👤 Yuhui 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, Junkai 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, 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

Current status of career adaptability among Chinese cardiovascular specialist nurses: a latent profile analysis.

Yanling Du, Chao Wu, Ziyue Gai +6 more · 2025 · BMC nursing · BioMed Central · added 2026-04-24
This study aimed to explore the career adaptability status of cardiovascular specialist nurses (CSNs) through latent profile analysis (LPA), identify distinct subgroups and their demographic features, Show more
This study aimed to explore the career adaptability status of cardiovascular specialist nurses (CSNs) through latent profile analysis (LPA), identify distinct subgroups and their demographic features, and determine factors influencing different adaptability categories. CSNs play a vital role in treating and rehabilitating patients with cardiovascular conditions. However, the existing literature offers limited insights into the career adaptability of CSNs in China. A multicenter, cross-sectional survey involving 659 Chinese CSNs was conducted. LPA was utilized to classify career adaptability profiles based on responses to the Career Adaptation Abilities Scale Short Form (CAAS-SF). Influencing factors were assessed using the Conditions of Work Effectiveness Questionnaire-II (CWEQ-II) and the General Self-Efficacy Scale (GSES). Differences among identified profiles were analyzed through ANOVA, chi-square tests, and multinomial logistic regression to explore relevant socio-demographic characteristics and influencing variables. A four-profile model provided the best fit, identifying groups labeled as “high adaptability” (Class 4, These findings provide evidence to assist nursing administrators in developing training programs to enhance CSNs’ career adaptability. The variables identified as associated with profile membership may enable more tailored training strategies. Show less
📄 PDF DOI: 10.1186/s12912-025-03887-z
LPA

Copper metabolism-related biomarkers and therapeutic targets for diabetic nephropathy.

Qiaofang Yan, Yuanyuan Du, Fei Huang +9 more · 2025 · PeerJ · added 2026-04-24
Diabetic nephropathy (DN) is the most intractable complication of diabetes. Despite decades of research, accurate diagnostic markers and effective therapeutic drugs are still elusive. Abnormal copper Show more
Diabetic nephropathy (DN) is the most intractable complication of diabetes. Despite decades of research, accurate diagnostic markers and effective therapeutic drugs are still elusive. Abnormal copper metabolism is also implicated in diabetes and its complications. This study aims to identify copper metabolism-related biomarkers and potential drugs for DN. DN datasets and copper metabolism-related genes (CMGs) were obtained from Gene Expression Omnibus (GEO) and GeneCards. Differentially expressed CMGs (DE-CMGs) were identified using the limma package and the Venn algorithm. Functional enrichment analysis and protein-protein interaction (PPI) network were performed to identify candidate hub genes. The single gene with an area under the receiver operating characteristic (ROC) curve > 0.7 was identified as a potential diagnostic biomarker of DN. Finally, these biomarkers were validated by quantitative real-time polymerase chain reaction (qRT-PCR) in high-glucose-treated human proximal tubular (HK-2) cells. These validated hub genes were used to construct a combined prediction model, confirmed by additional GSE30528 and GSE30529 datasets. The correlation analysis between the expression level of the hub genes and the estimated glomerular filtration rate (eGFR) was carried out. Additionally, immune cell infiltration and potential target drugs were investigated for these biomarkers. Five hub genes associated with copper metabolism, namely CD36, CCL2, CASP3, LPL, and APOC3, were identified as biomarkers for the early diagnosis of DN. Utilizing multiple biomarkers enhanced diagnostic accuracy and specificity. CD36, CCL2, and CASP3 correlated negatively with eGFR levels, while LPL and APOC3 correlated positively. Additionally, these hub genes were significantly linked to various immune cell types, including macrophages M1 and M2, T cells, gamma delta resting dendritic cells, neutrophils, and NK cells. Furthermore, 15 agents targeting these biomarkers were retrieved from the DrugBank database. Our study identified key genes possibly related to copper metabolism in the pathological mechanism of DN that could serve as novel targets for the diagnosis and therapy of DN. Show less
📄 PDF DOI: 10.7717/peerj.20468
APOC3

METTL3-dependent DLG2 inhibits the malignant progression of cervical cancer by inactivating the Hippo/YAP signaling.

