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Project description:Kombucha Tea (KT), a fermented tea with roots in traditional Chinese medicine, has surged in worldwide popularity due to its purported health benefits. KT contains a symbiotic culture of yeast and bacterial species, many of which are considered human probiotics. The molecular basis of the health benefits of KT has yet to be thoroughly explored in any animal model. We establishC. elegansas a model to query the molecular interactions between Kombucha-associated microbes (KTM) and the host. We find that worms have an established gut microbiome after consuming a KTM-exclusive diet that mirrors the microbial community found in the fermenting culture. Remarkably, animals consuming KTMs display strikingly reduced lipid levels, yet develop and reproduce similarly toE. coli-fed animals. Critically, consumption of a non-fermenting mix of KT microbial isolates (Kombucha microbe mix) resulted in elevated fat accumulation, suggesting that KTMs do not impair nutrient absorption. To identify the host metabolic pathways altered by KTMs, we performed mRNA-seq on KTM-fed animals, finding widespread changes in lipid metabolism genes. Specifically, we found that three lysosomal lipase genes are significantly upregulated in these animals. These lipases, LIPL-1-3, have been previously shown to promote lipophagy via catabolism of lipid droplets. Consistently, KTM-fed animals display reduced levels of triglycerides and smaller lipid droplet sizes. We propose that KTM-fed animals exhibit a fasting-like metabolic state, even in the presence of sufficient nutrient availability, possibly through induction of lipophagy. Elucidating the host metabolic response to KT consumption will provide unprecedented insight into how this popular fermented beverage may impact human health and inform its use in complementary healthcare plans.
2024-01-17 | GSE236037 | GEO
Project description:Background: Plasmapheresis/rituximab-based desensitization therapy has successfully reduced anti-ABO antibody levels and suppressed antibody-mediated rejection (AMR) in ABO-incompatible (ABOi) kidney transplantation (KT). However, high titers of anti-ABO antibodies in some patients are refractory to standard desensitization, leading to loss of KT opportunities or AMR. Methods: Eculizumab-based desensitization was used to rescue high-titer ABOi KT patients refractory to plasmapheresis/rituximab-based desensitization. Results: The initial titers of anti-ABO IgG antibodies in the two patients were 1:512 and >1:1024; the final pre-transplant titers after desensitization were 1:128 and 1:64. Both patients received eculizumab from the day of KT to two or four weeks post-KT and maintained stable renal function up to one-year post-transplantation without overt infectious complications, despite early episodes of suspicious AMR or borderline T cell-mediated rejection. Molecular phenotype analysis of allograft biopsies using the Banff Human Organ Transplant gene panel revealed that gene expression patterns in the ABOi KT with eculizumab group overlapped with those in the ABOi KT with AMR group more than in the ABOi KT without AMR group, except for complement pathway-related gene expression. Anti-ABO antibody titers decreased to low levels 1–3 months post-transplant in the eculizumab group in parallel with decreasing anti-B-specific B cells at this time point. Conclusions: Short-term eculizumab-based desensitization therapy is promising for rescuing ABOi KT recipients with unacceptably high anti-ABO antibody titers refractory to plasmapheresis-based desensitization therapy.
2024-10-15 | GSE274052 | GEO
Project description:It was analyzed whole genome microarray data to describe the changes in gene transcription profile in human MCF-7 cancer cells under the influence of fatty acid extracts from CLA-enriched and non-enriched egg yolks.Those results might be found useful in assessing the application of CLA-enriched egg as a nutraceutics in cancer prevention. Six-condition experiment: CLA, KT, cis9,trans11-CLA, trans10,cis12-CLA, KT+cis9,trans11-CLA and KT+trans10,cis12-CLA vs MCF-7 adenocarcinoma cell line. Two control of expreriment. Three biological replicates and three technical replicates.
2015-01-30 | E-GEOD-65397 | biostudies-arrayexpress
Project description:Microbiome and behaviour interactions in a naturally inbred fish
| PRJEB76690 | ENA
Project description:Effects of micropollutants on Asellus aquaticus and its microbiome
| PRJEB66514 | ENA
Project description:Cotton Leaf Curl Disease Suppression by Interspecies Microbiome Transplantation
| PRJEB68138 | ENA
Project description:Strains and Metagenomics of the contaminated soil microbiome, SYMBIOREM PROJECT
| PRJEB75648 | ENA
Project description:Proper chromosome segregation is required to ensure genomic and chromosomal stability. The centromere is a unique chromatin domain present throughout the cell cycle on each chromosome defined by the CENP-A nucleosome. Centromeres (CEN) are responsible for recruiting the kinetochore (KT) during mitosis, ultimately regulating spindle attachment and mitotic checkpoint function. Upregulation of many genes that encode CEN/KT proteins is commonly observed in cancer. Here, we show although FOXM1 occupies the promoters of many CEN/KT genes with MYBL2, occupancy is insufficient alone to drive the FOXM1 correlated transcriptional program. We show that CENP-F, a component of the outer kinetochore, functions with FOXM1 to coregulate G2/M transcription and proper chromosome segregation. Loss of CENP-F results in alteration of chromatin accessibility at G2/M genes, including CENP-A, and leads to reduced FOXM1-MBB complex formation. The FOXM1-CENP-F transcriptional coordination is a cancer-specific function. We observed that a few CEN/KT genes escape FOXM1 regulation such as CENP-C which when upregulated with CENP-A, leads to increased chromosome misegregation and cell death. Together, we show that the FOXM1 and CENP-F coordinately regulate G2/M gene expression, and this coordination is specific to a subset of genes to allow for proliferation and maintenance of chromosome stability for cancer cell survival.
2024-06-01 | GSE252506 | GEO
Project description:Proper chromosome segregation is required to ensure genomic and chromosomal stability. The centromere is a unique chromatin domain present throughout the cell cycle on each chromosome defined by the CENP-A nucleosome. Centromeres (CEN) are responsible for recruiting the kinetochore (KT) during mitosis, ultimately regulating spindle attachment and mitotic checkpoint function. Upregulation of many genes that encode CEN/KT proteins is commonly observed in cancer. Here, we show although FOXM1 occupies the promoters of many CEN/KT genes with MYBL2, occupancy is insufficient alone to drive the FOXM1 correlated transcriptional program. We show that CENP-F, a component of the outer kinetochore, functions with FOXM1 to coregulate G2/M transcription and proper chromosome segregation. Loss of CENP-F results in alteration of chromatin accessibility at G2/M genes, including CENP-A, and leads to reduced FOXM1-MBB complex formation. The FOXM1-CENP-F transcriptional coordination is a cancer-specific function. We observed that a few CEN/KT genes escape FOXM1 regulation such as CENP-C which when upregulated with CENP-A, leads to increased chromosome misegregation and cell death. Together, we show that the FOXM1 and CENP-F coordinately regulate G2/M gene expression, and this coordination is specific to a subset of genes to allow for proliferation and maintenance of chromosome stability for cancer cell survival.
2024-06-01 | GSE252598 | GEO