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10篇 您的检索式:作者名="LIN Jinye"
    题名 作者 年代 出处 被引量
1Hybrid quantum private communication with continuous-variable and discrete-variable signals显示文摘The quantum key distribution(QKD) has been entering the practical application era. Subsequently, hybrid quantum private communication with discrete-variable signals, continuous-variable signals, and classic optical signals becomes inevitable in the practical scenario. In this paper, we experimentally investigated the mutual effects between the discrete-variable QKD(DVQKD) and the continuous-variable QKD(CVQKD) via a fiber channel. The experimental results show that the DVQKD will be influenced by the continuous-variable quantum signals and classic optical signals, while the CVQKD is not sensitive to the discrete-variable quantum signals.LIU WeiQi PENG JinYe WANG Chao CAO ZhengWen HUANG Duan LIN DaKai HUANG Peng ZENG GuiHua 2015Science China(Physics,Mechanics & Astronomy)2015,58,2:4
2A PID type fuzzy controller with self-tuning scaling factors 显示文摘WOO Zhiwei CHUNG Hungyuan LIN Jinye 2000Fuzzy Sets and Systems2000,115,3:1
3Decellularized Disc Hydrogels for hBMSCs tissue-specific differentiation and tissue regeneration显示文摘Tissue specificity,a key factor in the decellularized tissue matrix(DTM),has shown bioactive functionalities in tuning cell fate-e.g.,the differentiation of mesenchymal stem cells.Notably,cell fate is also determined by the living microenvironment,including material composition and spatial characteristics.Herein,two neighboring tissues within intervertebral discs,the nucleus pulposus(NP)and annulus fibrosus(AF),were carefully processed into DTM hydrogels(abbreviated DNP-G and DAF-G,respectively)to determine the tissue-specific effects on stem cell fate,such as specific components and different culturing methods,as well as in vivo regeneration.Distinct differences in their protein compositions were identified by proteomic analysis.Interestingly,the fate of human bone marrow mesenchymal stem cells(hBMSCs)also responds to both culturing methods and composition.Generally,hBMSCs cultured with DNP-G(3D)differentiated into NP-like cells,while hBMSCs cultured with DAF-G(2D)underwent AF-like differentiation,indicating a close correlation with the native microenvironments of NP and AF cells,respectively.Furthermore,we found that the integrin-mediated RhoA/LATS/YAP1 signaling pathway was activated in DAF-G(2D)-induced AF-specific differentiation.Additionally,the activation of YAP1 determined the tendency of NP-or AF-specific differentiation and played opposite regulatory effects.Finally,DNP-G and DAF-G specifically promoted tissue regeneration in NP degeneration and AF defect rat models,respectively.In conclusion,DNP-G and DAF-G can specifically determine the fate of stem cells through the integrin-mediated RhoA/LATS/YAP1 signaling pathway,and this tissue specificity is both compositional and spatial,supporting the utilization of tissue-specific DTM in advanced treatments of intervertebral disc degeneration.Yizhong Peng Xiangcheng Qing Hui Lin Donghua Huang Jinye Li Shuo Tian Sheng Liu Xiao Lv Kaige Ma Rui Li Zilong Rao Ying Bai Songfeng Chen Ming Lei Daping Quan Zengwu Shao 2021Bioactive Materials2021,6,10:1
4Overexpression of Akt/Akt can modulate chemotherapy-induee apoptosis显示文摘Page C Lin HJ Jiny 2000Anticancer Res2000,20,1:1
5Tumour suppressor SIRT3 deacetylates and activates Manganese superoxide dismutase to scavenge ROS显示文摘CHEN YAOHUI ZHANG JINYE LIN YAN 2011EMBO Reports2011,12,6:1