Mei Pu, Xia Xiao, Shasha Lv +6 more · 2025 · Hereditas · BioMed Central · added 2026-04-24
Discs large homolog 2 (DLG2) has been implicated in cancer development, yet its role in cervical cancer remains unclear. This study aims to explore the regulatory mechanism of DLG2 in cervical cancer Show more
Discs large homolog 2 (DLG2) has been implicated in cancer development, yet its role in cervical cancer remains unclear. This study aims to explore the regulatory mechanism of DLG2 in cervical cancer and its clinical implications. Quantitative reverse transcription polymerase chain reaction and western blotting assays were employed to detect RNA and protein expression, respectively. Colony formation assay, 5-Ethynyl-2'-deoxyuridine assay, flow cytometry, and transwell assays were conducted for cell functional analysis. A xenograft mouse model assay was performed to analyze tumor tumorigenesis in vivo. m6A RNA immunoprecipitation assay was used to analyze the association of METTL3 and DLG2. DLG2 was underexpressed in cervical cancer tissues and cells. Elevating DLG2 levels significantly suppressed cervical cancer cell proliferation, migration, and invasion, while promoting apoptosis. Additionally, DLG2 overexpression led to the deactivation of the Hippo/YAP signaling pathway. In vivo, DLG2 overexpression was shown to reduce tumor formation. We also discovered that METTL3 destabilized DLG2 mRNA through an m6A-dependent mechanism. Moreover, lowering DLG2 expression mitigated the effects of METTL3 silencing on cervical cancer cell malignancy. DLG2 acted as a tumor suppressor in cervical cancer by inhibiting the Hippo/YAP signaling pathway. The METTL3-dependent regulation of DLG2 mRNA stability could be a critical factor in cervical cancer progression. Show less
📄 PDF DOI: 10.1186/s41065-025-00365-z
DLG2

LIPG-mediated regulation of lipid deposition and proliferation in goat intramuscular preadipocytes involves the PPARα signaling pathway.

Yinggui Wang, Lian Huang, JiangJiang Zhu +6 more · 2025 · PloS one · PLOS · added 2026-04-24
Endothelial lipase (LIPG), a member of the triglyceride lipase family, plays an essential role in human diseases and lipid metabolism. However, its function in goat intramuscular fat (IMF) deposition Show more
Endothelial lipase (LIPG), a member of the triglyceride lipase family, plays an essential role in human diseases and lipid metabolism. However, its function in goat intramuscular fat (IMF) deposition remains unclear. In this study, we investigated the role of the LIPG gene in IMF deposition by knocking down and overexpressing it in goat intramuscular preadipocytes. We successfully cloned the full-length LIPG gene, which spans 2,131 bp, including a 94 bp 5' untranslated region (5'UTR), a 1,503 bp coding sequence (CDS), and a 534 bp 3' untranslated region (3'UTR). Tissue expression profiles showed that LIPG is expressed in the heart, liver, spleen, Kidney, longest dorsal muscle, and small intestine tissues of goats. LIPG knockdown significantly inhibited both the proliferation of intramuscular preadipocytes and lipid deposition. Moreover, LIPG knockdown markedly decreased mRNA expression of FASN, LPL, CPT1A, CPT1B, FABP3, while increasing the mRNA expression of ATGL, ACOX1, FADS1, and ELOVL6. These findings were further corroborated through LIPG overexpression experiments. Using RNA sequencing (RNA-seq), we identified 1695 differentially expressed genes (DEGs) between the negative control (NC) and LIPG knockdown (Si-LIPG) groups, with KEGG pathway analysis revealing significant enrichment in the PPAR signaling pathway. Additionally, LIPG knockdown significantly upregulated the expression of both mRNA and protein levels of PPARα. The PPARα agonist WY14643 was able to reverse the enhanced lipid deposition induced by LIPG overexpression. In conclusion, our study highlights a key role for LIPG in the regulation of goat intramuscular preadipocyte proliferation and lipid deposition, potentially through the PPARα signaling pathway. These findings provide new insights into the regulatory mechanisms governing IMF deposition and suggest potential strategies for improving goat meat quality. Show less
📄 PDF DOI: 10.1371/journal.pone.0317953
FADS1

Acupuncture combined with repetitive transcranial magnetic stimulation for the treatment of post-stroke cognitive impairment: a systematic review and meta-analysis with trial sequential analysis.

