B2d53baf-ec6d-4530-b0df-8266eddd6c00 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001004965 | EGA |
REPOSITORIES: EGA
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Project description:Model dependent on changing parameters.
There are 3 disease states: Healthy, Sick, and Dead, where the Dead state is terminal.
The yearly transition probabilities are:
Healthy to Dead: Age/1000; Healthy to Sick: according to function F1 depending on Age and Male parameters; Sick to Healthy: 0.1; Sick to Dead: according to function F2 depending on Age and Male parameters. Pre-Transition Rules: Age increased by 1 each cycle.
Initial conditions: Healthy = (50 Male, 50 Female with Age =1,2,…,50 for each individual), Sick = (0,0) and Dead = (0,0).
Output: Number of men and women in each disease state for years 1-10 and their ages in each state.
2019-01-30 | MODEL1803120005 | BioModels
Project description:To determine whether extracellular vesicles were also present in human disease, we isolated and evaluated extracellular vesicles from synovial fluid from normal and OA patients at relatively advanced ages (70 - 80 years). Here we report the altered expression of synovial fluid extracellular vesicles-derived miRNAs in osteoarthritis compared to normal patients with age-relate degeneration to investigate potential biomarkers for OA diagnosis. The OA donors had clinical evidence of OA based on pain that led to total joint arthroplasty.
2019-02-18 | GSE126677 | GEO
Project description:Model with functions depending on Age, Male, BP (Blood Pressure).
There are 3 disease states: Healthy, Sick, and Dead, where the Dead state is terminal. The yearly transition probabilities are: Healthy to Dead: Age/1000; Healthy to Sick: According to function F1 depending on Age and Male and BP; Sick to Healthy: 0.1; Sick to Dead: according to function F2 depending on Age and Male.
Pre-Transition Rules: Age increased by 1 and BP by Age/10 each simulation cycle. Post-Transition Rules: Treatment = BP>140 , becomes 1 when BP crosses 140 threshold; BP =BP-Treatment*10 , meaning a drop of 10 once treatment is applied; CostThisYear = Age + \Treatment*10 , cost depends on age and if treatment was taken; Cost= Cost + CostThisYear , it accumulates cost over time.
Initial conditions: Healthy = (50 Male, 50 Female with Age =1,2,...,50 for each individual), BP =120, Sick = (0,0) and Dead = (0,0).
Output: Number of men and women in each disease state for years 1-10 and their ages and costs in each state. A stratified report by male and female and young – up to age 30 and old above age 30 is produced.
2019-01-30 | MODEL1803120006 | BioModels
Project description:Breast cancer is an age-related cancer in women with two peaks, one at 50 and one at 70 years of age. Here we used two conditional genetically engineered mouse models of breast cancer risk to study mammary gland transcriptional changes that occur as female mice age from 12 to 30 months of age, paralleling aging from 58 to 85 years of age in women. The two models express either mammary epithelial cell-targeted Estrogen Receptor (ER) alpha (Esr1) or Aromatase (CYP19A1A) over-expression beginning at age 12 or 18 months of age. Both of these risk factors increase estrogen pathway signaling, either directly though the receptor or by increasing local estrogen production. The goals of the study are to determine how quickly significant transcriptional changes occur in the mammary gland following transgene induction, to determine how the transcriptome becomes modified as the mice age past reproductive senescence through old and very old life stages, and to identify similarities and differences in the transcriptomes between the two risk conditions at different ages and conditions. The first specific objective of this transcriptome-based study is to identify significantly differentially expressed genes within each model between different ages and times of transgene induction. This includes transcriptional changes induced by 1 week, 6, 12 and 18 months of transgene expression with transgene expression initiated at age 12 months as well as transcriptional changes induced by 1 week and 6 months of transgene expression initiated at age 18 months. The second specific objective is to compare the two models at different ages (12, 18, 24 and 30 months of age) and different transgene induction times (6, 12 and 18 months) to identify differentially expressed genes between the models. Comparative control mice from each model include age 18- and 24-month-old mice without transgene induction.
2022-08-22 | GSE201767 | GEO
Project description:Sevoflurane is the most commonly used general anesthetic in pediatric surgery, but it has the potential to be neurotoxic. Previous research found that long-term or multiple sevoflurane exposures could cause cognitive deficits in newborn mice but not adult mice, whereas short-term or single inhalations had little effect on cognitive function at both ages. The mechanisms behind these effects, however, are unclear. In the current study, 6- and 60-day-old C57bl mice in the sevoflurane groups were given 3% sevoflurane plus 60% oxygen for three consecutive days, each lasting 2 hours, while those in the control group only got 60% oxygen. The cortex tissues were harvested on the 8th or 62nd day. The tandem mass tags (TMT)pro-based quantitative proteomics combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysi were applied to analyze the influences of multiple sevoflurane anesthesia on the cerebral cortex in mice with various ages. A total of 6247 proteins were measured using the combined quantitative proteomics methods of TMTpro-labeled and LC-MS/MS, 443 of which were associated to the age-dependent neurotoxic mechanism of repeated sevoflurane anesthesia. Our findings would help to further the mechanistic study of age-dependent anesthetic neurotoxicity and contribute to seek for effective protection in the developing brain under general anesthesia.
