Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30979700.fastq.gz | Fastqsanger.gz | |||
| SRR30979701.fastq.gz | Fastqsanger.gz | |||
| SRR30979702.fastq.gz | Fastqsanger.gz | |||
| SRR30979703.fastq.gz | Fastqsanger.gz | |||
| SRR30979704.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:We fed control mice and Slc7a11-LTG mice methionine and Choline Deficient (MCD) to induce NASH. Whole-genome RNA sequencing were then performed in the livers of control and LTG mice fed with MCD.
2025-09-09 | GSE213182 | GEO
Project description:Malformations of cortical development (MCD) are present in up to 40% of children with pharmacoresistant epilepsy. Although epilepsy surgery can be successful in a subset of children, not all forms of MCD are operable. Understanding the genetic and neurobiological mechanisms underlying MCD and MCD-related epilepsy are necessary for the development of novel anti-epilepsy drugs. The tish (telencephalic internal structural heterotopia) rat is a unique model of MCD and spontaneous seizures, but the underlying genetic mutation has been, heretofore, unknown. DNA and RNA-sequencing revealed that a deletion encompassing a previously unannotated exon markedly diminished EML1 transcript and protein abundance in the tish brain. Developmental electrographic characterization of the tish rat demonstrated spontaneous spike-wave discharge (SWD) bursts beginning as early as postnatal day (P) 17. A dihybrid cross demonstrated that the mutantEml1 allele segregates with the observed dysplastic cortex and SWD bursts in monogenic autosomal recessive frequencies. Our data link the development of the bilateral, heterotopic dysplastic cortex of the tish rat to a mutation in Eml1 and provide a novel rat model of MCD.
2020-03-28 | GSE147663 | GEO
Project description:The microRNAs expression was markedly altered with the MCD diet. Using a custom microarray platform, we analyzed the expression levels of 1135 mouse microRNA probes in liver tissue that were fed MCD diet.
2015-03-01 | E-GEOD-55593 | biostudies-arrayexpress
Project description:<p>Nonalcoholic fatty liver disease (NAFLD) is a major public health problem due to the high incidence affecting approximately one-third of the world’s population. NAFLD is usually linked to obesity and excessive weight. A subset of patients with NAFLD express normal or low body mass index; thus, the condition is called nonobese NAFLD or lean NAFLD. However, patients and healthcare professionals have little awareness and understanding of NAFLD in nonobese individuals. Furthermore, preclinical results from nonobese animal models with NAFLD are unclear. Gut microbiota and their metabolites in nonobese/lean NAFLD patients differ from those in obese NAFLD patients. Therefore, we analyzed the biochemical indices, intestinal flora and intestinal metabolites in a nonobese NAFLD mouse model established using a methionine-choline deficient (MCD) diet. The significantly lean MCD mice had a remarkable fatty liver with lower serum triglyceride and free fatty acid levels as well as higher alanine transaminase and aspartate transaminase levels than normal mice. 16s RNA sequencing of fecal DNA showed that the overall richness and diversity of the intestinal flora decreased in MCD mice, whereas the Firmicutes/Bacteroidota ratio was increased. <em>g_Tuzzerella, s_Bifidobacterium pseudolongum</em> and <em>s_Faecalibaculum rodentium</em> were the predominant species in nonobese NAFLD mice. Fecal metabolomics using LC-MS/MS revealed the potential biomarkers for the prognosis and diagnosis of nonobese NAFLD, including high levels of tyramine glucuronide, 9,12,13-TriHOME and pantetheine 4'-phosphate, and low levels of 3-carbamoyl-2-phenylpropionaldehyde, N-succinyl-L,L-2,6-diaminopimelate, 4-methyl-5-thiazoleethanol, homogentisic acid and estriol. Our findings could be useful to identify and develop drugs to treat nonobese NAFLD and lean NAFLD.</p>
2024-02-27 | MTBLS9365 | MetaboLights
Project description:Metabolic dysfunction-associated steatohepatitis (MASH) is a leading cause of cirrhosis and liver related mortality, but it remains unclear how nutrient stresses drive coordinated transcriptional remodeling in the pathogenesis of MASH. Clinical studies reported that methionine and choline deficiency (MCD) promotes chronic liver diseases. Multiple types of MCD diets have been adopted to establish MASH mouse models. However, how methionine and choline deficiency modulates cell-intrinsic transcriptional responses across parenchymal and nonparenchymal liver cell types, and whether these effects recapitulate human MASH, remains unclear. Here, we generated a customized MCD cell culture medium to induce nutrient stress in HepG2 cells, endothelial cells, bone marrow derived macrophages, and hepatic stellate cells (HSCs). RNA sequencing was performed to characterize transcriptional regulations in response to MCD. Across cell types, lack of methionine and choline induced transcriptional program of inflammatory and stress response and suppressed metabolic pathways and cell-cycle progression, suggesting a proliferation pause as a compensatory stress-adaptive response that preserves cell viability and essential functions. In addition to these shared responses, MCD stress also caused distinct cell type-specific outputs that could contribute to the pathogenesis of MASH. Integrated analysis of these datasets with human MASH liver single nucleus transcriptomic data demonstrated that MCD condition recapitulates multiple pathophysiological features of human MASH, including the elevated inflammation, enhanced hepatocyte death, disrupted redox balance, altered metabolic homeostasis, and HSC activation. These findings not only uncover how MCD stress promotes MASH progression, but also provide a conceptual basis to guide future use of MCD diet-induced models in MASH studies.
2026-03-25 | GSE319635 | GEO
Project description:To search for biomarkers to differentiate Adult-Onset Steroid Sensitive focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD). Compared the profiles of glomerular transcriptomes between patients with FSGS and patients with MCD using microarray analysis. This dataset is part of the TransQST collection.
2017-01-04 | E-GEOD-69814 | biostudies-arrayexpress