Xiaomeng Zhang, Jie Wang, Wen Pan +4 more · 2025 · Frontiers in neurology · Frontiers · added 2026-04-24
This study aimed to comprehensively evaluate the clinical effectiveness and safety of acupuncture combined with repetitive transcranial magnetic stimulation (rTMS) in treating post-stroke cognitive im Show more
This study aimed to comprehensively evaluate the clinical effectiveness and safety of acupuncture combined with repetitive transcranial magnetic stimulation (rTMS) in treating post-stroke cognitive impairment (PSCI) through meta-analysis and trial sequential analysis (TSA), moreover to provide an evidence-based basis for the treatment of PSCI in clinical practice. The study conducted a comprehensive search of eight major domestic and international databases, including PubMed, Cochrane Library, Embase, Web of Science, China National Knowledge Infrastructure (CNKI), Wanfang Data, VIP and China Biology Medicine (CBM). Four English and four Chinese databases of randomized controlled trials of acupuncture combined with rTMS for the treatment of PSCI from inception until July 2025. Systematic reviews and meta-analyses were conducted based on the Cochrane systematic review method by using RevMan5.4 and Stata/MP 18.0, and trial sequential analyses were performed by TSA 0.9. Sixteen RCTs involving 1,058 patients were included, including 532 patients in the experimental group and 526 patients in the control group. Meta-analysis results showed that the experimental group had a higher clinical effectiveness rate in treating patients with PSCI compared to the control group [RR = 1.29, 95% CI (1.08, 1.55), Acupuncture combined with rTMS can improve cognitive function, regulate daily living ability, and regulate neurotransmitter levels in patients with PSCI, which is worthy recommended in the clinic. However, due to limitations in sample size, inclusion quality and incomplete reporting, it is worth noting that more rigorously designed and high-quality studies are needed to further validate these conclusions. Show less
📄 PDF DOI: 10.3389/fneur.2025.1663452
BDNF

Quantitative proteomic analysis reveals key proteins involved in radiation-induced brain injury.

Jing Liu, Junshuang Wang, Shuang Lv +7 more · 2025 · PloS one · PLOS · added 2026-04-24
Radiation-induced brain injury (RIBI) is a significant complication following radiotherapy for brain tumors, leading to neurocognitive deficits and other neurological impairments. This study aims to i Show more
Radiation-induced brain injury (RIBI) is a significant complication following radiotherapy for brain tumors, leading to neurocognitive deficits and other neurological impairments. This study aims to identify potential biomarkers and therapeutic targets for RIBI by utilizing advanced proteomic techniques to explore the molecular mechanisms underlying RIBI. A rat model of RIBI was established and subjected to whole-brain irradiation (30 Gy). Tandem mass tagging (TMT)-based quantitative proteomics, combined with high-resolution mass spectrometry, was used to identify differentially expressed proteins (DEPs) in the brain tissues of irradiated rats. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted to identify the biological processes and pathways involved. Protein-protein interaction (PPI) networks were constructed to identify key hub proteins. A total of 35 DEPs were identified, including PHLDA3, APOE and CPE. GO enrichment analysis revealed that the DEPs were mainly involved in lipid transport, cell adhesion, and metabolic processes. KEGG analysis highlighted the enrichment of pathways related to metabolism, tight junctions, and PPAR signaling. APOE was identified as a key hub protein through PPI network analysis, indicating its potential role in RIBI pathophysiology. Immunohistochemistry further validated the increased expression of PHLDA3, APOE, and CPE in the brain tissue of irradiated rats. This study provides valuable insights into the molecular mechanisms of RIBI by identifying key proteins and their associated pathways. The findings suggest that these proteins, particularly APOE and PHLDA3, could serve as potential biomarkers and therapeutic targets for clinical intervention in RIBI. These results not only enhance our understanding of RIBI's molecular pathology but also open new avenues for the development of targeted therapies to mitigate radiation-induced neurotoxicity. Show less
📄 PDF DOI: 10.1371/journal.pone.0337608
APOE

Integration of gut microbiome and lipid metabolism reveals the anti-cancer effects of pentadecanoic acid on bladder cancer.

