http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Songhua Wang (검색결과 4 건)
- 무료
- 기관 내 무료
- 유료
-
Study on grinding mechanism and machining technology of Si3N4 ceramic spindle
Songhua Li,Chuang Li,Minghe Liu,Yonghua Wang,Chuang Zuo,Hao Zhang,Yifeng Gao 한양대학교 청정에너지연구소 2023 Journal of Ceramic Processing Research Vol.24 No.6
In order to improve the machining accuracy of the cylindrical surface of silicon nitride ceramic spindle, the machining technologyof the cylindrical surface of ceramic spindle was studied by high-speed universal cylindrical grinder in this experiment. Firstly, the primary and secondary order of the influence of various factors on the surface roughness of ceramic spindleis determined by orthogonal experiment, then the influence law of single grinding parameter on the surface roughness ofceramic spindle is explored by single factor experiment, and the prediction model of the grinding surface roughness value ofceramic spindle is calculated by numerical analysis software, and finally the optimal processing parameters of the cylindricalsurface of ceramic spindle are obtained. The experimental results show that the grinding surface roughness of silicon nitrideceramic spindle first decreases and then increases with the increase of grinding wheel linear speed and workpiece linearspeed, and then increases with the increase of transverse feed speed and axial feed speed. The relative error between the predictedvalue of the prediction model and the actual measured value is less than 5%, which shows that the prediction modelhas a good prediction effect and provides a theoretical basis for actual machining
-
Li-Hua Yao,Jinxiu Wang,Chao Liu,Shanshan Wei,Guoyin Li,Songhua Wang,Wei Meng,Zhi-Bin Liu,Li-Ping Huang 대한약리학회 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6
Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer’s disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. β-Amyloid (Aβ) and ibotenic acid (IBO)–induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed Aβ + IBO–induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in Aβ + IBO–induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against Aβ + IBO–induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine A1 receptor–specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the Aβ + IBO–induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of A1R is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.
-
Yao, Li-Hua,Wang, Jinxiu,Liu, Chao,Wei, Shanshan,Li, Guoyin,Wang, Songhua,Meng, Wei,Liu, Zhi-Bin,Huang, Li-Ping The Korean Society of Pharmacology 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6
Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer's disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. ${\beta}$-Amyloid ($A{\beta}$) and ibotenic acid (IBO)-induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in $A{\beta}$ + IBO-induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine $A_1$ receptor-specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the $A{\beta}$ + IBO-induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of $A_1R$ is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.
-
Li-Hua Yao,Jinxiu Wang,Chao Liu,Shanshan Wei,Guoyin Li,Songhua Wang,Wei Meng,Zhi-Bin Liu,Li-Ping Huang 대한약리학회 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6
Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer’s disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. β-Amyloid (Aβ) and ibotenic acid (IBO)–induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed Aβ + IBO–induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in Aβ + IBO–induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against Aβ + IBO–induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine A1 receptor–specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the Aβ + IBO–induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of A1R is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.
연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
