Project description:Whole Genome Metabolism of "Chroococcidiopsis thermalis"
This is a whole genome metabolism model of Chroococcidiopsis thermalis.
This model has been automatically generated by the SuBliMinaL Toolbox
and libAnnotationSBML using information coming from from KEGG (release 66, April 2013, accessed via the resource's web services interface) and, where relevant, augmented with metabolic pathway information extracted from MetaCyc (version 17.0, March 2013).
This model has been produced by the path2models
project and is currently hosted on BioModels Database
and identified by: BMID000000142554
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.
Project description:We investigated how Tfh cells contribute to the breakdown of peripheral immune tolerance and the formation of autoimmune lesions in a murine model of SS. Our results indicate a yet unreported mechanism of autoreactive response through Tfh cells in a SS model mouse, and it will be supportive for understanding the pathogenesis of autoimmunity. Overall design: Two-condition experiment, purified CD4+ CD25- T cells from spleen of non-thymectomied NFS/sld (Control) vs. purified CD4+ CD25- T cells from spleen of thymectomied NFS/sld (SS model).
Project description:described in: Pharmacokinetic-pharmacodynamic modeling of caffeine: Tolerance to pressor effects
Shi J, Benowitz NL, Denaro CP and Sheiner LB. ;Clin. Pharmacol. Ther. 1993 Jan;53(1):6-14. PMID:8422743;
We propose a parametric pharmacokinetic-pharmacodynamic model for caffeine that quantifies the development of tolerance to the pressor effect of the drug and characterizes the mean behavior and inter-individual variation of both pharmacokinetics and pressor effect. Our study in a small group of subjects indicates that acute tolerance develops to the pressor effect of caffeine and that both the pressor effect and tolerance occur after some time delay relative to changes in plasma caffeine concentration. The half-life of equilibration of effect with plasma caffeine concentration is about 20 minutes. The half-life of development and regression of tolerance is estimated to be about 1 hour, and the model suggests that tolerance, at its fullest, causes more than a 90 percent reduction of initial (nontolerant) effect. Whereas tolerance to the pressor effect of caffeine develops in habitual coffee drinkers, the pressor response is regained after relatively brief periods of abstinence. Because of the rapid development and regression of tolerance, the pressor response to caffeine depends on how much caffeine is consumed, the schedule of consumption, and the elimination half-life of caffeine.
Caffeine intake in this version is modelled as cups of coffee drunk at regular intervals (parameter t_interval). The amount of caffeine per cup is determined by the parameter cupsize. The body weight of the person drinking is given by the parameter bodyweight.
The even coffee cup occures delayed to the drinking of each cup, as the availability of the caffeine in the digestive tract is assumed to be delayed to the ingestion by the time t_lag.
Project description:Many plant researchers have applied genomic tools to model species to identify abiotic stress responsive genes that might be useful for improving stress tolerance in crops. However, it is unclear whether this translational approach will be successful given the complexity of abiotic stress tolerance. We carried out a functional genomic (ionomic, transcriptomic and metabolomic) comparison of three model and three forage species of the genus Lotus with varying tolerance to salinity. Transcriptome analysis showed that about 60 % of expressed genes were responsive to salt treatment in one or more of the six species tested, but less than 1 % was responsive in all genotypes. Therefore, genotype-specific responses overshadowed conserved transcriptional responses to salinity and represent an impediment to translational genomics. Fortunately, 'triangulation' from multiple species enabled the identification of a core set of conserved and tolerant-specific responses that could provide durable tolerance across genotypes.
Project description:To assess the effect of sleep deprivation on glucose metabolism and elucidate the mechanism, we established the mouse model wth C57BL/6J that is useful for the intervention on sleep deprivation associated diabetes and evaluate the liver metabolism and gene expression. Single six hours sleep deprivation induced increased hepatic glucose production assessed by pyruvate tolerance test and the hepatic triglyceride content was significantly higher in the sleep deprivation group than freely sleeping control group. Liver metabolites such as ketone bodies were increased in sleep deprivation group. Some gene expressions which associated with lipogenesis were increased. Overall design: In order to disturb the sleep, the cage changing method, the water platform method and the gentle handling method was performed using the C57BL/6J male mice. Intraperitoreal glucose tolerance tests were performed with each model. Using the model which shown impaired glucose tolerance by sleep deprivation, the plasma glucose and insulin levels were evaluated. Triglyceride content assay, metabolomics analysis, gene expression analysis by real-time PCR and gene microarray were also performed with liver tissue.