Ya-Ting Chen, Jing Sui, Yu Yang +16 more · 2025 · BMC medicine · BioMed Central · added 2026-04-24
Pentadecanoic acid (PEA), an odd-chain fatty acid derived from diet by the gut microbiome, has garnered increasing attention for its systemic health-promoting properties. Its potential role in bladder Show more
Pentadecanoic acid (PEA), an odd-chain fatty acid derived from diet by the gut microbiome, has garnered increasing attention for its systemic health-promoting properties. Its potential role in bladder cancer (BC) occurrence and invasion, however, remains unclear. Large-scale cohorts' analyses were performed to assess the association between dietary PEA and BC occurrence and invasion. In vitro and in vivo experiments, including EJ and T24 BC cell assays and a BBN-induced mouse model, were conducted to experimentally assess the impact of PEA on BC. Serum proteomics, gut microbiome, and targeted fecal lipidomics analyses were employed to explore the underlying mechanisms. Dietary PEA was negatively associated with BC occurrence and invasion in cohort analyses. PEA suppressed EJ and T24 BC cell migration, invasion, and proliferation, while inhibiting BC development in a BBN-induced mouse model. In vivo serum proteomics identified differentially expressed lipid-related proteins (e.g., Apoe and Apob) following PEA treatment, implicating its modulation of lipid metabolism pathways. Considering the essential role of the gut-bladder axis, the gut microbiome analysis exhibited that PEA markedly altered bacteria (e.g., g_Alistipes) and fungi (e.g., o_Erysiphales, g_Teberdinia, and g_Gibberella), with concomitant lipid metabolism changes. Furthermore, targeted fecal lipidomics demonstrated the shifts in key lipids, such as phosphatidylethanolamines (PE) involved in essential lipid clusters, suggesting regulation by gut microbiome linked to BC development. Collectively, our findings demonstrate that PEA mitigates BC by reshaping the gut microbiome and modulating lipid metabolism, providing new insights into its molecular and therapeutic potential. Show less
📄 PDF DOI: 10.1186/s12916-025-04554-5
APOB

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

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

Erdafitinib inhibits the tumorigenicity of MDA-MB-231 triple-negative breast cancer cells by inducing TRIM25/ubiquitin-dependent degradation of FGFR4.

Qing Luo, Li Zhang, Yue Hao +11 more · 2025 · Breast cancer research : BCR · BioMed Central · added 2026-04-24
Triple-negative breast cancer (TNBC) is the most malignant subtype of breast cancer (BC), characterized by limited treatment options and poor clinical outcomes. Aberrant FGFR signaling has been implic Show more
Triple-negative breast cancer (TNBC) is the most malignant subtype of breast cancer (BC), characterized by limited treatment options and poor clinical outcomes. Aberrant FGFR signaling has been implicated in TNBC; however, the therapeutic potential of targeting FGFRs for TNBC treatment remains unclear. This study investigated the anti-cancer activity of the selective pan-FGFR inhibitor Erdafitinib and its underlying mechanisms using both in vitro and in vivo models. The results demonstrated that Erdafitinib suppressed TNBC tumorigenicity by promoting FGFR1/4 degradation, generating reactive oxygen species (ROS), inducing DNA damage, and ultimately triggering cell death. Mechanistic analyses revealed that Erdafitinib facilitated FGFR1/4 degradation through ubiquitination, enhanced interaction between TRIM25 and FGFR1/4, and subsequent lysosomal degradation. Furthermore, RNA-seq data from the TCGA and GEO databases, along with paired tumor tissues from TNBC patients, indicated that FGFR4 was significantly upregulated in TNBC. Notably, co-knockdown of FGFR1 and FGFR4 induced cytotoxicity in MDA-MB-231 cells, highlighting the therapeutic relevance of FGFR1/4 degradation by Erdafitinib in TNBC. These findings provide novel insights into the mechanisms underlying the anti-cancer efficacy of Erdafitinib, supporting its potential as a promising therapeutic agent for TNBC. Show less
📄 PDF DOI: 10.1186/s13058-025-02086-7
FGFR1

Systemic inflammation modulates lipoprotein(a)-associated coronary stenosis in the chronic coronary syndromes.

