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| 1 | The role of autophagy in cardiac hypertrophy显示文摘Autophagy 从更低的优核质在自然被保存到哺乳动物并且是一重要自我吃, degradative processthat 贡献过剩材料的消除。心脏的肥大被过量 proteinsynthesis,增加的 cardiomyocyte 尺寸,和变厚的室的墙首先描绘并且是支持 arrhythmiaand 心失败的一个主要风险因素。在最近的年里, cardiomyocyte autophagy 被认为在控制 hypertrophicresponse 起一个作用。然而,在心脏的肥大的 cardiomyocyte autophagy 的有益或加重的角色仍然是在心脏的肥大的 cardiomyocyte autophagy 的准确机制进一步要求的 controversial.The 学习。在这评论,我们在心脏的肥大与 autophagy 联系的 summarizethe 争吵并且在心脏的肥大的 thedevelopment 提供卓见进 autophagy 的角色。我们断定未来研究应该强调在 autophagy andthe 之间的关系心脏的肥大的不同阶段,以及 autophagic 流动和选择 autophagy。Autophagy 将是为心脏的肥大的一个 potentialtherapeutic 目标。 | Lanfang Li Jin Xu Lu He Lijun Peng Qiaoqing Zhong Linxi Chen Zhisheng Jiang | 2016 | Acta Biochimica et Biophysica Sinica2016，48，6： | 30 |
| 2 | Energy-Optimal and Delay-Bounded Computation Offloading in Mobile Edge Computing with Heterogeneous Clouds显示文摘By Mobile Edge Computing(MEC), computation-intensive tasks are offloaded from mobile devices to cloud servers, and thus the energy consumption of mobile devices can be notably reduced. In this paper, we study task offloading in multi-user MEC systems with heterogeneous clouds, including edge clouds and remote clouds. Tasks are forwarded from mobile devices to edge clouds via wireless channels, and they can be further forwarded to remote clouds via the Internet. Our objective is to minimize the total energy consumption of multiple mobile devices, subject to bounded-delay requirements of tasks. Based on dynamic programming, we propose an algorithm that minimizes the energy consumption, by jointly allocating bandwidth and computational resources to mobile devices. The algorithm is of pseudo-polynomial complexity. To further reduce the complexity, we propose an approximation algorithm with energy discretization, and its total energy consumption is proved to be within a bounded gap from the optimum. Simulation results show that, nearly 82.7% energy of mobile devices can be saved by task offloading compared with mobile device execution. | Tianchu Zhao Sheng Zhou Linqi Song Zhiyuan Jiang Xueying Guo Zhisheng Niu | 2020 | China Communications2020，17，5： | 18 |
| 3 | Oxidized low-density lipoprotein activates adipophilin through ERK1/2 signal pathway in RAW264.7 cells显示文摘它被报导了那氧化低密度的脂蛋白(Ox-LDL ) 能增加 adipophilin 的表示。然而,详细机制充分没被理解。这研究的目的是在 adipophilin 表示和细胞内部的类脂化合物微滴累积上调查 Ox-LDL 的机制。一个鼠标像巨噬细胞的房间线, RAW264.7,全部被使用,并且 Ox-LDL 以一种剂量依赖者方式导致了 adipophilin 表示,这被发现。而且, Ox-LDL 导致了 peroxisome 激活 proliferator 的受体 --(PPAR ) 表示和 PPAR 特定的禁止者 T0070907 没废除 Ox-LDL-induced adipophilin 表示,而是特定的收缩筋 GW1929。而且, Ox-LDL 导致了 ERK1/2 的 phosphorylation,并且由 PD98059 的 ERK1/2-specific 抑制压制了 Ox-LDL-induced PPAR 和 adipophilin 表示。结果显示出那 ERK1/2 或 PPAR 特定的抑制减少了细胞内部的类脂化合物微滴的数量。同时, PPAR 特定的收缩筋增加了细胞内部的类脂化合物微滴。这些结果建议 Ox-LDL-induced 经由 ERK1/2 激活在 adipophilin 水平增加是在 RAW264.7 房间导致细胞内部的类脂化合物微滴的更大的数量的机制之一,它显示 adipophilin 涉及动脉粥样硬化患者前进。 | Qingnan Liu Zhibing Dai Zhiqiang Liu Xiaohui Liu Chaoke Tang Zuo Wang Guanghui Yi Lushan Liu Zhisheng Jiang Yongzong Yang Zhonghua Yuan | 2010 | Acta Biochimica et Biophysica Sinica2010，42，9： | 13 |
