Josep Ramon Alonso

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Mitochondria constitute a source of reactive oxygen species. We tested whether mitochondrial function from human circulating lymphocytes is affected by smoking habit and if this could be associated with an increase in oxidative damage of biological membranes. We prospectively studied 35 smokers and 35 non-smoking healthy individuals matched by age and sex,(More)
Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of the mitochondrial respiratory chain of skeletal muscle mitochondria(More)
Smoking causes a decrease of mitochondrial complex IV activity in chronic smokers. However, it is not known if this toxic effect is due to the acute effect of cigarette smoke itself or is a secondary phenomenon related to other smoking factors. The study assessed mitochondrial respiratory chain function in peripheral blood mononuclear cells of 15 healthy(More)
BACKGROUND AND OBJECTIVE Many experimental studies in animals have demonstrated that carbon monoxide (CO) has the ability to bind to complex IV of the mitochondrial respiratory chain (MRC) inhibiting its function. It is unknown, however, if this situation is also present in patients who are admitted to an emergency department because of acute CO poisoning.(More)
AIM The aim of the study was to establish a triage flowchart to rule out acute coronary syndrome (ACS) among patients with chest pain (CP) arriving on an Emergency Department (ED). PATIENTS AND METHOD This prospective observational study included 1000 consecutive patients with CP arriving on an ED CP unit. Demographic and clinical characteristics along(More)
OBJECTIVE Chronic smoking has been associated with diverse mitochondrial respiratory chain (MRC) dysfunction in lymphocytes, although inhibition of complex IV activity is the most consistent and relevant finding. These mitochondrial abnormalities have been proposed to contribute to pathogenesis of diseases associated with tobacco consumption. We assessed(More)
Increased oxidative damage seems to be a relevant mechanism in the pathophysiology of patients with an acute carbon monoxide (CO) poisoning. We have investigated the degree of membrane oxidative damage through the assessment of lipid peroxidation in circulating lymphocytes from five patients acutely intoxicated by CO. Since mitochondria are a major source(More)
BACKGROUND Harmful effects of chronic ethanol intake on liver mitochondria have been clearly demonstrated; however, mitochondria from skeletal muscle are preserved, and the effect of ethanol on heart mitochondria remains controversial. We assessed individual enzyme activity of mitochondrial respiratory chain (MRC) complexes and membrane oxidative damage of(More)
To analyze adhesion molecule expression on peripheral blood mononuclear cells (PBMCs) and on different lymphocyte subpopulations (CD2+, CD8+, CD19+, and CD56+ subsets) in chronic alcoholism, 30 well-nourished chronic alcoholics without ethanol-related diseases and 30 matched controls were included in the study. Adhesion molecules that mediate adhesion to(More)
BACKGROUND In the last few years, rare cases of acute quadriplegic myopathy (AQM*) with myosin-deficient muscle fibres occurring after solid organ transplantation has been reported. The aim of the present study was to review all cases of AQM with myosin deficient fibres seen at our institution among a large series of patients after orthotopic liver(More)