👤 Yanping Zhang

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Also published as: Lanyue Zhang, Zemin Zhang, Kangning Zhang, Fan Zhang, Xianpeng Zhang, Xiaoxia Zhang, Suping Zhang, Jingtian Zhang, Jianzhao Zhang, Guoan Zhang, Bowei Zhang, Mengshi Zhang, Shijun Zhang, Nieke Zhang, Guoguo Zhang, J R Zhang, Hongbin Zhang, Xiao-Ming Zhang, Baojing Zhang, Linjing Zhang, Xiao-bo Zhang, Dai Zhang, Rongchao Zhang, Guang-Qiong Zhang, Jixing Zhang, Xiaomei Zhang, Honghua Zhang, Lixia Zhang, Jinhua Zhang, Xiaotong Zhang, Shu Zhang, Ming Zhang, Jianeng Zhang, Xintao Zhang, T Zhang, Li-Ke Zhang, Miaoran Zhang, Jinfeng Zhang, Shi Zhang, Lingxiao Zhang, Xiaoli Zhang, Hongjie Zhang, Bosheng Zhang, Qingfeng Zhang, Xiaofei Zhang, Tonghua Zhang, Huiting Zhang, Yuning Zhang, Yangfan Zhang, Guiping Zhang, Junying Zhang, Xiaojie Zhang, Yu-Chi Zhang, Yumin Zhang, Daming Zhang, Hongquan Zhang, Youzhong Zhang, Jianghong Zhang, Zhenzhen Zhang, Yixia Zhang, Yuebo Zhang, Yijing Zhang, Wenji Zhang, Xianjing Zhang, Menghuan Zhang, Xinwu Zhang, Xinyi Zhang, Fujun Zhang, Wen-Hong Zhang, Dayi Zhang, Xiongze Zhang, Qiaojun Zhang, F P Zhang, Sanbao Zhang, Nianxiang Zhang, Ya Zhang, Wenyang Zhang, Yunmei Zhang, Qingrun Zhang, Hailing Zhang, X X Zhang, Xiao-Yu Zhang, Zhihui Zhang, Youyi Zhang, Haokun Zhang, Jason Z Zhang, Jing-Nan Zhang, Han Zhang, Caiyu Zhang, Jianhong Zhang, Wenlu Zhang, Guang Zhang, Xinran Zhang, Xiaoxi Zhang, Kongyong Zhang, Xiuming Zhang, Jiaxing Zhang, Zhaobo Zhang, Wenkui Zhang, Yintang Zhang, Wen-Jie Zhang, Zhong-Yin Zhang, Ziding Zhang, XiaoLin Zhang, Xiao-Meng Zhang, Wenwen Zhang, Jinfang Zhang, Jinliang Zhang, Xiaoyuan Zhang, Jieming Zhang, Jiannan Zhang, Tianshu Zhang, Xinheng Zhang, Shitian Zhang, Su Zhang, Wen-Xuan Zhang, Qiuyue Zhang, Bohua Zhang, C Zhang, P Zhang, Huaqi Zhang, Fuqiang Zhang, Ruihong Zhang, Shanchun Zhang, Mingjun Zhang, Aiguo Zhang, Dong Zhang, Xipeng Zhang, Lingqiang Zhang, Yonglong Zhang, Haonan Zhang, Chengyu Zhang, Xutong Zhang, Cathy C Zhang, Zhao Zhang, Xinhan Zhang, Yulong Zhang, Guowei Zhang, Yi-Min Zhang, Lizhi Zhang, Licheng Zhang, Chunhai Zhang, Rui Long Zhang, Junwei Zhang, Zhao-Ming Zhang, Lianqin Zhang, Yiyao Zhang, X Zhang, Caiyi Zhang, Xiangwu Zhang, Haoxing Zhang, Ge Zhang, Shi-Qian Zhang, Ang Zhang, Zhi-Jun Zhang, Tao Zhang, Guofang Zhang, Yinzhi Zhang, Hu Zhang, Zhuzhen Zhang, Zewei Zhang, Qingqing Zhang, Liyi Zhang, S Y Zhang, Junjing Zhang, Yongjuan Zhang, Chao-Hua Zhang, Mingyu Zhang, Kaiyi Zhang, Xuelong Zhang, Juntai Zhang, Shanxiang Zhang, Liyuan Zhang, Siyuan Zhang, Ya-Long Zhang, Mingfa Zhang, Yashuo Zhang, Chengbo Zhang, Ziqi Zhang, Jianping Zhang, Chenmin Zhang, Juliang Zhang, Xingong Zhang, Kailing Zhang, Hengrui Zhang, Yachen Zhang, Changlong Zhang, Mo-Ruo Zhang, Hanyin Zhang, Jianyong Zhang, Boxiang Zhang, Jiangyan Zhang, Mingjiong Zhang, Guan-Yan Zhang, Mingming Zhang, Meng-Ying Zhang, Zhengfen Zhang, Gui-Ping Zhang, John Z H Zhang, Hai-Liang Zhang, Z Zhang, Kunning Zhang, Fukang Zhang, Yaping Zhang, Guangyong Zhang, Shasha Zhang, Hongrui Zhang, Jianwu Zhang, Shou-Peng Zhang, Nasha Zhang, Huiqing Zhang, Chuanxin Zhang, Ke Zhang, Anqi Zhang, Haomin Zhang, Yuanping Zhang, Mengmin Zhang, Junsheng Zhang, Xinmin Zhang, Enming Zhang, Chen-Yang Zhang, Qian Jun Zhang, Guo-Wei Zhang, Zhongqi Zhang, Yawei Zhang, Yang Zhang, Yueqi Zhang, Haitao Zhang, Zhen-Shan Zhang, Wencheng Zhang, Ai Zhang, Yuetong Zhang, Jinzhou Zhang, Guo-Fang Zhang, Jingmei Zhang, Fengxu Zhang, Lei Zhang, Quan Zhang, Zhenqiang Zhang, Shengchi Zhang, Shuer Zhang, Haiyang Zhang, Xiuzhen Zhang, Chenfei Zhang, Heping Zhang, Pingmei Zhang, Yichi Zhang, Junxing Zhang, Kainan Zhang, Long Zhang, Joyce Zhang, Cheng-Lin Zhang, Zhen-Dong Zhang, Fei-Ran Zhang, Tongran Zhang, F Zhang, Hongtao Zhang, Haijiao Zhang, Dongmei Zhang, Yuzhou Zhang, Zhiming Zhang, Shuangjie Zhang, Fuquan Zhang, M X Zhang, Chengkai Zhang, Chengshi Zhang, Luyun Zhang, Jinlong Zhang, Yanxia Zhang, Xiong Zhang, Luning Zhang, Jiayu Zhang, Zuoyi Zhang, H L Zhang, Pei-Zhuo Zhang, Geng Zhang, Caiying Zhang, Qifan Zhang, Wenya Zhang, Xiao-yan Zhang, Lijie Zhang, Fengwei Zhang, Yanhong Zhang, Leo H Zhang, Yongjiu Zhang, Jiachen Zhang, Jianmin Zhang, Zhaomin Zhang, Lechi Zhang, Bangzhou Zhang, Hongxia Zhang, Xuehui Zhang, Zhenglang Zhang, Qiyong Zhang, M M Zhang, Jianjun Zhang, Guangxin Zhang, Ninghan Zhang, Ruiqi Zhang, Jianduan Zhang, Yi-Ge Zhang, Qian-Qian Zhang, Pu-Hong Zhang, Meishan Zhang, Yun-Xiang Zhang, Lirong Zhang, Yan-Qing Zhang, Xiuwen Zhang, Yunhe Zhang, Shuxia Zhang, Kang Zhang, Yongping Zhang, Chen-Yan Zhang, Yihan Zhang, Yingmei Zhang, Jin-Yu Zhang, Xianhua Zhang, Xiao Zhang, Panpan Zhang, Haowen Zhang, Zhiqiang Zhang, Huili Zhang, Yushan Zhang, Yinzhuang Zhang, Zhiyan Zhang, Bingye Zhang, Ruihao Zhang, Kunyi Zhang, Lian-Lian Zhang, Jin-Jing Zhang, Yikai Zhang, Zhaohui Zhang, Hongxin Zhang, Leilei Zhang, Rong Zhang, Xiaonyun Zhang, Haotian Zhang, Chuankuo Zhang, Chong Zhang, Le-Le Zhang, Y Y Zhang, Chao Zhang, Hao-Chen Zhang, Yating Zhang, Jishui Zhang, Wenbo Zhang, Furen Zhang, Jinfan Zhang, Fen Zhang, Yajie Zhang, Chunxia Zhang, Xiu-Li Zhang, Tong-Cun Zhang, Tongxin Zhang, Le Zhang, Churen Zhang, Hongmei Zhang, Xin-Xin Zhang, Huiyuan Zhang, Yiqian Zhang, Aihua Zhang, Qingling Zhang, Yanman Zhang, Jianguang Zhang, Jiaying Zhang, Mingyang Zhang, Guangyuan Zhang, Xinping Zhang, Naixia Zhang, Yi-Hua Zhang, Xuebin Zhang, Tongxue Zhang, Jianshe Zhang, Chenyan Zhang, Yingying Zhang, Michael Zhang, Mengmeng Zhang, Fengshuo Zhang, Yi J Zhang, Cun Zhang, Xiuping Zhang, Shao Zhang, Dong-cui Zhang, Huijun Zhang, Yuan-Yuan Zhang, Chongguo Zhang, Huanxia Zhang, Niankai Zhang, Mengna Zhang, Lianjun Zhang, Anwei Zhang, Xiaoning Zhang, Huafeng Zhang, Xiao-Qi Zhang, Junmin Zhang, Jiecheng Zhang, Qi-Lei Zhang, Ruotian Zhang, Hejun Zhang, Yongsheng Zhang, Mengqi Zhang, Yuxin Zhang, Zengqiang Zhang, Lili Zhang, Ying Zhang, Yi-yi Zhang, Yanxiang Zhang, Hailin Zhang, Yi Ping Zhang, Zhongyang Zhang, Yunhai Zhang, Aimei Zhang, Sai Zhang, Ruixin Zhang, Naijin Zhang, Hanwen Zhang, Yanfei Zhang, Guangliang Zhang, Qihong Zhang, Kaitai Zhang, Xiao-Hua Zhang, Yanqiao Zhang, Xuan Zhang, Suyang Zhang, Jianchao Zhang, Rongcai Zhang, Weiping J Zhang, Chun-Lan Zhang, Duowen Zhang, Chenggang Zhang, Chao-Sheng Zhang, Xiangyang Zhang, Weizhou Zhang, Jianwen Zhang, Yan Zhang, Xijiang Zhang, Yi-Qi Zhang, Wanqi Zhang, Hengyuan Zhang, Zhewei Zhang, Haiwei Zhang, Guangqiong Zhang, Zhiyao Zhang, Ren Zhang, Mengdi Zhang, Shuangxin Zhang, Kan Zhang, Clarence K Zhang, Qishu Zhang, Jinyi Zhang, Tie-mei Zhang, Tuo Zhang, Runyun Zhang, Hongsen Zhang, Hong-Yu Zhang, Mingyuan Zhang, Jingmian Zhang, Lei-Sheng Zhang, Xinyue Zhang, Qingxue Zhang, Meng-Wen Zhang, YiJie Zhang, Xieyi Zhang, Guoxin Zhang, Xinling Zhang, Hengming Zhang, Jinquan Zhang, Zhangjin Zhang, Xi'an Zhang, Kejian Zhang, Liang-Rong Zhang, Baojun Zhang, Yanchao Zhang, Yan-Ling Zhang, Litao Zhang, Xia Zhang, Ruizhong Zhang, Tongwu Zhang, Lingling Zhang, Guicheng Zhang, Caihong Zhang, Yongyan Zhang, Guang-Xian Zhang, Q Y Zhang, Chris Zhiyi Zhang, Feng Zhang, Chuantao Zhang, Yanyi Zhang, Suzhen Zhang, Jimei Zhang, Shuo Zhang, Yue Zhang, W X Zhang, Xuefei Zhang, Haifeng Zhang, Xuehai Zhang, Richard Zhang, Qing-Hui Zhang, Runze Zhang, Chuchu Zhang, Minyue Zhang, Naiqi Zhang, Yong-Liang Zhang, Chang-Hua Zhang, Minying Zhang, Yuansheng Zhang, Maomao Zhang, Yixin Zhang, Hongyi Zhang, Qimin Zhang, Hongyuan Zhang, Quan-bin Zhang, Jianhui Zhang, Tingxue Zhang, Pili Zhang, Zhuohua Zhang, Yunfeng Zhang, Yanlin Zhang, X-T Zhang, Guofu Zhang, Yiren Zhang, Jingyu Zhang, Peiyi Zhang, S Z Zhang, Yajing Zhang, Juqing Zhang, Luzheng Zhang, Yuanzhuang Zhang, Kaihua Zhang, Ming-Liang Zhang, Weisen Zhang, Yupei Zhang, Luwen Zhang, Ruoxuan Zhang, Xiao Min Zhang, Yongxing Zhang, Muqing Zhang, Mingxue Zhang, Guolong Zhang, Jiquan Zhang, Wenjing Zhang, Ziyang Zhang, Changteng Zhang, Jieping Zhang, Jinglu Zhang, Honghe Zhang, Donna Zhang, Yandong Zhang, Chunjun Zhang, Fei Zhang, Jiajing Zhang, Xiaoming Zhang, Jingdan Zhang, Caiping Zhang, Mengzhao Zhang, Si Zhang, Jiankun Zhang, Boqing Zhang, Wang-Dong Zhang, Xindang Zhang, Jiahe Zhang, Qiannan Zhang, Zhibo Zhang, Zijing Zhang, Mei Zhang, Guiliang Zhang, Kaichuang Zhang, Dawei Zhang, Weihua Zhang, Yuhua Zhang, Xuezhi Zhang, Shu-Yang Zhang, Jun-Jie Zhang, Xin-Ye Zhang, Luoping Zhang, Yun Zhang, Jiayan Zhang, Yifan Zhang, Songying Zhang, Xinhua Zhang, Meng Zhang, Yani Zhang, Yuchao Zhang, Lijun Zhang, Zongwang Zhang, Pei Zhang, Peiqin Zhang, Guixiang Zhang, Ruiling Zhang, Liwen Zhang, Ming-Yu Zhang, Ziyu Zhang, Yanyu