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Advanced age per se is a major risk factor for cardiovascular disease (CVD). Apart from the chronic exposure to known cardiovascular risk factors, intrinsic aging of the cardiovascular system amplifies the vulnerability to various stressors, ultimately favoring the development of CVD in late life. The process of cardiac aging involves derangements in multiple cellular pathways. Among these, impairments in mitochondrial function arising from failure of mitochondrial quality control are considered to be a major contributing factor to heart senescence. Besides being less bioenergetically efficient, damaged mitochondria produce larger amounts of reactive oxygen species and are more prone to induce apoptosis. This results in oxidative damage to cardiomyocyte components and dismissal of postmitotic and virtually irreplaceable cardiac cells. The chapter summarizes the current knowledge about prominent mechanisms and consequences of mitochondrial decay and failure of mitochondrial quality control in the context of cardiac aging. The therapeutic potential of targeting specific mitochondrial pathways is also discussed.

Introduction We evaluated the gene expression levels of atrogin-1, MuRF1, myostatin, follistatin, activin A, and inhibin alpha in skeletal muscle samples of patients with gastric cancer and controls. Methods We studied 38 cancer patients and 12 controls who underwent surgery for gastric adenocarcinoma and benign abdominal diseases, respectively. A biopsy specimen was obtained from the rectus abdominis muscle from all participants. The relative gene expression of atrogin-1, MuRF1, myostatin, follistatin, activin A, and inhibin alpha was determined by qRT-PCR analysis. Results Atrogin-1 and MuRF1 mRNA expression was similar between cancer patients and controls and was unaffected by the disease stage or the severity of body weight loss. Transcript levels of myostatin and follistatin did not differ between cases and controls and were similar across disease stages and categories of weight loss. Finally, no differences were detected in activin A and inhibin alpha gene expression between cancer patients and controls. Discussion In skeletal muscle, the gene expression of atrogin-1, MuRF1, myostatin, follistatin, activin A, and inhibin alpha is not affected by the presence of cancer. The expression of atrophy-related genes is unaffected by the disease stage and the degree of weight loss. © 2013 Wiley Periodicals, Inc.

The impact of alcohol on brain morphology was studied in a large group of cognitively intact people whose consumption of alcohol was below the threshold for abuse. Participants were 367 healthy subjects, aged 18 years or older, who underwent magnetic resonance imaging (MRI) for reasons other than cognitive impairment. MRI analyses were carried out using SPM8 software on the MATLAB 7.9 platform. Gray matter (GM) and white matter (WM) volumes were normalized for intracranial volume. Participants were interviewed about their lifetime consumption of alcohol, nicotine and other available illicit substances. Direct WM and GM comparisons between alcohol users and non-users did not detect significant differences. Differences also did not emerge from multiple regression analyses or in the subgroup aged 65 or older. Based on this study's findings, we cannot infer a detrimental effect of alcohol on the brain of normal adults. These data may be considered to provide reference information for clinical studies.

We evaluated the gene expression levels of atrogin-1, MuRF1, myostatin, follistatin, activin A, and inhibin alpha in skeletal muscle samples of patients with gastric cancer and controls.