Gene or cell doping is defined by the World Anti-Doping Agency (WADA) as "the non-therapeutic use of genes, genetic elements and/or cells that have the capacity to enhance athletic performance". New research in genetics and genomics will be used not only to diagnose and treat disease, but also to attempt to enhance human performance. In recent years, gene therapy has shown progress and positive results that have highlighted the potential misuse of this technology and the debate of 'gene doping'. Gene therapies developed for the treatment of diseases such as anaemia (the gene for erythropoietin), muscular dystrophy (the gene for insulin-like growth factor-1) and peripheral vascular diseases (the gene for vascular endothelial growth factor) are potential doping methods. With progress in gene technology, many other genes with this potential will be discovered. For this reason, it is important to develop timely legal regulations and to research the field of gene doping in order to develop methods of detection. To protect the health of athletes and to ensure equal competitive conditions, the International Olympic Committee, WADA and International Sports Federations have accepted performance-enhancing substances and methods as being doping, and have forbidden them. Nevertheless, the desire to win causes athletes to misuse these drugs and methods. This paper reviews the current status of gene doping and candidate performance enhancement genes, and also the use of gene therapy in sports medicine and ethics of genetic enhancement.
The aim of this study was to evaluate aerobic exercise capacity, cardiac features and function in a group of asthmatic children who underwent medical treatment. Dynamic exercise testing was done to evaluate aerobic exercise capacity. Echocardiography was performed to identify the effects that asthma-induced pulmonary changes have on respiratory and cardiac function in these patients. The study involved 20 asthmatic children (aged 7-16 years) who were followed at our hospital and 20 age- and sex-matched, healthy control subjects. Sixteen of the asthma cases were moderate and four were severe. All 40 subjects underwent similar series of assessments: multiple modes of echocardiography, treadmill stress testing, pulmonary function testing. The means for forced expiratory volume in 1 sec, forced expiratory flow 25-75%, maximal voluntary ventilation and inspiratory capacity were all significantly higher in the control group. The patient group had significantly lower mean maximal oxygen uptake and mean endurance time than the controls but there were no significant differences between the groups with respect to respiratory exchange ratio or the ventilatory threshold. The control group means for ejection fraction, fractional shortening, left ventricular mass, and left ventricular mass index were significantly higher than the corresponding patient group results. Children with moderate or severe asthma have lower aerobic capacity than healthy children of the same age. The data suggest that most of these children have normal diastolic cardiac function, but exhibit impaired systolic function and have lower LVM than healthy peers of the same age.
The side of the pneumonectomy and previous tuberculosis were the two most important risk factors independent of the bronchial closure methods. The incidence of BPF was much higher after right pneumonectomy than after left pneumonectomy. The high mortality and morbidity rates show that the treatment of BPF is still not satisfactory.
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