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44 results on '"Dong, Zhixia"'

18. Diagnosis and segmentation effect of the ME-NBI-based deep learning model on gastric neoplasms in patients with suspected superficial lesions - a multicenter study

Author

Liu, Leheng, primary, Dong, Zhixia, additional, Cheng, Jinnian, additional, Bu, Xiongzhu, additional, Qiu, Kaili, additional, Yang, Chuan, additional, Wang, Jing, additional, Niu, Wenlu, additional, Wu, Xiaowan, additional, Xu, Jingxian, additional, Mao, Tiancheng, additional, Lu, Lungen, additional, Wan, Xinjian, additional, and Zhou, Hui, additional

Published
2023
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34. A study on the influence of Wechat marketing on attitudes of super-market consumers

Author

Zheng Qiujin, Xu Anxin, Zheng Haitang, and Dong Zhixia

Subjects
Descriptive statistics, Applied Mathematics, Field (Bourdieu), 0502 economics and business, 05 social sciences, 050211 marketing, Advertising, Business, Marketing, 050203 business & management, Analysis, Analysis method, Test (assessment)
Abstract

This paper is dedicated to analyze the influence of WeChat marketing on supermarket consumer attitudes. Through the field questionnaire investigations, this paper uses descriptive statistics and empirical statistics analysis methods to test the factors of consumers’ attitudes. It also puts forward some strategies to increase levels of consumer trust, improve the wording attraction of WeChat marketing and enhance peoples’ involvement in We Chat Public Platform.

Published
2016

35. ETS translocation variant 5 (ETV5) promotes CD4+T cell-mediated intestinal inflammation and fibrosis in inflammatory bowel diseases

Author

Shi, Yan, Ma, Caiyun, Wu, Shan, Ye, Xin, Zhuang, Qian, Ning, Min, Xia, Jie, Shen, Shuang, Dong, Zhixia, Chen, Dafan, Liu, Zhanju, and Wan, Xinjian

Abstract

ETS translocation variant 5 (ETV5) has been implicated in the pathogenesis of inflammatory bowel disease (IBD). However, the exact roles of ETV5 in regulating CD4+T cell-mediated intestinal inflammation and fibrosis formation remain unclear. Here, we reveal that ETV5 overexpression induced IL-9 and its transcription factor IRF4 expression in naïve IBD CD4+T cells under Th9-polarizing conditions. Silencing of IRF4 inhibited ETV5-induced IL-9 expression. CD4+T cell-specific ETV5 deletion (CKO) ameliorated intestinal inflammation and fibrosis in TNBS-induced experimental colitis and CD4+T cell-transferred Rag1-/-colitis mice, characterized by less CD4+T cell infiltration, lower fibroblast activation and collagen deposition in the colonic tissues. Furthermore, IL-9 treatment aggressive TNBS-induced intestinal fibrosis in CKO and wild type (WT) control mice. In vitro, human intestinal fibroblasts cocultured with ETV5 overexpressed-Th9 cells expressed higher levels of collagen I and III, whereas an inclusion of anti-IL-9 antibody could reverse this effect. RNA sequencing analysis demonstrated that IL-9 upregulated TAF1 expression in human intestinal fibroblasts. Clinic data showed that number of α-SMA+TAF1+fibroblasts are higher in inflamed mucosa of IBD patients. Importantly, TAF1 siRNA treatment suppressed IL-9-mediated profibrotic effect in vitro. These findings reveal that CD4+T cell-derived ETV5 promotes intestinal inflammation and fibrosis through upregulating IL-9-mediated intestinal inflammatory and fibrotic response in IBD. Thus, the ETV5/IL-9 signal pathway in T cells might represent a novel therapeutic target for intestinal inflammation and fibrosis in IBD.

Published
2024
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41. MSCs with ACE II gene affect apoptosis pathway of acute lung injury induced by bleomycin.

Author

Zhang, Xiaomiao, Gao, Fengying, Li, Qian, Dong, Zhixia, Sun, Bo, Hou, Lili, Li, Zhuozhe, and Liu, Zhenwei

Subjects
LUNG injury treatment, APOPTOSIS prevention, MESENCHYMAL stem cells, ANGIOTENSIN converting enzyme, BLEOMYCIN, BCL-2 genes, CELLULAR signal transduction, THERAPEUTICS
Abstract

