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Ji-Hae Park,Do-Gyeong Lee,Seung-Woo Yeon,Hyuk-Sang Kwon,Jong-Hee Ko,Dong-Jin Shin,Han-Sol Park,Yong-Soon Kim,Myun-Ho Bang,NAM-IN BAEK 대한약학회 2011 Archives of Pharmacal Research Vol.34 No.4
The silkworm (Bombyx mori L.) droppings were extracted with 80% aqueous MeOH, and the concentrated extract was partitioned in succession with EtOAc, n-BuOH, and H_2O. From the EtOAc fraction, five megastigmane sesquiterpenes were isolated through repeated silica gel and ODS column chromatography. According to the results of spectroscopic data, such as NMR, MS, and IR, the chemical structures of the isolated compounds were determined as (3S,5R,8R)-3,5-dihydroxymegastigma-6,7-dien-9-one (1), (S)-dehydrovomifoliol (2), (6R,7E,9R)-9-hydroxy-4,7-megastigmadien-3-one (3), (3S,5R,6S,7E)-3,5,6-trihydroxy-7-megastigmen-9-one (4), (6R,9R)-9-hydroxy-4-megastigmen-3-one (5). Compounds 2 through 5 were isolated for the first time from silkworm droppings. GC/MS analysis indicated silkworm powder contained compound 3, and mulberry leaves contained compound 4. Compounds 1 and 5 increased the expression of heme oxygenase-1 and SIRT1 in HepG2 and HEK239 cells, respectively. Heme oxygenase-1 is considered to be an antioxidant enzyme that catabolizes heme to carbon monoxide, free iron and biliverdin, while SIRT1 is the mammalian homologue of the yeast silent information regulator (Sir)-2, which are involved in the suppression of inflammatory mediators or factors that may be used to improve atopy-related symptoms.
Diphenylhydantoin에 의한 중증 재생불량성 빈혈
김한성 ( Kim Han Seong ),한경근 ( Han Gyeong Geun ),김종현 ( Kim Jong Hyeon ),김경환 ( Kim Gyeong Hwan ),조강일 ( Jo Gang Il ),정찬수 ( Jeong Chan Su ),정철호 ( Jeong Cheol Ho ),제영성 ( Je Yeong Seong ),임창현 ( Im Chang Hyeon 대한내과학회 1993 대한내과학회지 Vol.44 No.5
Since 1938, Diphenylhydantoin (DPH) has remained one of the most widely used anticonvulsants for treatment and prevention of seizures. DPH may induce serious damage to the hematopoietic system. Especially, DPH induced severe aplastic anemia is one of the most severe complication and its incidence is extremely rare. We recently expreienced one case of severe aplastic anemia in 52-year-old woman following administration of DPH. Litreature was reviewed briefly.
홍삼 생약 복합물(KTNG0345)의 피부 주름개선에 관한 작용기전
소승호(Seung-Ho So),이성계(Seong-Kye Lee),황의일(Eui-Il Hwang),구본석(Bon-Suk Koo),한경호(Gyeong-Ho Han),정진호(Jin Ho Chung),이민정(Min-Jung Lee),김나미(Na-Mi Kim) 고려인삼학회 2008 Journal of Ginseng Research Vol.32 No.1
본 실험은 홍삼 혼합물 (KTNG0345)을 이용한 주름 예방 및 개선효과가 있는 건강기능 식품을 개발하기 위한 기초자료로 활용하기 위하여 시료를 경구투여한 무모생쥐의 피부조직으로부터 MMP-3의 발현양상과 작용 메커니즘을 연구하였다. MMP-3의 발현정도는 농도 의존적으로 현저한 감소를 나타내었으며, 유전자와 단백질 모두에서 동일한 양상을 보였다. PAK는 변화가 없었지만, p38, p-p38 그리고 c-Jun, p-c-Jun을 통계적으로 유의하게 감소시킴으로써 MMPs의 발현 감소를 가져온 것으로 보인다. 뿐만 아니라 자외선에 의한 TNF-α의 생성 또는 유입을 억제함으로써 TNF-α receptor에 의해 매개되는 신호전달 경로를 둔화시켜 MMPs의 발현을 감소시킨 것으로 보인다. 