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      • KCI등재

        The Shear Behavior of Double-superposed Panels Reinforced with Different Shear Connectors

        Wenying Zhang,Lianping Yang,Shaole Yu,Junsheng Yan 대한토목학회 2018 KSCE JOURNAL OF CIVIL ENGINEERING Vol.22 No.10

        The shear behavior of a new type of sandwich structure, double-superposed panels, is investigated by conducting push-out test and finite element analysis in this paper. Experiments have been carried out to characterize the effect on the shear behavior of two different shear connector configurations: truss connector and tic-tac-toe connector. Based on finite element analysis, a parameter study is conducted, with the major parameters considered being the diameter, height and pitch of shear connector. Test results indicate that the delamination between the precast layers and core layer is the main failure mode for all specimens, and the crack formation and crack development between the two interfaces is not in synch. It’s also revealed that the specimens with tic-tac-toe connections present higher ultimate shear strength, as well as better ductility during the process of failure, compared to those with truss connections. The results of the numerical simulations show that the ultimate shear strength and the ductility of both connector configurations increases as the diameter of the shear connector increases; increasement in height of shear connector has a negligible effect on the shear behavior; when the pitch length is increased, the ultimate shear strength of the truss connector specimen increases, which is the inverse behavior of the specimen with tic-tac-toe connector.

      • KCI등재

        Role of autophagy in diabetes and endoplasmic reticulum stress of pancreatic β-cells

        Wenying Quan,Yu-Mi Lim,Myung-Shik Lee 생화학분자생물학회 2012 Experimental and molecular medicine Vol.44 No.2

        Type 2 diabetes mellitus is characterized by insulin resistance and failure of pancreatic β-cells producing insulin. Autophagy plays a crucial role in cellular homeostasis through degradation and recycling of organelles such as mitochondria or endoplasmic reticulum (ER). Here we discussed the role of β-cell autophagy in development of diabetes, based on our own studies using mice with β-cell-specific deletion of Atg7(autophagy-related 7 ), an important autophagy gene,and studies by others. β-cell-specific Atg7-null mice showed reduction in β-cell mass and pancreatic insulin content. Insulin secretory function ex vivo was also impaired, which might be related to organelle dysfunction associated with autophagy deficiency. As a result, β-cell-specific Atg7-null mice showed hypoinsulinemia and hyperglycemia. However, diabetes never developed in those mice. Obesity and/or lipid are physiological ER stresses that can precipitate β-cell dysfunction. Our recent studies showed that β-cellspecific Atg7-null mice, when bred with ob/ob mice, indeed become diabetic. Thus, autophagy deficiency in β-cells could be a precipitating factor in the progression from obesity to diabetes due to inappropriate response to obesity-induced ER stress.

      • KCI등재

        Identification and Characterization of Pathogenic and Endophytic Fungal Species Associated with Pokkah Boeng Disease of Sugarcane

        Angelyn Hilton,Huanming Zhang,Wenying Yu,Won-Bo Shim 한국식물병리학회 2017 Plant Pathology Journal Vol.33 No.3

        Pokkah Boeng is a serious disease of sugarcane, which can lead to devastating yield losses in crop-producing regions, including southern China. However, there is still uncertainty about the causal agent of the disease. Our aim was to isolate and characterize the pathogen through morphological, physiological, and molecular analyses. We isolated sugarcane-colonizing fungi in Fujian, China. Isolated fungi were first assessed for their cell wall degrading enzyme capabilities, and five isolates were identified for further analysis. Internal transcribed spacer sequencing revealed that these five strains are Fusarium, Alternaria, Phoma, Phomopsis, and Epicoccum. The Fusarium isolate was further identified as F. verticillioides after Calmodulin and EF-1α gene sequencing and microscopic morphology study. Pathogenicity assay confirmed that F. verticillioides was directly responsible for disease on sugarcane. Co-inoculation of F. verticillioides with other isolated fungi did not lead to a significant difference in disease severity, refuting the idea that other cellulolytic fungi can increase disease severity as an endophyte. This is the first report characterizing pathogenic F. verticillioides on sugarcane in southern China.

      • SCIEKCI등재

        Identification and Characterization of Pathogenic and Endophytic Fungal Species Associated with Pokkah Boeng Disease of Sugarcane

        Hilton, Angelyn,Zhang, Huanming,Yu, Wenying,Shim, Won-Bo The Korean Society of Plant Pathology 2017 Plant Pathology Journal Vol.33 No.3

        Pokkah Boeng is a serious disease of sugarcane, which can lead to devastating yield losses in crop-producing regions, including southern China. However, there is still uncertainty about the causal agent of the disease. Our aim was to isolate and characterize the pathogen through morphological, physiological, and molecular analyses. We isolated sugarcane-colonizing fungi in Fujian, China. Isolated fungi were first assessed for their cell wall degrading enzyme capabilities, and five isolates were identified for further analysis. Internal transcribed spacer sequencing revealed that these five strains are Fusarium, Alternaria, Phoma, Phomopsis, and Epicoccum. The Fusarium isolate was further identified as F. verticillioides after Calmodulin and EF-$1{\alpha}$ gene sequencing and microscopic morphology study. Pathogenicity assay confirmed that F. verticillioides was directly responsible for disease on sugarcane. Co-inoculation of F. verticillioides with other isolated fungi did not lead to a significant difference in disease severity, refuting the idea that other cellulolytic fungi can increase disease severity as an endophyte. This is the first report characterizing pathogenic F. verticillioides on sugarcane in southern China.

      • SCISCIESCOPUS

        Amyloidogenic peptide oligomer accumulation in autophagy-deficient β cells induces diabetes.

        Kim, Jinyoung,Cheon, Hwanju,Jeong, Yeon Taek,Quan, Wenying,Kim, Kook Hwan,Cho, Jae Min,Lim, Yu-Mi,Oh, Seung Hoon,Jin, Sang-Man,Kim, Jae Hyeon,Lee, Moon-Kyu,Kim, Sunshin,Komatsu, Masaaki,Kang, Sang-Woo American Society for Clinical Investigation 2014 The Journal of clinical investigation Vol.124 No.8

        <P>Islet amyloid accumulation is a hallmark of human type 2 diabetes (T2D). In contrast to human islet amyloid polypeptide (hIAPP), murine islet amyloid polypeptide (mIAPP) does not exhibit amyloidogenic propensity. Because autophagy is important in the clearance of amyloid-like proteins, we studied transgenic mice with β cell-specific expression of hIAPP to evaluate the contribution of autophagy in T2D-associated accumulation of hIAPP. In mice with β cell-specific expression of hIAPP, a deficiency in autophagy resulted in development of overt diabetes, which was not observed in mice expressing hIAPP alone or lacking autophagy alone. Furthermore, lack of autophagy in hIAPP-expressing animals resulted in hIAPP oligomer and amyloid accumulation in pancreatic islets, leading to increased death and decreased mass of β cells. Expression of hIAPP in purified monkey islet cells or a murine β cell line resulted in pro-hIAPP dimer formation, while dimer formation was absent or reduced dramatically in cells expressing either nonamyloidogenic mIAPP or nonfibrillar mutant hIAPP. In autophagy-deficient cells, accumulation of pro-hIAPP dimers increased markedly, and pro-hIAPP trimers were detected in the detergent-insoluble fraction. Enhancement of autophagy improved the metabolic profile of hIAPP-expressing mice fed a high-fat diet. These results suggest that autophagy promotes clearance of amyloidogenic hIAPP, autophagy deficiency exacerbates pathogenesis of human T2D, and autophagy enhancers have therapeutic potential for islet amyloid accumulation-associated human T2D.</P>

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