[Postpartum progression of anxiety and depression levels in mothers of premature newborns].

Objective: The postpartum period represents a vulnerable time for women's mental health, especially for those with complications and prematurity. This study aims to explore the evolution of depression and anxiety levels during the 12 weeks postpartum in mothers of premature babies.

Design: Prospective study of two parallel cohorts.

Molecular and cellular events in alcohol-induced muscle disease.

Alcohol consumption induces a dose-dependent noxious effect on skeletal muscle, leading to progressive functional and structural damage of myocytes, with concomitant reductions in lean body mass. Nearly half of high-dose chronic alcohol consumers develop alcoholic skeletal myopathy. The pathogenic mechanisms that lie between alcohol intake and loss of muscle tissue involve multiple pathways, making the elucidation of the disease somewhat difficult.

Up-regulation of myocardial L-type Ca2+ channel in chronic alcoholic subjects without cardiomyopathy.

Background: Excessive ethanol intake is one of the most frequent causes of acquired dilated cardiomyopathy in developed countries. L-type Ca(2+) channels, involved in excitation-contraction coupling, are disturbed in animal models of persistent ethanol consumption. This study was designed to evaluate the density and function of myocardial L-type Ca(2+) channel receptors in organ donors with chronic alcoholism and controls.

Evidence of apoptosis in alcoholic cardiomyopathy.

Apoptosis is a mechanism of cell death implicated in the pathogenesis of alcohol-induced organ damage. Experimental studies have suggested alcohol-mediated apoptosis in the cardiac muscle, and there is evidence of skeletal muscle apoptosis in long-term high-dose alcohol consumers. The relation between skeletal and cardiac muscle damage in alcoholism led us to consider the pathogenic role of apoptosis in alcoholic dilated cardiomyopathy.