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      • Imidazole이 내독소에 의한 Shock폐에 미치는 효과

        최재유,이상한,한치동,곽정식,손태중 慶北大學校 醫科大學 1991 慶北醫大誌 Vol.32 No.2

        Thromboxane synthetase 억제제인 imidazole이 내독소에 의한 쇽폐에 미치는 영향을 규명하기 위해 토끼에 내독소 4.0㎎/㎏을 정맥으로 투여한 후 1, 4 및 8시간에, 그리고 내독소 4.0㎎/㎏을 정맥으로 투여한 직후 imidazole 50㎎/㎏/2hr의 양으로 2시간마다 정맥으로 투여하면서 내독소 투여후 1, 4 및 8시간에 각각 3마리씩 전자현미경으로 관찰하였다. 그 성적을 요약하면 다음과 같다. 내독소 투여후에는 Ⅰ형 폐포세포 표면의 불규칙화, 내피세포의 종창 및 간질의 부종이 일어났으며 이는 내독소 투여후 4∼8시간에 가장 현저하였다. 내독소 및 imidazole 병합투여군에서는 4시간 이후 내피세포의 종창과 간질의 부종이 일어났으며 그 정도는 내독소 단독투여군에 비해 경하였다. 이상의 소견으로 보아 thromboxane A_2의 합성 억제는 내독소에 의한 폐상해를 상당히 경감시킨다고 인정된다. This study was carried out to investigate the effect of imidazole, known as a inhibitor of thromboxane synthetase, on shock lung induced by E. coli endotoxin. White rabbits were intravenously injected 4.0㎎/㎏ of E. coli O26:B6 lypopolysaccharide. The lungs were observed 1, 4, 10 hours after injection. The other rabbits were given same dose of endotoxin simultaneously with imidazole, 50㎎/㎏ continously injections. The results were summarized as follows: After endotoxin injection, irregularity of the surface of type Ⅰ appeared. These changes were more pronounced 4 to 8 hours after injection. In the lungs of endotoxin and imidazole injected group, endothelial swelling and interstitial edema occurred 4 hours after injections. But these changes were mild in degree compared to endotoxin injected group. From these results, it is concluded that inhibition of thromboxane A_2 synthesis can suppress the endothelial injury and pulmonary edema induced by endotoxin.

      • KCI등재

        한국인 정신분열병 환자의 지연성 운동장애와 $CYP2D6^*4$ 및 $CYP2D6^*10$ 다형성들의 연합에 대한 고찰

        우성일,강동우,서한길,김봉조,이인상,정근화,박소영,정치영,이환철,정경천,손진욱,Woo, Sung-Il,Kang, Dong-Woo,Seo, Han-Gil,Kim, Bong-Jo,Lee, In-Sang,Jeong, Geun-Hoa,Park, So-Young,Jung, Chi-Yeong,Lee, Hwan-Cheol,Jeong, Kyeong-Cheon,Sohn, 대한생물정신의학회 2000 생물정신의학 Vol.7 No.2

        P450 CYP2D6 enzyme(=debrisoquine hydroxylase) is known to metabolize many neuroleptics and some genetic polymorphisms in the CYP2D6 gene were reported to be associated with tardive dyskinesia(TD). We investigeted the association of two genetic polymorphisms in the CYP2D6 gene, $CYP2D6^*4$ and $CYP2D6^*10$, with TD in Korean schizophrenic subjects. Subjects consisted of 71 Korean schizophrenics and TD was evaluated using the Abnormal Involuntary Movement Scale (AIMS). There were no statistically significant differences in the demographic variables of age, male to female percentage and the current antipsychotic(CPZ equivalent) dose between the group with TD and the group without TD. But the duration of antipsychotic drug exposure was significantly higher in the group without TD(p=0.000, by independent t-test). The mean AIMS score in the group with TD was $11.2{\pm}6.6$(S.D.). Genotypings for the presence of $CYP2D6^*4$ and $CYP2D6^*10$ were done using PCR amplifications and endonuclease digestions. There were no statistically significant genotypic and alleleic associations between TD and $CYP2D6^*4$(by chisquare tests), and between TD and $CYP2D6^*10$(by chi-square tests). These results indicate that the $CYP2D6^*4$ and $CYP2D6^*10$ polymorphisms have no significant roles in the causation of TD.

