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1,759 results on '"Xia,Juan"'

209. Correlation Between Abdominal Fat Distribution and Serum Uric Acid in Patients Recently Diagnosed with Type 2 Diabetes

Author

Wang,Hong-Ping, Xu,Yuan-Ying, Xu,Bi-Lin, Lu,Jun, Xia,Juan, Shen,Tian, Fang,Ji, Lei,Tao, Wang,Hong-Ping, Xu,Yuan-Ying, Xu,Bi-Lin, Lu,Jun, Xia,Juan, Shen,Tian, Fang,Ji, and Lei,Tao

Abstract

Hong-Ping Wang,1,&ast; Yuan-Ying Xu,1,&ast; Bi-Lin Xu,1 Jun Lu,1 Juan Xia,1 Tian Shen,1 Ji Fang,1,2 Tao Lei1 1Department of Endocrinology, Putuo Hospital, Shanghai University of Traditonal Chinese Medicine, Shanghai, 200333, People’s Republic of China; 2Department of Nephrology, Putuo Hospital, Shanghai University of Traditonal Chinese Medicine, Shanghai, 200333, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Tao Lei, Department of Endocrinology, Putuo Hospital, Shanghai University of Traditonal Chinese Medicine, No. 164 of Lanxi Road, Putuo District, Shanghai, 200333, People’s Republic of China, Tel +86 021-22233222-58142, Email leitao5899@126.com Ji Fang, Department of Nephrology, Putuo Hospital, Shanghai University of Traditonal Chinese Medicine, No. 164 of Lanxi Road, Putuo District, Shanghai, 200333, People’s Republic of China, Tel +86 021-22233222-58082, Email 13601833102@163.comObjective: To investigated the link between the distribution of abdominal fat and the concentration of serum uric acid (SUA) in individuals recently diagnosed with type 2 diabetes.Methods: Studied 364 individuals had been diagnosed with type 2 diabetes within one month, and evaluated factors such as the distribution of fat in the abdomen, indicators related to glucose and lipid metabolism. The participants’ SUA concentrations were divided into a normal control group (CG) and a hyperuricemia group (HG).Results: The HG group had elevated abdominal subcutaneous fat area (SFA), visceral fat content (VFA), body mass index (BMI), fasting blood glucose (FBG), 2-hour postprandial blood glucose (PBG), glycosylated albumin (GA), serum creatinine (SCr), triacylglycerol (TG), and lower values in glomerular filtration rate (eGFR), high-density lipoprotein cholesterol (HDL-C) when compared to the CG group (P < 0.05). Among the obese individuals, the hyperuricemia subgroup exhibited higher measurements in waistline, hipline, VFA

Published
2023

229. Supplementary Data from Calnexin Impairs the Antitumor Immunity of CD4+ and CD8+ T Cells

Author

Chen, Yichen, primary, Ma, Da, primary, Wang, Xi, primary, Fang, Juan, primary, Liu, Xiangqi, primary, Song, Jingjing, primary, Li, Xinye, primary, Ren, Xianyue, primary, Li, Qiusheng, primary, Li, Qunxing, primary, Wen, Shuqiong, primary, Luo, Liqun, primary, Xia, Juan, primary, Cui, Jun, primary, Zeng, Gucheng, primary, Chen, Lieping, primary, Cheng, Bin, primary, and Wang, Zhi, primary

Published
2023
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231. Data from Calnexin Impairs the Antitumor Immunity of CD4+ and CD8+ T Cells

Author

Chen, Yichen, primary, Ma, Da, primary, Wang, Xi, primary, Fang, Juan, primary, Liu, Xiangqi, primary, Song, Jingjing, primary, Li, Xinye, primary, Ren, Xianyue, primary, Li, Qiusheng, primary, Li, Qunxing, primary, Wen, Shuqiong, primary, Luo, Liqun, primary, Xia, Juan, primary, Cui, Jun, primary, Zeng, Gucheng, primary, Chen, Lieping, primary, Cheng, Bin, primary, and Wang, Zhi, primary

Published
2023
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236. Identifying, Resolving, and Quantifying Anisotropy in ReS 2 Nanomechanical Resonators

Author

Xu, Bo, primary, Zhu, Jiankai, additional, Xiao, Fei, additional, Jiao, Chenyin, additional, Liang, Yachun, additional, Wen, Ting, additional, Wu, Song, additional, Zhang, Zejuan, additional, Lin, Lin, additional, Pei, Shenghai, additional, Jia, Hao, additional, Chen, Ying, additional, Ren, Ziming, additional, Wei, Xueyong, additional, Huang, Wen, additional, Xia, Juan, additional, and Wang, Zenghui, additional

Published
2023
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239. Repurposing Dihydroartemisinin to Combat Oral Squamous Cell Carcinoma, Associated with Mitochondrial Dysfunction and Oxidative Stress

