👤 Junkai Zhang

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

Stem Cell-Derived Exosomes Improve Neurological Dysfunction in a Rat Model of Moderate-to-Severe Cerebral Palsy.

Tingting Peng, Huijuan Lin, Xiaoli Zeng +16 more · 2026 · Stem cell reviews and reports · Springer · added 2026-04-24
Cerebral palsy (CP), the most prevalent pediatric motor disorder with significant cognitive comorbidity (> 50%), lacks therapies addressing both impairments in moderate-to-severe cases. This study dem Show more
Cerebral palsy (CP), the most prevalent pediatric motor disorder with significant cognitive comorbidity (> 50%), lacks therapies addressing both impairments in moderate-to-severe cases. This study demonstrates that human umbilical cord mesenchymal stem cell-derived exosomes (hUCMSC-Exos) exert profound therapeutic effects in a rat model of moderate-to-severe CP established via bilateral carotid artery occlusion with hypoxia. Intravenously administered hUCMSC-Exos displayed sustained brain retention and significantly restored motor coordination and cognitive function. The recovery was primarily mediated through enhanced remyelination driven by promoted oligodendrocyte maturation and differentiation (elevated oligodendrocyte lineage transcription factor 2 and myelin basic protein). Concurrently, the treatment attenuated key pathological processes involving sustained neuroinflammatory responses (reduced ionized calcium-binding adapter molecule 1, tumor necrosis factor-α, and interleukin-6) while elevating brain-derived neurotrophic factor. Our findings establish hUCMSC-Exos as a promising dual-modality therapy for moderate-to-severe CP, mechanistically linked to robust remyelination and coordinated modulation of core disease mechanisms. Show less
no PDF DOI: 10.1007/s12015-026-11072-1
BDNF cerebral palsy exosomes mesenchymal stem cells neurological disorders neuroscience pediatric motor disorder stem cells

Retigabine ameliorates CRS-induced depressive-like behaviors and cognitive impairment by inhibiting endoplasmic reticulum stress-mediated apoptosis.

Jing Zhang, Yi-Heng Li, Jin-Jing Zhang +4 more · 2026 · Brain research bulletin · Elsevier · added 2026-04-24
Retigabine (RTG) shows notable neuroprotective efficacy in multiple brain injury models; however, its interplay with endoplasmic reticulum stress (ERS) is poorly understood. This study was designed to Show more
Retigabine (RTG) shows notable neuroprotective efficacy in multiple brain injury models; however, its interplay with endoplasmic reticulum stress (ERS) is poorly understood. This study was designed to explore the therapeutic potential of RTG against CRS-induced depression-like behaviors and cognitive deficits in mice and to uncover the associated molecular mechanisms. A depression-like and cognitive impairment model was established in C57BL/6 male mice using chronic restraint stress (CRS). Six-week-old C57BL/6 male mice were randomly assigned to the following groups: control (Con), model (CRS), RTG (10 mg/kg), XE-991 (2 mg/kg) or tunicamycin (Tm, 2 mg/kg). Behavioral tests were conducted to assess depression-like behaviors and cognitive function. Hippocampal neuronal morphology was examined by H&E and immunofluorescence staining, while changes in endoplasmic reticulum stress (ERS)-related signaling pathways were analyzed by Western blot. Retigabine treatment reduced hippocampal neuronal damage and the expression of ERS-related factors (GRP78, CHOP) and the pro-apoptotic factor BAX in CRS-induced mice, while it increased the levels of BDNF. These effects were antagonized by XE-991 and the ERS agonist tunicamycin (Tm). Retigabine may alleviate CRS-induced depressive-like behaviors and cognitive impairment by inhibiting ERS-mediated apoptosis, suggesting its potential as a novel therapeutic strategy for depression. Show less
no PDF DOI: 10.1016/j.brainresbull.2026.111798
BDNF apoptosis behaviors cognitive impairment depression endoplasmic reticulum stress neuroprotection stress

Sox11 deficiency induces paravertebral muscle injury and scoliosis via Mlxipl upregulation.

Ruohao Wu, Wenting Tang, Yu Li +5 more · 2026 · Genes & diseases · Elsevier · added 2026-04-24
📄 PDF DOI: 10.1016/j.gendis.2025.101970
MLXIPL

Efferocytosis deficiency exacerbates local inflammation and predicts recurrence in chronic rhinosinusitis with nasal polyps.

Shuang Liang, Bing Yan, Shen Shen +3 more · 2026 · The Journal of allergy and clinical immunology · Elsevier · added 2026-04-24
The role of efferocytosis in chronic rhinosinusitis (CRS), particularly CRS with nasal polyps (CRSwNP), remains poorly understood. We comprehensively characterized efferocytosis in CRS and determined Show more
The role of efferocytosis in chronic rhinosinusitis (CRS), particularly CRS with nasal polyps (CRSwNP), remains poorly understood. We comprehensively characterized efferocytosis in CRS and determined its association with inflammatory endotypes and clinical outcomes in CRSwNP. Efferocytosis-related marker expression between nasal polyps and healthy nasal mucosa was detected by quantitative real-time PCR and immunohistochemistry. Public single-cell RNA sequencing profiles of CRS were reanalyzed to dissect efferocytosis at single-cell resolution. Associations between efferocytosis and tissue inflammation were evaluated by Spearman correlation. Regression models and receiver operating characteristic analyses assessed the predictive capability of efferocytosis for CRSwNP recurrence. Compared with controls, CRSwNP exhibited widespread efferocytosis deficiency, including "find me" signals (CX3CR1, S1PRs, P2RY2, GPR132), "eat me" signals (ITGAV, MerTK, Tim1, ADGRB1), "don't eat me" signal CD300a, postengulfment signals (ABCA1, NR1H3/2, PPARδ/γ), and bridging molecule MFGE8. Macrophages, the principal efferocytic cells, shifted from homeostatic C3 Insufficient phagocytosis and increased antiphagocytosis activity are hallmarks of efferocytosis deficiency in CRS and are associated with the severity of inflammation and the clinical outcome of CRSwNP. Show less
no PDF DOI: 10.1016/j.jaci.2025.12.1016
NR1H3

Effectiveness, safety, and biomarker dynamics of lecanemab in Chinese Alzheimer's disease population: a multicenter real-world study.

Wang Liao, Qun Yu, Bin Chen +33 more · 2026 · Alzheimer's & dementia : the journal of the Alzheimer's Association · Wiley · added 2026-04-24
Lecanemab, an anti-amyloid beta (Aβ) protofibril antibody, was introduced in China in 2024, but its real-world performance remains unknown. In this prospective, multicenter study across 21 sites, 261 Show more
Lecanemab, an anti-amyloid beta (Aβ) protofibril antibody, was introduced in China in 2024, but its real-world performance remains unknown. In this prospective, multicenter study across 21 sites, 261 Alzheimer's disease patients (mild cognitive impairment to moderate dementia) received biweekly lecanemab (10 mg/kg). A matched Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort served as comparator. Cognitive tests, plasma biomarkers, and optional amyloid/tau positron emission tomography (PET) were assessed over 6 months. Lecanemab significantly attenuated cognitive decline versus ADNI. Plasma Aβ42, Aβ40, phosphorylated tau 217 (p‑tau217), glial fibrillary acidic protein (GFAP), and ratios showed robust changes; a p‑tau217 reduction correlated with amyloid PET clearance (mean -22.1 Centiloid; 29.2% turned amyloid-negative). Apolipoprotein E (APOE) ε4 non-carriers showed greater improvements. Infusion reactions occurred in 11.1% and amyloid-related imaging abnormalities in 9.2% (1.6% symptomatic), with no stage-related safety differences. Lecanemab was effective and well tolerated in real-world Chinese patients. Plasma p‑tau217 may serve as a sensitive, minimally invasive treatment-response biomarker. Show less
📄 PDF DOI: 10.1002/alz.71231
APOE

Association of uric acid-to-HDL cholesterol ratio and coronary atherosclerotic heart disease in patients with and without CKD.

