Lihua Qiu Similar Datasets
Project description:label-free raw data of heart and muscle samples from yellowfin tuna
2021-11-19 | PXD029854 | iProX
Project description:Thiele2013 - Heart muscle myocytes
The model of heart muscle myocytes metabolism is derived from the community-driven global reconstruction of human metabolism (version 2.02, MODEL1109130000
).
This model is described in the article:
A community-driven global reconstruction of human metabolism.
Thiele I, et al
.
Nature Biotechnology
Abstract:
Multiple models of human metabolism have been reconstructed, but each represents only a subset of our knowledge. Here we describe Recon 2, a community-driven,
consensus 'metabolic reconstruction', which is the most comprehensive representation of human metabolism that is applicable to computational modeling. Compared
with its predecessors, the reconstruction has improved topological and functional features, including ~2x more reactions and ~1.7x more unique metabolites. Using
Recon 2 we predicted changes in metabolite biomarkers for 49 inborn errors of metabolism with 77% accuracy when compared to experimental data. Mapping metabolomic
data and drug information onto Recon 2 demonstrates its potential for integrating and analyzing diverse data types. Using protein expression data, we automatically
generated a compendium of 65 cell type-specific models, providing a basis for manual curation or investigation of cell-specific metabolic properties. Recon 2 will
facilitate many future biomedical studies and is freely available at http://humanmetabolism.org/.
This model is hosted on BioModels Database
and identified by: MODEL1310110056
.
To cite BioModels Database, please use: BioModels Database: An enhanced,
curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer
to CC0 Public Domain Dedication
for more information.
2005-01-01 | MODEL1310110056 | BioModels
Project description:To investigate the pathological significance of excess oxidative stress in the heart, we generated heart/muscle-specific manganese superoxide dismutase (MnSOD) -deficient mice on a C57BL/6 background using the Cre-loxP system uder the control of the muscle reatin kinase (MCK) promoter. The mutant mice developed progressive congestive heart failure with dilated cardiomyopathy and physical disability and died with a median survival rate of 15.4 ± 4.0 weeks. The pathological changes in our model were compatible with human cardiac aging. To investigate the transcriptional alterations in the mutant heart, we carried out an Affymetrix microarray analysis for comparison between the mutant and normal heart at 16 weeks of age. Keywords = Mn-SOD Keywords = manganese superoxide dismutase Keywords = knockout Keywords = heart failure Keywords = heart Keywords = muscle Keywords: parallel sample
2005-02-05 | GSE2236 | GEO
Project description:PRM analysis of RPL39L, RPL10L and RPL3L in 9 mouse tissues, including testis, fat, brain, liver, kidney, lung, skeletal muscle, heart and spleen; PRM analysis of RPL39 and RPL39L, RPL10 and RPL10L, and RPL22 and RPL22L1 in testicular cells; PRM analysis of RPL39L and RPL39 in RibosomeRPL39L-/- and wild type mouse spermatocytes and spermatids; PRM analysis of 17 down-regulated proteins and 1 unchanged protein (DYNC1LI2) in RibosomeRPL39L-/- testes; PRM analysis of RPL39 and RPL39L in GC-1 ribosomes, and RibosomeRPL39L-/- and wild type N2a ribosomes, Consistency between the observed and expected signal ratios of the light and heavy peptides by PRM in serial dilution experiments. Bovine serum albumin (BSA) as a negative control.
2022-09-30 | PXD020922 | Pride
Project description:Providencia alcalifaciens strain:PRM-2 Genome sequencing and assembly
| PRJNA437544 | ENA
Project description:Heart failure is a multisystem syndrome caused by structural and functional defects in multiple tissues. The study aims to identify differentially regulated genes in skeletal muscle of heart failure patients. Here, we obtained biopsies from the pectoralis major muscle and performed RNA sequencing to profile the gene expression patterns from six heart failure patients and three healthy controls.
2020-09-07 | E-MTAB-8531 | biostudies-arrayexpress
Project description:TK2 deficiency causes severe mtDNA depeltion in several tissues, including skeletal muscle and heart. TK2 knockout mice grow slower and their skeletal muscles appeared significantly underdeveloped, whereas heart was close to normal size. We used microarrays in order to compare the transcriptomes in skeletal muscle and heart tissue of 11 days-old TK2 knockout pups with the sames tissues of wild-type pups at the same age. We collected skeletal muscle from the hind limb and hearts of three 11 days-old TK2 knockout and three wild-type pups and extracted total RNA. These RNA samples were used for hybridization in Affymetrix arrays.