| 4 | Hypoxia promotes bone marrow-derived mesenchymal stem cell proliferation through apelin/APJ/autophagy pathway显示文摘骨头导出髓的间充质的干细胞(BMSC ) 是有增长和区别的能力进间充质的系房间的 multipotent 祖先的一张人口。规章的肽 apelin 是为 G 联合蛋白质的受体 APJ 的内长的 ligand。Apelin,能提高 BMSC 增长,在许多房间类型上有 mitogenic 效果。我们假设了增加的 apelin/APJ 可能涉及导致组织缺氧的 BMSC 增长的出现和发展。从到 10-week-old C57BL/6J 老鼠的 8- 的骨头髓的 BMSC 在 normoxia (21% 氧) 或组织缺氧(1% 氧) 下面是有教养的状况。房间增长被 3-(4,5-dimethylthiazol-2-yl ) 决定 -2,5-diphenyltetrazolium 溴化物试金和 5-bromo-2-deoxyuridine 试金。组织缺氧可诱导的因素(HIF ) 的表情 -1, apelin, APJ, Beclin-1,和 LC3II/LC3I 被西方的污点分析检测。结果建议组织缺氧以一种时间依赖者方式提高了 BMSC 的增长。HIF-1, apelin, APJ, Beclin-1,和 LC3II/LC3I 的表情在组织缺氧导致的 BMSC 被增加。禁止了 apelin, APJ, Beclin-1,和 LC3II/LC3I 的导致组织缺氧的表情的小介入 RNA (siRNA )-HIF-1 阻止了导致组织缺氧的 BMSC 增长。禁止了 Beclin-1 和 LC3II/LC3I 的导致组织缺氧的表情的 siRNA-APJ 颠倒了导致组织缺氧的 BMSC 增长。siRNA-Beclin-1 也废除了导致组织缺氧的房间增长。这些数据建议表明小径的 apelin/APJ/autophagy 可能涉及导致组织缺氧的 BMSC 增长。 | Lanfang Li Lifang Li Zidong Zhang Zhisheng Jiang | 2015 | Acta Biochimica et Biophysica Sinica2015，47，5： | 10 |
| 5 | OxLDL up-regulates Niemann-Pick type C1 expression through ERK1/2/COX-2/ PPARα-signaling pathway in macrophages显示文摘NiemannPick 类型 C1 (NPC1 ) 主要位于迟了的 endosome/lysosome 的膜并且从迟了的 endosome/lysosome 控制细胞内部的胆固醇 trafficking 到血浆膜。它被报导了那氧化低密度的脂蛋白(oxLDL ) 罐头起来调整 NPC1 表情。然而,详细机制充分没被理解。在这研究,我们在 THP-1 巨噬细胞在 NPC1 表示上调查了 oxLDL 刺激的效果。我们的结果显示出在 mRNA 和蛋白质的起来调整的 NPC1 表示在一个剂量依赖者和时间依赖者举止铺平的那 oxLDL。另外, oxLDL 也导致了细胞外的调整信号的 kinase 1/2 (ERK1/2 ) 的 phosphorylation。有 oxLDL 的处理显著地在巨噬细胞增加了 cyclooxygenase-2 (COX-2 ) mRNA 和蛋白质表示,并且这些增加被 ERK1/2 禁止者 PD98059 或 ERK1/2 压制小介入 RNA (siRNA ) 处理。OxLDL 起来调整在 mRNA 和蛋白质的激活 proliferator 的受体(PPAR ) 铺平的 peroxisome 的表示,它能被 COX-2 siRNA 或 COX-2 禁止者 NS398 处理在这些巨噬细胞废除。OxLDL 戏剧性地提高了细胞的胆固醇流出,它被禁止 ERK1/2 或 COX-2 废除。另外,导致 oxLDL 的 NPC1 表示和细胞的胆固醇流出被 PPAR siRNA 或 GW6471 颠倒, PPAR 的一个对手。一起拿,这些结果提供证据那 oxLDL 罐头起来调整通过在巨噬细胞的 ERK1/2/COX-2/PPAR-signaling 小径的 NPC1 的表示。 | Xiaohua Yu Xiaoxu Li Guojun Zhao Ji Xiao Zhongcheng Mo Kai Yin Zhisheng Jiang Yuchang Fu Xiaohui Zha Chaoke Tang | 2012 | Acta Biochimica et Biophysica Sinica2012，44，2： | 6 |
| 6 | Pannexin-1 channels and their emerging functions in cardiovascular diseases显示文摘Pannexin-1, Pannexin-2,和 Pannexin-3 是形成隧道的 glycoprotein 的 Pannexin 家庭的三个成员。他们的主要功能是由他们形成单个膜的隧道的能力的 dened。Pannexin-1 无所不在地在整个身体在许多房间和机关存在并且在循环系统是特殊分布式的,当 Pannexin-2 和 Pannexin-3 的表情主要被限制为机关和纸巾时。Pannexin-1 oligomers 被显示了是连接细胞内部、细胞外的分隔空间的功能的单个膜隧道并且不是在同位格的膜的细胞间的隧道。Pannexin-1 的生理的函数是连接到充当一个 paracrine 信号的腺苷 triphosphate 流出,并且在许多房间类型调整细胞的 inflammasomes 在下面生理并且 pathophysiological 条件。然而,仍然有要探索的许多功能。这评论总结最近的报告并且在心血管的疾病讨论 Pannexin-1 的角色,包括局部缺血,心律不齐,心脏的纤维变性,和高血压。Pannexin-1 在心血管的疾病作为一个令人激动的、临床上相关的目标被建议了。 | Lanfang Li Lu He Di Wu Linxi Chen Zhisheng Jiang | 2015 | Acta Biochimica et Biophysica Sinica2015，47，6： | 4 |
| 7 | Influence ofthe reaction conditions on the solid-state graft copolymeri-zation of methyl methacrylate and polyethylene/polypro-pylene in situ alloys显示文摘 | Fu Zhisheng Xu Junting Jiang Guoxin | 2005 | Journal of Applied Polymer Sci-ence2005，98，1： | 1 |