6Endogenous repair theory enriches construction strategies for orthopaedic biomaterials:a narrative review显示文摘The development of tissue engineering has led to new strategies for mitigating clinical problems;however,the design of the tissue engineering materials remains a challenge.The limited sources and inadequate function,potential risk of microbial or pathogen contamination,and high cost of cell expansion impair the efficacy and limit the application of exogenous cells in tissue engineering.However,endogenous cells in native tissues have been reported to be capable of spontaneous repair of the damaged tissue.These cells exhibit remarkable plasticity,and thus can differentiate or be reprogrammed to alter their phenotype and function after stimulation.After a comprehensive review,we found that the plasticity of these cells plays a major role in establishing the cell source in the mechanism involved in tissue regeneration.Tissue engineering materials that focus on assisting and promoting the natural self-repair function of endogenous cells may break through the limitations of exogenous seed cells and further expand the applications of tissue engineering materials in tissue repair.This review discusses the effects of endogenous cells,especially stem cells,on injured tissue repairing,and highlights the potential utilisation of endogenous repair in orthopaedic biomaterial constructions for bone,cartilage,and intervertebral disc regeneration.Yizhong Peng Jinye Li Hui Lin Shuo Tian Sheng Liu Feifei Pu Lei Zhao Kaige Ma Xiangcheng Qing Zengwu Shao 2021Biomaterials Translational2021,2,4:1
7Low glucose metabolite 3-phosphoglycerate switches PHGDH from serine synthesis to p53 activation to control cell fate显示文摘Glycolytic intermediary metabolites such as fructose-1,6-bisphosphate can serve as signals,controlling metabolic states beyond energy metabolism.However,whether glycolytic metabolites also play a role in controlling cell fate remains unexplored.Here,we find that low levels of glycolytic metabolite 3-phosphoglycerate(3-PGA)can switch phosphoglycerate dehydrogenase(PHGDH)from cataplerosis serine synthesis to pro-apoptotic activation of p53.PHGDH is a p53-binding protein,and when unoccupied by 3-PGA interacts with the scaffold protein AXIN in complex with the kinase HIPK2,both of which are also p53-binding proteins.This leads to the formation of a multivalent p53-binding complex that allows HIPK2 to specifically phosphorylate p53-Ser46 and thereby promote apoptosis.Furthermore,we show that PHGDH mutants(R135W and V261M)that are constitutively bound to 3-PGA abolish p53 activation even under low glucose conditions,while the mutants(T57A and T78A)unable to bind 3-PGA cause constitutive p53 activation and apoptosis in hepatocellular carcinoma(HCC)cells,even in the presence of high glucose.In vivo,PHGDH-T57A induces apoptosis and inhibits the growth of diethylnitrosamine-induced mouse HCC,whereas PHGDH-R135W prevents apoptosis and promotes HCC growth,and knockout of Trp53 abolishes these effects above.Importantly,caloric restriction that lowers whole-body glucose levels can impede HCC growth dependent on PHGDH.Together,these results unveil a mechanism by which glucose availability autonomously controls p53 activity,providing a new paradigm of cell fate control by metabolic substrate availability.Yu-Qing Wu Chen-Song Zhang Jinye Xiong Dong-Qi Cai Chen-Zhe Wang Yu Wang Yan-Hui Liu Yu Wang Yiming Li Jian Wu Jianfeng Wu Bin Lan Xuefeng Wang Siwei Chen Xianglei Cao Xiaoyan Wei Hui-Hui Hu Huiling Guo Yaxin Yu Abdul Ghafoor Changchuan Xie Yaying Wu Zheni Xu Cixiong Zhang Mingxia Zhu Xi Huang Xiufeng Sun Shu-Yong Lin Hai-Long Piao Jianyin Zhou Sheng-Cai Lin 2023Cell Research2023,33,11:0
