👤 Jia 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, 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

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

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

Shared genetic loci connect cardiovascular disease with blood pressure and lipid traits in East Asian populations.

Peng Zhong, Chumeng Zhang, Qinfeng Wu +1 more · 2025 · Frontiers in genetics · Frontiers · added 2026-04-24
Cardiovascular diseases (CVDs), including myocardial infarction (MI), heart failure (HF), atrial fibrillation (AF), and arrhythmia, are major contributors to global mortality and often share overlappi Show more
Cardiovascular diseases (CVDs), including myocardial infarction (MI), heart failure (HF), atrial fibrillation (AF), and arrhythmia, are major contributors to global mortality and often share overlapping risk factors and pathophysiological mechanisms. While genome-wide association studies (GWAS) have identified many loci for individual CVDs, the shared genetic architecture across related traits-particularly in East Asian populations-remains underexplored. We integrated large-scale GWAS summary statistics from East Asian populations to perform genome-wide and local genetic correlation analyses across four CVD phenotypes and five cardiometabolic traits (blood pressure and lipid levels). Using stratified LD score regression, we assessed tissue-specific heritability enrichment. Multi-trait analysis of GWAS (MTAG) was then employed to identify pleiotropic loci associated with multiple traits, with functional annotation and expression quantitative trait loci (eQTL) data used to explore biological relevance. We observed extensive genetic correlations among CVDs and between CVDs and cardiometabolic traits, with HF showing the strongest connections to both MI and arrhythmia. Notable genome-wide correlations were found between MI and SBP (rg = 0.35, Our findings provide comprehensive insight into the shared genetic determinants of cardiovascular and metabolic diseases in East Asian populations. The identification of pleiotropic and ancestry-specific loci, along with tissue-specific regulatory patterns, underscores the need for integrative multi-trait and population-informed approaches in cardiovascular genetics and risk prediction. Show less
📄 PDF DOI: 10.3389/fgene.2025.1635378
MC4R

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

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

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

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

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

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

Lp(a) levels and ischemic stroke recurrence in type 2 diabetes mellitus.

Aichun Cheng, Fangyuan Zhang, Aoming Jin +5 more · 2025 · Diabetology & metabolic syndrome · BioMed Central · added 2026-04-24
We investigated the association between lipoprotein(a) [Lp(a)] levels and stroke recurrence in type 2 diabetes mellitus (T2DM) patients with recent acute ischemic stroke or transient ischemic attack ( Show more
We investigated the association between lipoprotein(a) [Lp(a)] levels and stroke recurrence in type 2 diabetes mellitus (T2DM) patients with recent acute ischemic stroke or transient ischemic attack (TIA). This study included 3,311 T2DM patients with recent acute ischemic stroke or TIA and complete Lp(a) data from the Third China National Stroke Registry. The patients were categorized into three groups based on the 40th and 70th percentiles of the Lp(a): ≤13.1, 13.1 to 29.2 and ≥ 29.2 mg/dL. The primary outcome was stroke recurrence within one year, with incident cases further classified as either ischemic or hemorrhagic. Cox proportional hazards regression and restricted cubic splines were used to evaluate these associations. A total of 3311 patients (2142 men, 64.69%, median age 63) were analyzed. Restricted cubic spline analysis revealed a U-shaped relationship between Lp(a) levels and the risk of stroke recurrence. After adjusting for cardiovascular risk factors, patients with Lp(a) levels ≤ 13.1 mg/dL or ≥ 29.2 mg/dL had hazard ratios of 1.34 (95% confidence interval (CI), 1.02-1.76) and 1.35 (95% CI, 1.01-1.79), respectively, for total stroke compared to those with Lp(a) levels between 13.1 and 29.2 mg/dL. The corresponding hazard ratios were 1.36 (95% CI, 1.02-1.81) and 1.36 (95% CI, 1.01-1.83) for ischemic stroke and 0.88 (95% CI, 0.37-2.09) and 0.77 (95% CI, 0.31-1.94) for hemorrhagic stroke, respectively. Both low and high levels of Lp(a) are associated with an increased risk of stroke recurrence in T2DM patients with a recent history of acute ischemic stroke or TIA, demonstrating a U-shaped relationship. Show less
📄 PDF DOI: 10.1186/s13098-025-02005-y
LPA

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

Physiological response and lipid metabolism induced by re-feeding in Jian carp (Cyprinus carpio var. Jian) subjected to short-term starvation.

