Ontology highlight
ABSTRACT:
PROVIDER: PRJNA574574 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10199639_1.fastq.gz | Fastqsanger.gz | |||
| SRR10199639_2.fastq.gz | Fastqsanger.gz | |||
| SRR10199640_1.fastq.gz | Fastqsanger.gz | |||
| SRR10199640_2.fastq.gz | Fastqsanger.gz | |||
| SRR10199641_1.fastq.gz | Fastqsanger.gz |
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Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.
2020-11-30 | E-MTAB-8739 | biostudies-arrayexpress
Project description:HuMiChip was used to analyze human oral and gut microbiomes, showing significantly different functional gene profiles between oral and gut microbiome. The results were used to demonstarte the usefulness of applying HuMiChip to human microbiome studies.
2014-02-04 | E-GEOD-54290 | biostudies-arrayexpress
Project description:Cocaine use disorder represents a public health crisis with no FDA-approved medications for its treatment. A growing body of research has detailed the important connections between the brain and the resident population of bacteria in the gut, the gut microbiome in psychiatric disease models. Acute depletion of gut bacteria results in enhanced reward in a mouse cocaine place preference model, and repletion of bacterially-derived short-chain fatty acid (SCFA) metabolites reverses this effect. However, the role of the gut microbiome and its metabolites in modulating cocaine-seeking behavior after prolonged abstinence is unknown. Given that relapse prevention is the most clinically challenging issue in treating substance use disorders, studies examining the effects of microbiome manipulations in relapse-relevant models are critical. Here, Sprague-Dawley rats received either untreated water or antibiotics to deplete the gut microbiome and its metabolites. Rats were trained to self-administer cocaine and subjected to either within-session threshold testing to evaluate motivation for cocaine or 21 days of abstinence followed by a cue-induced cocaine-seeking task to model relapse behavior. Microbiome depletion did not affect cocaine acquisition on an FR1 schedule. However, microbiome-depleted subjects exhibited significantly enhanced motivation for low dose cocaine on a within-session threshold task. Similarly, microbiome depletion increased cue-induced cocaine-seeking following prolonged abstinence. In the absence of a normal microbiome, repletion of bacterially-derived SCFA metabolites reversed the behavioral and transcriptional changes associated with microbiome depletion. These findings suggest that gut bacteria, via their metabolites, are key regulators of drug-seeking behaviors, positioning the microbiome as a potential translational research target.
2024-05-01 | GSE227980 | GEO
Project description:Gestational diabetes mellitus (GDM) is considered as the early stage of type 2 diabetes mellitus. In this study, we compared the demographic and clinical data between six GDM and six NGT (healthy controls) and found the HOMA-IR was increased in GDM. Previously, many researches had proved that omental adipose tissues dysfunction could induce insulin resistance. Thus, in order to investigate the cause of the insulin resistance in GDM, label-free proteomics was used to discover differentially expressed proteins in omental adipose tissues between GDM and NGT. A total of 3529 proteins identified, including 66 significantly changed proteins. Adipocyte plasma membrane associated protein (APMAP also called C20orf3) was one of changed proteins and down regulated in GDM omental adipose tissues. Further, mature 3T3-L1 adipocytes were used to simulate omental adipocytes and we found that inhibited the expression of APMAP by RNAi would impaired the insulin signaling and activated the NFkB signaling in adipocytes. These results indicated that the decreased of APMAP in mental adipose tissues may be important in process of the insulin resistance in GDM.
2016-02-02 | PXD003095 | Pride
Project description:Gestational diabetes mellitus (GDM) is considered as the early stage of type 2 diabetes mellitus. In this study, we compared the demographic and clinical data between six GDM and six NGT (healthy controls) and found the HOMA-IR was increased in GDM. Previously, many researches had proved that omental adipose tissues dysfunction could induce insulin resistance. Thus, in order to investigate the cause of the insulin resistance in GDM, label-free proteomics was used to discover differentially expressed proteins in omental adipose tissues between GDM and NGT. A total of 3529 proteins identified, including 66 significantly changed proteins. Adipocyte plasma membrane associated protein (APMAP also called C20orf3) was one of changed proteins and down regulated in GDM omental adipose tissues. Further, mature 3T3-L1 adipocytes were used to simulate omental adipocytes and we found that inhibited the expression of APMAP by RNAi would impaired the insulin signaling and activated the NFkB signaling in adipocytes. These results indicated that the decreased of APMAP in mental adipose tissues may be important in process of the insulin resistance in GDM.
2017-03-29 | MSV000080798 | MassIVE
Project description:Background Alterations of the gut microbiome have been linked to multiple chronic diseases. However, the drivers of such changes remain largely unknown. The oral cavity acts as a major route of exposure to exogenous factors including pathogens, and processes therein may affect the communities in the subsequent compartments of the gastrointestinal tract. Here, we perform strain-resolved, integrated multi-omic analyses of saliva and stool samples collected from eight families with multiple cases of type 1 diabetes mellitus (T1DM). Results We identified distinct oral microbiota mostly reflecting competition between streptococcal species. More specifically, we found a decreased abundance of the commensal Streptococcus salivarius in the oral cavity of T1DM individuals, which is linked to its apparent competition with the pathobiont Streptococcus mutans. The decrease in S. salivarius in the oral cavity was also associated with its decrease in the gut as well as higher abundances in facultative anaerobes including Enterobacteria. In addition, we found evidence of gut inflammation in T1DM as reflected in the expression profiles of the Enterobacteria as well as in the human gut proteome. Finally, we were able to follow transmitted strain-variants from the oral cavity to the gut at the metagenomic, metatranscriptomic and metaproteomic levels, highlighting not only the transfer, but also the activity of the transmitted taxa along the gastrointestinal tract. Conclusions Alterations of the oral microbiome in the context of T1DM impact the microbial communities in the lower gut, in particular through the reduction of “oral-to-gut” transfer of Streptococcus salivarius. Our results indicate that the observed oral-cavity-driven gut microbiome changes may contribute towards the inflammatory processes involved in T1DM. Through the integration of multi-omic analyses, we resolve strain-variant “mouth-to-gut” transfer in a disease context.
2022-10-05 | PXD031579 | Pride
Project description:Diabetes Mellitus Type 1 miRnome
| PRJEB51173 | ENA