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Cui Xun,Gao Likun,Lu Cheng-Hsin,Ma Rui,Yang Yingkui,Lin Zhiqun 나노기술연구협의회 2022 Nano Convergence Vol.9 No.34
Single-metal-atom catalysts (SMACs) have garnered extensive attention for various electrocatalytic applications, owing to their maximum atom-utilization efficiency, tunable electronic structure, and remarkable catalytic performance. In particular, carbon-based SMACs exhibit optimal electrocatalytic activity for the oxygen reduction reaction (ORR) which is of paramount importance for several sustainable energy conversion and generation technologies, such as fuel cells and metal-air batteries. Despite continuous endeavors in developing various advanced carbon-based SMACs for electrocatalytic ORR, the rational regulation of coordination structure and thus the electronic structure of carbon-based SMACs remains challenging. In this review, we critically examine the role of coordination structure, including local coordination structure (i.e., metal atomic centers and the first coordination shell) and extended local coordination structure (i.e., the second and higher coordination shells), on the rational design of carbon-based SMACs for high-efficiency electrocatalytic ORR. Insights into the relevance between coordination structures and their intrinsic ORR activities are emphatically exemplified and discussed. Finally, we also propose the major challenges and future perspectives in the rational design of advanced carbon-based SMACs for electrocatalytic ORR. This review aims to emphasize the significance of coordination structure and deepen the insightful understanding of structure-performance relationships.
폐열(肺熱)을 치료(治療)하는 약물의 기미론(氣味論)적 약리분석(藥理分析)에 대한 고찰(考察)
최훈 ( Xun Cui ),이청학 ( Cheong Hak Lee ) 한약응용학회 2010 한약응용학회지 Vol.10 No.2
In Traditional Oriental Medicine, the drug treatment has been explained by the thoery of "Qiweilun(氣味論)". So we studied on the drug treatment of drugs to treat FeiRe(肺熱) by "Qiweilun(氣味論)" When FeiRe(肺熱) was caused by "Wai Gan Feng Re(外感風熱)", we make a conclusion that use Mori Folium, Lonicerae Flos, Gypsum Fibrosum. And when FeiRe(肺熱) was caused by "Shi Re(實熱)", we make a conclusion that use Gardeniae Fructus, Scutellariae Radix, Fritillariae Bulbus, Anemarrhenae Rhizoma, Asparagi Radix. When FeiRe(肺熱) was caused by "Fei Zhong Fu Huo(肺中伏火)", we make a conclusion that use Adenophorae Radix, Trichosanthis Semen, Lilii Herba. When FeiRe(肺熱) was caused by "Xu Re(虛熱)", we make a conclusion that use Ophiopogonis Radix, Trichosanthis Radix.
崔勳,柳熙台 대한동의생리학회,대한동의병리학회 2002 동의생리병리학회지 Vol.16 No.3
Senile involution is divided into two classes : physiological senile involution and pathological senile involution. Physiological senile involution is a natural process of vital action of decreasing Vital Essence and Energy in kidney that is a necessary physiological phenomenon. Pathological senile involution is an evidence of impairment of True Qi of internal human body. Human vital action is a changing process of life, senility, sickness, and death. In other words, this is a natural process of being full and decreasing of Vital Essence and Energy in kidney, and True Qi of human body decides this process. The Vital Essence and Energy in kidney vary, and they are influenced and restricted by various elements. The time of a senile involution varies individually. Human body protects and makes efforts not to leak out True Qi in effective ways. We can postpone a limit of time of physiological senile involution phenomenon. This is called "Health Preservation" - resistance against senile involution.
심방 이뇨 호르몬 유리에 미치는 cytochalasin B의 영향
최훈,안해선,조경우 의과학연구소 2000 全北醫大論文集 Vol.24 No.1
It has recently been proposed that the secretion of atrial natriuretic peptide(ANP) is regualted by a "two-step sequential mechanism". In order to demonstrate the role of actin microfilaments in the regulation of ANP secretion, an attempt was made to investigate the effects of cytochalasin B on the stretch-activated ANP secretion from perfused rabbit atria. Atrial stretch-and-release stimulated ANP secretion with concomitant extracellular fluid (ECF) translocation, and elevated the concentration of ANP in the interstitium. Cytochalasin B suppressed the stretch-activated ANP secretion and elevation of the ANP concentration without change in the ECF translocation. These data suggest that cytochalasin B ingibits ANP release from the atrital myocytes and that the actin microfilaments may be involved in the mechanomolecular signal transduction of the stretch-activated ANP secretion. (Key words : atrial natriuretic peptide, ANP, atria, secretion, release)
Zhao Xun,Cui De-Jun,Yang Liu-chan,Yuan Wen-Qiang,Yan Fang 한국조직공학과 재생의학회 2022 조직공학과 재생의학 Vol.19 No.5
BACKGROUND: This study commenced to uncover the role of long non-coding RNA FBXL19 antisense RNA 1 (FBXL19-AS1) in the development of ulcerative colitis (UC) and its possible mechanism. METHODS: FBXL19-AS1 expression in the colonic sigmoid mucosa of UC patients was detected. A colitis model was induced in mice using 5% dextran sodium sulfate. Hematoxylin–eosin staining was performed for histopathological examination. Apoptosis was detected by Tunel staining and tissue fibrosis was detected by immunohistochemistry. Also, intestinal permeability was examined. The concentrations of inflammatory factors IL-1b and IL-18 were detected by enzyme-linked immunosorbent assay. The relationship between FBXL19-AS1, miR-339-3p and RHOB was verified by RNA immunoprecipitation assay and dual luciferase reporter assay. RESULTS: The expression of FBXL19-AS1 was increased in dextran sodium sulfate (DSS)-induced colitis mouse model. FBXL19-AS1 interference or miR-339-3p overexpression inhibited DSS-induced colonic epithelial cell apoptosis and inflammatory response, and improved intestinal epithelial barrier defects, thereby ameliorating DSS-induced colitis injury in mice. FBXL19-AS1 sponged miR-339-3p while miR-339-3p targeted RHOB. Overexpression of RHOB reversed the protective effect of inhibition of FBXL19-AS1 on DSS-induced colitis in mice. CONCLUSION: FBXL19-AS1 reduces miR-339-3p-mediated targeting of RHOB and aggravates intestinal epithelial barrier defect in DSS-induced colitis in mice.