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탄광부 진폐증 환자에서 맞춤형 호흡 재활 치료 프로그램의 임상적 효용성
정희 ( Hee Cheong ),이정민 ( Jeong Min Lee ),박인기 ( In Ki park ),김종규 ( Jong Kyu Kim ),전근재 ( Geun Jae Jeon ),김주령 ( Ju Ryung Kim ),김지홍 ( Ji Hong Kim ),최병용 ( Byoong Yong Choi ) 대한내과학회 2014 대한내과학회지 Vol.87 No.6
Background/Aims: It is unknown whether pulmonary rehabilitation (PR) is an effective intervention to manage coal worker pneumoconiosis (CWP). We evaluated the efficacy and safety of an individualized PR program in 53 patients with CWP hospitalized in two medical institutions. Methods: The PR program consisted of upper and lower extremity exercises to improve exercise endurance and skeletal musculoskeletal strength. All subjects performed treadmill and ergometer exercise with steady loading weights three times/week for 12 weeks. The following tests were performed before and after the study to investigate the efficacy of the PR program: modified Borg scale, pulmonary function test, mid-thigh circumference, maximum muscular strength, 6-min walk distance (6MWD), and the St. George’s Respiratory Questionnaire (SGRQ), Korean version. Results: Forty patients (75.5%) completed their PR programs. They improved significantly on the modified Borg scale, mid thigh circumference, maximum muscular strength, 6MWD (all p < 0.000), and SGRQ (p = 0.007), however, no significant improvement was observed on the pulmonary function test. A significant improvement in dyspnea (p = 0.004) and 6MWD (p = 0.002) was observed in 12 patients with forced expiratory volume in 1 sec < 60%. The PR program with smoking cessation resulted in significantly more improvement on the 6MWD (p < 0.0001) and the SGRQ score (p = 0.002), as compared to those of patients who did not quit smoking. Conclusions: Our results show that an individualized 12-week PR program improves exercise capacity and quality of life for patients with CWP. (Korean J Med 2014,87:690-697)
위엥쥐스,김주령,정태숙,류희문,석대은 충남대학교 약학대학 의약품개발연구소 2002 藥學論文集 Vol.17 No.-
Paraoxonase (PON), an enzyme associated with high density lipoprotein (HDL), is known to protect low density lipoprotein (LDL) from lipid peroxidation involving copper ion. However, PON activity was observed to decrease during LDL oxidation. Here, we attempted to elucidate the possible mechanism for the inactivation of PON. PON was partially purified from human plasma, and subjected to various oxidant systems. PON activity, based on the hydrolysis of phenyl acetate, decreased slightly after the exposure to H_2O_2 or ascorbate, while oxidants such as peroxynitrite or HOCl had no remarkable effect. Inclusion of Cu^2+ in the incubation with ascorbate (0.3∼1 mM) led to a rapid decrease of activity in a time-and concentration-dependent manner. In comparison, ascorbate/Cu^2+ system was much more effective than ascorbate/Fe^2+ system in inactivating PON. A further study indicates that general hydroxyl radical scavengers such as mannitol, ethanol or benzoate failed to prevent the PON inactivation. Based on these results, it is proposed that the PON inactivation during LDL oxidation may be ascribed mainly to the Cu^2+-catalyzed oxidation.
Cumene hydroperoxide에 의한 paraoxonase 1의 산화적 불활성화에 대한 보호 방안
스, 위엥쥐,류희문,김주령,석대은 충남대학교 약학대학 의약품개발연구소 2003 藥學論文集 Vol.18 No.-
Paraoxonase 1 (PON1), an enzyme associated with high density lipoprotein (HDL), is known to protect low density lipoprotein (LDL) from lipid peroxidation involving copper ion. However, Paraoxonase 1 activity was observed to decrease during LDL oxidation. Here, the inactivation of PON1 by various peroxides was examined. Paraoxonase 1, purified from human plasma, was subjected to cumene hydroperoxide, hydrogen peroxide or tert-butyl hydroperoxide. PON activity, based on the hydrolysis of phenyl acetate, decreased by approximately 40 and 38 %, respectively, after the exposure to 2mM cumene hydroperoxide and hydrogen peroxide, while tert-butyl hydroperoxide had no remarkable inhibitory effect. Next, the compounds capable of preventing against cumene hydroperoxide-induced inactivation of PONl were screened. While quercetin or phenyl acetate failed to protect PON1, lauric acid or calcium chloride was found to protect PONl from cumene hydroperoxide-induced inactivation. Especially, lauric acid appeared to show the greater protection than the other fatty acids tested. In further study, lauric acid showed a dose-dependent protection with an E& value of around 35 μM. Based on these results, It is proposed that the alky hydroperoxide-induced inactivation of Paraoxonase 1 can be prevented by a proper fatty acid recipe.