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- 저자 : Si Wen Zheng (검색결과 9 건)
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Mutation of IPO13 causes recessive ocular coloboma, microphthalmia, and cataract
Xiu-Feng Huang,Lue Xiang,Wan Cheng,Fei-Fei Cheng,Kai-Wen He,Bo-Wen Zhang,Si-Si Zheng,Ru-Yi Han,Yi-Han Zheng,Xiao-Tao Xu,Huan-Yun Yu,Wenjuan Zhuang,Yuk Fai Leung,Zi-Bing Jin 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Ocular coloboma is a developmental structural defect of the eye that often occurs as complex ocular anomalies. However, its genetic etiology remains largely unexplored. Here we report the identification of mutation (c.331C>T, p. R111C) in the IPO13 gene in a consanguineous family with ocular coloboma, microphthalmia, and cataract by a combination of whole-exome sequencing and homozygosity mapping. IPO13 encodes an importin-B family protein and has been proven to be associated with the pathogenesis of coloboma and microphthalmia. We found that Ipo13 was expressed in the cornea, sclera, lens, and retina in mice. Additionally, the mRNA expression level of Ipo13 decreased significantly in the patient compared with its expression in a healthy individual. Morpholinooligonucleotide- induced knockdown of ipo13 in zebrafish caused dose-dependent microphthalmia and coloboma, which is highly similar to the ocular phenotypes in the patient. Moreover, both visual motor response and optokinetic response were impaired severely. Notably, these ocular phenotypes in ipo13-deficient zebrafish could be rescued remarkably by full-length ipo13 mRNA, suggesting that the phenotypes observed in zebrafish were due to insufficient ipo13 function. Altogether, our findings demonstrate, for the first time, a new role of IPO13 in eye morphogenesis and that loss of function of IPO13 could lead to ocular coloboma, microphthalmia, and cataract in humans and zebrafish.
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Si-Qi Dong,Tong-Min Wang,Jiang-Bo Zhang,Yong-Qiao He,Wen-Qiong Xue,Zi-Yi Wu,Da-Wei Yang,Lian-Jing Cao,Jing-Wen Huang,Xi-Zhao Li,Pei-Fen Zhang,Xiao-Hui Zheng,Wei-Hua Jia 대한암학회 2021 Cancer Research and Treatment Vol.53 No.3
Purpose Capecitabine is an extensively used oral prodrug of 5-fluorouracil in treatment of colon cancer and is known to cause hand-foot syndrome (HFS). As the target enzyme for capecitabine, thymidylate synthase (TYMS) plays a key role for 5-fluorouracil metabolism and has been associated with some side effects caused by capecitabine. The aim of our study is to identify the possible genetic predictors of capecitabine-induced HFS (CAP-HFS) in Chinese colorectal cancer patients.Materials and Methods Whole exons of TYMS were sequenced for 288 extreme phenotype HFS patients, including 144 severe or early-onset (first 2 cycles) moderate HFS extreme cases and 144 extreme controls with no reported HFS. The associations between polymorphisms and CAP-HFS were analyzed using logistic regression under an additive model.Results We identified a novel risk mutation (c.1A>G, chr18:657743), was associated with severe HFS in an extreme case who was affected during the first cycle of treatment. Moreover, we identified three new variants, rs3786362, rs699517, rs2790, and two previously reported variants, 5’VNTR 2R/3R and 3′-untranslated region 6-bp ins-del, which were significantly associated with CAP-HFS (p < 0.05). In silico analysis revealed that the effect of these polymorphisms in the TYMS region on the development of HFS might not be restricted solely to the regulation of TYMS expression, but also the TYMS catalytic activity through the indirect effect on ENOSF1 expression.Conclusion This study identified new polymorphisms in TYMS gene significantly associated with CAP-HFS, which may serve as useful genetic predictors for CAP-HFS and help to elucidate the underlying mechanism of HFS.