Zhang, Junping Zhang, Chu-Yue Zhang, Taoyuan Zhang, Lu-Pei Zhang, Junkai Zhang, Chunqing Zhang, S Zhang, Baohu Zhang, Songlin Zhang, Liu Zhang, H F Zhang, Ruixia Zhang, Zhi-Xin Zhang, Hongyan Zhang, Jingfa Zhang, Jing-Lve Zhang, Xiaochen Zhang, Xiangzheng Zhang, Jianbo Zhang, Yiliang Zhang, Yuanhui Zhang, Bo-Ya Zhang, Xiaofeng Zhang, Yanbing Zhang, K Zhang, Zhemei Zhang, Meixian Zhang, Hanqi Zhang, Fangmei Zhang, Mingyao Zhang, Fuxing Zhang, Mengxi Zhang, Yunjia Zhang, Lin Zhang, Weifeng Zhang, Guangji Zhang, Tian Zhang, Meiling Zhang, Xiaobao Zhang, Dongsheng Zhang, Luyao Zhang, Xiaopei Zhang, Zihan Zhang, Bing-Qi Zhang, Kui-ming Zhang, Yanru Zhang, Mingjie Zhang, Lupei Zhang, Junjie Zhang, Xiaocui Zhang, Yali Zhang, Yongheng Zhang, Guilin Zhang, Xiuse Zhang, Shu-Ming Zhang, Yuxia Zhang, Qiuting Zhang, Danning Zhang, Zhi-Jie Zhang, Siqi Zhang, Rongxu Zhang, Tingying Zhang, Claire Y Zhang, Mingxuan Zhang, Lianxin Zhang, Ding Zhang, Lichuan Zhang, Yuejuan Zhang, Dingkai Zhang, Li-Fen Zhang, Zhenyu Zhang, Yingna Zhang, Yuanhao Zhang, Linyou Zhang, Lintao Zhang, Shubing Zhang, Xufang Zhang, Lei-Lei Zhang, Zhi-Peng Zhang, Xiaomeng Zhang, Guoliang Zhang, Xujun Zhang, Ji Yao Zhang, Mengnan Zhang, Shenglan Zhang, Ningkun Zhang, Zhimin Zhang, Zhiwen Zhang, Jiming Zhang, Chuanfu Zhang, Yongwei Zhang, Mao Zhang, PeiFeng Zhang, Jia-Xuan Zhang, Shiyun Zhang, Genxi Zhang, Qingjiong Zhang, Duo Zhang, Qunyuan Zhang, Yan-Chun Zhang, Yongguo Zhang, Qi Zhang, Yaozhengtai Zhang, W G Zhang, Yu-Bo Zhang, Bowen Zhang, Wangping Zhang, Xinhe Zhang, Jinrui Zhang, Yuhan Zhang, Yangqianwen Zhang, Miao-Miao Zhang, Ya-Juan Zhang, Rui Xue Zhang, Dachuan Zhang, Ji Zhang, Chunxiao Zhang, Yaming Zhang, Xinrui Zhang, Bochuan Zhang, Yurou Zhang, Zhuoya Zhang, Ming-Zhu Zhang, Song-Yang Zhang, Ruiyang Zhang, Yang-Yang Zhang, Jinjin Zhang, Xinhong Zhang, Guijie Zhang, Jifa Zhang, Hai Zhang, Dong-Mei Zhang, Jian-Ping Zhang, Zi-Jian Zhang, Xixun Zhang, Haiying Zhang, Guoming Zhang, Jianfa Zhang, Zhi-Qing Zhang, Zhe Zhang, Qilong Zhang, Yingyi Zhang, Xincheng Zhang, Shiquan Zhang, Junhan Zhang, Hai-Ying Zhang, Xiuyun Zhang, Tiefeng Zhang, Chaoyue Zhang, Hailian Zhang, Yunqi Zhang, Zhanjie Zhang, Mei-Ya Zhang, Da-Qi Zhang, Yiheng Zhang, Qingjun Zhang, Wenting Zhang, Ruoshi Zhang, Xiaoyu Zhang, Chenhui Zhang, Baorong Zhang, Yong-Guo Zhang, Xuemin Zhang, Xu Dong Zhang, Jun-Xiao Zhang, Jingshuang Zhang, Zhi-Chang Zhang, Qihao Zhang, Tonghui Zhang, Guanglei Zhang, Jia Zhang, Shiyu Zhang, Hua Zhang, Xue-Ping Zhang, Xiao Bin Zhang, Chunhong Zhang, Huayong Zhang, Jixia Zhang, Tianxiao Zhang, Daoyong Zhang, Xinlei Zhang, Yilin Zhang, Rulin Zhang, Chi Zhang, Cuijuan Zhang, Shanshan Zhang, ChaoDong Zhang, Shaohua Zhang, Quanqi Zhang, Tianxi Zhang, Xinan Zhang, Q-D Zhang, Bingkun Zhang, Haiyue Zhang, Lihua Zhang, Simin Zhang, L Zhang, Nisi Zhang, Guanghui Zhang, Chen-Song Zhang, Rugang Zhang, H-F Zhang, Qi-Ai Zhang, Jiangtao Zhang, Cai Zhang, Youying Zhang, Guimin Zhang, Haopeng Zhang, Wanyu Zhang, Guo-Xiong Zhang, Wenru Zhang, Guoqiang Zhang, Xiuqing Zhang, K Y Zhang, Xinbo Zhang, Weilong Zhang, Tongcun Zhang, Ranran Zhang, Qing-Zhu Zhang, Wanying Zhang, Junpei Zhang, Yonghong Zhang, Hailou Zhang, Qingna Zhang, Tiehua Zhang, Hai-Gang Zhang, Shuwei Zhang, Jiahai Zhang, Hong-Sheng Zhang, Mo Zhang, Mengren Zhang, Renshuai Zhang, Xiao-Jun Zhang, Xinxin Zhang, Pengfei Zhang, Jin-Man Zhang, Shikai Zhang, Wenchao Zhang, Jianxin Zhang, Junzhi Zhang, Jiangang Zhang, Qian ZHANG, Peilin Zhang, Pengpeng Zhang, Daxin Zhang, Shuaishuai Zhang, Kai-Jie Zhang, Ruizhi Zhang, Yutong Zhang, Lanlan Zhang, Huijie Zhang, Jianxia Zhang, Yuxi Zhang, Dong-Hui Zhang, Hai-Bo Zhang, Zhonglin Zhang, Mengjie Zhang, Suya Zhang, Jinwei Zhang, Genglin Zhang, Yun-Feng Zhang, Yubin Zhang, Nong Zhang, Joe Z Zhang, Yupeng Zhang, De-Jun Zhang, Ganlin Zhang, Yanmin Zhang, Jin-Ge Zhang, Qingchuan Zhang, ShiSong Zhang, Yichen Zhang, Yafang Zhang, Lian Zhang, Liwei Zhang, Xuelian Zhang, Yinjiang Zhang, Xiaowan Zhang, Yeqian Zhang, Zaifeng Zhang, Zhehua Zhang, Jianing Zhang, Chen Zhang, Jiejie Zhang, Zhanhao Zhang, Donghui Zhang, Dinghu Zhang, Guochao Zhang, Guohui Zhang, Yingchao Zhang, Zikai Zhang, Danfeng Zhang, Hongmin Zhang, Jinming Zhang, Liying Zhang, Yu Zhang, Liguo Zhang, Yujing Zhang, Jun-Xiu Zhang, Yuanxi Zhang, Peichun Zhang, Yangyu Zhang, Xue-Qing Zhang, Fu-Ping Zhang, Terry Jianguo Zhang, Hongyou Zhang, Xuejiao Zhang, Zhijiao Zhang, Wenhong Zhang, Kezhong Zhang, Yihang Zhang, Qianhui Zhang, Sizhong Zhang, Mingchang Zhang, Shulong Zhang, Kaiming Zhang, Haiming Zhang, Bo-Heng Zhang, Yingzi Zhang, Chunxiang Zhang, Xiayin Zhang, Yumeng Zhang, Hongrong Zhang, Junyu Zhang, Peng-Fei Zhang, Yuanyuan Zhang, Ci Zhang, Zhanming Zhang, Yuanxiang Zhang, Hao-Yu Zhang, Jingzhe Zhang, Junxia Zhang, Xiaogang Zhang, Bingbing Zhang, Liyin Zhang, Shuang Zhang, Cuilin Zhang, Yi-Hang Zhang, Lichao Zhang, Chengnan Zhang, Chengcheng Zhang, Qianru Zhang, Bei Zhang, Manjin Zhang, Mengni Zhang, Hongyang Zhang, Yimin Zhang, Bojian Zhang, Junhui Zhang, Dianzheng Zhang, Chaoqiang Zhang, Huiyu Zhang, Wenjia Zhang, Xin-Yuan Zhang, Yun-Lin Zhang, Yangyang Zhang, Ning-Ping Zhang, Cheng-Wei Zhang, Yaoyao Zhang, Wenguang Zhang, Wei-Jia Zhang, Qiangsheng Zhang, Hongbing Zhang, Xuehong Zhang, Xin Zhang, Xueluo Zhang, Lining Zhang, Fugui Zhang, Hongzhou Zhang, Xinquan Zhang, Huhan Zhang, Gaoxin Zhang, Zhen-lin Zhang, Gong Zhang, Weiling Zhang, Yu-Qiu Zhang, Yulin Zhang, Zhengyun Zhang, Ting Ting Zhang, Xiaofan Zhang, Li Zhang, Zhiyong Zhang, Jieqiong Zhang, Tianlong Zhang, Yingang Zhang, Tianyang Zhang, Yahua Zhang, Weikang Zhang, Zhu-Qin Zhang, Junlong Zhang, Jingwei Zhang, Zenglei Zhang, Chuankuan Zhang, Liangliang Zhang, Guo-Fu Zhang, Wangang Zhang, Peng Zhang, Yaguang Zhang, Xinruo Zhang, Xu-Jun Zhang, Zhihong Zhang, Tianye Zhang, Zhiqiao Zhang, Zhuorong Zhang, Fa Zhang, Min Zhang, Ru Zhang, Yifang Zhang, Jin-Ru Zhang, Yibo Zhang, DanDan Zhang, M H Zhang, Shengnan Zhang, Jiayuan Zhang, Bao-Rong Zhang, Chengxiong Zhang, Ke-Wen Zhang, Zixiong Zhang, Q Zhang, Fred Zhang, G-Y Zhang, Ting-Ting Zhang, Shengli Zhang, Jie Zhang, Nan Yang Zhang, Zhijun Zhang, Bangke Zhang, Hui Z Zhang, Dekai Zhang, Xiaojia Zhang, Jiao Zhang, He Zhang, Bofang Zhang, Jiayi Zhang, Xianxian Zhang, Tianliang Zhang, Zhongheng Zhang, Shiyao Zhang, Xiaojing Zhang, Jinglan Zhang, Minfang Zhang, Xiujie Zhang, Xinhai Zhang, Wenkai Zhang, Feifei Zhang, Chunyan Zhang, Hong-Zhen Zhang, Tingting Zhang, Shuya Zhang, Chao-Yang Zhang, Shang Zhang, Jingrong Zhang, Zheyuan Zhang, Wen-Xin Zhang, Xueying Zhang, W Zhang, Jiangmei Zhang, Shuai-Nan Zhang, Shiping Zhang, Kai Zhang, Y L Zhang, Zhuo-Ya Zhang, Ling-Yu Zhang, Huan-Tian Zhang, Ying E Zhang, Mengliang Zhang, Jingying Zhang, Jingsong Zhang, Yunsheng Zhang, Xuxiang Zhang, Mengyuan Zhang, Xiang Yang Zhang, Hua-Min Zhang, Chenguang Zhang, Ziyue Zhang, Bohao Zhang, Xiulan Zhang, Xiaorong Zhang, Peng-Cheng Zhang, Famin Zhang, Hao Zhang, Yong-hong Zhang, Xiangbin Zhang, Weichen Zhang, Yuheng Zhang, Xu Zhang, Jiang Zhang, Xinjiang Zhang, Chen-Qi Zhang, Lingyan Zhang, Beiyu Zhang, Haipeng Zhang, Dongxin Zhang, Yuzhu Zhang, Cong Zhang, Haihong Zhang, Yanhua Zhang, Jitai Zhang, Shaozhen Zhang, Xinfu Zhang, Pengcheng Zhang, Ruth Zhang, Guangping Zhang, Ben Zhang, Run Zhang, Chan-na Zhang, Jiawen Zhang, Wuhu Zhang, Minhong Zhang, Jiyang Zhang, Dingyi Zhang, Guangxian Zhang, Haolin Zhang, Pei-Weng Zhang, Shu-Zhen Zhang, Yiqing Zhang, Xiu Qi Zhang, Jianguo Zhang, Zhixin Zhang, M Zhang, Muzi Zhang, Huayu Zhang, Jianwei Zhang, Xunming Zhang, Da-Wei Zhang, L F Zhang, Claire Zhang, Xiping Zhang, Yanan Zhang, Z-K Zhang, Jun-ying Zhang, Kaituo Zhang, Peijing Zhang, MeiLu Zhang, Zizhen Zhang, Fengxi Zhang, Yi-Yue Zhang, Melissa C Zhang, Bin Zhang, Xuebao Zhang, Dongjian Zhang, Sophia L Zhang, Anying Zhang, Siyue Zhang, Deyin Zhang, Yuehong Zhang, Lan Zhang, Xiao-Lei Zhang, Dongjie Zhang, Hailei Zhang, Jingting Zhang, Leli Zhang, Lichen Zhang, Haozheng Zhang, Shenqian Zhang, Yin-Hong Zhang, Xuejun C Zhang, Qiu Zhang, Kaiwen Zhang, Joshua Zhang, Fushun Zhang, Hailong Zhang, Haiyan Zhang, Chengfei Zhang, Melody Zhang, Xiaojian Zhang, Shangxiong Zhang, Zhijian Zhang, Zhishuai Zhang, Qingchao Zhang, Zhiwang Zhang, Liming Zhang, Baoren Zhang, Xiuyue Zhang, Huajia Zhang, Yaxin Zhang, Sibin Zhang, Anan Zhang, Linyuan Zhang, Mingai Zhang, Muxin Zhang, Zhongxu Zhang, Xinlin Zhang, Nana Zhang, Xiaoying Zhang, Guodong Zhang, Hong-Xing Zhang, Shaofei Zhang, Fomin Zhang, Jianhai Zhang, Xindong Zhang, Zhenfeng Zhang, Mei-Fang Zhang, Wanjiang Zhang, Naisheng Zhang, Xiaojun