      • KCI등재
      • KCI등재
      • SCISCIESCOPUS

        Ameliorative effect of <i>Alnus japonica</i> ethanol extract on colitis through the inhibition of inflammatory responses and attenuation of intestinal barrier disruption <i>in vivo</i> and <i>in vitro</i>

        Chi, Jin Hua,Kim, Young Ho,Sohn, Dong Hwan,Seo, Geom Seog,Lee, Sung Hee Elsevier 2018 BIOMEDICINE AND PHARMACOTHERAPY Vol.108 No.-

        <P><B>Abstract</B></P> <P>Inflammatory bowel disease (IBD) is chronic inflammation of the gastrointestinal tract caused by high levels of pro-inflammatory cytokines and epithelial barrier dysfunction. <I>Alnus japonica</I> Steud. (Betulaceae) has been used in traditional Asian medicine. However, the potential of <I>A. japonica</I> for the treatment of intestinal inflammation has not been investigated. This study investigated the effects of ethanol extract from <I>A. japonica</I> bark (AJE) on colonic mucosa injury in mice with dextran sodium sulfate (DSS)-induced colitis. Treatment with AJE ameliorated pathological damage and the histopathologic features of DSS-induced colitis. The administration of AJE also inhibits DSS-induced pro-inflammatory cytokines expression, including interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and cyclooxygenase (COX)-2. Notably, AJE administration attenuated the reduction of tight junction proteins, zonula occludens (ZO)-1 and occludin, in DSS-induced colitis. In addition, AJE increased heme oxygenase (HO)-1 expression and prevented DSS-induced apoptosis in colonic epithelial cells. Furthermore, <I>in vitro</I> studies demonstrated that AJE inhibits TNF-α-induced IL-8, IL-1β, and COX-2 expression in human intestinal epithelial HT-29 cells and <I>tert</I>-butyl hydroperoxide-induced reduction of ZO-1 and occludin expression in human intestinal epithelial Caco-2 cells. AJE-induced HO-1 protein expression was also found in both HT-29 and Caco-2 cells. Taken together, our findings demonstrated that AJE inhibits intestinal inflammation and protects against intestinal barrier disruption in mice with DSS-induced colitis <I>in vivo</I> and human intestinal epithelial cells <I>in vitro</I>. These results suggest that AJE might have beneficial effects for the treatment of IBD.</P> <P><B>Highlights</B></P> <P> <UL> <LI> AJE attenuates the severity of DSS-induced colitis mice. </LI> <LI> AJE suppresses expression of pro-inflammatory mediators in DSS-induced colitis mice. </LI> <LI> AJE protects intestinal barrier integrity in DSS-induced colitis mice. </LI> <LI> AJE increases HO-1 expression in mouse colonic epithelial cells. </LI> <LI> AJE inhibits inflammation and protects loss of TJ proteins of human IEC cells. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

      • SCISCIE

        A mother and daughter with the p.R443X mutation of mucopolysaccharidosis type II: Genotype and phenotype analysis

        Sohn, Young Bae,Kim, Su Jin,Park, Sung Won,Park, Hyung‐,Doo,Ki, Chang‐,Seok,Kim, Chi Hwa,Huh, Seung Won,Yeau, Sunghee,Paik, Kyung‐,Hoon,Jin, Dong,Kyu Wiley Subscription Services, Inc., A Wiley Company 2010 AMERICAN JOURNAL OF MEDICAL GENETICS PART A Vol.a152 No.12

        <P><B>Abstract</B></P><P>Mucopolysaccharidosis type II (Hunter syndrome) is a lysosomal storage disease caused by a deficiency of iduronate‐2‐sulfatase. Most reported patients are males because of X‐linked recessive inheritance pattern. Only a few female patients with Hunter syndrome have been reported, and there is no prior report of offspring from a patient with Hunter syndrome. In this report, we describe a woman with mild manifestations of Hunter syndrome who gave birth to a daughter. Both the mother and daughter carried the p.R443X mutation in exon 9 of the <I>ID2S</I> gene. Iduronate‐2‐sulfatase activity in the mother was as low as that found in male Hunter syndrome patients, but it was in the low‐normal range in her daughter. Unlike her mother, the daughter did not show any physical signs of Hunter syndrome, and urinary excretion of glycosaminoglycan was within normal range. However, she had severe pulmonary vein stenosis with pulmonary hypertension and a large atrial septal defect and died at 11 months of age. © 2010 Wiley‐Liss, Inc.</P>

