http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
비글개에서 인체 재조합 적혈구 조혈인자 , rHuEPO 의 아만성 정맥독성에 관한 연구
조명행(Myung Haing Cho),성하정(Ha Jung Seong),김형식(Hyung Sik Kim),곽승준(Seung Jun Kwack),천선아(Sun Ah Chun),한하수(Ha Su Han),임소영(So Young Lim),안미영(Mi Young Ahn),김원배(Won Bae Kim),김병문(Byoung Moon Kim),안병옥(Byoung Ok 한국응용약물학회 1998 Biomolecules & Therapeutics(구 응용약물학회지) Vol.6 No.3
The subchronic toxicity study of rHuEPO, a newly developed recombinant erythropoietin, was investigated for 13 weeks in Beagle dogs intravenously treated with doses of 100, 500 and 2,500 IU/㎏/day. There were no significant changes in body weight, food intake, physical and opthalmic examination, urine analysis, etc. Any toxic response was not observed except for enlarged spleen and extramedullary hematopoiesis. These results indicate that the no-observed adverse effect level (NOAEL) of rHuEPO is 100 IU/㎏ in Beagle dogs.
호중구 감소증을 유도한 마우스에서의 유전자 재조합 인과립구 콜로니자극인자의 효과
조명행(Myung Haing Cho),유아선(Ah Sun Yu),방명주(Ming Zhu Fang),곽형일(Hyung Il Kwak),성하정(Ha Jung Seong),강관엽(Koan Yeob Kang),최승진(Seung Jin Choi),정경환(Kyung Hwan Jung),박두홍(Doo Hong Park),안길환(Gil Hwan Ahn) 한국응용약물학회 1998 Biomolecules & Therapeutics(구 응용약물학회지) Vol.6 No.2
Administration of 3 type KGCs [recombinant human granulocyte colony-stimulating factor (rhGCSF)] to mice with cyclophosphamide (CPA)-induced neutropenia for 4 consecutive days from the day after the CPA dosing (100 mg/kg) resulted in a dose dependent increase in the peripheral blood neutrophil count 6 hours after the final KGC injection. Within the KGC dose range of 0.1 to 40 ㎍ per mouse per day, there was a sigmoidal relationship between the logarithm of the dose and the peripheral blood neutrophil count (relative value for neutrophil count of the basal dose) in the treated mice. The sigmoidal relationship of test KGC preparations shows that there is a saturation point in terms of efficacy. Compared with effect of KGC-Orange, Green, and Blue, KGC-Orange recovers neutrophils more effectively than the others do.
비글개에서 인체 재조합 적혈구 조혈인자, rHu-EPO의 급성독성에 관한 연구
조명행,성하정,김형식,곽승준,천선아,임소영,김원배,김병문,안병옥,이병무,Cho, Myung-Hang,Seong, Ha-Jung,Kim, Hyung-Sik,Kwack, Seung-Jun,Chun, Sun-Ah,Lim, So-Young,Kim, Won-Bae,Kim, Byoung-Moon,Ahn, Byoung-Ok,Lee, Byung-Mu 한국독성학회 1996 Toxicological Research Vol.12 No.2
The acute toxicity of rHu-EPO, newly developed recombinant erythropoietin, was tested in beagle dogs. rHu-EPO, when administered intravenously at 25, 000 IU/kg, did not cause any death. Also, rHu-EPO did not induce any change of body weight, food intake and clinical signs compared to controls. There were no significant changes in hematological, urine analysis and pathological examination. These results showed that rHu-EPO did not induce any remarkable toxic response and the $LD_50$ was greater than 25, 000 IU/kg in beagle dogs.
비글개에서 인체 재조합 적혈구 조혈인자 , rHu-EPO 의 아급성정맥독성시험
조명행(Myung Hang Cho),성하정(Ha Jung Seong),김형식(Hyung Sik Kim),곽승준(Seung Jun Kwack),임소영(So Young Lim),천선아(Sun Ah Chun),김원배(Won Bae Kim),김병문(Byoung Moon Kim),안병옥(Byoung Ok Ahn),이병무(Byung Mu Lee) 한국응용약물학회 1996 Biomolecules & Therapeutics(구 응용약물학회지) Vol.4 No.4
The subacute toxicity was investigated in Sprague-Dawley rats orally treated with KDRD-010 at the doses of 0.056, 0.28, and 1.4 g/㎏ for one month. There were no clinical signs and pathological changes compared with control group. Body weights were not significantly changed between control and treatment groups. In hematological and biochemical serum parameters, all mean values appear to be within the normal range. In pathological examinations, hemorrhages of lung was observed in one male rat at low dose group and one female rat at high dose group of KDRD-010, but it was not considered to be caused by KDRD-010. These results suggest that KDRD-010 dose not induce any significant subacute oral toxicities in Sprague-Dawley rats.
