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      • KCI등재

        Protective strategy for the caudate lobe bile duct during left hemihepatectomy based on imaging data analysis

        Zhengyi Wu*,Liang Sun*,Ke Ning,Zhendong Chen,Zhipeng Wu,Hanqing Yang,Jinlong Yan*,Xiangbao Yin* 대한외과학회 2023 Annals of Surgical Treatment and Research(ASRT) Vol.105 No.6

        Purpose: This study was performed to analyze the rule of confluence of the caudate lobe bile duct (CLD) into the left hepatic duct (LHD) and to discuss the protective strategy during left hemihepatectomy. Methods: MRI of 400 patients and T-tube angiography images of 100 patients were collected, and the imaging rules of the confluence of the CLD into the LHD were summarized. The clinical data of 33 patients who underwent left hemihepatectomy using the protective strategy were analyzed. Results: MRI and T-tube angiography images showed that the length from the confluence point of the CLD into the LHD to the confluence of the left and right hepatic ducts was 1.19 ± 0.40 cm and 1.26 ± 0.39 cm, respectively. The average angle between the longitudinal axis of the 2 bile ducts was 68.27° ± 22.59° and 66.58 ± 22.88°, respectively. Coronal and cross-sectional images showed that inflow from the foot side to the cranial side was noted in 79.8% and 82.0% of patients, respectively, and inflow from the dorsal to the ventral side was observed in 84.5% and 88.0%, respectively. Based on these imaging rules, the safe transection length and plane were summarized, and the CLD was effectively protected in 33 cases of left hemihepatectomy. Conclusion: In left hemihepatectomy, the LHD should be transected at least 1.5 cm away from the confluence of the left and right hepatic ducts, and the plane of transection should be oblique to the dorsal side at an angle of 45° with the LHD, these parameters represent an effective strategy to protect the CLD.

      • KCI등재

        Few-shot transfer learning with attention for intelligent fault diagnosis of bearing

        Yao Hu,Qingyu Xiong,Qiwu Zhu,Zhengyi Yang,Zhiyuan Zhang,Dan Wu,Zihui Wu 대한기계학회 2022 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.36 No.12

        The bearing is one of the key components in modern industrial equipment. In the past few years, many studies have been carried out on bearing diagnosis through datadriven methods. However, there are two practical problems. First, under actual working conditions, the lack of fault samples is a major factor that hinders the application of these methods in industrial environments. Second, there is a lack of full utilization of a priori knowledge in the current stage of methods using relational networks for fault diagnosis. It is manifested by the incompleteness of the relational network structure. To address these problems, we present a new diagnosis method based on few-shot learning, which is suitable for the environment where the data is scarce. In this method, we train the model with the data generated by the artificial damaged bearings instead of the data from the real bearing. We experimentally validate the performance improvement of the complete relational network structure. It is able to perform the few-shot learning task better. In addition, we also reduce the global feature discrepancy by introducing an attention mechanism to improve the performance of the model. And the impact of the number of layers of the attention mechanism on the model is also discussed in detail. In this paper, our model performs better under the same experimental conditions compared with other transfer learning models.

      • Gene Expression Profiles of HeLa Cells Impacted by Hepatitis C Virus Non-structural Protein NS4B

        Zheng, Yi,Ye, Lin-Bai,Liu, Jing,Jing, Wei,Timani, Khalid A.,Yang, Xiao-Jun,Yang, Fan,Wang, Wei,Gao, Bo,Wu, Zhen-Hui Korean Society for Biochemistry and Molecular Biol 2005 Journal of biochemistry and molecular biology Vol.38 No.2