      • 子宮筋腫의 結合組織의 超微形態學的 變化

        韓治東,郭精植,孫泰重 慶北大學校 醫科大學 1986 慶北醫大誌 Vol.27 No.3

        저자는 인체에서 적출된 자궁근종을 전자현미경으로 관찰하여 자궁근종의 기질조직의 미세형태학적 변화를 검색하고 자궁근종의 기질조직의 특징과 종양의 생물학적 성장과의 관계를 규명하고자 하였으며 그 결과는 다음과 같다. 자궁근종의 간질은 대부분 교원조직으로 형성되었으며 그 양은 정상자궁보다 증가되었고 교원섬유의 배열이 불규칙한 곳이 있었따. 다당류를 함유한 간질조직은 기저판과 교원섬유가 대부분이었고 기질물질에는 거의 볼 수 없었다. 탄력조직은 종양의 간질조직에 거의 없었으며 종양이 변성된 곳에는 교원섬유의 양이 감소되었으며 유기적인 구조물은 없었다. 이러한 소견으로 보아 자궁근종이 간질조직은 풍부한 교원조직으로 형성되었으며 종양의 2차적인 변성은 종양세포에서 유래된 collagenase의 역할에 의할 것이라 생각된다. The author studied on the ultrastructure of connective tissues of uterine leiomyoma extracted from the patients to investigate characteristics of connective tissues in the leiomyoma and its correlation with biological behavior of the tumor. PAM stain for study of polysccharides and Kajikawa stain for elastic tissue were performed. The interstitium of the leiomyoma was almostly composed of collagen and its amount was more abundant than that in normal myometrium. Focal disarrangement of collagen fibrils appeared. On PAM stain, collagen fibers and basal lamina of the tumor cells were positively stained. The elastic tissue was very scanty without areas aroung blood vessels. In areas of degenerated tumor tissue, the collagen fibers were decreased in amount and no organoid structures were present. Based on these findings, the interstitium of uterine leiomyoma was composed mainly of collagen tissue. It would be considered that the secondary degeneration of the uterine leiomyoma was caused by collagenase derived from the tumor cells.

      • Anti-Inflammatory and Cytoprotective Effects of TMC-256C1 from Marine-Derived Fungus <i>Aspergillus</i> sp. SF-6354 via up-Regulation of Heme Oxygenase-1 in Murine Hippocampal and Microglial Cell Lines

        Kim, Dong-Cheol,Cho, Kwang-Ho,Ko, Wonmin,Yoon, Chi-Su,Sohn, Jae Hak,Yim, Joung Han,Kim, Youn-Chul,Oh, Hyuncheol MDPI AG 2016 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.17 No.4

        <P>In the course of searching for bioactive secondary metabolites from marine fungi, TMC-256C1 was isolated from an ethyl acetate extract of the marine-derived fungus <I>Aspergillus</I> sp. SF6354. TMC-256C1 displayed anti-neuroinflammatory effect in BV2 microglial cells induced by lipopolysaccharides (LPS) as well as neuroprotective effect against glutamate-stimulated neurotoxicity in mouse hippocampal HT22 cells. TMC-256C1 was shown to develop a cellular resistance to oxidative damage caused by glutamate-induced cytotoxicity and reactive oxygen species (ROS) generation in HT22 cells, and suppress the inflammation process in LPS-stimulated BV2 cells. Furthermore, the neuroprotective and anti-neuroinflammatory activities of TMC-256C1 were associated with upregulated expression of heme oxygenase (HO)-1 and nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) in HT22 and BV2 cells. We also found that TMC-256C1 activated p38 mitogen-activated protein kinases (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways in HT22 and BV2 cells. These results demonstrated that TMC-256C1 activates HO-1 protein expression, probably by increasing nuclear Nrf2 levels via the activation of the p38 MAPK and PI3K/Akt pathways.</P>

      • KCI등재

        복강내 및 복강외 방광파열과 소장파열이 동반된 직장천통

        김용정,지훈상,손승국,윤동섭,심희수,임대진,권민수 대한외상학회 1997 大韓外傷學會誌 Vol.10 No.2

        Rectal impalement is even more unusual form of rectal injury. The typical mechanism of injury is a jump or a fall onto an impaling object, such as a fence or rake. This type of injury may range from simple rectal perforation with minimal soft tissue injury to severe rectal impalement, characterized by transfixion by the impaling object with resultant extensive perineal trauma and multiple organ damage. Because rectal injuries in civilians are uncommon, there remain considerable differences of opinion ahout the need for their repair as well as the optimal type of colostomy, method of drainage, and role of irrigation. We report a case of rectal impalement with associated intrapeirtoneal, extraperitoneal bladder perofration and ileal perforation caused hy through and through mechanism. Operatively, the anterior rectal tear was closed primarily transanally with interrupted two layer vicryl sutures. The diverting colostomy and presacral drainage were not performed. The defects of bladder were closed with running chromic sutures. A suprapubic tube was placed. Postoperatively, the patient did well and discharged on postoperative day 14. We believe this to he the first reported case of rectal impalement causing intraperitoneal, extraperitoneal bladder perforation and ileal perforation.

      • SCISCIESCOPUS

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