| 8 | TRIM65 E3 ligase targets VCAM-1 degradation to limit LPS-induced lung inflammation显示文摘Although the adhesion molecules-mediated leukocyte adherence and infiltration into tissues is an important step of inflammation,the post-translational regulation of these proteins on the endothelial cells is poorly understood.Here,we report that TRIM65,an ubiquitin E3 iigase of tripartite protein family,selectively targets vascular cell adhesion molecule 1(VCAM-1)and promotes its ubiq-uitination and degradation,by which it critically controls the duration and magnitude of sepsis-induced pulmonary inflammation.TRIM65 is constitutively expressed in human vascular endothelial cells.During TNFa-induced endothelial activation,the protein levels ofTRIM65 and VCAM-1 are inversely correlated.Expression of wild-type TRIM65,but not expression of aTRIM65 mutant that lacks E3 ubiquitin ligase function in endothelial cells,promotes VCAM-1 ubiquitination and degradation,whereas small interference RNA-mediated knockdown of TRIM65 attenuates VCAM-1 protein degradation.Further experiments show that TRIM65 directly interacts with VCAM-1 protein and directs its polyubiquitination,by which TRIM65 controls monocyte adherence and infiltration into tissues during inflammation.Importantly,TRIM65-deficient mice are more sensitive to lipopolysaccharide-induced death,due to sustained and severe pulmonary inflammation.Taken together,our studies suggest that TRIM65-mediated degradation of VCAM-1 represents a potential mechanism that controls the duration and magnitude of infiammation. | Yong Li Xuan Huang Fang Guo Tianhua Lei Shitao Li Paula Monaghan-Nichols Zhisheng jiang Hong-Bo Xin Mingui Fu | 2020 | Journal of Molecular Cell Biology2020，12，3： | 1 |
| 9 | A joint call for actions to advance taxonomy in China显示文摘Taxonomy plays an important role in understanding the origin, evolution, and ecological functionality of biodiversity. There are large number of unknown species yet to be described by taxonomists, which together with their ecosystem services cannot be effectively protected prior to description. Despite this, taxonomy has been increasingly underrated insufficient funds and permanent positions to retain young talents. Further, the impact factordriven evaluation systems in China exacerbate this downward trend, so alternative evaluation metrics are urgently necessary. When the current generation of outstanding taxonomists retires,there will be too few remaining taxonomists left to train the next generation. In light of these challenges, all co-authors worked together on this paper to analyze the current situation of taxonomy and put out a joint call for immediate actions to advance taxonomy in China. | Chaodong Zhu Arong Luo Ming Bai Michael COrr Zhonge Hou Siqin Ge Jun Chen Yibo Hu Xuming Zhou Gexia Qiao Hongzhi Kong Limin Lu Xiaohua Jin Lei Cai Xinli Wei Ruilin Zhao Wei Miao Qingfeng Wang Zhongli Sha Qiang Lin Meng Qu Jianping Jiang Jiatang Li Jing Che Xuelong Jiang Xiaoyong Chen Lianming Gao Zongxin Ren Chunlei Xiang Shixiao Luo Donghui Wu Dong Liu Yanqiong Peng Tao Su Chenyang Cai Tianqi Zhu Wanzhi Cai Xingyue Liu Hu Li Huaijun Xue Zhen Ye Xuexin Chen Pu Tang Shujun Wei Hong Pang Qiang Xie Feng Zhang Feng Zhang Xianjin Peng Aibing Zhang Taiping Gao Changfa Zhou Chen Shao Libin Ma Zhaoming Wei Yunxia Luan Ziwei Yin Wu Dai Cong Wei Xiaolei Huang Jingxian Liu Xiangsheng Chen Tianci Yi Zhisheng Zhang Zhulidezi Aishan Qin Li Hongying Hu | 2022 | Zoological Systematics2022，47，3： | 1 |