Lu Shen, Wenqing Zhai, Ping Jiang +6 more · 2025 · American journal of preventive cardiology · Elsevier · added 2026-04-24
Recent researches highlight the interdependence of lipoprotein(a) [Lp(a)] and Lp(a)-associated cardiovascular risk with the background inflammatory burden. This study aimed to investigate whether syst Show more
Recent researches highlight the interdependence of lipoprotein(a) [Lp(a)] and Lp(a)-associated cardiovascular risk with the background inflammatory burden. This study aimed to investigate whether systemic inflammation modulates Lp(a)-associated coronary stenosis in chronic coronary syndromes (CCS). A total of 1513 participants undergoing angiography at a tertiary cardiology center in China were included in our retrospective, cross-sectional study. Participants were categorized into normal, mild, and severe groups based on the Gensini Scores, which quantitatively assess stenosis severity. Multinomial logistic models were calculated according to accompanying systemic inflammation concentration. Participants with elevated Lp(a) levels had a high coronary stenosis risk: fully adjusted model odds ratios (ORs) [95% confidence intervals (CIs)] for the mild vs. normal and severe vs. normal groups were 1.47 (1.11-1.96) and 1.68 (1.21-2.33). Notably, the strongest Lp(a)-coronary stenosis associations after multi-variable adjustment persisted only in low inflammation concentration [systemic inflammation response index (SIRI) < 0.64)] [mild vs. normal, OR 2.03, 95% CI 1.17-3.54, Elevated Lp(a) correlates with coronary stenosis only in low inflammation concentration. Considering systemic inflammation in personalized Lp(a)-lowering therapies is more conducive for CCS managements. Show less
📄 PDF DOI: 10.1016/j.ajpc.2025.101324
LPA

A new species of the genus

Tao Zhang, Siyu Yang, Haijun Jiang +7 more · 2025 · ZooKeys · added 2026-04-24
The genus
📄 PDF DOI: 10.3897/zookeys.1262.164459
APOB

Effects of supplementation with vitamin D

Jiawei Li, Ximei Li, Jiamin Tian +5 more · 2025 · Frontiers in veterinary science · Frontiers · added 2026-04-24
Lower intramuscular fat (IMF) and excessive abdominal fat reduce carcass quality in broilers. The study aimed to investigate the effects of dietary VD
📄 PDF DOI: 10.3389/fvets.2025.1542637
APOB

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

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

CD11c+ microglia: From basic research to clinical application.

Zipeng Zhou, Yongfei Zhao, Xiangyi Fan +8 more · 2025 · Neural regeneration research · added 2026-04-24
CD11c+ microglia are a functionally specialized subpopulation of microglia that play a crucial role in the pathophysiological processes of various central nervous system diseases. This review synthesi Show more
CD11c+ microglia are a functionally specialized subpopulation of microglia that play a crucial role in the pathophysiological processes of various central nervous system diseases. This review synthesizes compelling evidence that CD11c+ microglia exhibit unique transcriptomic and phagocytic characteristics. These characteristics distinguish them from homeostatic microglia and support their specialized functions. During development, CD11c+ microglia are crucial for the maturation of oligodendrocytes and the integrity of white matter, particularly in regions such as the corpus callosum and cerebellum. In preclinical models of neurodegenerative diseases (such as Alzheimer's disease and amyotrophic lateral sclerosis) and central nervous system injuries (such as stroke and spinal cord injury), they are consistently associated with neuroprotective phenotypes. CD11c+ microglia exhibit enhanced phagocytic capacity near amyloid plaques and damaged neurons, helping to clear pathological protein aggregates and cell debris, thereby reducing neurotoxicity and promoting a repair environment. The current consensus is that specific microenvironmental cues, particularly hazard signaling molecules (DAMPs) and cytokines (such as interferon-γ), are the main drivers of the differentiation and activation of CD11c+ microglia. Among these, the TREM2-APOE signaling axis is a key and widely accepted regulatory pathway for their survival, proliferation, and functional status. The plasticity of CD11c+ microglia is regulated by multiple signaling pathways, including CSF1R, SIRPα-CD47, IFN-γ, and the complement cascade. Emerging therapeutic strategies aim to regulate their activities through gene targeting, metabolic intervention, and immune regulation using TREM2 agonists, CSF1R inhibitors, or nanopharmacological methods. However, challenges remain in defining specific CD11c+ biomarkers, understanding environment-dependent functions, and achieving targeted delivery. Future prospects depend on clearly addressing individual developmental issues, deciphering the molecular switches that control phenotypic plasticity, and developing highly specific therapeutic strategies to leverage their beneficial functions, thereby paving the way for new intervention methods for neurological diseases. Show less
no PDF DOI: 10.4103/NRR.NRR-D-25-00868
APOE

