• Journal of Korean Medical classics
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• v.4
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• pp.19-73
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• 1990

Today, many people are more interested in preventing the disease than curing it. Chi-Kung (氣功) is the way of Life-Cultivation (養生法) peculiar to the orient, it is reported in china that Chi-Kung has an excellent curative value not only in curing the disease but also in preventing it. But the full-scale study of Chi-Kung is not be made up to now in Korea, so I studied the developmental history of chinese Chi-Kung through the oriental medical books. From this study, I reached the following conclusions ; 1. Chi-Kung is naturally derived from the self-preservation instinct to adapt oneself to circumstances of the nature, but in the investigation from the documentational records, it is originated in the treatment method of the Sam-Huang-O-Jae (三皇五帝 )period to cure the abnormal circulation of the vital force and blood caused by damp (濕). 2. As the principle and the method of the Life-Cultivation of the Chun-chu-Jeon-Kook (春秋戰國) periods were recorded in Huang-Jae-Nai-Gyung (黃帝內徑) detailly and the remedy examples by ancient Chi-Kung such as Tao-Yin (導引), Haeng-Chi (行氣) were presented, we considered that theoretical basis of the development of Life-cultivation and Chi-Kung study was furnished in that period. 3. A famous doctor, Hwa-Ta (華陀) lived in Han dynasty, researched the theory and practice of Tao-Yin transmitted from the former generations, as that result, he formed a kind of medical gymnastics what is called O-Keum-Hi (五禽戱). It is considered that 'O-Keum-Hi' is a Tao-Yin method developed more practically and systemetically than the Tao-Yin appeared in the 'Jang-Ja' (莊子) or 'Hoy-Nam-Ja' (淮南子). 4. In Wui-Jin-Nambook Jo (魏晋南北朝) periods, the contents of Chi-Kung were more abundant under the influence of Buddhism (佛敎) and Taoism (道敎). Galhong (葛洪), the author of 'Po-Bak-Ja' (抱朴子) arranged the ancient Chi-Kung method systematically first of all, Tao-Goeng-Gyung (陶宏景), the author of 'Yang-Seong-Yeun-Myung-Rok' (養性延命錄) recorded the 'Yook-Ja-Geul' (六字訣) first time. 5. There is a new development of Chi-Kung therapy in Soo-Tang-Odae (隋唐五代) pefiods, especially So-Won-Bang (巢元方), the author of 'Jey-Byung-Won-Hwu-Ron' (諸病源候論) collected aimost all of the Chi-Kung method, for curing the disease formed before soo (隋) period. From that fact, we supposed that Chi-Kung was utilized more widely in curing the disease. 6. 'So-Ju-Cheon-Hwa-Hu-Peob' (小周天火候法) was adopted as the best orthodox approach under the influence of Nae-Tan-Taoist (道敎內丹學派) in Song-Keum-Won (宋金元) periods, especially in the song dynasty, 'Pal-Dan-Geum' (八段錦) was appeared and assignment of six-Chi (六氣) for bowel and viscera in the 'Yook-Ja-Geul' (六字訣) was decided firmly, that is to say Lung-Si (肺-呬), Heart-Kha (心-呵), Spleen-Hoa (脾-呼), Liver-Hoe (肝-噓), Kidneychui (賢-吹), Three-Burner-shi (三焦-嘻). 7. In Myung-Cheong (明淸) periods, The general practitioner applied the principle of 'Byun-Jeng-Ron-Chi' (辨證論治) to the Chi-Kung field, and after Myeong dynasty the style of doing 'Yook-Ja-Gyel' (六字訣) was developed to the moving style. 8. Today, in china, the study on the Chi-Kung is being progressed constantly under the positive assistance of government, Chi-Kung-Hak (氣功學) has taking its place as a branch of study step by step. It is considered that the establishment of Chi-Kung-Hak Classroom (氣功學教室) and Medical Chi-Kung Center (氣功療法室) for special and systematic research are needed, at the same time the settlement of institutional system for training the Chi-Kung technician (氣功師) is also needed.

