Similar Datasets
Project description:Aliarcobacter butzleri ED-1 Genome sequencing
| PRJDA61719 | ENA
Project description:Hypsibius dujardini strain:ED Genome sequencing
| PRJEA78171 | ENA
Project description:Diaphorobacter sp. ED-3 Genome sequencing and assembly
| PRJNA915479 | ENA
Project description:Escherichia coli strain:ED collection Raw sequence reads
| PRJNA643386 | ENA
Project description:(Erectile dysfunction) ED during the radical prostatectomy (RP) treatment is caused by surgical injury of the cavernous nerve which is the final neuronal pathways of penile erection. We performed microarray experiment focused on theto understanding the gene signature alteration in the corporal cavernous tissue of the CNI-induced ED rat model.
2012-12-31 | GSE31247 | GEO
Project description:USP21 belongs to ubiquitin specific protease (USP) family. To dissect the molecular mechanisms that regulated by USP21 overexpression in PDAC cells, we conducted RNA-seq analysis of iKPC PDAC cells overexpressing wild-type USP21 (WT-USP21) and enzyme dead USP21 (ED-USP21).
2019-09-04 | GSE134686 | GEO
Project description:Enterococcus devriesei strain:Ed-CK-24 Genome sequencing
| PRJNA1099446 | ENA
Project description:Aliarcobacter butzleri strain:ED-1 | isolate:Okinawa Genome sequencing
| PRJNA553057 | ENA
Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress
Project description:Purpose: Previously, we have reported the effectiveness of elemental diet (ED) Elental® against radiotherapy- or chemoradiotherapy- induced oral mucositis (Support Care Cancer 2016, Mol Clin Oncol 2019). However, administration of additional nutrition or ED in oral cancer patients might also provide extra nutrition for cancer cells, which could result in cancer development. At present, it is still unclear whether the beneficial effect of ED can be expected to surpass its possible harmful effect on oral cancer treatment. In the present study, we tried to clarify whether Elental® has different effects on human oral keratinocyte (HOK) cells compared to oral squamous cell carcinoma (OSCC) cells (HSC2). Method: Gene expression profiles of HOK cells and HSC2 cells treated with Elental® were generated by deep sequencing. Results: Whole transcriptome analysis data suggested that Elental® helped in the proliferation and survival of HOK through the induction of ERK. Moreover, Elental® added stress to HSC2 through the induction of endoplasmic reticulum stress response marker, BiP. Our results showed that Elental® might add stress to HSC2, and provide growth stimulation to HOK. Conclusion: Whole transcriptome analysis showed different gene expression profile between HOK cells and HSC2 cells treated with Elental®, suggesting that effects of Elental® might differ between normal oral cells and oral cancer cells.
2021-07-31 | GSE151420 | GEO