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Jung, Dae Young,Lee, Heasuk,Jung, Bo-Young,Ock, Jiyeon,Lee, Myung-Shik,Lee, Won-Ha,Suk, Kyoungho American Association of Immunologists 2005 Journal of Immunology Vol.174 No.10
<P>TLRs mediate diverse signaling after recognition of evolutionary conserved pathogen-associated molecular patterns such as LPS and lipopeptides. Both TLR2 and TLR4 are known to trigger a protective immune response as well as cellular apoptosis. In this study, we present evidence that TLR4, but not TLR2, mediates an autoregulatory apoptosis of activated microglia. Brain microglia underwent apoptosis upon stimulation with TLR4 ligand (LPS), but not TLR2 ligands (Pam(3)Cys-Ser-Lys(4), peptidoglycan, and lipoteichoic acid). Based on studies using TLR2-deficient or TLR4 mutant mice and TLR dominant-negative mutants, we also demonstrated that TLR4, but not TLR2, is necessary for microglial apoptosis. The critical difference between TLR2 and TLR4 signalings in microglia was IFN regulatory factor-3 (IRF-3) activation, followed by IFN-beta expression: while TLR4 agonist induced the activation of IRF-3/IFN-beta pathway, TLR2 did not. Nevertheless, both TLR2 and TLR4 agonists strongly induced NF-kappaB activation and NO production in microglia. Neutralizing Ab against IFN-beta attenuated TLR4-mediated microglial apoptosis. IFN-beta alone, however, did not induce a significant cell death. Meanwhile, TLR2 activation induced microglial apoptosis with help of IFN-beta, indicating that IFN-beta production following IRF-3 activation determines the apoptogenic action of TLR signaling. TLR4-mediated microglial apoptosis was mediated by MyD88 and Toll/IL-1R domain-containing adaptor-inducing IFN-beta, and was associated with caspase-11 and -3 activation rather than Fas-associated death domain protein/caspase-8 pathway. Taken together, TLR4 appears to signal a microglial apoptosis via autocrine/paracrine IFN-beta production, which may act as an apoptotic sensitizer.</P>
Clinicopathologic Characteristics of T-cell Non-Hodgkin`s Lymphoma: A Single Institution Experience
( Ock Bae Ko ),( Dae Ho Lee ),( Sang We Kim ),( Jung Shin Lee ),( Shin Kim ),( Joo Ryung Huh ),( Cheol Won Suh ) 대한내과학회 2009 The Korean Journal of Internal Medicine Vol.24 No.2
Background/Aims: Although the incidence of T-cell non-Hodgkin`s lymphoma (NHL) is higher in Far East Asia than in Western countries, its incidence and clinical course in Korea are not well-defined. Therefore, we assessed the relative frequency and clinical features of T-cell NHL in Korea. Methods: We performed a retrospetcive analysis of 586 patients with NHL. Results: 101 (17.2%) had T-cell NHL. The most frequent subtypes of T-cell NHL were extranodal NK/T-cell lymphoma, nasal type (NASAL), peripheral T-cell lymphoma, unspecified type (PTCL-U), and anaplastic large cell lymphoma, T/null cell, primary systemic type (ALCL). The seven pathological subtypes could be classified into three prognostic subgroups. When patients with the three most frequent subtypes were grouped together, their survival was reflected in the International Prognostic Index (IPI) scores. Univariate analysis of IPI elements and other clinical features showed that clinical stage and extranodal sites were significant predictors of survival. Cox multivariate analysis showed that the number of extranodal sites was the only independent prognostic indicator. Conclusions: The relative frequency of T-cell NHL seems to be decreasing in Korea, although NASAL remains frequent. Korean patients with ALCL appear to have an unfavorable prognosis. Large-scale studies are warranted for Korean patients with T-cell NHL. (Korean J Intern Med 2009;24:128-134)
Induction of microglial apoptosis by corticotropin-releasing hormone
Ock, Jiyeon,Lee, Heasuk,Kim, Sangseop,Lee, Won-Ha,Choi, Dong-Kug,Park, Eun Jung,Kim, Sang-Hyun,Kim, In Kyeom,Suk, Kyoungho Raven Press [etc.] 2006 Journal of neurochemistry Vol.98 No.3
<P>Abstract</P><P>Neuropeptides are short-chain peptides found in brain tissue, some of which function as neurotransmitters and others as hormones. Neuropeptides may directly or indirectly modulate glial functions in the CNS. In the present study, effects of various neuropeptides on the viability and inflammatory activation of cultured microglia were investigated. Vasoactive intestinal peptide, substance P, cholecystokinin and neuropeptide Y did not affect microglial cell viability, whereas corticotropin-releasing hormone (CRH) induced a classical apoptosis of mouse microglia in culture as shown by nuclear condensation and fragmentation, terminal deoxynucleotidyl transferase dUTP nick-end labeling, and cleavage of caspase 3 and poly(ADP-ribose) polymerase protein. CRH, however, did not influence nitric oxide production or expression of inflammatory genes including those encoding cytokines and chemokines, indicating that CRH did not affect the inflammatory activation of microglia. The CRH-induced microglial apoptosis appeared to involve a mitochondrial pathway and reactive oxygen species, based on the mitochondrial membrane potential change, caspase 9 activation and sensitivity to antioxidants. Taken together, our results indicate that the stress neuropeptide CRH may regulate neuroinflammation by inducing the apoptosis of microglia, the major cellular source of inflammatory mediators in the CNS.</P>
