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      • KCI등재

        Intestinal lymphangiectasia in a Yorkshire terrier dog: clinical outcome, clinicopathological and histopathological findings

        Duna Hwang,Chul Park,Byeong-Teck Kang,Jong-Hyun Yoo3,Soon-Wuk Jeong,Jung-Hyang Sur,박희명 한국임상수의학회 2006 한국임상수의학회지 Vol.23 No.3

        A 7-year-old, 3.16 kg intact male Yorkshire terrier had the history of abdominal distension, diarrhea, andweight loss. On the basis of history takings, physical examination, laboratory tests, radiography, ultrasonography,exploratory laparotomy, and histopathological examination, the dog was diagnosed definitely as intestinallymphangiectasia. In this case, signs and results are consistent with those of other reports, but some clinicopathologicalfindings such as hypocalcemia and hypocholesterolemia are not. This means that the findings were not completelyin accord with the typical ones of intestinal lymphangiectasia in this dog. Prednisolone was prescribed to treat. However,it was not effective sufficiently. Thus, azathioprine was added to the regimen used in the first trial, and it was quiteefficient in inducing remission in intestinal lymphangiectasia. The clinical signs were improved to the combined therapy. This case report demonstrates that the combined therapy for intestinal lymphangiectasia can be used as an alternativeto only glucocorticoid therapy.

      • PDMS와 유리를 이용한 제한효 반응용 마이크로바이오칩 개발

        허영선,염혜정,조철호,안유민,황승용 한양대학교 이학기술연구소 2005 이학기술연구지 Vol.8 No.-

        최근 생화학 심험 분야에서 초미세 구조를 이용한 소형화 분야가 두드러지게 나타나고 있다. 소형화의 가증 큰 이점은 적은 양의 시료가 사용되기 때문에 실험 비용이 줄어들 뿐 아니라 실험 시간이 단축 된다는 것이다. 게다가 하나의 칩으로 바이오 실험의 모든 단계가 수행되는 랩 온어 칩의 통합을 위한 가능성을 나타내어 준다, 우리는 제한 효소 반응 실험에 응용하기 위해 새로운 마이크로바이오칩을 개발하였다, 이 마이크로 바이오칩은 PDMS와 유리를 사용해 제작하였고 총 실험 반응 양의 10㎕이다, 마이크로바이오칩을 이용한 제한효소 실험은 일반적으로 행해지는 실험 방법에 비해 반응 시간과 시료 양을 단축하는데 성공적이었다. In recent years, significant advances emerged in the area of miniaturzation of biochemical experiment using micro fabricated structures The key sdvantages of the miniaturization would be reduces assay costs due to the low consumpation of expensive reagent and increased experiment speed The additional benefits can be intergrated into Lab-on -a chip in which all the steps necessary in bio assays is performed in a single chip We have developed a novel Microbiochip for th application of Restriction Enzyme cut reaction The Microbiochip with reaction volum of 10 ㎕was fabricated using PDMS/glass The Restriction Enzyme cut reaciton using the microbiochip was successfully done with less time sample compared to the conventioal way

      • SCIESCOPUSKCI등재

        Kaposi's Sarcoma-Associated Herpesvirus Infection of Endothelial Progenitor Cells Impairs Angiogenic Activity In Vitro

        Yoo, Seung-Chul,Kim, Sil,Yoo, Seung-Min,Hwang, In-Taek,Cho, Hae-Wol,Lee, Myung-Shin 한국미생물학회 2011 The journal of microbiology Vol.49 No.2

        A recent study reported that endothelial progenitor cells (EPCs) are one of the reservoirs of Kaposi's sarcoma associated herpesvirus (KSHV). Although EPCs are closely linked to angiogenesis and vasculogenesis, little is known about the angiogenic potential of KSHV in EPCs. In this study, we used EPCs isolated from human umbilical cord blood to show that early infection by KSHV in vitro impaired the neovascularization of EPCs in matrigel. Our results suggest that KSHV may disrupt the angiogenic potential of EPCs and that the disseminated infection of KSHV could be associated with EPC dysfunction.

