Muscle - atypical diabetes protein expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE634 | GEO | 2004/03/01
SECONDARY ACCESSION(S): PRJNA87543
REPOSITORIES: GEO
Similar Datasets
Project description:Skeletal muscle biopsies from atypical diabetics at presentation and remission. Protein expression determined with antibody arrays
2010-06-09 | E-GEOD-634 | biostudies-arrayexpress
Project description:The current study aimed to address the hypothesis that programmed expression of key miRNAs in skeletal muscle mediates the development of insulin resistance, and consequently long-term health. We thus examined microRNA signatures in skeletal muscle of unmedicated newly diagnosed human pre-diabetics and type 2 diabetics. Skeletal muscle biopsies were obtained from the vastus lateralis from males with pre-diabetes (PD, n=5) or type 2 diabetes mellitus (T2DM, n=6) along with age and sex-matched healthy volunteers (H, n=5). Ramaciotti Centre for Genomics (UNSW, sydney, Australia)
2015-04-25 | E-GEOD-68224 | biostudies-arrayexpress
Project description:The current study aimed to address the hypothesis that programmed expression of key miRNAs in skeletal muscle mediates the development of insulin resistance, and consequently long-term health. We thus examined microRNA signatures in skeletal muscle of unmedicated newly diagnosed human pre-diabetics and type 2 diabetics.
2015-04-25 | GSE68224 | GEO
Project description:Type 2 diabetes is one of the most prevalent metabolic disorders. It is characterised by insulin resistance in peripheral tissues. Skeletal muscle is one of the tissues that affect by insulin resistance. Therefore, the study aims to identify differentially regulated genes in skeletal muscle of type 2 diabetes patients. Here, we obtained biopsies from the pectoralis major muscle and performed RNA sequencing to profile the gene expression patterns from four patients with diabetes and three healthy controls.
2024-03-30 | E-MTAB-8917 | biostudies-arrayexpress
Project description:Human skeletal muscle was obtained from five individuals: Two hyperglycaemic type 2 diabetics, one diabetic subjects with normal fasting glucose and two healthy control subjects matched for age and BMI.
2007-12-10 | E-MEXP-1270 | biostudies-arrayexpress
Project description:Despite improved therapy, approximately one-fifth of children with acute T-lymphoblastic leukemia (T-ALL) succumb to the disease, suggesting unrecognized biologic heterogeneity that may contribute to drug resistance. We studied leukemic cells, collected at diagnosis, to identify features that could define this high-risk subgroup. A total of 139 patients with T-ALL were treated consecutively from 1992 to 2006 at this institution. Their leukemic cells were examined with multiparameter flow cytometry, single nucleotide polymorphism arrays and other methods of genomic analysis. Survival rates and probabilities of treatment failure were calculated for subgroups considered to have biologically distinct forms of T-ALL. The lymphoblasts of 17 patients (12.2%) had immunophenotypes that clearly differed from those of the remaining patients. Most striking features were the low or absent expression of common T-lineage markers (CD5, CD1a and CD8), and expression of myeloid and stem cell markers, suggesting stem-cell like properties. These atypical blasts also showed a distinct gene expression profile and increased genomic instability overall. Patients with this form of T-ALL had a very low probability of surviving for 10 years after diagnosis: 19% ± 12% (mean ± SE) versus 84% ± 6% for all other patients ( P<0.001). The cumulative incidence of remission failure / hematologic relapse was 72% ± 16% versus 10% ± 3% (P < 0.001). A subset of children with T-ALL have atypical blast cell immunophenotypes that predict a dire outcome with use of standard intensive chemotherapy. Alternative treatment strategies are need for patients with this sybtype of leukemia. Experiment Overall Design: 55 Diagnostic T-ALL samples were analyzed
2008-10-25 | E-GEOD-8879 | biostudies-arrayexpress
Project description:Plasmodium falciparum malaria is a deadly infectious disease for which we have no licensed vaccine. Antibodies confer protection against malaria and individuals exposed to P. falciparum acquire protective antibodies, but only after years of repeated infections. We recently showed that malaria exposure is associated with a large expansion of a population of atypical memory B cells (MBCs) that phenotypically resemble B cell populations expanded in chronic viral infections, including HIV. At present the relationship of atypical MBCs to classical MBCs and their function are not known. We provide evidence that the expressed VH gene repertoires and somatic hypermutation rates of atypical and classical MBCs are indistinguishable, indicating the two populations are closely related developmentally. Atypical MBCs can be distinguished by their expression of multiple inhibitory receptors, including Fc receptor-like-5. B cell receptor (BCR) signaling is stunted in atypical MBCs, resulting in impaired Ca2+ mobilization, proliferation and cytokine production. Atypical MBCs do not spontaneously secrete antibodies and cannot be stimulated to differentiate into antibody-secreting cells in vitro. These results suggest that in individuals chronically exposed to malaria, atypical MBCs differentiate from classical MBCs and assume a phenotype refractory to BCR-mediated activation, potentially contributing to the inefficient acquisition of immunity to malaria. Comparison of human atypical B cell versus classical B cell versus naïve B cell.