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Zheng Si,Yanlong Li,Lifeng Wen,Xiaoqi Du 대한토목학회 2020 KSCE JOURNAL OF CIVIL ENGINEERING Vol.24 No.8
Mass concrete structures are prone to suffer temperature destruction during construction and operation because of their own mechanical properties and the role of cement hydration; therefore, the law of temperature field and temperature stress changes is crucial. This paper is based on the heat conduction theory and contact friction element theory under general external load. The heat conduction matrix, node thermal load vector, equivalent stiffness-constraint matrix and equivalent load vector of the contact friction element are each added to the whole heat conduction matrix, thermal load vector and total stiffness matrix, and the total load vector according to the finite element integration rule to establish the thermal-stress calculation model of the contact friction element. Combined with the Qi River inverted siphon project, this paper analyzed the temperature field and temperature stress using the three-dimensional finite element method, considering the changes of concrete thermodynamic parameters with age and the outside air temperature and other conditions, and obtained the distribution and variation in temperature field and temperature stress during the construction of an inverted siphon. The research results are of great significance for temperature control and crack prevention of inverted siphon structures. The thermal-stress calculation model of the contact friction element overcomes the limitations that it is difficult to use the current contact surface model to perform the temperature field simulation and further improves the application of the contact friction element model in the simulation of the temperature field and the temperature stress of mass concrete.
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Yi-Qing Ni,Wen-Qiang Liu,En-Ze Rui,Lei Yuan,Si-Yi Chen,You-Liang Zheng 국제구조공학회 2023 Smart Structures and Systems, An International Jou Vol.31 No.4
To assess structural condition in a non-destructive manner, computer vision-based structural health monitoring (SHM) has become a focus. Compared to traditional contact-type sensors, the advantages of computer vision-based measurement systems include lower installation costs and broader measurement areas. In this study, we propose a novel computer vision-based vibration measurement and coarse-to-fine damage assessment method for truss bridges. First, a deep learning model FairMOT is introduced to track the regions of interest (ROIs) that include joints to enhance the automation performance compared with traditional target tracking algorithms. To calculate the displacement of the tracked ROIs accurately, a normalized cross-correlation method is adopted to fine-tune the offset, while the Harris corner matching is utilized to correct the vibration displacement errors caused by the non-parallel between the truss plane and the image plane. Then, based on the advantages of the stochastic damage locating vector (SDLV) and Bayesian inference-based stochastic model updating (BISMU), they are combined to achieve the coarse-to-fine localization of the truss bridge's damaged elements. Finally, the severity quantification of the damaged components is performed by the BI-SMU. The experiment results show that the proposed method can accurately recognize the vibration displacement and evaluate the structural damage.
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TAZ as a novel regulator of oxidative damage in decidualization via Nrf2/ARE/Foxo1 pathway
Yu Hai-Fan,Zheng Lian-Wen,Yang Zhan-Qing,Wang Yu-Si,Wang Ting-Ting,Yue Zhan-Peng,Guo Bin 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-
TAZ, as a crucial effector of Hippo pathway, is required for spermatogenesis and fertilization, but little is known regarding its physiological function in uterine decidualization. In this study, we showed that TAZ was localized in the decidua, where it promoted stromal cell proliferation followed by accelerated G1/S phase transition via Ccnd3 and Cdk4 and induced the expression or activity of stromal differentiation markers Prl8a2, Prl3c1 and ALP, indicating the importance of TAZ in decidualization. Knockdown of TAZ impeded HB-EGF induction of stromal cell proliferation and differentiation. Under oxidative stress, TAZ protected stromal differentiation against oxidative damage by reducing intracellular ROS and enhancing cellular antioxidant capacity dependent on the Nrf2/ARE/Foxo1 pathway. TAZ strengthened the transcriptional activity of Nrf2 which directly bound to the antioxidant response element (ARE) of Foxo1 promoter region. Additionally, silencing TAZ caused accumulation of intracellular ROS through heightening NOX activity whose blockade by APO reversed the disruption in stromal differentiation. Further analysis revealed that TAZ might restore mitochondrial function, as indicated by the increase in ATP level, mtDNA copy number and mitochondrial membrane potential with the reduction in mitochondrial superoxide. Additionally, TAZ modulated the activities of mitochondrial respiratory chain complexes I and III whose suppression by ROT and AA resulted in the inability of TAZ to defend against oxidative damage to stromal differentiation. Moreover, TAZ prevented stromal cell apoptosis by upregulating Bcl2 expression and inhibiting Casp3 activity and Bax expression. In summary, TAZ might mediate HB-EGF function in uterine decidualization through Ccnd3 and ameliorate oxidative damage to stromal cell differentiation via Nrf2/ARE/Foxo1 pathway.