Cancer-associated adipocytes mediate CD8

Sumiya Dalangood, Cegui Hu, Chenwei Yuan +10 more · 2025 · Cell reports · Elsevier · added 2026-04-24
Cancer-associated adipocytes (CAAs) reprogram the metabolic status of the tumor microenvironment (TME). The metabolic crosstalk between CAAs and CD8
no PDF DOI: 10.1016/j.celrep.2025.116526
FGFR1

TRIM21-driven K63-linked ubiquitination of RBM38c, as a novel interactor of BECN1, contributes to DNA damage-induced autophagy.

Lishenglan Xia, Yusheng Xing, Xinjia Ye +6 more · 2025 · Cell death and differentiation · Nature · added 2026-04-24
Autophagy is essential in DNA damage response by limiting damage, but its responsive activation remains unclear. RBM38 (RBM38a), an RNA-binding protein, regulates mRNA metabolism and plays a key role Show more
Autophagy is essential in DNA damage response by limiting damage, but its responsive activation remains unclear. RBM38 (RBM38a), an RNA-binding protein, regulates mRNA metabolism and plays a key role in controlling cell cycle progression, senescence, and cancer. In this study, we uncovered a novel primate-specific isoform, RBM38c, with 32 extra amino acids from exon 2, which imparts a distinct capacity to promote autophagy upon DNA damage. TP53 increases RBM38c expression upon DNA damage, while TRIM21 facilitates its K63-linked ubiquitination at lysine (K) 35. Activated RBM38c enhances its interaction with BECN1, promoting the formation of the ATG14-containing PtdIns3K-C1 complex and thus autophagy initiation. A K35R mutation or TRIM21 deficiency impairs RBM38c ubiquitination, preventing autophagy activation upon DNA damage. Moreover, RBM38c-driven autophagy protects cells from DNA damage-induced apoptosis and promotes survival, with this beneficial effect susceptible to suppression by the autophagy inhibitor 3-methyladenine. Consequently, depleting RBM38c enhances the efficacy of DNA-damaging drugs by impairing autophagy and increasing DNA damage. Clinical lung cancer samples show a positive correlation between RBM38c expression and LC3 expression, and this correlation is linked to chemotherapy resistance. Together, our study reveals a novel mechanism for DNA damage-induced autophagy, involving K63-linked ubiquitination of RBM38c as a critical interactor with BECN1. Show less
no PDF DOI: 10.1038/s41418-025-01480-0
PIK3C3

Esketamine relieves postoperative depression and pain indicators in patients undergoing laparoscopic total hysterectomy.