OCK, Sun-A,LEE, Yeon-Mi,PARK, Ji-Sung,SHIVAKUMAR, Sharath Belame,MOON, Seon-Woung,SUNG, Nak-Ju,LEE, Won-Jae,JANG, Si-Jung,PARK, Ju-Mi,LEE, Seung-Chan,LEE, Sung-Lim,RHO, Gyu-Jin JAPANESE SOCIETY OF VETERINARY SCIENCE 2016 The Journal of veterinary medical science Vol.78 No.6
<P>The biological properties of mesenchymal stem cells (MSCs) are influenced by donor age, gender and/or tissue sources. The present study investigated the cellular and molecular properties of porcine mesenchymal stromal/stem cells <B>(</B>MSCs) isolated from different tissues (adipose & dermal skin) and sex at different ages (1 week & 8 months after birth) with similar genetic and environmental backgrounds. MSCs were analyzed for alkaline phosphatase (AP) activity, CD90 and Oct3/4 expression, <I>in vitro</I> differentiation ability, senescence-associated <I>β</I>-galactosidase (SA-<I>β</I>-Gal) activity, telomeric properties, cell cycle status and expression of senescence (IL6, c-myc, TGFβ, p53 and p21)- and apoptosis (Bak and Bcl2)-related proteins. An age-dependent decline in AP activity and adipogenesis was observed in all MSCs, except for male A-MSCs. CD90 expression did not change, but SA<I>-β</I>-Gal activity increased with advancement in age, except in A-MSCs. Telomeric properties were similar in all MSCs, whereas expression levels of Oct3/4 protein declined with the advancement in age. p21 expression was increased with increase in donor age. Male derived cells have shown higher IL6 expression. The expression of p53 was slightly lower in MSCs of dermal tissue than in adipose tissue. Bak was expressed in all MSCs regardless of age, but up regulation of Bcl2 was observed in DS-MSCs derived at 1 week after birth. In conclusion, adipose tissue-derived MSCs from young female individuals were found to be more resistant to senescence under <I>in vitro</I> culture conditions.</P>
F2211-04 생체조직공학적 의료제품(TEMPs)에 대한 표준 분류
소정원 ( Jung Won So ),김순희 ( Soon Hee Kim ),백미옥 ( Mi Ock Baek ),노혜원 ( Hye Won Roh ),이나리 ( Na Ri Lee ),유규하 ( Gyu Ha Ryu ),조양하 ( Yang Ha Cho ),이승진 ( Seung Jin Lee ),강길선 ( Gil Son Khang ) 한국조직공학과 재생의학회 2008 조직공학과 재생의학 Vol.5 No.1
Tissue engineered medical products (TEMPs) are those protocols and products developed for use in the human body as biological substitutes to restore, maintain, or improve tissue function. So TEMPs may achieve a therapeutic potential from cells, biomolecules, scaffolds, and other materials, and processed tissue and derivatives used in various combinations or alone. Since interactions may occur among the components used in TEMPs, new standard descriptions, test methods, and practices are needed to aid the evaluation of these interactions. Therefore this technical report the aspects of tissue engineered medical that will be developed as standards.
So Jung Lee,Ji Young Park,Ki Seok Choi,Chan Young Ock,Kyung Sook Hong,Yoon Jae Kim,Jun Won Chung,Ki-Baik Hahm 고려인삼학회 2010 Journal of Ginseng Research Vol.34 No.2
This clinical study was performed to evaluate whether supplementation of proton pump inhibitor (PPI)-based triple therapy with Korean red ginseng can enhance Helicobacter pylori (H. pylori) eradication and reduce levels of halitosis-associated volatile sulfur compounds (VSCs) in the stomach. Seventy-six patients were randomized into an eradication regimen-only group (n=45) or an eradication regimen plus 10 weeks of Korean red ginseng supplementation group (n=31). The eradication regimen consisted of PPI b.i.d., clarithromycin 500 ㎎ b.i.d., and amoxicillin 1 g b.i.d.. for seven days. Korean red ginseng supplementation commenced on the last day of the eradication regimen. ¹³C-urea breath test and halimeter measurements were performed prior to protocol repetition. By intention-to-treat analysis, the H. pylori eradication rate in the Korean red ginseng group (77.4%, 24 of 31) was higher than that in the control group (45.0%, 26 of 45). However, by per protocol analysis, the eradication rate in the Korean red ginseng group was significantly higher than that in the control group (92.3%, 24/26 vs. 69.4%, 26/38; p<0.05). H. pylori infection was significantly associated with increased VSC levels. However, VSC levels decreased significantly in the Korean red ginseng group (p<0.05). In conclusion, supplementation of triple therapy with Korean red ginseng increased the H. pylori eradication rate and led to significant reductions in VSC levels, suggesting the usefulness of this substance in combating H. pylori infection.