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14.6 A GeV ^28Si 중이온이 원자핵건판내에서 발생시킨 핵반응에서 생성된 2차입자의 발생각 분포
김종오,김태연,남신우,신택수,우종관,이세병,임계엽,장세덕,조재희,천병구,임인택,김기영 慶尙大學校 기초과학연구소 1990 基礎科學硏究所報 Vol.6 No.-
14.6A GeV^28Si 중이온이 원자핵 건판내에서 발생시킨 N_h=1인 핵반응에서 생성된 47개의 파쇄 α 입자와 537개의 단일하전 2차입자의 발생각들을 측정하여 변수 exp(γ-η_b)의 포괄적 분포를 회귀함수 dN=exp[a+χ{exp(γ-η_b)d{exp(γ-η_b)}로 적합시켰다. 여기서 의사신속도 γ=arctanh(cosθ)=-ln tan(θ/2)이고, 입사 중이온의 신속도 η_b=3.445이다. 그 적합결과 파쇄 α입자의 경우 χ=-0.052±0.011이고, 파쇄 p입자의 경우 χ=-0.141±0.015이었다. For LS emission angles of 47 α fragments and 537 single-charged shower particles, produced by the N_h (the number of heavyprongs)=1 interactions of 14.6 A GeV^28Si nuclei in the nuclear emulsion, the distribution of the parameter exp(γ-η_b) is well expressed by dN=exp[a+χ{exp(γ-η_b)d{exp(γ-η_b)}with χ=-0.052±0.011 for αfragments and χ=-0.141±0.015 for p 'fragments', where the pseudorapidity of secondaries γ=arctanh(cosθ)=-ln tan(θ/2) and the rapidity of incident heavy ions, η_b=3.445.
Kim, E-K,Seo, H-S,Chae, M-J,Jeon, I-S,Song, B-Y,Park, Y-J,Ahn, H M,Yun, C-O,Kang, C-Y Macmillan Publishers Limited 2014 Gene therapy Vol.21 No.1
For successful clinical tumor immunotherapy outcomes, strong immune responses against tumor antigens must be generated. Cell-based vaccines compromise one strategy with which to induce appropriate strong immune responses. Previously, we established a natural killer T-cell (NKT) ligand-loaded, adenoviral vector-transduced B-cell-based anticancer cellular vaccine. To enhance tumor antigen delivery to B cells, we established a modified adenoviral vector (Ad-k35) that encoded a truncated form of the breast cancer antigen Her2/neu (Ad-k35HM) in which fiber structure was substituted with adenovirus serotype 35. We observed increased tumor antigen expression with Ad-k35HM in both human and murine B cells. In addition, an Ad-k35HM-transduced B-cell vaccine elicited strong antigen-specific cellular and humoral immune responses that were further enhanced with the additional loading of soluble NKT ligand KBC009. An Ad-k35HM-transduced, KBC009-loaded B-cell vaccine efficiently suppressed the in vivo growth of established tumors in a mouse model. Moreover, the vaccine elicited human leukocyte antigen (HLA)-A2 epitope-specific cytotoxic T-cell responses in B6.Cg (CB)-Tg (HLA-A/H2-D) 2Enge/Jat mice. These findings indicated that the Ad-k35 could be appropriate for the preclinical and clinical development of B-cell-based anticancer immunotherapies.
Caspase-3 activation as a key factor for HBx-transformed cell death
Kim, A.,Kwon, O. S.,Kim, S. O.,He, L.,Bae, E. Y.,Lee, M. S.,Jeong, S. J.,Shim, J. H.,Yoon, D. Y.,Kim, C. H.,Moon, A.,Kim, K. E.,Ahn, J. S.,Kim, B. Y. Blackwell Publishing Ltd 2008 Cell proliferation Vol.41 No.5
<P>Abstract. </P><P><I>Objectives</I>: Nuclear factor-kappa B (NF-&kgr;B) activation has been associated with the tumorigenic growth of hepatitis B virus X protein (HBx)-transformed cells. This study was aimed to find a key target for treatment of HBx-mediated cancers. <I>Materials and methods</I>: NF-&kgr;B activation, endoplasmic reticulum-stress (ER-stress), caspase-3 activation, and cell proliferation were evaluated after Chang/HBx cells permanently expressing HBx viral protein were treated with inhibitors of NF-&kgr;B, proteasome and DNA topoisomerase. <I>Results</I>: Inhibition of NF-&kgr;B transcriptional activity by transient transfection with mutant plasmids encoding Akt1 and glycogen synthase kinase-3&bgr; (GSK-3&bgr;), or by treatment with chemical inhibitors, wortmannin and LY294002, showed little effect on the survival of Chang/HBx cells. Furthermore, I&kgr;Bα (S32/36A) mutant plasmid or other NF-&kgr;B inhibitors, 1-pyrrolidinecarbonidithioic acid and sulphasalazine, were also shown to have little effect on