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中国植物学会于1981年11月21日至27日在四川省成都市召开了有61名代表参加的草原生态学研究方法学术讨论会。大会收到包括植物群落结构调查研究、第一性生产力测定、第二性生产力测定、光合作用测定、物质与水分循环、热值测定、数学生态等有关内容的研究方法论文和报告34篇。其中有18篇论文在大会上作了报告。在小组讨论中,代表们就第一性生产力测定、水分与物质循环、光合作用测定 相似文献
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Foroughi Kobra Jahanbani Sarvin Nazarnezhad Simin Khastar Hossein Jafarisani Moslem Tashakori Mersedeh Kazemi Seyedeh Sareh 《International journal of peptide research and therapeutics》2020,26(2):1115-1126
International Journal of Peptide Research and Therapeutics - Survivin is a unique member of the inhibitor of apoptosis protein family. Research has approved Survivin’s ability to interact... 相似文献
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Changjian Zuo Zongxiang Hu Rui Qi Jiajie Liu Zhibo Li Junliang Lu Cheng Dong Kai Yang Weiyuan Huang Cong Chen Zhibo Song Sicheng Song Yaoming Yu Jiaxin Zheng Feng Pan 《Liver Transplantation》2020,10(34)
The relatively low capacity and capacity fade of spinel LiMn2O4 (LMO) limit its application as a cathode material for lithium‐ion batteries. Extending the potential window of LMO below 3 V to access double capacity would be fantastic but hard to be realized, as it will lead to fast capacity loss due to the serious Jahn–Teller distortion. Here using experiments combined with extensive ab initio calculations, it is proved that there is a cooperative effect among individual Jahn–Teller distortions of Mn3+O6 octahedrons in LMO, named as cooperative Jahn–Teller distortion (CJTD) in the text, which is the difficulty to access the capacity beyond one lithium intercalation. It is further proposed that the cationic disordering (excess Li at Mn sites and Li/Mn exchange) can intrinsically suppress the CJTD of Mn3+O6 octahedrons. The cationic disordering can break the symmetry of Mn3+ arrangements to disrupt the correlation of distortions arising from individual JT centers and prevent the Mn3+? O bonds distorting along one direction. Interestingly, with the suppressed CJTD, the original octahedral vacancies in spinel LMO are activated and can serve as extra Li‐ion storage sites to access the double capacity with good reversible cycling stability in microsized LMO. 相似文献
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Self-assembled DNA nanostructures have shown remarkable potential in the engineering of biosensing interfaces, which can improve the performance of various biosensors. In particular, by exploiting the structural rigidity and programmability of the framework nucleic acids with high precision, molecular recognition on the electrochemical biosensing interface has been significantly enhanced, leading to the development of highly sensitive and specific biosensors for nucleic acids, small molecules,proteins, and cells. In this review, we summarize recent advances in DNA framework-engineered biosensing interfaces and the application of corresponding electrochemical biosensors. 相似文献
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Jinwang Ye Yaling Yin Huanhuan Liu Lin Fang Xiaoqing Tao Linyu Wei Yue Zuo Ying Yin Dan Ke Jian‐Zhi Wang 《Aging cell》2020,19(1)
Intraneuronal accumulation of wild‐type tau plays a key role in Alzheimer's disease, while the mechanisms underlying tauopathy and memory impairment remain unclear. Here, we report that overexpressing full‐length wild‐type human tau (hTau) in mouse hippocampus induces learning and memory deficits with remarkably reduced levels of multiple synapse‐ and memory‐associated proteins. Overexpressing hTau inhibits the activity of protein kinase A (PKA) and decreases the phosphorylation level of cAMP‐response element binding protein (CREB), GluA1, and TrkB with reduced BDNF mRNA and protein levels both in vitro and in vivo. Simultaneously, overexpressing hTau increased PKAR2α (an inhibitory subunit of PKA) in nuclear fraction and inactivated proteasome activity. With an increased association of PKAR2α with PA28γ (a nuclear proteasome activator), the formation of PA28γ‐20S proteasome complex remarkably decreased in the nuclear fraction, followed by a reduced interaction of PKAR2α with 20S proteasome. Both downregulating PKAR2α by shRNA and upregulating proteasome by expressing PA28γ rescued hTau‐induced PKA inhibition and CREB dephosphorylation, and upregulating PKA improved hTau‐induced cognitive deficits in mice. Together, these data reveal that intracellular tau accumulation induces synapse and memory impairments by inhibiting PKA/CREB/BDNF/TrkB and PKA/GluA1 signaling, and deficit of PA28γ‐20S proteasome complex formation contributes to PKAR2α elevation and PKA inhibition. 相似文献
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