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Growth hormone promotes the reconstruction of injured axons in the hypothalamo-neurohypophyseal system
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作者 Kai Li Zhanpeng Feng +11 位作者 Zhiwei Xiong Jun Pan Mingfeng Zhou Weizhao Li Yichao Ou Guangsen Wu Mengjie Che Haodong Gong Junjie Peng xingqin wang Songtao Qi Junxiang Peng 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第10期2249-2258,共10页
Previous studies have shown that growth hormone can regulate hypothalamic energy metabolism, stress, and hormone release. Therefore, growth hormone has great potential for treating hypothalamic injury. In this study, ... Previous studies have shown that growth hormone can regulate hypothalamic energy metabolism, stress, and hormone release. Therefore, growth hormone has great potential for treating hypothalamic injury. In this study, we established a specific hypothalamic axon injury model by inducing hypothalamic pituitary stalk electric lesions in male mice. We then treated mice by intraperitoneal administration of growth hormone. Our results showed that growth hormone increased the expression of insulin-like growth factor 1 and its receptors, and promoted the survival of hypothalamic neurons, axonal regeneration, and vascular reconstruction from the median eminence through the posterior pituitary. Altogether, this alleviated hypothalamic injury-caused central diabetes insipidus and anxiety. These results suggest that growth hormone can promote axonal reconstruction after hypothalamic injury by regulating the growth hormone-insulin-like growth factor 1 axis. 展开更多
关键词 arginine vasopressin growth hormone hypothalamo-neurohypophyseal system HYPOTHALAMUS injury insulin-like growth factor 1 OXYTOCIN regeneration
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Insight into the Electrochemical Behaviors of NCM811|SiO-Gr Pouch Battery through Thickness Variation
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作者 xingqin wang Youzhi Song +5 位作者 Hao Cui Jianhong Liu Hua Huo Li wang Yunzhi Gao Xiangming He 《Energy & Environmental Materials》 SCIE EI CAS CSCD 2023年第5期211-218,共8页
LiNi0.8Co0.1Mn0.1O2(NCM811)|SiOx-graphite(SiO-Gr.)battery chemistry is of intensive attention because its achievable practical energy density is approaching impressively 300 Wh Kg^(-1).However,it still suffers rapid c... LiNi0.8Co0.1Mn0.1O2(NCM811)|SiOx-graphite(SiO-Gr.)battery chemistry is of intensive attention because its achievable practical energy density is approaching impressively 300 Wh Kg^(-1).However,it still suffers rapid capacity fades during repeated cycles,both chemical,electrochemical and mechanical irreversibility contribute.A comprehensive understanding behind the fading behavior of the cell chemistry is required before fully realize the benefits of this chemistry.Herein,the in-situ thickness variation is introduced as a diagnostic technique and is performed on 5-55 Ah NCM811|SiO-Gr cells.With the help of Li reference electrode and in-situ X-ray diffraction device,the correspondence between thickness variation and the electrode potential is carefully investigated.Firstly,the NCM811|SiO-Gr cell is characterized with the maximum cell thickness at around 80%state-of-charge(SOC)in the discharge process,rather than at 100%SOC.Secondly,the electrochemical behaviors during rate charge/discharge are diagnosed,and a Li platting signal is resolved from thickness variation profile at 2C.This work confirms that the thickness monitoring is a nondestructive and informative complement to conventional diagnostic techniques for failure analysis of pouch cells. 展开更多
关键词 diagnostic technique electrochemical behavior NCM811 cathode Si-containing anode thickness variation
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Chaperone-mediated autophagy and neurodegeneration:connections,mechanisms,and therapeutic implications 被引量:4
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作者 Xiaolei Liu Sihua Huang +3 位作者 xingqin wang Beisha Tang Wenming Li Zixu Mao 《Neuroscience Bulletin》 SCIE CAS CSCD 2015年第4期407-415,共9页
Lysosomes degrade dysfunctional intracellular components via three pathways: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). Unlike the other two, CMA degrades cytosolic proteins with a reco... Lysosomes degrade dysfunctional intracellular components via three pathways: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). Unlike the other two, CMA degrades cytosolic proteins with a recognized KFERQ-like motif in lysosomes and is important for cellular homeostasis. CMA activity declines with age and is altered in neurodegenerative diseases. Its impairment leads to the accumulation of aggregated proteins, some of which may be directly tied to the pathogenic processes of neurodegenerative diseases. Its induction may accelerate the clearance of pathogenic proteins and promote cell survival, representing a potential therapeutic approach for the treatment of neurodegenerative diseases. In this review, we summarize the current findings on how CMA is involved in neurodegenerative diseases, especially in Parkinson's disease. 展开更多
关键词 AUTOPHAGY chaperone-mediated autophagy neurodegenerative disorder Parkinson's disease risk factors mutant proteins therapeutic target
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