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| 1 | Ventilation Structure Optimization and Performance Analyses of Permanent Magnet Wind Generators显示文摘为了提高永磁风力发电机的通风冷却效果,以一台2.5 MW永磁风力发电机为例,基于计算流体力学(computational fluid dynamics,CFD)以及传热传质学基本理论,根据流–热协同机理,建立了包括外部通风系统的三维流体流动与传热的求解模型。应用有限体积元法,对电机通风冷却性能进行了数值研究,并与实验数据进行对比分析,实验结果验证了计算结果的准确性以及求解方法的合理性。通过改变电机内径向通风沟结构尺寸,提出4种优化方案,通过对不同结构方案条件下通风冷却性能进行对比研究,给出了发电机最佳的结构方案。所得结论可以为永磁风力发电机通风结构的设计提供参考。 | DING Shuye GUO Baocheng SUN Zhaoqiong | 2013 | 中国电机工程学报2013，33，9： | 8 |
| 2 | Diagnostic numerical simulation of large hydro generator with insulation aging显示文摘 | Li Weili Ding Shuye Zhou Feng | 2008 | Heat Transfer Engineering2008，29，10： | 1 |
| 3 | Numerical Calculation of Multicoupled Fields in Large Salient Synchronous Generator 显示文摘 | LI Weili DING Shuye JIN Huiyang | 2007 | iEEE Transactions on Magnetics2007，43，4： | 1 |
| 4 | Diagnostic numerical simulation of large hydro generator with insulation aging 显示文摘 | Weili Li Shuye Ding Feng Zhou | 2008 | Heat TransferEngineering2008，29，10： | 1 |
| 5 | Calculation and Analysis of Fluid Flow and Heat Transfer for Large Doubly-fed Wind Generator显示文摘 | DING Shuye SUN Zhaoqiong DENG Lei | 2011 | Proceedings of the 6th International Forum on Strategic Technology2011，1，： | 1 |
| 6 | Human IFN-k Inhibited Respiratory RNA Virus Replication Dependent on Cell-to-Cell Interaction in the Early Phase显示文摘Background:Interferon kappa(IFN-k)is a type I interferon(IFN-I)that inhibits virus replication by evoking interferon-stimulated genes(ISGs).However,as an evolutionarily ancient interferon,IFN-k may function differently from the later emerged interferon-a and b.Methods:Conventional molecular biology methods were used to determine the localization of IFN-k and its structure and function.In addition,we employed RT-PCR,western blot,and RNA-Seq technologies to characterize the ISGs expression profile and antiviral activities exerted by IFN-k or IFN-a2.Results:Human IFN-k exists in two forms upon ectopic expression,one located on the cell membrane and the other secreted outside the cells.The membrane-anchored IFN-k showed the ability to induce ISGs and curtail RNA virus replication,whereas the secreted IFN-k failed to do so.Structural analyses indicated that 1-27aa at the N-terminus was the signal peptide,and 28-37aa was predicted as the transmembrane region.However,our data demonstrated that both of them were not associated with membrane localization of IFN-k;the former influenced the expression and secretion of IFN-k,and the latter had an impact on the induction of ISGs.In addition,prokaryotic purified soluble mature human IFN-k was also capable of inducing ISGs and inhibiting RNA virus replication.Importantly,human IFN-k induced a faster ISG response but with a lower intensity and a shorter half-life than the response of IFN-a2.In contrast,IFN-a2 started to function later but was stronger and more durable than IFN-k.Conclusions:Human IFN-k-induced ISG response and inhibited respiratory RNA virus replication dependent on cell-to-cell interactions.In addition,compared with IFN-a2,IFN-k exerted effects more rapidly in the early phase,with less intensity and a shorter half-life.Therefore,IFN-k may constitute the first line of IFN-I against respiratory virus infections. | Weihui Fu Peng Sun Jun Fan Longfei Ding Songhua Yuan Guanxing Zhai Miaomiao Zhang Chenli Qiu Shuye Zhang Xiaoyan Zhang Jianqing Xu | 2022 | Infectious Diseases & Immunity2022，2，2： | 0 |
| 7 | UHRF1/DNMT1—MZF1 axis-modulated intragenic site-specific CpGI methylation confers divergent expression and opposing functions of PRSS3 isoforms in lung cancer显示文摘As confusion mounts over RNA isoforms involved in phenotypic plasticity,aberrant CpG methylation-mediated disruption of alternative splicing is increasingly recognized as a driver of intratumor heterogeneity(ITH).Protease serine 3(PRSS3),possessing four splice variants(PRSS3-SVs;PRSS3-V1—V4),is an indispensable trypsin that shows paradoxical effects on cancer development.Here,we found that PRSS3 transcripts and their isoforms were divergently expressed in lung cancer,exhibiting opposing functions and clinical outcomes,namely,oncogenic PRSS3-V1 and PRSS3-V2 versus tumorsuppressive PRSS3-V3,by targeting different downstream genes.We identified an intragenic CpG island(iCpGI)in PRSS3.Hypermethylation of iCpGI was mediated by UHRF1/DNMT1 complex interference with the binding of myeloid zinc finger 1(MZF1)to regulate PRSS3 transcription.The garlic-derived compound diallyl trisulfide cooperated with 5-aza-2'-deoxycytidine to exert antitumor effects in lung adenocarcinoma cells through site-specific iCpGI demethylation specifically allowing MZF1 to upregulate PRSS3-V3 expression.Epigenetic silencing of PRSS3-V3 via i CpGI methylation(iCpGIm)in BALF and tumor tissues was associated with early clinical progression in patients with lung cancer but not in those with squamous cell carcinoma or inflammatory disease.Thus,UHRF1/DNMT1—MZF1 axismodulated site-specific iCpGIm regulates divergent expression of PRSS3-SVs,conferring nongenetic functional ITH,with implications for early detection of lung cancer and targeted therapies. | Shuye Lin Hanli Xu Lin Qin Mengdi Pang Ziyu Wang Meng Gu Lishu Zhang Cong Zhao Xuefeng Hao Zhiyun Zhang Weimin Ding Jianke Ren Jiaqiang Huang | 2023 | Acta Pharmaceutica Sinica B2023，13，5： | 0 |
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