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| 1 | Microstructure and composition evolution of a single-crystal superalloy caused by elements interdiffusion with an overlay NiCrAlY coating on oxidation显示文摘MCrAlY(M=Ni and/or Co)overlay coating is widely used as a protective coating against high temperature oxidation and corrosion.However,due to its big difference in chemical composition with the underlying superalloy,elements interdiffusion occurs inevitably.One of the direct results is the formation of interdiffusion zone(IDZ)and secondary reaction zone(SRZ)with a high density of fine topological closed-packed phases(TCPs),weakening dramatically the mechanical properties of the alloy substrate.It is by now the main problem of modern high-temperature metallic coatings,but there are still hardly any reports studying the formation,growth and transformation of IDZ and SRZ in deep,as well as the precipitation of TCPs.In this work,a typical NiCrAlY coating is deposited by arc ion plating on a single-crystal superalloy N5.Elements interdiffusion between them and its relationship on microstructure were clarified.Cr rather than Al from the coating diffuses into the alloy at high temperatures and segregates immediately beneath their interface,contributing largely to the formation of IDZ.Simultaneously,diffusion of Ni from the deep alloy to IDZ leads to the formation and continuous expansion of SRZ. | Lanlan Yang Minghui Chen Jinlong Wang Yanxin Qiao Pingyi Guo Shenglong Zhu Fuhui Wang | 2020 | Journal of Materials Science & Technology2020，42，10： | 7 |
| 2 | Peripheral Lymphocyte Subsets as a Marker of Parkinson's Disease in a Chinese Population显示文摘In this study, we conducted a clinical analysis of lymphocyte subtypes in 268 patients with Parkinson's disease(PD) to assess their clinical impact as a potential marker of advanced PD in Chinese patients. The participants comprised 268 sporadic PD patients and 268 healthy controls. The numbers of natural killer(NK) cells and CD3+, CD3+CD4+, CD3+CD8+, and CD19+ lymphocytes from peripheral blood were determined by immunostaining and flow cytometric analysis and the percentages of these CD+ T cells were calculated. The ratio of regulatory T(Treg)/helper T 17(Th17) lymphocytes from 64 PD patients and 46 controls was determined by flow cytometric analysis.The results showed that the percentage of NK cells was higher in advanced PD patients than in controls(22.92% ±10.08% versus 19.76% ± 10.09%, P = 0.006), while CD3+ T cells are decreased(62.93% ± 9.27% versus65.75% ± 9.13%, P = 0.005). The percentage of CD19+B cells in male patients was lower(P = 0.021) than in female patients, whereas NK cells were increased(P \ 0.0001). The scores on the Unified Parkinson's Disease Rating Scale(UPDRS) and the Non-Motor Symptoms Scale in late-onset PD patients were significantly higher than those in earlyonset patients(P = 0.024 and P = 0.007, respectively). The percentage of CD19+ B cells in patients with UPDRS scores[24 was lower than in those with scores \24(10.17% ±4.19% versus 12.22% ± 5.39%, P = 0.009). In addition, the Treg/Th17 ratio in female patients was higher than that in female controls(13.88 ± 6.32 versus 9.94 ± 4.06, P =0.042). These results suggest that the percentages of NK cells,CD3+ T cells, and CD19+ B cells along with the Treg/Th17 ratio in peripheral blood may be used to predict the risk of PD in Chinese individuals and provide fresh avenues for novel diagnostic biomarkers and therapeutic designs. | Luan Cen Chaohao Yang Shuxuan Huang Miaomiao Zhou Xiaolu Tang Kaiping Li Wenyuan Guo Zhuohua Wu Mingshu Mo Yousheng Xiao Xiang Chen Xinling Yang Qinhui Huang Chaojun Chen Shaogang Qu Pingyi Xu | 2017 | Neuroscience Bulletin2017，33，5： | 5 |
| 3 | Chaperone-mediated Autophagy Regulates Cell Growth by Targeting SMAD3 in Glioma显示文摘Previous studies suggest that the reduction of SMAD3(mothers against decapentaplegic homolog 3)has a great impact on tumor development,but its exact pathological function remains unclear.In this study,we found that the protein level of SMAD3 was greatly reduced in human-grade IV glioblastoma tissues,in which LAMP2A(lysosome-associated membrane protein type 2A)was significantly up-regulated.LAMP2A is a key ratelimiting protein of chaperone-mediated autophagy(CMA),a lysosome pathway of protein degradation that is activated in glioma.We carefully analyzed the amino-acid sequence of SMAD3 and found that it contained a pentapeptide motif biochemically related to KFERQ,which has been proposed to be a targeting sequence for CMA.In vitro,we confirmed that SMAD3 was degraded in either serum-free or KFERQ motif deleted condition,which was regulated by LAMP2A and interacted with HSC70(heat shock cognate 71 kDa protein).Using isolated lysosomes,amino-acid residues 75 and 128 of SMAD3 were found to be of importance for this process,which affected the CMA pathway in which SMAD3 was involved.Similarly,down-regulating SMAD3 or up-regulating LAMP2A in cultured glioma cells enhanced their proliferation and invasion.Taken together,these results suggest that excessive activation of CMA regulates glioma cell growth by promoting the degradation of SMAD3.Therefore,targeting the SMAD3-LAMP2Amediated CMA-lysosome pathway may be a promising approach in anti-cancer therapy. | Hanqun Liu Yuxuan Yong Xingjian Li Panghai Ye Kai Tao Guoyou Peng Mingshu Mo Wenyuan Guo Xiang Chen Yangfu Luo Yuwan Lin Jiewen Qiu Ziling Zhang Liuyan Ding Miaomiao Zhou Xinling Yang Lin Lu Qian Yang Pingyi Xu | 2022 | Neuroscience Bulletin2022，38，6： | 0 |
