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Hwang, Seongsoo,Choi, Eun Joo,You, Seungkwon,Choi, Yun-Jaie,Min, Kwan-Sik,Yoon, Jong-Taek Asian Australasian Association of Animal Productio 2006 Animal Bioscience Vol.19 No.11
This study was performed to determine the developmental potentials of nuclear transfer (NT) embryos using life-span extended cells transfected with a foreign gene as donor cells. A life-span extended bovine embryonic fibroblast cell line was transfected with an expression vector in which the human type II collagen (BOMAR) and ear fibroblasts were used as a donor cell. Cytogenetic analysis was performed to analyze the chromosomal abnormality of donor cells. The fusion rate of 1.8 kV/cm for $15{\mu}sec$ given twice was significantly higher than that of other groups (p<0.05) and the embryos lysed were significantly higher after 1.8 kV/cm for $20{\mu}sec$ given once compared to other groups (p<0.01). The blastocyst development in the ear cell group was statistically significant compared to both BOMAR groups (p<0.01). Both BOMAR groups cultured more than 40 passages (>40 passages) had a lower number of chromosomes; however, fresh granulosa cell (GC) and BOMAR groups cultured less than 20 passages had normal chromosome numbers. Both >40 passages BOMAR groups had numerous obscure debris in metaphase spreads. The transfected foreign gene was expressed in all BOMAR groups, but not in the GC group. Based on these results, the lower developmental potential of NT embryos using life-span extended donor cells transfected with a foreign gene might be a cause of chromosomal abnormality in donor cells.
Nonenzymatic Degradation of RNA by Polyvinylpyrrolidone
You, Sung-Sik,Ryu, Hyeong-Won,Hwang, Seung-Jin,Jang, Hyun,Cho, Young,Ko, Thong-Sung 충남대학교 기초과학연구소 1995 忠南科學硏究誌 Vol.22 No.1
Nonenzymatic degradation of Baker's yeast RNA by polyvinylpyrrolidone (PVP) was tested, according to the procedure for the assay of ribonuclease activity, described by McDonald (1955) using MacFadyen's reagent. Significant catalytic activity of PVP for the RNA-cleavage was observed. The plot of the reaction rate vs. PVP concentration showed a bell-shaped pattern.
급성심근경색환자에서 최초증상으로부터 재관류요법결정까지의 시간경과
황성오,임경수,이부수,김영식,안무업,유병수,윤정환,박금수,최경훈 대한응급의학회 1994 대한응급의학회지 Vol.5 No.1
To investigate the potential causes of delays between onset of chest pain and provision of reperfusion therapy. We measured time intervals of prehospital phase and in emergency department in 149 patients with acute myocardial infarction. Data were collected by interview with patients for prehospital time delays and time records in emergency department. The results were followings : Patients who admitted to our hospital prior to 6 hours from chest pain were 519(34%). Mean prehospital dealy time of total patients was 548 minutes. Mean prehospital delay time of direct visit patients was shorter than transported patients(357 vs 595 minutes, p<0.05). In direct visit patients, patient delay time was shorter in reperfusion group than non-reperfusion group(117 vs 481 Minutes, p<0.001). In transported patients, patients dealy time and first hos-pital delay time were shorter in reperfusion group than non-reperfusion group(116 vs 294 minutes in patient dealy time, 70 vs 227 minutes in first hospital dealy time, p<0.05 respectively). Transportation time and dealy time in emergency department were not different between both groups. In conclusion, time dealys in patients not receiving reperfusion therapy was attributed to prolonged patient delay time and first hospital dealy time in prehospital phase.
Hwang, Jungwon,Kim, Byoung Sik,Jang, Song Yee,Lim, Jong Gyu,You, Dong-Ju,Jung, Hyun Suk,Oh, Tae-Kwang,Lee, Jie-Oh,Choi, Sang Ho,Kim, Myung Hee National Academy of Sciences 2013 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.110 No.30
<P>Pathogenic and commensal bacteria that experience limited nutrient availability in their host have evolved sophisticated systems to catabolize the mucin sugar N-acetylneuraminic acid, thereby facilitating their survival and colonization. The correct function of the associated catabolic machinery is particularly crucial for the pathogenesis of enteropathogenic bacteria during infection, although the molecular mechanisms involved with the regulation of the catabolic machinery are unknown. This study reports the complex structure of NanR, a repressor of the N-acetylneuraminate (nan) genes responsible for N-acetylneuraminic acid catabolism, and its regulatory ligand, N-acetylmannosamine 6-phosphate (ManNAc-6P), in the human pathogenic bacterium Vibrio vulnificus. Structural studies combined with electron microscopic, biochemical, and in vivo analysis demonstrated that NanR forms a dimer in which the two monomers create an arched tunnel-like DNA-binding space, which contains positively charged residues that interact with the nan promoter. The interaction between the NanR dimer and DNA is alleviated by the ManNAc-6P-mediated relocation of residues in the ligand-binding domain of NanR, which subsequently relieves the repressive effect of NanR and induces the transcription of the nan genes. Survival studies in which mice were challenged with a ManNAc-6P-binding-defective mutant strain of V. vulnificus demonstrated that this relocation of NanR residues is critical for V. vulnificus pathogenesis. In summary, this study presents a model of the mechanism that regulates sialic acid catabolism via NanR in V. vulnificus.</P>
Triazole계 농약 Difenoconazole이 Xenopus Laevis의 초기 배 발생에 미치는 독성 영향
이유화 ( You Hwa Lee ),윤춘식 ( Chun Sik Yoon ),이미주 ( Mi Ju Lee ),황용기 ( Yong Gi Hwang ),정선우 ( Seon Woo Cheong ) 한국환경과학회 2011 한국환경과학회지 Vol.20 No.10
We investigated the toxic effects of difenoconazole on the development in the African clawed frog, Xenopus laevis. To test the toxic effects, frog embryo teratogenesis assays using Xenopus were performed. Embryos were exposed to various concentrations of difenoconazole (0-30 μM). LC100 for difenoconazole was 30 μM, and the LC50 determined by probit analysis was 27.19 μM. Exposure to difenoconazole concentrations ≥5 μM resulted in 10 different types of severe external malformation. Histological examinations revealed dysplasia of the eye, heart, liver, somatic muscle, and swelling of the pronephric ducts. The tissue-specific toxic effects were investigated with an animal cap assay. Blood cells were normally induced at a high frequency by mSCF and activin A. However, the induction of blood cells was strongly inhibited by the addition of difenoconazole. Electron micrographs of tested embryos showed the degeneration of somatic muscle and the shrinkage of microvilli on pronephric duct. The gene expression of cultivated animal cap explants was investigated by reverse transcriptase-polymerase chain reaction (RT-PCR). It revealed that the expression of the blood-specific marker(β -globin Ⅱ) and muscle-specific marker (XMA) were more strongly inhibited than the neural-specific marker(XEn2) by the addition of difenoconazole.