Search

Abstract: The smoke of cigarettes represents an important accelerator of the aging process, both directly through complex mechanisms mediated prevalently by excessive formation of free radicals, and indirectly by favoring the appearance of various pathologies in which smoke is a recognized risk factor. This means that smoke compromises not only life expectancy, but also the quality of the life, favoring the occurrence of non-autosufficiency. Smoking is an important risk factor for many diseases, such as cancer, cardiovascular and respiratory diseases. These are also the main causes of death in the industrialized Countries, where the habit of smoking is also largely diffused. Non-smokers have a much higher life expectancy than smokers, and the suspension of smoking is accompanied, even in the elderly, by an increase in the survival time due to the reduction of smoke-induced biological damage. Therefore, cigarette smoking is opposing the longevity, particularly the extreme one, as it is confirmed by the observations obtained on centenarians. Among them, smoking is extremely rare, and even when it occurs among them, it is correlated almost exclusively to bad health conditions and non-autosufficiency, indicating that it compromises health status and the quality of life even in extremely long living subjects. Considering the demonstrated beneficial effects of suspension of smoking, all practitioners and geriatricians in particular, should promote the abstinence from smoking as a behavioral norm for a correct life style. Non-smokers can delay the appearance of diseases and of the aging process, thus attaining longevity; further, non-smoking habit allows genetically predisposed subjects to reach the extreme longevity and maintain an acceptable health status and autosufficiency. [Copyright &y& Elsevier]

Abstract: Chronic heart failure (CHF) is a complex and heterogeneous clinical syndrome and because of its rising incidence and prevalence, it can be considered a global epidemic. Interleukin (IL)-22 is a pro-inflammatory cytokine, belonging to the IL-10 family. Forty-seven consecutive older patients, hospitalized with an admitting diagnosis of CHF at the Geriatric Medicine Unit (University of Messina, Italy), from 01/01/06 to 30/06/06, were enrolled in the study. Serum concentrations of IL-22 were measured by a quantitative enzyme immunoassay technique. IL-22 levels in all CHF patients were significantly higher than those in controls, in particular, only the II and III NYHA class had IL-22 values significantly higher than the controls, whereas there was no difference between the IL-22 levels of NYHA class IV and the controls. The reason may be the declining immune function in CHF older patients, in fact we can hypothesize that the fall in IL-22 levels, with the progression of NYHA class, is due to the reduced ability in CHF patients to respond to infections, as IL-22 has anti-microbial properties. We detected different outcomes correlated to different IL-22 levels, and the Kaplan–Meier curves suggest a trend. [Copyright &y& Elsevier]

OBJECTIVE: To evaluate the relationship between plasma leptin and the tumor necrosis factor-α (TNFα), TNF receptor p60 (TNF-R1) and TNF receptor p80 (TNF-R2) concentrations in obese subjects. DESIGN: Case-control study. SETTING: Outpatient’s Service for Prevention and Treatment of Obesity at the University Hospital. MEASUREMENTS: Body mass index (BMI), waist circumference, hip circumference, waist-to-hip ratio (WHR), fasting plasma glucose, fasting plasma insulin, homeostasis model assessment of insulin resistance (HOMA IR), plasma leptin, TNF α, TNF-R1 and TNF-R2 concentrations were evaluated in obese subjects (n=42) and in age- and gender-matched, lean healthy controls (n=16). RESULTS: In obese subjects, fasting plasma glucose and insulin, HOMA IR, plasma leptin, TNFα, TNF-R1 and TNF-R2 concentrations were significantly higher than in controls. Furthermore, females showed higher leptin, TNF-R1 and TNF-R2 plasma concentrations compared to males, in both control and obese subjects. In control subjects, plasma leptin concentrations showed a direct correlation with BMI (r=0.74, P<0.001), hip circumference (r=0.94, P<0.001), TNF-R1 (r=0.79, P<0.001) and TNF-R2 (r=0.64, P<0.01), and a negative correlation with WHR (r=-0.58, P<0.05). In obese subjects, we found a direct correlation between plasma leptin concentrations and BMI (r=0.67, P<0.001), hip circumference (r=0.66, P<0.001), fasting glucose (r=0.37, P<0.05), fasting insulin (r=0.31, P<0.05), HOMA IR (r=0.38, P<0.05), TNF-R1 (r=0.71, P<0.001) and TNR-R2 (r=0.66, P<0.001), while a negative correlation was found between circulating leptin and WHR (r=-0.44, P<0.01). In multivariate analysis, plasma leptin concentrations were significantly associated with BMI (P=0.015) and gender (P=0.047) in the control group, while in obese subjects, plasma leptin showed a significant association with BMI (P=0.019) and TNF-R1 (P=0.012). CONCLUSIONS: Our results are consistent with the hypothesis that... [ABSTRACT FROM AUTHOR]