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Evaluation of a Apo-1/Fas promoter polymorphism in Korean stroke patients
Jung-ChulSeo,Sang-WonHan,Chang-SikYin,Hyung-KyunKoh,Chang-HwanKim,Ee-HwaKim,Kang-HyunLeem,Hyang-SookLee,Hi-JoonPark,Soon-AeKim,Bong-KeunChoe,Hee-JaeLee,Sung-VinYim,Chang-JuKim,Joo-HoChung 생화학분자생물학회 2002 Experimental and molecular medicine Vol.34 No.4
Apoptosis has been implicated in the pathogenesis ofneurodegenerative diseases such as stroke and Alzhe-imer's disease. Apo-1/Fas gene is one of the mediatorsof apoptosis in stroke. MvaI polymorphism is the firstpolymorphic marker identified in the Apo-1/Fas genepromoter, which was typed by PCR and folowed byMvaI digestion and gel electrophoresis. DNA isolatedfrom peripheral blood collected from 91 strokepatients and 103 healthy blood donors was used forgenotypes of GG, GA and AA by sequence specificprimer PCR. MvaI polymorphism was examined basedon Fas gene promotor region by restriction fragmentlength polymorphism (RFLP). The Fas-G genotypewas the least frequent in patients with stroke andhealthy controls (P= 0.57). In normal Korean controlsthe MvaI polymorphism GA, AA and GG were 48.6%,34.9% and 16.5%. In stroke patients were 56.2%, 29.6%and 14.2% respectively. And the allelic frequencies ofMvaI*2 (G) alle were les frequent than MvaI*1 (A)alle in patients with stroke and healthy controls(P= 0.76). In normal Korean controls MvaI*1 (A) andMvaI*2 (G) alles were 59.2% and 40.8%. In strokepatients were 57.6% and 42.4%, respectively. Ourresults, pending confirmation in a larger study, indi-cate that the Fas genotype may not apear to be a riskfactor for stroke in Korean stroke patients.
Si-YunRyu,Bit-NaKang,Sung-whanCho,Hwa-youngSon,Kyu-ShikJeong,Sang-JoonPark,Sung-HoKim,Se-RaKim,Tae-HwanKim,Mi-youngAn,Ho-Jun Kim 대한수의학회 2002 Journal of Veterinary Science Vol.3 No.4
The detrimental effects of environmental pollutantson the health of the individual are generally accepted,although the mechanisms of these effects remain tobe incompletely understood.In the present study,weexamined the effects of B[a]P,2-BP,phenol and TCDDon proinflammatory cytokine gene expression in micespleen cells which were stimulated with anti-CD3.10-9M TCDD increased IFNγ and TNFα gene expression,but suppressed IL-1 gene expression. 10-6M phenolinhibited IL-1, IL-6 and TNFα gene expression, and10-6M of 2-BP downregulated TNFα gene expression.However, 10-6M of B[a]P did not influence on IL-1,IL-6,IFNγ and TNFα gene expression. These findingssuggest that TCDD may impair the immune functionsof mice by enhancing proinflammatory cytokines pro-duction, whereas phenol and 2-BP may impair thefunctions by inhibiting the production of thesecytokines.
Rodenticide Poisoning in a Cocker Spaniel Dog
Hai-Jie Yang,Won-Il Jeong,Da-Hee Jeong,Sun-Hee Do,Dong-Hwan Kim,Myung-Hee Sohn,Dong-Wei Yuan,Il-Hwa Hong,Youg-Sook Son,Sang-JoonPark,Tae-Hwan Kim,Kil-Soo Kim,Keun-Woo Lee,Kyu-Shik Jeong 한국실험동물학회 2005 Laboratory Animal Research Vol.21 No.1
A dead Cocker Spaniel, a one-year-old male, was presented from a local animal hospital to the College of Veterinary Medicine, Kyungpook National University with a history of vomiting right after the ingestion of the anti-coagulant rodenticide 14 days before. At necropsy, the thorax was filled with uncoagulated blood and the thymus was markedly hemorrhagic. Hemorrhages were also found in the subcutaneous or mesenteric adipose tissues and the submucosal layers of the intestine and stomach. The spleen was atrophied. In microscopy, hemorrhages were detected in the thymus, submucose of the stomach and intestine, and adipose tissues around several organs such as the heart, kidney, and intestines. However, hemorrhages, were not detected in lungs. Centrilobular necrosis was observed in the liver. In conclusion, the cause of death was severe hemorrhages, which might have been due to the reabsorption of a small amount of anti-coagulant rodenticide that still remained in the body after vomiting. Therefore, the diagnosis was decided as intoxication with anti-coagulant rodenticide.