Chang-Hao Sun, Xin-Yu Zhu, Zhi-Long Wang +5 more · 2026 · BMC cardiovascular disorders · BioMed Central · added 2026-04-24
The ratio of uric acid to high-density lipoprotein cholesterol (UHR) is a novel comprehensive indicator related to dyslipidemia. However, the association between UHR and coronary artery disease (CAD) Show more
The ratio of uric acid to high-density lipoprotein cholesterol (UHR) is a novel comprehensive indicator related to dyslipidemia. However, the association between UHR and coronary artery disease (CAD) risk in patients with chronic kidney disease (CKD) remains unclear. After matching based on age and gender propensity scores, 2124 subjects were included and divided into the CKD group (708 cases) and the non-CKD group (1416 cases). The predictive performance of UHR for CAD was evaluated by the area under the curve (AUC), and the independent association between UHR and the risk of CAD onset was analyzed using a multivariate logistic regression model. The correlation and dose-response relationship between the ratio of uric acid to high-density lipoprotein cholesterol (UHR) and the risk of CAD were analyzed using LOESS fitting and restricted cubic spline (RCS) analysis. After matching, the multiple lipid-related indices (Triglycerides (TG), Remnant Cholesterol (RC), Atherogenic Index (AI), Atherogenic Index of Plasma (AIP), Triglyceride Glucose Index (TyG), Lipoprotein Composite Index (LCI), Triglyceride to High-Density Lipoprotein Cholesterol Ratio (TG/HDL-C), Total Cholesterol to High-Density Lipoprotein Cholesterol Ratio (TC/HDL-C), Low-Density Lipoprotein Cholesterol to High-Density Lipoprotein Cholesterol Ratio (LDL-C/HDL-C), UHR) in the CKD group were significantly higher than those in the non-CKD group. The AUC analysis showed that HDL-C, AIP, TG/HDL-C, and UHR had strong predictive performance in the overall cohort and the non-CKD group, while in the CKD group, HDL-C, AI, and TC/HDL-C are better predictive indicators. After adjusting for all confounding factors, multivariate regression analysis revealed that HDL-C, apolipoprotein A-1 (APOA-1), and the APOA-1/APOB ratio were independent protective factors for CAD in the entire cohort. Among them, the protective effect of HDL-C was the most stable (overall population aOR = 0.26, 95% CI: 0.17-0.39, p < 0.001), and it was significantly in both the CKD (aOR = 0.18, 95% CI: 0.09-0.40, p < 0.001) and non-CKD subgroups (aOR = 0.31, 95% CI: 0.18-0.52, p < 0.001). In CKD, UHR is significantly correlated with CAD (aOR = 6.23, 95% CI: 1.89-20.60, p = 0.003), and the association was more significant in the non-CKD group (aOR = 15.15, 95% CI: 4.20-54.72, p < 0.001). CKD status significantly modified the association between UHR and CAD (P for interaction = 0.015). LOESS fitting suggested that UHR was positively correlated with the probability of CAD occurrence (the correlation was more significant at low UHR, and it slowed down when UHR > 0.5, r = 0.2, p < 0.001), and negatively correlated with eGFR (r = -0.38, p < 0.001). RCS analysis confirmed a significant nonlinear association between UHR and CAD (overall P < 0.001, nonlinear P = 0.002), and the risk of CAD increased when UHR was > 0.41 in CKD patients. UHR is an independent risk factor for coronary heart disease, with higher adjusted OR values and more significant independent risk effects in non-CKD populations. Show less
no PDF DOI: 10.1186/s12872-026-05838-1
APOB

Fibroblast growth factor 21 (FGF21) promoter methylation drives the progression of chronic hepatitis B by mediating oxidative stress and inflammatory immunity.

Xue Li, Feng Zhang, Hanxu Zhu +5 more · 2026 · Microbiology spectrum · added 2026-04-24
Hepatitis B virus (HBV) infection can cause liver damage through oxidative stress (OS) and immune-inflammatory responses. This study aims to explore the clinical significance of fibroblast growth fact Show more
Hepatitis B virus (HBV) infection can cause liver damage through oxidative stress (OS) and immune-inflammatory responses. This study aims to explore the clinical significance of fibroblast growth factor 21 (FGF21) in the development and progression of chronic hepatitis B (CHB). A total of 336 participants were recruited, including 320 CHB patients and 16 healthy controls. The expression of FGF21, immune cytokines, and OS-related molecules in peripheral blood mononuclear cells (PBMCs) was detected using real-time quantitative polymerase chain reaction. The methylation level of the FGF21 gene promoter in PBMCs was detected using TaqMan probe-based quantitative methylation-specific PCR. The expression level of FGF21 in the peripheral blood of CHB patients was higher than that of HC, but the methylation level of the FGF21 promoter was lower than that of HC, especially in patients during the immune activation phase. The mRNA expression levels of CXCR3 and CCL5 in PBMCs of CHB patients during the immune activation and reactivation phases were higher than those in other clinical stages. Single-cell analysis revealed that CXCR3 and CCL5 expression in the immune tolerance and immune activation phases with high HBsAg expression was closely related to T lymphocytes (T cells) and natural killer cells (NK cells) and was highly expressed in CD4 and CD8 T cells and NK cells. In addition, the mRNA expression levels of Nrf2 and GPX4 in the reactivation phase were higher than those in other clinical stages. The mRNA expression level and methylation level of FGF21 in PBMCs of CHB patients were correlated with the viral load, immune inflammation, and OS levels during the antiviral treatment course of CHB. The methylation level of the FGF21 promoter has the potential to become a non-invasive biomarker for monitoring the progress of antiviral treatment in CHB.IMPORTANCEThis study conducted an in-depth exploration of the application of methylation detection technology, analyzing its value and driving mechanism in the oxidative stress and immune-inflammatory balance during the course of chronic hepatitis B. The study analyzed the methylation patterns of the FGF21 promoter and the expression levels of its receptor FGFR1, as well as the expression levels of chemokines CXCR3, CCL5, and oxidative stress factors GPX4 and Nrf2 in the immune tolerance period, immune clearance period, immune control period, and reactivation period of chronic hepatitis B. It clarified the association between these molecules and the FGF21/FGFR1 axis and revealed the synergistic or antagonistic mechanisms of these molecules in the oxidative stress and inflammatory vicious cycle. At the same time, this study also explored the value of FGF21 promoter methylation in disease diagnosis and prognosis, providing a theoretical basis for evaluating the antiviral treatment effect and disease progression of chronic hepatitis B. Show less
📄 PDF DOI: 10.1128/spectrum.02769-25
FGFR1

Transcriptomic and functional evidence reveals dual-module immune response of human-nasal staphylococcus aureus in Koi Carp (Cyprinus carpio).