Author

Shi, Shanwei, primary, Luo, Huigen, additional, Ji, Yuna, additional, Ouyang, Huiya, additional, Wang, Zheng, additional, Wang, Xinchen, additional, Hu, Renjie, additional, Wang, Lihong, additional, Wang, Yun, additional, Xia, Juan, additional, Cheng, Bin, additional, Bao, Baicheng, additional, Li, Xin, additional, Liao, Guiqing, additional, and Xu, Baoshan, additional

Published
2023
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240. Achieving 1.2 fm/Hz1/2 Displacement Sensitivity with Laser Interferometry in Two-Dimensional Nanomechanical Resonators: Pathways towards Quantum-Noise-Limited Measurement at Room Temperature

Author

Zhu, Jiankai, primary, Wang, Luming, additional, Wu, Jiaqi, additional, Liang, Yachun, additional, Xiao, Fei, additional, Xu, Bo, additional, Zhang, Zejuan, additional, Fan, Xiulian, additional, Zhou, Yu, additional, Xia, Juan, additional, and Wang, Zenghui, additional

Published
2023
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246. Data from Loss of VOPP1 Contributes to BET Inhibitor Acquired Resistance in Non–Small Cell Lung Cancer Cells

Author

Ze-Hong Miao, Ying-Qing Wang, Chang-Qing Tian, Xia-Juan Huan, Qian Wu, and Lin Sun

Abstract

Inhibitors targeting bromodomain and extraterminal (BET) proteins are promising anticancer drugs. The emergence of drug resistance during treatments will impair their therapeutic effectiveness. To investigate the mechanisms of acquired resistance to BET inhibitors (BETi), we generated a series of drug-resistant sublines by exposing non–small cell lung cancer (NSCLC) NCI-H1975 cells to the BETi ABBV-075. These sublines displayed cross-resistance to other tested BETis, increased migration abilities, reduced growth rates accompanied by an increased proportion of cells in G1 phase and decreased apoptotic responses to BETis. Changes in RNA expression and gene mutation profiles in the resistant variants indicate that emergence of BETi resistance is multifactorial. Importantly, all the tested ABBV-075–resistant variants showed loss of vesicular overexpressed in cancer prosurvival protein 1 (VOPP1) and an increase in the antiapoptotic BCL-2 protein. By knockdown, knockout, and reconstitution of VOPP1 in resistant cells, their parental cells, and other NSCLC cells, we confirmed that the loss of VOPP1 contributed to BETi resistance. Moreover, knockout of VOPP1 in the parental cells caused the increased expression of BCL-2, and the latter directly mediated BETi resistance. Through combined treatments with BETis and BCL-2 inhibitors (BCL-2i), we demonstrated that BCL-2is synergistically sensitized resistant cells to BETis.Implications:Based on these results, for the first time, we establish a causal link from VOPP1 loss to BCL-2 gain and then to BETi resistance, which provides new insights into BETi resistance and paves the way for further testing to circumvent BETi resistance.

Published
2023
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248. Data from MCL-1 Degradation Mediated by JNK Activation via MEKK1/TAK1-MKK4 Contributes to Anticancer Activity of New Tubulin Inhibitor MT189

Author

Ze-Hong Miao, Jing-Kang Shen, Jian Ding, Yi Chen, Lin-Jiang Tong, Lan-Ping Ma, Xia-Juan Huan, Jun-Mei Yi, Tao Meng, Ying-Qing Wang, and Wei Wang

Abstract

Colchicine site–targeted tubulin inhibitors are a promising type of anticancer drugs. MT189 is a new derivative of MT119, a previously reported colchicine site–binding antitubulin agent. In this study, MT189 was demonstrated to retain the property of MT119 in disrupting microtubulin via binding to the colchicine site, causing mitotic arrest and inducing apoptosis, and to display 8.7-fold enhanced proliferative inhibition in a panel of cancer cells. MT189 was shown to elicit in vivo anticancer effects on MDA-MB-231 xenografts in nude mice, and the tumor growth was suppressed by 35.9% over 14 days. MT189 led to degradation of MCL-1, a member of the antiapoptotic BCL-2 protein family. Its overexpression reduced but its silenced expression increased the apoptotic induction followed by the treatment with MT189. Moreover, the treatment with MT189 caused activation of the MEKK1/TAK1–MKK4–JNK signaling pathway. The activated JNK resulted in phosphorylation of MCL-1, which facilitated its ubiquitination-mediated degradation. Our results show that MT189 inhibits microtubulin polymerization by binding to the colchicine site. Relief of apoptotic suppression by MCL-1 degradation together with mitotic arrest contributes to the anticancer activity of MT189. Mol Cancer Ther; 13(6); 1480–91. ©2014 AACR.

Published
2023
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