👤 Bowen 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, 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, Yanping 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

Primary cutaneous CD8+ aggressive epidermotropic cytotoxic T-cell lymphoma with novel FGFR1 fusion treated with pemigatinib.

Carlos A Torres-Cabala, Julia Arreola Yescas, Yue Zhang +11 more · 2025 · Blood advances · added 2026-04-24
📄 PDF DOI: 10.1182/bloodadvances.2024014928
FGFR1

The role of serun lipid, cytokine production in sudden sensorineural hearing loss.

Xiaoqing Zhang, Zhihua Xu, Yehai Liu · 2025 · Cytotechnology · Springer · added 2026-04-24
Sudden sensorineural hearing loss (SSNHL) has serious harm to human hearing health, where blood lipid and inflammatory levels may play a key role in it. Thus, the purpose of this investigation was to Show more
Sudden sensorineural hearing loss (SSNHL) has serious harm to human hearing health, where blood lipid and inflammatory levels may play a key role in it. Thus, the purpose of this investigation was to assess the connection between inflammatory and lipid variables and SSNHL. Patients diagnosed with SSNHL had an analysis of serum lipid parameters, such as total cholesterol (TC), triglycerides, HDL-C, LDL-C, apolipoprotein A (apo A), apolipoprotein B (apo B), and lipoprotein A (Lp(a)), as well as inflammatory factors like TNF-α and IL-10. After that, risk factor analysis was carried out utilizing univariate, multivariate regression, and LASSO retrospective modeling. In all, 72 SSNHL patients and 67 healthy control individuals were involved. The LDL/HDL, total cholesterol, ApoB, LP(a), IL-10, TNF-α, and IFN-γ considerably higher in the SSNHL group than in the healthy control group, however, nervonic acid and coenzyme Q were decreased significantly in SSNHL than Control group. The multivariate logistic regression model's analysis using multifactorial retrospective modeling revealed significant changes in LDL, LDL/HDL, IL-10, and TNF-α. In addition, in the LASSO regression model, the model demonstrated high discrimination, as evidenced by the C-index for the cohort's prediction nomogram, which was 0.998 (95% CI, 0.154-1.115) and confirmed to be 0.925 following bootstrapping validation. Finally, IL-10 and LDL/HDL were the main risk factors in SSNHL. LDL/HDL and IL-10 may be closely related to SSNHL's progress and should be evaluated promptly before treating patients with SSNHL. Show less
no PDF DOI: 10.1007/s10616-025-00722-w
APOB

Cholesterol induced-mitochondrial calcium dysregulation facilitates atherosclerosis by promoting lipid accumulation in vascular smooth muscle cells.

Zhiwang Zhang, Fan Yang, Wei Wang +7 more · 2025 · Molecular biomedicine · BioMed Central · added 2026-04-24
Mitochondria play an essential role in regulating various physiological functions including bioenergetics, calcium homeostasis, redox signaling, and lipid metabolism and also are involved in the patho Show more
Mitochondria play an essential role in regulating various physiological functions including bioenergetics, calcium homeostasis, redox signaling, and lipid metabolism and also are involved in the pathogenesis of cardiovascular diseases. However, the relationship between mitochondrial calcium homeostasis in vascular smooth muscle cells (VSMCs) and atherosclerosis remains poorly understood. Here, we demonstrate that cholesterol induces mitochondrial calcium overload and lipid accumulation in VSMCs, which is resulted from dysregulation of mitochondrial calcium uniporter (MCU), as evidenced by genetic and pharmacologic inhibition of MCU. Furthermore, MCU inhibitors alleviate Western diet-induced atherosclerosis in ApoE-/- mice. Mechanistically, high-fat and high-cholesterol diets induce the contact between mitochondria and the endoplasmic reticulum (ER) in VSMCs as indicated by transmission electron microscopy, proximity ligation assay and immunofluorescence staining, which increases the formation of mitochondria-associated membranes (MAMs), leading to Ca2 + release from the ER into the mitochondria and thus elevating Ca2 + in the mitochondria. Using mitochondrial calcium uptake 1 (MICU1) mutant and Ca2 + detection assay, we confirmed that this increased Ca2 + binds to MICU1, a blocker of MCU, to impair its ability to block MCU, thus enabling the MCU to remain open and resulting in mitochondrial calcium overload. Further, mitochondrial calcium overload dysregulates fatty acid β-oxidation by modulating medium-chain acyl-CoA dehydrogenase (ACADM), thereby leading to lipid deposition. The inhibition of MCU alleviates the pathological changes elecited by cholesterol. Our findings unveil the previously unrecognized role of MAM-MICU1-MCU axis in cholesterol-induced mitochondrial calcium overload and atherosclerosis, indicating that MCU represents a promising therapeutic target for the treatment of atherosclerosis. Show less
📄 PDF DOI: 10.1186/s43556-025-00384-2
APOE

Qingre Sanjie Formula alleviates atherosclerosis by promoting LXR-α/ABCG5/G8-mediated reverse cholesterol transport and bile acid synthesis.

Xiao Li, Xianglong Huang, Keyan Song +5 more · 2025 · Phytomedicine : international journal of phytotherapy and phytopharmacology · Elsevier · added 2026-04-24
Atherosclerosis is the leading cause of cardiovascular disease-related morbidity and mortality. The traditional Chinese medicine Qingre Sanjie Formula (QRSJF), composed of Prunellae Spica, Sargassum, Show more
Atherosclerosis is the leading cause of cardiovascular disease-related morbidity and mortality. The traditional Chinese medicine Qingre Sanjie Formula (QRSJF), composed of Prunellae Spica, Sargassum, Fritillariae Thunbergii Bulbus, Leonuri Herba, and Forsythiae Fructus, has shown efficacy in treating cardiovascular diseases, although its mechanisms are unclear. This study aimed to explore the protective effects of QRSJF against atherosclerosis and the mechanisms involved. The composition of QRSJF was analyzed using Ultra Performance Liquid Chromatography Quadrupole Time-of-Flight Mass Spectrometry. An 8-week high-fat diet (HFD)-induced atherosclerosis model was established in ApoE Both low- and high-dose QRSJF effectively attenuated dyslipidemia and decreased serum inflammatory cytokine levels in HFD-fed ApoE QRSJF improves dyslipidemia and reduces atherosclerotic plaque in ApoE Show less
no PDF DOI: 10.1016/j.phymed.2025.156691
NR1H3

Integrated meta-analysis and network pharmacology analysis: evaluation of Zhigancao decoction as treatment for diabetic cardiomyopathy.

