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      • 체외배양한 인제대정맥혈관내피세포에서 R. tsutsugamushi 감염이 Tissue Factor와 Type 1 Plasminogen Activator Inhibitor의 발현에 미치는 영향에 관한 연구

        김미란,기선호,배현주,장우현,박선양,최강원 대한감염학회 1995 감염 Vol.27 No.4

        목적:쯔쯔가무시질환시 생기는 전신혈액응고장애의 병인 기전이 rickettsia의 침투에 의한 혈관내피세포의 손상, 그에 따른 tissue factor의 발현, 뒤이은 tissue type plasminogen activator(tPA)의 분비와 보상기전으로 type 1 plasminogen activator inhibitor(PAI-1)이 분비되는 과정으로 생각하고 이를 보고자 연구를 시행하였다. 방법:체외배양한 혈관내피세포에 순수분리한 Rickettsia tsutsugamushi를 감염시킨후 상층액에서 ELISA법으로 tPA와 PAI-1을 측정하였고 혈관내피세포 단층배양에서 면역형광법으로 tissue factor를 측정하였으며 PAI-1 유전자의 발현을 확인하고자 Northern blot analysis로 PAI-1 mRNA를 확인하였다. 결과: 1) PAI-1 R. tsutsugamushi를 감염시킨후 24시간에 가장 높은 농도를 보이며 그 증가량은 정상대조군에 비해 2.5배에서 4.7배까지 증가 하였다. 2) R. tsutsugamushi를 감염시킨후 혈관내피세포에서 분비되는 tPA의 분비는 정상대조군에 비해 유의한 차이를 보이지 않았다. 3) Northern blot analysis에 의한 PAI-1 mRNA의 발현 검색 결과 정상대조군에 비해 R. tsutsugamush가 감염된 혈관내피세포에서는 PAI-1의 발현이 2.5배 정도 증가하였다. 4) 혈관내피세포 단층배양에 R. tsutsugamushi를 감염시킨후 24시간에 tissue factor단일클론 항체와 FITC-conjugated anti mouse IgG를 이용한 간접 면역형광항체법으로 tissue factor를 측정한 결과 혈관내피세포 표면에서 tissue factor의 존재를 확인할 수 있었다. 결론:단층배양한 혈관내피세포에 R. tsutsugamushi를 감염시켰을 때 tissue factor가 발현되었고 PAI-1의 분비가 증가하여 24시간에 가장 많이 분비되었다. 그러나 tPA의 분비는 정상대조군에 비해 유의한 차이를 보이지 않았다. Nothern blot analysis를 통한 PAI-1 mRNA의 발현 검색 결과 PAI-1이 새로이 생성되어 분비됨을 확인하였다. Background:Tissue type plasminogen activator(tPA), type 1 plasminogen activator inhibitor (PAI-1), and von Willebrand factor are known to be released into the sera of patients in disseminated intravascular coagulation(DIC). The main pathologic mechanism of tsutsugamushi disease is the vasculitis by direct endothelial cell invasion by R. tsutsugamushi which dosen't have endotoxin. It is suspected that the mechanisms of DIC and activation of plasminogen activation system are different from those of sepsis by other organisms. which is caused by endotoxin. We suspect that direct rickettsial invasion of endothelial cells causes endothelial cell damage, tissue factor release, which is followed by DIC, and tPA and PAI-1 are released as compensatory mechanism. Methods:We cultured endothelial cells from human umbilical cord vein, infected them with purified R. tsutsugamushi Gilliam strain, checked tPA and PAI-1 by ELISA in culture supernatant. Then we observed the tissue factor expression on cultured endothelial cell monolayer by indirect IF stain. PAI-1 gene expression was evaluated by northern blot analysis. Results: 1) PAI-1 level showed gradual increase up to 240ng/ml (2.5-4.7 fold increase) in 24 hours. 2) tPA level showed no significant change with time. 3) PAI-1 gene expression increased 2.5 fold by northern blot analysis. 4) Tissue factor was expressed on the endothelial cells infected with R. tsutsugamushi. Conclusion: R. tsutsugamushi infection induces expression of tissue factor on endothelial cells and PAI-1 synthesis and it would contribute to DIC mechanism in tsutsugamushi disease in part. But it has no direct effect on tPA release.