ICR마우스에서 phenytoin의 최기형성 및 dimethyl sulfoxide의 항최기형 효과
이재권,이창업,이문한,류판동,조명행,성하정,박진봉,Lee, Jae-kwon,Lee, Chang-eop,Lee, Mun-han,Ryu, Pan-dong,Cho, Myung-haing,Sung, Ha-jung,Park, Jin-bong 대한수의학회 1994 大韓獸醫學會誌 Vol.34 No.4
Phenytoin(PHT), a commonly prescribed anticonvulsant, has been known as a teratogen in experimental animals and human. However, PHT has strain-specific teratogenic effects for mice and human. Dimethyl sulfoxids(DMSO) has been known to antagonize the teratogenic effects of secalonic acid D, a toxic mold metabolite that has similar teratogenic effects to PHT. Therefore, this study was performed to examine the embryopathic effects of PHT in terms of treatment period and the antiteratogenic effect of DMSO in ICR mice. PHT(75mg/kg, BW) was administered intrapetitoneally on day 10, 10-11 and 10-12 of gestation with or without DMSO(2ml/kg, BW), and the fetal malformation was observed on day 18. Major malformation of fetuses treated with PHT on day 10, 10-11 and 10-12 of gestation was cleft palate, and the percentages of fetus with cleft palate were 14.5%, 31.7% and 51.7%, respectively. Also, there was a significant decrease of cleft palate from 51.7% in PHT alone group to 30.8% in PHT plus DMSO group. Our findings suggest that cleft palate is one of major malformation by PHT treatment in ICR mouse and DMSO has strong antiteratogenic effect.
Phenytoin의 태아 구개열 유발과 모체 혈청 Corticosterone 증가에 대한 Dimethyl Sulfoxide 억제 작용
이재권,이창업,이문한,류판동,이영재,성하정,Lee, Jae-Kwon,Lee, Chang-Eop,Lee, Mun-Han,Ryu, Pan-Dong,Lee, Young-Jae,Sung, Ha-Jung 한국독성학회 1992 Toxicological Research Vol.8 No.2
It is well known that phenytoin (PHT), a commonly prescribed anticonvulsant, has teratogenicity in experimental animals and human. The major malformation induced by PHT in mouse is cleft palate. The mechanisms of the embryotoxic effects of PHT are unknown. However, PHT and synthetic glucocorticoids share several features with respect to their teratogenicity, and it was known that PHT increased maternal corticosterone level. Therefore PHT-induced cleft palate may be mediated indirectly by elevated maternal corticosterone. Recently it was reported that secalonic acid Dinduced cleft palate and elevated endogenous corticosterone level, and that such effects were antagonized by DMSO. The purpose of this work was to investigate whether the elevated maternal corticosterone is associated with the teratogenicity of PHT in the ICR mouse fetuses by treatment with PHT or PHT plus DMSO. PHT (74mg/kg, BW) was daily administered intraperitoneally on day 10~12 of gestation with and without DMSO(2ml/kg, BW), and the fetal malformation was observed on day 18. Maternal serum corticosterone and fetal PHT levels were determined by HPLC. The results are summarized as follows. 1)The percentage of cleft palate incidense in fetuses following treatment with PHT on day 10~12 of gestation was 51.7%. 2)There was a significant decrement in the cleft palate incidence in fetuses to 30.8% in the group treated with PHT plus DMSO compared with 51.7% in that with PHT alone. 3) Maternal serum corticosterone levels following treatment with PHT on day 10~12 of gestation increased by 116~343% compared with that of vehicle control. Such effect was antagonized by DMSO. 4)PHT concentration in the fetuses was not affected by DMSO. These results suggest that PHT-induced cleft-palate in fetuses seems to be closely associated with the elevation of maternal corticosterone level.