Project description:Interventions: Patients with spleen deficiency and qi stagnation syndrome SDQSS:NA;Patients with DHS with damp-heat accumulation syndrome:NA;Patients with SPOS with stasis and internal resistance syndrome:NA;Patients with SKYDS of Spleen and Kidney Yang Deficiency Syndrome:NA;Patients with liver-kidney yin deficiency syndrome LKYDS:NA;QBDS patients with deficiency of both qi and blood syndrome:NA
Primary outcome(s): Serum metabolites;Fecal microbiome;lipidomics
Study Design: Diagnostic test for accuracy
Project description:FLORINASH - The role of intestinal microflora in non-alcoholic fatty liver disease (NAFLD) EU FP7-HEALTH, project number 241913<br>Florinash examined the role on the gut microbiota in NAFLD. Metagenomic, proteomic, metabolomic and transcriptomic data were integrated to give provide a systems biology approach to disease-associated studies. Liver biopsies were obtained from patients undergoing bariatric surgery; one was used to diagnose NAFLD, the other was used to examine the host transcriptome in NAFLD. This dataset is part of the TransQST collection.
Project description:Interventions: Syndrome of spleen qi deficiency1:Chinese medicine of Supplementing Qi and nourishing spleen;Syndrome of spleen qi deficiency2:no;Flat syndrome group:no;Qi deficiency constitution:no
Primary outcome(s): Symptom score;Serum TTR expression
Study Design: Case-Control study
Project description:In this study, the spleen deficiency syndrome rat model was built with reserpine injection method. At first, the intervention effect of SJZD on spleen deficiency syndrome was preliminary evaluation through pharmacodynamics study. By comparing the differences proteins of liver tissues by label-free proteomics techniques, the differentially expressed proteins of spleen deficiency syndrome and SJZD intervention spleen deficiency syndrome were screened. At last, differentially expressed proteins were analyzed with bioinformatics analysis method, the potential target proteins of spleen deficiency syndrome and SJZD intervention spleen deficiency syndrome were excavated. At the same time, the corresponding metabolic pathways and biological molecular interaction network was established. We hope to probe the mechanisms of SJZD intervention spleen deficiency syndrome from the aspect of proteomic to provide a scientific basis for the clinical diagnosis and treatment of spleen deficiency syndrome.
Project description:Vitamin D, in addition to calcium/phosphate metabolism and bone homeostasis regulation, has antiproliferative, anti-inflammatory and antifibrotic properties. These protective actions may have an impact in the progression of chronic liver disease including NAFLD (Non-alcoholic fatty liver disease). Vitamin D deficiency is associated with metabolic syndrome components, such as insulin resistance and dyslipidemia. NAFLD is often considered as the hepatic manifestation of metabolic syndrome, and a growing body of research suggests a relationship between vitamin D deficiency and NAFLD, with low levels of 25(OH)D associated with hepatic inflammation, and the severity and progression of NAFLD.
Project description:The intestinal mucus layer produced by goblet cells is a critical component of innate immunity. The key host factors and regulatory mechanisms controlling goblet cell function in mucus layer formation remain poorly understood. This study identifies a function for the microprotein FXYD domain-containing transport regulator 3 (FXYD3) in goblet cells in regulating mucus layer formation to maintain intestinal homeostasis. Deficiency of FXYD3 in mouse intestinal epithelial cellsresults in a damaged mucus barrier, leading to microbiota dysbiosis and increased susceptibility to colitis. Mechanistically, FXYD3 interacts with endoplasmic reticulum Ca2+-ATPase SERCA2 to enhances its pump activity. FXYD3 deficiency causes defects in ER Ca2+ homeostasis and mucin glycosylation, impairing mucus layer integrity. Furthermore, metabolites of gut microbiota, propionate and butyrate promoteFXYD3 expression. In ulcerative colitis (UC) patients, FXYD3 expression is significantly downregulated and correlats with disease severity. These findings indicat FXYD3 is a key mediator of host-microbiota interactions for intestinal health.
Project description:Irritable Bowel Syndrome (IBS) is a disorder of the gut-brain axis, characterized by altered gut function and frequent psychiatric co-morbidity. Although altered intestinal microbiome profiles have been documented, their relevance to the clinical expression of IBS is unknown. To evaluate a functional role of the microbiota, we colonized germ-free mice with fecal microbiota from healthy controls or IBS patients with accompanying anxiety, and monitored gut function and behavior. Mouse microbiota profiles clustered according to their human donors. Despite having taxonomically similar composition as controls, mice with IBS microbiota had distinct serum metabolomic profiles related to neuro- and immunomodulation. Mice with IBS, but not control microbiota, exhibited faster gastrointestinal transit, intestinal barrier dysfunction, innate immune activation and anxiety-like behavior. These results support the notion that the microbiota contributes to both intestinal and behavioral manifestations of IBS and rationalize the use of microbiota-directed therapies in ameliorating IBS.
2017-03-02 | GSE61841 | GEO
Project description:Gut microbiota characteristics of obese Polycystic ovary syndrome patients