Kangshou Ji, Meizi Han, Mingqian Yang +2 more · 2025 · Frontiers in cardiovascular medicine · Frontiers · added 2026-04-24
Zhigancao Decoction (ZGCD) is derived from "Treatise on Febrile Diseases" and is traditionally prescribed for treating a variety of cardiovascular conditions. As of now, there are no data to support i Show more
Zhigancao Decoction (ZGCD) is derived from "Treatise on Febrile Diseases" and is traditionally prescribed for treating a variety of cardiovascular conditions. As of now, there are no data to support its use as a treatment for diabetic cardiomyopathy (DCM) and the mechanism behind the effect is unclear as well. In the present study, clinical evidence for the efficacy of ZGCD in patients with DCM was examined using a meta-analysis and its underlying anti-DCM molecular mechanisms were explored via network pharmacology. The current study utilized an extensive search strategy encompassing various domestic and foreign databases databases to retrieve pertinent articles published up to June 2024. In light of this, a thorough evaluation of the benefits and safety of Zhigancao decoction (ZGCD) was conducted in this study using RevMan and Stata. Subsequently, a number of active compounds and target genes for ZGCD were gathered from the TCMSP and BATMAN-TCM databases, while the main targets for DCM were obtained from databases such as GenCards, OMIM, TTD, and DrugBank. To select core genes, protein-protein interaction networks were generated using the STRING platform, and enrichment analyses were completed using the Metascape platform. Meta-analysis results were ultimately derived from 9 studies involving 661 patients in total. In comparison with WM therapy alone, the pooled results showed that ZGCD significantly enhanced overall effectiveness. Additionally, the utilization of ZGCD was leading to a reduction in LVEDV, LVESV and LVDD, also a greater increase in LVEF. Meanwhile, the utilization of ZGCD during intervention was more effective in reducing SBP, and DBP. In addition, the ZGCD showed potential in reducing the occurrence of adverse events. In the context of network pharmacology, five constituents of ZGCD-namely lysine, quercetin, gamma-aminobutyric acid, stigmasterol, and beta-sitosterol-are posited to exert anti-diabetic cardiomyopathy (anti-DCM) effects through interactions with the molecular targets ASS1, SERPINE1, CACNA2D1, AVP, APOB, ICAM1, EGFR, TNNC1, F2, F10, IGF1, TNNI2, CAV1, INSR, and INS. The primary mechanisms by which ZGCD may achieve its anti-DCM effects are likely mediated via the AGEs/RAGE signaling pathway, as well as through pathways related to lipid metabolism and atherosclerosis. In comparison to WM therapy alone, ZGCD demonstrates greater efficacy and safety in the management of DCM. ZGCD not only significantly reduces blood pressure, but also enhances cardiac function while producing fewer adverse effects. The therapeutic effects of ZGCD on DCM can likely be ascribed to its capacity to modulate the AGEs-RAGE signaling pathway, as well as its efficacy in enhancing lipid metabolism and mitigating atherosclerosis. identifier (INPLASY202430133). Show less
📄 PDF DOI: 10.3389/fcvm.2025.1454647
APOB

Causal inference of CLEC5A and ISG20 in atherosclerosis: integrating Mendelian randomization and eQTL evidence.

Ya Zhang, Qian Tian, Yuan Zhu +5 more · 2025 · Frontiers in immunology · Frontiers · added 2026-04-24
Atherosclerosis (AS) is a vascular disorder characterized by lipid accumulation and chronic inflammation, with pathogenesis closely linked to genetic factors and immune regulatory mechanisms. This stu Show more
Atherosclerosis (AS) is a vascular disorder characterized by lipid accumulation and chronic inflammation, with pathogenesis closely linked to genetic factors and immune regulatory mechanisms. This study comprehensively identified ASassociated genes by integrating data from the Gene Expression Omnibus (GEO) database and expression quantitative trait locus (eQTL) analyses, complemented by Mendelian randomization (MR) analysis, followed by experimental validation of their functional roles. Results indicated significant upregulation of CLEC5A and ISG20 in patients with AS, with MR analysis revealing positive causal relationships between both genes and AS risk (CLEC5A: OR = 1.001, P = 0.047; ISG20: OR = 1.001, P = 0.030), while HOXA2 showed a negative causal association. Functional enrichment analysis highlighted CLEC5A and ISG20's involvement in immune responses, inflammatory pathways, and lipid metabolism regulation. Experimental validation in oxidized low-density lipoprotein (ox-LDL)-stimulated macrophages and apolipoprotein E-deficient (ApoE This study represents the first to elucidate the molecular mechanism by which ISG20 promotes AS progression through macrophage lipid accumulation and inflammatory responses, positioning it as a potential novel therapeutic target for AS. Show less
📄 PDF DOI: 10.3389/fimmu.2025.1644135
APOE

LXRα agonists ameliorates acute rejection after liver transplantation via ABCA1/MAPK and PI3K/AKT/mTOR signaling axis in macrophages.

Xiaoyan Qin, Dingheng Hu, Qi Li +6 more · 2025 · Molecular medicine (Cambridge, Mass.) · BioMed Central · added 2026-04-24
Liver X receptor α (LXRα) plays an important role in inflammatory immune response induced by hepatic ischemia-reperfusion injury (IRI) and acute rejection (AR). Macrophage M1-polarization play an impo Show more
Liver X receptor α (LXRα) plays an important role in inflammatory immune response induced by hepatic ischemia-reperfusion injury (IRI) and acute rejection (AR). Macrophage M1-polarization play an important role in the occurrence and development of AR. Although the activation of LXR has anti-inflammatory effects, the role of LXRα in AR after liver transplantation (LT) has not been elucidated. We aimed to investigate LXRα anti-inflammatory and macrophage polarization regulation effects and mechanisms in acute rejection rat models. LXRα anti-inflammatory and liver function protective effects was initially measured in primary Kupffer cells and LT rat models. Subsequently, a flow cytometry assay was used to detect the regulation effect of LXRα in macrophage polarization. HE staining, TUNEL and ELISA were used to evaluate the co-treatment effects of TO901317 and tacrolimus on hepatic apoptosis and liver acute rejection after LT. In this study, we found that LPS can inhibit the expression of LXRα and activate MAPK pathway and PI3K/AKT/mTOR. We also found that LXRα agonist (TO901317) could improve liver function and rat survival after LT by activating the level of ABCA1 and inhibiting MAPK. TO901317 could inhibit macrophage M1-polarization by activating PI3K/AKT/mTOR signal pathway to improve the liver lesion of AR rats after liver transplantation. Additionally, co-treatment with TO901317 and tacrolimus more effectively alleviated the damaging effects of AR following LT than either drug alone. Our results suggest that the activation of LXRα can improve liver function and rat survival after LT by regulate ABCA1/MAPK and PI3K/AKT/mTOR signaling axis in macrophages. Show less
no PDF DOI: 10.1186/s10020-025-01153-1
NR1H3

CRISPR/Cas9-mediated CH2 deletion of Fel d1 triggers transcriptomic reprogramming and disease-associated pathways in feline cells.