Yu Zhang, Gang Jiang, Wenrong Feng +4 more · 2025 · Comparative biochemistry and physiology. Part A, Molecular & integrative physiology · Elsevier · added 2026-04-24
The effects of starvation and re-feeding on Jian carp (Cyprinus carpio var. Jian) remain incompletely understood. This study investigated changes in growth performance, liver antioxidant capacity, int Show more
The effects of starvation and re-feeding on Jian carp (Cyprinus carpio var. Jian) remain incompletely understood. This study investigated changes in growth performance, liver antioxidant capacity, intestinal morphology, fatty acid profile, and expression of genes related to lipid metabolism. Juvenile C. carpio var. Jian, with initial body weight of 29.50 ± 2.00 g, were reared in 15 cylindrical culture barrels (200L) at a stocking density of 10 fish per barrel. These fish were subjected to five feeding regimes: a continuous feeding group (control group, treatment A), complete fasting (treatment B), 1, 2, and 3 days starvation within one week, followed by re-feeding 6 days (treatment C), 5 days (treatment D), and 4 days (treatment E). The results indicated significantly lower growth performance in C. carpio var. Jian in treatments B and E compared to the control and treatment C (P < 0.05). Intestinal length (only 627 ± 13.14 μm in treatment B) was significantly reduced, and an increase in vacuoles was observed in C. carpio var. Jian with the prolonged starvation. Antioxidant enzyme activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were significantly (P < 0.05) improved in treatment C when compared with treatments B, D and E.. In contrast, malondialdehyde (MDA) value was lowest (12.62 ± 0.60 nmol/mL) in treatment B. Furthermore, continuous starvation significantly decreased the total lipid and fatty acids contents in the muscle (P < 0.05). Compared with the control group, the reduction of total lipid and fatty acids contents was 31.53 % and 4.57 %, respectively, particularly affecting n3PUFA and n6PUFA. However, after one-day re-feeding, these contents resumed. Lipid metabolism is closely related to fish health, while in the current study, the genes related to lipid metabolism including lipoprotein lipase (LPL), 6-phosphogluconate dehydrogenase (G6PD), and peroxisome proliferator-activated receptor alpha (PPARα) did not differ significantly in treatment C compared to the control group (P > 0.05). In contrast, expressions in treatments B, D, and E were significantly reduced (P < 0.05). Taken together, prolonged starvation (>one day per week) not only affected the growth, which may further disrupt the intestinal structure, weaken antioxidant capacity, but also attenuate lipid deposition. Show less
no PDF DOI: 10.1016/j.cbpa.2025.111832
LPL

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

Genetic findings of children with congenital heart diseases using chromosomal microarray and trio-based whole exome sequencing.

Rui Guo, Chunhong Duan, Mehdi Zarrei +9 more · 2025 · Scientific reports · Nature · added 2026-04-24
Congenital heart disease (CHD) is the most common type of birth defects in humans. Genetic factors have been identified as an important contributor to the etiology of CHD. However, the underlying gene Show more
Congenital heart disease (CHD) is the most common type of birth defects in humans. Genetic factors have been identified as an important contributor to the etiology of CHD. However, the underlying genetic causes in most individuals remain unclear. Here, 101 individuals with CHD and their unaffected parents were included in this study. Chromosomal microarray analysis (CMA) as a first-tier clinical diagnostic tool was applied for all affected individuals, followed by trio-based whole exome sequencing (WES) of 76 probands and proband-only WES of 3 probands. We detected aneuploidies in 2 individuals (trisomy 21 and monosomy X), 21 pathogenic and likely pathogenic copy number variants (CNVs) in 19 individuals, and pathogenic and likely pathogenic SNVs/InDels in 8 individuals. The combined genetic diagnostic yield was 28.7%, including 20.8% with chromosomal abnormalities and 7.9% with sequence-level variants. Eighteen CNVs in 17 individuals were associated with 13 recurrent chromosomal microdeletion/microduplication syndromes, the most common being 22q11.2 deletion syndrome. Pathogenic/likely pathogenic sequence-level variants were identified in 8 genes, including GATA6, FLNA, KANSL1, TRAF7, KAT6A, PKD1L1, RIT1, and SMAD6. Trio sequencing facilitated the identification of pathogenic variation (55.6% were de novo missense variants). In individuals with extracardiac features, the overall detection rate was significantly higher (61.5%) than in individuals with isolated CHD (17.3%) (P = 4.6 × 10 Show less
📄 PDF DOI: 10.1038/s41598-025-06977-9
KANSL1

