Ontology highlight
ABSTRACT:
PROVIDER: PRJNA577204 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10270478_1.fastq.gz | Fastqsanger.gz | |||
| SRR10270478_2.fastq.gz | Fastqsanger.gz | |||
| SRR10270479_1.fastq.gz | Fastqsanger.gz | |||
| SRR10270479_2.fastq.gz | Fastqsanger.gz | |||
| SRR10270480_1.fastq.gz | Fastqsanger.gz |
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Project description:As one of the most important environmental factors, heat stress (HS) has been found to affect various biological activities of organisms such as growth, signal transmission, primary metabolism and secondary metabolism. Ganoderma lucidum has become a potential model system for evaluating how environmental factors regulate the secondary metabolism of basidiomycetes. Previous research showed that HS can induce the biosynthesis of ganoderic acids (GAs). In this study, we found the existence of hydrogen sulfide in Ganoderma lucidum; moreover, HS increased GAs biosynthesis and could affect the hydrogen sulfide content. We found that sodium hydrosulfide (NaHS), an exogenous donor of hydrogen sulfide, could revert the increased GAs biosynthesis elicited by HS. This result indicated that an increased content of hydrogen sulfide, within limits, was associated with HS-induced GAs biosynthesis. Our results further showed that the GAs content was increased in CBS-silenced strains and could be reverted to WT strain levels by the addition of NaHS. Transcriptomic analyses indicated that that H2S can affect various intracellular signal pathways and physiological processes in G. lucidum. Further studies showed that H2S could affect the intracellular calcium concentration and thus regulate the biosynthesis of GAs. This study demonstrated that hydrogen sulfide is involved in the regulation of secondary metabolic processes induced by heat stress in filamentous fungi.
2021-10-12 | GSE121270 | GEO
Project description:Interventions: Case series:nill;The control group:nill
Primary outcome(s): Hydrogen sulfide;Pathological diagnosis
Study Design: Case-Control study
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Project description:The aim of this experiment was to determine how exposure of Hydrogen sulfide impacts gene expression in Mycobacterium tuberculosis. RNA was isolated from actively growing mycobacterial cells (0.6-0.8 OD600) using Trizol according to established protocols (27). Briefly, cells were exposed to 25 µM GYY4137 for 1 hr under carefully controlled conditions (n=3/group) and RNA isolated. Unexposed cells received spent GYY4137 (without any capacity to produce Hydrogen sulfide).
2020-01-04 | E-MTAB-7421 | biostudies-arrayexpress
Project description:Hypertension is a major risk factor for chronic kidney disease (CKD) and renal inflammation is an integral part in this pathology. Hydrogen sulfide (H2S) has been shown to mitigate renal damage through reduction in blood pressure and reactive oxygen species; however, the exact mechanisms are not clear. While several studies have underlined the role of epigenetics in renal inflammation and dysfunction, the mechanisms through which epigenetic regulators play role in hypertension are not well defined. We used microarrays to detail the global programme of gene expression underlying hypertension in the kidney and how hydrogen sulfide supplementation alleviates these effects.
2016-12-23 | GSE92857 | GEO
Project description:Stress response of Methylococcus capsulatus str.Bath toward hydrogen sulfide (H2S) was investigated via physiological study and transcriptomic profiling. M. capsulatus (Bath) can grow and tolerate up to 0.75%vol H2S in headspace. Vast change in pH suggests biological relevant sulfide oxidation. Dozens of H2S-sensitive genes were identified from comparison of cell transcriptome in different H2S concentrations. Mc sulfide quinone reductase (SQR) and persulfide dioxygenase were found to be active during sulfide detoxification. Moreover, xoxF, a novel lanthanide(Ln)-dependent methanol dehydrogenase (MDH) was overexpressed in H2S while mxaF, a calcium-dependent MDH, was down-regulated, and such MDH switch phenomenon is also well known to be induced by addition of lanthanide via an as-yet-unknown mechanism. Activities in quorum sensing and RND efflux pump also suggest their role in sulfide detoxification, and might provide insight on the xoxF/mxaF switch mechanism.
