Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1053635 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27235200.fastq.gz | Fastqsanger.gz | |||
| SRR27235200_1.fastq.gz | Fastqsanger.gz | |||
| SRR27235200_2.fastq.gz | Fastqsanger.gz | |||
| SRR27235300.fastq.gz | Fastqsanger.gz | |||
| SRR27235300_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 450 |
Similar Datasets
Project description:We recruited 24 Mongolian volunteers,6 of which were T2D cases(sample T1-T6), 6 were prediabetes cases(sample P1-P6), and 12 were health cases(sample C1-C12). The metagenomic analysis of gut microbiota from the volunteers’ fecal samples was performed. We compared the microbial differences in the three groups, and analyzed the differences of the stool microbial function.
2022-07-30 | E-MTAB-11957 | biostudies-arrayexpress
Project description:Type 2 diabetes (T2D), one of the most common metabolic diseases, is the result of insulin resistance or impaired insulin secretion by mitochondrial dysfunctions. Mitochondrial DNA (mtDNA) polymorphisms play an important role in physiological and pathological characteristics of T2D, however, their mechanism is poorly understood. To directly identify candidate mtDNA variants associated with T2D at the genome-wide level, we constructed forty libraries from ten patients with T2D and thirty control individuals for deep sequencing. We characterized their mtDNA atlas, and analyzed their single nucleotide polymorphisms (MtSNPs), insertions and deletions (InDels), and screened potential mtDNA mutation sites associated with T2D. We found ten mtDNA polymorphisms at nucleotides 489T > C, 3105AC > A, 3107N > C, 8701A > G, 9540T > C, 10398A > G, 10400C > T, 10873T > C, 12705C > T and 14783T > C that showed a significant difference between patients and control subjects. Therefore, our results characterize mtDNA atlas of patients with T2D, and further demonstrate that mtDNA variants are participated in the pathophysiology of T2D and other diseases. In addition, mtDNA variants may be candidate molecular biomarkers of T2D, and they may be valuable for early diagnosis of T2D in the future.
2022-08-30 | GSE136892 | GEO
Project description:Abnormalities in glucose metabolism that precede the onset of type 2 diabetes (T2D) activate immune cells, leading to elevated inflammatory factors and chronic inflammation. However, no single-cell RNA sequencing (scRNA-seq) studies have characterized the properties and networks of individual immune cells in T2D. Here, we analyzed peripheral blood mononuclear cells (PBMCs) from healthy controls and T2D patients by scRNA-seq. We found that CD14 monocytes in T2D patients were in a pro-inflammatory state and intermediate monocytes expressed more MHC class II genes. In T2D patients, cytotoxic CD4 T cells, effector memory CD8 T cells, and γδ T cells have increased cytotoxicity and clonal expansion. B cells were characterized by increased differentiation into intermediate B cells, plasma cells, and isotype class switching with increased expression of soluble antibody genes. These results suggest that monocytes, T cells, and B cells could interact to induce chronic inflammation in T2D patients with pro-inflammatory characteristics.
2024-06-12 | GSE268210 | GEO
Project description:To identify the potential regulators in the progression of diabetic nephropathy (DN), we performed RNA sequencing of blood samples from healthy volunteers, patients with T2D, and patients with DN. Further analyses revealed that FTO was significantly downregulated in blood samples of T2D and DN patients, while the expression of other erasers, writers or readers remained unchanged between disease and healthy groups . Our study thus provides potential molecular mechanisms for DN progression and association of differential gene expression with the functional and structural changes observed in patients with DN.
2024-01-13 | GSE154881 | GEO
Project description:Proteomic data from moose fistulated rumen; metagenomic and viral sequencing performed; metabolic pathways reconstructed
2018-07-03 | PXD008667 | Pride
Project description:Next-Generation-Sequencing (NGS) technologies have led to important improvement in the detection of new or unrecognized infective agents, related to infectious diseases. In this context, NGS high-throughput technology can be used to achieve a comprehensive and unbiased sequencing of the nucleic acids present in a clinical sample (i.e. tissues). Metagenomic shotgun sequencing has emerged as powerful high-throughput approaches to analyze and survey microbial composition in the field of infectious diseases. By directly sequencing millions of nucleic acid molecules in a sample and matching the sequences to those available in databases, pathogens of an infectious disease can be inferred. Despite the large amount of metagenomic shotgun data produced, there is a lack of a comprehensive and easy-use pipeline for data analysis that avoid annoying and complicated bioinformatics steps. Here we present HOME-BIO, a modular and exhaustive pipeline for analysis of biological entity estimation, specific designed for shotgun sequenced clinical samples. HOME-BIO analysis provides comprehensive taxonomy classification by querying different source database and carry out main steps in metagenomic investigation. HOME-BIO is a powerful tool in the hand of biologist without computational experience, which are focused on metagenomic analysis. Its easy-to-use intrinsic characteristic allows users to simply import raw sequenced reads file and obtain taxonomy profile of their samples.