      • SCISCIESCOPUS

        Memory Impairment in Estrogen Receptor α Knockout Mice Through Accumulation of Amyloid-β Peptides

        Hwang, Chul Ju,Yun, Hyung-Mun,Park, Kyung-Ran,Song, Ju Kyung,Seo, Hyun Ok,Hyun, Byung Kook,Choi, Dong Young,Yoo, Hwan-Soo,Oh, Ki-Wan,Hwang, Dae Yeun,Han, Sang-Bae,Hong, Jin Tae Springer US 2015 Molecular Neurobiology Vol.52 No.1

        <P>Estrogen has been known to reduce the development of Alzheimer’s disease (AD). However, exact mechanisms are not clear. We investigated whether estrogen can increase amyloid-beta (Aβ) degradation and affects Aβ-induced memory impairment in an estrogen deficiency model. Estrogen receptor alpha (ERα) knockout mice and wild-type mice were intracerebroventricular (ICV) infused with Aβ (300 pmol) for 2 weeks. Cognitive function was then assessed by the Morris water maze test and passive avoidance test. In addition, Western blot analysis, immunostaining, immunofluorescence staining, ELISA, and enzyme activity assays were used to examine the degree of Aβ deposition in the brains of ERα knockout mice. In our present study, Aβ was accumulated more in the ERα knockout mice brain and greatly worsened memory impairment and glial activation as well as neurogenic inflammation. These results suggest that estrogen may protect memory impairment by stimulating the degradation of Aβ and down-regulate neurogenic inflammation as well as amyloidogenesis.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1007/s12035-014-8853-z) contains supplementary material, which is available to authorized users.</P>

      • Medicinal Chemistry : Memory Impairment in Estrogen Receptor α Knockout Mice Through Accumulation of Amyloid-β Peptides

        ( Chul Ju Hwang ),( Hyung Mun Yun ),( Kyung Ran Park ),( Ju Kyung Song ),( Hyun Ok Seo ),( Byung Kook Hyun ),( Dong Young Choi ),( Hwan Soo Yoo ),( Ki Wan Oh ),( Dae Yeun Hwang ),( Sang Bae Han ),( Ji 영남대학교 약품개발연구소 2015 영남대학교 약품개발연구소 연구업적집 Vol.25 No.-

        Estrogen has been known to reduce the development of Alzheimer’s disease (AD). However, exact mechanisms are not clear. We investigated whether estrogen can increase amyloid-beta (Aβ) degradation and affects Aβ- induced memory impairment in an estrogen deficiency model. Estrogen receptor alpha (ERα) knockout mice and wild-type mice were intracerebroventricular (ICV) infused with Aβ (300 pmol) for 2 weeks. Cognitive function was then assessed by the Morris water maze test and passive avoidance test. In addition, Western blot analysis, immunostaining, immunofluorescence staining, ELISA, and enzyme activity assays were used to examine the degree of Aβ deposition in the brains of ERα knockout mice. In our present study, Aβ was accumulated more in the ERα knockout mice brain and greatly worsened memory impairment and glial activation as well as neurogenic inflammation. These results suggest that estrogen may protect memory impairment by stimulating the degradation of Aβ and down-regulate neurogenic inflammation as well as amyloidogenesis.

      • KCI등재

        직장암의 수술 후 방사선 치료 시 국소 재발의 임상 병리적 예후 인자

        최철원(Chul Won Choi),김미숙(Mi Sook Kim),류성렬(Seong Yul Yoo),조철구(Chul Koo Cho),양광모(Kwang Mo Yang),유형준(Hyung Jun Yoo),서영석(Young Seok Seo),김민석(Min Suk Kim),이승숙(Seung Sook Lee),황대용(Dae Yong Hwang),문선미(Sun Mi M 대한방사선종양학회 2006 Radiation Oncology Journal Vol.24 No.4

