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      • KCI등재후보

        우측 수신증을 동반한 골반내 방선균증 1예

        정명아,서유승,양진수,박준섭,윤진훈,이중건,이준승,이영규,김동희,조성범,주종은 대한신장학회 2002 Kidney Research and Clinical Practice Vol.21 No.2

        Pelvic actinomycosis is a chronic granulomatous suppurative disease caused by an anaerobic grampositive organism Actinomyces israelii. It is com-monly associated with an intrauterine device(IUD) and can mimick pelvic or intra-abdominal malignant neoplasm. Ureteral obstruction leading to hydronephrosis is a rare complication of tubo-ovarian abscess. We experienced a case of hydronephrosis as a complication of pelvic actinomycotic abscess. The patient was a 46-year-old women presenting with fever and right flank pain. Leukocytosis and pyuria were present and a hydronephrosis was diagnosed by intravenous pyelography. Ultrasonography and a computerised tomography revealed a mass in right adnexum compressing the right ureter. Removal of retroperitoneal abscess and salphingo-oophorectomy were done and the diagnosis of actinomycosis was made by pathologic finding of resected mass. Postoperatively, the patient was treated with second-generation cephalosporin successfully. (Korean J Nephrol 2002;21(2):337-340)

      • 하악 고정성 임프란트를 이용한 퇴축된 하악골의 수복

        정영진,박원희,안원준,이명렬,이영수,유광희,심광섭 한양대학교 의과대학 1997 한양의대 학술지 Vol.17 No.2

        Transmandibular implants are used limitedly such as on remaining symphyseal basal bone of atrophic mandible, on the bony defect of symphyseal area due to trauma or tumor as surgical implants. Among the more recent advances in oral implantology are the Fixed Mandibular Implant (FMI)based on the pioneering studies and clinical applications by Irwin Small of the USA and the development very high success rates for providing attachments and abutments in areas of the oral cavity severely compromised by either atrophy or surgical loss of osseous tissues. We will present a case report of regabilitation of totally edentulous mandible with advanced alveolar atrophy using Fixed Mandibular implant (F.M.I).

      • Effect of zinc oxide nanoparticles on dams and embryo–fetal development in rats

        Hong, Jeong-Sup,Park, Myeong-Kyu,Kim, Min-Seok,Lim, Jeong-Hyeon,Park, Gil-Jong,Maeng, Eun-Ho,Shin, Jae-Ho,Kim, Yu-Ri,Kim, Meyoung-Kon,Lee, Jong-Kwon,Park, Jin-A,Kim, Jong-Choon,Shin, Ho-Chul Dove Medical Press 2014 INTERNATIONAL JOURNAL OF NANOMEDICINE Vol.9 No.2

        <P>This study investigated the potential adverse effects of zinc oxide nanoparticles (ZnO<SUP>SM20[−]</SUP> NPs; negatively charged, 20 nm) on pregnant dams and embryo–fetal development after maternal exposure over the period of gestational days 5–19 with Sprague Dawley rats. ZnO<SUP>SM20(−)</SUP> NPs were administered to pregnant rats by gavage at 0 mg/kg/day, 100 mg/kg/day, 200 mg/kg/day, and 400 mg/kg/day. All dams were subjected to caesarean section on gestational day 20, and all the fetuses were examined for external, visceral, and skeletal alterations. Toxicity in the dams manifested as significantly decreased body weight at 400 mg/kg/day and decreased liver weight, and increased adrenal glands weight at 200 mg/kg/day and 400 mg/kg/day. However, no treatment-related difference in the number of corpora lutea, the number of implantation sites, the implantation rate (%), resorption, dead fetuses, litter size, fetal deaths, fetal and placental weights, and sex ratio were observed between the groups. Morphological examinations of the fetuses demonstrated no significant difference in the incidences of abnormalities between the groups. No significant difference was found in the Zn content of fetal tissue between the control and high-dose groups. These results showed that a 15-day repeated oral dose of ZnO<SUP>SM20(−)</SUP> was minimally maternotoxic at dose of 200 mg/kg/day and 400 mg/kg/day.</P>

      • KCI등재SCISCIE
      • Negative Regulation of Type I IFN Expression by OASL1 Permits Chronic Viral Infection and CD8 <sup>+</sup> T-Cell Exhaustion

        Lee, Myeong Sup,Park, Chan Hee,Jeong, Yun Hee,Kim, Young-Joon,Ha, Sang-Jun Public Library of Science 2013 PLoS pathogens Vol.9 No.7