Zhang, Meixia Zhang, Hui Zhang, Dong-Wei Zhang, Qiuyang Zhang, Ming-Jun Zhang, Fangting Zhang, Jingxi Zhang, Ruixue Zhang, Mingyue Zhang, Zongxiang Zhang, Yingqi Zhang, Jingqi Zhang, Tong Xuan Zhang, Hanrui Zhang, You-Zhi Zhang, Wendi Zhang, Yunxia Zhang, Chuting Zhang, Xueguang Zhang, Hongliang Zhang, Haojie Zhang, Yanli Zhang, Huanmin Zhang, Zeng Zhang, H Y Zhang, Wancong Zhang, Yi-Xuan Zhang, Xu-Chao Zhang, Mei-Ling Zhang, Xiaoling Zhang, Qiang-Sheng Zhang, Cai-Ling Zhang, Chang Zhang, Xiaotun Zhang, Tianyi Zhang, Sainan Zhang, Guili Zhang, Weibo Zhang, Fangyuan Zhang, Yazhuo Zhang, Zeyuan Zhang, Xiujun Zhang, Stephen X Zhang, Zhaoxue Zhang, Ting Zhang, Rui-Ning Zhang, Xiaoxue Zhang, Hainan Zhang, Zhiye Zhang, Lanfang Zhang, Lingna Zhang, Weimin Zhang, Qingyue Zhang, Limei Zhang, Yuan-Wei Zhang, Haisan Zhang, Yinghui Zhang, Yujia Zhang, Ming-Ming Zhang, Shaoyang Zhang, Jing-Fa Zhang, Hui-Jun Zhang, Jian-Xu Zhang, Yunhui Zhang, Zhiyuan Zhang, Junhua Zhang, Qunfeng Zhang, Boping Zhang, Yaoyang Zhang, Mengxue Zhang, Yinhao Zhang, Hongying Zhang, Jingyue Zhang, Quanfu Zhang, Menghui Zhang, Xueqian Zhang, Keyong Zhang, Zian Zhang, Ning Zhang, Lishuang Zhang, Congen Zhang, Shurui Zhang, Shengding Zhang, Yuping Zhang, Mengyue Zhang, Yuyu Zhang, Ying-Qian Zhang, Huiru Zhang, Jingli Zhang, Wentao Zhang, Haoran Zhang, Sheng-Qiang Zhang, Zhikun Zhang, Yiwen Zhang, Daguo Zhang, R Zhang, June Zhang, Changjing Zhang, Yanna Zhang, Lingjie Zhang, Shuijun Zhang, Zhaohuai Zhang, Xudan Zhang, Jing-Qiu Zhang, Jieying Zhang, Zhihan Zhang, Jiasheng Zhang, Ningzhen Zhang, Menghao Zhang, Xin-Yan Zhang, Yiwei Zhang, Stanley Weihua Zhang, Hongjin Zhang, Shi-Yao Zhang, Zengfu Zhang, Yongfang Zhang, Hongzhong Zhang, Dongdong Zhang, Shuyang Zhang, Qiao-Xia Zhang, Meidi Zhang, Yanfen Zhang, Xinwei Zhang, An-Qi Zhang, Zhaotian Zhang, Yuyan Zhang, Yuwei Zhang, Yusen Zhang, Yin Jiang Zhang, Youti Zhang, Yingli Zhang, Yumei Zhang, Wenxiang Zhang, Yanfeng Zhang, Benyou Zhang, Tianxin Zhang, Duoduo Zhang, Xiao-Chang Zhang, Wei-Na Zhang, Jin Zhang, Ruiying Zhang, Liyu Zhang, Hongxing Zhang, Sen Zhang, Xuting Zhang, Qianjun Zhang, Yunfan Zhang, X-Y Zhang, Zu-Xuan Zhang, Yanbin Zhang, Xiao-Ling Zhang, Xinjun Zhang, An Zhang, Yanting Zhang, Shi-Han Zhang, Nan Zhang, Shaochun Zhang, Shi-Jie Zhang, Qiong Zhang, Xinyao Zhang, Yadong Zhang, Shushan Zhang, Jinying Zhang, Xiaotian Zhang, Jinhui Zhang, Shucong Zhang, Qiwei Zhang, Weiyu Zhang, X Y Zhang, Wenxi Zhang, Gang Zhang, Shan-Shan Zhang, Weilin Zhang, Chenglong Zhang, Andrew Zhang, Jingru Zhang, Zhaoqi Zhang, Yafeng Zhang, Bi-Tian Zhang, Liqian Zhang, Hefang Zhang, Meimei Zhang, Gan Zhang, Jinyu Zhang, Boxi Zhang, Jinghui Zhang, Zhengliang Zhang, Xiao-Xuan Zhang, Deyi Zhang, Chaoyang Zhang, Kunshan Zhang, Chen-Xi Zhang, Wenxin Zhang, Zhenzhu Zhang, Zaijun Zhang, Liyan Zhang, M J Zhang, Qiang Zhang, Zhentao Zhang, Wenzhong Zhang, Chenxi Zhang, Bo Zhang, Jianling Zhang, Vita Zhang, Ji-Yuan Zhang, Yonglian Zhang, Guorui Zhang, Junling Zhang, Xiao Yu Cindy Zhang, Haihua Zhang, Wenyi Zhang, Yidan Zhang, Tiejun Zhang, Yanjiao Zhang, Renhe Zhang, Ximei Zhang, Yiting Zhang, Menglu Zhang, Xiao-Chong Zhang, Jia-Bao Zhang, Shupeng Zhang, Ruilin Zhang, Donghua Zhang, Shiti Zhang, Zilu Zhang, Tiane Zhang, Xiang Zhang, Tongtong Zhang, Shengming Zhang, Y Zhang, Yu-Yu Zhang, Zengdi Zhang, Laihong Zhang, Ruxuan Zhang, Danhua Zhang, Youjin Zhang, Yuke Zhang, Sheng-Xiao Zhang, Zhongxin Zhang, Yuting Zhang, Shihan Zhang, Jinsong Zhang, Xiaolei Zhang, Yu Chen Zhang, Yefan Zhang, Jianmei Zhang, J-Y Zhang, Minghao Zhang, Yafei Zhang, Huawen Zhang, Junxiao Zhang, Jinsu Zhang, Yuxuan Zhang, Zhen Zhang, Cheng Cheng Zhang, Jingyao Zhang, Yi-Chi Zhang, Dongyan Zhang, Haoyuan Zhang, Yiyi Zhang, Yi-Ming Zhang, J Zhang, Mingdi Zhang, Huiping Zhang, Shuchen Zhang, Tongfu Zhang, Yaling Zhang, Huibing Zhang, Hugang Zhang, Danyang Zhang, Yuhao Zhang, Xibo Zhang, Keyi Zhang, Xiaozhe Zhang, Hongjia Zhang, Chenrui Zhang, Chaobao Zhang, Dan Zhang, Changhui Zhang, Wei-Yi Zhang, Simeng Zhang, Lianfeng Zhang, Qingtian Zhang, Xiuxing Zhang, Yongguang Zhang, Changjiang Zhang, Jinxiu Zhang, Xiling Zhang, Zhan-Xiong Zhang, Tianpeng Zhang, Mingzhao Zhang, Dan-Dan Zhang, Renbo Zhang, Yujin Zhang, Xiaochun Zhang, Xinjing Zhang, Yufang Zhang, Zhongwei Zhang, Lina Zhang, Enhui Zhang, Ningning Zhang, Yunfei Zhang, Jiqiang Zhang, Ping Zhang, Jing-Bo Zhang, Zeming Zhang, Jicai Zhang, Yikun Zhang, Fuyang Zhang, Yuanchao Zhang, Sihe Zhang, Haixia Zhang, Zaiqi Zhang, Shilei Zhang, Yayong Zhang, Wenlong Zhang, Zhiguo Zhang, Jiajia Zhang, Hansi Zhang, Yerui Zhang, Zhong-Yuan Zhang, Xiaoqing Zhang, Yuchi Zhang, Yu-Qi Zhang, Shun-Bo Zhang, Xueqin Zhang, Tian-Yu Zhang, Fengxia Zhang, Tengfang Zhang, Shiyi Zhang, Li-ping Zhang, Changquan Zhang, Rusi Zhang, Xueqia Zhang, Yimei Zhang, Ziyin Zhang, Chungu Zhang, Yufeng Zhang, Lingyu Zhang, Sisi Zhang, Changhua Zhang, Xue Zhang, Wen Zhang, Changwang Zhang, XiaoYi Zhang, Keyu Zhang, Runxiang Zhang, C D Zhang, Xi-Feng Zhang, Dadong Zhang, XueWu Zhang, Ziguo Zhang, Zhuqing Zhang, Shuhong Zhang, Di Zhang, J B Zhang, Ningzhi Zhang, Yiwan Zhang, Jennifer Y Zhang, Jiaxin Zhang, Peiwen Zhang, Hanchao Zhang, Tao-Lan Zhang, Sujiang Zhang, Chenyi Zhang, Yizhi Zhang, H D Zhang, Xu-Mei Zhang, Longzhen Zhang, Shiwu Zhang, Longlong Zhang, Pumin Zhang, Fuhan Zhang, Yingjie Zhang, Yong Zhang, H P Zhang, Feixue Zhang, Yuyuan Zhang, Kai-Qiang Zhang, Ye Zhang, Yujiao Zhang, Ruiqian Zhang, Hanxu Zhang, Zhengyu Zhang, Xiuyin Zhang, Tongshuo Zhang, Aijun Zhang, Lanjun Zhang, Mi Zhang, Gu Zhang, JingZi Zhang, Sheng Zhang, Man Zhang, Xinqiao Zhang, Ruikun Zhang, Hai-Feng Zhang, Zongping Zhang, Da Zhang, Xingyu Zhang, Shuanglu Zhang, Shun Zhang, Haoyu Zhang, Chuanyong Zhang, Rey M Zhang, Dongying Zhang, Yunqiang Zhang, Huifang Zhang, Shengye Zhang, Mingxiang Zhang, Wenjuan Zhang, Pinggen Zhang, John H Zhang, Chong-Hui Zhang, Ran Zhang, Minghui Zhang, Wencong Zhang, Ruiyan Zhang, Tianfeng Zhang, Yihao Zhang, Nu Zhang, Shenqi Zhang, Yao-Hua Zhang, Ai-Min Zhang, Shaozhao Zhang, Zhao-Huan Zhang, Jiacheng Zhang, Shao-Qi Zhang, Tian-Guang Zhang, Jibin Zhang, Chenjie Zhang, Meiwei Zhang, Sixue Zhang, Yongchang Zhang, Ying-Lin Zhang, Hongju Zhang, Xianhong Zhang, Ming-Rong Zhang, Benjian Zhang, Binbin Zhang, Meiyu Zhang, Shuwan Zhang, Weizheng Zhang, Yuyanan Zhang, Zhen-Jie Zhang, Hong Zhang, Qian-Wen Zhang, Chuan Zhang, Zhijing Zhang, Xiaoxin Zhang, Yexiang Zhang, Yonghui Zhang, Mingying Zhang, Qin Zhang, Chengrui Zhang, Zijiao Zhang, Xueli Zhang, Yizhe Zhang, Qingyun Zhang, Nannan Zhang, Shuyuan Zhang, Linan Zhang, Jifeng Zhang, Qilu Zhang, Xudong Zhang, Zhanyi Zhang, Shenglei Zhang, Xueping Zhang, Rongguang Zhang, Bing Zhang, Y H Zhang, Yu-Fei Zhang, Zhaocong Zhang, Haibo Zhang, Guojun Zhang, Na Zhang, Lijian Zhang, Huixin Zhang, Yuanzhen Zhang, Yaxuan Zhang, Liangdong Zhang, Donglei Zhang, Huilin Zhang, Shanhong Zhang, Xinyu Zhang, Jianming Zhang, Jiehao Zhang, Weiqin Zhang, Huizhen Zhang, Xian-Li Zhang, Libo Zhang, Guomin Zhang, Jianglin Zhang, Yu-Jing Zhang, Fuming Zhang, Guangye Zhang, Zhezhe Zhang, Qingshuang Zhang, Xianglian Zhang, Saidan Zhang, Mei-Qing Zhang, Shunfen Zhang, Xueming Zhang, Ling Zhang, Hanyu Zhang, Bao-Fu Zhang, XiHe Zhang, Rongxin Zhang, Karen Zhang, Liang Zhang, Junqing Zhang, Yuanqiang Zhang, Pengbo Zhang, H Zhang, Jingdong Zhang, Wenxue Zhang, Xiaocong Zhang, Jia-Su Zhang, Ya-Li Zhang, Haisen Zhang, Meijia Zhang, Jingliang Zhang, Qianqian Zhang, Yonggen Zhang, Shunming Zhang, Aileen Zhang, Hanwang Zhang, Zhihao Zhang, Zhi-Shuai Zhang, Xinlong Zhang, Jintao Zhang, Jingxue Zhang, Yinci Zhang, L-S Zhang, Ailin Zhang, Shuli Zhang, Zhizhong Zhang, Kewen Zhang, Jishou Zhang, Lusha Zhang, Guosen Zhang, Qinghong Zhang, Mengqiu Zhang, Shichao Zhang, Suming Zhang, Chengxiang Zhang, Linlin Zhang, Zhengbin Zhang, Mianzhi Zhang, Ziyi Zhang, En Zhang, Zhiqian Zhang, Chonghe Zhang, Dong-Ying Zhang, Hong-Jie Zhang, Bingqiang Zhang, Jingyi Zhang, Jianan Zhang, Yuying Zhang, Chunling Zhang, Jianbin Zhang, Kaige Zhang, Ying-Jun Zhang, Yue-Bo Zhang, Zicheng Zhang, Cuiyu Zhang, Jiuwei Zhang, Zishuo Zhang, Yihui Zhang, Jia-Si Zhang, Chenlin Zhang, Deqiang Zhang, Zhengxiang Zhang, Luo Zhang, Lilei Zhang, Tianyu Zhang, Keshan Zhang, Qunchen Zhang, Xinlu Zhang, Yuqing Zhang, Guisen Zhang, Mengguo Zhang, N Zhang, Zhi-Shuo Zhang, Lv-Lang Zhang, Lucia Zhang, Hongjuan Zhang, Quanquan Zhang, Shuyi Zhang, Chuyue Zhang, Junfeng Zhang, Hai-Man Zhang, Chun Zhang, Lihong Zhang, Kui Zhang, Hongcai Zhang, Zhuqin Zhang, Yongliang Zhang, Yueru Zhang, Zufa Zhang, Xinye