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

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

PDZ domains of PATJ facilitate immunological synapse formation to promote T cell activation.

Xinxin Xiong, Danyang Wang, Liping Xu +7 more · 2025 · Journal for immunotherapy of cancer · added 2026-04-24
The highly organized structures of the immunological synapse (IS) are crucial for T cell activation. PDZ domains might be involved in the formation of the IS by serving as docking sites for protein in Show more
The highly organized structures of the immunological synapse (IS) are crucial for T cell activation. PDZ domains might be involved in the formation of the IS by serving as docking sites for protein interactions. In this study, we investigate the role of the PALS1-associated tight junction protein (PATJ), which contains 10 PDZ domains, in the formation of IS and its subsequent impact on T cell activation. To elucidate the function of PATJ, we generated murine models with conditional T cell-specific knockout of We observed a rapid increase in PATJ expression during T cell activation. Conditional knockout of Our study reveals an important role of PATJ in the formation of IS and provides an approach to improve the efficacy of CAR-T therapy. Show less
no PDF DOI: 10.1136/jitc-2024-010966
PATJ

Identification and prognostic potential of lactylation-related genes in sepsis: implications of the RBM25-acly axis.

Yu Li, Tao Zhang, Lin Zhou +4 more · 2025 · International immunopharmacology · Elsevier · added 2026-04-24
Elevated circulating lactate serves as a critical biomarker in sepsis, yet the epigenetic mechanisms by which lactate influences disease progression remain unclear. This study aims to identify lactate Show more
Elevated circulating lactate serves as a critical biomarker in sepsis, yet the epigenetic mechanisms by which lactate influences disease progression remain unclear. This study aims to identify lactate-associated genes in sepsis, decode their regulatory roles, and assess their potential as therapeutic targets. We performed transcriptome-wide bioinformatic analyses to identify lactylation-related differentially expressed genes (DEGs) between sepsis patients and healthy controls. Pathway enrichment highlighted immune signaling circuits. Five DEGs (ZC3H4, RBM10, PCBP2, RBM25, HNRNPM) were prioritized via ROC analysis, and their combined expression formed a prognostic signature with strong predictive power (AUC > 0.85). Validation in murine sepsis-induced acute lung injury (ALI) models (cecal ligation-puncture and LPS challenge) confirmed significant upregulation of these five genes by qRT-PCR. RBM25 was selected for deeper functional study. Mechanistic assays implicate an RBM25-Acly axis that couples altered metabolism to histone lactylation and transcriptional reprogramming. Notably, we propose the RBM25-Acly axis that couples altered metabolism to histone lactylation and transcriptional reprogramming. Our work uncovers a novel metabolic-epigenetic circuit in sepsis driven by lactylation, with RBM25 and its regulation of ACLY as a key node. The lactylation-based gene signature offers a high-fidelity prognostic tool, and targeting the RBM25-Acly pathway may open new therapeutic avenues. These findings lay a foundation for precision interventions that integrate metabolic and epigenetic strategies in sepsis care. Show less
no PDF DOI: 10.1016/j.intimp.2025.115177
ZC3H4

Genetic evidence for the liver-brain axis: lipid metabolism and neurodegenerative disease risk.