2012-07-30 | E-GEOD-38449 | biostudies-arrayexpress
Project description:Compairsion of transcriptional profiles of heart and skeletal muscle tissue of fetal rhesus monkey exposed to maternal Bisphenol A or vehicle during early or late gestaion. Maternal exposure to the endocrine disrupting chemical, bisphenol A (BPA) affects the development of multiple organ systems in rodents and monkeys. However, effects of BPA exposure on cardiac and skeletal muscle development have not been assessed. Given that maternal BPA crosses placenta and reaches developing fetus, examining the physiological consequences of gestational exposure during development is of research significance. Therefore, we evaluate the effects of daily, oral BPA exposure of pregnant rhesus monkeys (Macaca mulatta) on the fetal heart and skeletal muscle transcriptome. Pregnant monkeys were administered daily oral doses (400 M-BM-5g/kg body weight) of BPA during early (50 M-bM-^@M-^S100 M-BM-1 2 days post conception, dpc) or late (100 M-BM-1 2 dpc - term), gestation. At the end of treatment, fetal heart tissues; left ventricle (LV), right ventricle (RV), left atrium (LA), right atrium (RA) and skeletal muscle; biceps femoris (BFM), were collected. Transcriptome expression was assessed using genome-wide microarray in each of the tissues and compared paired-wise between the BPA and matched control fetuses. Our results show that maternal BPA exposure alters transcriptional profile of several coding and non-coding genes in fetal heart and skeletal muscle. Pregnant rhesus monkey were administered a daily oral dose of 400 M-NM-<g/kg. body weight of Bisphenol A (BPA) or vehicle (CON) either during early (50M-bM-^@M-^S100 M-BM-1 2 days) or late (100 M-BM-1 2 daysM-bM-^@M-^Sterm) gestation. Gene expression profiles of each of the heart chambers (left ventricle, LV; right ventricle, RV; left atrium, LA; and right atrium, RA) and skeletal muscle (biceps femoris, BFM) were analyzed using microarrays and compared between the BPA exposed and matched control fetuses. A total of 12 samples were analyzed for each tissue; LV, RV, LA, RA and BFM. This includes 6 samples at each time period (early vs. late gestation) and 3 biological replicates for each treatment (BPA, n=3; control, n=3).
2014-07-01 | E-GEOD-53393 | biostudies-arrayexpress
Project description:RNA interference (RNAi) is a promising gene therapy strategy for targeting dominant mutations. This therapy leverages small hairpin RNAs (shRNAs) to knock down gene expression; however, delivery of too much shRNA can disrupt the processing of endogenous microRNAs (miRNAs), and lead to toxicity. In this study, we sought to understand the effect that excessive shRNAs have on muscle miRNAs by transducing several constructs in mice and performing small RNA sequencing on their muscle and liver tissues. We found that shRNA expression was highest in the heart, and that when shRNAs accumulated to about 27% of total small RNAs, mice experienced substantial cardiomyopathy. At this level in the heart, shRNAs in other muscle tissues were only ~1.8-7.6% of total miRNAs. Regardless of treatment, the predominant heart microRNAs remained stable across samples, while the lower-expressed miR-451 – one of the only microRNAs processed in a Dicer-independent manner – changed in direct correlation with shRNA level and toxicity. Our data suggest that certain muscle miRNAs compete with exogenous shRNAs, leading to the observed cardiomyopathy, and that the mechanism of cardiotoxicity in these mice in response shRNA treatment was in contrast to what has been previously shown in the liver. Quantifying microRNA profiles after excessive shRNA delivery illuminates the host response to rAAV-shRNA, allowing for safer and more robust therapeutic gene knockdown, and gives us insight into the basic functions of muscle microRNAs.
2019-12-30 | GSE129896 | GEO
Project description:Caspases, proteolytic enzymes involved in cell death could play a role independent of cell death in the developing heart in this datasheet we include the expression data obtained from dissected heart muscle (ventricle) of wild type mice and mice knockout for caspase-3,-7 24 samples. genotypes: wild type and cardiac-specific conditional caspase-3 and -7 KO. Age: 1-2-day-old; 30-day-old (aprox 3 male, 3 female/genotype and age).
2015-12-31 | E-GEOD-63023 | biostudies-arrayexpress