Zhang, Zhong-Bai Zhang, Kejun Zhang, Huimao Zhang, Ruo-Xin Zhang, Pengwei Zhang, Xinfeng Zhang, Zhaohuan Zhang, Shu-Fan Zhang, Lukuan Zhang, Xiu-Peng Zhang, Zhaohua Zhang, Yiping Zhang, Chengwu Zhang, Hang Zhang, Yao Zhang, Wenming Zhang, Luanluan Zhang, Haicheng Zhang, Yanming Zhang, Yajun Zhang, Xingen Zhang, Honglei Zhang, Xingyuan Zhang, Sumei Zhang, Wenyuan Zhang, Rong-Kai Zhang, Guixia Zhang, Jianliang Zhang, QiYue Zhang, Xinbao Zhang, Qinghua Zhang, Jianting Zhang, Xingxing Zhang, Xueyi Zhang, Yi-Wei Zhang, Weijian Zhang, Detao Zhang, Shaofeng Zhang, Yina Zhang, Yu-Hui Zhang, Zhou Zhang, Bo-Fei Zhang, Bixia Zhang, Yuyang Zhang, Chuanmao Zhang, Hongya Zhang, Shuai Zhang, XiaoPing Zhang, Huabing Zhang, Yili Zhang, Dianbo Zhang, Huiying Zhang, Qiuxia Zhang, Xiyu Zhang, Chenyang Zhang, Wanting Zhang, Ni Zhang, Rongying Zhang, Zebang Zhang, Fengshi Zhang, Wannian Zhang, Xiao-Yong Zhang, Xue-Qin Zhang, Chunli Zhang, Ti Zhang, Lifan Zhang, Guanqun Zhang, Erchen Zhang, Chenhong Zhang, Xiaopo Zhang, Dingyu Zhang, Lie Zhang, Mingfeng Zhang, Lu-Yang Zhang, M Q Zhang, Yvonne Zhang, Sheng-Hong Zhang, Li-Jie Zhang, Huanqing Zhang, Shen Zhang, Jun Zhang, Qiguo Zhang, Teng Zhang, Haikuo Zhang, Gary Zhang, Ziping Zhang, Bei-Bei Zhang, Changlin Zhang, Aimin Zhang, Xiao-Feng Zhang, Zepeng Zhang, Zixuan Zhang, Yuan Zhang, Xiaolong Zhang, Junpeng Zhang, Boya Zhang, Fuyuan Zhang, Xiao-Qian Zhang, Zongquan Zhang, Hongyun Zhang, Yaqi Zhang, Tinghu Zhang, Xingyi Zhang, Kejia Zhang, Qiaofang Zhang, Zhicong Zhang, Xiao-Lin Zhang, Gumuyang Zhang, Xingang Zhang, Honghong Zhang, Haoyue Zhang, Shuran Zhang, Hai-Han Zhang, Yihong Zhang, Zhishang Zhang, Qing Zhang, Wenhua Zhang, Chenlu Zhang, G Zhang, Yalan Zhang, Xiaodan Zhang, Geyang Zhang, Lianbo Zhang, Aixiang Zhang, Yujie Zhang, Xiushan Zhang, Xuening Zhang, Xiao-Wei Zhang, Lulu Zhang, Linda S Zhang, Jue Zhang, Linli Zhang, Hongting Zhang, Mengjia Zhang, Huayang Zhang, Cuihua Zhang, Liuwei Zhang, Jing Jing Zhang, Wen-Jing Zhang, Shimao Zhang, Xuewei Zhang, Jingning Zhang, Wanjun Zhang, Yaoxin Zhang, Mingzhen Zhang, Jingxuan Zhang, Mei-Zhen Zhang, Lin-Jie Zhang, Yongfeng Zhang, Lida Zhang, Xuemei Zhang, Ziheng Zhang, Sha Zhang, Jin-Rui Zhang, Wenhao Zhang, Yue-Ming Zhang, Ping-Fan Zhang, Wenjun Zhang, Yutian Zhang, Jiankang Zhang, Xiaobo Zhang, Xian-Man Zhang, Xilin Zhang, Chun-Mei Zhang, Junyan Zhang, Xiu-Juan Zhang, Bingxue Zhang, Liyun Zhang, Dingdong Zhang, Shuye Zhang, Zilong Zhang, Lijuan Zhang, Fang Zhang, Yunli Zhang, Yonggang Zhang, Jinze Zhang, Ling Xia Zhang, Xiaochang Zhang, Chenzi Zhang, Zi-Feng Zhang, Zai-Rong Zhang, Xueting Zhang, Liping Zhang, Xiupeng Zhang, Yanling Zhang, Qiaoxuan Zhang, Donna D Zhang, Zhenhua Zhang, Bohong Zhang, Wenhui Zhang, Shouyue Zhang, Chunguang Zhang, Jingwen Zhang, Jiuxuan Zhang, Xinke Zhang, David Y Zhang, Qun Zhang, Qingyu Zhang, Jian Zhang, Kejin Zhang, Shenglai Zhang, Jiupan Zhang, Xiaosheng Zhang, Mengzhen Zhang, Jinjing Zhang, Youwen Zhang, Yu-Jie Zhang, Alex R Zhang, Yanyan Zhang, Igor Ying Zhang, Kangjun Zhang, Guihua Zhang, Shaojun Zhang, Jianqiong Zhang, Xuexi Zhang, Sifan Zhang, Shuyan Zhang, Xin-Hui Zhang, Xiaobiao Zhang, Junyi Zhang, Susie Zhang, Fubo Zhang, Pan-Pan Zhang, Zhiyu Zhang, Taojun Zhang, Dongfeng Zhang, Dong-juan Zhang, Yi-Feng Zhang, Pan Zhang, Dapeng Zhang, Yukun Zhang, Yingnan Zhang, Yi-Wen Zhang, Tiantian Zhang, Weiwei Zhang, Yuanyi Zhang, Xiaotian Michelle Zhang, Bikui Zhang, Zhihua Zhang, Yadi Zhang, Xingan Zhang, Rui Zhang, Kang-Ling Zhang, Yiguo Zhang, Hongwu Zhang, Hua-Xiong Zhang, Wenqian Zhang, Caishi Zhang, Nan-Nan Zhang, Zhong Zhang, Jingxiao Zhang, Xiaoqi Zhang, Limin Zhang, Zhiyi Zhang, Xiongjun Zhang, Yunqing Zhang, Zhenhao Zhang, Xiuqin Zhang, Zhi Zhang, Chunying Zhang, Fengqing Zhang, Zhanjun Zhang, Zhengxing Zhang, Lixing Zhang, Haojun Zhang, Licui Zhang, Lele Zhang, YiPei Zhang, Shining Zhang, Xiaoyun Zhang, Yannan Zhang, Weili Zhang, Yitian Zhang, Hongfeng Zhang, Yanghui Zhang, Zhifei Zhang, Guo-Liang Zhang, Xiaoxian Zhang, Jiawei Zhang, Jimmy Zhang, Xingxu Zhang, Haohao Zhang, Leiying Zhang, Jihang Zhang, Hui-Wen Zhang, Yongbao Zhang, Ruohan Zhang, Zhuojun Zhang, Rui-fang Zhang, Youmin Zhang, Jing-Zhan Zhang, Dong-qiang Zhang, Yameng Zhang, Xuewen Zhang, Zhiyun Zhang, Jamie Zhang, Yunhang Zhang, Mingyi Zhang, Yujuan Zhang, Lanju Zhang, Longxin Zhang, Runcheng Zhang, Yiyuan Zhang, Hongfu Zhang, Xian-Bo Zhang, Xiao-Hong Zhang, Zhong-Yi Zhang, Si-Zhong Zhang, Yongfa Zhang, Qingcheng Zhang, Yeting Zhang, Guang-Ya Zhang, Juan-Juan Zhang, Mengxian Zhang, Hailiang Zhang, Yuzhi Zhang, Shuge Zhang, Peijun Zhang, Jian-Guo Zhang, Xiaowei Zhang, Yidong Zhang, Zheng Zhang, Zengtie Zhang, Xiangfei Zhang, Dengke Zhang, Xiaohui Zhang, Zhewen Zhang, Jing Zhang, Danyan Zhang, Juan Zhang, Mingyang A Zhang, Xiangsong Zhang, Yingze Zhang, Wen Jun Zhang, Wenbin Zhang, Qi-Min Zhang, X N Zhang, Junli Zhang, Jianying Zhang, Jiaqi Zhang, Yuemei Zhang, Huaiyong Zhang, Yuehua Zhang, Ruisan Zhang, Huihui Zhang, Dalong Zhang, Xiaohong Zhang, Zhongyi Zhang, Rongyu Zhang, Chenming Zhang, Yaru Zhang, Xueya Zhang, Jingping Zhang, Keke Zhang, YuHong Zhang, Junran Zhang, Xingwei Zhang, Biao Zhang, Song Zhang, Xiaodong Zhang, Shiwen Zhang, Kuo Zhang, Yongqiang Zhang, Xiao-Cheng Zhang, Ruyi Zhang, Tong Zhang, Shi-Meng Zhang, Junxiu Zhang, Jun-Feng Zhang, Guo-Guo Zhang, David Zhang, Zhiru Zhang, Kailin Zhang, Zhuo Zhang, Huiming Zhang, Zhuang Zhang, Caiqing Zhang, Jingchuan Zhang, Zixu Zhang, Ruxiang Zhang, Channa Zhang, Shu-Min Zhang, Xiaohan Zhang, Shengkun Zhang, Chunhua Zhang, Xixi Zhang, Xiaoyan Zhang, C H Zhang, Haijun Zhang, H X Zhang, Jingyuan Zhang, Weipeng Zhang, Yipeng Zhang, Ao Zhang, Yaodong Zhang, Mingxiu Zhang, Weiyi Zhang, Xiaoxiao Zhang, Delai Zhang, Mu Zhang, Yanquan Zhang, Liangming Zhang, Yuling Zhang, Jerry Z Zhang, Bicheng Zhang, Lijiao Zhang, Yige Zhang, Yanju Zhang, Shan Zhang, Kaihui Zhang, Chaoke Zhang, Zhenlin Zhang, Tangjuan Zhang, Lingli Zhang, Yuqi Zhang, Luo-Meng Zhang, Haiwang Zhang, Haibing Zhang, Miao Zhang, Miaomiao Zhang, Yimeng Zhang, Anli Zhang, Yun-Sheng Zhang, Yamin Zhang, Yongchao Zhang, Huize Zhang, Yingqian Zhang, Ruizhe Zhang, Wei Zhang, Yongci Zhang, Zhen-Tao Zhang, Daolai Zhang, Zeyan Zhang, Zhaoping Zhang, Xing Zhang, Zhicheng Zhang, Yuanqing Zhang, Zhiping Zhang, J Y Zhang, Yibin Zhang, Rui Yan Zhang, Lun Zhang, Yirong Zhang, Zewen Zhang, Yiming Zhang, Yongxiang Zhang, Xiaoyue Zhang, Xinlian Zhang, Baotong Zhang, Ruimin Zhang, Guohua Zhang, Xiao-Shuo Zhang, Ya-Meng Zhang, Zhenyang Zhang, Lifang Zhang, Shaochuan Zhang, Mingtong Zhang, Kefen Zhang, Tonghan Zhang, Xiaojin Zhang, Qiangyan Zhang, Renliang Zhang, Meng-Jie Zhang, Zhaofeng Zhang, Jiayin Zhang, Guoying Zhang, Guoping Zhang, Chumeng Zhang, Weixia Zhang, Yu-Zhe Zhang, A-Mei Zhang, YuHang Zhang, Xiaokui Zhang, Hui Hua Zhang, Rongrong Zhang, Boyan Zhang, Jiabi Zhang, Zijian Zhang, Xing Yu Zhang, Shou-Mei Zhang, Shu-Dong Zhang, Minzhu Zhang, Yongpeng Zhang, Yuchen Zhang, Yin Zhang, Hanting Zhang, Lantian Zhang, Jing-Chang Zhang, Jiahao Zhang, Zengrong Zhang, Shao Kang Zhang, Cheng Zhang, Jiuchun Zhang, Huawei Zhang, Xueyan Zhang, Huimin Zhang, Bei B Zhang, Saifei Zhang, Qinjun Zhang, Leili Zhang, Yuru Zhang, Huan Zhang, Haojian Zhang, Leitao Zhang, Minghang Zhang, Junru Zhang, Lu Zhang, Heng Zhang, Weiguo Zhang, Pingchuan Zhang, Amy L Zhang, Alaina Zhang, Fanghong Zhang, Yuzhe Zhang, Jinbiao Zhang, Junmei Zhang, Sheng-Dao Zhang, Liuming Zhang, Chenshuang Zhang, Mengying Zhang, Q L Zhang, Xian Zhang, Ke-lan Zhang, Rui-Nan Zhang, Huaqiu Zhang, Minzhi Zhang, Junhang Zhang, Chen-Ran Zhang, Wenli Zhang, Dian Ming Zhang, Jiachao Zhang, Yanjun Zhang, Linbo Zhang, Yunpeng Zhang, Y-H Zhang, Xiaolan Zhang, Yun-Mei Zhang, Bolin Zhang, Jianhua Zhang, Zhigang Zhang, Dongyang Zhang, Jingchun Zhang, Zekun Zhang, Huanyu Zhang, Guoli Zhang, Lufei Zhang, Qingquan Zhang, Deng-Feng Zhang, Xi Zhang, Yi Zhang, Yakun Zhang, Shu-Fang Zhang, Kun Zhang, Ruoying Zhang, Qun-Feng Zhang, Peizhen Zhang, Zhongjie Zhang, Yuhui Zhang, Yongyun Zhang, Xiaofang Zhang, Pengyuan Zhang, Guozhi Zhang, Lianmei Zhang, Jingjing Zhang, Xiaomin Zhang, Shujun Zhang, Weina Zhang, Mingqi Zhang, Sulin Zhang, Yongjie Zhang, Cuiping Zhang, Shiqi Zhang, Qingxiu Zhang, Chengsheng Zhang, Lunan Zhang, Jianxiang Zhang, Zengli Zhang, Haibei Zhang, Guoqing Zhang, Houbin Zhang, Jiaming Zhang, Chun-Qing Zhang, Zhixia Zhang, Xuhao Zhang, Xiangyu Zhang, Yan-Min Zhang, Xiuxiu Zhang, Guofeng Zhang, Bao Long Zhang, Chenan Zhang, Yucai Zhang, Can Zhang, Xingcai Zhang, Xinglai Zhang, H W Zhang, Zhu Zhang, Yuebin Zhang
articles

