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Limited Effect of CpG ODN in Preventing Type 1 Diabetes in NOD Mice
이병준,김수기,김문규,박은섭,조현철,심명숙,김미진,신영구,정춘희 연세대학교의과대학 2005 Yonsei medical journal Vol.46 No.3
Type 1 diabetes is considered as Th1 cell mediated autoimmune disease and the suppression of Th1 cells or the activation of Th2 cells has been regarded as a plausible immunologic intervention for the prevention of type 1 diabetogenesis in a rodent model. CpG ODN is an immunostimulatory sequence primarily present in bacterial DNA, viral DNA and BCG. CpG ODN is conventionally classified as a Th1 cell activator, which has been clinically applied to cancer, allergy and infectious disease. Recently, there was a promising report of that CpG ODN administration suppressed the development of type 1 diabetes in NOD mice by inducing Th2 cell mediated cytokine. However, the antidiabetogenic effect of CpG ODN on NOD mice is controversial. Thus, two studies were serially undertaken with various kinds of CpG motif to find a more optimal sequence and administration method. In the first study, CpG ODN was vaccinated four times and pancreatic inflammation and the quantity of serum insulin subsequently evaluated. In the second study, the amounts of IFN γ and IL-4 in sera were measured as representative cytokines of Th1 and Th2 cells, respectively. As a result, vaccination or continuous injection of CpG ODN failed to show a preventive effect on type 1 diabetogenesis in NOD mice. Structural differences of CpG ODN also had no affect on the result. CpG ODN also consistently showed affect on the pancreatic pathology. The productions of IFN γ and IL-4 were detected only in the K and D type CpG ODN administration groups. Comparison of the two cytokines leads to the conclusion that CpG ODN generated a Th1-weighted response in both study groups. It was assumed that CpG ODN failed to produce Th2-weighted cytokine milieu, which can overcome the genetically determined phenotype of NOD mice. Given these results, it was concluded that the immunotherapeutic application of CpG ODN on Type 1 diabetes had clear limitations.
스마트 항로표지 시스템의 고가용성을 보장하는 마이크로 서비스 아키텍처 기반 장애 관리 방안
조인표,이승준,오지원,박은섭,이재규,이상엽 한국항해항만학회 2023 한국항해항만학회 학술대회논문집 Vol.2023 No.1
본 논문은 해상 안전을 유지하는 중요한 역할을 수행하는 스마트 항로표지 시스템의 높은 가용성을 유지하기 위해 제안된 장애관리 방안에 대한 연구이다. 스마트 항로표지 시스템은 고가용성을 요구하는 시스템으로, 시스템의 건전성을 유지하고 장애 발생 시 빠른 대응이 필요하다. 따라서, 이 논문에서는 마이크로 서비스 아키텍처 기반의 방안을 제안한다. 이를 통해 장애 발생 시 해당 서비스만 중단되고, 다른 서비스는 계속 운영될 수 있어 시스템 전체의 가용성과 신뢰성을 높일 수 있다. 본 연구에서는 모니터링 및 로깅 시스템을 도입하여 빠른 대응이 가능하도록 하며, 또한, 다양한 장애 관리 방안을 제시한다. 이를 통해 스마트 항로표지 시스템의 고가용성을 확보하여 안정적인운영을 보장하는 데 기여할 수 있다.
The Effect of Dehydroepiandrosterone on Isoproterenol-induced Cardiomyopathy in Rats
정지훈,김찬웅,임성혁,신용규,박경화,박은섭 대한약리학회 2006 The Korean Journal of Physiology & Pharmacology Vol.10 No.2
We evaluated therapeutic and preventive properties of dehydroepiandrosterone (DHEA), a weak androgenic steroid, against isoproterenol-induced cardiomyopathy. The cardiomyopathy was induced by daily i.p. administration of isoproterenol to rats for five days. One group of rats were given with daily s.c. for 5 days during isoproterenol and the other group with daily s.c. DHEA for total 10 days, including 5 days before and during isoproterenol. The animals were killed after each treatment, and cardiac muscle failure was evaluated using histopathologic examination and biochemical indices. DHEA was found to reduce the damaged area and inhibit the elevation in the serum levels of glutamic oxaloacetic transaminase (SGOT), lactate dehydrogenase (LDH), skeletal muscle creatine kinase (CK) and heart creatine kinase (CK-MB) induced by isoproterenol. We also assayed widely used oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase and glutathion peroxidase (GPx). DHEA decreased the escalated level of TBARS and enhanced the anti oxidant defense reaction with an increase in Mn-SOD and Cu/Zn-SOD. On the other hand, the treatment with DHEA did not affect catalase and GPx activity. The present study indicates that DHEA has a therapeutic and preventive effect against isoproterenol-induced cardiomyopathy and its effects may depend largely on the increase in SOD activity.