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Han, Jae Yoon,Jeong, Eun Young,Kim, Yoon Sook,Roh, Gu Seob,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung Wiley Subscription Services, Inc., A Wiley Company 2008 JOURNAL OF NEUROSCIENCE RESEARCH - Vol.86 No.14
<P>Activation of the c-jun N-terminal kinase (JNK) is known to be an important step during ethanol-induced cell death, but it has yet to be identified how JNK regulates apoptosis. Therefore, we investigated the mechanism by which JNK induces cell death following ethanol treatment. Ethanol (6 g/kg, 20% in saline) was administered subcutaneously to postnatal 7 day rat pups. Twelve hours after the first ethanol administration, rat pups were decapitated, and extracts of total protein from cerebral cortices were prepared. Ethanol exposure induced phosphorylation of JNK but did not affect the expression levels of pro- and antiapoptotic proteins. Furthermore, interactions of phospho-JNK (p-JNK) with 14-3-3 as well as with Bad were enhanced in the cerebral cortices of ethanol-treated rats. Pretreatment with JNK inhibitor (SP600125) of SH-SY5Y cells inhibited JNK phosphorylation and interaction between p-JNK and 14-3-3 resulting from ethanol. Furthermore, 14-3-3 interaction with Bad was diminished in the cerebral cortices of ethanol-treated rats. These findings suggest that JNK induces Bad release from 14-3-3 by inhibiting their interaction. After this event, Bad binds to Bcl-xL, releasing Bax from Bcl-xL and leading to cell death. We hypothesize that JNK may play an important role during ethanol-induced cell death via the inhibition of antiapoptotic function of 14-3-3 as well as activation of proapoptotic function of Bad. © 2008 Wiley-Liss, Inc.</P>
Fabrication of Mn-ferrite nanoparticles from MnO colloids
Han, Anna,Choi, Donghyuk,Kim, Taehei,Lee, Jei Hee,Kim, Jai Keun,Yoon, Mi Jin,Choi, Kyeong Sook,Kim, Sang-Wook Royal Society of Chemistry 2009 Chemical communications Vol.2009 No.44
<P>The reaction mechanism for conversion of MnO nanoparticles to Mn-ferrite nanoparticles was studied, which involved sequential consumption of MnO and the growth of ferrite. The method could be applied to other ferrite nanoparticles including cobalt ferrite.</P> <P>Graphic Abstract</P><P>The reaction mechanism for conversion of MnO nanoparticles to Mn-ferrite nanoparticles was studied, which involved sequential consumption of MnO and the growth of ferrite. The method could be applied to other ferrite nanoparticles including cobalt ferrite. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=b914881g'> </P>
Han, Myoung Sook,Chung, Kun Wook,Cheon, Hyae Gyeong,Rhee, Sang Dal,Yoon, Chang-Hwan,Lee, Moon-Kyu,Kim, Kwang-Won,Lee, Myung-Shik American Diabetes Association 2009 Diabetes Vol.58 No.2
<P><B>OBJECTIVE—</B>Imatinib has been reported to induce regression of type 2 diabetes in chronic leukemia patients. However, the mechanism of diabetes amelioration by imatinib is unknown, and it is uncertain whether imatinib has effects on type 2 diabetes itself without other confounding diseases like leukemia. We studied the effect of imatinib on diabetes in <I>db/db</I> mice and investigated possible mechanism's underlying improved glycemic control by imatinib.</P><P><B>RESEARCH DESIGN AND METHODS—</B>Glucose tolerance and insulin tolerance tests were done after daily intraperitoneal injection of 25 mg/kg imatinib into <I>db/db</I> and C57BL/6 mice for 4 weeks. Insulin signaling and endoplasmic reticulum stress responses were studied by Western blotting. β-Cell mass and apoptotic β-cell number were determined by combined terminal deoxynucleotidyl transferase–mediated dUTP nick-end labeling (TUNEL) staining and insulin immunohistochemistry. The in vitro effect of imatinib was studied using HepG2 cells.</P><P><B>RESULTS—</B>Imatinib induced remission of diabetes in <I>db/db</I> mice and amelioration of insulin resistance. Expression of endoplasmic reticulum stress markers in the liver and adipose tissues of <I>db/db</I> mice, such as phospho-PERK, phospho-eIF2α, TRB3, CHOP, and phospho–c-Jun NH<SUB>2</SUB>-terminal kinase, was reduced by imatinib. Insulin receptor substrate-1 tyrosine phosphorylation and Akt phosphorylation after insulin administration were improved by imatinib. Serum aminotransferase levels and hepatic triglyceride contents were decreased by imatinib. Pancreatic β-cell mass was increased by imatinib, accompanied by decreased TUNEL<SUP>+</SUP> β-cell and increased BrdU<SUP>+</SUP> β-cell numbers. Imatinib attenuated endoplasmic reticulum stress in hepatoma cells in vitro.</P><P><B>CONCLUSIONS—</B>Imatinib ameliorated endoplasmic reticulum stress and induced remission of diabetes in <I>db/db</I> mice. Imatinib or related compounds could be used as therapeutic agents against type 2 diabetes and metabolic syndrome.</P>
