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Báo cáo hóa học: Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity
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Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity
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Báo cáo hóa học: " Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity"Vermeulen et al. Journal of Translational Medicine 2010, 8:93http://www.translational-medicine.com/content/8/1/93 RESEARCH Open AccessPatients with chronic fatigue syndromeperformed worse than controls in a controlledrepeated exercise study despite a normaloxidative phosphorylation capacityRuud CW Vermeulen1*, Ruud M Kurk1, Frans C Visser1, Wim Sluiter2, Hans R Scholte3 Abstract Background: The aim of this study was to investigate the possibility that a decreased mitochondrial ATP synthesis causes muscular and mental fatigue and plays a role in the pathophysiology of the chronic fatigue syndrome (CFS/ME). Methods: Female patients (n = 15) and controls (n = 15) performed a cardiopulmonary exercise test (CPET) by cycling at a continuously increased work rate till maximal exertion. The CPET was repeated 24 h later. Before the tests, blood was taken for the isolation of peripheral blood mononuclear cells (PBMC), which were processed in a special way to preserve their oxidative phosphorylation, which was tested later in the presence of ADP and phosphate in permeabilized cells with glutamate, malate and malonate plus or minus the complex I inhibitor rotenone, and succinate with rotenone plus or minus the complex II inhibitor malonate in order to measure the ATP production via Complex I and II, respectively. Plasma CK was determined as a surrogate measure of a decreased oxidative phosphorylation in muscle, since the previous finding that in a group of patients with external ophthalmoplegia the oxygen consumption by isolated muscle mitochondria correlated negatively with plasma creatine kinase, 24 h after exercise. Results: At both exercise tests the patients reached the anaerobic threshold and the maximal exercise at a much lower oxygen consumption than the controls and this worsened in the second test. This implies an increase of lactate, the product of anaerobic glycolysis, and a decrease of the mitochondrial ATP production in the patients. In the past this was also found in patients with defects in the mitochondrial oxidative phosphorylation. However the oxidative phosphorylation in PBMC was similar in CFS/ME patients and controls. The plasma creatine kinase levels before and 24 h after exercise were low in patients and controls, suggesting normality of the muscular mitochondrial oxidative phosphorylation. Conclusion: The decrease in mitochondrial ATP synthesis in the CFS/ME patients is not caused by a defect in the enzyme complexes catalyzing oxidative phosphorylation, but in another factor. Trial registration: Clinical trials registration number: NL16031.040.07.Background explained, not caused by exercise, insufficiently relievedChronic fatigue syndrome/myalgic encephalopathy (CFS/ by rest and causing a major reduction in physical capa-ME) as a syndrome was defined in consensus meetings city. The additional symptoms of the syndrome wereby Fukuda et al [1]. Fatigue was the major criterion in the headache, pain in muscles and joints, unrefreshing sleep,definition. It was described as suddenly occurring, not postexertional malaise, sore throat, painful lymph glands and insufficient concentration. The combination of fati- gue and four or more of the additional symptoms lasting* Correspondence: rv@cvscentrum.nl at least for 6 months, sufficed for the diagnosis of CFS/1 CFS/ME and Pain Research Center Amsterdam, Waalstraat 25-31, 1078 BR ME. The main exclusion cri terion for CFS/ME, was theAmsterdam, The NetherlandsFull list of author information is available at the end of the article © 2010 Vermeulen et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Vermeulen et al. Journal of Translational Medicine 2010, 8:93 ...
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Báo cáo hóa học: " Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity"Vermeulen et al. Journal of Translational Medicine 2010, 8:93http://www.translational-medicine.com/content/8/1/93 RESEARCH Open AccessPatients with chronic fatigue syndromeperformed worse than controls in a controlledrepeated exercise study despite a normaloxidative phosphorylation capacityRuud CW Vermeulen1*, Ruud M Kurk1, Frans C Visser1, Wim Sluiter2, Hans R Scholte3 Abstract Background: The aim of this study was to investigate the possibility that a decreased mitochondrial ATP synthesis causes muscular and mental fatigue and plays a role in the pathophysiology of the chronic fatigue syndrome (CFS/ME). Methods: Female patients (n = 15) and controls (n = 15) performed a cardiopulmonary exercise test (CPET) by cycling at a continuously increased work rate till maximal exertion. The CPET was repeated 24 h later. Before the tests, blood was taken for the isolation of peripheral blood mononuclear cells (PBMC), which were processed in a special way to preserve their oxidative phosphorylation, which was tested later in the presence of ADP and phosphate in permeabilized cells with glutamate, malate and malonate plus or minus the complex I inhibitor rotenone, and succinate with rotenone plus or minus the complex II inhibitor malonate in order to measure the ATP production via Complex I and II, respectively. Plasma CK was determined as a surrogate measure of a decreased oxidative phosphorylation in muscle, since the previous finding that in a group of patients with external ophthalmoplegia the oxygen consumption by isolated muscle mitochondria correlated negatively with plasma creatine kinase, 24 h after exercise. Results: At both exercise tests the patients reached the anaerobic threshold and the maximal exercise at a much lower oxygen consumption than the controls and this worsened in the second test. This implies an increase of lactate, the product of anaerobic glycolysis, and a decrease of the mitochondrial ATP production in the patients. In the past this was also found in patients with defects in the mitochondrial oxidative phosphorylation. However the oxidative phosphorylation in PBMC was similar in CFS/ME patients and controls. The plasma creatine kinase levels before and 24 h after exercise were low in patients and controls, suggesting normality of the muscular mitochondrial oxidative phosphorylation. Conclusion: The decrease in mitochondrial ATP synthesis in the CFS/ME patients is not caused by a defect in the enzyme complexes catalyzing oxidative phosphorylation, but in another factor. Trial registration: Clinical trials registration number: NL16031.040.07.Background explained, not caused by exercise, insufficiently relievedChronic fatigue syndrome/myalgic encephalopathy (CFS/ by rest and causing a major reduction in physical capa-ME) as a syndrome was defined in consensus meetings city. The additional symptoms of the syndrome wereby Fukuda et al [1]. Fatigue was the major criterion in the headache, pain in muscles and joints, unrefreshing sleep,definition. It was described as suddenly occurring, not postexertional malaise, sore throat, painful lymph glands and insufficient concentration. The combination of fati- gue and four or more of the additional symptoms lasting* Correspondence: rv@cvscentrum.nl at least for 6 months, sufficed for the diagnosis of CFS/1 CFS/ME and Pain Research Center Amsterdam, Waalstraat 25-31, 1078 BR ME. The main exclusion cri terion for CFS/ME, was theAmsterdam, The NetherlandsFull list of author information is available at the end of the article © 2010 Vermeulen et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Vermeulen et al. Journal of Translational Medicine 2010, 8:93 ...
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