Purpose: The aim of this study was to evaluate the effect and related mechanisms of Mesenchymal stem cells (MSCs) and Angiotensin converting enzyme II (ACE II) on acute lung injury (ALI). Methods: MSCs were separated from umbilical cord cells, and the changes of phenotype before and after ACE II silence were observed using Flow Cytometer. ALI model was induced by 10 mg/mL bleomycin in 60 Balb/c mice, and the rest 8 mice were regarded as the baseline group. The mice were randomly divided into four groups ( n = 15): control, ACE II, stem, and stem + ACE II. The apoptotic index (AI) was calculated using TUNEL, and the detection of protein and mRNA of Bax, Bak and p53, Bcl-2, Grp78, CHOP and Caspase 12 were used by western-blot and RT-PCR, respectively. Results: The umbilical cord cells differentiated into stable MSCs about 14 days, and ACE II transfection reached a peak at the 5th day after transfection. ACE II silence did not affect the phenotype of MSCs. All the proteins and mRNAs expression except Bcl-2 in the stem and stem + ACE II were significantly lower than those in control from 8 h ( p < 0.05, p < 0.01), while Bcl-2 exhibited an opposite trend. Stem + ACE II performed a better effect than single stem in most indexes, including AI ( p < 0.05, p < 0.01). Conclusions: The co-administration of MSCs and ACE II can significantly suppress apoptosis in ALI mice, and may be an effective clinical treatment for ALI. [ABSTRACT FROM AUTHOR]

Published
2015
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42. “Fatty” or “steatotic”: position statement from a linguistic perspective by the Chinese-speaking community

