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동형 모더나이트 상에서 일산화탄소 산화반응에 대한 속도론
정명수,이창용,최고열,하백현 漢陽大學校 環境科學硏究所 1989 環境科學論文集 Vol.10 No.-
모더나이트에 동을 이온교환 및 담지시킨 후 환원·산화 처리를 하여 동의 상태를 변화시킨 촉매에 대해 일산화탄소 산화반응의 속도론적인 고찰을 행하였다. 이온교환 촉매나 담지촉매 모두 동의 상태와는 관계없이 일산화탄소에 관한 반응차수는 1차이고 산소에 관한 반응차수는 0차였다. 이온교환 촉매의 경우는 수소로 환원시켜 동이 금속상태로 존재할때와 이를 재산화시켜 산화동 상태로 존재할때는 활성화에너지가 각각 16.4 및 20.3으로 비교적 큰 값을 나타냈으나 동의 담지촉매의 경우는 동이 금속일 때나 산화물 상태 모두 12∼13kcal/mole로 비슷한 값을 나타냈으며 이온교환 촉매보다 상당히 감소함을 알 수 있었다. 이와 같은 결과는 이온교환 촉매의 경우는 동이 제올라이트내부에 대부분 존재하는 반면, 담지촉매의 경우는 제올라이트 결정 표면에 존재하기 때문에 활성을 증가시키는 것으로 생각된다. Kinetics of oxidation of carbon monoxide over copper mordenite was carried out at the temperature range between 373K-443K in the micro-catalytic reactor. The experimental results indicated that the reaction order, with respect to carbon monoxide and oxygen was first and zero order respectively, regardless of the valence states such as copper metal, copper ion and copper oxide on the mordenite. The activation energy for metal-copper mordenite which is obtained by the ion-exchange revealed 20kcal/mol. But if this was reoxidized under the oxygen it decreased to 16.6kcal/mol. The activation energy of metal-copper mordenite which was obtained by impregnation and its reoxidized one under the oxygen were 12.2kcal/mol and 13.3kcal/mol respectively.
고분자 전해질형 연료전지에서 Hot Pressing 조건의 영향
이태희,이승재,조원일,노용우,고영태,최경환 한국화학공학회 1996 Korean Chemical Engineering Research(HWAHAK KONGHA Vol.34 No.1
고분자 전해질형 연료전지에서 고분자막/전극 어셈블리를 hot pressing 조건을 달리하여 제조하고 그 성능을 반응면적 5㎠인 단위전지에서 측정하였다. 전지의 성능은 고분자막과 전극간의 접합이 가능한 온도 범위에서 hot pressing온도가 낮을수록, hat Pressing 압력이 높을수록 향상되었다. 즉, 고분자 전해질형 연료전지의 성능은 고분자 전해질 내의 수분 함량 증가, 고분자막/전극간 접촉저항 감소 및 얇은 고분자막을 사용한 전해질의 이온저항 감소 등으로 향상시킬 수 있었다. For a proton exchange membrane fuel cell, membrane and electrode assemblies were fabricated by different hot pressing conditions and those performances were observed in a unit cell having 5 ㎠ active electrode area. The cell performance increased with lower hot pressing temperature in the range of temperature having intimate contact between membrane and electrodes and with higher hot pressing pressure. Namely, the performance of proton exchange membrane fuel cell could be raised with higher water content in the membrane, with lower contact resistance between membrane and electrodes and with lower ion resistance of the electrolyte using thinner membrane.
WDNM1 is associated with differentiation and apoptosis of mammary epithelial cells.
Kho, Yoonjung,Kim, Sungchan,Yoon, Byung Sun,Moon, Jai-Hee,Kwak, Sungwook,Park, Gyuman,Woo, Junghee,Oh, Sejong,Hong, Kichang,Kim, Saehun,Kim, Hyunggee,You, Seungkwon,Choi, Yunjaie Marcel Dekker 2008 Animal biotechnology Vol.19 No.2
<P>In this study, we show that expression of the Westmead DMBA8 nonmetastatic cDNA 1 (WDNM1) gene was increased upon SFM and/or TNFalpha treatment, with a corresponding increase in apoptotic cells, and gradually decreased following re-stimulation with serum in HC11 mammary epithelial cells. TNFalpha induced WDNM1 expression showed the NFkappaB-dependent mechanism since it's expression was abrogated in IkappaBalphaM (super-repressor of NFkappaB)-transfected cells, but not those transfected with control vector. Furthermore, overexpression of WDNM1 suppressed growth and differentiation, and accelerated apoptosis of HC11 cells. Thus, our results demonstrate that WDNM1 gene expression, regulated by the TNFalpha-NFkappaB signal pathway, is associated with HC11 cell apoptosis.</P>
Kho, A Ra,Kim, Ok Joon,Jeong, Jeong Hyun,Yu, Ji Min,Kim, Hye Sun,Choi, Bo Young,Suh, Sang Won,Chung, Tae Nyoung Elsevier 2018 Brain Research Vol.1689 No.-
<P><B>Abstract</B></P> <P><B>Background</B></P> <P>Global cerebral ischemia (GCI) is a major obstacle for cardiac arrest survival. Recent studies have suggested the possibility of mesenchymal stem cell (MSC) as a novel therapeutic option for GCI, but these results were limited to the neuroprotective effects of MSCs. Therefore, we aimed to investigate specific characteristics of neurogenesis after transient GCI, and to assess the effect of MSC on these characteristics.</P> <P><B>Methods</B></P> <P>Adult male Sprague–Dawley rats were subjected to 7 min of transient GCI and randomized into 7 groups: baseline, MSC, and control administered groups, to be analyzed at 2, 3, and 4 weeks after GCI, respectively. The same interventions were repeated for sham operated animals. Rats were euthanized at the designated time after GCI.</P> <P><B>Results</B></P> <P>A comparison of GCI and sham groups without MSC treatment, showed that the counts of bromodeoxyuridine (BrdU)- and doublecortin (DCX)-positive cells were significantly increased in the GCI group at 1 week after insult, but the trend was reversed at 3 weeks after insult. The counts of BrdU-, Ki67- and DCX-positive cells and the intensity of zinc translocator 3 (ZnT3) were all significantly higher in the MSC-treated group than those in the control group at 3 weeks after GCI. The count of NeuN-positive cells in the hippocampus was significantly increased in the MSC group at 4 weeks after GCI.