Lin-Yi Qu, Fu-Shi Quan, Shu-Ming Shi +6 more · 2025 · Frontiers in cell and developmental biology · Frontiers · added 2026-04-24
Fel d1, the major cat allergen responsible for over 90% of human IgE-mediated allergies, has an incompletely defined physiological role. To explore its function and assess the feasibility of producing Show more
Fel d1, the major cat allergen responsible for over 90% of human IgE-mediated allergies, has an incompletely defined physiological role. To explore its function and assess the feasibility of producing hypoallergenic cats, we knocked out the CH2 domain of Fel d1 using CRISPR/Cas9 in feline skin cells. An optimized sgRNA introduced a frameshift mutation, with knockout efficiency validated by sequencing, qRT-PCR, and Western blot. Transcriptomic alterations were profiled by RNA-seq, and functional consequences were investigated via GO, KEGG, and GSEA analyses. Key findings were confirmed by qPCR, and phenotypes were assessed using CCK-8, EdU, and flow cytometry. The approach successfully generated a three-base insertion, resulting in near-complete loss of CH2 mRNA and Fel d1 protein. RNA-seq identified 3,469 differentially expressed genes (DEGs), with significant enrichment in pathways for hypertrophic cardiomyopathy (HCM) and rheumatoid arthritis (RA). Key genes in these pathways (e.g., Show less
📄 PDF DOI: 10.3389/fcell.2025.1716808
MYBPC3

Core competencies and training needs of specialist-nurse clinical educators: a latent profile analysis.

Junye Tian, Meng Zhang, Lichuan Zhang +3 more · 2025 · BMC nursing · BioMed Central · added 2026-04-24
The competency of specialist nurse clinical educators is crucial for the effectiveness of specialist nurse training programmes. However, variability in teaching competency and training needs among edu Show more
The competency of specialist nurse clinical educators is crucial for the effectiveness of specialist nurse training programmes. However, variability in teaching competency and training needs among educators remains insufficiently studied, especially in the context of rapidly evolving healthcare education in China. This study aimed to identify distinct core competency profiles among clinical educators for specialist nurses, examine associated socio-demographic factors, and explore differences in training needs across profiles. A cross-sectional online survey was conducted with 3,945 specialist nurse clinical educators from 30 Chinese regions. The Chinese version of the Nurse Educator Core Competency Scale (NECCS) and a self-developed training needs questionnaire were used. Latent Profile Analysis (LPA) identified competency subgroups, while multinomial logistic regression and Kruskal-Wallis tests examined associated variables and training needs. Latent Profile Analysis identified three competency profiles: foundational (8.6%), intermediate (43.0%), and advanced (48.4%), with mean scores of 43.89, 68.24, and 91.68, respectively. Educators without prior training were significantly more likely to belong to the foundational (OR = 3.195, p < 0.001) and intermediate (OR = 1.676, p < 0.001) groups compared to those with training experience. Advanced-competency educators showed the highest demand for curriculum design training, with 75% rating it as highly necessary. In contrast, educators in the intermediate group identified clinical teaching methods and techniques as their top training need (58.7%). Those in the foundational group prioritised common pedagogical methods and instructional technologies (54.7%). Clinical educator competencies vary by background characteristics and training exposure. Tailored, competency-based training is needed to address these gaps and enhance the quality of specialist nursing education. Show less
📄 PDF DOI: 10.1186/s12912-025-04006-8
LPA

ANGPTL4: A Comprehensive Review of 25 Years of Research.

Pedro Ramos, Qiongyu Shi, Jeremy Kleberg +3 more · 2025 · Cancers · MDPI · added 2026-04-24
Angiopoietin-like 4 (ANGPTL4) is a secreted glycoprotein that was discovered in 2000 by three independent laboratories. In the ensuing two and a half decades, extensive work has been conducted to dete Show more
Angiopoietin-like 4 (ANGPTL4) is a secreted glycoprotein that was discovered in 2000 by three independent laboratories. In the ensuing two and a half decades, extensive work has been conducted to determine its physiological and pathological functions. ANGPTL4 has been shown to be involved in many biological processes, including glucose and lipid metabolism, angiogenesis, and wound healing, with implications in diseases such as type 2 diabetes, cardiovascular (e.g., atherosclerosis) and renal diseases, and cancer. For instance, ANGPTL4 is upregulated in several cancers, including renal cell carcinoma, breast cancer, and colorectal cancer. Interestingly, ANGPTL4 has been shown to exhibit both pro-tumor-promoting tumor growth, cell survival, angiogenesis and metastasis-as well as anti-tumor activities, underscoring its complex roles in cancer biology. This review examines the comprehensive biological functions of ANGPTL4 and its contributions to disease mechanisms with a specific emphasis on cancer, as well as its potential as a therapeutic target across different types of human cancers. Show less
📄 PDF DOI: 10.3390/cancers17142364
ANGPTL4

Defining the surgical curative time window: identifying patients with an absence of recurrence for 5 years following surgical resection of stage I invasive non-small cell lung cancer.