| 10 | Apelin/APJ system: a novel promising therapy target for thrombotic diseases显示文摘APJ,它是开始与最靠近的相同作为基因识别了到血管收缩素 II 类型 1 受体,是七 transmembrane G 联合蛋白质的受体。Apelin 是原来从牛的胃摘录孤立的 APJ 的内长的 ligand。有 apelin 的几 isoforms。Apelin preproproteins 包含 77 氨基酸的残余,它能被劈开形成更短的 bioactive isoforms 包括 apelin-36, apelin-17, apelin-13, apelin-12 等等。Apelin/APJ 受体广泛地在中央神经系统和外部纸巾被散布。Apelin/APJ 系统在大量生理、病理学的函数包含。例如, apelin 经由 NO/cGMP-dependent 机制降低血压。Apelin-13 在 cardiomyocytes 维持对 ischemia/reperfusion 短暂的 Ca 2+ 。而且, apelin-13 经由 PI3K/AKT 激活支持房间增长和 angiogenesis [1,2 ] 。 | Lanfang Li Jin Xu Linxi Chen Zhisheng Jiang | 2016 | Acta Biochimica et Biophysica Sinica2016，48，6： | 1 |
| 11 | Millennial and orbital-scale changes in the East Asian monsoon over the past 224,000 years显示文摘 | Wang Yongjin Cheng Hai Edwards R L Kong Xinggong Shao Xiaohua Chen Shitao Wu Jiangying Jiang Xiuyang Wang Xianfeng An Zhisheng | | 0，，7182： | 1 |
| 12 | Grain-size distribution function of polymodal sediments in hydraulic and aeolian environments, and numerical partitioning of the sedimentary components显示文摘 | Donghuai Sun J Bloemendal D.K Rea J Vandenberghe Fuchu Jiang Zhisheng An Ruixia Su | 2002 | Sedimentary Geology2002，，3： | 1 |
| 13 | Hydrogen sulfide from adipose tissue is a novel insulin resistance regulator显示文摘 | Xuejuan Feng Yu Chen Jing Zhao Chaoshu Tang Zhisheng Jiang Bin Geng | 2009 | Biochemical and Biophysical Research Communications2009，，1： | 1 |
| 14 | Influence of the reaction conditions on the solid-state graft copolymerization of methyl methacrylate and polyethylene/polypropylene in situ alloys显示文摘 | Fu Zhisheng Xu Junting Jiang Guoxin | 2005 | Journal of Applied Polymer Science2005，98，1： | 1 |
| 15 | Receptor-mediated reticulophagy: a novel promising therapy target for diseases显示文摘Autophagy ? 一个高度保存的自我消化过程从更低的优核质正在发怒到哺乳动物。Autophagy 在错误褶层蛋白质总数和损坏细胞器的降级包含,它随后被再使用。在 autophagy 之上被开始,膜结构称为 phagophore, autophagosome 的先锋,逐渐地扩展并且吞没并且为降级把他们送到 vacuole/lysosome 错误褶层蛋白质或损坏细胞器。Autophagy 贡献幸存和死亡的过程。基本 autophagy 为维持细胞的动态平衡是必要的。在正常生理学期间,专业化细胞的功能由清除要求 autophagy 的规定错误褶层蛋白质或损坏细胞器。然而,过多并且 dysregulated autophagy 可以由于从 lysosomes 漏的酶导致 apoptosis 和甚至房间死亡[1 ] 。 | Lanfang Li Jin Xu Linxi Chen Zhisheng Jiang | 2016 | Acta Biochimica et Biophysica Sinica2016，48，8： | 0 |
| 16 | Formation conditions of Sinian–Cambrian large lithologic gas reservoirs in the north slope area of central Sichuan Basin,SW China显示文摘Based on analyses of characteristics,hydrocarbon charging history and geological conditions for the formation of Sinian-Cambrian reservoirs in the north slope area of central Sichuan paleo-uplift,the natural gas origin,accumulation evolution,accumulation pattern and formation conditions of large lithologic gas reservoirs have been investigated.Through comprehensive analyses of natural gas composition,carbon and hydrogen isotopic compositions,fluid inclusions,reservoir bitumen,and geological conditions such as lithofacies paleogeography and beach body characterization,it is concluded that:(1)The natural gas in the Sinian-Cambrian of the north slope area is mainly oil cracking gas,and different contribution ratios of multiple sets of source rocks lead to different geochemical characteristics of natural gas in different reservoirs.