        <▼1><P>The type I interferons (IFN-Is) are critical not only in early viral control but also in prolonged T-cell immune responses. However, chronic viral infections such as those of human immunodeficiency virus (HIV) and hepatitis C virus (HCV) in humans and lymphocytic choriomeningitis virus (LCMV) in mice overcome this early IFN-I barrier and induce viral persistence and exhaustion of T-cell function. Although various T-cell-intrinsic and -extrinsic factors are known to contribute to induction of chronic conditions, the roles of IFN-I negative regulators in chronic viral infections have been largely unexplored. Herein, we explored whether 2′–5′ oligoadenylate synthetase-like 1 (OASL1), a recently defined IFN-I negative regulator, plays a key role in the virus-specific T-cell response and viral defense against chronic LCMV. To this end, we infected <I>Oasl1</I> knockout and wild-type mice with LCMV CL-13 (a chronic virus) and monitored T-cell responses, serum cytokine levels, and viral titers. LCMV CL-13-infected <I>Oasl1</I> KO mice displayed a sustained level of serum IFN-I, which was primarily produced by splenic plasmacytoid dendritic cells, during the very early phase of infection (2–3 days post-infection). <I>Oasl1</I> deficiency also led to the accelerated elimination of viremia and induction of a functional antiviral CD8 T-cell response, which critically depended on IFN-I receptor signaling. Together, these results demonstrate that OASL1-mediated negative regulation of IFN-I production at an early phase of infection permits viral persistence and suppresses T-cell function, suggesting that IFN-I negative regulators, including OASL1, could be exciting new targets for preventing chronic viral infection.</P></▼1><▼2><P><B>Author Summary</B></P><P>Chronic viral infections, such as those of human immunodeficiency virus (HIV) and hepatitis C virus (HCV) in humans, remain serious health problems worldwide, necessitating alternative targets/reagents for better treatment. Although the production of and/or response to type I interferon (IFN-I), a critical antiviral reagent, are known to be dysregulated in chronic viral infections, no serious effort has been performed to determine whether any host IFN-I negative regulator can importantly contribute to inducing and/or maintaining chronic viral infections. In this study, we used a mouse model of chronic viral infection, lymphocytic choriomeningitis virus (LCMV) infection, and asked whether 2′–5′ oligoadenylate synthetase-like 1 (OASL1), a recently defined IFN-I negative regulator, plays a key role in the viral defense against chronic LCMV infection. Our data show that OASL1 suppresses IFN-I production during very early phase of infection, thus inhibits efficient viral control and the induction of functional virus-specific T-cell response, permitting viral persistence. These results indicate that OASL1-mediated suppression of IFN-I production is a critical step for permitting chronic viral infection and suggest that IFN-I negative regulators, including OASL1, could be exciting new targets for preventing chronic viral infection.</P></▼2>

      • Neutrophils Promote Mycobacterial Trehalose Dimycolate-Induced Lung Inflammation via the Mincle Pathway

        Lee, Wook-Bin,Kang, Ji-Seon,Yan, Ji-Jing,Lee, Myeong Sup,Jeon, Bo-Young,Cho, Sang-Nae,Kim, Young-Joon Public Library of Science 2012 PLoS pathogens Vol.8 No.4

        <▼1><P>Trehalose 6,6′-dimycolate (TDM), a cord factor of <I>Mycobacterium tuberculosis</I> (Mtb), is an important regulator of immune responses during Mtb infections. Macrophages recognize TDM through the Mincle receptor and initiate TDM-induced inflammatory responses, leading to lung granuloma formation. Although various immune cells are recruited to lung granulomas, the roles of other immune cells, especially during the initial process of TDM-induced inflammation, are not clear. In this study, Mincle signaling on neutrophils played an important role in TDM-induced lung inflammation by promoting adhesion and innate immune responses. Neutrophils were recruited during the early stage of lung inflammation following TDM-induced granuloma formation. Mincle expression on neutrophils was required for infiltration of TDM-challenged sites in a granuloma model induced by TDM-coated-beads. TDM-induced Mincle signaling on neutrophils increased cell adherence by enhancing F-actin polymerization and CD11b/CD18 surface expression. The TDM-induced effects were dependent on Src, Syk, and MAPK/ERK kinases (MEK). Moreover, coactivation of the Mincle and TLR2 pathways by TDM and Pam3CSK4 treatment synergistically induced CD11b/CD18 surface expression, reactive oxygen species, and TNFα production by neutrophils. These synergistically-enhanced immune responses correlated with the degree of Mincle expression on neutrophil surfaces. The physiological relevance of the Mincle-mediated anti-TDM immune response was confirmed by defective immune responses in Mincle<SUP>−/−</SUP> mice upon aerosol infections with Mtb. Mincle-mutant mice had higher inflammation levels and mycobacterial loads than WT mice. Neutrophil depletion with anti-Ly6G antibody caused a reduction in IL-6 and monocyte chemotactic protein-1 expression upon TDM treatment, and reduced levels of immune cell recruitment during the initial stage of infection. These findings suggest a new role of Mincle signaling on neutrophils during anti-mycobacterial responses.</P></▼1><▼2><P><B>Author Summary</B></P><P>Tuberculosis is one of the world's most pernicious diseases. <I>Mycobacterium tuberculosis</I> (Mtb), the causative agent of tuberculosis, has a lipid-rich cell wall that contains immunostimulatory properties. One of the lipid cell wall components, trehalose 6,6′-dimycolate (TDM), is a Mincle ligand and an immunogenic factor of Mtb that induces inflammatory responses leading to granuloma formation. Defining the major target and cellular functions of TDM may be requisite for delaying or preventing mycobacterial TDM-induced inflammation. Here, we demonstrated that neutrophils are important for the early phase of TDM-induced lung inflammation. Neutrophils are recruited during the initial stage of TDM-induced lung inflammation and Mincle is required for neutrophil access to TDM-challenged sites by enhancing neutrophil integrin expression, cytoskeleton remodeling, and cell adhesion. Furthermore, neutrophils aggravate TDM-induced lung inflammation by producing proinflammatory cytokines/chemokines. These findings open new perspectives for the role of Mincle signaling on neutrophils during TDM-induced inflammatory responses.</P></▼2>