Tong Li, Yang Zhang, Hong Hu +5 more · 2025 · Translational lung cancer research · added 2026-04-24
While most patients with stage I non-small cell lung cancer (NSCLC) remain recurrence-free after resection, some still develop recurrent disease. The surgical curative time window concept, defined as Show more
While most patients with stage I non-small cell lung cancer (NSCLC) remain recurrence-free after resection, some still develop recurrent disease. The surgical curative time window concept, defined as no recurrence through 5-year follow-up, helps identify potentially cured patients, yet predictive clinicopathologic features in stage I invasive NSCLC need clarification. This study sought to identify such features to enable risk-adapted surveillance. We analyzed a prospectively collected dataset of patients with stage I invasive NSCLC who underwent R0 resection between 2008 and 2015. Cox regression analysis was used to evaluate the association between clinicopathologic features and disease recurrence, aiming to identify independent prognostic factors. A total of 1,817 patients met the inclusion criteria. The 5-year cumulative incidence of recurrence was 14.6%. Female sex, tumor size ≤2 cm, lepidic-predominant adenocarcinoma (LPA) histologic type, presence of a ground-glass opacity (GGO) component, and solid component size ≤10 mm were identified as independent prognostic factors. A risk stratification system was subsequently developed, classifying patients into two groups: a low-risk group (with ≥4 factors; n=341) and an elevated-risk group (with <4 factors; n=1,476). Kaplan-Meier analysis revealed statistically significant differences in recurrence-free survival (RFS), overall survival (OS), and lung cancer-specific survival (LCSS) between the two groups (P<0.001). The low-risk group is considered to represent the population within the surgical curative time window. Patients with stage I invasive NSCLC who meet at least four of the following five criteria-female sex, tumor size ≤2 cm, solid component ≤10 mm, presence of a GGO component, and LPA histologic type-may be considered within the "surgical curative time window" and may therefore qualify for reduced surveillance intensity. Show less
📄 PDF DOI: 10.21037/tlcr-2025-894
LPA

Body Fat Distribution and Ectopic Fat Accumulation as Mediator of Diabetogenic Action of Lipid-Modifying Drugs: A Mediation Mendelian Randomization Study.

Yuanlong Hu, Xinhai Cui, Mengkai Lu +11 more · 2025 · Mayo Clinic proceedings · Elsevier · added 2026-04-24
To investigate the causal relationship between various lipid-modifying drugs and new-onset diabetes, as well as the mediators contributing to this relationship. Mediation Mendelian randomization was p Show more
To investigate the causal relationship between various lipid-modifying drugs and new-onset diabetes, as well as the mediators contributing to this relationship. Mediation Mendelian randomization was performed to investigate the causal effect of lipid-modifying drug targets on type 2 diabetes (T2D) outcomes and the proportion of this association that is mediated through ectopic fat accumulation traits. Specific sets of variants in or near genes that encode 11 lipid-modifying drug targets (LDLR, HMGCR, NPC1L1, PCSK9, APOB, ABCG5/ABCG8, LPL, PPARA, ANGPTL3, APOC3, and CETP; for expansion of gene symbols, use search tool at www.genenames.org) were extracted. Random effects inverse variance weighted were performed to evaluate the causal effects among outcomes. Mediation analyses were performed to identify the mediators of the association between lipid-modifying drugs and T2D. The study was conducted from November 10, 2023, to April 2, 2024 RESULTS: The genetic mimicry of HMGCR and APOB inhibition was associated with an increased T2D risk, whereas the genetic mimicry of LPL enhancement was linked to a lower T2D risk. Gluteofemoral adipose tissue volume was a mediator for explaining 9.52% (P=.002), 16.90% (P=.03), and 10.50% (P=.003) of the total effect of HMGCR, APOB, and LPL on T2D susceptibility, respectively. Liver fat was a mediator for explaining 21.12% (P=.005), 12.28% (P=.03), and 9.84% (P=.005) of the total effect of HMGCR, APOB, and LPL on T2D susceptibility, respectively. Our findings support the hypothesis that liver fat and gluteofemoral adipose tissue play a mediating role in the prodiabetic effects of HMGCR and APOB inhibition, as well as in the antidiabetic effects of LPL enhancement. Show less
no PDF DOI: 10.1016/j.mayocp.2024.10.018
APOB

Activation of AMPK by GLP-1R agonists mitigates Alzheimer-related phenotypes in transgenic mice.

Yun Zhang, Huaqiu Chen, Yijia Feng +14 more · 2025 · Nature aging · Nature · added 2026-04-24
Individuals with type 2 diabetes mellitus have an increased risk of developing Alzheimer's disease (AD). GLP-1 receptor agonists (GLP-1RAs) are used for glycemic control in diabetes and show potential Show more
Individuals with type 2 diabetes mellitus have an increased risk of developing Alzheimer's disease (AD). GLP-1 receptor agonists (GLP-1RAs) are used for glycemic control in diabetes and show potential neuroprotective properties, but their effects on AD and the underlying mechanisms are not well understood. Here we demonstrate that GLP-1RAs can alleviate AD-related phenotypes by activating 5' AMP-activated protein kinase (AMPK) signaling. We found that plasma GLP-1 levels were decreased in AD model mice and negatively correlated with amyloid-beta (Aβ) load in patients with AD. Enhancing GLP-1 signaling through GLP-1RAs increased CaMKK2-AMPK signaling, which subsequently reduced BACE1-mediated cleavage of amyloid precursor protein (APP) and Aβ generation. GLP-1RAs also increased AMPK activity in microglia, inhibiting neuroinflammation and promoting Aβ phagocytosis. Consequently, GLP-1RAs inhibited plaque formation and improved memory deficits in AD model mice. Our findings indicate that AMPK activation mediates the effects of GLP-1RAs on AD, highlighting the therapeutic potential of GLP-1RAs for the treatment of AD. Show less
📄 PDF DOI: 10.1038/s43587-025-00869-3
BACE1

Serum IL-27 and GDF15 levels in second trimester are associated with adverse pregnancy outcomes.

Xue Li, Luping Liu, Li Jiang +7 more · 2025 · Journal of molecular cell biology · Oxford University Press · added 2026-04-24
📄 PDF DOI: 10.1093/jmcb/mjae053
IL27

Exploring clinical and genetic evidence in association between unsaturated fatty acids and acne.