• Journal of Food Hygiene and Safety
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• v.6 no.1
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• pp.1-12
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• 1991

Fischer 344 rats aged six weeks were diYided into four groups and group 1, 2, and 3 of rats were given an intraperitoneal injection of diethylnitrosamine at 200 mg/kg body weight and group 4 was given saline alone. Two weeks after beginning of the experiment, group 1 and 2 of rats were begun to feed on diets containing 0.02% 2-acetylaminofluorene as a promoter for four weeks. Three weeks after beginning of the experiment, all groups were performed partial hepatectomy. During the last two weeks, group 1 and 3 of rats were received subcutaneously 3 consecutive weekly doses of iron dextran at 0.125 ml/100 g body weight. Subcutaneous injection of iron dextran resulted in hepatic siderosis in group 1 and 3 of rats. Pre neoplastic nodules were identified histopathologically by two markers, resistance to exogenous iron accumulation and glutathione S-transeferase placental form (GST-P) activity, while early carcinogen induced foci were hardly resistant to iron accumulation and though a few lesions were identified, it could hardly be distincted from normal hepatocytes of surroundings. However, GST-P positive nodules as well as foci were clearly distincted from normal hepatic cells of surroundings. In the quantitative analysis of carcinogen-induced nodules and foci, more lesions were detected by immunohistochemical method for GST-P than by prussian blue staining for resistant to iron accumulation. It is concluded that immunohistochemical marker for GST-P is more sensitive and reliable than iron-resistance marker, and that iron-resistance is not useful marker for early detection of carcinogen-induced hepatic lesions.

• Tuberculosis and Respiratory Diseases
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• v.60 no.4
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• pp.451-463
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• 2006

Background : Reactive oxygen species (ROS) take center stage as executers in ventilator-induced lung injury (VILI). The protein with DNA-damage scanning activity, poly (ADP-ribose) polymerase-1 (PARP1), signals DNA rupture and participates in base-excision repair. Paradoxically,overactivation of PARP1 in response to massive genotoxic injury such as ROS can induce cell death through ${\beta}$ -nicotinamide adenine dinucleotide ($NAD^+$) depletion, resulting in inflammation. The purpose of this study is to investigate the role of PARP1 and the effect of its inhibitor in VILI. Methods : Forty-eight male C57BL/6 mice were divided into sham, lung protective ventilation(LPV), VILI, and PARP1 inhibitor (PJ34)+VILI (PJ34+VILI) groups. Mechanical ventilator setting for the LPV group was $PIP\;15cmH_2O$ + $PEEP\;3cmH_2O$ + RR 90/min + 2 hours. The VILI and PJ34+VILI groups were ventilated on a setting of $PIP\;40cmH_2O$ + $PEEP\;0cmH_2O$ + RR 90/min + 2 hours. As a PARP1 inhibitor for the PJ34+VILI group, 20 mg/Kg of PJ34 was treated intraperitoneally 2 hours before mechanical ventilation. Wet-to-dry weight ratio and acute lung injury (ALI) score were measured to determine the degree of VILI. PARP1 activity was evaluated by using an immunohistochemical method utilizing biotinylated NAD. Myeloperoxidase (MPO) activity and the concentration of inflammatory cytokines such as tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 were measured in bronchoalveolar lavage fluid (BALF). Results : In the PJ34+VILI group, PJ34 pretreatment significantly reduced the degree of lung injury, compared with the VILI group (p<0.05). The number of cells expressing PARP1 activity was significantly increased in the VILI group, but significantly decreased in the PJ34+VILI group (p=0.001). In BALF, MPO activity, $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6 were also significantly lower in the PJ34+VILI group (all, p<0.05). Conclusion : PARP1 overactivation plays a major role in the mechanism of VILI. PARP1 inhibitor prevents VILI, and decreases MPO activity and inflammatory cytokines.