497 research outputs found

    Cardiovascular and other causes of death as a function of lifestyle habits in a quasi extinct middle-aged male population. a 50-year follow-up study

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    Objectives: To relate major causes of death with lifestyle habits in an almost extinct male middle-aged population. Material and methods: A 40-59 aged male population of 1712 subjects was examined and followed-up for 50 years. Baseline smoking habits, working physical activity and dietary habits were related to 50 years mortality subdivided into 12 simple and 3 composite causes of death by Cox proportional hazard models. Duration of survival was related to the same characteristics by a multiple linear regression model. Results: Death rate in 50 years was of 97.5%. Out of 12 simple groups of causes of death, 6 were related to smoking habits, 3 to physical activity and 4 to dietary habits. Among composite groups of causes of death, hazard ratios (and their 95% confidence limits) of never smokers versus smokers were 0.68 (0.57-0.81) for major cardiovascular diseases; 0.65 (0.52-0.81) for all cancers; and 0.72 (0.64-0.81) for all-cause deaths. Hazard ratios of vigorous physical activity at work versus sedentary physical activity were 0.63 (0.49-0.80) for major cardiovascular diseases; 1.01 (0.72-1.41) for all cancers; and 0.76 (0.64-0.90) for all-cause deaths. Hazard ratios of Mediterranean Diet versus non-Mediterranean Diet were 0.68 (0.54-0.86) for major cardiovascular diseases; 0.54 (0.40-0.73) for all cancers; and 0.67 (0.57-0.78) for all-cause deaths. Expectancy of life was 12 years longer for men with the 3 best behaviors than for those with the 3 worst behaviors. Conclusions: Some lifestyle habits are strongly related to lifetime mortality

    Lifestyle behaviour and lifetime incidence of heart diseases

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    Objectives: Investigate the relationship of some behavioural characteristics of a male population with lifetime incidence of heart diseases. Material and methods: In the Italian Rural Areas of the Seven Countries Study of Cardiovascular Diseases, 1677 heart disease-freemen aged 40–59 yearswere followed up during 50 years for lifetime incidence of heart disease up to the age of 90 years. They were classified as coronary heart disease (CHD) and heart diseases of uncertain etiology (HDUE). Baseline cigarette smoking habits (non-smokers and ex-smokers, moderate smokers, heavy smokers), physical activity (sedentary, moderate, vigorous) and eating habits (non-Mediterranean Diet, Prudent Diet and Mediterranean Diet) were related to incidence of heart disease. Results: Incidence of CHD and HDUE up to the age of 90 years was 28.8 and 17.7%, respectively. Univariate and multivariate analyses showed strong association of behavioural characteristics with CHD incidence, but not with HDUE incidence. Cox proportional hazard rates for CHD were 1.45 (95% confidence intervals, CI: 1.11– 1.90) for heavy smokers versus non-smokers; 0.67 (CI 0.50–0.89) for vigorous activity versus sedentary habits and 0.62 (CI 0.47–0.83) for Mediterranean Diet versus non-Mediterranean Diet. Combining CHD cases with HDUE cases made the predictive picture similar to that of CHD. When some basic risk factors were added to the model results remained substantially unaltered, despite the existence of some correlations of behaviours with risk factors. Conclusions: Behavioural factors including cigarette smoking, physical activity and diet are strong predictors of lifetime incidence of common heart diseases even adding other traditional risk factors

    The pro-autophagic protein AMBRA1 coordinates cell cycle progression by regulating CCND (cyclin D) stability

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    The scaffold protein AMBRA1 regulates the early steps of autophagosome formation and cell growth, and its deficiency is associated with neurodevelopmental defects and cancer. In a recent study, we show that AMBRA1 is a key factor in the upstream branch of the MYCN-MYC and CDK4-CDK6-dependent regulation of G1/S phase transition. Indeed, in the developing neuroepithelium, in neural stem cells, and in cancer cells, we demonstrate that AMBRA1 regulates the expression of D-type cyclins by controlling both their proteasomal degradation and their MYCN-MYC-mediated transcription. Also, we show that this regulation axis maintains genome integrity during DNA replication, and we identify a possible line of treatment for tumors downregulating AMBRA1 and/or overexpressing CCND1 (cyclin D1), by demonstrating that AMBRA1-depleted cells carry an AMBRA1-loss-specific lethal sensitivity to CHEK1 inhibition. Interestingly, we show that this aspect is specific for AMBRA1 loss, because ATG7 knockdown does not display the same response to CHEK1 inhibitors. Hence, our findings underscore that the AMBRA1-CCND1 pathway represents a novel crucial mechanism of cell cycle regulation, deeply interconnected with genomic stability in development and cancer
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