probe signals constantly present in multiple sample types.
Specimen part
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