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The aim of the study was to find out predispositions to eating disorders (ED) such as anorexia and bulimia nervosa in girls between 14-19 years, going to grammar or secondary school. 189 girls were to answer questions of Eating Attitude Test 26 (EAT26) and fill a questionnaire prepared by authors of the study. Both questionnaires were anonymous. 19 girls (10,1%) attained 20 and more points and were qualified as EAT26+ what means predispositions to eating disorders. Body Mass Index (BMI) was used to estimate a state of nutrition. In the group EAT26+ most of the girls (57,9%) presented proper weight-height proportions.
In the present study, we examined cardiac and regional haemodynamic effects of endothelin-1 (ET-1), a potent vasoconstrictive factor, in a rat model of pressure-controlled irreversible haemorrhagic shock resulting in the death of all control animals within 30 min. Experiments were carried out in male ethylurethane-anaesthetised Wistar rats subjected to hypotension of 20-25 mmHg, which resulted in bradycardia, an extreme decrease in cardiac index (CI) and an increase in total peripheral resistance index (TPRI), with reductions in renal (RBF), hindquarters (HBF) and mesenteric blood flow (MBF). ET-1 (50, 200 pmol/kg) administered intravenously at 5 min of critical hypotension produced increases in mean arterial pressure (MAP) and heart rate (HR), which were significantly higher than those in normotensive animals, and a 100% survival at 2 h after treatment. The effects were accompanied by a rise in CI, a decrease in TPRI, with increases in RBF and HBF and persistently lowered MBF, and an increase in circulating blood volume 20 min after treatment. The cardiovascular effects of ET-1 were inhibited by the ETA receptor antagonist BQ-123 (1 mg/kg), while the ETB receptor antagonist BQ-788 (3 mg/kg) had no effect. In conclusion, ET-1 acting via ETA receptors produces reversal of haemorrhagic hypotension in rats due to the mobilisation of blood from venous reservoirs, with the improvements in cardiac function and the perfusion of peripheral tissues.
The increase in the blood-brain barrier (BBB)permeability and a developing cerebral oedema due to the ischemic infarction appear a few hours,and intensify during a few days,after closing the carotid arteries.It fails to be clear,however,what causes the increase in the microvessels damage,and whether the damage is a secondary result of the vasoactive substances released by the neurones and glia cells damaged by the ischemia.CRH,which plays an essential role in integrative the nervous,endocrine, and immunological systems,has a positive effect on the decrease in the permeability of the BBB damaged by various physical and chemical factors.Therefore,the examination of the CRH role in the cerebral ischemia may prove useful for explaining the processes taking place in the foci of the cerebral infarction and their environment. The experiment was carried out on rats which,20 minutes before closing of both internal carotid arteries,was administered 10 µg CRH to cerebrospinal fluid via cisterna magna of the brain.The BBB permeability was measured 30 minutes,3 hours,3 days,and 7 days after closing the arteries.The experiment has shown the CRH protective effect on the BBB and its consequent effect on the decrease in the BBB permeability which appears in the 3 hours after closing the arteries (p<0.05),and is high significant during the chronic phase of the cerebral ischemia (p<0.03).It can be thus concluded that CRH,by affecting directly the endothelium of the cerebral vessels, decreases the endothelial damage in the acute phase of the ischemia.The decrease is noted to be more significant in the chronic phase of the ischemia;such an effect can be attributed to CRH stimulating the hypothalamic-adrenal axis,and to the secondary activation of the mechanisms decreasing the BBB permeability.
Angiogenesis and VEGF play a major role in many repair processes such as healing of gastric ulceration.The present study was undertaken to assess the dynamics of changes in VEGF expression and angiogenesis in stress-induced gastric ulcers in rats. Acute gastric ulceration was induced using a water-immersion and restraint stress method. The VEGF expression, angiogenesis, size of area and depth of ulcers in gastric speciments were evaluated. The study shows that as early as one day after the development of ulcers there is a significant increase in both the expression of the VEGF protein and the number of newly formed microvessels, while an abrupt decrease in VEGF expression, observed on the fifth day, results in a decreased intensity of angiogenesis. Moreover, it has been demonstrated that the increase in VEGF expression and angiogenesis is accompanied by a reduction in the size of area and depth of stress-induced ulcers in rats. Six days after ulcer development both VEGF expression and angiogenesis return to normal levels.
The aim of the study was to evaluate prevalence and risk factors of sight defects in students of dentistry using a questionnaire and base-line eye examination. Myopia was observed in 44 (50,00 %) students, hypermetropia in 3 (3,41%) students. None of spherical refraction defects was observed in 41 (46,59%) examined. There were 34 (77,27%) women and 10 (22,73%) men in the group with the diagnosed myopia. Observed myopia was qualified as low or medium grade. The low grade myopia was diagnosed in 38 students (86,36%) and the medium grade in 6 cases (13,64%). In 11 (25,00%) cases it was noticed for the first time. The statistical analysis indicated familial occurance of refraction defect in subjects.
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