Zeyu Wang, Zixiao Yin, Guangyong Sun +2 more · 2025 · Lipids in health and disease · BioMed Central · added 2026-04-24
The liver‒brain axis is critical in neurodegenerative diseases (NDs), with lipid metabolism influencing neuroinflammation and microglial function. A systematic investigation of the genetic relationshi Show more
The liver‒brain axis is critical in neurodegenerative diseases (NDs), with lipid metabolism influencing neuroinflammation and microglial function. A systematic investigation of the genetic relationship between lipid metabolism abnormalities and ND, namely, Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS), is lacking. To assess potential causal links between ND and six lipid parameters, two-sample Mendelian randomization (MR) was used. Large-scale European ancestry GWAS data for lipid parameters and ND (AD, ALS, PD, and MS) were used. Genetic variants demonstrating significant correlations (P < 5 × 10 MR via the inverse-variance weighted method revealed causal effects of cholesterol (CHOL, OR = 1.10, 95% CI: 1.03-1.18, P = 4.23 × 10⁻ Higher CHOL and LDLC levels were associated with increased ALS risk, suggesting a potential causal link, and supporting the liver‒brain axis hypothesis in ND. Current genetic evidence does not support a significant role for lipid metabolism in PD and MS etiology, suggesting the relationship between lipid metabolism and other NDs may be more complex and warrants further investigation. Show less
📄 PDF DOI: 10.1186/s12944-025-02455-3
APOB

Genetic association analysis between LDL-c lowering drugs and portal hypertension using Mendelian randomization analysis.

Qing-Ao Xiao, Xiao-Long Li, Lei Qin +1 more · 2025 · Scientific reports · Nature · added 2026-04-24
Clinical guidelines recommend the use of statins to reduce portal pressure and alleviate portal hypertension (PH). However, there is a lack of population-level studies on the use of non-statin Low-Den Show more
Clinical guidelines recommend the use of statins to reduce portal pressure and alleviate portal hypertension (PH). However, there is a lack of population-level studies on the use of non-statin Low-Density Lipoprotein Cholesterol (LDL-c) reduction agents for the treatment of PH. This study utilized a novel method, Mendelian Randomization (MR) analysis, to investigate the impact of commonly used LDL-c-lowering medications on PH. Instrumental variables (IVs) for eight lipid-lowering drug-related genes were extracted from three large-scale LDL-c databases of Genome-Wide Association Studies (GWAS), followed by MR analysis. The MR results indicated that, compared to normal individuals, lower expression of CETP and NPC1L1 in whole blood (result of meta-analysis: CETP [OR: 0.322, 95%CI:0.130-0.795, P = 1.396e-02], NPC1L1 [OR: 0.057, 95%CI: 0.022-0.146, P = 2.670e-09]) is associated with reduced portal pressure. The IVs of target genes were subjected to MR analysis with coronary atherosclerosis (CAD) as a positive control, confirming that the IVs can effectively substitute for the biological function of the target gene, thereby further enhancing the reliability of the results. Subsequently, Summary-based Mendelian Randomization (SMR) analysis was conducted by using expression quantitative trait loci (eQTL) data to validate the results of the MR analysis. The SMR results suggested that only NPC1L1 is associated with PH (OR: 0.648, 95%CI: 0.472-0.891, P Show less
📄 PDF DOI: 10.1038/s41598-025-08153-5
CETP

Potential mechanisms and therapeutic effect of dietary resveratrol supplementation on the spleen organ of chicken in chronic unpredictable mild stress transcriptomic analysis.