2022-12-08 | PXD037294 | Pride
Project description:Rhodopsin P23H mutation is the most comment mutation causing autosomal dominant retinitis pigmentosa in the USA. The goal of this project is to compare the transcriptome changes of the Rhodopsin P23H knock-in mouse model of adRP to the wildtype control at different ages. The transcriptomic profile will help us understand the molecular events along the pathophysiology of reititis pigmentosa in this mouse model. We include the RNA seq data of Rhodopsin P23H heterozygous mouse retinas at 1, 3 and 6 months of age to compare with age-matched wildtype mouse retinas. N=3 and each sample is from an individual animal.
2024-12-01 | GSE281959 | GEO
Project description:Low glutathione levels are associated with crystallin oxidation in age-related nuclear cataract (ARNC). To understand the role of cysteine residue oxidation, we used the novel approach of comparing human cataracts with glutathione-depleted LEGSKO mouse lenses for intra- vs. intermolecular disulfide crosslinks using 2D-PAGE and proteomics, and then systematically identified in vivo and in vitro all disulfide forming sites using ICAT labeling method coupled with proteomics. Crystallins rich in intramolecular disulfides were abundant at young age in human and WT mouse lens but shifted to multimeric intermolecular disulfides at older age. The shift was ~4x accelerated in LEGSKO lens. Most cysteine disulfides in β-crystallins (except βA4 in human) were highly conserved in mouse and human and could be generated by oxidation with H2O2, while γ-crystallin oxidation selectively affected γC23/42/79/80/154, γD42/33 and γS83/115/130 in human cataracts, and γB79/80/110, γD19/109, γF19/79, γE19, γS83/130 and γN26/128 in mouse. Analysis based on available crystal structure suggests that conformational changes are needed to expose C42, C79/80, C154 in γC; C42, C33 in γD, and C83, C115 and C130 in γS. In conclusion, while the β-crystallin disulfidome is highly conserved in ARNC and LEGSKO mouse, and reproducible by in vitro oxidation, some of the disulfide formation sites in γ-crystallins necessitate prior conformational changes. Overall, the LEGSKO mouse model is closely reminiscent of ARNC.
2015-10-16 | PXD002658 | Pride
Project description:Aging was long assumed to be a passive and stochastic process caused by random damage accumulation, however，such theories fail to explain the program-like features of the aging process. Measuring the aging process in C. elegans at individual level provides an opportunity to analyze both the programmed (age-related changes at population level) and stochastic (inter-individual differences in isogenic population) components during the aging process. Here, we performed quantitative proteomic analyses on more than 150 worm individuals of different ages and aged individuals with different mobility. The analysis of inter-individual variations helps dissect the programmed and stochastic components during the aging process, and key proteins underlying the lifespan plasticity among the genetically identical worm individuals. Using a high temporal resolution single worm proteomic landscape, we found that the aging process was non-linearly progressed, with each stage marked by distinct age-related changes. The fast-aging individuals are depleted with such secreted proteins and over-activation of lysosome degradation processes, providing a first molecular link for the programmed enhanced offspring growth and death of the parent individual. This mechanistic link indicates that programmed events at least in part explain the heterogeneity of adult aging.
2023-11-14 | PXD039330 | Pride
Project description:The Uppsala Longitudinal Study of Adult Men (ULSAM) study is an ongoing, longitudinal, epidemiologic study started in 1970 and based on men born between 1920 and 1924 in Uppsala, Sweden which were invited to participate at age 50 (N=2,841) [PMID: 9484991]; 81.7% (N=2,322) participated. Individuals were reinvestigated at the ages of 60, 70, 77, 82 and 88 years. Information collected includes a medical questionnaire, blood pressure and anthropometric measurements, glucose tolerance test and 24-hour ambulatory blood pressure. Metbaolomics has been performed on plasma samples from age 70. In the final analysis we included samples from 1,138 individuals.
2015-03-23 | MTBLS124 | MetaboLights
Project description:ST-segment elevated myocardial infarction (STEMI) is one of the most severe forms of cardiovascular heart diseases. In the present study, we aim to describe differential expressed plasma exosome-miRNAs in patients with post-STEMI 3-6 months. Methods: Consecutive patients with ages from 40 to 80 years and 25 males among them 3-6 months after STEMI (n=11) were compared to sex-matched healthy control (n=10). The mean age of the patient was 64.71±10.40 years and 89.2% were male. Compared to the healthy control group, the plasma exosome-miRNAs were assessed by using microarray assay (IIIumnia Hiseq 2500). Profile of plasma exosome-miRNAs related to heart diseases was established both in the patient and control groups. The specificity of the lowest expressed exosome-miRNAs for all subjects was evaluated by using a quantitative real-time polymerase chain (qPCR). plasma exosomes miRNAs were obtained from STEMI patients after 3-6 months and healthy subjects
2022-06-29 | GSE185729 | GEO