Author

Miao, Lei, Ye, Shu-Mian, Fan, Jian-Gao, Seto, Wai-Kay, Yu, Hon Ho, Yu, Ming-Lung, Kao, Jia-Horng, Boon-Bee Goh, George, Young, Dan Yock, Wong, Yu Jun, Chan, Wah-Kheong, Yang, Wah, Jia, Jidong, Lau, George, Wei, Lai, Shi, Junping, Zhang, Huijie, Bi, Yan, Pik-Shan Kong, Alice, Pan, Calvin Q., Zheng, Ming-Hua, Liang, Huiqing, Yang, Ling, Li, Xinhua, Zeng, Qing-Lei, Gao, Rong, Hu, Songhao, Yan, Bi, Jin, Xiaozhi, Li, Gang, Chen, En-Qiang, Hu, Dandan, Fan, Xiaotang, Hu, Peng, Chang, Xiangrong, Jin, Yihui, Cai, Yijing, Chen, Liangmiao, Wen, Qianjun, Sun, Jian, Xu, Hexiang, Li, Junfeng, Yang, Yongping, Huang, Ang, Zhang, Dongmei, Tan, Lin, Li, Dongdong, Zhu, Yueyong, Cai, Chenxi, Gu, Xuemei, Shen, Jilong, Zhong, Jianhong, Li, Lu, Li, Zhenzhen, Ma, Chiye, Liu, Yaming, Zhang, Yimin, Zhao, Lei, Han, Juqiang, Chen, Tao, Zhang, Qiang, Yang, Song, Zhang, Le, Chen, Lanlan, Feng, Gong, Wang, Qixia, Hao, Kunyan, Lu, Qinghua, Mao, Yimin, Zhong, Yandan, Wang, Ningjian, Xin, Yongning, Yu, Yongtao, Qi, Xingshun, Wang, Ke, He, Yingli, Du, Mulong, Zou, Zhengsheng, Xia, Mingfeng, Zhao, Suxian, Zhao, Jingjie, Xie, Wen, Zhang, Yao, Ji, Mao, Richeng, Du, Qingwei, Chen, Haitao, Song, Yongfeng, Wang, Cunchuan, Lu, Yan, Song, Yu, Zhang, Chi, Shi, Li, Mak, Lungyi, Chen, Li, Xu, Liang, Yuan, Hai-Yang, Hong, Liang, Hai, Li, Wu, Xiaoning, Yang, Naibin, Li, Jing-Wei, Jiejin, Zou, Zhuolin, Zheng, Wen, Zhao, Jian, Zhang, Xiang, Huang, Chen-Xiao, Yao, Ying, Yuan, Bao-Hong, Huang, Shanshan, Min, Lian, Chai, Jin, Hong, Wandong, Miao, Kai-Wen, Xiao, Tie, Chen, Shun-Ping, Ye, Feng, Song, Yuhu, Zhang, Jinshun, Zhou, Xiao-Dong, Wang, Mingwei, Dai, Kai, Lou, Jianjun, Duan, Xu, Yu, Hongyan, Jin, Xi, Fu, Liyun, Zhang, Yanliang, Ye, Junzhao, Liu, Feng, Chen, Qin-Fen, Zhou, Yong-Hai, Duan, Xiaohua, Zhang, Qun, Zhang, Faming, Cao, Zhujun, Li, Yingxu, Sun, Dan-Qin, Hu, Ai-Rong, Liu, Fenghua, Chen, Yuanwen, Zhang, Dianbao, Gao, Feng, Ye, Hua, Rao, Huiying, Luo, Kaizhong, Dai, Zhijuan, Wang, Chia-Chi, Tang, Shanhong, Hua, Jing, Deng, Cunliang, Zhou, Ling, Fan, Yu-Chen, Wu, Mingyue, Lu, Hongyan, Zhang, Xiaoxun, Zhang, Huai, Ni, Yan, Kei Ng, Stephen Ka, Li, Chunming, Liu, Chang, Zhang, Xia, Shi, Yu, Yan, Hongmei, Xu, Jinghang, Zhou, Yu-Jie, Cheng, Yuan, Bai, Honglian, Hu, Xiang, Gao, Yufeng, Lin, Biaoyang, Gu, Guangxiang, Chen, Jin, Hu, Xiaoli, Yuan, Xiwei, Wang, Jie, Chen, Qiang, Yiling, Li, Zhu, Xiao Jia, Chen, Xu, Zhu, Yongfen, Liu, Xiaolin, Wang, Bing, Cai, Mingyan, Chen, Enguang, Chen, Jun, Chen, Jingshe, Deng, Hong, Chen, Xiaoxin, Chen, Yingxiao, Cheng, Xinran, Chen, Fei, Ding, Yang, Dong, Zhixia, Ding, Yanhua, Qingxian, Cai, Deng, Zerun, Cai, Tingchen, Chen, Yaxi, Chen, Zhongwei, Chen, Xing, Huang, Jiaofeng, Huang, Mingxing, Fu, Lei, Jin, Jianhong, Geng, Bin, Chen, Yu, Chen, Ruicong, Jin, Weimin, Li, Dongliang, Jin, Xianghong, Li, Jian-Jun, Zhang, Jie, Matsiyit, Alimjan, Wang, Guiqi, Gao, Tian, Zhang, Shu, Yan, Wenmao, Liu, Jie, Chen, Peng, Hu, Hao, Li, Ming, Yuan, Ping Ge, Chen, Yi, Dong, Zhiyong, Li, Xiaopeng, Lin, Su, Li, Jie, Li Ang, Xujing, Liu, Xin, Liu, Shousheng, Li, Min-Dian, Qian, Hui, Qi, Minghua, Peng, Liang, Luo, Fei, Dang, Shuangsuo, Mao, Xianhua, Sheng, Qiyue, Lyu, Jiaojian, Liu, Chenghai, Qi, Kemin, Ma, Honglei, Lu, Zhonghua, Pan, Qiong, Miao, Qing, Li, Xiaosong, Lin, Huapeng, Shui, Guanghou, Qu, Shen, Fei, Wang, Liu, Chang-Hai, Xia, Fan, Wang, Dan, Pan, Ziyan, Hu, Fangzheng, Xu, Long, Xiong, Qing-Fang, Yang, Rui-Xu, Wang, Qi, Chen, Ligang, W Ang, Danny, Ren, Wanhua, Tong, Xiaofei, You, Ningning, Xing, Yanqing, Sun, Chao, Yu, Zhuo, Shuangxu, Xu, Honghai, Sun, Yi, Zhang, Taotao, Wu, Wei, Zhang, Yingmei, Ye, Qing, Zhang, Zhongheng, Yan, Jie, Zhou, Bengjie, Liu, Weiqiang, Li, Yongguo, Zhao, Lili, Lei, Siyi, Zhu, Guangqi, Ouyang, Huang, Zhou, Yaoyao, Yin, Jianhui, Xia, Yongsheng, He, Qiancheng, Zhang, Xiaoyong, Yang, Qiao, Yao, Libin, Pan, Xiazhen, Wang, Xiaodong, Li, Yangyang, Zhu, Shenghao, Zhao, Xinyan, Chen, Sui-Dan, Zhu, Jiansheng, Zeng, Jing, Tang, Liangjie, Hu, Kunpeng, Yang, Wanshui, Huang, Bingyuan, Zhuang, Chengle, Xun, Yunhao, Zhou, Jianghua, Xu, Wenjing, Wu, Bian, Zhang, Xuewu, He, Yong, Mei, Zubing, Xia, Zefeng, Lu, Bin Feng, Li, Qiang, Li, Jia, Yan, Xuebing, Wen, Zhengrong, Liu, Wenyue, Xu, Dongsheng, Chen, Huiting, Wang, Jing, Song, Juan, Peng, Jie, Chen, Jionghuang, Li, Shuchen, Zheng, Yongping, Zhi-Zhi, Xing, Tang, Jieting, Liu, Chuan, Chen, Chao, Guicheng, Wu, Ye, Quanzhong, Ka, Li, Zhou, Yuping, Jia, Xiaoli, Zou, Ziyuan, Zu, Fuqiang, Cai, Yongqian, Chen, Yunzhi, Chu, Jinguo, Yan, Bing, Wang, Tie, Pan, Qiuwei, Xie, Lingling, Zeng, Xufen, Liu, Bingrong, Su, Minghua, Mu, Yibing, Zeng, Menghua, Guo, Yuntong, Yang, Yongfeng, Zhang, Xiaoguan, Wu, Shike, Pan, Jin-Shui, Cao, Li, Feng, Wenhuan, Yubin, Yang, Wang, Na, Lu, Xiaolan, Lu, Guanhua, Xiong, Jianbo, Zhuang, Jianbin, Shi, Guojun, Zhu, Yanfei, Ying, Xing, Qiao, Zengpei, Zhang, Rui, Li, Yuting, Lei, Yuanli, Xixi, Wu, Tian, Na, Lian, Liyou, Zhang, Binbin, Xiaozhu, Huang, Yan, Chen, Wenying, Liu, Kun, Zhang, Ruinan, Lai, Qintao, Wang, Fudi, Wen, Caiyun, Zhang, Xinlei, Wu, Lili, Liang, Yaqin, Jie, You, Xinzhejin, Zeng, Qiqiang, Zhu, Qiang, Chao, Zheng, Shou, Lan, Jin, Wei-Lin, Ye, Chenhui, Han, Yu, Xie, Gangqiao, Zhao, Jing, Ye, Chunyan, Wang, Hua, Song, Lintao, Feng, Juan, Huang, Yubei, Su, Wen, Bai, Juli, Wong, Vincent, Wang, Huifeng, Ming, Wai-Kit, Yu, Yue-Cheng, Jin, Yan, Zhao, Yan, Gao, Lilian, Liangwang, Chen, Hanbin, Ruifangwang, Tang, Yuhan, Chen, Gang, Liu, Dabin, Cai, Xiaobo, Xue, Feng, Yang, Qinhe, Sun, Guangyong, Zhu, Chunxia, Huang, Zhifeng, Zhou, Hongwen, Xiao, Xiao, Hou, Xin, He, Jie, Ji, Dong, Xiao, Huanming, Chi, Xiaoling, Zou, Huaibin, Shi, Yiwen, Fan, Xingliang, Hu, Xiaoyu, Huang, Zhouqin, Cao, Haixia, Jiang, Jingjing, Zhao, Qiang, Chen, Wei, Li, Shi Bo, Zhang, Fan, Chen, Zhiyun, Liu, Jinfeng, Li, Shibo, Liu, Jing, Li, Li, Li, Ruyu, Kun, Ya, Xiao, ErHui, Wang, Tingyao, Wang, Chunjiong, Aili, Aikebaier, Liu, Xiaoxia, Ding, Ran, Zhu, Chonggui, Zeng, Xin, Wu, Miao, Li, Zhen, Yang, Tao, Qin, Yunfei, Sun, Lihua, Xu, Ying, Fu, Xianghui, and Li, Yongyin