Han, Sun Sook,Jung, Cheol Hee,Lee, Sang Chul,Jung, Hae Jung,Kim, Yang Hyun Blackwell Publishing Ltd 2010 SKIN RESEARCH AND TECHNOLOGY Vol.16 No.2
<P>Background</P><P>Changes in the temperature distribution of the skin follows herpes zoster (HZ). Infrared thermography is a non-invasive, non-ionizing diagnostic tool that provides information about normal and abnormal functioning of the sensory and sympathetic nervous systems. This study examined the usefulness of infrared thermography as a predictor of post-herpetic neuralgia (PHN).</P><P>Methods</P><P>Infrared thermography was performed on the affected body regions of 110 patients who had been diagnosed with acute HZ. Demographic data collected included age, gender, time of skin lesions onset, development of PHN, and comorbidities. The temperature differences between the unaffected and affected dermatome were calculated. Differences >0.6 °C for the mean temperature across the face and trunk were considered abnormal.</P><P>Results</P><P>The affected side was warmer in 35 patients and cooler in 33 patients than the contralateral side. A patient's age and disease duration affected treatment outcomes. However, the temperature differences were not correlated with pain severity, disease duration, allodynia, development of PHN, and use of antiviral agents (<I>P</I>>0.05).</P><P>Conclusion</P><P>A patient's age and disease duration are the most important factors predicting PHN progression, irrespective of thermal findings, and PHN cannot be predicted by infrared thermal imaging.</P>
ALGORITHM FOR FINDING 90/150 TRIDIAGONAL MATRICES
Sung Jin CHO,Un Sook CHOI,Han Doo KIM,Yoon Hee HWANG,Jin Gyoung KIM 한국산업응용수학회 2006 한국산업응용수학회 학술대회 논문집 Vol.1 No.2
In this paper, we propose a new method for finding 90/150 Linear Hybrid Group Cellular Automata(LHGCA) for CA-polynomials.
Rhabdomyomatous Mesenchymal Hamartoma of the Vagina
HAN, SUNG HYUB,SONG, HEE JIN,HONG, WON KYU,LEE, HYEON SOOK,CHOI, GWANG SEONG,SHIN, JEONG HYUN Blackwell Publishing Ltd 2009 Pediatric dermatology Vol.26 No.6
<P>Abstract: </P><P>Rhabomyomatous mesenchymal hamartoma (RMH) is a rare hamartomatous lesion in the dermis and subcutaneous tissue. We report a case of solitary RMH occurring on the vagina of a newborn infant.</P>
N-Acetylphytosphingosine Enhances the Radiosensitivity of Tumor Cells by Increasing Apoptosis
Han, Young Soo,Kim, Yun Hwa,Yun, Yeon Sook,Jeon, Soo Jin,Kim, Ki Sung,Hong, Sung Hee,Park, Chang Soe,Song, Jie Young Trans Tech Publications, Ltd. 2005 Key Engineering Materials Vol.277 No.-
<P>Ceramides are well-known second messengers which mediate apoptosis, proliferation, differentiation in mammalian cells, but the physiological roles of phytosphingosines are poorly understood. We hypothesized that one of the phytosphingosine derivatives, N-acetylphytosphingosine (NAPS) can induce apoptosis in human leukemia Jurkat cell line and increase apoptosis in irradiated MDA-MB-231 cells. We first examined the effect of NAPS on apoptosis of Jurkat cells. NAPS had a more rapid and stronger apoptotic effect than C2-ceramide in Jurkat cells and significant increase of apoptosis was observed at 3 h after treatment. In contrast, the apoptosis induced by C2-ceramide was observed only after 16 h of treatment. NAPS induced apoptosis was mediated by caspase 3 and 8 activation and inhibited by z-VAD-fmk. Ceramide plays a pivotal role in radiation induced apoptosis. We postulated that exogenous treatment of NAPS sensitizes tumor cells to ionizing radiation, since NAPS might be used as a more effective alternative to C2-ceramide. As expected, NAPS decreased clonogenic survival of irradiated MDA-MB-231 cells dose dependently, and apoptosis of irradiated cells in the presence of NAPS was increased through the caspase activation. Taken together, NAPS is an effective apoptosis-inducing agent, which can be readily synthesized from yeast sources, and is a potent alternative to ceramide for the further study of ceramide associated signaling and the development of radiosensitizing agent.</P>