Farooque Laghari, Qingqing Chang, Haoran Zhang +5 more · 2025 · Poultry science · Elsevier · added 2026-04-24
Chronic unpredictable mild stress (CUMS) affects chicken immune system and welfare, causing huge losses of growth performance and welfare. Resveratrol (RSV), an antioxidant and anti-inflammatory natur Show more
Chronic unpredictable mild stress (CUMS) affects chicken immune system and welfare, causing huge losses of growth performance and welfare. Resveratrol (RSV), an antioxidant and anti-inflammatory natural plant polyphenol, is widely used for the prevention of stress related disease. The aim of this study is to explore the therapeutic effect of RSV on spleen damage in CUMS. We successfully constructed a CUMS model. A total of 288 healthy one-day-old chicks were used in this study and were divided in 3 groups, control, CUMS and CUMS+RSV group. During 42 days of age, spleen tissue samples were collected and analyzed. Transmission electron microscope (TEM), Hematoxylin and eosin (H&E) staining, immunofluorescence, qRT- PCR, Western blots, immunohistochemical staining and RNA- sequencing (RNA-seq) technology was used to determine any changes and analyzed the mRNA and enrichment pathways. Histopathology and ultrastructure showed there was a severe damage of tissues. The results of RNA-seq showed that a total of 206, 267 and 211 DEGs were identified (log2 Fold Change| >1, P < 0.05) in control -vs- CUMS group, CUMS -vs- CUMS+RSV group and control -vs- CUMS+RSV group, respectively. Through Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of the SDEGs, two immune/stress- related pathways including PPAR signaling pathway and neuroactive ligand receptor interaction were selected. The genes related to PPAR signaling pathway identified were PLIN1, MMP1, ANGPTL4 and FABP4 and Neuroactive ligand-receptor interaction genes were GRPR, NTSR1, KNG1 and AGT. The PLIN1, MMP1, ANGPTL4, FABP4, GRPR, KNG1 and AGT were up regulated and NTSR1 was down regulated in CUMS group. When compared to CUMS -vs- CUMS+RSV group, PLIN1, FABP4, KNG1 and AGT were down regulated genes and NTSR1 was up regulated gene. Taken together, KEGG pathway analyses of DEGs, verified by qRT-PCR and Western blots, the current study suggested that these data reveal the promising role of RSV in the prevention and therapy of a wide variety of tissue damage and PPAR signaling pathway, neuroactive ligand-receptor interaction in chronic unpredictable mild stress. Show less
📄 PDF DOI: 10.1016/j.psj.2025.104940
ANGPTL4

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

Therapeutic effect and potential mechanism of Fufang Danshen dripping pills for stable coronary heart disease: a randomized controlled trial.

Li-Qin Meng, Pei-Ying Huang, Qing-Min Li +7 more · 2025 · Frontiers in cardiovascular medicine · Frontiers · added 2026-04-24
The efficacy and mechanism of Fufang Danshen dripping pills (FFDS) in the secondary prevention of stable coronary heart disease (SCHD) is currently undetermined. This study aims to investigate the eff Show more
The efficacy and mechanism of Fufang Danshen dripping pills (FFDS) in the secondary prevention of stable coronary heart disease (SCHD) is currently undetermined. This study aims to investigate the efficacy and preliminary mechanism by which FFDS may impact the progression of SCHD. Based on randomization, we administered oral FFDS to 30 patients with SCHD in addition to conventional treatment for 30 days. After treatment, three-months major adverse cardiovascular events (MACE) were assessed as the primary outcome. Additionally, we evaluated the patients' Seattle Angina Questionnaire score, blood pressure, circulating levels of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, C-reactive protein, platelets, alanine aminotransferase, aspartate aminotransferase, serum creatinine, and fasting blood glucose as the secondary outcomes. Furthermore, we utilized mass spectrometry analysis, network pharmacology, and lipidomics to predict the potential mechanisms of FFDS in the treatment of SCHD. Following treatment, FFDS demonstrated significant improvements in serum triglyceride levels ( In individuals with SCHD, the administration of FFDS has been shown to effectively reduce circulating triglyceride levels and decrease the frequency of angina episodes. This therapeutic effect is likely due to the active components of FFDS targeting key proteins: LPL, CD36, FABPpm, L-FABP, LCAT, and CEPT. https://www.chictr.org.cn/, identifier (ChiCTR2400080149). Show less
📄 PDF DOI: 10.3389/fcvm.2025.1506917
LPL

Discovery of First Branched-Chain Ketoacid Dehydrogenase Kinase (BDK) Inhibitor Clinical Candidate PF-07328948.