Mei Li, Zeqing Xu, Jiarui Zeng +6 more · 2026 · International journal of medical microbiology : IJMM · Elsevier · added 2026-04-24
Staphylococcus aureus is a significant pathogen that poses a threat to both human and animal health. Its pathogenicity in humans has been extensively studied, however, the signaling pathways and key g Show more
Staphylococcus aureus is a significant pathogen that poses a threat to both human and animal health. Its pathogenicity in humans has been extensively studied, however, the signaling pathways and key genes in Koi Carp responding to S. aureus from human rhinitis remain unclear. In this study, we established an intraperitoneal infection model in koi carp (Cyprinus carpio) using an S. aureus isolate from patients with rhinitis and integrated RNA-seq, qPCR, and ELISA to dissect the host response. Our findings reveal a dual-module immune evasion strategy employed by S. aureus in koi carp. Module I: The pathogen down-regulated the entire complement coagulation cascade (C3, C9, CFH, F7/9/10) and apolipoprotein-mediated opsonins (APOA1, APOB, APOC1/2), thereby crippling innate clearance. Module II: The host mounted a restricted but potent counter-response, characterized by type I IFN signalling (gvin1, MHC-I), NK/T-cell co-stimulation (CD244, SLAMF5), and the selective induction of IL-8 and IL-1β, while IL-6, IL-10, and TNF-α remained unchanged. Functionally, serum superoxide dismutase (SOD), catalase (CAT), and lysozyme (LZM) activities surged, confirming an oxidative burst, whereas splenic CD22R protein decreased, indicating B-cell disinhibition. These results establish a molecular basis for understanding the interaction between human-derived S. aureus and the immune system of aquatic organisms. Show less
no PDF DOI: 10.1016/j.ijmm.2026.151707
APOB

Phytochemical profiling and molecular interactions of Parishins a and C as potent AChE inhibitors from red Gastrodia elata.

Ming Chen, Yuchi Zhang, Jingying Xu +7 more · 2026 · Biophysical chemistry · Elsevier · added 2026-04-24
Current in vitro enzyme inhibition assays often involve subjective data analysis based on the researcher's experience. In this study, we developed a multi-dimensional quantitative integration platform Show more
Current in vitro enzyme inhibition assays often involve subjective data analysis based on the researcher's experience. In this study, we developed a multi-dimensional quantitative integration platform (MDQIP) that uses a model to objectively calculate and rank compound activities, addressing the limitations of traditional "experience-driven" evaluations, accelerates the screening and evaluation of potential AChE inhibitors from Red Gastrodia elata, offering a more efficient approach to drug discovery. Ultrafiltration-LC screening identified parishin A as having the most stable binding, with binding degree and recovery rates of 98.85% and 99.39%, respectively. Molecular docking revealed that parishins A and C were the strongest AChE inhibitors, exhibiting stable binding through hydrogen bonds, π-alkyl, and π-π interactions. Molecular dynamics simulations confirmed the stability of these compounds, with binding energies of -82.65 ± 4.24 and - 80.69 ± 4.19 kcal/mol. Enzyme kinetics showed that parishins A and C are mixed-type inhibitors, with IC Show less
no PDF DOI: 10.1016/j.bpc.2026.107617
BACE1

Effects of Combined Psychological and Functional Exercise Interventions on Emotion, Life Quality, and Brain-Derived Neurotrophic Factor Levels in Patients With Parkinson's Disease: A Randomized Controlled Trial.

Tao Ding, Jing Zhang, Xue Jiang +1 more · 2026 · International journal of psychiatry in medicine · SAGE Publications · added 2026-04-24
ObjectiveTo evaluate the effects of a combined psychological and functional exercise intervention on emotion, quality of life, and brain-derived neurotrophic factor (BDNF) levels in patients with Park Show more
ObjectiveTo evaluate the effects of a combined psychological and functional exercise intervention on emotion, quality of life, and brain-derived neurotrophic factor (BDNF) levels in patients with Parkinson's disease (PD).MethodsIn this randomized controlled trial, 172 patients with PD were randomly assigned into 2 groups with 86 patients in each group. The control group received routine care, while the intervention group received a 12-week intervention combining psychological support with functional exercise in addition to routine care. Hamilton Anxiety Scale (HAMA), Hamilton Depression Scale (HAMD), Parkinson's Disease Questionnaire-39 (PDQ-39), Barthel Index, Movement Disorder Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS), and serum BDNF levels were assessed before and after the intervention. Adherence rates were also determined for each group. Spearman correlation analysis was used to examine associations between changes in BDNF (ΔBDNF) and changes in HAMA (ΔHAMA) and HAMD (ΔHAMD) scores.ResultsAt the end of the 12-week clinical trial, the intervention group demonstrated significantly lower HAMA, HAMD, PDQ-39, and MDS-UPDRS scores ( Show less
no PDF DOI: 10.1177/00912174261422307
BDNF brain-derived neurotrophic factor exercise neurology neuroscience parkinson's disease psychology rehabilitation

Metabolomics Identified Caloric Restriction-associated Glycerophospholipid Alterations in ApoE-/- Mice.

Zi-Yu Wei, He-Ping Wang, Song Tang +10 more · 2026 · Genomics, proteomics & bioinformatics · Oxford University Press · added 2026-04-24
Caloric restriction (CR) improves metabolic health and reduces the risk of aging-related vascular diseases. However, the systematic metabolic reprogramming associated with CR remains unclear. To addre Show more
Caloric restriction (CR) improves metabolic health and reduces the risk of aging-related vascular diseases. However, the systematic metabolic reprogramming associated with CR remains unclear. To address this, we performed multi-tissue metabolomic profiling (liver, heart, and serum) in apolipoprotein E-deficient (ApoE-/-) mice subjected to CR. Metabolomic analyses of the multiple tissues revealed that glycerophospholipid metabolism pathway was consistently modulated by CR. To explore its relevance in vascular diseases, we performed serum metabolomic profiling in an abdominal aortic aneurysm (AAA) model induced by angiotensin Ⅱ (AngⅡ) infusion in ApoE-/- mice. The level of lysophosphatidylethanolamine (LPE) (16:0/0:0), a metabolite in the glycerophospholipid metabolism pathway, was elevated during AAA progression and significantly reduced by CR intervention, suggesting its potential as a vascular disease risk factor. Notably, glycerophospholipid metabolism and LPE (16:0) were significantly associated with vascular diseases and aging-related indicators in human multi-omics data, including public transcriptomic and lipidomic, and our serum multi-omics profiling of 76 healthy aged individuals. Collectively, our findings establish glycerophospholipid metabolism and LPE (16:0) as systemic signatures of CR with diagnostic potential. They highlight a crucial link between systemic metabolism and vascular remodeling and remodeling-associated vascular diseases, while also functioning as indicators of systemic aging. Show less
no PDF DOI: 10.1093/gpbjnl/qzag030
APOE

Hepatic GAL1 deficiency alleviates steatosis via WWP2-mediated PARP1 degradation and activation of the SIRT1-CPT1A pathway.