        목 적: 진행된 직장암의 수술 후 보조적 방사선 치료를 시행한 환자에서 국소 재발한 군의 병리학적 예후 인자를 규명함으로써 향후 치료 방침의 결정에 도움이 되고자 하였다. 대상 및 방법: 1993년 2월부터 2001년 12월까지 원자력의학원에서 수술을 시행한 후 병기 3기 이상으로 방사선치료 및 항암 요법을 시행 받은 직장암 환자 110명을 대상으로 검체를 모두 조사하여 면역조직화학검사가 가능한 총 54명을 대상으로 하였다. 이중 국소전이가 발견된 군이 14명, 발견되지 않은 군이 40명이었다. 이들의 조직 검체를 대상으로 종양의 침윤 깊이, 종양의 조직학적 등급, 임파절 침윤 여부, 혈관 침윤 여부, 신경 침윤 여부 등의 병리적인 특징 및 p53, Ki-67, c-erb, ezrin, c-met, phospho-S6K, S100A4, HIF-1 alpha의 다양한 암 유전자의 발현양상을 단변량 분석 및 다변량 분석, hierarchical clustering 분석 기법을 사용하여 치료 후 예후와 관련된 인자를 찾았다.결 론: 병리학적 예후 인자 중 단변량 분석상 종양 침윤 깊이, 종양의 등급, 혈관 침범이 의미 있었고 다변량 분석상 침윤의 깊이가 5.5 mm 이하, 혈관 침윤이 없는 경우가 국소 재발이 낮은 군이었다. 면역조직화학검사 결과의 단변량 분석상 c-met 양성, HIF-1 alpha 양성이 국소 재발률이 높은 예후 인자였고 다변량 분석상 c-met이 의미 있는 예후 인자였다. Hierarchical clustering을 통해서 조사한 결과 HIF-1 alpha, c-met 및 종양 침윤 깊이가 국소재발과 관련된 인자로써 국소 재발을 한 군의 71.4%가 3가지 인자 중 2개 이상을 가지고 있는 반면 국소 재발을 하지 않은 군에서는 27.5%가 2개 이상을 가지고 있었다. 결 론: 국소적으로 진행되어 방사선 치료를 시행해야 하는 직장암 환자군 중에서 HIF-1 alpha 양성, c-met 양성,종양 침윤 깊이 5.5 mm 이상의 병리학적 예후 인자를 두 개 이상 가지는 환자는 국소 재발의 가능성이 높다. 이러한 인자가 방사선치료 저항군의 지표로써 유용한지에 대한 전향적 연구가 향후 필요할 것이다. Purpose: To evaluate the pathological prognostic factors related to local recurrence after radical surgery and adjuvant radiation therapy in advanced rectal cancer. Materials and Methods: Fifty-four patients with advanced rectal cancer who were treated with radical surgery followed by adjuvant radiotherapy and chemotherapy between February 1993 and December 2001 were enrolled in this study. Among these patients, 14 patients experienced local recurrence. Tissue specimens of the patients were obtained to determine pathologic parameters such as histological grade, depth of invasion, venous invasion, lymphatic invasion, neural invasion and immunohistopathological analysis for expression of p53, Ki-67, c-erb, ezrin, c-met, phosphorylated S6 kinase, S100A4, and HIF-1 alpha. The correlation of these parameters with the tumor response to radiotherapy was statistically analyzed using the chi-square test, multivariate analysis, and the hierarchical clustering method. Results: In univariate analysis, the histological tumor grade, venous invasion, invasion depth of the tumor and the over expression of c-met and HIF-1 alpha were accompanied with radioresistance that was found to be statistically significant. In multivariate analysis, venous invasion, invasion depth of tumor and over expression of c-met were also accompanied with radioresistance that was found to be statistically significant. By analysis with hierarchical clustering, the invasion depth of the tumor, and the over expression of c-met and HIF-1 alpha were factors found to be related to local recurrence. Whereas 71.4% of patients with local recurrence had 2 or more these factors, only 27.5% of patients without local recurrence had 2 or more of these factors. Conclusion: In advanced rectal cancer patients treated by radical surgery and adjuvant chemo-radiation therapy, the poor prognostic factors found to be related to local recurrence were HIF-1 alpha positive, c-met positive, and an invasion depth more than 5.5 mm. A prospective study is necessary to confirm whether these factors would be useful clinical parameters to measure and predict a radio-resistance group of patients.

      • KCI등재

        증례 : 소화기 ; Hemosuccus Pancreaticus 1예

        유은수 ( Eun Soo Yoo ),유병무 ( Byung Moo Yoo ),유은정 ( Eun Jung Yoo ),윤소영 ( So Young Yoon ),양민재 ( Min Jae Yang ),황재철 ( Jae Chul Hwang ),김진홍 ( Jin Hong Kim ) 대한내과학회 2016 대한내과학회지 Vol.90 No.5

        HP는 혈액이 췌관을 통하여 주 유두부로 배출되는 상부위장관 출혈로, 드문 빈도와 증상의 간헐성으로 인해 정확한초기 진단이 어려운 경우가 많으나, 상부위장관 출혈 환자에서 십이지장내에 출혈이 관찰되는 경우 반드시 감별이 필요한 질환이다. 가성동맥류의 경우 급성 및 만성 췌장염에 의한효소 작용으로 혈관벽이 손상되어 발생하나, 진성동맥류의 경우 동맥경화로 인한 혈관벽 확장이 주요 기전으로, 진성동맥류로 인한 HP 발생 가능성 역시 고려되어야 하겠다. 기존의 보고와는 달리 저자들은 만성 음주력 없이 비장동맥의 진성동맥류에 의하여 발생한 HP 1예를 경험하였고 이를 성공적으로 치료하고 최종 병리학적 소견을 확인하였기에 문헌고찰과 함께 증례를 보고하는 바이다. Hemosuccus pancreaticus, defined as bleeding from the papilla of Vater via the pancreatic duct, is a rare cause of recurrent upper gastrointestinal bleeding. We report the case of a 67.year.old man with recurrent gastrointestinal bleeding, who was subsequently diagnosed with hemosuccus pancreaticus caused by rupture of a true splenic artery aneurysm. The patient had chronic pancreatitis after considerable delay and unnecessary surgical small bowel exploration. The patient was cured with distal pancreatectomy because concomitant arcuate ligament syndrome precluded the angiographic approach via the celiac trunk, and tortuous dilatation of the distal pancreatic duct could not exclude the main duct type of intraductal papillary mucinous neoplasm (IPMN). In the surgical specimen, the pancreatic duct contained a hematoma and was lined by normal epithelium, indicating rupture of the splenic artery aneurysm that bled into the pancreatic duct. (Korean J Med 2016;90:421-426)