Li Zhang, Yadong Li, Yunjing Pu +3 more · 2025 · European journal of nutrition · Springer · added 2026-04-24
This study aims to comprehensively analyze the intricate relationship between unsaturated fatty acids (UFAs, particularly omega-3 and omega-6 UFAs) and acne, from their clinical therapeutic effects to Show more
This study aims to comprehensively analyze the intricate relationship between unsaturated fatty acids (UFAs, particularly omega-3 and omega-6 UFAs) and acne, from their clinical therapeutic effects to their underlying genetic regulatory mechanisms, to elucidate the role of UFAs in acne pathogenesis. Clinical evidence synthesis: we systematically reviewed randomized controlled trials (RCTs) to evaluate the impact of UFA supplementation on acne treatment outcomes. Genetic analysis: two-sample Mendelian randomization (MR) analysis we used to investigate causal relationships between serum UFA metabolites and acne, identifying potential key regulatory enzymes. The synthesis of these RCT studies confirmed that UFA supplementation improved acne conditions. MR analysis revealed causal links between three serum UFA metabolites and acne, with dihomo-gamma-linolenic acid (DGLA) (OR = 8.457; 95% CI: 2.367-30.214; P-value = 0.001) as a risk factor and arachidonic acid (AA) (OR = 0.209; 95% CI: 0.071-0.618; P-value = 0.005) and eicosapentaenoic acid (EPA) (OR = 0.318; 95% CI: 0.102-0.991; P-value = 0.048) as protective factors. Functional annotation suggested enzymes such as Δ5 desaturase (FADS1) and Δ6 desaturase (FADS2) may play a role in acne regulation. This study offers evidence that supports a connection between UFAs and acne, examining this relationship from both clinical and genetic angles. These findings highlight the role of specific UFAs and their associated metabolic enzymes in the development of acne. Omega-3 UFAs seem to have a protective effect against acne, whereas certain types and ratios of omega-6 UFAs might contribute to acne formation. The varied impacts of UFAs on acne could be attributed to disease processes mediated by specific enzymes. However, the study's limitations include its genetic analysis being primarily based on European populations, which limits the applicability of the findings to other groups. Future research should aim to include a more diverse range of participants to improve the generalizability of the results. Show less
📄 PDF DOI: 10.1007/s00394-025-03647-4
FADS1

APOE

Minnuo Cai, Hang Lei, Yuetong Zhang +4 more · 2025 · medRxiv : the preprint server for health sciences · added 2026-04-24
The role of APOE- We integrated a systematic meta-analysis of 18 studies ( The meta-analysis confirmed significant atrophy in APOE- APOE-
📄 PDF DOI: 10.64898/2025.12.08.25341534
APOE

Neuromodulatory Effects of Arecoline on Anxiety-like Behavior in Mice Exposed to Chronic Unpredictable Mild Stress.

Xiangfei Zhang, Danyang Wang, Jingwen Cui +3 more · 2025 · International journal of molecular sciences · MDPI · added 2026-04-24
Chronic stress disrupts neuroendocrine regulation, neurotransmitter balance, and neuronal redox homeostasis, thereby contributing to the development of anxiety-related neuropathology. Arecoline, the p Show more
Chronic stress disrupts neuroendocrine regulation, neurotransmitter balance, and neuronal redox homeostasis, thereby contributing to the development of anxiety-related neuropathology. Arecoline, the predominant alkaloid of Show less
📄 PDF DOI: 10.3390/ijms27010371
BDNF

Nuclear-Localized BCKDK Facilitates Homologous Recombination Repair to Support Breast Cancer Progression and Therapy Resistance.

Haiying Liu, Jiaqian Feng, Tingting Pan +10 more · 2025 · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Wiley · added 2026-04-24
Homologous recombination repair (HRR) is crucial for maintaining genomic stability by repairing DNA damage. Despite its importance, HRR's role in cancer progression is not fully elucidated. Here, this Show more
Homologous recombination repair (HRR) is crucial for maintaining genomic stability by repairing DNA damage. Despite its importance, HRR's role in cancer progression is not fully elucidated. Here, this work shows that nuclear-localized branched-chain α-ketoacid dehydrogenase kinase (BCKDK) acts as a modulator of HRR, promoting cell resistance against DNA damage-inducing therapy in breast cancer. Mechanistically, this work demonstrates that BCKDK is localized in the nucleus and phosphorylates RNF8 at Ser157, preventing the ubiquitin-mediated degradation of RAD51, thereby facilitating HRR-mediated DNA repair under replication stress. Notably, aberrant expression of the BCKDK/p-RNF8/RAD51 axis correlates with breast cancer progression and poor patient survival. Furthermore, this work identifies a small molecule inhibitor of BCKDK, GSK180736A, that disrupts its HRR function and exhibits strong tumor suppression when combined with DNA damage-inducing drugs. Collectively, this study reveals a new role of BCKDK in regulating HRR, independent of its metabolic function, presenting it as a potential therapeutic target and predictive biomarker in breast cancer. Show less
📄 PDF DOI: 10.1002/advs.202416590
BCKDK

Role of GNL3L in lung cancer: Mediating proliferation and progression through NF-κB pathway activation and upregulation of Slug, MMP2, and MMP9.

Qian Wang, Xiao-Qi Zhang, Shan-Shan Liu +4 more · 2025 · Experimental cell research · Elsevier · added 2026-04-24
The precise involvement of Guanine Nucleotide-Binding Protein-Like 3-Like Protein (GNL3L) in lung cancer progression and invasion remains unclear. In this study, we explored the impact and underlying Show more
The precise involvement of Guanine Nucleotide-Binding Protein-Like 3-Like Protein (GNL3L) in lung cancer progression and invasion remains unclear. In this study, we explored the impact and underlying mechanisms of GNL3L on the proliferation, migration, and invasion of lung adenocarcinoma (LUAD), and evaluated the therapeutic potential of targeting GNL3L. Inhibition of GNL3L expression led to a notable decrease in the in vitro proliferation, migration, and invasion of A549 and H1299 non-small cell lung cancer (NSCLC) cells. Meanwhile, GNL3L silencing could significantly reduce the tumor volume of the nude mice and improve the outcomes of tumor-bearing mice in vivo. Additionally, inhibition of GNL3L expression dramatically suppressed NF-κB activation and Slug, MMP2, and MMP9 expression. Overexpression of Slug or treatment of the GNL3L-deficient cells with NF-κB activator can partially restore the growth suppressed by GNL3L deficiency, and combined treatment with Slug overexpression and NF-κB activator could totally restore the suppressed cell growth caused by GNL3L deficiency. Moreover, the overexpression of MMP2 or MMP9 could partially enhance the reduced migration and invasion caused by GNL3L deficiency, and this GNL3L-deficiency-caused suppression of migration and invasion can be totally restored by the overexpression of MMP2 and MMP9 together. These results strongly indicated that GNL3L has the capability to activate the NF-κB and increase Slug, MMP2, and MMP9 expression, which in turn could stimulate the proliferation, migration, and invasion of lung cancer cells. NF-κB activation and Slug, MMP2, and MMP9 expression enhanced by GNL3L, leading to the promotion of proliferation, migration, and invasion of lung cancer cells, indicating the therapeutic implications and potential significance of these pathways in the progression and invasion of NSCLCs that overexpress GNL3L protein. Show less
no PDF DOI: 10.1016/j.yexcr.2025.114630
SNAI1

Regulation of perinatal estrogen levels on primordial follicle formation and activation in mouse.