2015-05-07 | E-GEOD-65928 | biostudies-arrayexpress
Project description:Muscle biopsies taken from vastus lateralis muscle of 30 normal subjects and 19 FSHD subjects (see PubMed ID 17151338) Affymetrix U133A and U133B arrays were scanned both before (S1) and after (S2) antibody enhancement. Effects of age and sex in normal subjects reported previously under GSE362, GSE674, and GSE9676. Keywords: facioscapulohumeral dystrophy, skeletal muscle
2008-03-08 | GSE10760 | GEO
Project description:Mechanistic insights into the molecular events by which exercise enhances the skeletal muscle phenotype are lacking, particularly in the context of type 2 diabetes. Here we unravel a fundamental role for exercise-responsive cytokines (exerkines) on skeletal muscle development and growth in individuals with normal glucose tolerance or type 2 diabetes. Acute exercise triggered an inflammatory response in skeletal muscle, concomitant with an infiltration of immune cells. These exercise effects were potentiated in type 2 diabetes. In response to contraction or hypoxia, cytokines were mainly produced by endothelial cells and macrophages. The chemokine CXCL12 was induced by hypoxia in endothelial cells, as well as by conditioned medium from contracted myotubes in macrophages. We found that CXCL12 was associated with skeletal muscle remodeling after exercise and differentiation of cultured muscle. Collectively, acute aerobic exercise mounts a non-canonical inflammatory response, with an atypical production of exerkines, which is potentiated in type 2 diabetes.
2022-07-06 | GSE202295 | GEO
Project description:Despite improved therapy, approximately one-fifth of children with acute T-lymphoblastic leukemia (T-ALL) succumb to the disease, suggesting unrecognized biologic heterogeneity that may contribute to drug resistance. We studied leukemic cells, collected at diagnosis, to identify features that could define this high-risk subgroup. A total of 139 patients with T-ALL were treated consecutively from 1992 to 2006 at this institution. Their leukemic cells were examined with multiparameter flow cytometry, single nucleotide polymorphism arrays and other methods of genomic analysis. Survival rates and probabilities of treatment failure were calculated for subgroups considered to have biologically distinct forms of T-ALL. The lymphoblasts of 17 patients (12.2%) had immunophenotypes that clearly differed from those of the remaining patients. Most striking features were the low or absent expression of common T-lineage markers (CD5, CD1a and CD8), and expression of myeloid and stem cell markers, suggesting stem-cell like properties. These atypical blasts also showed a distinct gene expression profile and increased genomic instability overall. Patients with this form of T-ALL had a very low probability of surviving for 10 years after diagnosis: 19% ± 12% (mean ± SE) versus 84% ± 6% for all other patients ( P<0.001). The cumulative incidence of remission failure / hematologic relapse was 72% ± 16% versus 10% ± 3% (P < 0.001). A subset of children with T-ALL have atypical blast cell immunophenotypes that predict a dire outcome with use of standard intensive chemotherapy. Alternative treatment strategies are need for patients with this sybtype of leukemia. Keywords: Analysis of gene expression profiles of typical versus atypical T-ALL
2009-05-15 | GSE8879 | GEO