the cell proliferation. By contrast, proteasome inhibitor-1 (Pro1) and MG132 enhanced the HBx-induced ER-stress response and the subsequent activation of caspase-12, -9 and -3 and reduced cell proliferation. Camptothecin (CPT), however, triggered activation of caspase-3 without induction of caspase-12, and reduced cell proliferation. In addition, CPT-induced cell death was reversed by pre-treatment with z-DEVD, a caspase-3-specific inhibitor. <I>Conclusions</I>: Detailed exploitation of the regulators of caspase-3 activation could open the gate for finding an efficient target for development of anticancer therapeutics against HBx-transformed hepatocellular carcinoma.</P>
200 GeV/핵자 유황이온과 핵건판핵의 충돌에 의해 생성된 헬륨 파쇄핵의 극한파쇄 연구
김동철,송진섭,윤천실,정성헌,박인곤,김종오,김철수,김태연,이승희,조재희,천병구,김재률,김준원,김태익,박명렬,장한일,임인택 慶尙大學校 기초과학연구소 1992 基礎科學硏究所報 Vol.8 No.-
고에너지 중이온 원자핵과 핵건판의 충돌에서, 200GeV/핵자 유황이온에 의해 생성된 파쇄 헬륨핵(Z=2)의 실험실계의 방출각 분포는 표적핵에 무관한 회귀공식. dN=exp[a+k exp(η-y_b)]d[exp(η-y_b)]로 잘 표현된다. 여기에서 의사신속도 η=-ln[tan(θ/2)]이고, y_b는 실험실계의 입사입자(^32S)의 신속도이다. 이 공식에 의한 적합에서 k=-0.057±0.008로 얻어진다. 즉, 핵건판과 고에너지 중이온의 충돌에서 파쇄 헬륨핵의 exp(η-y_b)의 분포는 "극한파쇄" 현상을 잘 설명하고 있다. The angular distribution of emission angle θ of helium (Z=2) produced in the collisions of incident particles of 200 GeV/nucleon ^32S in nuclear emulsion is well expressed by dN=exp[a+k exp(η-y_b)]d[exp(η-y_b)] where the pseudorapidity is η=-ln[tan(θ/2)], the laboratory system primary rapidity is y_b, and k=-0.057+0.008. The shape of this frequency of occurrence distributions in terms of exp(η-y_b) attests to the validity of the concept of "limiting fragmentation" for helium projectile fragments produced in the projectile fragmentation regions of heavy ion collisions in nuclear emulsion.
Selective novel inverse agonists for human GPR43 augment GLP-1 secretion
Park, B.O.,Kim, S.H.,Kong, G.Y.,Kim, D.H.,Kwon, M.S.,Lee, S.U.,Kim, M.O.,Cho, S.,Lee, S.,Lee, H.J.,Han, S.B.,Kwak, Y.S.,Lee, S.B.,Kim, S. North-Holland ; Elsevier Science Ltd 2016 european journal of pharmacology Vol.771 No.-
<P>GPR43/Free Fatty Acid Receptor 2 (FFAR2) is known to be activated by short-chain fatty acids and be coupled to G(i), and G(q), family of heterotrimeric G proteins. GPR43 is mainly expressed in neutrophils, adipocytes and enteroendocrine cells, implicated to be involved in inflammation, obesity and type 2 diabetes. However, several groups have reported the contradictory data about the physiological functions of GPR43, so that its roles in vivo remain unclear. Here, we demonstrate that a novel compound of pyrimidinecarboxamide class named as BTI-A-404 is a selective and potent competitive inverse agonist of human GPR43, but not the murine ortholog. Through structure-activity relationship (SAR), we also found active compound named as BTI-A-292. These regulators increased the cyclic AMP level and reduced acetate-induced cytoplasmic Ca2+ level. Furthermore, we show that they modulated the downstream signaling pathways of GPR43, such as ERK, p38 MAPK, and NF-kappa B. It was surprising that two compounds augmented the secretion of glucagon-like peptide 1 (GLP-1) in NCI-H716 cell line. Collectively, these novel and specific competitive inhibitors regulate all aspects of GPR43 signaling and the results underscore the therapeutic potential of them. (C) 2015 Elsevier B.V. All rights reserved.</P>
HBeAg양성인 만성 B형 간염 환자에서 alpha-interferon치료후 반응형태와 장기적 결과, 그리고 lamivudine의 가치
김현영 ( H. Y. Kim ),김성훈 ( S. H. Kim ),윤병철 ( B. C. Yoon ),이상욱 ( S. O. Lee ),한병훈 ( B. H. Han ) 대한소화기학회 2002 대한소화기학회 춘계학술대회 Vol.2002 No.-
<목적> HBeAg 양성 만성 B형 간염환자에서 alpha-interferon과 lamivudine의 효과 판정기준과 장기적 효과에 대한 연구는 아직까지도 제한적이다. 이에 연자들은 HBeAg 양성인 만성 B형 간염 환자들에서 alpha-interferon의 장기적 효과와 효과판정 기준, 그리고 치료 실패 군에서 lamivudine의 가치를 확인하기 위해서 다음과 같은 연구를 시행하였다. <방법> HBeAg양성 만성B형간염으로 진단받고 alpha-int