Rui Xu, Lu Yin, Yiqian Zhang +6 more · 2025 · American journal of physiology. Endocrinology and metabolism · added 2026-04-24
Primordial follicle formation and activation are key for the reproductive ability of females. In mice, primordial follicles are formed and begin to activate during the perinatal period, when the level Show more
Primordial follicle formation and activation are key for the reproductive ability of females. In mice, primordial follicles are formed and begin to activate during the perinatal period, when the levels of estrogen are fluctuating. Whether estrogen plays a role in primordial follicle formation and activation, and its mechanism are still not fully elucidated. In this study, estrogen remained at high levels before birth and declined after birth. When fetal mouse ovaries (E16.5) were cultured in vitro, higher levels (10 nM) of estrogen maintained the germ cell cysts, prevented primordial follicles from forming prematurely, and promoted the full differentiation of oocytes. Furthermore, it was found that estrogen-regulated JNK-signal pathway through both nuclear and membrane receptors, thereby inhibited the degradation of E-cadherin and maintained the germ cell cysts. After birth, ovarian estrogen concentration decreases and is accompanied by the activation of primordial follicles. Hence, the ovaries of newborn mice (P3) were treated with lower concentrations (0.1 nM) of estrogen to investigate the effect of estrogen on primordial follicle activation. The results demonstrated that estrogen regulated the protein expression of cAMP synthase adenylyl cyclase 3 (ADCY3) through the membrane receptor G-protein-coupled estrogen receptor (GPER), increased the level of cAMP in the ovary, and activated the cAMP-PKA signaling pathway to promote the activation of primordial follicles. This study revealed the regulatory role of perinatal estrogen levels on primordial follicle formation and activation before and after birth, which would help to better understand the potential physiological effect of estrogen in vivo. Show less
no PDF DOI: 10.1152/ajpendo.00026.2025
ADCY3

Long-read sequencing of 945 Han individuals identifies structural variants associated with phenotypic diversity and disease susceptibility.

Jiao Gong, Huiru Sun, Kaiyuan Wang +26 more · 2025 · Nature communications · Nature · added 2026-04-24
Genomic structural variants (SVs) are a major source of genetic diversity in humans. Here, through long-read sequencing of 945 Han Chinese genomes, we identify 111,288 SVs, including 24.56% unreported Show more
Genomic structural variants (SVs) are a major source of genetic diversity in humans. Here, through long-read sequencing of 945 Han Chinese genomes, we identify 111,288 SVs, including 24.56% unreported variants, many with predicted functional importance. By integrating human population-level phenotypic and multi-omics data as well as two humanized mouse models, we demonstrate the causal roles of two SVs: one SV that emerges at the common ancestor of modern humans, Neanderthals, and Denisovans in GSDMD for bone mineral density and one modern-human-specific SV in WWP2 impacting height, weight, fat, craniofacial phenotypes and immunity. Our results suggest that the GSDMD SV could serve as a rapid and cost-effective biomarker for assessing the risk of cisplatin-induced acute kidney injury. The functional conservation from human to mouse and widespread signals of positive natural selection suggest that both SVs likely influence local adaptation, phenotypic diversity, and disease susceptibility across diverse human populations. Show less
no PDF DOI: 10.1038/s41467-025-56661-9
WWP2

Nose-to-brain delivery of targeted lipid nanoparticles as two-pronged

Yanyan Xu, Xiangtong Ye, Yanfeng Du +8 more · 2025 · Acta pharmaceutica Sinica. B · Elsevier · added 2026-04-24
Alzheimer's disease (AD), characterized by
📄 PDF DOI: 10.1016/j.apsb.2025.02.035
BACE1

Exogenous lactate infusion enhanced VMH neuroplasticity and visceral fat reduction via PGC-1α-ERα pathway in female rats.

Shuai Tian, Jing Han, Zhaomin Zhang +3 more · 2025 · European journal of applied physiology · Springer · added 2026-04-24
High-intensity exercise promotes visceral adipose tissue (VAT) breakdown in females via the hypothalamic ERα pathway, and exogenous lactate infusion combined with aerobic training (AT) mimics this eff Show more
High-intensity exercise promotes visceral adipose tissue (VAT) breakdown in females via the hypothalamic ERα pathway, and exogenous lactate infusion combined with aerobic training (AT) mimics this effect. However, whether lactate administration can independently mediate hypothalamic plasticity and VAT catabolism as a standalone nutritional strategy remains unexplored. Firstly, using a two-factor design (Lactate × AT) in female SD rats, we showed that long-term exogenous lactate infusion independently induced co-expression of Estrogen receptor α (ERα) and Brain-derived neurotrophic factor (BDNF) in the ventromedial hypothalamus (VMH) and elevated local field potential spectral power in specific bands. These neural adaptations were accompanied by increased resting metabolic rate, enhanced fat oxidation, and enhanced lipolysis, thereby preventing excessive VAT accumulation induced by a high-fat diet. Furthermore, pharmacological inhibition confirmed that Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-α (PGC-1α) acts as a co-upstream signal of ERα and BDNF mediating this process. Our findings reveal that standalone lactate administration induces functional plasticity and metabolic reprogramming through the VMH PGC-1α-ERα pathway, independent of exercise, and effectively suppresses pathological VAT accumulation in female rats. This study identifies potential nutritional interventions and mechanistic targets for preventing female-centered obesity. Show less
📄 PDF DOI: 10.1007/s00421-025-06097-2
BDNF

SIPA1L3 via its PDZ domain inhibits the tight junction-associated AMOT-Patj to promote a malignant phenotype in NSCLC.