Downregulated RRS1 inhibits invasion and metastasis of BT549 through RPL11‑c‑Myc‑SNAIL axis.

Runze Wang, Cuixiu Peng, Junying Song +8 more · 2022 · International journal of oncology · added 2026-04-24
Regulator of ribosome synthesis 1 (RRS1) is a key factor in ribosome biosynthesis and other cellular functions. High level of RRS1 in breast cancer cell lines is associated with increased cell prolife Show more
Regulator of ribosome synthesis 1 (RRS1) is a key factor in ribosome biosynthesis and other cellular functions. High level of RRS1 in breast cancer cell lines is associated with increased cell proliferation, invasion and migration. RRS1 controls the assembly of the 60s subunit and maturation of 25S rRNA during ribosome biosynthesis. In this study, lentiviral transfection of sh‑RNA was used to knock down the level of RRS1, to detect the effect of RRS1 on cell function and to explore the specific mechanism of RRS1 affecting cell invasion and metastasis by COIP and dual‑luciferase reporter gene assays. The present study found that RRS1 knockdown reduced the accumulation of ribosome protein L11 (RPL11) in the nucleolus, which then migrated to the nucleoplasm and bound to c‑Myc. This inhibited trans‑activation of SNAIL by c‑Myc and eventually decreased the invasion and metastasis capacity of the human breast cancer cell line BT549. Taken together, RRS1 regulates invasion and metastasis of human breast cancer cells through the RPL11‑c‑Myc‑SNAIL axis. The findings are of great significance for exploring the mechanism of breast cancer invasion and metastasis and the corresponding regulatory factors. Show less
no PDF DOI: 10.3892/ijo.2022.5323
SNAI1

Silencing of AKIP1 Suppresses the Proliferation, Migration, and Epithelial-Mesenchymal Transition Process of Glioma Cells by Upregulating DLG2.

ZhaoHui Chen, Haitao Wen, Jinwei Zhang +2 more · 2022 · BioMed research international · added 2026-04-24
Gliomas, the most prevalent brain tumors, account for nearly one-third of the all brain and central nervous system (CNS) tumors diagnosed in the USA. The purpose of this study was to discuss the impor Show more
Gliomas, the most prevalent brain tumors, account for nearly one-third of the all brain and central nervous system (CNS) tumors diagnosed in the USA. The purpose of this study was to discuss the important role of A kinase-interacting protein 1 (AKIP1) in glioma and reveal the potential mechanism. After prediction by CCLE, the expression of AKIP1 was determined by qRT-PCR and western blot. The impacts of AKIP1 knockdown on the proliferation, migration, and invasion were then measured by MTT, colony formation assay, wound healing, and transwell assays. Western blot was used to assess the protein levels of migration and epithelial-mesenchymal transition- (EMT-) related factors. Subsequently, the expression of Disks Large Homolog 2 (DLG2) was predicted by bioinformatics analyses, and the interaction between AKIP1 and DLG2 was confirmed by IP assay, qRT-PCR, and western blot. Finally, DLG2 was further downregulated in glioma cells to detect the association between AKIP1 and DLG2 in the cellular functions of glioma. It was demonstrated that AKIP1 exhibited a high level in glioma cells, and interference of AKIP1 led to reductions in the proliferation, migration, invasion, and EMT of glioma cells. DLG2, which was lowly expressed in glioma cells, demonstrated a negative link to AKIP2. Inhibition of both AKIP2 and DLG2 counteracted the inhibited cellular behaviors on account of AKIP1 interference. To be concluded, this study presented evidence that AKIP1 silencing suppressed the progression of glioma via targeting DLG2, which could provide novel insights to impede the development of glioma. Show less
📄 PDF DOI: 10.1155/2022/5648011
DLG2

mTOR pathway gene mutations predict response to immune checkpoint inhibitors in multiple cancers.

Lei Cheng, Yanan Wang, Lixin Qiu +10 more · 2022 · Journal of translational medicine · BioMed Central · added 2026-04-24
mTOR pathway is known to promote cancer malignancy and influence cancer immunity but is unknown for its role in immune checkpoint inhibitors (ICI) therapy. Using Memorial Sloan-Kettering Cancer Center Show more
mTOR pathway is known to promote cancer malignancy and influence cancer immunity but is unknown for its role in immune checkpoint inhibitors (ICI) therapy. Using Memorial Sloan-Kettering Cancer Center dataset (MSKCC), we extracted mTOR pathway gene mutations for stepwise Cox regression in 1661 cancer patients received ICI. We associated the mutation of the gene signature resulted from the stepwise Cox regression with the 1661 patients' survival. Other 553 ICI-treated patients were collected from 6 cohorts for validation. We also performed this survival association in patients without ICI treatment from MSKCC as discovery (n = 2244) and The Cancer Genome Atlas (TCGA) as validation (n = 763). Pathway enrichment analysis were performed using transcriptome profiles from TCGA and IMvigor210 trial to investigate the potential mechanism. We identified 8 genes involved in mTOR pathway, including FGFR2, PIK3C3, FGFR4, FGFR1, FGF3, AKT1, mTOR, and RPTOR, resulted from stepwise Cox regression in discovery (n = 1661). In both discovery (n = 1661) and validation (n = 553), the mutation of the 8-gene signature was associated with better survival of the patients treated with ICI, which was independent of tumor mutation burden (TMB) and mainly attributed to the missense mutations. This survival association was not observed in patients without ICI therapy. Intriguingly, the mutation of the 8-gene signature was associated with increased TMB and PD1/PD-L1 expression. Immunologically, pathways involved in anti-tumor immune response were enriched in presence of this mutational signature in mTOR pathway, leading to increased infiltration of immune effector cells (e.g., CD8 + T cells, NK cells, and M1 macrophages), but decreased infiltration of immune inhibitory M2 macrophages. These results suggested that mTOR pathway gene mutations were predictive of better survival upon ICI treatment in multiple cancers, likely by its association with enhanced anti-tumor immunity. Larger studies are warranted to validate our findings. Show less
no PDF DOI: 10.1186/s12967-022-03436-1
PIK3C3

dSec16 Acting in Insulin-like Peptide Producing Cells Controls Energy Homeostasis in Drosophila.

Ruo-Xin Zhang, Sha-Sha Li, An-Qi Li +3 more · 2022 · Life (Basel, Switzerland) · MDPI · added 2026-04-24
Many studies show that genetics play a major contribution to the onset of obesity. Human genome-wide association studies (GWASs) have identified hundreds of genes that are associated with obesity. How Show more
Many studies show that genetics play a major contribution to the onset of obesity. Human genome-wide association studies (GWASs) have identified hundreds of genes that are associated with obesity. However, the majority of them have not been functionally validated. Show less
no PDF DOI: 10.3390/life13010081
SEC16B

Effect of high glucose on glycosaminoglycans in cultured retinal endothelial cells and rat retina.

Gaganpreet Kaur, Yuefan Song, Ke Xia +4 more · 2022 · Glycobiology · Oxford University Press · added 2026-04-24
The endothelial glycocalyx regulates vascular permeability, inflammation, and coagulation, and acts as a mechanosensor. The loss of glycocalyx can cause endothelial injury and contribute to several mi Show more
The endothelial glycocalyx regulates vascular permeability, inflammation, and coagulation, and acts as a mechanosensor. The loss of glycocalyx can cause endothelial injury and contribute to several microvascular complications and, therefore, may promote diabetic retinopathy. Studies have shown a partial loss of retinal glycocalyx in diabetes, but with few molecular details of the changes in glycosaminoglycan (GAG) composition. Therefore, the purpose of our study was to investigate the effect of hyperglycemia on GAGs of the retinal endothelial glycocalyx. GAGs were isolated from rat retinal microvascular endothelial cells (RRMECs), media, and retinas, followed by liquid chromatography-mass spectrometry assays. Quantitative real-time polymerase chain reaction was used to study mRNA transcripts of the enzymes involved in GAG biosynthesis. Hyperglycemia significantly increased the shedding of heparan sulfate (HS), chondroitin sulfate (CS), and hyaluronic acid (HA). There were no changes to the levels of HS in RRMEC monolayers grown in high-glucose media, but the levels of CS and HA decreased dramatically. Similarly, while HA decreased in the retinas of diabetic rats, the total GAG and CS levels increased. Hyperglycemia in RRMECs caused a significant increase in the mRNA levels of the enzymes involved in GAG biosynthesis (including EXTL-1,2,3, EXT-1,2, ChSY-1,3, and HAS-2,3), with these increases potentially being compensatory responses to overall glycocalyx loss. Both RRMECs and retinas of diabetic rats exhibited glucose-induced alterations in the disaccharide compositions and sulfation of HS and CS, with the changes in sulfation including N,6-O-sulfation on HS and 4-O-sulfation on CS. Show less
no PDF DOI: 10.1093/glycob/cwac029
EXT1

Implications of structural right ventricular involvement in patients with hypertrophic cardiomyopathy.

Yu Zhang, Yuming Zhu, Mo Zhang +9 more · 2022 · European heart journal. Quality of care & clinical outcomes · Oxford University Press · added 2026-04-24
In the clinical practice, the right ventricular (RV) manifestations have received less attention in hypertrophic cardiomyopathy (HCM). This paper aimed to evaluate the risk prediction value and geneti Show more
In the clinical practice, the right ventricular (RV) manifestations have received less attention in hypertrophic cardiomyopathy (HCM). This paper aimed to evaluate the risk prediction value and genetic characteristics of RV involvement in HCM patients. A total of 893 patients with HCM were recruited. RV hypertrophy, RV obstruction, and RV late gadolinium enhancement were evaluated by echocardiography and/or cardiac magnetic resonance. Patients with any of the above structural abnormalities were identified as having RV involvement. All patients were followed with a median follow-up time of 3.0 years. The primary endpoint was cardiovascular death; the secondary endpoints were all-cause death and heart failure (HF)-related death. Survival analyses were conducted to evaluate the associations between RV involvement and the endpoints. Genetic testing was performed on 669 patients. RV involvement was recognized in 114 of 893 patients (12.8%). Survival analyses demonstrated that RV involvement was an independent risk factor for cardiovascular death (P = 0.002), all-cause death (P = 0.011), and HF-related death (P = 0.004). These outcome results were then confirmed by a sensitivity analysis. Genetic testing revealed a higher frequency of genotype-positive in patients with RV involvement (57.0% vs. 31.0%, P < 0.001), and the P/LP variants of MYBPC3 were more frequently identified in patients with RV involvement (30.4% vs. 12.0%, P < 0.001). Logistic analyses indicated the independent correlation between RV involvement and these genetic factors. RV involvement was an independent risk factor for cardiovascular death, all-cause death and HF-related death in HCM patients. Genetic factors might contribute to RV involvement in HCM. Show less
no PDF DOI: 10.1093/ehjqcco/qcac008
MYBPC3

Mechanism of Glycans Modulating Cholesteryl Ester Transfer Protein: Unveiled by Molecular Dynamics Simulation.

