The metabolic syndrome (MS) is a conglomerate of interrelated risk factors-including obesity, atherogenic dyslipidemia, arterial hypertension, and insulin resistance-which exponentially increase the risk of developing cardiovascular disease and type 2 diabetes mellitus. The purpose of this study was to determine the prevalence of MS according to the criteria published by the International Diabetes Federation, in individuals of both sexes over 18 years of age. This is a cross-sectional study based on MS prevalence in a representative sample from the Maracaibo district, Zulia State. The population of Maracaibo, according to the last census in 2001, was 1,219,927 habitants, with a 2007 population estimation of 1,428,043 habitants according to the National Institute of Statistics (NIS). Likewise, NIS projects that for the year 2009, 59.7% of the population of Venezuela will have individuals over 18 years of age. Using these data, the sample for Maracaibo District corresponds to 1986 individuals with or above 18 years of age. The data recollection was conducted by health professionals and medicine students, previously trained. The participants were subject to inquiry previous written consent and a medical examination, and qualitative variables such as smoking habit, socioeconomic status, physical activity, race, alcoholism, and nutritional habits, and quantitative ones like blood pressure, anthropometry, and blood works were determined. There is clear evidence that there is a lack of research and validated values to use as reference in our country and maybe in Latin America. Taking into account all that has been exposed here, this study will serve as a pilot for the numerous statistical determinations that will soon come afterward, providing first-hand accurate evidence on the behavior of the MS in the Latin American populace.

Our results suggest that exposure to cigarette smoke increases NO synthesis, such that NO may act in a compensatory way as an inhibitor of lipid peroxidation. Smoking also activates other antioxidative mechanisms such as involving vitamin C. These protective mechanisms appear to be enough in preventing accumulation of oxidative products such as MDA and avoiding oxidative damage.

Multimorbidity is an emerging topic in public health policy because of its increasing prevalence and socio-economic impact. However, the age- and gender-dependent trends of disease associations at fine resolution, and the underlying genetic factors, remain incompletely understood. Here, by analyzing disease networks from electronic medical records of primary health care, we identify key conditions and shared genetic factors influencing multimorbidity. Three types of diseases are outlined: “central”, which include chronic and non-chronic conditions, have higher cumulative risks of disease associations; “community roots” have lower cumulative risks, but inform on continuing clustered disease associations with age; and “seeds of bursts”, which most are chronic, reveal outbreaks of disease associations leading to multimorbidity. The diseases with a major impact on multimorbidity are caused by genes that occupy central positions in the network of human disease genes. Alteration of lipid metabolism connects breast cancer, diabetic neuropathy and nutritional anemia. Evaluation of key disease associations by a genome-wide association study identifies shared genetic factors and further supports causal commonalities between nervous system diseases and nutritional anemias. This study also reveals many shared genetic signals with other diseases. Collectively, our results depict novel population-based multimorbidity patterns, identify key diseases within them, and highlight pleiotropy influencing multimorbidity.

Serum levels of malondialdehyde increase, and serum levels of nitric oxide diminish within 24 hours after the onset of thrombotic stroke onset. This suggests that serum malondialdehyde level could be used as potentially reliable and sensitive marker for reperfusion, whereas nitric oxide levels could acts as potential biochemical sensor for nonreflow phenomenon.

Lipoprotein (a) [Lp(a)] was discovered by Kare Berg in 1963 from the study of low-density lipoprotein genetic variants. Lp(a) contains a unique protein, apolipoprotein(a), which is linked to the Apo B-100 through a disulfide bond that gives it a great structural homology with plasminogen, and confers it atherogenic and atherothrombotic properties. Interest in Lp(a) has increased because an important association between high plasma levels of Lp(a) and coronary artery disease and cerebral vascular disorders has been demonstrated. Numerous case control studies have confirmed that hyper-Lp(a) is a risk factor for premature cardiovascular disease. Lp(a) is identified as a genetic trait with autosomal transmission, codified by one of the most studied polymorphic genes in humans. It has been demonstrated that variations in this gene are a major factor in the serum levels of Lp(a). Variations differ considerably between individuals and sex across populations. Various approaches to drug treatment using fibric acid derivatives, growth hormone, insulin-like growth factor-1, alcohol extracted soy protein, niacin, and exercise have been proven to decrease Lp(a) in high risk patients, but none has really been an effective therapeutic option for successfully reducing Lp(a) plasma levels.