Yuqi Li, Ruikai Li, Peng Wang +6 more · 2026 · Biochimica et biophysica acta. Molecular basis of disease · Elsevier · added 2026-04-24
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a highly prevalent chronic liver disease worldwide and is closely associated with obesity, diabetes, and other metabolic disorders. Show more
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a highly prevalent chronic liver disease worldwide and is closely associated with obesity, diabetes, and other metabolic disorders. Because MASLD progression poses serious health risks, elucidating the underlying mechanisms is essential to guide early intervention and therapeutic strategies. Proteomic analysis was used to identity high-fat diet (HFD)-induced proteins in mouse liver. Galectin-1 (GAL1) expression was assessed via immunohistochemistry in human liver tissues. Liver-specific GAL1-deficient mice were generated using adeno-associated virus. Mice were fed either a chow diet or an HFD. Functional studies were performed in cell lines using western blotting, RT-qPCR, immunofluorescence, co-immunoprecipitation, mass spectrometry, and molecular docking analysis. GAL1 expression was elevated in liver tissues from patients with MASLD and in mouse models. Liver-specific GAL1 knockdown alleviated hepatic steatosis and enhanced fatty acid oxidation (FAO). Mechanistically, GAL1 competitively bound to the BRCT domain of poly (ADP-ribose) polymerase 1 (PARP1), thereby interfering with its interaction with the WW domain -containing E3 ubiquitin protein ligase 2 (WWP2). Hepatic GAL1 knockdown promoted the PARP1 -WWP2 interaction and subsequently facilitated ubiquitin-dependent degradation of PARP1. This degradation led to increased NAD Hepatic deficiency of GAL1 alleviates hepatic steatosis by enhancing FAO through promotion of ubiquitin-dependent PARP1 degradation, thereby restoring NAD Show less
no PDF DOI: 10.1016/j.bbadis.2026.168237
WWP2

A novel GIPR/GLP-1R dual agonist improves systemic metabolism through differentially regulating inflammation and lipid metabolism in obesity.

Feng Zhang, Wei Chen, Huiying Wang +10 more · 2026 · Journal of advanced research · Elsevier · added 2026-04-24
Dual GIP/GLP-1 receptor agonists have gained significant attention in clinical applications because of their remarkable efficacy in reducing obesity and type 2 diabetes. However, the mechanisms by whi Show more
Dual GIP/GLP-1 receptor agonists have gained significant attention in clinical applications because of their remarkable efficacy in reducing obesity and type 2 diabetes. However, the mechanisms by which these dual agonists affect systemic metabolism remain elusive. To investigate the effects of a novel dual-receptor agonist, THDBH120, on systemic metabolism in obese individuals and the specific roles of GIPR and GLP-1R in modulating systemic and adipose tissue metabolism. To evaluate the intrinsic properties of THDBH120, we conducted a potency assay by using HEK293 cell lines overexpressing either human GIPR or GLP-1R and measured the accumulation of cAMP as a downstream second messenger following receptor activation. To evaluate the efficacy of THDBH120 on systemic metabolism, we used obese rodents and nonhuman primate species that received various doses and frequencies of THDBH120. To determine the metabolic roles of GLP-1R and GIPR in mediating the beneficial effects of THDBH120, we used GLP-1R- and GIPR-knockout mouse models treated with THDBH120, the GLP-1R agonist semaglutide, or the GIPR agonist LAGIPRA and performed transcriptomic sequencing analyses of adipose tissues. THDBH120 is a novel long-acting dual GIPR/GLP-1R agonist that has superior weight loss and metabolic improvement effects in rodents and mammals. The activation of GLP-1R by semaglutide or THDBH120 improved lipid metabolism, whereas the activation of GIPR by LAGIPRA or THDBH120 alleviated inflammation. THDBH120 improved lipid metabolism via GLP-1R-mediated pathways and mitigated inflammation by activating GIPR-associated pathways in the adipose tissues of obese mice. Both GLP-1R and GIPR are important in mediating the beneficial effects of dual receptors on systemic metabolism. THDBH120 is a novel long-acting dual GIPR/GLP-1R agonist that has potential clinical applications. Show less
no PDF DOI: 10.1016/j.jare.2026.02.006
GIPR

Dual intestinal-hepatic modulation by phenolic acids improves metabolic-dysfunction associated steatohepatitis.

Peter U Amadi, Justice O Osuoha, Joy A Amadi +11 more · 2026 · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · Elsevier · added 2026-04-24
Metabolic-dysfunction associated steatohepatitis (MASH) arises from sustained triglyceride overload of the intestine-liver axis, yet current therapies rarely coordinate intestinal lipid entry with hep Show more
Metabolic-dysfunction associated steatohepatitis (MASH) arises from sustained triglyceride overload of the intestine-liver axis, yet current therapies rarely coordinate intestinal lipid entry with hepatic triglyceride disposal. Here we identify a phenolic-acid fraction as a dual-compartment metabolic modulator that couples intestinal lipase inhibition to CPT1α-PPARα-dependent hepatic β-oxidation across species. Across species, we investigated the kinetics and metabolic actions of a phenolic fraction (PhAM) using recombinant lipase systems, epithelial transport assays, hepatocyte models, pharmacokinetics, diet-induced metabolic disease paradigms, quantitative histopathology, and a 24-week randomized placebo-controlled clinical trial. PhAM selectively suppresses pancreatic and intestinal lipases non-competitively, lowering V_max with minimal K_m change, resembling some features of orlistat, but via a distinct, non-covalent mechanism. In Caco-2 monolayers and ex vivo loops, it reduces apical-to-basolateral fatty-acid flux, depletes intracellular triglycerides, and limits luminal-to-plasma lipid transfer. PhAM is orally bioavailable, with measurable plasma exposure and prolonged intestinal residence. Under high-fat feeding, it increases fecal fat loss, attenuates post-lipid-load triglyceride excursions, and lowers hepatic triglycerides without altering ApoB secretion. Its triglyceride-lowering effect requires CPT1α-dependent mitochondrial import and PPARα activation, elevates β-hydroxybutyrate, and induces oxidative genes while sparing lipogenesis. In chronic MASH, PhAM reduces steatosis, ballooning, inflammation, and metabolic-dysfunction associated steatotic liver disease (MASLD) Activity Score. A 24-week clinical subgroup, defined by ultrasound and transaminase enrichment, showed dose-responsive improvements in ultrasonographic steatosis and metabolic biomarkers. Collectively, these findings define PhAM as a phenolic-acid-based agent that aligns intestinal lipid restriction with hepatic oxidative unloading, offering a mechanistically coherent framework for potentially addressing steatotic liver disease-associated metabolic features. Show less
no PDF DOI: 10.1016/j.biopha.2026.119070
APOB

Endoplasmic reticulum stress mediates oxidative stress-driven endothelial impairment and atherogenesis induced by sodium perfluorononenoxybenzene sulfonate exposure.