8Anti-fatigue Effect of Water Extract from Centella asiatica(L.)Urban on Mice显示文摘[Objectives]To study the anti-fatigue effect of water extract from Centella asiatica(L.)Urban on mice.[Methods]After intragastric administration of low,medium and high concentration of water extract from Centella asiatica(L.)Urban for 14 d,the rotarod time and the content of serum lactic acid in mice were determined,respectively.[Results]Compared with the control group,the rotarod time of mice in the low and medium concentration groups was significantly prolonged(P<0.05),but there was no significant difference between the control group and the high concentration group;the content of serum lactic acid in the medium concentration group was significantly lower than that in the control group(P<0.01),but there was no significant difference between low concentration group and high concentration group and the control group.[Conclusions]A certain concentration of water extract from Centella asiatica(L.)Urban had a good anti-fatigue effect.Chunmei MO Jinye LIN Yanfang MA Jiajie ZHOU Ling LIANG Nian LIN Suoyi HUANG Gang XIAO 2023Medicinal Plant2023,14,1:0
9Corrigendum to‘Decellularized disc hydrogels for hBMSC tissue-specific differentiation and tissue regeneration’[Bioactive Materials 6(2021)3541-3556]显示文摘The authors regret missing out the below change in the acknowledgment section of the article.The original sentence reads as'This work was supported by the Major Research Plan of National Natural Science Foundation of China[No.91649204],the National Key Research and Development Program of China[2016YFC1100100],…'and the same has been corrected to'This work was supported by the National Key Research and Development Program of China[2016YFC1100100],the Major Research Plan of National Natural Science Foundation of China[No.91649204],…'and the same has been corrected to'This work was supported by the National Key Research and Development Program of China[2016YFC1100100],the Major Research Plan of National Natural Science Foundation of China[No.91649204],…'.Yizhong Peng Xiangcheng Qing Hui Lin Donghua Huang Jinye Li Shuo Tian Sheng Liu Xiao Lv Kaige Ma Rui Li Zilong Rao Ying Bai Songfeng Chen Ming Lei Daping Quan Zengwu Shao 2022Bioactive Materials2022,7,2:0
10Hierarchical inhibition of mTORC1 by glucose starvation-triggered AXIN lysosomal translocation and by AMPK显示文摘When glucose is replete,mammalian/mechanistic target of rapamycin complex 1(mTORC1)is active and anchored to the lysosomal surface via the two GTPases,Ras-related GTPase(RAG)and Ras homolog enriched in brain(Rheb),which are regulated by Ragulator and tuberous sclerosis complex 2(TSC2),respectively.When glucose is low,aldolase senses low fructose-1,6-bisphosphate level and promotes the translocation of AXIN−liver kinase B1(LKB1)to the lysosomal surface,which leads to the activation of AMP-activated protein kinase(AMPK)and the inhibition of RAGs,sundering mTORC1 from the lysosome and causing its inactivation.AMPK can also inactivate mTORC1 by phosphorylating Raptor and TSC2.However,the hierarchy of AXIN-and AMPK-mediated inhibition of mTORC1 remains poorly defined.Here,we show that AXIN translocation does not require AMPK expression or activity.In glucose starvation conditions,knockout of AXIN extended the half-life of mTORC1 inhibition from 15 to 60 min,whereas knockout of AMPK only extended it to 30 min.RAGBGTP(constitutively active RAGB)almost entirely blocked the lysosomal dissociation and inhibition of mTORC1 under glucose starvation,but it did not inhibit AMPK,indicating that under these conditions,it is AXIN lysosomal translocation that inhibits mTORC1,and it does so via inhibition of RAGs.5-aminoimidazole-4-carboxamide ribonucleoside(AICAR),a mimetic of AMP,which activates both cytosolic AMPK and lysosomal AMPK,fully inhibited mTORC1 even when it is stably anchored to the lysosome by RAGBGTP,whereas glucose starvation mildly inhibited such anchored mTORC1.Together,we demonstrate that the lysosomal translocation of AXIN plays a primary role in glucose starvation-triggered inhibition of mTORC1 by inhibiting RAGs,and that AMPK activity inhibits mTORC1 through phosphorylating Raptor and TSC2,especially under severe stress.Mengqi Li Xiaoyan Wei Jinye Xiong Jin-Wei Feng Chen-Song Zhang Sheng-Cai Lin 2023Life Metabolism2023,2,3:0
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