Dongxiao Hao, He Wang, Yongjian Zang +3 more · 2022 · Journal of chemical information and modeling · ACS Publications · added 2026-04-24
Inhibition of the cholesteryl ester transfer protein (CETP) has been considered as a promising way for the treatment of cardiovascular disease (CVD) for three decades. However, clinical trials of seve Show more
Inhibition of the cholesteryl ester transfer protein (CETP) has been considered as a promising way for the treatment of cardiovascular disease (CVD) for three decades. However, clinical trials of several CETP inhibitors with various potencies have been marginally successful at best, raising doubts on the target drugability of CETP. The in-depth understanding of the glycosylated CETP structure could be beneficial to more definitive descriptions of the CETP function and the underlying mechanism. In this work, large-scale molecular dynamics simulations were performed to thoroughly explore the mechanism of glycans modulating CETP. Here, the extensive simulation results intensely suggest that glycan88 tends to assist CETP in forming a continuous tunnel throughout interacting with the upper-right region of the N-barrel, while it also could prevent the formation of a continuous tunnel by swinging toward the right-rear of the N-barrel. Furthermore, glycan240 formed stable H-bonds with Helix-B and might further stabilize the central cavity of CETP. Furthermore, the nonspecific involvement of the hydroxyl groups from the various glycans with protein core interactions and the similar influence of different glycans trapped at similar regions on the protein structure suggest that physiological glycan may lead to a similar effect. This study would provide valuable insights into devising novel methods for CVD treatment targeting CETP and functional studies about glycosylation for other systems. Show less
no PDF DOI: 10.1021/acs.jcim.1c00233
CETP

Apolipoprotein A-IV Has Bi-Functional Actions in Alcoholic Hepatitis by Regulating Hepatocyte Injury and Immune Cell Infiltration.

Wan-Hong Li, Li Zhang, Yue-Ying Li +6 more · 2022 · International journal of molecular sciences · MDPI · added 2026-04-24
Alcohol abuse can lead to alcoholic hepatitis (AH), a worldwide public health issue with high morbidity and mortality. Here, we identified apolipoprotein A-IV (APOA4) as a biomarker and potential ther Show more
Alcohol abuse can lead to alcoholic hepatitis (AH), a worldwide public health issue with high morbidity and mortality. Here, we identified apolipoprotein A-IV (APOA4) as a biomarker and potential therapeutic target for AH. APOA4 expression was detected by Gene Expression Omnibus (GEO) databases, Immunohistochemistry, and qRT-PCR in AH. Bioinformatics Methods (protein-protein interaction (PPI) network, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and Gene Set Enrichment Analysis (GSEA) were used to show down-stream gene and pathways of APOA4 in AH. AML-12 cells were used to evaluate the biological function of APOA4 using an ELISA kit (AST, ALT, and IL-1β) and flow cytometry (ROS activity). Both in vivo and in vitro, APOA4 expression was significantly elevated in the AH model induced by alcohol (ETOH). AML-12 cell damage was specifically repaired by APOA4 deficiency, while AST, ALT, and IL-1β activity that was increased by ETOH (200 µmol, 12 h) were suppressed. APOA4 inhibition increased intracellular ROS induced by ETOH, which was detected by flow cytometry. Functional and PPI network analyses showed Fcgamma receptor (FCGR) and platelet activation signaling were potential downstream pathways. We identified Show less
📄 PDF DOI: 10.3390/ijms24010670
APOA4

FADS1 overexpression promotes fatty acid synthesis and triacylglycerol accumulation

Jiangtao Huang, Yuexin Shao, Xueyang Zong +4 more · 2022 · Food & function · Royal Society of Chemistry · added 2026-04-24
Delta-5 desaturase (D5D), encoded by the fatty acid desaturase 1 (FADS1) gene, is a rate-limiting enzyme in polyunsaturated fatty acid (PUFA) synthesis that influences the PUFA levels in milk fat. How Show more
Delta-5 desaturase (D5D), encoded by the fatty acid desaturase 1 (FADS1) gene, is a rate-limiting enzyme in polyunsaturated fatty acid (PUFA) synthesis that influences the PUFA levels in milk fat. However, the function and molecular mechanism of FADS1 in milk fat metabolism remain largely unknown. The Show less
no PDF DOI: 10.1039/d2fo00246a
FADS1

Coronary artery disease risk factors affected by RNA modification-related genetic variants.

Ru Li, Huan Zhang, Fan Tang +6 more · 2022 · Frontiers in cardiovascular medicine · Frontiers · added 2026-04-24
Single nucleotide polymorphisms that affect RNA modification (RNAm-SNPs) may have functional roles in coronary artery disease (CAD). The aim of this study was to identify RNAm-SNPs in CAD susceptibili Show more
Single nucleotide polymorphisms that affect RNA modification (RNAm-SNPs) may have functional roles in coronary artery disease (CAD). The aim of this study was to identify RNAm-SNPs in CAD susceptibility loci and highlight potential risk factors. CAD-associated RNAm-SNPs were identified in the CARDIoGRAMplusC4D and UK Biobank genome-wide association studies. Gene expression and circulating protein levels affected by the RNAm-SNPs were identified by QTL analyses. Cell experiments and Mendelian randomization (MR) methods were applied to test whether the gene expression levels were associated with CAD. We identified 81 RNAm-SNPs that were associated with CAD or acute myocardial infarction (AMI), including m The present study identified RNAm-SNPs in CAD susceptibility genes, gene expression and circulating proteins as risk factors for CAD and suggested that RNA modification may play a role in the pathogenesis of CAD. Show less
📄 PDF DOI: 10.3389/fcvm.2022.985121
DHX36

Large-Scale Targeted Sequencing Study of Ischemic Stroke in the Han Chinese Population.

Mengyao Shi, Tanika N Kelly, Zhengbao Zhu +16 more · 2022 · Journal of the American Heart Association · added 2026-04-24
Background Ischemic stroke is likely caused by interactions of multiple genes and environmental determinants. However, large-scale sequencing studies to discern functional genetic variants and their i Show more
Background Ischemic stroke is likely caused by interactions of multiple genes and environmental determinants. However, large-scale sequencing studies to discern functional genetic variants and their interactions with clinical and lifestyle risk factors on ischemic stroke are limited. Methods and Results We sequenced functional regions of 740 previously identified genes associated with atherosclerotic disease among 999 ischemic stroke cases and 1001 controls of Chinese ancestry. Multiple logistic regression models were used to examine the associations between variants and ischemic stroke and test interactions between variants and clinical and lifestyle risk factors. Functional variants achieving suggestive significance were replicated in an independent sample of 4724 ischemic stroke cases and 5029 controls. Driven by variant main effects, each minor allele of the correlated rs174535, rs174545, and rs3834458 variants at Show less
📄 PDF DOI: 10.1161/JAHA.122.025245
FADS1

IL-27 attenuates airway inflammation and epithelial-mesenchymal transition in allergic asthmatic mice possibly via the RhoA/ROCK signalling pathway.

Chuanjun Huang, Yan Sun, Na Liu +5 more · 2022 · European cytokine network · added 2026-04-24
Asthma is an airway disease characterized by airflow limitation and various additional clinical manifestations. Repeated inflammatory stimulation of the airways leads to epithelial-mesenchymal transit Show more
Asthma is an airway disease characterized by airflow limitation and various additional clinical manifestations. Repeated inflammatory stimulation of the airways leads to epithelial-mesenchymal transition (EMT) which aggravates subepithelial fibrosis during the process of airway remodelling and enhances resistance to corticosteroids and bronchodilators in refractory asthma. There is growing evidence that IL-27 modulates airway remodelling, however, the molecular mechanisms involving IL-27 and EMT are poorly understood. The objective of this study was to investigate the effects of IL-27 on ovalbumin (OVA)-challenged asthmatic mice in vivo and TGF-β1-induced EMT in 16HBE cells in vitro. Airway inflammation, mucus secretion, and collagen deposition were analysed by conventional pathological techniques. The ratio of Th17 and Th9 cells in the spleen of mice was measured using flow cytometry, ELISA was performed for cytokine analysis to identify EMT-related molecules and signalling pathways, and other molecular and cellular techniques were used to explore the functional mechanism involving IL-27 and EMT. Airway inflammation in asthmatic mice was significantly alleviated by IL-27, with downregulation of RhoA and ROCK, upregulation of E-cadherin, and a decrease of vimentin and α-SMA expression, compared to asthmatic mice. Moreover, the frequency of Th17 and Th9 cells in the spleen of asthmatic mice decreased following treatment with IL-27. In TGF-β1-induced 16HBE cells, the addition of IL-27 was shown to inhibit EMT, based on the expression of E-cadherin, vimentin, and α-SMA. Intranasal administration of IL-27 attenuates airway inflammation and EMT in a murine model of allergic asthma possibly by downregulating the RhoA/ROCK signalling pathway. Show less
no PDF DOI: 10.1684/ecn.2021.0476
IL27

Glucose-Dependent Insulinotropic Polypeptide and Substance P Mediate Emetic Response Induction by Masked Trichothecene Deoxynivalenol-3-Glucoside through Ca

Zihui Qin, Hua Zhang, Qinghua Wu +5 more · 2022 · Toxins · MDPI · added 2026-04-24
Deoxynivalenol (DON), the most naturally-occurring trichothecenes, may affect animal and human health by causing vomiting as a hallmark of food poisoning. Deoxynivalenol-3-glucoside (D3G) usually co-o Show more
Deoxynivalenol (DON), the most naturally-occurring trichothecenes, may affect animal and human health by causing vomiting as a hallmark of food poisoning. Deoxynivalenol-3-glucoside (D3G) usually co-occurs with DON as its glucosylated form and is another emerging food safety issue in recent years. However, the toxicity of D3G is not fully understood compared to DON, especially in emetic potency. The goals of this research were to (1) compare emetic effects to D3G by oral and intraperitoneal (IP) routes and relate emetic effects to brain-gut peptides glucose-dependent insulinotropic polypeptide (GIP) and substance P (SP) in mink; (2) determine the roles of calcium-sensing receptor (CaSR) and transient receptor potential (TRP) channel in D3G's emetic effect. Both oral and IP exposure to D3G elicited marked emetic events. This emetic response corresponded to an elevation of GIP and SP. Blocking the GIP receptor (GIPR) diminished emetic response induction by GIP and D3G. The neurokinin 1 receptor (NK-1R) inhibitor Emend Show less
📄 PDF DOI: 10.3390/toxins14060371
GIPR

The genetic polymorphisms of key genes in WNT pathway (LRP5 and AXIN1) was associated with osteoporosis susceptibility in Chinese Han population.

Yongsheng Cui, Xinglv Hu, Chen Zhang +1 more · 2022 · Endocrine · Springer · added 2026-04-24
Genetic factors play a critical role in the pathogenesis of osteoporosis. The imbalance of WNT/β-catenin will cause the occurrence of osteoporosis. LRP5 and AXIN1 play an important role in the classic Show more
Genetic factors play a critical role in the pathogenesis of osteoporosis. The imbalance of WNT/β-catenin will cause the occurrence of osteoporosis. LRP5 and AXIN1 play an important role in the classical Wnt/β-catenin signaling pathway. Our study was aimed to determine the association between five candidate single nucleotide polymorphisms (SNPs) of LRP5 or AXIN1 and osteoporosis susceptibility in Chinese Han population. A total of 599 osteoporosis patients and 599 healthy individuals were recruited for this case-control study. Agena MassARRAY was used to genotype SNPs. The association between SNPs and osteoporosis susceptibility in different genetic models was analyzed by PLINK software. We used false-positive report probability (FPRP) analysis to detect whether the positive results were just chance or noteworthy observations. Multifactor dimension reduction (MDR) was used to analyze the interaction of SNP-SNP in the osteoporosis risk. Finally, haplotype analysis was performed by plink1.07 and Haploview software. We found that LRP5 rs11228240, AXIN1 rs2301522, and rs9921222 were significantly associated with the osteoporosis susceptibility. The results of subgroup analysis showed that LRP5 rs11228240 (protective factor) and AXIN1 rs2301522 (risk factor) were associated with the susceptibility of osteoporosis among participants who were age >60 years, female or BMI ≤ 24; AXIN1 rs9921222 significantly increased the risk of osteoporosis among participants with BMI ≤ 24. The genotype A The LRP5-rs11228240, AXIN1-rs2301522, and AXIN1- rs9921222 were associated with osteoporosis susceptibility in Chinese Han population. Show less
📄 PDF DOI: 10.1007/s12020-021-02866-z
AXIN1

ATF3 -activated accelerating effect of LINC00941/lncIAPF on fibroblast-to-myofibroblast differentiation by blocking autophagy depending on ELAVL1/HuR in pulmonary fibrosis.

Jinjin Zhang, Haixia Wang, Hongbin Chen +6 more · 2022 · Autophagy · Taylor & Francis · added 2026-04-24
Idiopathic pulmonary fibrosis (IPF) is characterized by lung scarring and has no effective treatment. Fibroblast-to-myofibroblast differentiation and myofibroblast proliferation and migration are majo Show more
Idiopathic pulmonary fibrosis (IPF) is characterized by lung scarring and has no effective treatment. Fibroblast-to-myofibroblast differentiation and myofibroblast proliferation and migration are major clinical manifestations of this disease; hence, blocking these processes is a practical treatment strategy. Here, highly upregulated Show less
📄 PDF DOI: 10.1080/15548627.2022.2046448
CLN3

Oridonin alleviates hyperbilirubinemia through activating LXRα-UGT1A1 axis.

