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- 저자 : Haihua Hu (검색결과 5 건)
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Representing Topic-Comment Structures in Chinese
( Haihua Pan ),( Jianhua Hu ) 한국언어정보학회 2002 국제 워크샵 Vol.2002 No.-
Shi (2000) claims that topics must be related to a syntactic position in the comment, thus denying the existence of dangling topics in Chinese. Under Shi``s analysis, the dangling topic sentences in Chinese are not topic-comment but subject-predicate sentences. However, Shi``s arguments are not without problems. In this paper we argue that topics in Chinese can be licensed not only by a syntactic gap but also by a semantic gap/variable without syntactic realization. Under our analysis, all the dangling topics discussed in Shi (2000) are, in fact, not subjects but topics licensed by a semantic gap/variable that can turn the relevant comment into an open predicate, thus licensing dangling topics and deriving well-formed topic-comment constructions. Our analysis fares better than Shi``s in not only unifying the licensing mechanism of a topic to an open predicate without considering how the open predicate is derived, but also unifying the treatment of normal and dangling topics in Chinese.
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Jingjuan Hu,Haihua Luo,Jieyan Wang,Wenli Tang,Junqi Lu,Shan Wu,Zhi Xiong,Guizhi Yang,Zhenguo Chen,Tian Lan,Hongwei Zhou,Jing Nie,Yong Jiang,Peng Chen 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
Chronic high-salt diet-associated renal injury is a key risk factor for the development of hypertension. However, the mechanism by which salt triggers kidney damage is poorly understood. Our study investigated how high salt (HS) intake triggers early renal injury by considering the ‘gut-kidney axis’. We fed mice 2% NaCl in drinking water continuously for 8 weeks to induce early renal injury. We found that the ‘quantitative’ and ‘qualitative’ levels of the intestinal microflora were significantly altered after chronic HS feeding, which indicated the occurrence of enteric dysbiosis. In addition, intestinal immunological gene expression was impaired in mice with HS intake. Gut permeability elevation and enteric bacterial translocation into the kidney were detected after chronic HS feeding. Gut bacteria depletion by non-absorbable antibiotic administration restored HS loadinginduced gut leakiness, renal injury and systolic blood pressure elevation. The fecal microbiota from mice fed chronic HS could independently cause gut leakiness and renal injury. Our current work provides a novel insight into the mechanism of HS-induced renal injury by investigating the role of the intestine with enteric bacteria and gut permeability and clearly illustrates that chronic HS loading elicited renal injury and dysfunction that was dependent on the intestine.
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Yanwei Sui,Man Zhang,Haihua Hu,Yuanming Zhang,Jiqiu Qi,Fuxiang Wei,Qingkun Meng,Yezeng He,Yaojian Ren,Zhi Sun 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2018 NANO Vol.13 No.12
The interconnected three-dimensional Ni–Co–S nanosheets were successfully deposited on ZnO nanorods by a one-step potentiostatic electrodeposition. The Ni–Co–S nanosheets provide a large electrode/electrolyte interfacial area which has adequate electroactive sites for redox reactions. Electrochemical characterization of the ZnO@Ni–Co–S core–shell nanorods presents high specifc capacitance (1302.5 F/g and 1085 F/g at a current density of 1 A/g and 20 A/g), excellent rate capabilities (83.3% retention at 20 A/g) and great cycling stability (65% retention after 5000 cycles at a current density of 30 A/g). The outstanding electrochemical performance of the as-prepared electrode material also can be ascribed to these reasons that the special structure improved electrical conductivity and allowed the fast diffusion of electrolyte ions.
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MicroRNA-206 Protects against Myocardial Ischaemia-Reperfusion Injury in Rats by Targeting Gadd45β
Zhai, Changlin,Qian, Qang,Tang, Guanmin,Han, Bingjiang,Hu, Huilin,Yin, Dong,Pan, Haihua,Zhang, Song Korean Society for Molecular and Cellular Biology 2017 Molecules and cells Vol.40 No.12
MicroRNAs are widely involved in the pathogenesis of cardiovascular diseases through regulating gene expression via translational inhibition or degradation of their target mRNAs. Recent studies have indicated a critical role of microRNA-206 in myocardial ischaemia-reperfusion (I/R) injury. However, the function of miR-206 in myocardial I/R injury is currently unclear. The present study was aimed to identify the specific role of miR-206 in myocardial I/R injury and explore the underlying molecular mechanism. Our results revealed that the expression level of miR-206 was significantly decreased both in rat I/R group and H9c2 cells subjected to hypoxia/reoxygenation (H/R) compared with the corresponding control. Overexpression of miR-206 observably decreased infarct size and inhibited the cardiomyocyte apoptosis induced by I/R injury. Furthermore, bioinformatics analysis, luciferase activity and western blot assay proved that $Gadd45{\beta}$ (growth arrest DNA damage-inducible gene $45{\beta}$) was a direct target gene of miR-206. In addition, the expression of pro-apoptotic-related genes, such as p53, Bax and cleaved caspase3, was decreased in association with the down-regulation of $Gadd45{\beta}$. In summary, this study demonstrates that miR-206 could protect against myocardial I/R injury by targeting $Gadd45{\beta}$.
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MicroRNA-206 Protects against Myocardial Ischaemia-Reperfusion Injury in Rats by Targeting Gadd45β
Changlin Zhai,Qang Qian,Guanmin Tang,Bingjiang Han,Huilin Hu,Dong Yin,Haihua Pan,Song Zhang 한국분자세포생물학회 2017 Molecules and cells Vol.40 No.12
MicroRNAs are widely involved in the pathogenesis of cardiovascular diseases through regulating gene expression via translational inhibition or degradation of their target mRNAs. Recent studies have indicated a critical role of microRNA-206 in myocardial ischaemia-reperfusion (I/R) injury. However, the function of miR-206 in myocardial I/R injury is currently un-clear. The present study was aimed to identify the specific role of miR-206 in myocardial I/R injury and explore the underlying molecular mechanism. Our results revealed that the expres-sion level of miR-206 was significantly decreased both in rat I/R group and H9c2 cells subjected to hypoxia/reoxygenation (H/R) compared with the corresponding control. Overexpression of miR-206 observably decreased infarct size and inhibited the cardiomyocyte apoptosis induced by I/R injury. Furthermore, bioinformatics analysis, luciferase activity and western blot assay proved that Gadd45beta (growth arrest DNA damage-inducible gene 45beta) was a direct target gene of miR-206. In addition, the expression of pro-apoptotic-related genes, such as p53, Bax and cleaved caspase3, was decreased in association with the down-regulation of Gadd45beta. In summary, this study demonstrates that miR-206 could protect against myocardial I/R injury by targeting Gadd45beta.
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