Boxiang Zhang, Zeming Liu, Qing Li +4 more · 2026 · Environmental research · Elsevier · added 2026-04-24
Sodium perfluorononenoxybenzene sulfonate (OBS), a substitute for perfluorooctane sulfonate (PFOS), has been frequently detected in the environment and human blood. Although OBS exposure has been iden Show more
Sodium perfluorononenoxybenzene sulfonate (OBS), a substitute for perfluorooctane sulfonate (PFOS), has been frequently detected in the environment and human blood. Although OBS exposure has been identified as a novel risk factor for atherosclerosis associated with endothelial dysfunction, the underlying molecular mechanisms remain unclear. In this study, in vitro experiments using human umbilical vein endothelial cells (HUVECs) demonstrated that OBS exposure induced oxidative stress, activated the PERK-eIF2α-ATF4 axis of endoplasmic reticulum stress (ERS) and triggered NF-κB signaling. Pharmacological inhibition with N-acetylcysteine (NAC, an antioxidant), 4-phenylbutyric acid (4-PBA, an ERS inhibitor), and BAY 11-7082 (an inhibitor for NF-κB signaling pathway) revealed a sequential pathogenic cascade, in which oxidative stress acts upstream to initiate ERS and compromise endothelial barrier function, leading to NF-κB activation, which drives inflammatory responses, monocyte adhesion, and impaired endothelial migration. Consistent with these findings, in vivo experiments in ApoE Show less
no PDF DOI: 10.1016/j.envres.2026.124344
APOE

Dendrobine attenuates postoperative cognitive dysfunction by inhibiting Runx1-mediated NF-κB signaling pathway.

Dong Ji, Qingyu Sun, Chengcheng Zhang +5 more · 2026 · Brain research bulletin · Elsevier · added 2026-04-24
Postoperative cognitive dysfunction (POCD) in older adults is strongly linked to neuroinflammation driven by microglial activation and NF-κB signaling. Runx1 has emerged as an upstream regulator of NF Show more
Postoperative cognitive dysfunction (POCD) in older adults is strongly linked to neuroinflammation driven by microglial activation and NF-κB signaling. Runx1 has emerged as an upstream regulator of NF-κB, but its role in POCD is unknown. Dendrobine, a sesquiterpenoid alkaloid from Dendrobium species, exhibits anti-inflammatory and neuroprotective activity. POCD was induced in aged C57BL/6 mice via sevoflurane anesthesia combined with exploratory laparotomy. Dendrobine (10 or 20 mg/kg) was administered, and cognitive outcomes were evaluated by Morris Water Maze and Novel Object Recognition. RNA sequencing, Western blotting, immunofluorescence, and in vitro microglia-neuron co-culture systems were employed to investigate inflammatory responses, apoptosis, synaptic plasticity, and signaling pathway activation. Functional roles of Runx1 were validated via siRNA knockdown, pharmacological inhibition (Ro5-3335), and overexpression in BV2 cells. Dendrobine improved spatial and recognition memory in POCD mice, reduced hippocampal microglial activation, proinflammatory cytokine expression (TNF-α, IL-1β, IL-6), and neuronal apoptosis while enhancing synaptic protein levels (BDNF, PSD95, SYN1). Transcriptomic and KEGG analyses revealed suppression of NF-κB signaling by dendrobine, with Runx1 identified as an upstream modulator. Dendrobine downregulated Runx1 expression in vivo and in vitro. Runx1 inhibition enhanced dendrobine's anti-inflammatory effects, whereas RUNX1 overexpression abolished them. Dendrobine ameliorates POCD by inhibiting the Runx1/NF-κB signaling pathway, suppressing neuroinflammation, promoting synaptic resilience, and preventing neuronal apoptosis. Runx1 appears to act as a key upstream mediator of NF-κB signaling in POCD. Targeting the Runx1/NF-κB axis represents a promising strategy for perioperative neuroprotection. Show less
no PDF DOI: 10.1016/j.brainresbull.2026.111746
BDNF microglial activation neuroinflammation neuroprotection nf-kb signaling postoperative cognitive dysfunction sesquiterpenoid

Novel Protective Role for Gut Microbiota-derived Metabolite PAGln in Doxorubicin-induced Cardiotoxicity.

Jie Huang, Xingyuan Hou, Ni Zhou +7 more · 2026 · Cardiovascular drugs and therapy · Springer · added 2026-04-24
Doxorubicin (Dox) is a classic anthracycline chemotherapy drug with cause cumulative and dose-dependent cardiotoxicity. This study aimed to investigate the potential role and molecular mechanism of ph Show more
Doxorubicin (Dox) is a classic anthracycline chemotherapy drug with cause cumulative and dose-dependent cardiotoxicity. This study aimed to investigate the potential role and molecular mechanism of phenylacetylglutamine (PAGln), a novel gut microbiota metabolite, in Dox-induced cardiotoxicity (DIC). DIC models were established in vivo and in vitro, and a series of experiments were performed to verify the cardioprotective effect of PAGln. RNA sequencing (RNA-seq) was employed to explore the mechanism of PAGln in DIC. Subsequently, the differentially expressed genes (DEGs) were subjected to comprehensive analysis using diverse public databases, and RT-PCR was used to confirm the expression levels of the candidate genes. Finally, molecular docking techniques were used for validation. PAGln effectively prevented both in vivo and in vitro Dox-induced myocardial injury and cell apoptosis. RNA-seq results showed that 40 genes were up-regulated and 54 down-regulated in the Dox group compared to the Con group, displaying opposite changes in the Dox + PAGln group. Enrichment analysis highlighted several mechanisms by which PAGln alleviated Dox-induced cardiotoxicity, including the lipid metabolic process, calcium-mediated signaling, positive regulation of store-operated calcium channel activity, and hypertrophic cardiomyopathy. In vitro and in vivo experiments confirmed that PAGln treatment could reverse the changes in the expression levels of Klb, Ece2, Nmnat2, Casq1, Pak1, and Apob in Dox. Molecular docking results showed that these genes had good binding activity with PAGln. PAGln shows potential in alleviating Dox-induced cardiotoxicity, with Ece2 identified as key regulatory molecules related to endothelial dysfunction. Show less
📄 PDF DOI: 10.1007/s10557-024-07665-y
APOB

Transcriptome Analysis of Different Stages in the Early Ovarian Development of the Greater Amberjack (

Qiuxia Deng, Yang Huang, Xiaoying Ru +10 more · 2026 · Animals : an open access journal from MDPI · MDPI · added 2026-04-24
The greater amberjack (
📄 PDF DOI: 10.3390/ani16050709
HSD17B12

BDNF and NLRP3 signaling differentially regulate formation and retrieval of nitrous oxide (N

Huarong Shen, Yatong Shi, Jiancheng Xu +7 more · 2026 · International immunopharmacology · Elsevier · added 2026-04-24
The formation and retrieval of reward memories within the hippocampus are critical mechanisms underlying the development of substance use disorder. Nitrous oxide (N
no PDF DOI: 10.1016/j.intimp.2026.116327
BDNF bdnf hippocampus nitrous oxide nlrp3 substance use disorder

Association between vaginal microbiota in early pregnancy and gestational diabetes mellitus: a nested case-control study.