Zhikun Zhan, Fahong Dai, Tao Zhang +6 more · 2022 · Pharmacological research · Elsevier · added 2026-04-24
Hyperbilirubinemia is a serious hazard to human health due to its neurotoxicity and lethality. So far, successful therapy for hyperbilirubinemia with fewer side effects is still lacking. In this study Show more
Hyperbilirubinemia is a serious hazard to human health due to its neurotoxicity and lethality. So far, successful therapy for hyperbilirubinemia with fewer side effects is still lacking. In this study, we aimed to clarify the effects of oridonin (Ori), an active diterpenoid extracted from Rabdosia rubescens, on hyperbilirubinemia and revealed the underlying molecular mechanism in vivo and in vitro. Here, we showed that liver X receptor alpha (LXRα) deletion eliminated the protective effect of Ori on phenylhydrazine hydrochloride-induced hyperbilirubinemia mice, indicating that LXRα acted as a key target for Ori treatment of hyperbilirubinemia. Ori significantly increased the expression of LXRα and UDP-glucuronosyltransferase 1A1 (UGT1A1) in the liver of wild-type (WT) mice, which were lost in LXRα Show less
no PDF DOI: 10.1016/j.phrs.2022.106188
NR1H3

Development and Validation of a Hypoxia-related Prognostic Model for Ovarian Cancer.

Linling Xie, Meijun Pan, Zhaoping Zhang +8 more · 2022 · Recent patents on anti-cancer drug discovery · Bentham Science · added 2026-04-24
The high heterogeneity of ovarian cancer (OC) brings great difficulties to its early diagnosis and prognostic forecast. There is an urgent need to establish a prognostic model of OC based on clinicopa Show more
The high heterogeneity of ovarian cancer (OC) brings great difficulties to its early diagnosis and prognostic forecast. There is an urgent need to establish a prognostic model of OC based on clinicopathological features and genomics. We identified hypoxia-related differentially expressed genes (DEGs) between OC tissues from The Cancer Genome Atlas (TCGA) and normal tissues from the Genotype-Tissue Expression (GTEx). LASSO Cox regression analysis was applied for building a prognostic model in the TCGA-GTEx cohorts, and its predictive value was validated in the GEO-OC cohort. Functional enrichment analysis was performed to investigate the underlying mechanisms. By constructing a hypoxia model of the SKOV3 cell line and applying qRT-PCR, we investigated the relationship between hypoxia with two novel genes in the prognostic model (ISG20 and ANGPTL4). Twelve prognostic hypoxia-related DEGs were identified, and nine of them were selected to establish a prognostic model. OC patients were stratified into two risk groups, and the high-risk group showed reduced survival time compared to the low-risk group upon survival analysis. Univariate and multivariate Cox regression analysis demonstrated that the risk score was an independent risk factor for overall survival. The biological function of the identified prognostic hypoxia-related gene signature was involved in immune cell infiltration. Low expression of ISG20 was observed in the CoCl Our findings showed that this hypoxia-related gene signature could serve as a satisfactory prognostic classifier for OC and will be beneficial to the research and development of targeted therapeutic strategies. Show less
no PDF DOI: 10.2174/1574892817666220623154831
ANGPTL4

DYNLT3 overexpression induces apoptosis and inhibits cell growth and migration

Jianan Zhang, Qi Shen, Lu Xia +2 more · 2022 · Frontiers in oncology · Frontiers · added 2026-04-24
The role of the dynein light chain Tctex-type 3 (DYNLT3) protein in the biological behavior of cervical cancer and its relative molecular mechanisms were investigated. Immunohistochemical staining was Show more
The role of the dynein light chain Tctex-type 3 (DYNLT3) protein in the biological behavior of cervical cancer and its relative molecular mechanisms were investigated. Immunohistochemical staining was used to detect DYNLT3 protein expression in cervical cancer tissues. Cell proliferation and apoptosis rates and invasiveness and migratory capacities were determined by CCK-8 assays, BrdU staining assays and colony formation assays, fluorescence activated cell sorting (FACS), wound healing assays, and Transwell invasion assays of cervical cancer cells after DYNLT3 modulation. The expression levels of Wnt signaling pathway- and EMT-related proteins were examined by Western blotting. Furthermore, the effects of DYNLT3 on the tumorigenicity and metastasis of cervical cancer in nude mice were analyzed by performing immunohistochemistry, and we found that the expression level of the DYNLT3 protein was higher in human normal cervical tissues than in cervical cancer tissues. Overexpression of DYNLT3 obviously attenuated the proliferation, migration and invasion of CaSki and SiHa cells, and promoted cell apoptosis. Upregulation of DYNLT3 expression markedly decreased the expression of Wnt signaling pathway-related proteins (Dvl2, Dvl3, p-LRP6, Wnt3a, Wnt5a/b, Naked1, Naked2, β-catenin and C-Myc) and EMT-related proteins (N-cadherin, SOX2, OCT4, vimentin and Snail), and increased the expression of E-cadherin and Axin1. However, the opposite results were observed after down-regulation of DYNLT3 expression. Up-regulation of DYNLT3 expression significantly inhibited tumor growth in a nude mouse model, while downregulation of DYNLT3 showed the opposite results. In addition, the major metastatic site of cervical cancer cells in mice was the lung, and downregulation of DYNLT3 expression increased cancer metastasis Show less
📄 PDF DOI: 10.3389/fonc.2022.889238
AXIN1

Half-Life Extension and Biodistribution Modulation of Biotherapeutics via Red Blood Cell Hitch-Hiking with Novel Anti-Band 3 Single-Domain Antibodies.

Toan D Nguyen, Brandon M Bordeau, Yu Zhang +2 more · 2022 · International journal of molecular sciences · MDPI · added 2026-04-24
Small therapeutic proteins are receiving increased interest as therapeutic drugs; however, their clinical success has been limited due to their rapid elimination. Here, we report a half-life extension Show more
Small therapeutic proteins are receiving increased interest as therapeutic drugs; however, their clinical success has been limited due to their rapid elimination. Here, we report a half-life extension strategy via strategy via red blood cell red blood cell (RBC) hitch-hiking. This manuscript details the development and characterization of novel anti-RBC single-domain antibodies (sdAbs), their genetic fusion to therapeutic antibody fragments (TAF) as bispecific fusion constructs, and their influence on TAF pharmacokinetics and biodistribution. Several sdAbs specific to the band 3 antigen were generated via phage-display technology. Binding affinity to RBCs was assessed via flow cytometry. Affinity maturation via random mutagenesis was carried out to improve the binding affinity of the sdAbs. Bi-specific constructs were generated by fusing the anti-RBC sdAbs with anti-tissue necrosis factor alpha (TNF-α) TAF via the use of a glycine-serine flexible linker, and assessments for binding were performed via enzyme-linked immunosorbent assay and flow cytometry. Pharmacokinetics of anti-RBC sdAbs and fusion constructs were evaluated following intravenous bolus dosing in mice at a 1 mg/kg dose. Two RBC-binding sdAbs, RB12 and RE8, were developed. These two clones showed high binding affinity to human RBC with an estimated K Show less
no PDF DOI: 10.3390/ijms24010475
RMC1

Novel pathogenic variant of MYBPC3 responsible for hypertrophic cardiomyopathy.

Xiaofei Yang, Zhenghao Li, Qingfa Wang +2 more · 2022 · Cardiology in the young · added 2026-04-24
This study aims to investigate the pathogenic gene variant in a family with hypertrophic cardiomyopathy by using whole-exome sequencing and to explore the relationship between the gene variant and cli Show more
This study aims to investigate the pathogenic gene variant in a family with hypertrophic cardiomyopathy by using whole-exome sequencing and to explore the relationship between the gene variant and clinical phenotype. Peripheral blood was collected from a family with hypertrophic cardiomyopathy, and deoxyribonucleic acid was extracted. The possible pathogenic genes were detected by whole-exome sequencing, and the variant was verified by Sanger sequencing. Functional change in the variant was predicted by bioinformatics software. Clinical data of the family members are analysed simultaneously. The proband carries a novel heterozygous nonsense variant of MYBPC3:c.2731G > T (p.E911X). The analysis of amino acid conservation suggests that the variation is highly conserved. The three-dimensional protein structure shows that the variant in MYBPC3 results in the incompleteness of the fibronectintype-III2 (p872-967) domain and deletion of Ig-like C2-type 6 (p971-1065) and fibronectin type-III 3 and Ig-like C2-type 7 (p1181-1274) domains, in which p1253-1268 is predicted to have a transmembrane helix structure. Clinical data indicate that the phenotypes of variant carriers with hypertrophic cardiomyopathy are diverse, suggesting the functional damages to the protein of MYBPC3. The phenotypes of variant carriers with hypertrophic cardiomyopathy caused by the novel variant in MYBPC3: c.2731G > T (p.E911X) exhibit variable severity and clinical manifestations. Whole-exome sequencing can be used to comprehensive screen hypertrophic cardiomyopathy genes and provide a strong basis for early screening and accurate diagnosis and treatment of hypertrophic cardiomyopathy in children. Show less
no PDF DOI: 10.1017/S1047951121002468
MYBPC3

GREM1 is required to maintain cellular heterogeneity in pancreatic cancer.

Linxiang Lan, Theodore Evan, Huafu Li +18 more · 2022 · Nature · Nature · added 2026-04-24
Pancreatic ductal adenocarcinoma (PDAC) shows pronounced epithelial and mesenchymal cancer cell populations
no PDF DOI: 10.1038/s41586-022-04888-7
SNAI1

Diagnostic Value of Inflammatory Markers and Cytokines in Neonatal Sepsis.

Lijie Wu, Jinku Li, Lili Ping +4 more · 2022 · Evidence-based complementary and alternative medicine : eCAM · added 2026-04-24
To explore the diagnosis value of inflammatory markers and cytokines in neonatal sepsis. In this retrospective analysis, 90 cases of neonatal sepsis admitted to our hospital from April 2019 to April 2 Show more
To explore the diagnosis value of inflammatory markers and cytokines in neonatal sepsis. In this retrospective analysis, 90 cases of neonatal sepsis admitted to our hospital from April 2019 to April 2021 were included in the observation group, and 70 healthy neonates who received routine physical examinations in our hospital during the same period were recruited as the control group. Comparison and analysis of inflammatory markers and cytokines levels between the two groups were performed on days 1, 3, and 7 after the onset. Flow cytometry was used to measure the white blood cells (WBCs) and percentage of neutrophils (N%), immunoturbidimetry was used to determine C-reactive protein (CRP), immunochromatographic analysis was used to determine procalcitonin (PCT) in plasma, and the enzyme-linked immunosorbent assay was used to determine interleukin-27 (IL-27), interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor- Compared with healthy controls, neonatal sepsis resulted in significantly higher levels of WBC, N%, PCT, and CRP on days 1, 3, and 7 after onset. The levels of WBC, N%, and PCT were continuously decreased from day 1 to day 7, while the levels of CRP were increased on day 1 and day 3 but declined on day 7 ( Neonatal sepsis was associated with fluctuating levels of WBC, N%, PCT, CRP, IL-27, IL-6, IL-10, and TNF- Show less
📄 PDF DOI: 10.1155/2022/4143101
IL27

WNT5A promotes the metastasis of esophageal squamous cell carcinoma by activating the HDAC7/SNAIL signaling pathway.

Yingtong Feng, Zhiqiang Ma, Minghong Pan +14 more · 2022 · Cell death & disease · Nature · added 2026-04-24
Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers worldwide, with high incidence and mortality rates and low survival rates. However, the detailed molecular mechanism of ESCC Show more
Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers worldwide, with high incidence and mortality rates and low survival rates. However, the detailed molecular mechanism of ESCC progression remains unclear. Here, we first showed significantly higher WNT5A and SNAIL expression in ESCC samples than in corresponding paracancerous samples. High WNT5A and SNAIL expression levels correlated positively with lymphatic metastasis and poor prognosis for patients with ESCC based on immunohistochemical (IHC) staining of 145 paired ESCC samples. Spearman's correlation analyses confirmed the strong positive correlation between WNT5A and SNAIL expression, and patients with ESCC presenting coexpression of WNT5A and SNAIL had the worst prognosis. Then, we verified that the upregulation of WNT5A promoted ESCC cell metastasis in vivo and in vitro, suggesting that WNT5A might be a promising therapeutic target for the prevention of ESCC. Furthermore, WNT5A overexpression induced the epithelial-mesenchymal transition via histone deacetylase 7 (HDAC7) upregulation, and HDAC7 silencing significantly reversed WNT5A-induced SNAIL upregulation and ESCC cell metastasis. In addition, we used HDAC7 inhibitors (SAHA and TMP269) to further confirm that HDAC7 participates in WNT5A-mediated carcinogenesis. Based on these results, HDAC7 is involved in WNT5A-mediated ESCC progression, and approaches targeting WNT5A and HDAC7 might be potential therapeutic strategies for ESCC. Show less
no PDF DOI: 10.1038/s41419-022-04901-x
SNAI1

Anti-LINGO-1 antibody treatment alleviates cognitive deficits and promotes maturation of oligodendrocytes in the hippocampus of APP/PS1 mice.