| 4 | CHCHD2 maintains mitochondrial contact site and cristae organizing system stability and protects against mitochondrial dysfunction in an experimental model of Parkinson’s disease显示文摘Background:Parkinson’s disease(PD)is the second most common neurodegenerative disease after Alzheimer’s dementia.Mitochondrial dysfunction is involved in the pathology of PD.Coiled-coil-helix-coiled-coil-helix domain-containing 2(CHCHD2)was identified as associated with autosomal dominant PD.However,the mechanism of CHCHD2 in PD remains unclear.Methods:Short hairpin RNA(ShRNA)-mediated CHCHD2 knockdown or lentivirus-mediated CHCHD2 overexpression was performed to investigate the impact of CHCHD2 on mitochondrial morphology and function in neuronal tumor cell lines represented with human neuroblastoma(SHSY5Y)and HeLa cells.Blue-native polyacrylamide gel electrophoresis(PAGE)and two-dimensional sodium dodecyl sulfate-PAGE analysis were used to illustrate the role of CHCHD2 in mitochondrial contact site and cristae organizing system(MICOS).Co-immunoprecipitation and immunoblotting were used to address the interaction between CHCHD2 and Mic10.Serotype injection of adeno-associated vector-mediated CHCHD2 and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)administration were used to examine the influence of CHCHD2 in vivo.Results:We found that the overexpression of CHCHD2 can protect against methyl-4-phenylpyridinium(MPP+)-induced mitochondrial dysfunction and inhibit the loss of dopaminergic neurons in the MPTP-induced mouse model.Furthermore,we identified that CHCHD2 interacted with Mic10,and overexpression of CHCHD2 can protect against MPP+-induced MICOS impairment,while knockdown of CHCHD2 impaired the stability of MICOS.Conclusion:This study indicated that CHCHD2 could interact with Mic10 and maintain the stability of the MICOS complex,which contributes to protecting mitochondrial function in PD. | Lin Lu Hengxu Mao Miaomiao Zhou Yuwan Lin Wei Dai Jiewen Qiu Yousheng Xiao Mingshu Mo Xiaoqin Zhu Zhuohua Wu Zhong Pei Wenyuan Guo Pingyi Xu Xiang Chen | 2022 | Chinese Medical Journal2022，，13： | 0 |
| 5 | Preparation and properties of Ni-W-P-TiO_(2)nanocomposite coatings developed by a sol-enhanced electroplating method显示文摘Several Ni-W-P-TiO_(2) nanocomposite coatings were developed by the sol-enhanced electroplating method. The phase and elemental compositions of coatings were determined, and the surface and cross-section morphology were characterized. The mechanical and corrosion performance were systematically tested. The results revealed the addition of 5 ml·L^(-1) TiO_(2) sol caused a compact coating surface,while higher concentrations of TiO_(2) reduced the coating thickness and led to the inferior surface microstructure. The comparison in physiochemical properties of prepared coatings confirmed the superior performance of the Ni-W-P-TiO_(2) nanocomposite coating at 5 ml·L^(-1) TiO_(2) sol addition. Under this condition, the best mechanical properties were achieved when abrasive wear was the dominating wearresistance mechanism, and the best corrosion resistance was obtained due to its smooth and compact surface microstructure. | Zhen He Yu Zhou Yuxin Wang Pingyi Guo Wensen Jiang Caizhen Yao Xin Shu | 2022 | Chinese Journal of Chemical Engineering2022，35，4： | 0 |
| 6 | CHCHD2 Thr61Ile mutation impairs F1F0-ATPase assembly in in vitro and in vivo models of Parkinson's disease显示文摘Mitochondrial dysfunction is a significant pathological alte ration that occurs in Parkinson's disease(PD),and the Thr61lle(T61I)mutation in coiled-coil helix coiled-coil helix domain containing 2(CHCHD2),a crucial mitochondrial protein,has been reported to cause Parkinson's disease.FIFO-ATPase participates in the synthesis of cellular adenosine triphosphate(ATP)and plays a central role in mitochondrial energy metabolism.However,the specific roles of wild-type(WT)CHCHD2 and T611-mutant CHCHD2 in regulating F1FO-ATPase activity in Parkinson's disease,as well as whether CHCHD2 or CHCHD2 T61I affects mitochondrial function through regulating F1FO-ATPase activity,remain unclea r.Therefore,in this study,we expressed WT CHCHD2 and T61l-mutant CHCHD2 in an MPP^(+)-induced SH-SY5Y cell model of PD.We found that CHCHD2 protected mitochondria from developing MPP^(+)-induced dysfunction.Under normal conditions,ove rexpression of WT CHCHD2 promoted F1FO-ATPase assembly,while T61I-mutant CHCHD2 appeared to have lost the ability to regulate F1FO-ATPase assembly.In addition,mass spectrometry and immunoprecipitation showed that there was an interaction between CHCHD2 and F1FO-ATPase.Three weeks after transfection with AAV-CHCHD2 T61I,we intraperitoneally injected 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine into mice to establish an animal model of chronic Parkinson's disease and found that exogenous expression of the mutant protein worsened the behavioral deficits and dopaminergic neurodegeneration seen in this model.These findings suggest that WT CHCHD2 can alleviate mitochondrial dysfunction in PD by maintaining F1F0-ATPase structure and function. | Xiang Chen Yuwan Lin Zhiling Zhang Yuting Tang Panghai Ye Wei Dai Wenlong Zhang Hanqun Liu Guoyou Peng Shuxuan Huang Jiewen Qiu Wenyuan Guo Xiaoqin Zhu Zhuohua Wu Yaoyun Kuang Pingyi Xu Miaomiao Zhou | 2024 | Neural Regeneration Research2024，19，1： | 0 |
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