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Your search keyword '"Zhao, Bingbin"' showing total 14 results
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14 results on '"Zhao, Bingbin"'

7. Bridging “Office-Based Care” With the “Virtual Practice Care Model”: Evolving Care for Chronic Kidney Disease Patients in the COVID-19 Pandemic—And Beyond

Author

Zhao, Bingbin, primary, Zhang, Lei, additional, Ji, Peili, additional, Lin, Jianfeng, additional, Han, Jianfang, additional, Li, Jiaying, additional, Zhou, Zijuan, additional, Wang, Haiyun, additional, Qiu, Ling, additional, Hong, Xia, additional, Williams, Winfred, additional, and Chen, Limeng, additional

Published
2020
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12. Ethical dilemma of identity disclosure faced by medical students in clinical clerkships: A nationwide multicenter study in China

Author

Zhao, Yi, primary, Cao, Yihan, additional, Che, Lu, additional, Fu, Qining, additional, Song, Shuang, additional, Zhao, Bingbin, additional, Zhang, Shuo, additional, Zhang, Weiwen, additional, Li, Xiang, additional, Choi, Stephanie, additional, Zhao, Jun, additional, Zhang, Hanwen, additional, Li, Yunzhu, additional, Xu, Haopeng, additional, and Pan, Hui, additional

Published
2018
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14. Frequent SLC12A3mutations in Chinese Gitelman syndrome patients: structure and function disorder

Author

Jiang, Lanping, Peng, Xiaoyan, Zhao, Bingbin, Zhang, Lei, Xu, Lubin, Li, Xuemei, Nie, Min, and Chen, Limeng

Abstract

This study was conducted to identify the frequent mutations from reported Chinese Gitelman syndrome (GS) patients, to predict the three-dimensional structure change of human Na–Cl co-transporter (hNCC), and to test the activity of these mutations and some novel mutations in vitroand in vivo.SLC12A3gene mutations in Chinese GS patients previously reported in the PubMed, China National Knowledge Infrastructure, and Wanfang database were summarized. Predicted configurations of wild type (WT) and mutant proteins were achieved using the I-TASSER workplace. Six missense mutations (T60M, L215F, D486N, N534K, Q617R, and R928C) were generated by site-directed mutagenesis. 22Na+uptake experiment was carried out in the Xenopus laevisoocyte expression system. In the study, 35 GS patients and 20 healthy volunteers underwent the thiazide test.T60M, T163M, D486N, R913Q, R928C, and R959frameshift were frequent SLC12A3gene mutations (mutated frequency >3%) in 310 Chinese GS families. The protein’s three-dimensional structure was predicted to be altered in all mutations. Compared with WT hNCC, the thiazide-sensitive 22Na+ uptake was significantly diminished for all six mutations: T60M 22 ± 9.2%, R928C 29 ± 12%, L215F 38 ± 14%, N534K 41 ± 15.5%, Q617R 63 ± 22.1%, and D486N 77 ± 20.4%. In thiazide test, the net increase in chloride fractional excretion in 20 healthy controls was significantly higher than GS patients with or without T60M or D486N mutations.Frequent mutations (T60M, D486N, and R928C) and novel mutations (L215F, N534K, and Q617R) lead to protein structure alternation and protein dysfunction verified by 22Na+ uptake experimentin vitroand thiazide test on the patients.

Published
2022
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