Age- and Gender-Based Studies of Trace Metal Levels and Various Enzymes Associated with Myocardial Infarction

The present investigation deals with the determination of various serum enzymes known to be elevated during myocardial infarction (MI) and estimation of selected metals like Cu, Cr, Co, Fe, Pb, and Mg by flame atomic absorption spectrophotometry. The data obtained thereby were processed for the determination of correlation coefficient matrix among the cardiac enzymes and the serum metals. The study evidenced the accumulation of Pb during MI and reduction in the level of Fe. A significant negative correlation was observed between Cu and creatine kinase-MB. The data were also segregated into various groups to study the influence of age and gender on the levels of selected parameters. In both the genders, the age of the patients was found to be correlated significantly with various cardiac enzymes. In case of male patients, the most significant correlation was observed between age and blood sugar at random. The other significant correlations among the male patients included Cr–CPK, Cr–creatine kinase-MB, Fe–age, and others. In female patients, the pairs of studied parameters that exhibited significant correlations included age–lactic dehydrogenase, creatine phosphokinase isoenzyme–aspartate aminotransferase, lactic dehydrogenase–creatine phosphokinase isoenzymes, Pb-Fe, and Cu-Co in addition to others.     

Anorexigen-induced pulmonary hypertension and the serotonin (5-HT) hypothesis: lessons for the future in pathogenesis

Pulmonary surfactant is a surface active material composed of both lipids and proteins that is produced by alveolar type II pneumocytes. Abnormalities of surfactant in the immature lung or in the acutely inflamed mature lung are well described. However, in a variety of subacute diseases of the mature lung, abnormalities of lung surfactant may also be of importance. These diseases include chronic obstructive pulmonary disease, asthma, cystic fibrosis, interstitial lung disease, pneumonia, and alveolar proteinosis. Understanding of the mechanisms that disturb the lung surfactant system may lead to novel rational therapies for these diseases.