Lin Wang, Bin-Xue Wang, Rui Zhang +2 more · 2025 · Medicine · added 2026-04-24
Signal-induced proliferation-associated 1 like 3 (SIPA1L3) is a member of the protein family. Very limited data are currently available regarding the role of SIPA1L3 in human carcinoma. Therefore, in Show more
Signal-induced proliferation-associated 1 like 3 (SIPA1L3) is a member of the protein family. Very limited data are currently available regarding the role of SIPA1L3 in human carcinoma. Therefore, in this study, we investigated the expression pattern and function of SIPA1L3 in non-small cell lung cancer (NSCLC). We analyzed the distribution of SIPA1L3 in NSCLC specimens by immunohistochemistry, the relationship between SIPA1L3 expression and patient clinicopathological features, and investigated the effect of SIPA1L3 on cell growth and invasion in vivo and in vitro using small interfering RNA. Western blotting and immunoprecipitation were performed to demonstrate the interaction between SIPA1L3 and tight junction-associated angiomotin (AMOT) and Pals1-associtated tight junction protein. We found that SIPA1L3 was overexpressed in NSCLC clinical tissue samples and was associated with several clinicopathological factors. SIPA1L3 affects the proliferation and invasion of cancer cells both in vivo and in vitro. Using a SIPA1L3 mutant, we found that SIPA1L3 interacts with AMOT through its PDZ domain, which inhibits the binding of AMOT to Pals1-associtated tight junction protein and further decreases AMOT anchoring to tight junctions. Our findings suggested that SIPA1L3 promotes tumorigenesis in lung cancer cells through its PDZ domain-mediated interaction with AMOT, suggesting that SIPA1L3 is a novel candidate gene that contributes to the malignant phenotype of lung cancer. Show less
no PDF DOI: 10.1097/MD.0000000000045095
PATJ

Associations between 24-hour movement behaviors and physical fitness in adolescents: A cross-sectional study using objective and subjective measures.

Zhiqiang Ren, Yutai Cai, Qiaoman Mo +5 more · 2025 · Journal of sports sciences · Taylor & Francis · added 2026-04-24
This study aimed to investigate the association between objectively and subjectively measured 24-hour movement behaviors and physical fitness, and explore how the reallocation of time between 24-hour Show more
This study aimed to investigate the association between objectively and subjectively measured 24-hour movement behaviors and physical fitness, and explore how the reallocation of time between 24-hour movement behaviors is associated with changes in physical fitness in adolescents. A total of 690 adolescents aged 14-17 years (55% girls) were included in this cross-sectional study conducted in Foshan, China. Moderate-to-vigorous physical activity (MVPA), light physical activity (LPA), sedentary behavior, and sleep were assessed using accelerometers in combination with a questionnaire. Physical fitness was tested through body mass index, forced vital capacity, 50-m sprint, standing long jump, sit-and-reach, gender-specific 800/1000-m run, and pull-ups/sit-ups. MVPA was significantly associated with better performance in the 50-m sprint ( Show less
no PDF DOI: 10.1080/02640414.2025.2567791
LPA

Targeting TRIM15-mediated Axin1 depolymerization suppresses Wnt signaling and inhibits colorectal cancer growth.

Hangfei Liang, Fanghong Zheng, Jincheng Wu +5 more · 2025 · Cell death & disease · Nature · added 2026-04-24
Axin1 plays a critical role in regulating the Wnt/β-catenin signaling pathway and cancer progression, and its polymerization is indispensable for the assembly of the β-catenin destruction complex. How Show more
Axin1 plays a critical role in regulating the Wnt/β-catenin signaling pathway and cancer progression, and its polymerization is indispensable for the assembly of the β-catenin destruction complex. However, the mechanisms that control Axin1 polymerization are limited. Here, we reveal that TRIM15 interferes with the polymerization of Axin1, thereby promoting Wnt activation and colorectal cancer growth. Mechanistically, TRIM15 strongly interacts with Axin1 through its coiled-coil domain to disrupt the polymerization among Axin1 molecules. Manipulation of TRIM15 expression dramatically weakens Wnt signaling, cell proliferation, and tumor growth. Furthermore, conditional genetic ablation of Trim15 in mice inhibits tumor formation in both AOM/DSS-induced and Apc Show less
📄 PDF DOI: 10.1038/s41419-025-08400-7
AXIN1

ANGPTL3 nanobody-FGF21 fusion protein ameliorates metabolic dysfunction-associated fatty liver disease via regulation of lipid and glucose metabolism and attenuation of oxidative stress.

Yuanzhen Zhang, Xiaozhi Hu, Zhonglian Cao +10 more · 2025 · International journal of biological macromolecules · Elsevier · added 2026-04-24
Metabolic dysfunction-associated fatty liver disease (MAFLD), driven by dyslipidemia and hepatic lipid deposition, has become a major public health concern. Angiopoietin-like protein 3 (ANGPTL3), a li Show more
Metabolic dysfunction-associated fatty liver disease (MAFLD), driven by dyslipidemia and hepatic lipid deposition, has become a major public health concern. Angiopoietin-like protein 3 (ANGPTL3), a lipoprotein lipase (LPL) activity inhibitor, can inhibit triglycerides (TGs) decomposition, and fibroblast growth factor 21 (FGF21) enhances fatty acids' β-oxidation in liver. We constructed a novel fusion protein combining the anti-ANGPTL3 nanobody FD03 and FGF21 (FD03-FGF21), which exerted appropriate binding affinities to ANGPTL3 and β-Klotho respectively. Our results showed FD03-FGF21 restored bioactivity of LPL which inhibited by ANGPTL3 and activated downstream pathway of FGF21 in iLite FGF21 assay-ready cells. Next, FD03-FGF21 showed a significant therapeutic effect in MAFLD mice, including attenuation of metabolic dyslipidemia, hepatic lipid accumulation, and impaired glucose tolerance. Compared to other treatments, FD03-FGF21 achieved the most significant therapeutic effect with a 79.78 % attenuation of low-density lipoprotein cholesterol (LDL-C) and a 95.8 % reduction of hepatic lipid accumulation. Mechanistically, transcriptomic analysis revealed that differential expression genes (DEGs) were principally clustered into lipid metabolism and oxidative stress pathways after the fusion protein treatment, especially the key lipid metabolism genes of LDLR and CD36 were significantly upregulated and downregulated respectively, as confirmed by WB. Furthermore, lipidomic and metabolomic analysis indicated the fusion protein ameliorated disorders in lipid and protein metabolism mainly through the downregulation of DG and upregulation of PC. Hepatic oxidative stress and inflammation were significantly reduced after administration of the fusion protein in MAFLD mice. Collectively, FD03-FGF21 represents an effective therapeutic strategy for MAFLD therapy through ameliorating lipid metabolism and oxidative stress. Show less
no PDF DOI: 10.1016/j.ijbiomac.2025.148726
LPL

Surufatinib in advanced neuroendocrine tumours: Final overall survival from two randomised, double-blind, placebo-controlled phase 3 studies (SANET-ep and SANET-p).