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Yin Bin Chen,Yu Fang Wang,Wei Hou,Ying-Ping Wang,Sheng-Yuan Xiao,Yang Yang Fu,Jia Wang,Si Wen Zheng,Pei-He Zheng 고려인삼학회 2017 Journal of Ginseng Research Vol.41 No.2
Background: Both ginsenoside Re and B-complex vitamins are widely used as nutritional supplements. They are often taken together so as to fully utilize their antifatigue and refreshing effects, respectively. Whether actually a drugenutrient interaction exists between ginsenoside Re and B-complex vitamins is still unknown. The objective of this study was to simultaneously investigate the effect of B-complex vitamins on the antifatigue activity and bioavailability of ginsenoside Re after their oral administration. The study results will provide valuable theoretical guidance for the combined utilization of ginseng and B-complex vitamins. Methods: Ginsenoside Re with or without B-complex vitamins was orally administered to mice to evaluate its antifatigue effects and to rats to evaluate its bioavailability. The antifatigue activity was evaluated by the weight-loaded swimming test and biochemical parameters, including hepatic glycogen, plasma urea nitrogen, and blood lactic acid. The concentration of ginsenoside Re in plasma was determined by liquid chromatographyetandem mass spectrometry. Results: No antifatigue effect of ginsenoside Re was noted when ginsenoside Re in combination with Bcomplex vitamins was orally administered to mice. B-complex vitamins caused to a reduction in the bioavailability of ginsenoside Re with the area under the concentrationetime curve from zero to infinity markedly decreasing from 11,830.85 2,366.47 h$ng/mL to 890.55 372.94 h$ng/mL. Conclusion: The results suggested that there were pharmacokinetic and pharmacodynamic drugenutrient interactions between ginsenoside Re and B-complex vitamins. B-complex vitamins can significantly weaken the antifatigue effect and decrease the bioavailability of ginsenoside Re when simultaneously administered orally.
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Chen, Yin Bin,Wang, Yu Fang,Hou, Wei,Wang, Ying Ping,Xiao, Sheng Yuan,Fu, Yang Yang,Wang, Jia,Zheng, Si Wen,Zheng, Pei He The Korean Society of Ginseng 2017 Journal of Ginseng Research Vol.41 No.2
Background: Both ginsenoside Re and B-complex vitamins are widely used as nutritional supplements. They are often taken together so as to fully utilize their antifatigue and refreshing effects, respectively. Whether actually a drug-nutrient interaction exists between ginsenoside Re and B-complex vitamins is still unknown. The objective of this study was to simultaneously investigate the effect of B-complex vitamins on the antifatigue activity and bioavailability of ginsenoside Re after their oral administration. The study results will provide valuable theoretical guidance for the combined utilization of ginseng and B-complex vitamins. Methods: Ginsenoside Re with or without B-complex vitamins was orally administered to mice to evaluate its antifatigue effects and to rats to evaluate its bioavailability. The antifatigue activity was evaluated by the weight-loaded swimming test and biochemical parameters, including hepatic glycogen, plasma urea nitrogen, and blood lactic acid. The concentration of ginsenoside Re in plasma was determined by liquid chromatography-tandem mass spectrometry. Results: No antifatigue effect of ginsenoside Re was noted when ginsenoside Re in combination with B-complex vitamins was orally administered to mice. B-complex vitamins caused to a reduction in the bioavailability of ginsenoside Re with the area under the concentration-time curve from zero to infinity markedly decreasing from $11,830.85{\pm}2,366.47h{\cdot}ng/mL$ to $890.55{\pm}372.94h{\cdot}ng/mL$. Conclusion: The results suggested that there were pharmacokinetic and pharmacodynamic drug-nutrient interactions between ginsenoside Re and B-complex vitamins. B-complex vitamins can significantly weaken the antifatigue effect and decrease the bioavailability of ginsenoside Re when simultaneously administered orally.
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