Kevin J Filipski, Luis A Martinez-Alsina, Matthew R Reese +31 more · 2025 · Journal of medicinal chemistry · ACS Publications · added 2026-04-24
Inhibition of branched-chain ketoacid dehydrogenase kinase (BDK or BCKDK), a negative regulator of branched-chain amino acid (BCAA) metabolism, is hypothesized to treat cardio-metabolic diseases. From Show more
Inhibition of branched-chain ketoacid dehydrogenase kinase (BDK or BCKDK), a negative regulator of branched-chain amino acid (BCAA) metabolism, is hypothesized to treat cardio-metabolic diseases. From a starting point with potential idiosyncratic toxicity risk, modification to a benzothiophene core and discovery of a cryptic pocket allowed for improved potency with 3-aryl substitution to arrive at PF-07328948, which was largely devoid of protein covalent binding liability. This BDK inhibitor was shown also to be a BDK degrader in cells and in vivo rodent studies. Plasma biomarkers, including BCAAs and branched-chain ketoacids (BCKAs), were lowered in vivo with enhanced pharmacodynamic effect upon chronic dosing due to BDK degradation. This molecule improves metabolic and heart failure end points in rodent models. PF-07328948 is the first known selective BDK inhibitor candidate to be examined in clinical studies, with Phase 1 single ascending dose data showing good tolerability and a pharmacokinetic profile commensurate with once-daily dosing. Show less
no PDF DOI: 10.1021/acs.jmedchem.4c02230
BCKDK

LRRK2 G2019S mutation contributes to mitochondrial transfer dysfunction in a Drp1-STX17-dependent manner.

Mei Ding, Fen Wang, Lan-Lan Jiang +11 more · 2025 · Translational neurodegeneration · BioMed Central · added 2026-04-24
Previous studies have shown that astrocytes can transfer healthy mitochondria to dopaminergic (DA) neurons, which may serve as an intrinsic neuroprotective mechanism in Parkinson's disease (PD). LRRK2 Show more
Previous studies have shown that astrocytes can transfer healthy mitochondria to dopaminergic (DA) neurons, which may serve as an intrinsic neuroprotective mechanism in Parkinson's disease (PD). LRRK2 G2019S is the most common pathogenic mutation associated with PD. In this study, we explored whether mitochondrial transfer is influenced by genetic and environmental factors and whether dysfunction in this process is one of the mechanisms of the pathogenic LRRK2 G2019S mutation. DA neurons and astrocytes were differentiated from induced pluripotent stem cells generated from the peripheral blood of a healthy individual and a PD patient carrying the LRRK2 G2019S mutation. A coculture system of astrocytes and DA neurons was established to explore the pathogenic mechanisms of LRRK2 G2019S. Exposure to the environmental toxin rotenone impaired mitochondrial transfer from astrocytes to DA neurons. Compared with the co-culture system from the healthy participant, the co-culture system harboring the LRRK2 G2019S mutation experienced more pronounced damage. Specifically, STX17 was colocalized with the mitochondrial outer membrane marker TOM20, and its knockdown caused damage to mitochondrial transfer. Drp1 interacted with STX17. LRRK2 G2019S-mutant astrocytes exhibited markedly increased phosphorylation of Drp1 at Ser616 upon rotenone exposure. Moreover, the degree of colocalization of STX17 with TOM20 decreased. The Drp1 phosphorylation inhibitor DUSP6 restored the colocalization of STX17 and TOM20, as well as the mitochondrial transfer efficiency and neuronal survival. The impairment of mitochondrial transfer is a potential pathogenic mechanism associated with LRRK2 G2019S mutation. The molecular mechanisms of mitochondrial transfer were observed to occur through a Drp1-STX17-dependent pathway. Notably, inhibitors for Drp1 Ser616 phosphorylation may offer neuroprotection through mitigating mitochondrial transfer impairments. This study provides novel insights into the pathogenesis of PD and the development of new therapeutic targets. Show less
📄 PDF DOI: 10.1186/s40035-025-00525-1
DUSP6

Opposing mechanisms by which miRNAs mediate distinct Nrf1 and Nrf2 regulation of epithelial-mesenchymal transition in hepatocellular carcinoma.