Xiang Hong, Mengjie Zhao, Furong Tan +5 more · 2026 · BMC microbiology · BioMed Central · added 2026-04-24
To investigate the association between vaginal microbiota structure in early pregnancy and gestational diabetes mellitus (GDM) and to characterize microbial signatures for early screening for GDM. The Show more
To investigate the association between vaginal microbiota structure in early pregnancy and gestational diabetes mellitus (GDM) and to characterize microbial signatures for early screening for GDM. The present study was a nested case-control study recruiting pregnant women from the Nanjing Gulou Maternal-Child Health Center, China. Vaginal swabs were collected before 20 weeks of gestation for 16S rRNA sequencing. Following 1:3 propensity score matching, 45 GDM cases and 135 controls were enrolled. The final analysis included 42 GDM cases and 121 controls. A random forest model was used to explore the genera of vaginal differential microbiota associated with GDM. Based on these findings, latent profile analysis (LPA) was conducted to explore potential types of vaginal microbiota, and logistic regression was used to analyze the association between vaginal microbiota types and GDM. The GDM group exhibited elevated alpha diversity (Chao1 index, The composition and structure of vaginal microbiota in early pregnancy are different in the two groups. The vaginal microbiota in early pregnancy, which is characterized by co-dominated by The online version contains supplementary material available at 10.1186/s12866-026-04910-2. Show less
📄 PDF DOI: 10.1186/s12866-026-04910-2
LPA

Si-Ni-San alleviates depressive-like behaviors in adolescent male mice by restoring DRN-NAc serotonergic circuit function and 5-HT4R-dependent synaptic plasticity.

Yue Wang, Zuyi Liu, Jiayi Wu +12 more · 2026 · Phytomedicine : international journal of phytotherapy and phytopharmacology · Elsevier · added 2026-04-24
Early-life stress (ELS) is a key risk factor for adolescent depression. Si-Ni-San (SNS), a classic traditional Chinese medicine formula, has shown antidepressant potential, yet its effects on the dors Show more
Early-life stress (ELS) is a key risk factor for adolescent depression. Si-Ni-San (SNS), a classic traditional Chinese medicine formula, has shown antidepressant potential, yet its effects on the dorsal raphe nucleus (DRN)-nucleus accumbens (NAc) serotonergic circuit remain unclear. This study aimed to investigate whether SNS alleviates adolescent depression by restoring DRN-NAc serotonergic circuit function and to identify the serotonin receptor mediating its synaptic effects in the NAc. Firstly, the antidepressant efficacy of SNS was evaluated in a mouse model of ELS. Subsequently, its underlying mechanism was explored through integrated neurophysiological, molecular, and pharmacological analyses. Depressive- and anxiety-like behaviors were assessed using behavioral tests (sucrose preference, tail suspension, forced swim, open field, and elevated plus maze). In vivo electrophysiolog was employed to monitor DRN neuronal activity. Chemogenetic manipulation was employed to regulate the DRN-NAc serotonergic circuit, while 5-HT4R function was assessed through pharmacological intervention and viral knockdown. Synaptic and molecular mechanisms were examined using Western blotting, qPCR, ELISA, and immunofluorescence. SNS alleviated depressive-like behaviors, enhanced neural activity and low-frequency oscillations in the DRN, and restored 5-hydroxytryptamine (5-HT) levels in the NAc. Mechanistically, SNS upregulated tryptophan hydroxylase 2 (TPH2) while downregulating indoleamine 2,3-dioxygenase 1 (IDO1), thus promoting 5-HT synthesis. Critically, the antidepressant effects of SNS were blocked by either chemogenetic inhibition of the DRN-NAc serotonergic circuit or pharmacological blockade of 5-HT4R in the NAc. Meanwhile, the knockdown of 5-HT4R abolished the ameliorative effects of SNS on depressive-like behaviors and associated synaptic remodeling, including the upregulation of brain-derived neurotrophic factor, postsynaptic density protein 95, and mushroom spine density. These results demonstrate that SNS alleviates depressive-like behaviors in adolescent male mice by restoring DRN-NAc serotonergic circuit function, enhancing 5-HT bioavailability, and promoting 5-HT4R-dependent synaptic plasticity in the NAc, revealing a circuit- and receptor-specific therapeutic mechanism. Show less
no PDF DOI: 10.1016/j.phymed.2026.158088
BDNF adolescent depression depression neuroscience serotonergic circuit serotonin synaptic plasticity traditional chinese medicine

FGF21 Promotes Thermogenesis by Browning Thermogenic Adipose Tissue during Cold Exposure.

Chen-Xi Li, Chuan-Fei Tan, Qi-Min Zhang +3 more · 2026 · Annals of nutrition & metabolism · added 2026-04-24
The global obesity epidemic necessitates therapies that enhance energy expenditure. Non-shivering thermogenesis (NST) in brown/beige adipose tissue represents a promising target, with fibroblast growt Show more
The global obesity epidemic necessitates therapies that enhance energy expenditure. Non-shivering thermogenesis (NST) in brown/beige adipose tissue represents a promising target, with fibroblast growth factor 21 (FGF21) emerging as a critical regulator linking environmental stimuli to adipose plasticity and mitochondrial function. However, the precise mechanisms of FGF21 secretion and its specific role in adipose tissue browning and subsequent NST potentiation remain incompletely elucidated. FGF21 regulates NST via distinct spatiotemporal mechanisms. Acute cold exposure triggers hepatic FGF21 secretion through a β FGF21 exhibits dual regulation: hepatic (acute lipid mobilization) and adipose-based (chronic browning); adipose-targeted FGF21 delivery is essential for therapeutic efficacy, and future studies should integrate FGF21 with UCP1-independent pathways (e.g., creatine/succinate cycles) to advance obesity treatment. Show less
no PDF DOI: 10.1159/000548868
FGFR1

Excess apolipoprotein B predicts long-term survival in statin-treated CAD irrespective of achieved LDL-C levels: a pooled cohort analysis.