</P> <P><B>Conclusions</B></P> <P>GCI induces transient neurogenesis, followed by an anergic state. MSC may counteract this anergy of neurogenesis and result in an increase in intact neurons in later stages.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Neurogenesis increased after global cerebral ischemia but decreased soon. </LI> <LI> MSC administration counteracted the decrease of neurogenesis activity. </LI> <LI> Counteraction of MSC to anergy of neurogenesis resulted in more intact neurons. </LI> <LI> Effect of MSC on neurogenesis activity is consistent with ZnT3 expression. </LI> </UL> </P>
Kho, Minjung,Lee, Jung Eun,Song, Yun-Mi,Lee, Kayoung,Kim, Kyunga,Yang, Sarah,Joung, Hyojee,Sung, Joohon American Society for Clinical Nutrition 2013 The American journal of clinical nutrition Vol.98 No.6
<P><B>Background:</B> Salt is essential in our diet, but excess intake is a well-established risk factor for hypertension. The presence and importance of genetic contributions to salt intake, however, are not well understood.</P><P><B>Objective:</B> The aim of this study was to examine whether a genetic predisposition and an environmental influence exist for sodium intake and salt habit.</P><P><B>Design:</B> In a twin-family cohort, half-day urine samples from 1204 individuals (133 pairs of monozygotic twins, 29 pairs of dizygotic twins, and 880 singletons) were collected to assess 24-h sodium intakes. Daily total sodium intake, sodium density per calorie (Na-D), and salt habit questions were analyzed with adjustment for other epidemiologic characteristics. We calculated heritability (h2) and intraclass correlations to examine the genetic and shared environmental contributions to total sodium intake traits.</P><P><B>Results:</B> The average sodium intake was 208.4 ± 107.0 mmol/d. Men had a higher absolute sodium intake (242.6 ± 117.4 mmol/d), but Na-D did not differ by sex. Moderate genetic influences existed (h2 = 0.31–0.34) for sodium intake and Na-D. We also found that sharing current residence rather than being a family member explained 22% of the variance in Na-D.</P><P><B>Conclusion:</B> Our findings suggest that both genetic predisposition and shared environment contribute to sodium intakes and salt habits alike.</P>
Effects of Protocatechuic Acid (PCA) on Global Cerebral Ischemia-Induced Hippocampal Neuronal Death
Kho, A Ra,Choi, Bo Young,Lee, Song Hee,Hong, Dae Ki,Lee, Sang Hwon,Jeong, Jeong Hyun,Park, Kyoung-Ha,Song, Hong Ki,Choi, Hui Chul,Suh, Sang Won MDPI 2018 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.19 No.5
<P>Global cerebral ischemia (GCI) is one of the main causes of hippocampal neuronal death. Ischemic damage can be rescued by early blood reperfusion. However, under some circumstances reperfusion itself can trigger a cell death process that is initiated by the reintroduction of blood, followed by the production of superoxide, a blood–brain barrier (BBB) disruption and microglial activation. Protocatechuic acid (PCA) is a major metabolite of the antioxidant polyphenols, which have been discovered in green tea. PCA has been shown to have antioxidant effects on healthy cells and anti-proliferative effects on tumor cells. To test whether PCA can prevent ischemia-induced hippocampal neuronal death, rats were injected with PCA (30 mg/kg/day) per oral (p.o) for one week after global ischemia. To evaluate degenerating neurons, oxidative stress, microglial activation and BBB disruption, we performed Fluoro-Jade B (FJB), 4-hydroxynonenal (4HNE), CD11b, GFAP and IgG staining. In the present study, we found that PCA significantly decreased degenerating neuronal cell death, oxidative stress, microglial activation, astrocyte activation and BBB disruption compared with the vehicle-treated group after ischemia. In addition, an ischemia-induced reduction in glutathione (GSH) concentration in hippocampal neurons was recovered by PCA administration. Therefore, the administration of PCA may be further investigated as a promising tool for decreasing hippocampal neuronal death after global cerebral ischemia.</P>
Kho, Dohng-Hyo,Lee, Jeong-Kug The Korean Society for Microbiology and Biotechnol 1997 Journal of microbiology and biotechnology Vol.7 No.5
A transposon Tn5 mutant of Rhodobacter sphaeroides 2.4.1 was isolated for its impaired ability of growth on minimal medium containing ${\beta}$-hydroxybutyric acid as a sole carbon source. The mutant, R. sphaeroides S7 showed approximately 6-fold decrease in ${\beta}$-hydroxybutyrate dehydrogenase activity compared with that of wild type. In R. sphaeroides S7 the Tn5 was located in DNA region corresponding to a 4.2-kb EcoRI DNA fragment of R. sphaeroides 2.4.1 chromosome.