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43. Amelioration of nonalcoholic fatty liver disease by inhibiting the deubiquitylating enzyme RPN11.

Author

Zhou B, Luo Y, Bi H, Zhang N, Ma M, Dong Z, Ji N, Zhang S, Wang X, Liu Y, Guo X, Wei W, Xie C, Wu L, Wan X, Zheng MH, Zhao B, Li Y, Hu C, and Lu Y

Abstract

Nonalcoholic fatty liver disease (NAFLD), including its more severe manifestation nonalcoholic steatohepatitis (NASH), is a global public health challenge. Here, we explore the role of deubiquitinating enzyme RPN11 in NAFLD and NASH. Hepatocyte-specific RPN11 knockout mice are protected from diet-induced liver steatosis, insulin resistance, and steatohepatitis. Mechanistically, RPN11 deubiquitinates and stabilizes METTL3 to enhance the m6A modification and expression of acyl-coenzyme A (CoA) synthetase short-chain family member 3 (ACSS3), which generates propionyl-CoA to upregulate lipid metabolism genes via histone propionylation. The RPN11-METTL3-ACSS3-histone propionylation pathway is activated in the livers of patients with NAFLD. Pharmacological inhibition of RPN11 by Capzimin ameliorated NAFLD, NASH, and related metabolic disorders in mice and reduced lipid contents in human hepatocytes cultured in 2D and 3D. These results demonstrate that RPN11 is a novel regulator of NAFLD/NASH and that suppressing RPN11 has therapeutic potential for the treatment., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Published
2024
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44. A unique case of well-differentiated gastric-type adenocarcinoma coexisting with a gastric adenocarcinoma of the fundic gland in a Helicobacter pylori-uninfected stomach.

Author

Dong Z, Wu S, Xia J, Liu D, Qian Y, and Wan X

Subjects
Humans, Gastric Mucosa pathology, Helicobacter pylori, Stomach Neoplasms complications, Stomach Neoplasms pathology, Adenocarcinoma complications, Adenocarcinoma pathology, Helicobacter Infections complications, Helicobacter Infections diagnosis
Abstract

Competing Interests: The authors declare that they have no conflict of interest.

Published
2023
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