Wei Pan, Xiaozhao Lu, Ziwei Zhou +14 more · 2026 · Lipids in health and disease · BioMed Central · added 2026-04-24
Residual cardiovascular risk persists in statin-treated patients with coronary artery disease (CAD), even when low-density lipoprotein cholesterol (LDL-C) targets are met. Excess apolipoprotein B (apo Show more
Residual cardiovascular risk persists in statin-treated patients with coronary artery disease (CAD), even when low-density lipoprotein cholesterol (LDL-C) targets are met. Excess apolipoprotein B (apoB), defined as measured apoB minus LDL-C-predicted apoB, may capture atherogenic particle burden beyond LDL-C, but its prognostic value for long-term mortality in secondary prevention remains uncertain. We conducted a pooled analysis of two nationwide Chinese cohorts (CIN-II and RED-CARPET) comprising 68,616 statin-treated CAD patients. Excess apoB was calculated using an internal reference population (triglycerides ≤ 1.0 mmol/L). Associations with all-cause and cardiovascular mortality were assessed using multivariable Cox models, with adjustment for clinical covariates including nutritional status. External validation was performed in 13,702 participants from the UK Biobank. Over a median follow-up of 5.2 years, 10,835 deaths occurred (5,090 cardiovascular). Each 1-standard deviation (15.4 mg/dL) increase in excess apoB was associated with a 12% higher risk of all-cause mortality (adjusted hazard ratio [aHR] 1.12, 95% CI 1.06-1.18) and a 24% higher risk of cardiovascular mortality (aHR 1.24, 95% CI 1.15-1.34). Patients in the highest excess apoB quartile (≥ 11.5 mg/dL) had significantly worse survival. Notably, these associations persisted consistently across all achieved LDL-C strata (< 2.0 to > 4.0 mmol/L). These findings were robustly confirmed in the external validation cohort. Excess apoB is an independent predictor of long-term mortality in statin-treated CAD patients, even among those with well-controlled LDL-C. Its incorporation into risk assessment could improve prognostic stratification and guide personalized management in secondary prevention. CIN-II: ClinicalTrials.gov, NCT05050877 (Retrospectively registered, 21 September 2021); RED-CARPET: Chinese Clinical Trial Registry, ChiCTR2000039901 (Prospectively registered, 14 November 2020). The UK Biobank study is covered by generic ethical approval from the NHS National Research Ethics Service (Ref: 99231). Show less
no PDF DOI: 10.1186/s12944-026-02928-z
APOB

NRXN3 regulates pyroptosis in intrahepatic cholangiocarcinoma via mediating the phospho-dependent ubiquitination and degradation of caspase-3.

Tao Zhou, Yaodong Zhang, Tianlin Wang +9 more · 2026 · Journal of advanced research · Elsevier · added 2026-04-24
Intrahepatic cholangiocarcinoma (ICC) remains one of the most lethal malignancies with an increasing incidence worldwide. Gemcitabine has been considered the standard first-line chemotherapeutic agent Show more
Intrahepatic cholangiocarcinoma (ICC) remains one of the most lethal malignancies with an increasing incidence worldwide. Gemcitabine has been considered the standard first-line chemotherapeutic agent for ICC but the therapeutic response is unsatisfactory due to the development of chemoresistance. Caspase-3-mediated pyroptosis has been reported to play significant roles in chemotherapeutic response but the relevant therapeutic strategy remains unstated due to the unclear molecular mechanisms under pyroptosis in ICC. This study was designed to comprehensively explore the crucial role and underlying mechanisms of NRXN3 in pyroptosis and chemosensitivity of ICC. We performed genome-scale CRISPR-Cas9 screen integrated with transcriptomic analysis to identify key regulators of pyroptosis and gemcitabine sensitivity in ICC. In vitro and in vivo experiments were employed to investigate the effects of NRXN3 on gemcitabine-induced pyroptosis. RNA-seq and IP-MS were conducted to explore the mechanisms of NRXN3-regulated pyroptosis and chemosensitivity. NRXN3 was identified to be a critical contributor to pyroptosis and chemosensitivity in ICC. Low NRXN3 expression correlates with poor prognosis and worse therapeutic response. Mechanistically, NRXN3 competitively blocks caspase-3 binding to the RSK1 serine/threonine-protein kinase, thereby inhibiting RSK1-dependent phosphorylation of caspase-3 at T152. Inhibition of caspase-3 phosphorylation impairs its interaction with the ubiquitin ligase component FBXO1 and enhances its stability, thus facilitating caspase-3/GSDME-dependent pyroptotic cell death and chemosensitivity. Furthermore, administration of an RSK1 inhibitor or caspase-3 activator boosts the efficacy of gemcitabine in murine models of ICC. NRXN3 plays a crucial role in maintaining chemotherapy-induced pyroptosis in ICC. Targeting the NRXN3/RSK1/FBXO1/caspase-3 axis emerges as a promising strategy for ICC treatment, with the potential to improve chemosensitivity and survival. Show less
no PDF DOI: 10.1016/j.jare.2025.04.040
NRXN3

Targeting FGFR signaling overcomes therapeutic resistance and immune evasion in oncogenic PIK3CA-driven serous-like endometrial cancer.

Xin Cheng, Changli Qian, Erica Holdridge +18 more · 2026 · bioRxiv : the preprint server for biology · added 2026-04-24
Serous endometrial cancer (SEC) is an aggressive subtype of endometrial cancer (EC) with poor prognosis and limited treatment options. Here, we developed a clinically relevant, immunocompetent serous- Show more
Serous endometrial cancer (SEC) is an aggressive subtype of endometrial cancer (EC) with poor prognosis and limited treatment options. Here, we developed a clinically relevant, immunocompetent serous-like mouse model incorporating oncogenic Show less
no PDF DOI: 10.64898/2026.02.16.706009
FGFR1

The association of Alzheimer's disease-related SNPs with mild cognitive impairment susceptibility in the Chinese population.

Zhilan Xie, Wuzi Tu, Xiao-Fei Ye +3 more · 2026 · Scientific reports · Nature · added 2026-04-24
Previous Genome-wide association studies have identified several single nucleotide polymorphisms (SNPs) associated with Alzheimer's disease (AD), whereas their associations with mild cognitive impairm Show more
Previous Genome-wide association studies have identified several single nucleotide polymorphisms (SNPs) associated with Alzheimer's disease (AD), whereas their associations with mild cognitive impairment (MCI) remain unclear. To evaluate the associations between 100 representative AD-associated SNPs and susceptibility to MCI in the Chinese population. We recruited 200 MCI patients and 200 cognitively-healthy controls from the community, matched for age and sex. Associations between SNPs and MCI risk were estimated using lasso regression, adjusted for APOE status, using different genetic models. Fifteen SNPs in nine genes (including CLU, SORL1, PICALM, BDNF, NOS3, MTHFR, TOMM40, BIN1, and PVRL2) were associated with MCI in single-SNP analysis. In the multi-SNP association test, rs1801133 and rs9331888 of CLU were consistently associated with MCI risk in the dominant model. TOMM40 rs2075650 (G) was associated with MCI risk in the dominant model by age and education (OR = 2.41, 95%CI = 1.27-4.59), but disappeared when further adjusted for APOEε4 status. PICALM rs561655 (G) (OR = 0.52, 95%CI = 0.30-0.92) and NOS3 rs1549758 (T) (OR = 0.53, 95%CI = 0.30-0.94) were identified as protective genetic factors of MCI for the first time in dominant model combined with the APOEε4 allele. Moreover, MTHFR rs1801133 (A) and CLU rs9331888 (G) showed more susceptibility to MCI in the additive model. SORL1 rs641120(G) showed a protective effect, whereas BIN1 rs5733839 consistently showed a risk effect for MCI in the overdominant model, regardless of APOEε4 status. This study suggests that some AD-associated SNPs are associated with cognitive decline and may have important implications for future studies. Show less
📄 PDF DOI: 10.1038/s41598-026-37309-0
BDNF

SOX5 Overexpression in Schwann Cell Combined With Chitosan-Based Conduit Promotes Peripheral Nerve Regeneration.

