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There is a specific antagonism between an aging organism and neoplasia, in which the tumor is considered to influence the local tissue. It returns to some atavistic features, including the thermodynamic approach (2nd law of thermodynamics, Fig. 1), causing the rejuvenation of the surrounding tissue. The existence of various theories of oncogenesis entitles their supplementation with the theory of inflammaging: an entropic inflammation that can potentially have an indirect influence on the oncogenesis. This theory covers the effects of various causes of aging, including genetically programmed changes, telomere dependent processes and damage of genome, epigenome and proteome particles. The paper describes the patomechanism of inflammaging, including the role of mitochondria (point mutations and deletions especially in mtDNA), oxidative stress with overproduction and accumulation of free radicals and NFkB factor (nuclear factor kappa-light chain-enhancer of activated B cells) and the possibility of the influence of inflammaging on oncogenesis (Fig. 2). The inflamma-ging is programmed by hypothalamus using the immune-neuro-endocrine system, including gonadotropin releasing hormone (GnRH) that inhibits the NFkB factor with the inactivation of kinase IKK-beta. Regardless of that, the chronic inflammation, exceeding its defensive competence, lasts for years and can also be the beginning of neoplastic cells proliferation.
The article describes the principles of the insulin signaling pathway and the latest research results indicating the new role of insulin in modulating mitochondrial activity during muscle development. Myogenesis is considered to be an extensive energy-demanding process where mitochondria are the main source of ATP. Moreover, a number of reports emphasize that insulin is the most likely factor regulating prenatal muscle growth. Despite the fact that research into the affect of insulin onto myogenesis is incomplete, the role of mitochondria in muscle formation is thought to be essential in order to comprehend both whole-body growth and development. Insulin stimulates the expression of mitochondrial proteins in muscle cells whereas the activity of some targets of the insulin signaling pathway depends on ATP supply (e. g. mTOR). Similarly, alterations in available energy supply, resulting from the impaired function of mitochondria affect the cells sensitivity to insulin as well as leading to myopaties in the developing muscle tissue.
Purpose: The aim of the study was to evaluate the content of malondialdehyde (MDA) and the activity of the total antioxidant status (TAS) in the aqueous humor of dogs with senile cataract without general conditions. Material and methods: The population examined consisted of 40 dogs of various breeds and sexes, aged 10-16 years, diagnosed with senile cataracts, which qualified for cataract surgery. Samples of the aqueous humor were collected at the beginning of the operation, after the opening of the anterior chamber. MDA luminescence spectra were determined with a Perkin-Elmer LS 30 by the method of Yagi. TAS was measured by a colorimetric reagent kit Randox Total Antioxidant Status. Results: Our results showed a significant increase in malondialdehyde (MDA) levels and a significantly lower activity of the total antioxidant status (TAS) in the aqueous humor of dogs with senile cataract compared to the control group. Conclusions: The results indicate an increased peroxidation of lipids and a local weakening of the defensive system in the aqueous humor of dogs with senile cataract. These results suggest that these conditions may have an impact on the development of age-related cataract, and are compatible with the free-radical theory of the development of senile cataract.
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