Jun Jing, Meng-Ying Zhang, Wei-Hong Yin +4 more · 2025 · BMC anesthesiology · BioMed Central · added 2026-04-24
This study aimed to investigate the effects of perioperative esketamine on postoperative depression and pain in patients undergoing laparoscopic total hysterectomy. 135 patients undegoing laparoscopic Show more
This study aimed to investigate the effects of perioperative esketamine on postoperative depression and pain in patients undergoing laparoscopic total hysterectomy. 135 patients undegoing laparoscopic total hysterectomy were recruited and randomly allocated to three groups. Finally, a total of 127 patients were selected into the statistical analysis, with the final grouping information as follows: sufentanil group (S1, n = 44), sufentanil combined with 0.25 mg/kg esketamine group (SK1, n = 42) and sufentanil combined with 0.5 mg/kg esketamine group (SK2,n = 41) intraoperatively, then postoperative analgesia was maintained with sufentanil (2 µg/kg) via patient-controlled intravenous analgesia (PCIA) in all groups, while a 1 mg/kg dose of esketamine was added to the PCIA regimen for patients in groups SK1 and SK2. The peripheral blood serum brain-derived neurotrophic factor (BDNF) level, 5-hydroxytryptamine (5-HT) level, Hamilton Depression Scale (HAM-D) scores, visual analogue scale(VAS) scores and the number of PCIA button pressed times in perioperative period were collected. Meanwhile, the postoperative adverse effects including nausea, vomiting, dizziness, respiratory depression and hallucinations were collected and compared between the three groups. Relative to preoperative baseline levels, BDNF and 5-HT levels decreased at the 1th day(1d) post surgery in all groups(P < 0.05), and then followed by a gradual increase thereafter. Compared with S1 group, the SK1 and SK2 group showed significantly higher serum BDNF and 5-HT levels at 1d, 2d and 5d after operation (P < 0.05), and revealed even higher at 1d and 2d after operation in SK2 group(P < 0.05). The HAM-D scores at 1d, 2d and 5d post operation were significantly reduced in SK1 and SK2 group (P < 0.05) compared to S1 group, and decreased even lower at 1d and 2d postoperative in SK2 group(P < 0.05), but no significant difference was found among three groups at 1d before and the 7d after operation. Simultaneously, the VAS scores decreased significantly in SK1 and SK2 group at the 1th hour(1 h), 6 h, 12 h, 24 h, and 48 h after surgery (P < 0.05), and the PCIA button pressed times were also significantly reduced in SK1 and SK2 group (P < 0.05) during the postoperative 48 h. Furthermore, the SK1 and SK2 group showed the lower dosage of remifentanil during the surgery(P < 0.05). However, the postoperative adverse effects had no statistical differences among the three groups. The combined intraoperative and postoperative administration of esketamine was effective in alleviating postoperative depression and pain, without increasing adverse effects in patients undergoing laparoscopic total hysterectomy. Moreover, the 0.5 mg/kg dosage intraoperatively may have the better alleviation property of depression-related indicators. The study was registered with the Chinese Clinical Trial Registry at www.chictr.org.cn (registration date: October 31, 2022; registration number: ChiCTR2200065198). Show less
📄 PDF DOI: 10.1186/s12871-025-03570-5
BDNF

Establishment and characterization of liver-specific Apoa4-Cre and Cyp2c11-Cre rat models in juvenile and adult stages.

Wei Dong, Xiang Gao, Feifei Guan +4 more · 2025 · Animal models and experimental medicine · Wiley · added 2026-04-24
Liver diseases are a major contributor to both morbidity and mortality. Conditional knockout animals are always produced through crossing floxed animals with a tissue-specific Cre animal. The use of f Show more
Liver diseases are a major contributor to both morbidity and mortality. Conditional knockout animals are always produced through crossing floxed animals with a tissue-specific Cre animal. The use of floxed rat resource has rapidly increased, but the liver-specific Cre rat lines for studying liver diseases and interested genes are limited, especially in a spatially and temporally restricted manner. RNA sequencing and real-time polymerase chain reaction (PCR) were used to screen and confirm the presence of liver-specific genes. Apoa4-Cre rats and Cyp2c11-Cre rats were produced by CRISPR/Cas9 knockin. Rosa26-imCherry rats were employed to hybridize with the Cre rats to obtain the Apoa4-Cre/Rosa26-imCherry and Cyp2c11-Cre/Rosa26-imCherry rats. The temporal and spatial patterns of Cre expression were determined by the observation of red fluorescence on tissue sections. Hematoxylin-eosin stain was used to evaluate the liver histopathologic changes. The blood biochemical analysis of several liver enzymes and liver lipid profile was performed to evaluate the liver function of Cre rats. Apoa4 and Cyp2c11 were identified as two liver-specific genes. Apoa4-Cre and Cyp2c11-Cre rats were produced and hybridized with Rosa26-imCherry rats. The red fluorescence indicated that the Cre recombinases were specially expressed in the juvenile and adult liver and not in other organs of two hybridized rats. All the blood biochemical parameters except low-density lipoprotein (LDL) did not change significantly in the Cre rats. No histological alterations were detected in the livers of the Cre rats. Liver-specific Apoa4-Cre and Cyp2c11-Cre rats have been established successfully and could be used to study gene knockout, specifically in juvenile and adult liver. Show less
📄 PDF DOI: 10.1002/ame2.12504
APOA4

DHX36-mediated G-quadruplexes unwinding is essential for oocyte and early embryo development in mice.

