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등방성 이종재료 내의 Ⅴ-노치 균열에 대한 응력강도계수 결정에 관한 연구
조상봉,정휘원,김진광 경남대학교 신소재연구소 1999 論文集 Vol.11 No.-
접합계면 V-노치 균열 문제는 고유치와 고유벡터 문제로 수식화할 수 있다. V-노치 균열첨단에서 응력특이성을 가지는 고유치가 존재한다. 상반일 등고선 적분법(RWCIM)은 고유치와 관련된 고유벡터의 계수를 구하는 한 가지의 방법이다. 상반일 등고선 적분법을 이용하여 접합계면 균열의 응력확대계수를 구하도록 시도하였다. 상반일 등고선 적분법으로 구한 응력확대계수와 경계요소법과 변위외삽법을 이용하여 구한 결과를 비교하였다. An inteiface 17-notched crack problem can be formulated as a eigenvalue problem. there are the eigenvalues which give stress singularities at the V-notched crack tip. The RWCIM is a method of calculating the eigenvector coefficients associated with eigenvalues. Obtaining the stress intensity factors for an interface crack in dissimilar materials was examined by the RWCIM. The results obtained for stress intensity factors using RWCIM were compared with those obtained by using the displacement extrapolation method and the BEM.
Cho, Jeong Hwi,Tae, Hyun-Jin,Kim, In-Shik,Song, Minah,Kim, Hyunjung,Lee, Tae-Kyeong,Kim, Young-Myeong,Ryoo, Sungwoo,Kim, Dae Won,Lee, Choong-Hyun,Hwang, In Koo,Yan, Bing Chun,Kang, Il Jun,Won, Moo-Ho Academic Press 2019 Experimental neurology Vol.320 No.-
<P><B>Abstract</B></P> <P>Although multiple reports using animal models have confirmed that melatonin appears to promote neuroprotective effects following ischemia/reperfusion-induced brain injury, the relationship between its protective effects and activation of autophagy in Purkinje cells following asphyxial cardiac arrest and cardiopulmonary resuscitation (CA/CPR) remains unclear. Rats used in this study were randomly assigned to 6 groups as follows; vehicle-treated sham operated group, vehicle-treated asphyxial CA/CPR operated group, melatonin-treated sham operated group, melatonin-treated asphyxial CA/CPR operated group, PDOT (a MT2 melatonin receptor antagonist) plus (+) melatonin-treated sham operated group and PDOT+melatonin-treated asphyxial CA/CPR operated group. Melatonin (20 mg/kg, i.p., 4 times before CA and 3 times after CA) treatment significantly improved survival rate and neurological deficit compared with the vehicle-treated asphyxial CA/CPR rats (survival rates ≥40% vs 10%), showing that melatonin treatment exhibited protective effect against asphyxial CA/CPR-induced Purkinje cell death. The protective effect of melatonin against CA/CPR-induced Purkinje cell death paralleled a remarkable attenuation of autophagy-like processes (Beclin-1, Atg7 and LC3), as well as a dramatic reduction in superoxide anion radical (O<SUB>2</SUB>·-), intense enhancements of CuZn superoxide dismutase (SOD1) and MnSOD (SOD2) expressions. Furthermore, the protective effect was notably reversed by treatment with PDOT, which is a selective MT2 antagonist. In brief, melatonin conferred neuroprotection against asphyxial CA/CPR-induced Purkinje cell death via inhibiting autophagic activation by reducing expressions of O<SUB>2</SUB>·- and increasing expressions of antioxidant enzymes, and suggests that MT2 is involved in neuroprotective effect of melatonin against Purkinje cell death caused by asphyxial CA/CPR.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Melatonin prevents cerebellar Purkinje cell death following asphyxial cardiac arrest. </LI> <LI> Melatonin attenuates autophagy-like processes via MT2 receptor. </LI> <LI> Melatonin attenuates increase of superoxide anion radical via MT2 receptor. </LI> <LI> Melatonin maintains antioxidant enzymes expressions via MT2 receptor. </LI> </UL> </P>
Cho, Jeong-Hwi,Yan, Bing Chun,Lee, Young Joo,Park, Joon Ha,Ahn, Ji Hyeon,Kim, In Hye,Lee, Jae-Chul,Kim, Young-Myeong,Lee, Bonghee,Cho, Jun Hwi,Won, Moo-Ho Kluwer Academic/Plenum Publishers 2013 Neurochem Res Vol.38 No.5
<P>Beta-catenin, a transcription factor, plays a critical role in cell survival and degradation after stroke. In this study, we examined changes of expression in beta-catenin in the hippocampal CA1 region of the gerbil following 5 min of transient cerebral ischemia. We observed neuronal damage using cresyl violet staining, neuronal nuclei immunohistochemistry and Fluro-Jade B immunofluorescence. Four days after ischemia-reperfusion (I-R), most of pyramidal cells in the CA1 region were damaged. In addition, early damage in dendrites was detected 1 day after I-R by immunohistochemical staining for microtubule-associated protein 2 (MAP-2), and MAP-2 immunoreactivity was hardly detected in the CA1 region 4 days after I-R. We found that beta-catenin (a synapse-enriched cell adhesion molecule) was well expressed in dendrites before I-R. Its immunoreactivity was well colocalized with MAP-2. Chronological change of beta-catenin immunoreactivity was novelty in the present study. Twelve hours after I-R, its immunoreactivity was decreased in the stratum radiatum of the CA1 region, however, its immunoreactivity was increased 1 and 2 days after I-R, and decreased sharply 4 days after I-R. However, we did not find any change in beta-catenin immunoreactivity in the CA2 and CA3 region. In brief, we suggest that early change of beta-catenin expression in the stratum pyramidale of ischemic hippocampal CA1 region is associated with early dendrite damage following transient cerebral ischemia.</P>