      • KCI등재후보

        Thinning of the Corpus Callosum and Cerebellar Atrophy is Correlated with Phenotypic Severity in a Family

        Sanjeev Rajakulendran,Coro Paisán-Ruiz,Henry Houlden 대한신경과학회 2011 Journal of Clinical Neurology Vol.7 No.2

        Background:Mutations in the spatacsin gene are associated with spastic paraplegia type 11(SPG11), which is the most-common cause of autosomal recessive hereditary spastic paraplegia. Although SPG11 has diverse phenotypes, thinning of the corpus callosum is an important feature. Case Report:Clinical, genetic, and radiological evaluations were undertaken in a large family from Gujarat in North India with hereditary spastic paraplegia, whose affected members presented with varying degrees of spasticity, ataxia, and cognitive impairment. The clinical severity and the degree of corpus callosum and cerebellar atrophy varied among the four affected individuals in the family. Genetic testing of the affected members revealed recessive mutations in the spatacsin gene, consistent with a diagnosis of SPG11. Conclusions;We believe that the extent of corpus callosum thinning and cerebellar atrophy is correlated with disease severity in affected patients. The addition of extrapyramidal features in the most-affected members suggests that SPG11 exhibits considerable phenotypic heterogeneity.

      • KCI등재
      • SCIESCOPUSKCI등재

        The Effect of Agomelatine in Behavioral and Psychological Symptoms of Dementia

        Carol Sheei-Meei Wang(Carol Sheei-Meei Wang ),Kuo-Sheng Cheng(Kuo-Sheng Cheng),Chia-Hung Tang(Chia-Hung Tang),Ming-Chyi Pai(Ming-Chyi Pai),Pai-Lien Chen(Pai-Lien Chen),Pei-Fang Chien(Pei-Fang Chien) 대한정신약물학회 2022 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.20 No.4

        Objective: Moderate and severe behavioral and psychological symptoms of dementia (BPSD) often need medical treatment to improve symptoms. Agomelatine is a selective melatonergic (MT1/MT2) agonist that has normalizing effects on disturbed circadian rhythms and disrupted sleep−wake cycles. Its activity of 5HT-2C receptor antagonism is associated with lessening depression and anxiety and increasing slow-wave sleep. Based on past clinical records and current findings it suggests that agomelatine can improve BPSD for patients. This retrospective cohort study was designed to compare the BPSD before and after using agomelatine. Methods: Records of dementia cases who had ever received agomelatine treatment for BPSD in a general hospital setting during the past 2.5 years were identified and reviewed. Scores from before and after 3 months of treatment with agomelatine were collected for Neuropsychiatric Inventory (NPI), Brief Psychiatric Rating Scale (BPRS), and Clinical Global Impression (CGI) to compare and analyze the difference of psychological and behavioral symptoms pre- and post-agomelatine used. Results: Records of 144 cases of dementia with BPSD who had ever used agomelatine from January 2015 to June 2017 were collected. All of the 112 cases had BPRS and CGI scores, of which 75 cases had additional NPI scores. Among these 112 cases, the BPRS and CGI scores were significantly improved in all types of dementia. NPI scores indicated that the use of agomelatine alleviated obvious symptoms and decreased overall distress, especially in the depression/poor mood, anxiety, and sleep/night behavior. Conclusion: It is consistent with an effective result of agomelatine in improving BPSD.

