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| 1 | De novo mutation in ATP6V1B2 impairs lysosome acidification and causes dominant deafness-onychodystrophy syndrome显示文摘 | Yongyi Yuan Jianguo Zhang Qing Chang Jin Zeng Feng Xin Jianjun Wang Qingyan Zhu Jing Wu Jingqiao Lu Weiwei Guo Xukun Yan Hui Jiang Binfei Zhou Qi Li Xue Gao Huijun Yuan Shiming Yang Dongyi Han Zixu Mao Ping Chen Xi Lin Pu Dai | 2014 | Cell Research2014，24，11： | 13 |
| 2 | High-performance silicon−graphene hybrid plasmonic waveguide photodetectors beyond 1.55μm显示文摘Graphene has attracted much attention for the realization of high-speed photodetection for silicon photonics over a wide wavelength range.However,the reported fast graphene photodetectors mainly operate in the 1.55μm wavelength band.In this work,we propose and realize high-performance waveguide photodetectors based on bolometric/photoconductive effects by introducing an ultrathin wide silicon−graphene hybrid plasmonic waveguide,which enables efficient light absorption in graphene at 1.55μm and beyond.When operating at 2μm,the present photodetector has a responsivity of ~70 mA/W and a setup-limited 3 dB bandwidth of >20 GHz.When operating at 1.55μm,the present photodetector also works very well with a broad 3 dB bandwidth of >40 GHz(setup-limited)and a high responsivity of ~0.4 A/W even with a low bias voltage of−0.3 V.This work paves the way for achieving highresponsivity and high-speed silicon-graphene waveguide photodetection in the near/mid-infrared ranges,which has applications in optical communications,nonlinear photonics,and on-chip sensing. | Jingshu Guo Jiang Li Chaoyue Liu Yanlong Yin Wenhui Wang Zhenhua Ni Zhilei Fu Hui Yu Yang Xu Yaocheng Shi Yungui Ma Shiming Gao Limin Tong Daoxin Dai | 2020 | Light(Science & Applications)2020，9，1： | 10 |
| 3 | Expressions and their significance of PTTG and PC proteins in glioma显示文摘调查表情和他们转变基因(PTTG ) 和增殖的房间的垂体肿瘤的关系的目的在神经胶质瘤的原子抗原(PCNA ) 。PTTG 和 PCNA 的蛋白质表情被染色试金使用的免疫检测的方法在神经胶质瘤的 80 种情况中的 streptavidin-peroxidase (SP ) 方法。结果在等级的 PTTG 的积极的率我 IV gliomas 分别地是 56.3% , 68.2% , 80.8% ,和 100.0% ,并且 PTTG 的蛋白质表示与增加病理学的等级增加了(χ
2= 9.602, P <
0.05 ) ;PCNA 蛋白质的积极的率分别地是 37.5% , 54.5% , 69.2% ,和 93.8% ,并且 PCNA 的蛋白质表示与增加病理学的等级增加了(χ
2= 12.147, P <
0.01 ) 。PTTG 的表示与 PCNA 蛋白质的表示有积极关联(γ
= 0.557, P <
0.01 ) 。结论 PTTG 和 PCNA 蛋白质的表情与神经胶质瘤的恶意的度有关,并且可以在肿瘤发生和前进与对方一起合作并且能在神经胶质瘤被看作生物行为的指示物。 | Rufei Dai Shiming Zhang | 2009 | The Chinese-German Journal of Clinical Oncology2009，8，2： | 2 |
| 4 | Effect of hydrodynamic factors on ero-sion-corrosion destroy and structure optimization of high pres-sure air cooler tubes 显示文摘 | Zhen Dai Shen Shiming | 2006 | Journd of Pressure Equipment andSystems2006，，4： | 1 |
| 5 | Functional Mutation of SMAC / DIABLO , Encoding a Mitochondrial Proapoptotic Protein, Causes Human Progressive Hearing Loss DFNA64显示文摘 | Jing Cheng Yuhua Zhu Sudan He Yanping Lu Jing Chen Bing Han Marco Petrillo Kazimierz O. Wrzeszczynski Shiming Yang Pu Dai Suoqiang Zhai Dongyi Han Michael Q. Zhang Wei Li Xuezhong Liu Huawei Li Zheng-Yi Chen Huijun Yuan | 2011 | The American Journal of Human Genetics2011，，1： | 1 |
| 6 | The migration of the crustal deformation peak area in the eastern Himalayan Syntaxis inferred from present-day crustal deformation and morpho-tectonic markers显示文摘The present-day Global Positioning System(GPS)velocity field shows that the Indian Plate is not a complete rigid block,as its northeastern corner has been torn off and clockwise rotating relative to the main part.With the updated GPS velocity data,the Euler vector of the northeastern corner of the Indian Plate relative to the stable main plate is deduced as(89.566±0.06°E,26.131±0.05°N,1.34±0.11°/Myr).The peak area of the present-day crustal deformation is located in the Chayu deformation belt with the compressional dilation strain rate over 160 nanostrain/yr.However,the Namche-Barwa Syntaxis with the massive crustal thickening and intense surface erosion is generally considered to be the previous locus of the strongest compressional stress in the Eastern Himalayan Syntaxis over long geological timescales.Thus,there is a discrepancy between the previous and present-day crustal deformation peak areas.We argue the migration of the crustal deformation peak area with a total distance of about 120 km and ascribe it to the variation of stress conditions caused by northeast India’s clockwise rotation. | Ling Zhang Shiming Liang Xiaoping Yang Chenglong Dai | 2021 | Geodesy and Geodynamics2021，12，3： | 0 |