Hao Yang, Lin Jiang, Yi Zhang +13 more · 2022 · The Journal of comparative neurology · Wiley · added 2026-04-24
Leucine-rich repeat and immunoglobulin-like domain-containing nogo receptor-interacting protein 1 (LINGO-1), a negative regulator of oligodendrocyte differentiation and myelination, is associated with Show more
Leucine-rich repeat and immunoglobulin-like domain-containing nogo receptor-interacting protein 1 (LINGO-1), a negative regulator of oligodendrocyte differentiation and myelination, is associated with cognitive function, and its expression is highly upregulated in Alzheimer's disease (AD) patients. Anti-LINGO-1 antibody treatment can effectively antagonize the negative regulatory effect of LINGO-1. In this study, we aim to assess the effect of anti-LINGO-1 antibody treatment on cognition and hippocampal oligodendrocytes in an AD transgenic animal model. First, 10-month-old male amyloid-β (Aβ) protein precursor (APP)/presenilin 1 (PS1) mice were administered anti-LINGO-1 antibody for 8 weeks. Then, learning and memory abilities were assessed with the Morris water maze (MWM) and Y-maze tests, and Aβ deposition and hippocampal oligodendrocytes were investigated by immunohistochemistry, immunofluorescence, and stereology. We found that anti-LINGO-1 antibody alleviated the deficits in spatial learning and memory abilities and working and reference memory abilities, decreased the density of LINGO-1 positive cells, decreased Aβ deposition, significantly increased the number of mature oligodendrocytes and the density of myelin, reversed the abnormal increases in the number of oligodendrocyte lineage cells and the densities of oligodendrocytes precursor cells in APP/PS1 mice. Our results provide evidence that LINGO-1 might be involved in the process of oligodendrocyte dysmaturity in the hippocampus of AD mice, and that antagonizing LINGO-1 can alleviate cognitive deficits in APP/PS1 mice and decrease Aβ deposition and promote oligodendrocyte differentiation and maturation in the hippocampus of these mice. Our findings suggest that changes in LINGO-1 and oligodendrocytes in the hippocampus play important roles in the pathogenesis of AD and that antagonizing LINGO-1 might be a potential therapeutic strategy for AD. Show less
no PDF DOI: 10.1002/cne.25299
LINGO1

Gut microbiota and short chain fatty acids partially mediate the beneficial effects of inulin on metabolic disorders in obese ob/ob mice.

Jing Guo, Mengyuan Zhang, He Wang +5 more · 2022 · Journal of food biochemistry · Blackwell Publishing · added 2026-04-24
Mounting evidence has linked both obesity and metabolic disorders with dysbiosis of the gut microbiota. Dietary inulin is conducive to modulating this dysbiosis, and represents a potential means to im Show more
Mounting evidence has linked both obesity and metabolic disorders with dysbiosis of the gut microbiota. Dietary inulin is conducive to modulating this dysbiosis, and represents a potential means to improve disorders of glucose and lipid metabolism. However, the mechanisms underlying these improvements are largely unclear. Obese ob/ob mice were fed a standard chow, a low fiber diet (LFD) or a high fiber diet (HFD) for 4 weeks, and the body weight, fecal short chain fatty acids (SCFAs) level, and plasma and liver lipid profiles were analyzed. Oral glucose tolerance testing, and gut microbiota sequencing were also conducted. Dietary inulin improved the dysbiosis of the gut microbiota, attenuated the decrease in phylum Bacteroidetes, repressed the increase of phylum Firmicutes, and led to an increase in the ratio of Firmicutes/Bacteroidetes. At the family level, inulin promoted the expansion of SCFAs-producing Ruminococcaceae and Lachnospiraceae bacteria, which increased the fecal SCFAs concentrations. At the genus level, inulin increased the levels of Bacteroides and Bifidobacteria. Furthermore, our results revealed that there was enhanced expression of angiopoietin-like protein 4 (ANGPTL4), which might be induced by the higher production of SCFAs, and this may underlie the improvements in the disorders of glucose and lipid metabolism seen in mice with added dietary inulin. In conclusion, inulin may ameliorate metabolic disorders by remodeling the gut microbiota and increasing the production of SCFAs, which might be mediated by the ANGPTL4-related signaling pathway. Interventions targeting the gut microbiota warrant further investigation as a novel therapy for metabolic diseases. PRACTICAL APPLICATIONS: Mounting evidence has linked both obesity and metabolic disorders with dysbiosis of the gut microbiota. Dietary inulin is conducive to modulating this dysbiosis, and represents a potential means to improve disorders of glucose and lipid metabolism. However, the mechanisms underlying these improvements are largely unclear. In the present study, we investigated the effects of dietary fiber (inulin) on metabolic homeostasis using ob/ob mice. The results of our study demonstrate that inulin-induced remodeling of the gut microbiota resulted in increased production of short chain fatty acids (SCFAs), leading to the enhanced expression of angiopoietin-like protein 4 (ANGPTL4), which improved the glucose and lipid metabolism. Our results suggest that the gut microbiota, SCFAs and ANGPTL4 pathway at least partially mediate the beneficial effects of inulin on metabolic disorders in ob/ob mice. Show less
no PDF DOI: 10.1111/jfbc.14063
ANGPTL4

MACC1 promotes pancreatic cancer metastasis by interacting with the EMT regulator SNAI1.

Xianglian Zhang, Ya Luo, Yu Cen +5 more · 2022 · Cell death & disease · Nature · added 2026-04-24
Metastasis is the dominant cause of cancer-related mortality. Metastasis-associated with colon cancer protein 1 (MACC1) has been proven to play a critical role in cancer metastasis. However, the prome Show more
Metastasis is the dominant cause of cancer-related mortality. Metastasis-associated with colon cancer protein 1 (MACC1) has been proven to play a critical role in cancer metastasis. However, the prometastatic role of MACC1 in regulating the pancreatic cancer (PC) metastatic phenotype remains elusive. Here, we report that MACC1 is highly expressed in The Cancer Genome Atlas (TCGA) and tissue microarray (TMA) and identified as a good indicator for poor prognosis. Overexpression or knockdown of MACC1 in PC cells correspondingly promoted or inhibited pancreatic cancer cell migration and invasion in a MET proto-oncogene receptor tyrosine kinase (MET)-independent manner. Notably, knockdown of MACC1 in PC cells markedly decreased the liver metastatic lesions in a liver metastasis model. Mechanistically, MACC1 binds to the epithelial-mesenchymal transition (EMT) regulator snail family transcriptional repressor 1 (SNAI1) to drive EMT via upregulating the transcriptional activity of SNAI1, leading to the transactivation of fibronectin 1 (FN1) and the trans-repression of cadherin 1 (CDH1). Collectively, our results unveil a new mechanism by which MACC1 drives pancreatic cancer cell metastasis and suggest that the MACC1-SNAI1 complex-mediated mesenchymal transition may be a therapeutic target in pancreatic cancer. Show less
no PDF DOI: 10.1038/s41419-022-05285-8
SNAI1

MicroRNAs sequencing of plasma exosomes derived from patients with atrial fibrillation: miR-124-3p promotes cardiac fibroblast activation and proliferation by regulating AXIN1.

Pengju Zhu, Huilin Li, An Zhang +5 more · 2022 · Journal of physiology and biochemistry · Springer · added 2026-04-24
MicroRNAs (miRNAs) play an important role in the pathogenesis of atrial fibrillation (AF). Exosomal miRNAs may develop as promising biomarkers for AF. To explore significant exosomal miRNAs in AF, pla Show more
MicroRNAs (miRNAs) play an important role in the pathogenesis of atrial fibrillation (AF). Exosomal miRNAs may develop as promising biomarkers for AF. To explore significant exosomal miRNAs in AF, plasma exosomes were extracted from 3 patients with AF and 3 patients with sinus rhythm (SR), respectively. Differential expression of exosomal miRNAs were screened by high-throughput sequencing analysis and verified by qRT-PCR from 40 patients with AF and 40 patients with SR. The target genes prediction, biological function, and signaling pathways analysis were conducted by miRanda software, gene ontology (GO), and KEGG analysis. The results showed that there were 40 differently expressed exosomal miRNAs from AF patients compared with SR patients, of which 13 miRNAs were upregulated and 27 miRNAs were downregulated. qRT-PCR validation demonstrated that miR-124-3p, miR-378d, miR-2110, and miR-3180-3p were remarkably upregulated, while miR-223-5p, miR-574-3p, miR-125a-3p, and miR-1299 were downregulated. To explore the function of miR-124-3p associated with AF, plasma exosomes derived from AF patients were co-incubated with rat myocardial fibroblasts. The expression of miR-124-3p was upregulated in myocardial fibroblasts. The viability and proliferation of myocardial fibroblasts were elevated by transfecting with miR-124-3p overexpression plasmids using CCK8 and immunofluorescence-staining methods. AXIN1 was verified to be the target of miR-124-3p by luciferase assay in vitro. Expression of AXIN1 was reduced, while β-catenin, Collagen 1, and α-SMA were increased in myocardial fibroblasts with miR-124-3p overexpression. In conclusion, these findings suggested that circulating exosomal miRNAs may serve as novel biomarkers for AF, and miR-124-3p promotes fibroblast activation and proliferation through regulating WNT/β-catenin signaling pathway via AXIN1. Show less
📄 PDF DOI: 10.1007/s13105-021-00842-9
AXIN1

Identification and Characterization of Genes Related to the Prognosis of Hepatocellular Carcinoma Based on Single-Cell Sequencing.

Wenbiao Chen, Feng Zhang, Huixuan Xu +3 more · 2022 · Pathology oncology research : POR · Frontiers · added 2026-04-24
The heterogeneity of hepatocellular carcinoma (HCC) highlights the importance of precision therapy. In recent years, single-cell RNA sequencing has been used to reveal the expression of genes at the s Show more
The heterogeneity of hepatocellular carcinoma (HCC) highlights the importance of precision therapy. In recent years, single-cell RNA sequencing has been used to reveal the expression of genes at the single-cell level and comprehensively study cell heterogeneity. This study combined big data analytics and single-cell data mining to study the influence of genes on HCC prognosis. The cells and genes closely related to the HCC were screened through single-cell RNA sequencing (71,915 cells, including 34,414 tumor cells) and big data analysis. Comprehensive bioinformatics analysis of the key genes of HCC was conducted for molecular classification and multi-dimensional correlation analyses, and a prognostic model for HCC was established. Finally, the correlation between the prognostic model and clinicopathological features was analyzed. 16,880 specific cells, screened from the single-cell expression profile matrix, were divided into 20 sub-clusters. Cell typing revealed that 97% of these cells corresponded to HCC cell lines, demonstrating the high specificity of cells derived from single-cell sequencing. 2,038 genes with high variability were obtained. The 371 HCC samples were divided into two molecular clusters. Cluster 1 (C1) was associated with tumorigenesis, high immune score, immunotherapy targets (PD-L1 and CYLA-4), high pathological stage, and poor prognosis. Cluster 2 (C2) was related to metabolic and immune function, low immune score, low pathological stage, and good prognosis. Seven differentially expressed genes (CYP3A4, NR1I2, CYP2C9, TTR, APOC3, CYP1A2, and AFP) identified between the two molecular clusters were used to construct a prognostic model. We further validated the correlation between the seven key genes and clinical features, and the established prognostic model could effectively predict HCC prognosis. Our study identified seven key genes related to HCC that were used to construct a prognostic model through single-cell sequencing and big data analytics. This study provides new insights for further research on clinical targets of HCC and new biomarkers for clinical application. Show less
📄 PDF DOI: 10.3389/pore.2022.1610199
APOC3

Trans-ethnic genome-wide association study of blood metabolites in the Chronic Renal Insufficiency Cohort (CRIC) study.

Eugene P Rhee, Aditya Surapaneni, Zihe Zheng +24 more · 2022 · Kidney international · Elsevier · added 2026-04-24
Metabolomics genome wide association study (GWAS) help outline the genetic contribution to human metabolism. However, studies to date have focused on relatively healthy, population-based samples of Wh Show more
Metabolomics genome wide association study (GWAS) help outline the genetic contribution to human metabolism. However, studies to date have focused on relatively healthy, population-based samples of White individuals. Here, we conducted a GWAS of 537 blood metabolites measured in the Chronic Renal Insufficiency Cohort (CRIC) Study, with separate analyses in 822 White and 687 Black study participants. Trans-ethnic meta-analysis was then applied to improve fine-mapping of potential causal variants. Mean estimated glomerular filtration rate was 44.4 and 41.5 mL/min/1.73m Show less
📄 PDF DOI: 10.1016/j.kint.2022.01.014
FADS1

Comprehensive ceRNA network for MACF1 regulates osteoblast proliferation.

Shanfeng Jiang, Chong Yin, Kai Dang +3 more · 2022 · BMC genomics · BioMed Central · added 2026-04-24
Previous studies have shown that microtubule actin crosslinking factor 1 (MACF1) can regulate osteoblast proliferation and differentiation through non-coding RNA (ncRNA) in bone-forming osteoblasts. H Show more
Previous studies have shown that microtubule actin crosslinking factor 1 (MACF1) can regulate osteoblast proliferation and differentiation through non-coding RNA (ncRNA) in bone-forming osteoblasts. However, the role of MACF1 in targeting the competing endogenous RNA (ceRNA) network to regulate osteoblast differentiation remains poorly understood. Here, we profiled messenger RNA (mRNA), microRNA (miRNA), and long ncRNA (lncRNA) expression in MACF1 knockdown MC3TC‑E1 pre‑osteoblast cells. In total, 547 lncRNAs, 107 miRNAs, and 376 mRNAs were differentially expressed. Significantly altered lncRNAs, miRNAs, and mRNAs were primarily found on chromosome 2. A lncRNA-miRNA-mRNA network was constructed using a bioinformatics computational approach. The network indicated that mir-7063 and mir-7646 were the most potent ncRNA regulators and mef2c was the most potent target gene. Pathway enrichment analysis showed that the fluid shear stress and atherosclerosis, p53 signaling, and focal adhesion pathways were highly enriched and contributed to osteoblast proliferation. Importantly, the fluid shear stress and atherosclerosis pathway was co-regulated by lncRNAs and miRNAs. In this pathway, Dusp1 was regulated by AK079370, while Arhgef2 was regulated by mir-5101. Furthermore, Map3k5 was regulated by AK154638 and mir-466q simultaneously. AK003142 and mir-3082-5p as well as Ak141402 and mir-446 m-3p were identified as interacting pairs that regulate target genes. This study revealed the global expression profile of ceRNAs involved in the differentiation of MC3TC‑E1 osteoblasts induced by MACF1 deletion. These results indicate that loss of MACF1 activates a comprehensive ceRNA network to regulate osteoblast proliferation. Show less
📄 PDF DOI: 10.1186/s12864-022-08910-0
MACF1