      • KCI등재

        History and Epidemiology of Bacillary Dysentery in Korea: from Korean War to 2017

        Pai Hyunjoo 대한감염학회 2020 Infection and Chemotherapy Vol.52 No.1

        Dysentery has been a major illness for a long time in our country. During Korean war, bacillary dysentery was common illness as well as other infectious diseases such as typhus fever, and Shigella flexneri occupied more than 90% of the cases reported by UN forces. After the war, the Korean National Institute of Health began to monitor the disease as a legal communicable disease. The incidence of dysentery decreased gradually from 1960 through 1980s and consistently low until 1997, and common serotype has changed from S. flexneri to S. sonnei. However, a nationwide epidemic of dysentery occurred at 1998, peaking at 2,462 cases in 2000, and continued until 2004. Most cases were S. sonnei, but the proportion of S. flexneri existed changing with time. There were several major epidemic cases during the period, and the dysentery outbreaks in 1998 and 1999 were associated with nationwide school meal provision which began in 1998. According to the region, Juju island particularly showed a high incidence rate in the period. Since 2005, the nationwide dysentery epidemic was over and incidence of dysentery remained stably low. Recently, multi-drug resistant Shigella infection imported from Southeast Asia appeared, and it requires continuous monitoring and control.

      • Mathematical modeling of the phase behaviors of solid-polymer-electrolyte/salt systems in lithium secondary batteries: The nonrandomness effect

        Pai, Sung Jin,Bae, Young Chan,Kong, Sung Ho,Ryu, Si Ok Wiley Subscription Services, Inc., A Wiley Company 2004 Journal of applied polymer science Vol.94 No.1

        <P>We establish a new melting-point-depression theory, based on the modified-double-lattice model, that takes into account the local composition concept to describe the phase behaviors of solid-polymer-electrolyte/salt systems (modified-double-lattice/nonrandom model). In comparison with experimental data, quantitative descriptions of the proposed model show better agreement for the given systems than those of the modified-double-lattice model. The systems studied in this work are combinations of poly(ethylene oxide) and zinc halides and of poly(ethylene oxide) and LiCF<SUB>3</SUB>SO<SUB>3</SUB>. The results show that the nonrandomness effect of the salt distribution plays a major role in determining the eutectic points of the given systems. © 2004 Wiley Periodicals, Inc. J Appl Polym Sci 94: 231–237, 2004</P>

      • KCI등재
      • SCISCIESCOPUS

        Association of QnrB determinants and production of extended-spectrum beta-lactamases or plasmid-mediated AmpC beta-lactamases in clinical isolates of Klebsiella pneumoniae.

        Pai, Hyunjoo,Seo, Mi-Ran,Choi, Tae Yeal American Society for Microbiology 2007 Antimicrobial Agents and Chemotherapy Vol.51 No.1

        <P>Clinical isolates of Escherichia coli and Klebsiella pneumoniae producing extended-spectrum beta-lactamases or plasmid-mediated AmpC beta-lactamases were screened for qnrA and qnrB genes. QnrB was present in 54 of 54 DHA-1-producing K. pneumoniae isolates and 10 of 45 SHV-12-producing ones, suggesting that the distribution of plasmids conferring resistance to extended-spectrum cephalosporins and quinolones in clinical isolates of K. pneumoniae is widespread.</P>

      • Rac GTPases in Human Diseases

        Pai, Sung-Yun,Kim, Chaekyun,Williams, David A. IOS Press 2010 Disease markers Vol.29 No.3

        <P>Rho GTPases are members of the Ras superfamily of GTPases that regulate a wide variety of cellular functions. While Rho GTPase pathways have been implicated in various pathological conditions in humans, to date coding mutations in only the hematopoietic specific GTPase, <I>RAC2</I>, have been found to cause a human disease, a severe phagocytic immunodeficiency characterized by life-threatening infections in infancy. Interestingly, the phenotype was predicted by a mouse knock-out of <I>RAC2</I> and resembles leukocyte adhesion deficiency (LAD). Here we review Rho GTPases with a specific focus on Rac GTPases. In particular, we discuss a new understanding of the unique and overlapping roles of Rac2 in blood cells that has developed since the generation of mice deficient in Rac1, Rac2 and Rac3 proteins. We propose that Rac2 mutations leading to disease be termed LAD type IV.</P>

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