| 7 | Research on Mechanism of Diversified Investment and Financing in Building Ecological Cities显示文摘Ecological city is the advanced mode of harmonious development of city. Constant improvement is being made in the development of ecological city. However, building ecological city is an enormous project that calls for a huge amount of capital. The government fund is far from adequate. This paper probes into the fund issue and discusses in detail the mechanism of investment and financing in building ecological city from various aspects such as diversification of the investment subjects and the modes of financing. | Dai Shiming Lu Xiwu Qin Xing | 2008 | Chinese Journal of Population,Resources and Environment2008，6，1： | 0 |
| 8 | UTILITY OF VIBRANT SOUNDBRIDGE IN PATIENTS WITH CONGENITAL MIDDLE AND OUTER EAR DEFORMITIES | ZOU Yihui LI Jianan CHEN Aiting DAI Bu HAN Dongyi LIU Huizhan YANG Shiming | 2012 | Journal of Otology2012，7，2： | 0 |
| 9 | Cellularmetabolism: A key player in cancer ferroptosis显示文摘Cellular metabolism is the fundamental process by which cells maintain growth and self-renewal.It produces energy,furnishes raw materials,and intermedi-ates for biomolecule synthesis,and modulates enzyme activity to sustain normal cellular functions.Cellular metabolism is the foundation of cellular life processes and plays a regulatory role in various biological functions,including pro-grammed cell death.Ferroptosis is a recently discovered form of iron-dependent programmed cell death.The inhibition of ferroptosis plays a crucial role in tumorigenesis and tumor progression.However,the role of cellular metabolism,particularly glucose and amino acid metabolism,in cancer ferroptosis is not well understood.Here,we reviewed glucose,lipid,amino acid,iron and sele-nium metabolism involvement in cancer cell ferroptosis to elucidate the impact of different metabolic pathways on this process.Additionally,we provided a detailed overview of agents used to induce cancer ferroptosis.We explained that the metabolism of tumor cells plays a crucial role in maintaining intracellu-lar redox homeostasis and that disrupting the normal metabolic processes in these cells renders them more susceptible to iron-induced cell death,resulting in enhanced tumor cell killing.The combination of ferroptosis inducers and cel-lular metabolism inhibitors may be a novel approach to future cancer therapy and an important strategy to advance the development of treatments. | Xianjie Jiang Qiu Peng Mingjing Peng Linda Oyang Honghan Wang Qiang Liu Xuemeng Xu Nayiyuan Wu Shiming Tan Wenjuan Yang Yaqian Han Jinguan Lin Longzheng Xia Yanyan Tang Xia Luo Jie Dai Yujuan Zhou Qianjin Liao | 2024 | Cancer Communications2024，44，2： | 0 |
| 10 | TMEM106A transcriptionally regulated by promoter methylation is involved in invasion and metastasis of hepatocellular carcinoma显示文摘Expression of transmembrane protein 106A(TMEM106A)has been reported to be dysregulated in several types of cancers.However,the role of TMEM106A in hepatocellular carcinoma(HCC)is still unknown.In the present study,we demonstrate that TMEM106A is markedly downregulated in HCC compared with normal liver tissue.In particular,tumor-specific DNA methylation of TMEM106A is frequently observed in tumor tissues from HCC patients.Immunohistochemistry and pyrosequencing reveal a significant relationship between TMEM106A methylation and downregulation of protein expression.Receiver operating characteristic(ROC)curve analysis reveals that methylation of TMEM106A in tumor samples is different from that in non-malignant adjacent tissues of HCC patients.Moreover,HCC patients with TMEM106A hypermethylation have a poor clinical prognosis.5-Aza-2′-deoxycytidin treatment of hypermethylated TMEM106A in highly metastatic HCC cells increases the expression of TMEM106A.Functional assays reveal that overexpression of TMEM106A significantly suppresses the malignant behavior of HCC cells in vitro and decreases tumorigenicity and lung metastasis in vivo.Mechanistically,TMEM106A inhibits epithelial mesenchymal transition(EMT)of HCC cells through inactivation of the Erk1/2/Slug signaling pathway.In conclusion,our findings demonstrate that TMEM106A is an inhibitor of HCC EMT and metastasis,and TMEM106A is often transcriptionally downregulated by promoter methylation,which results in reduced levels of TMEM106A protein and predicts poor survival outcomes for HCC patients. | Shiming Shi Biao Wang Jinglei Wan Lina Song Guiqi Zhu Junxian Du Luxi Ye Qianqian Zhao Jialiang Cai Qing Chen Kun Xiao Jian He Lei Yu Zhi Dai | 2022 | Acta Biochimica et Biophysica Sinica2022，54，7： | 0 |
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