Jianming Xu, Lin Shen, Jie Li +28 more · 2025 · European journal of cancer (Oxford, England : 1990) · Elsevier · added 2026-04-24
SANET-ep (NCT02588170) and SANET-p (NCT02589821) demonstrated the efficacy and safety of surufatinib versus placebo in patients with advanced extra-pancreatic and pancreatic neuroendocrine tumours (NE Show more
SANET-ep (NCT02588170) and SANET-p (NCT02589821) demonstrated the efficacy and safety of surufatinib versus placebo in patients with advanced extra-pancreatic and pancreatic neuroendocrine tumours (NETs). Here, we present a pooled analysis of final overall survival (OS) from two randomised phase 3 studies. The SANET studies were randomised, placebo-controlled, double-blind, phase 3 studies in China, comparing the efficacy and safety of oral 300-mg surufatinib (n = 265) versus placebo (n = 133) in patients with unresectable/metastatic, well-differentiated NETs (grade 1/2). After progression of disease or study unblinding, patients receiving placebo crossed over/switched to open-label surufatinib. By pooling the data from the two studies, OS analysis was completed using Kaplan-Meier methodology and a Cox proportional hazards model in the intention-to-treat population. Exploratory analyses were performed using different models to correct the confounding effect introduced by crossover. Long-term safety was assessed. At study termination, 69 % of the placebo group had crossed over/switched to surufatinib. Median OS was 50.1 versus 46.8 months for patients initially on surufatinib versus those initially on placebo (stratified hazard ratio [HR] 0.935, 95 % confidence interval [CI] 0.684-1.278; p = 0.6727). After correcting the confounding effect introduced by crossover/switching, the HR ranged from 0.558 to 0.825. Commonly (≥10 %) reported treatment-related adverse events (grade 3/4) included hypertension and proteinuria. OS of patients initially on surufatinib was not significantly longer versus patients initially on placebo, likely due to the high amount of crossover from placebo to surufatinib. No new safety signals were observed. SANET-ep (NCT02588170) and SANET-p (NCT02589821). Show less
no PDF DOI: 10.1016/j.ejca.2025.115398
FGFR1

Biomimetic non-collagenous proteins-calcium phosphate complex with superior osteogenesis via regulating macrophage IL-27 secretion.

Shenglong Tan, Xinghong Luo, Yifan Wang +9 more · 2025 · Biomaterials · Elsevier · added 2026-04-24
Traumatic defects or non-union fractures presents a substantial challenge in the fields of tissue engineering and regenerative medicine. Although synthetic calcium phosphate-based biomaterials (CaPs) Show more
Traumatic defects or non-union fractures presents a substantial challenge in the fields of tissue engineering and regenerative medicine. Although synthetic calcium phosphate-based biomaterials (CaPs) such as dibasic calcium phosphate anhydrate (DCPA) are commonly employed for bone repair, their inadequate cellular immune responses significantly impede sustained degradation and optimal osteogenesis. In this study, drawing inspiration from the key structure of an acidic non-collagenous protein-CaP complex (ANCPs-CaP) essential for natural bone formation, we prepared biomimetic mineralized dibasic calcium phosphate (MDCPA). This preparation utilized plant-derived non-collagenous protein Zein as the organic template and acidic artificial saliva as the mineralization medium. Physicochemical property analysis revealed that MDCPA is a complex of Zein and DCPA, which mimics the composite of the natural ANCP-CaP. Moreover, MDCPA exhibited enhanced biodegradability and osteogenic potential. Mechanistic insight revealed that MDCPA can be phagocytized and degraded by macrophages via the FCγRIII receptor, leading to the release of interleukin 27 (IL-27), which promotes osteogenic differentiation by osteoimmunomodulation. The critical role of IL-27 in osteogenesis is further confirmed using IL-27 gene knockout mice. Additionally, MDCPA demonstrates effective healing of critical-sized defects in rat cranial bones within only 4 w, providing a promising basis and valuable insights for critical-sized bone defects regeneration. Show less
no PDF DOI: 10.1016/j.biomaterials.2024.122917
IL27

IL-27 attenuated macrophage injury and inflammation induced by Mycobacterium tuberculosis by activating autophagy.

Yushan Zhou, Yuxuan Zhang, Yanli Li +3 more · 2025 · In vitro cellular & developmental biology. Animal · Springer · added 2026-04-24
Interleukin-27 (IL-27) is a cytokine that is reported to be highly expressed in the peripheral blood of patients with pulmonary tuberculosis (PTB). IL-27-mediated signaling pathways, which exhibit ant Show more
Interleukin-27 (IL-27) is a cytokine that is reported to be highly expressed in the peripheral blood of patients with pulmonary tuberculosis (PTB). IL-27-mediated signaling pathways, which exhibit anti- Mycobacterium tuberculosis (Mtb) properties, have also been demonstrated in macrophages infected with Mtb. However, the exact mechanism remains unclear. This study aimed to clarify the potential molecular mechanisms through which IL-27 enhances macrophage resistance to Mtb infection. Both normal and PTB patients provided bronchoalveolar lavage fluid (BALF). Peripheral blood mononuclear cells (PBMCs) were isolated from healthy individuals and stimulated with 50 ng/mL macrophage-colony stimulating factor (M-CSF) to obtain monocyte-derived macrophages (MDMs). Using 100 ng/mL phorbol 12-myristate 13-acetate (PMA), THP-1 cells were induced to differentiate into THP-1-derived macrophage-like cells (TDMs). Both MDMs and TDMs were subsequently infected with the Mtb strain H37Rv and treated with 50 ng/mL IL-27 prior to infection. The damage and inflammation of macrophages were examined using flow cytometry, enzyme-linked immunosorbent assay (ELISA), and Western blotting. Patients with PTB had elevated levels of IL-27 in their BALF. Preconditioning with IL-27 was shown to reduce H37Rv-induced MDMs and TDMs apoptosis while also decreasing the levels of Cleaved Caspase-3, Bax and the proinflammatory cytokines TNF-α, IL-1β, and IL-6, promoting the expression of Bcl-2 and the anti-inflammatory factors IL-10 and IL-4. Silencing of the IL-27 receptor IL-27Ra increased macrophage damage and inflammation triggered by H37Rv. Mechanistically, IL-27 activates autophagy by inhibiting TLR4/NF-κB signaling and activating the PI3K/AKT signaling pathway, thereby inhibiting H37Rv-induced macrophage apoptosis and the inflammatory response. Our study suggests that IL-27 alleviates H37Rv-induced macrophage injury and the inflammatory response by activating autophagy and that IL-27 may be a new target for the treatment of PTB. Show less
📄 PDF DOI: 10.1007/s11626-024-00989-x
IL27