http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
서울의 Penicillinase Producing Neisseria Gonorrhoeae 발생빈도(1996)
김재홍,황동규,전재홍,김윤석,김중환,김용준,이창균,임동진,김현수,조창근,김경문,박상훈,전우형,김희성,이호정,차명수,김갑형,김형석,김석우,황지환,박병순,권오상,이민수,송기훈,성소영,이인섭,부태성 대한화학요법학회 1999 대한화학요법학회지 Vol.17 No.2
Background : In recent years, gonorrhea has been panedemic and remains one of the most commom STDs in the world, especially in developing countries. Objective & Methods: For the detection of a more effective therapeutic regimen and assessing the prevalence of PPNG, we have been trying to study the patients who have visited the VD Clinic of Choong-Ku Public Health Center in Seoul since 1980 by means of the chromogenic cephalosporin method. Results: In 1996, 139 strains of N. gonorrhoeae were isolated, among which 53(39.0%) were PPNG. Conclusion: Our results suggests that after a peak of 74.3% in 1993, the prevalence of PPNG in Seoul is gradually declining.
서울의 Penicillinase Producing Neisseria gonorrhoeae 발생빈도(1997)
김재홍,문득곤,김정수,김용준,임동진,박상훈,김희성,이민수,송기훈,김갑형,김형석,성소영,이인섭,김석우,황지환,조창근,김경문,부태성 대한화학요법학회 2000 대한화학요법학회지 Vol.18 No.3
Background : In recent years, gonorrhea has been pandemic and remains one of the most common STDs in the world, especially in developing countries. Objective & Methods : For the detection of a more effective therapeutic regimen and assessing the prevalence of PPNG, we have been trying to study the patients who have visited the Venereal Disease Clinic of Choong-Ku Public Health Center in Seoul since 1980 by means of the chromogenic cephalosporin method. Results : In 1997. 99 strains of N. gonorrhoeae were isolated, among which 45(45.5%) were PPNG. Conclusion : The prevalence of PPNG in Seoul, which had been decreased to 39% in 1996 after a peak of 74.3% in 1993, is increased to 45.5% in 1997.
SEK1 카이네이즈 과발현(overexpression)생쥐 대식세포주(RAW264,7)의 Nitric Oixde(NO)유도성 세포고사 (apoptosis) 기전에 관한 연구
정병학,소홍섭,박래길,정헌택 圓光大學校 醫科學硏究所 1998 圓光醫科學 Vol.14 No.2
Nitric oxide (NO) induces apoptotic cell death in murine RAW 264.7 macrophages. To A elucidate the NO-induced apoptotic mechanisms in SEK1/MKK4 overexpressed RAW 264.7 cells, we generated clones of RAW 264.7 cells which stably overexpressd kinase inactive SEK1 (RAW/SEK1-KI) or wild type SEK1 (RAW/SEK1-WT). Treatment of kinase inactive SEK1 transfected RAW 264.7 cells (RAW/SEK1-KI) with sodium nitroprusside (SNP), a NO donor, significantly decreased the cell viability than that of RAW control cells which were treated with the same amount of SNP. However, RAW/SEK1-WT cells were less susceptible to NO induced apoptosis. Furthermore, the treatment of NO with farnesyltransferase inhibitor (FTI) of Ras or MEK inhibitor (PD098059) significantly increased the apoptotic death of RAW/SEK1-KI. However, SB203580, a specific p38 inhibitor, did not affect NO-induced apoptosis of kinase inactive SEK1 transfected RAW 264.7 cells. For a while, caspase 3-like protease activity in NO plus FTI treated RAW/SEK1-KI cells were more increased than that of NO only. In addition, nuclear transcription factor kB (NFkB) was significantly activated in NO-treated RAW/SEK1-KI cells, whereas these transcriptional factor was not markedly activated in NO-treated RAW/SEK1-WT cells. Supershift analysis demonstrates that NFkB was composed of mainly p50 homodimer. Also pyrrolidine dithiocarbamate (PDTC), a strong inhibitor of NFkB, significantly inhibits the NO-induced apoptosis in RAW/SEK1-KI cells. Taken together, we suggest that SEK1 may play anti-apoptotic role in RAW cells from NO-induced apoptosis via the modulation of NFkB. In addition, in the absence of SEK1 kinase cascade activation, the viability of RAW cells may be mainly dependent on Ras/Raf/MEK/ERK pathway.
So, Hong-Seob,Park, Channy,Kim, Hyung-Jin,Lee, Jung-Han,Park, Sung-Yeol,Lee, Jai-Hyung,Lee, Zee-Won,Kim, Hyung-Min,Kalinec, Federico,Lim, David J.,Park, Raekil Elsevier/North-Holland,Biomedical Press 2005 Hearing research Vol.204 No.1-2
<P><B>Abstract</B></P><P>Changes in intracellular Ca<SUP>2+</SUP> level are involved in a number of intracellular events, including triggering of apoptosis. The role of intracellular calcium mobilization in cisplatin-induced hair cell death, however, is still unknown. In this study, the effect of calcium channel blocker flunarizine (Sibelium™), which is used to prescribe for vertigo and tinnitus, on cisplatin-induced hair cell death was investigated in a cochlear organ of Corti-derived cell line, HEI-OC1, and the neonatal (P2) rat organ of Corti explant. Cisplatin induced apoptotic cell death showing nuclear fragmentation, DNA ladder, and TUNEL positive in both HEI-OC1 and primary organ of Corti explant. Flunarizine significantly inhibited the cisplatin-induced apoptosis. Unexpectedly, flunarizine increased the intracellular calcium ([Ca<SUP>2+</SUP>]<SUB>i</SUB>) levels of HEI-OC1. However, the protective effect of flunarizine against cisplatin was not mediated by modulation of intracellular calcium level. Treatment of cisplatin resulted in ROS generation and lipid peroxidation in HEI-OC1. Flunarizine did not attenuate ROS production but inhibited lipid peroxidation and mitochondrial permeability transition in cisplatin-treated cells. This result suggests that the protective mechanism of flunarizine on cisplatin-induced cytotoxicity is associated with direct inhibition of lipid peroxidation and mitochondrial permeability transition.</P>
Sulfuretin Inhibits Ultraviolet B-induced MMP Expression in Human Dermal Fibroblasts
So, Hong-Seob,Kim, Seung-Hoon,Lee, Young-Rae The Physiological Society of Korean Medicine and T 2011 동의생리병리학회지 Vol.25 No.3
Sulfuretin is one of the main flavonoids produced by Rhusverniciflua. Sulfuretin has been shown to exhibit many pharmacological activities including anti-oxidant, anti-obesity, anti-inflammatory and anti-mutagenic activities. However, the anti-skin photoaging effects of sulfuretin has not yet been reported. In the present study, we investigated the inhibitory effect of sulfuretin on the expression levels of MMP-1 and -3 in the human dermal fibroblast cells. Western blot analysis and real-time PCR revealed sulfuretin inhibited UVB-induced MMP-1 and -3 expressions in a dose-dependent manner. UVB-induced MAPK/NF-${\kappa}B$/p50 activation and MMP expression were completely blocked by pretreatment of sulfuretin. Taken together, sulfuretin could prevent UVB-induced MMP expressions through inhibition of MAPK/NF-${\kappa}B$/p50 activation.