이렇게 KTNG0345는 복합적인 활성으로 작용하여 주름생성 억제 활성을 보이는 것으로 판단된다. UV irradiation causes skin-aging involving coarse wrinkles, thickening, dyspigmentation, and rough skin surface. These phenomena in complex skin tissue is controlled with receptor of cell surface growth factor and cytokine receptors. The activation of receptors induces multiple downstream signaling pathways including expression of MMPs (matrix metalloproteinases). This study was aimed to elucidate the mechanism for anti-wrinkle activity of Korean red ginseng, Torilis fructus and Corni fructus mixture (KTNG0345). In this animal study, we have investigated decreasing effects of Korean red ginseng mixture on MMP-3 synthesis through diminishing TNF-α signaling that express MMP-1, -3, and -9. c-Jun and c-fos as a component of transcription factor AP-1 (activator protein-1) were analyzed the expression level using real time PCR and western blotting. c-Jun was decreased dose dependent manner both gene and protein level where as cfos was not changed. In upstream, JNK and PAK was not changed, but p38 was decreased in down stream. MMP-3, final product in this pathway was significantly decreased in dose dependent manner. These results suggest that Korean red ginseng mixture have a anti-wrinkle activity through TNF-α mediated MMPs expression pathway.
A new miroestrol glycoside from the roots of Pueraria mirifica
Bang, Myun-Ho,Lee, Do-Gyeong,Baek, Yoon-Su,Cho, Jin-Gyeong,Han, Min-woo,Choi, Kyoung-Sook,Chung, Dae-Kyun,Ko, Sung-kwon,Oh, Chang-Hwan,Cho, Soo-Yeul,Chai, Kap-Yong,Kim, Jin-Ho,Baek, Nam-In Springer-Verlag 2013 Chemistry of natural compounds Vol.49 No.3
내시경으로 관찰된 식도 병변의 발생과 경비위관 거치의 상관관계 경피 내시경하 위루술을 시행한 185예의 임상적 고찰
김한숙 ( Kim Han Sug ),동석호 ( Dong Seog Ho ),정경환 ( Jeong Gyeong Hwan ),채명종 ( Chae Myeong Jong ),한요셉 ( Han Yo Seb ),정용희 ( Jeong Yong Hui ),이병욱 ( Lee Byeong Ug ),김효종 ( Kim Hyo Jong ),김병호 ( Kim Byeong Ho ),장 대한소화기학회 2003 대한소화기학회지 Vol.42 No.6
Background/Aims: Percutaneous endoscopic gastrostomy (PEG) is a method widely used for long-term enteral nutrition in dysphagia. Mostly, it is preceded by nasogastric intubation (NI) for short-term enteral nutrition; endoscopic findings associated with NI are encountered during PEG. The purpose of this study was to discuss such findings and to delineate a relationship between these findings, especially esophageal lesions and the duration of NI. Methods: This study involved 185 individuals who had undergone PEG at Kyung Hee Medical Center from January 1999 to May 2002. The medical records were examined retrospectively. Results: The dysfunction of the CNS comprised 98.4% of the causes of dysphagia. The duration of NI was 15.2 weeks on average, with median value of 8.7 weeks, indicating that PEG was performed relatively soon. Endoscopic findings revealed esophagitis in 63 cases, esophageal ulcers in 27 and active bleedings in another 10. The incidence of esophageal lesions was shown to be higher in subjects with duration of NI under 12 weeks than in those with duration over 12 weeks (p=0.032). Conclusions: PEG was carried out in many cases during the early stages of dysphagia, and NI-associated esophageal lesions appeared to be more prevalent within 12 weeks of NI duration. These results may be of help in deciding the timing of PEG. (Korean J Gastroenterol 2003;42:461-467)