Bo Ma, Fengshi Zhang, Junyu Su +4 more · 2026 · Journal of the peripheral nervous system : JPNS · Blackwell Publishing · added 2026-04-24
Severe peripheral nerve injury (PNI) remains a major clinical challenge, and functional recovery after conventional neurorrhaphy is often unsatisfactory due to fascicular mismatch, suture tension, and Show more
Severe peripheral nerve injury (PNI) remains a major clinical challenge, and functional recovery after conventional neurorrhaphy is often unsatisfactory due to fascicular mismatch, suture tension, and limited Schwann cell viability. To address these limitations, we previously developed a small-gap chitosan-based conduit that provides a controlled microenvironment for regenerative interventions. This study aimed to investigate whether SOX5 overexpression enhances Schwann cell regenerative potential and, when combined with this conduit, synergistically promotes peripheral nerve regeneration. Schwann cells were transduced with SOX5 lentivirus and assessed for proliferation, migration, and neurotrophic factor secretion in vitro. In a rat sciatic nerve transection model (2-mm gap), animals received a chitosan conduit with intraluminal injection of SOX5 lentivirus. Histological, electrophysiological, and behavioral assessments were conducted at 12 weeks post-surgery. SOX5 overexpression significantly enhanced Schwann cell proliferation, migration, and secretion of BDNF, NGF, CNTF, and VEGF, while maintaining the dedifferentiated repair phenotype. In vivo, the combination of SOX5 lentivirus and chitosan conduit improved axonal regeneration, reduced muscle atrophy, and increased conduction velocity and locomotor recovery relative to the empty conduit group. Lentivirus-mediated SOX5 overexpression drives Schwann cells toward a repair phenotype and, when integrated with a small-gap chitosan-based conduit, effectively promotes structural and functional nerve regeneration. Show less
no PDF DOI: 10.1111/jns.70120
BDNF chitosan nerve injury neuroregeneration peripheral nerve regeneration schwann cell sox5 tissue engineering

GSTM2 as the molecular linking of depression-driven colon cancer progression and chemoresistance: Reversal by Sinisan.

Na Li, Keying Chen, Bin Nie +14 more · 2026 · Phytomedicine : international journal of phytotherapy and phytopharmacology · Elsevier · added 2026-04-24
Depression has emerged as a concerning factor in colon cancer progression and treatment, yet its underlying mechanisms and therapeutic targets remain poorly defined. This study aimed to elucidate how Show more
Depression has emerged as a concerning factor in colon cancer progression and treatment, yet its underlying mechanisms and therapeutic targets remain poorly defined. This study aimed to elucidate how depression affects colon cancer progression and chemotherapeutic response, and to explore potential molecular targets and therapeutic interventions involving the traditional Chinese medicine formula Sinisan (SNS) and its bioactive component Quercetin. A mouse model combining depression and colon cancer was established to evaluate behavioral alterations, tumor progression, and pathological features. RNA sequencing was performed to screen the differentially expressed genes. The effects of corticosterone (CORT) on proliferation, colony formation, migration, and GSTM2 expression were examined in HCT116 cells, followed by functional validation through GSTM2 overexpression and inhibition assays. Molecular docking, molecular dynamics simulations, and surface plasmon resonance (SPR) were used to validate the binding of Quercetin to GSTM2. The therapeutic efficacy of SNS and Quercetin was assessed with respect to depressive symptoms, serum BDNF levels, NLRP3 inflammasome activity, and the potency of 5-fluorouracil (5-FU) chemotherapy. Mice with depression and colon cancer exhibited aggravated depressive behaviors and accelerated tumor progression. RNA-sequencing and network pharmacology analyses identified GSTM2 as a promising candidate target in colon cancer treatment, which was markedly down-regulated in the DP-CC group. CORT enhanced proliferation, colony formation, and migration of HCT116 cells while simultaneously suppressing GSTM2 expression. Conversely, GSTM2 levels negatively correlated with cell proliferation, colony formation, and chemoresistance in HCT116 cells. Treatment with SNS alleviated depressive symptoms, elevated serum BDNF, reduced NLRP3 inflammasome activity, and potentiated the efficacy of 5-FU chemotherapy. Quercetin, a bioactive component of SNS, bound to GSTM2 through hydrogen-bond and van-der-Waals interactions, up-regulated GSTM2 expression, and mitigated CORT-induced proliferation, colony formation, and chemoresistance. Our findings suggest that depression promotes colon-cancer progression by down-regulating GSTM2, whereas SNS restores GSTM2 expression and enhances chemotherapeutic response. Show less
no PDF DOI: 10.1016/j.phymed.2026.158113
BDNF cancer progression chemoresistance chemotherapy colon cancer depression gst

TUG1 suppresses neural repair subsequent to cerebral hemorrhage via the miR-381-3p/BDNF axis.

Fei Li, Xin Zhang, Hong Jiang +2 more · 2026 · Folia neuropathologica · added 2026-04-24
Intracerebral hemorrhage (ICH) has a high rate of death and disability. LncRNA-TUG1 is essential for the pathological changes secondary to ICH. The purpose of this work was to investigate the possible Show more
Intracerebral hemorrhage (ICH) has a high rate of death and disability. LncRNA-TUG1 is essential for the pathological changes secondary to ICH. The purpose of this work was to investigate the possible mechanism by which TUG1 inhibits neural repair subsequent to ICH through adjusting miR-381-3p/brain-derived neurotrophic factor (BDNF). After the ICH model was created, miR-381-3p agomir and pcDNA-TUG1 were injected. The neural function of rats was estimated using the modified neurological severity score. To quantify the expression of genes and proteins, western blotting, immunohistochemistry, and qRT-PCR were used. To confirm the interaction between TUG1 and miR-381-3p and between miR-381-3p and BDNF mRNA, a luciferase reporter assay was employed. In rats treated with miR-381-3p agomir, a trend of improvement in neurological dysfunction was observed, while the pcDNA-TUG1-treated ones showed deterioration. Furthermore, miR-381-3p agomir increased, while pcDNA-TUG1 reduced the expression level of BDNF in ICH rats. TUG1 and BDNF mRNA were validated to attach directly to miR-381-3p. Overexpressing TUG1 inhibited the level of BDNF by sponging miR-381-3p and antagonized its protective effect on neural repair in ICH rats. Our study suggests that TUG1 can sponge miR-381-3p to downregulate BDNF expression and inhibit neural repair following ICH, demonstrating a potential signaling pathway that is conducive to a better understanding of the pathological mechanisms of ICH. Show less
📄 PDF DOI: 10.5114/fn.2025.154414
BDNF bdnf cerebral hemorrhage ich lncrna mir-381-3p neural repair tug1

Corrigendum to "AdipoRon ameliorates anxiety- and depression-like behaviors in chronic restraint-stressed mice via AMPK-PPARα-BDNF-TrkB signaling" [Eur. J. Pharmacol. (2026) 1011 178468 doi: 10.1016/j.ejphar.2025.178468].

Y Li, S Han, T Xie +8 more · 2026 · European journal of pharmacology · Elsevier · added 2026-04-24
no PDF DOI: 10.1016/j.ejphar.2025.178493
BDNF ampk amyk anxiety bdnf depression pparα trk