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Escherichia coli 패혈증 환자에 합병된 대칭적 하지 말단 괴사증 1예
남해성,유진홍,권순석,민준기,조현선,박민경,심병주,남유정,이지인,김진수,길욱현,조근종,신완식 대한감염학회 2005 감염과 화학요법 Vol.37 No.6
We have encountered a rare case of symmetrical peripheral gangrene complicating Escherichia coli sepsis in a 47-years-old male. He was successfully treated with antibiotics, anticoagulants, and vasodilator. To our knowledge, this is the first report on symmetrical peripheral gangrene complicating E. coli sepsis in Korea.
Geun-Shik Lee 충북대학교 동물의학연구소 2013 Journal of Biomedical and Translational Research Vol.14 No.4
Inflammation mainly mediated by innate immune cells as the first line of host defense against pathogens is an acute response that limits tissue damage and eliminates pathogens in the body. In triggering inflammation, several pattern recognition receptors work together; membrane-associated Toll-like receptors, c-type lectin receptors, retinoic acid-inducible gene-like helicase receptors, absent in melanoma-like receptors, and cytosolic nucleotide-binding domain and leucine-rich repeat receptors. Among them, inflammasome is a newly trigger of inflammation in response to exogenous and endogenous stimuli and its activation leads to the assembly of multiprotein platforms composed of NLRP3 (NOD-like receptor family, pyrin domain containing 3), ASC (apoptosis associated speck-like protein containing a CARD), and procaspase 1. Thus, the activated inflammasome activates caspase 1, resulting in processing and secretion of interleukin (IL)-1β. Recent emerging data suggest that dysregulated metabolites, i.e., amyloids, ceramides, and cholesterol crystals, have been classified as inflammasome activators. In addition, IL-1β may play a critical role in the pathogenesis of chronic inflammation-induced disorders such as Alzheimer’s diseases, type 2 diabetes, and atheriosclerosis. This review introduces the basic concept of inflammasome activation and auto-inflammatory diseases. In addition, it discusses the updated signaling models of inflammasome activation that link metabolic dysfunction in order to outline future therapeutic approaches to inflammasome-mediating diseases.
Disruption of Stamp/Ttll5 Gene in Male Mice Causes Sperm Malformation and Infertility
Geun-Shik Lee,Yuanzheng He,Edward J. Dougherty,Maria Jimenez-Movilla,Matteo Avella,Sean erullon,David S. Sharlin,Chunhua Guo,Smita Auasthi,Zhenhuan Zhang,Stephen P. Armstrong,Edra C. London,Weiping Ch 한국동물생명공학회(구 한국동물번식학회) 2012 발생공학 국제심포지엄 및 학술대회 Vol.2012 No.1
Lee, Geun-Shik,Kim, Hoe-Jin,Jung, Yong-Woo,Choi, Kyung-Chul,Jeung, Eui-Bae Oxford University Press 2005 TOXICOLOGICAL SCIENCES Vol.84 No.2
<P>It has been demonstrated in our previous studies that <I>Calbindin-D<SUB>9k</SUB></I> (<I>CaBP-9k</I>) is a potent biomarker for screening estrogen-like chemicals in the rat model. Although treatments with 17beta-estradiol (E2) and endocrine disrupting compounds resulted in the up-regulation of uterine CaBP-9k, the mechanism of <I>CaBP-9k</I> induction by these compounds through two subtypes of estrogen receptors (ERα and ERβ) is unclear. Thus, in the present study, immature rats were treated with propyl pyrazole triol (PPT, an ERα-selective ligand), diarylpropionitrile (DPN, an ERβ-selective ligand), E2, or dimethyl sulfoxide (DMSO, a vehicle control) for three days in order to clarify which subtype of ER is involved in the uterine <I>CaBP-9k</I> induction. Following injection with these ER ligands, uterine <I>CaBP-9k</I> expression was analyzed by Northern blot and immunoblot assays. Uterine <I>CaBP-9k</I> expression is mainly mediated by PPT in a dose- and time-dependent manner in immature rats, whereas no significant alteration of the uterine <I>CaBP-9k</I> gene was observed after DPN treatment. In addition, an estrogenicity of PPT in inducing <I>CaBP-9k</I> expression was completely blocked by the anti-estrogen ICI 182,780, implying that uterine <I>CaBP-9k</I> is solely induced by ERα. A single treatment with PPT rapidly increased the protein levels of ERα and PR, an E2-mediated gene, in these tissues. Taken together, these results indicate that uterine <I>CaBP-9k</I> is induced by E2 and endocrine disrupting chemicals via the ERα pathway, but not ERβ, in the uterus of immature rats.</P>
Lee, DJoohyeong,Shin, Hyeji,Lee, Wonyou,Lee, Seung Tae,Lee, Geun-Shik,Hyun, Sang-Hwan,Lee, Eunsong The Korean Society of Veterinary Science 2017 大韓獸醫學會誌 Vol.57 No.2
This study was conducted to determine the effects of biophoton treatment during in vitro maturation (IVM) and/or in vitro culture (IVC) on oocyte maturation and embryonic development in pigs. An apparatus capable of generating homogeneous biophoton energy emissions was placed in an incubator. Initially, immature pig oocytes were matured in the biophoton-equipped incubator in medium 199 supplemented with cysteine, epidermal growth factor, insulin, and gonadotrophic hormones for 22 h, after which they were matured in hormone-free medium for an additional 22 hr. Next, IVM oocytes were induced for parthenogenesis (PA) or provided as cytoplasts for somatic cell nuclear transfer (SCNT). Treatment of oocytes with biophoton energy during IVM did not improve cumulus cell expansion, nuclear maturation, intraoocyte glutathione content, or mitochondrial distribution of oocytes. However, biophoton-treated oocytes showed higher (p < 0.05) blastocyst formation after PA than that in untreated oocytes (50.7% vs. 42.7%). In an additional experiment, SCNT embryos produced from biophoton-treated oocytes showed a greater (p < 0.05) number of cells in blastocysts (52.6 vs. 43.9) than that in untreated oocytes. Taken together, our results demonstrate that biophoton treatment during IVM improves developmental competence of PA- and SCNT-derived embryos.