      • Leukocyte-specific protein 1 regulates T-cell migration in rheumatoid arthritis

        Hwang, Seong-Hye,Jung, Seung-Hyun,Lee, Saseong,Choi, Susanna,Yoo, Seung-Ah,Park, Ji-Hwan,Hwang, Daehee,Shim, Seung Cheol,Sabbagh, Laurent,Kim, Ki-Jo,Park, Sung Hwan,Cho, Chul-Soo,Kim, Bong-Sung,Leng, National Academy of Sciences 2015 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.112 No.47

        <P><B>Significance</B></P><P>We screened rheumatoid arthritis (RA)-associated copy number variations (CNVs) across the whole genome and identified significant deletion variants encompassing leukocyte-specific protein 1 (LSP1) gene. Functional assays revealed that LSP1, induced by T-cell receptor activation, negatively regulates T-cell migration. Loss of <I>Lsp1</I> promotes T-cell migration into antigen-instilled tissues and draining lymph nodes in mice with T-cell–dependent chronic inflammation. Moreover, patients with RA show diminished expression of LSP1 in peripheral T cells with increased migratory capacity. To our knowledge, our work is the first to demonstrate how CNVs result in immune dysfunction and a disease phenotype, highlighting the importance of <I>LSP1</I> CNVs and LSP1 insufficiency in the pathogenesis of RA.</P><P>Copy number variations (CNVs) have been implicated in human diseases. However, it remains unclear how they affect immune dysfunction and autoimmune diseases, including rheumatoid arthritis (RA). Here, we identified a novel leukocyte-specific protein 1 (<I>LSP1</I>) deletion variant for RA susceptibility located in 11p15.5. We replicated that the copy number of LSP1 gene is significantly lower in patients with RA, which correlates positively with LSP1 protein expression levels. Differentially expressed genes in <I>Lsp1-</I>deficient primary T cells represent cell motility and immune and cytokine responses. Functional assays demonstrated that LSP1, induced by T-cell receptor activation, negatively regulates T-cell migration by reducing ERK activation in vitro. In mice with T-cell–dependent chronic inflammation, loss of <I>Lsp1</I> promotes migration of T cells into the target tissues as well as draining lymph nodes, exacerbating disease severity. Moreover, patients with RA show diminished expression of LSP1 in peripheral T cells with increased migratory capacity, suggesting that the defect in LSP1 signaling lowers the threshold for T-cell activation. To our knowledge, our work is the first to demonstrate how CNVs result in immune dysfunction and a disease phenotype. Particularly, our data highlight the importance of <I>LSP1</I> CNVs and LSP1 insufficiency in the pathogenesis of RA and provide previously unidentified insights into the mechanisms underlying T-cell migration toward the inflamed synovium in RA.</P>

      • SCIESCOPUSKCI등재

        Temporary placement of a newly designed, fully covered, self-expandable metal stent for refractory bile leaks.

        Hwang, Jae Chul,Kim, Jin Hong,Yoo, Byung Moo,Lim, Sun-Gyo,Kim, Jin Hun,Kim, Wook Hwan,Kim, Myung Wook Editorial Office of Gut and Liver 2011 Gut and Liver Vol.5 No.1

        <P>Bile leaks remain a significant cause of morbidity for patients undergoing laparoscopic cholecystectomy. Leakage from an injured duct of Luschka (subvesical duct) follows the cystic duct as the most common cause of postcholecystectomy bile leaks. Although endoscopic sphincterotomy, plastic-stent placement, or nasobiliary-drain placement are effective in healing biliary leaks, in patients in whom leakage persists and the symptoms worsen despite conventional endoscopic treatment, re-exploration with laparoscopy and ligation of the injured subvesical duct should be considered. We present herein the case of a 31-year-old woman with refractory bile leakage from a disrupted subvesical duct after cholecystectomy that could not be managed with endoscopic sphincterotomy and plastic-stent placement. A newly designed, fully covered, self-expandable metal stent (FC-SEMS) was successfully placed for the treatment of refractory bile leaks in this patient. It appears that temporary placement of an FC-SEMS is technically feasible and provides an effective alternative to surgical therapy for refractory bile leaks after cholecystectomy.</P>

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