2021-12-24 | GSE192351 | GEO
Project description:Inflammatory Bowel Disease (IBD) is a term describing a collection of conditions characterised by chronic inflammatory disorder of the gastrointestinal tract involving an inappropriate immune response to commensal microorganisms in a genetically susceptible host. Four kiwifruit extracts, aqueous and ethyl acetate extracts of gold kiwifruit (Actinidia chinensis) or green kiwifruit (A. deliciosa), have previously demonstrated anti-inflammatory activity using in vitro models of IBD. This study examined whether these kiwifruit extracts had immune modulating effects in vivo against inflammatory processes known to be increased in patients with IBD. KFEs were used as a dietary intervention in Il10-/- mice (an in vivo model of IBD) and the C57BL/6J background strain in a 3 x 2 factorial design. While all Il10-/- mice developed significant colonic inflammation compared to the C57BL/6J mice, this was not affected by the inclusion of KFE in the diet. Whole genome gene and protein expression level profiling indicated that KFEs influenced immune signalling pathways and metabolic processes within the colonic tissue; however, the effects were subtle. In particular, adaptive immune pathways were reduced by three out of four kiwifruit extracts, with greater reduction seen in the C57BL/6J mice. This suggests that while immune-modulating activity was present in vivo, KFEs did not reduce inflammatory processes relevant to IBD. Experimental design. Two experiments were conducted, one using extracts from gold kiwifruit and one using extracts from green kiwifruit. Within each experiment, both Il10-/- and C57 mice were randomly divided into three diet treatment groups, to ive the following 12 treatments: 1) Gold Kiwifruit Experiment, C57BL/6J mice, Control diet (AIN-76A), 2) Gold Kiwifruit Experiment, C57BL/6J mice, Aqueous Kiwifruit Extract Supplemented Diet (AIN-76A + 5% Aqueous KFE) 3) Gold Kiwifruit Experiment, C57BL/6J mice, Ethyl Acetate Kiwifruit Extract Supplemented Diet (AIN-76A + 0.11% Ethyl Acetate KFE) 4) Gold Kiwifruit Experiment, Il10-/- mice, Control diet (AIN-76A), 5) Gold Kiwifruit Experiment, Il10-/- mice, Aqueous Kiwifruit Extract Supplemented Diet (AIN-76A + 5% Aqueous KFE) 6) Gold Kiwifruit Experiment, Il10-/- mice, Ethyl Acetate Kiwifruit Extract Supplemented Diet (AIN-76A + 0.11% Ethyl Acetate KFE) 7) Green Kiwifruit Experiment, C57BL/6J mice, Control diet (AIN-76A), 8) Green Kiwifruit Experiment, C57BL/6J mice, Aqueous Kiwifruit Extract Supplemented Diet (AIN-76A + 5% Aqueous KFE) 9) Green Kiwifruit Experiment, C57BL/6J mice, Ethyl Acetate Kiwifruit Extract Supplemented Diet (AIN-76A + 0.11% Ethyl Acetate KFE) 10) Green Kiwifruit Experiment, Il10-/- mice, Control diet (AIN-76A), 11) Green Kiwifruit Experiment, Il10-/- mice, Aqueous Kiwifruit Extract Supplemented Diet (AIN-76A + 5% Aqueous KFE) 12) Green Kiwifruit Experiment, Il10-/- mice, Ethyl Acetate Kiwifruit Extract Supplemented Diet (AIN-76A + 0.11% Ethyl Acetate KFE) Six biological replicates were analysed from each treatment group, except for groups 3 and 7 where five replicates were analysed due to array quality issues with the sixth replicate. Each replicate contained mRNA from one mouse. A reference design was used, where each slide was hybridised with mRNA from one sample (green channel) and mRNA from a common reference pool (red channel).
2011-03-05 | E-GEOD-27684 | biostudies-arrayexpress
Project description:In this study we investigated the effect of two different agents producing hydrogen sulfide (H2S) on LPS-induced inflammatory mediators such as TNFa, NO and ROS. The agents (GYY4137 and sodium hydrosulfide) applied differ significantly by the kinetics of H2S release. In the investigation we compared the effects of H2S release on the LPS-induced inflammation exploring SH-SY5Y human neuroblastoma cell line and human promonocytic cell line, THP-1. Our data clearly show that both hydrogen sulfide producing agents significantly reduced the production of the investigated proinflammatory mediators when applied both before and after LPS administration. Furthermore, transcriptomic studies demonstrated that H2S release ameliorates the expression of multiple proinflammatory genes up-regulated due to LPS administration. However, the pattern of changes observed in transcriptome differs dramatically depending on the time of H2S release (before or after LPS-challenge).
2019-07-09 | GSE133942 | GEO
Project description:The purpose of this study is to detect the concentration of various gases，including hydrogen, methane, hydrogen sulfide, nitric oxide in different parts of the digestive tract by a safe and direct method, and to establish a human digestive tract gas profiles. Analyze the differences in gas components in different segments of the digestive tract in patients with different diseases, and analyze the correlation between specific gases and digestive tract diseases and non-specific symptoms.
| 14702 | ecrin-mdr-crc
Project description:Hydrogen sulfide (H2S) is well known to cause irritation and damage to airway following inhalation, but the mechanism by which H2S contributes to airway toxicity is unclear. We apply transcriptomics to demonstrate the possible effects, obtain valuable information about adverse health effects following H2S exposure and to study the molecular mechanisms of the gas toxicity in trachea.
2022-05-27 | GSE131820 | GEO
Project description:Hydrogen sulfide (H2S), a metabolic endproduct of sulfate-reducing bacteria in the large intestine, represents a genotoxic insult to the colonic epithelium, which may also be linked with chronic disorders such as ulcerative colitis and colorectal cancer. The present study defined the early (30 minutes) and late (4 hours) response of non-transformed human intestinal epithelial cells (FHs 74 Int) to sulfide. We measured the genotoxicity of Na2S using the single cell gel electrophoresis (comet) assay. Changes in gene expression were analyzed after exposure to a genotoxic–but not cytotoxic–concentration of sulfide (500 μM Na2S) using pathway specific quantitative RT-PCR gene arrays
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