2021-07-26 | E-MTAB-9189 | biostudies-arrayexpress
Project description:Next-Generation-Sequencing (NGS) technologies have led to important improvement in the detection of new or unrecognized infective agents, related to infectious diseases. In this context, NGS high-throughput technology can be used to achieve a comprehensive and unbiased sequencing of the nucleic acids present in a clinical sample (i.e. tissues). Metagenomic shotgun sequencing has emerged as powerful high-throughput approaches to analyze and survey microbial composition in the field of infectious diseases. By directly sequencing millions of nucleic acid molecules in a sample and matching the sequences to those available in databases, pathogens of an infectious disease can be inferred. Despite the large amount of metagenomic shotgun data produced, there is a lack of a comprehensive and easy-use pipeline for data analysis that avoid annoying and complicated bioinformatics steps. Here we present HOME-BIO, a modular and exhaustive pipeline for analysis of biological entity estimation, specific designed for shotgun sequenced clinical samples. HOME-BIO analysis provides comprehensive taxonomy classification by querying different source database and carry out main steps in metagenomic investigation. HOME-BIO is a powerful tool in the hand of biologist without computational experience, which are focused on metagenomic analysis. Its easy-to-use intrinsic characteristic allows users to simply import raw sequenced reads file and obtain taxonomy profile of their samples.
2021-07-26 | E-MTAB-9191 | biostudies-arrayexpress
Project description:The global prevalence of type 2 diabetes (T2D) is increasing, and it is contributing to the susceptibility to diabetes and its related epidemic in offspring. Although the impacts of paternal T2D on metabolism of offspring have been well established, the exact molecular and mechanistic basis that mediates these impacts remains largely unclear. Here we show that paternal T2D increases the susceptibility to diabetes in offspring through the gametic epigenetic alterations. Paternal T2D led to glucose intolerance and insulin resistance in offspring. Relative to controls, offspring of T2D fathers exhibited altered gene expression patterns in the pancreatic islets, with downregulation of several genes involved in glucose metabolism and insulin signaling pathway. Epigenomic profiling of offspring pancreatic islets revealed numerous changes in cytosine methylation depending on paternal T2D, including reproducible changes in methylation over several insulin signaling genes. Paternal T2D altered overall methylome patterns in sperm, with a large portion of differentially methylated genes overlapped with that of pancreatic islets in offspring. Our study revealed, for the first time, that T2D can be inherited transgenerationally through the mammalian germline by an epigenetic manner. Examination of the effect of paternal T2D on the DNA methylation in the pancreatic islets of offspring and in the sperm of father.
2013-01-02 | E-GEOD-43238 | biostudies-arrayexpress
Project description:Objective: We hypothesized that type 1 diabetes (T1D) is accompanied by changes in gene expression in peripheral blood mononuclear cells (PBMCs) due to dysregulation of adaptive and innate immunity, counterregulatory responses to immune dysregulation, insulin deficiency and hyperglycemia. Research Design and Methods: Microarray analysis was performed on PBMCs from 43 patients with newly diagnosed T1D, 12 patients with newly diagnosed type 2 diabetes (T2D) and 24 healthy controls. One and four month follow-up samples were obtained from 20 of the T1D patients. Results: Microarray analysis identified 282 genes differing in expression between newlydiagnosed T1D patients and controls at a false discovery rate of 0.05. Changes in expression of interleukin-1β (IL1B), early growth response gene 3 (EGR3), and prostaglandin-endoperoxide; synthase 2 (PTGS2) resolved within four months of insulin therapy and were also observed in T2D suggesting that they resulted from hyperglycemia. With use of a knowledge base, 81/282 genes could be placed within a network of interrelated genes with predicted functions including apoptosis and cell proliferation. IL1B and the MYC oncogene were the most highly-connected genes in the network. IL1B was highly overexpressed in both T1D and T2D, whereas MYC was dysregulated only in T1D. Conclusion: T1D and T2D likely share a final common pathway for beta cell dysfunction that includes secretion of interleukin-1β and prostaglandins by immune effector cells, exacerbating existing beta cell dysfunction, and causing further hyperglycemia. The results identify several targets for disease-modifying therapy of diabetes and potential biomarkers for monitoring treatment efficacy. Experiment Overall Design: We obtained blood samples from 24 healthy volunteers, 43 newly diagnosed T1D patients and 12 newly diagnosed T2D patients. All study participants were between the ages of 2 and 18 years. We collected samples one and four months after diagnosis from the last 20 of the T1D patients. For each time point one sample did not pass quality control and was dropped from the analysis. Patients with T2D were distinguished from T1D on the basis of age, body habitus, Experiment Overall Design: presence (11/12 patients) of acanthosis nigricans, family history of type 2 diabetes (11/12 patients), and absence of autoantibodies to insulin, IA-2, and GAD65. We allowed low titers of insulin antibodies in T2D patients (< 4 U/mL), which have been previously reported. All but two Experiment Overall Design: of the T1D patients with positive anti-insulin antibodies were also positive for at least one additional autoantibody.
2008-06-16 | E-GEOD-9006 | biostudies-arrayexpress