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Cardiovascular Dysfunction (cardiovascular + dysfunction)
Selected AbstractsClinical significance of geriatric sleep apnea syndromeGERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 4 2002Shinji Teramoto The prevalence of sleep apnea syndrome (SAS) is known to increase with advancing age, contributing to excessive daytime sleepiness, cardiovascular dysfunction and the impairment of health-related quality of life. However SAS is often undiagnosed and overlooked in the elderly. It is important to note that SAS is a differential diagnosis of insomnia, dementia, and depression in the elderly. For an accurate diagnosis of geriatric SAS, the apnea and hypopnea index as measured by polysomnography must be greater than 10 or 15. Many untoward effects of SAS on the health status of the elderly are considered to be clinically significant. Although it has been suggested that geriatric SAS has less effect on the mortality and morbidity of sufferers than does middle-aged SAS, sleep apnea in any age group, if severe and accompanied by symptoms, should be treated. However, the clinical significance of geriatric SAS should be further elucidated. [source] Identification and characterization of PEBP as a calpain substrateJOURNAL OF NEUROCHEMISTRY, Issue 4 2006Qinghua Chen Abstract Calpains are calcium- and thiol-dependent proteases whose dysregulation has been implicated in a number of diseases and conditions such as cardiovascular dysfunction, ischemic stroke, and Alzheimer's disease (AD). While the effects of calpain activity are evident, the precise mechanism(s) by which dysregulated calpain activity results in cellular degeneration are less clear. In order to determine the impact of calpain activity, there is a need to identify the range of specific calpain substrates. Using an in vitro proteomics approach we confirmed that phosphatidylethanolamine-binding protein (PEBP) as a novel in vitro and in situ calpain substrate. We also observed PEBP proteolysis in a model of brain injury in which calpain is clearly activated. In addition, with evidence of calpain dysregulation in AD, we quantitated protein levels of PEBP in postmortem brain samples from the hippocampus of AD and age-matched controls and found that PEBP levels were approximately 20% greater in AD. Finally, with previous evidence that PEBP may act as a serine protease inhibitor, we tested PEBP as an inhibitor of the proteasome and found that PEBP inhibited the chymostrypsin-like activity of the proteasome by ,30%. Together these data identify PEBP as a potential in vivo calpain substrate and indicate that increased PEBP levels may contribute to impaired proteasome function. [source] ENDOTHELINS AND NADPH OXIDASES IN THE CARDIOVASCULAR SYSTEMCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1 2008Karigowda J Dammanahalli SUMMARY 1The endothelin (ET) system and NADPH oxidase play important roles in the regulation of cardiovascular function, as well as in the pathogenesis of hypertension and other cardiovascular diseases. 2Endothelins activate NADPH oxidases and thereby increase superoxide production, resulting in oxidative stress and cardiovascular dysfunction. Thus, NADPH oxidases may mediate the role of endothelins in some cardiovascular diseases. However, the role of reactive oxygen species (ROS) in mediating ET-induced vasoconstriction and cardiovascular disease remains under debate, as evidenced by conflicting reports from different research teams. Conversely, activation of NADPH oxidase can stimulate ET secretion via ROS generation, which further enhances the cardiovascular effects of NADPH oxidase. However, little is known about how ROS activate the endothelin system. It seems that the relationship between ET-1 and ROS may vary with cardiovascular disorders. 3Endothelins activate NADPH oxidase via the ET receptor,proline-rich tyrosine kinase-2 (Pyk2),Rac1 pathway. Rac1 is an important regulator of NADPH oxidase. There is ample evidence supporting direct stimulation by Rac1 of NADPH oxidase activity. In addition, Rac1-induced cardiomyocyte hypertrophy is mediated by the generation of ROS. [source] Long-term circulatory and renal consequences of intrauterine growth restrictionACTA PAEDIATRICA, Issue 7 2005Umberto Simeoni Abstract Intrauterine growth restriction (IUGR) and probably also early postnatal altered nutrition in very-low-birthweight babies may, in the long term, be followed by the various disorders that are included in the metabolic syndrome. This discovery has raised a new paradigm about the background to cardiovascular disease, arterial hypertension, obesity, type 2 diabetes and dyslipidaemic disorders that play a prominent role in shortening human life. In this review article, present knowledge about the background to renal dysfunction as seen in IUGR is summarized. The way in which arterial hypertension and cardiovascular dysfunction may be programmed in IUGR is also speculated. Conclusion: During the last decade, knowledge of the long-term consequences of IUGR has increased at a very rapid rate. At present, it is most important not only to develop efficient methods of preventing and diagnosing IUGR, but to work out follow-up and treatment programmes for the control of the disorders which may follow this condition. Proper postnatal feeding and infant growth may be essential for long-term outcome. [source] | ||||||||||