(2)Although the both Sinian and Cambrian gas reservoirs in this area are lithologic gas reservoirs under monocline background,the former has normal-pressure and the latter has high-pressure.There are three types of source-reservoir-caprock combinations:single source with lower generation and upper reservoir,double sources with lower generation and upper reservoir or with side source and lateral reservoir,double sources with lower generation and upper reservoir or with upper generation and lower reservoir.The Permian-Triassic is the main generation period of oil,Early-Middle Jurassic is the main generation period of oil cracking gas and wet gas,and Late Jurassic-Cretaceous is the main generation period of dry gas.(3)The Sinian-Cambrian system of the north slope area has two favorable conditions for formation of large lithologic gas reservoirs,one is that the large scale beach facies reservoirs are located in the range of ancient oil reservoirs or near the source rocks,which is conducive to the'in-situ'large-scale accumulation of cracked gas in the paleo-oil reservoirs,the other is that the large scale mound-beach complex reservoirs and sealing layers of inter beach tight zones match effectively to form large lithologic traps under the slope background.The research results confirm that the north slope area has large multi-layer lithologic gas reservoirs with more than one trillion cubic meters of natural gas resources and great exploration potential. | WEI Guoqi XIE Zengye YANG Yu LI Jian YANG Wei ZHAO Luzi YANG Chunlong ZHANG Lu XIE Wuren JIANG Hua LI Zhisheng LI Jin GUO Jianying | 2022 | Petroleum Exploration and Development2022，49，5： | 0 |
| 17 | 支气管和肺动脉双袖状肺叶切除术治疗中央型肺癌的临床应用(英文)显示文摘Objective:The aim of our study was to introduce the surgical method and evaluate the efficacy of double sleeve lobectomy of the bronchus and the pulmonary artery in treatment for the central lung cancer. Method:From March 1995 to October 2010, double sleeve lobectomy of the bronchus and the pulmonary artery was performed in 45 cases with central lung cancer that involved the bronchial opening of an upper lobe of the lungs or the main bronchus and pulmonary artery but didn't involve any lower lobes. Among them, left upper lobectomy was performed in 37 cases, right medium-upper lobectomy was performed in 6 cases and right upper lobectomy was performed in 2 cases. Results:Postoperative complications were found in 12 cases. Among them, 3 cases were arrhythmia, 1 case was acute heart failure, 6 cases were obstructive pneumonia and pulmonary atelectasis, 2 cases were bronchial anastomotic fistula. Two cases died of cerebral infarction and massive hemoptysis respectively. Thirty-one cases were squamous carcinoma, 7 cases were adenocarcinoma, 4 cases were small cell lung cancer, 1 case was adenosquamous carcinoma, 1 case was sarcomatoid carcinomas, 1 case was mucinous adenocarcinoma. Ten cases were T3N0M0, 11 cases were T3N1M0, 17 cases were T3N2M0, 2 cases were T4N1M0, 5 cases were T4N2M0. The 1-year, 3-year, 5-year survival rates were 84.4% (38/45), 51.7% (15/29), 53.8% (7/13) respectively. Conclusion:The double sleeve lobectomy of the bronchus and the pulmonary artery can maximumly reserve the normal lung tissues while removing tumors, and avoid pneumonectomy. The surgery was safe and effective, while it required a high technique. | Yukang Kuang Laiduo Zeng Dongsheng Wang Binglin Yin Jiufa Wu Jian Huang Zhisheng He Jianfeng Zhu Feng Jiang Changying Guo | 2013 | The Chinese-German Journal of Clinical Oncology2013，12，6： | 0 |
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