Juan Chen, Jing Feng, Yuping Zhu +2 more · 2025 · RNA biology · Taylor & Francis · added 2026-04-24
Accumulation of various genetics and epigenetics alterations are accepted to result in the initiation and progression of hepatocellular carcinoma (HCC), and its high metastasis is viewed as a critical Show more
Accumulation of various genetics and epigenetics alterations are accepted to result in the initiation and progression of hepatocellular carcinoma (HCC), and its high metastasis is viewed as a critical bottleneck leading to its treatment failure. Amongst them, the microRNAs arising from the lack of the antioxidant transcription factor Nrf2 lead to cancer metastasis. However, much less is known about the regulation of microRNAs by Nrf1, even though it acts as an essential determinon of cell homoeostasis by governing the transcriptional expression of those driver genes contributing to the EMT involved in its metastasis. In this study, distinct EMT phenotypes resulted from specific knockouts of Nrf1 and Nrf2 in HepG2 cells, as accompanied by their differential migratory and invasive capabilities. The Show less
no PDF DOI: 10.1080/15476286.2025.2548628
SNAI1

Latent profile analysis of electronic health literacy and its impact on health promoting lifestyles among maintenance hemodialysis patients.

Lan Yang, Jinghua Yang, Hong Zhang +3 more · 2025 · Frontiers in public health · Frontiers · added 2026-04-24
Despite the critical role of e-Health literacy (eHL) in modern healthcare, current research predominantly concentrates on conditions such as cancer and diabetes, as well as outpatient care settings. H Show more
Despite the critical role of e-Health literacy (eHL) in modern healthcare, current research predominantly concentrates on conditions such as cancer and diabetes, as well as outpatient care settings. However, there remains a significant gap in studies specifically addressing the eHL needs of patients with maintenance hemodialysis (MHD). This study aims to explore the latent categories of eHL among MHD patients and its impact on health-promoting lifestyle (HPL). A survey was conducted using a convenience sampling method involving 500 MHD patients from three tertiary hospitals in Baoding. Data were analyzed using latent profile analysis (LPA) and a mixed regression model. This study showed that MHD patients could be classified into low (23.17%), middle (49.78%), and high (27.05%) eHL groups, with the three-class model showing optimal fit (AIC = 2321.213, BIC = 2271.168, entropy = 0.967). MHD Patients in the high literacy group scored significantly higher in all dimensions of e-HL and overall HPL (119.58 ± 13.86) compared to those in the low literacy group (91.82 ± 11.73) (all The findings suggest a heterogeneous stratification of eHL among MHD patients, closely linked to HPL. Stratified intervention strategies should be developed for different patient groups to potentially improve their health behaviors. The study provides evidence-based support for personalized health management. Show less
📄 PDF DOI: 10.3389/fpubh.2025.1630350
LPA

Identification of novel germline mutations in FUT7 and EXT1 linked with hereditary multiple exostoses.

Wan Peng, Gao-Fei Li, Guo-Wang Lin +11 more · 2025 · Oncogene · Nature · added 2026-04-24
Hereditary multiple exostoses (HME) is an autosomal dominant skeletal disorder primarily linked with mutations in Exostosin-1 (EXT1) and Exostosin-2 (EXT2) genes. However, not all HME cases can be exp Show more
Hereditary multiple exostoses (HME) is an autosomal dominant skeletal disorder primarily linked with mutations in Exostosin-1 (EXT1) and Exostosin-2 (EXT2) genes. However, not all HME cases can be explained by these mutations, and its pathogenic mechanisms are not fully understood. Herein, utilizing whole-exome sequencing and genetic screening with a family trio design, we identify two novel rare mutations co-segregating with HME in a Chinese family, including a nonsense mutation (c.204G>A, p.Trp68*) in EXT1 and a missense mutation (c.893T>G, p.Phe298Cys) in FUT7. Functional assays reveal that the FUT7 mutation affects the cellular localization of FUT7 protein and regulates cell proliferation. Notably, the simultaneous loss of fut7 and ext1 in a zebrafish model results in severe chondrodysplasia, indicating a functional link between FUT7 and EXT1 in chondrocyte regulation. Additionally, we unveil that FUT7 p.Phe298Cys reduces EXT1 expression through IL6/STAT3/SLUG axis at the transcription level and through ubiquitination-related proteasomal degradation at the protein level. Together, our findings not only identify novel germline mutations in FUT7 and EXT1 genes, but also highlight the critical interaction between these genes, suggesting a potential 'second-hit' mechanism over EXT1 mutations in HME pathogenesis. This insight enhances our understanding of the mechanisms underlying HME and opens new avenues for potential therapeutic interventions. Show less
📄 PDF DOI: 10.1038/s41388-024-03254-3
EXT1