        By a cDNA array representing 2308 signal transduction related genes, we studied the expression profiles of HeLa cells stably transfected by Hepatitis C virus nonstructural protein 4B (HCV-NS4B). The alterations of the expression of four genes were confirmed by real-time quantitative RT-PCR; and the aldo-keto reductase family 1, member C1 (AKR1C1) enzyme activity was detected in HCV-NS4B transiently transfected HeLa cells and Huh-7, a human hepatoma cell line. Of the 2,308 genes we examined, 34 were up-regulated and 56 were down-regulated. These 90 genes involved oncogenes, tumor suppressors, cell receptors, complements, adhesions, transcription and translation, cytoskeletion and cellular stress. The expression profiling suggested that multiple regulatory pathways were affected by HCV-NS4B directly or indirectly. And since these genes are related to carcinogenesis, host defense system and cell homeostatic mechanism, we can conclude that HCV-NS4B could play some important roles in the pathogenesis mechanism of HCV.

      • KCI등재

        Centromere protein N promotes lung adenocarcinoma progression by activating PI3K/AKT signaling pathway

        Zheng Yi,You Hui,Duan Jingzhu,Chen Biyu,Wu Chenlin,Chen Peipei,Wang Meifang 한국유전학회 2022 Genes & Genomics Vol.44 No.9

        Background: As an important member of centromere family, centromere associated protein N (CENPN) was abnormally expressed in varied malignant tumors. Objective: This paper aimed to analyze the expression and related mechanism of CENPN in lung adenocarcinoma (LUAD). Methods: The expression of CENPN in LUAD was analyzed by Gene Expression Profiling Interactive Analysis (GEPIA) database. The mRNA expression, protein expression, cell viability, cell invasion, cell apoptosis, cell stem like characteristics were detected by RT-PCR, western blot, CCK8 assay, transwell assay, flow cytometry and spheroidization assay, respectively. Finally, the pathological changes of xenograft were estimated by H&E staining, and the expression of proteins was detected by immunohistochemistry. Results: GEPIA analysis showed that the CENPN expression in LUAD was significantly higher than that in normal lung tissue, which was negatively correlated with the prognosis. These results were consistent with our clinical data. Besides, CENPN was highly expressed in LUAD cell lines. In addition, the upregulation of CENPN amplified the cell viability, stemness and invasive ability in PC9 cells. However, the knockdown of CENPN inhibited the cell activity, stemness, invasive ability with increased cell apoptosis in A549. Furthermore, CENPN could positively regulate the phosphorylation of PI3K and AKT. The PI3K inhibitor, 740Y-P, could reverse the effect of CENPN silencing on the expression of Ki-67, cleaved caspase 3, OCT4, and snail 1. Finally, the downregulation of CENPN restrained the growth of xenograft and inactivated the PI3K/AKT pathway. Conclusion: CENPN was abnormally overexpressed in LUAD, and promoted tumor progression of LUAD by affecting PI3K/AKT pathway.

      • SCIESCOPUSKCI등재

        Hepatitis C Virus Non-structural Protein NS4B Can Modulate an Unfolded Protein Response

        Zheng Yi,Gao Bo,Ye Li,Kong Lingbao,Jing Wei,Yang Xiaojun,Wu Zhenghui,Ye Linbai The Microbiological Society of Korea 2005 The journal of microbiology Vol.43 No.6

        Viral infection causes stress to the endoplasmic reticulum (ER). The response to endoplasmic reticulum stress, known as the unfolded protein response (UPR), is designed to eliminate misfolded proteins and allow the cell to recover. The role of hepatitis C virus (HCV) non-structural protein NS4B, a component of the HCV replicons that induce UPR, is incompletely understood. We demonstrate that HCV NS4B could induce activating transcription factor (ATF6) and inositol-requiring enzyme 1 (IRE1), to favor the HCV subreplicon and HCV viral replication. HCV NS4B activated the IRE1 pathway, as indicated by splicing of X box-binding protein (Xbp-1) mRNA. However, transcriptional activation of the XBP-1 target gene, EDEM (ER degradation-enhancing $\alpha-mannosidase-like$ protein, a protein degradation factor), was inhibited. These results imply that NS4B might induce UPR through ATF6 and IRE1-XBP1 pathways, but might also modify the outcome to benefit HCV or HCV subreplicon replication.

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