      • OASL1 inhibits translation of the type I interferon–regulating transcription factor IRF7

        Lee, Myeong Sup,Kim, Byungil,Oh, Goo Taeg,Kim, Young-Joon Nature Publishing Group, a division of Macmillan P 2013 Nature immunology Vol.14 No.4

        The production of type I interferon is essential for viral clearance but is kept under tight control to avoid unnecessary tissue damage from hyperinflammatory responses. Here we found that OASL1 inhibited translation of IRF7, the master transcription factor for type I interferon, and thus negatively regulated the robust production of type I interferon during viral infection. OASL1 inhibited the translation of IRF7 mRNA by binding to the 5′ untranslated region (UTR) of IRF7 and possibly by inhibiting scanning of the 43S preinitiation complex along the message. Oasl1<SUP>−/−</SUP> mice were resistant to viral infection because of the greater abundance of type I interferon, which suggests that OASL1 could be a potential therapeutic target for boosting the production of type I interferon during viral infection.

      • A randomized, open phase IV exploratory clinical trial to evaluate the efficacy and safety of acupuncture on the outcome of induction of ovulation in women with poor ovarian response : A study protocol for a randomized controlled trial

        Lee, Hoyoung,Choi, Tae-Young,Shim, Eun Hyoung,Choi, Jiae,Joo, Jong Kil,Joo, Bo Sun,Lee, Myeong Soo,Choi, Jun-Yong,Ha, Ki-Tae,You, Sooseong,Lee, Kyu Sup Wolters Kluwer Health 2018 Medicine Vol.97 No.34

        <P><B>Abstract</B></P><P><B>Introduction:</B></P><P>Women with infertility who have a poor ovarian responder (POR), characterized by a low number of retrieved oocytes after ovulation induction, often have a significantly reduced pregnancy rate after in vitro fertilization-embryo transfer (IVF-ET), due to the few transferred embryos. Acupuncture is a form of Korean Traditional Medicine. It involves the insertion of a microscopic needle at a specific point in the body, known as an acupuncture point or an acupoint. In this study, our purpose is to investigate how acupuncture affects the retrieval of mature oocytes after ovulation induction in patients with POR.</P><P><B>Methods and analysis:</B></P><P>This study will be a randomized clinical trial comprising an IVF-ET trial and an IVF-ET trial after acupuncture. Seventy patients will by enrolled and randomly assigned to either of the 2 groups. The study subjects will be required to be diagnosed as having POR. Participants will be divided into 2 groups: IVF-ET single treatment group, and acupuncture and IVF-ET combined treatment group. The study subjects will be required to participate in a 15-week trial involving 16 acupuncture treatments over a period of approximately 2 months before ovulation induction for oocyte retrieval. The primary assessment of all participants will be comparing the number of oocytes.</P><P><B>Result:</B></P><P>This treatment will be a therapeutic model for POR.</P><P><B>Discussion:</B></P><P>Our results will provide patients with POR as well as complementary and alternative medicine professionals, such as Korean medicine doctors, about the potential role of acupuncture in the treatment of POR. This will improve the quality of life in women with infertility and provide an important treatment option for patients with POR. Further studies can be performed to determine the optimal treatment for POR.</P>

      • SCISCIESCOPUS

        Signaling Pathways Downstream of Pattern-Recognition Receptors and Their Cross Talk

        Lee, Myeong Sup,Kim, Young-Joon Annual Reviews 2007 Annual review of biochemistry Vol.76 No.-

        Pattern-recognition receptors (PRRs) initiate innate immunity through pathogen recognition. Serum PRRs opsonize pathogens for enhanced phagocytic clearance. Toll-like receptors (TLRs) initiate common NF-&kgr;B/AP-1 and distinct IRF3/7 pathways to coordinate innate immunity and to initiate adaptive immunity against diverse pathogens. Cytoplasmic caspase-recruiting domain (CARD) helicases, such as RIG-I/MDA5, mediate antiviral immunity by inducing the production of type I interferons via the adaptor IPS-1, whereas nucleotide-binding oligomerization domain (NOD)-like receptors mediate mainly antibacterial immunity by activating NF-&kgr;B or inflammasomes. Dectin-1 is important for antifungal immunity, promoting phagocytosis and activating NF-&kgr;B. Potentially harmful TLR signaling pathways can be negatively regulated by negative feedback mechanisms and also by anti-inflammatory factors such as TGF&bgr;, interleukin (IL)-10, and steroids. Many combinations of TLR-TLR and TLR-NOD modulate inflammatory responses. TLRs and NALP3 interplay to produce mature IL-1&bgr;. Thus signaling pathways downstream of PRRs and their cross talk control immune responses in effective manners.

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