Yu-Xuan Jiao, Guo-Wei Bu, Yun-Wen Wu +6 more · 2025 · Science bulletin · Elsevier · added 2026-04-24
DHX36 plays a crucial role in regulating transcriptional and post-transcriptional processes through its interaction with G-quadruplexes (G4s). The mechanisms by which DHX36 regulates G4s vary across d Show more
DHX36 plays a crucial role in regulating transcriptional and post-transcriptional processes through its interaction with G-quadruplexes (G4s). The mechanisms by which DHX36 regulates G4s vary across different cell types and physiological conditions. Oocyte-specific conditional knockout (CKO) mice were utilized to study the impact of DHX36 deficiency on female fertility. The results show that the CKO mice exhibit severely impaired hormone response, ovulation, and complete infertility. The CKO germinal vesicle (GV) oocytes display large nucleoli, aberrant chromatin configuration, decreased chromatin accessibility, disturbed transcriptome, and inhibited meiosis progression. Following fertilization, the embryos derived from the CKO oocytes arrest at the zygote or 2-cell stage. Notably, we observed inadequate rRNA transcription in growing GV oocytes, as well as insufficient pre-rRNA processing and translation activity in fully-grown GV oocytes. Using a G4 probe and antibody, we found increased G4s formation at the chromatin and cytoplasm of CKO GV oocytes; these G4s mainly originate from the rDNA and pre-rRNA. Furthermore, the distribution of DHX36 was found to be spatiotemporally synchronized with that of pre-rRNA and G4s in early mouse embryos. In vitro experiments confirmed that DHX36 directly binds with pre-rRNA through the RHAU-specific motif (RSM). Overexpression of DHX36 could partially alleviate the pre-rRNA accumulation in fully-grown CKO oocytes. In conclusion, this study highlights the physiological significance of DHX36 in maintaining female fertility, underscoring its critical role in rRNA homeostasis and chromatin configuration through G4-unwinding mechanism in mouse oocytes. Show less
no PDF DOI: 10.1016/j.scib.2025.02.017
DHX36

Orlistat Confers Neuroprotection in Traumatic Brain Injury by Modulating Microglial Lipid Metabolism.

Chenxuan Yu, Yu Ni, Yuxuan Xiong +9 more · 2025 · Cells · MDPI · added 2026-04-24
Traumatic brain injury (TBI) represents a major cause of mortality and disability worldwide, particularly affecting young adults and elderly populations. This study investigates the neuroprotective po Show more
Traumatic brain injury (TBI) represents a major cause of mortality and disability worldwide, particularly affecting young adults and elderly populations. This study investigates the neuroprotective potential of orlistat (ORL), a gastrointestinal lipase inhibitor, in a murine TBI model. Behavioral, histological, and molecular analyses demonstrated that ORL significantly attenuated TBI-induced neurological damage. Microglial depletion experiments revealed that ORL's neuroprotective effects were largely mediated through microglial modulation. In vitro and in vivo studies showed that ORL suppressed microglial activation, phagocytosis, and migration. Single-cell RNA sequencing identified upregulation of lipoprotein lipase (LPL) in a TBI-induced microglial subpopulation. Molecular docking predicted ORL-LPL binding, suggesting direct enzymatic inhibition. Transcriptomic and metabolomic analyses further revealed ORL's modulation of microglial metabolic pathways and inflammatory responses. Our findings position ORL as a promising repurposed therapeutic for TBI through its novel mechanism of targeting microglial LPL-mediated neuroinflammation. Show less
📄 PDF DOI: 10.3390/cells14181469
LPL

The designer cytokine IC7Fc attenuates atherosclerosis development by targeting hyperlipidemia in mice.

Wietse In Het Panhuis, Ellen Thiemann, Daisy M A H van Dijk +27 more · 2025 · Science advances · Science · added 2026-04-24
The chimeric cytokine IC7Fc conveys the metabolic signaling properties of the glycoprotein 130 receptor cytokines interleukin-6 and ciliary neurotrophic factor via membrane-bound signaling. IC7Fc was Show more
The chimeric cytokine IC7Fc conveys the metabolic signaling properties of the glycoprotein 130 receptor cytokines interleukin-6 and ciliary neurotrophic factor via membrane-bound signaling. IC7Fc was previously shown to slow the progression of type 2 diabetes mellitus, and here, we demonstrate its effect on atherosclerotic development. In APOE*3-Leiden.CETP mice, an atherosclerosis-prone model with a humanized lipoprotein metabolism, IC7Fc markedly lowered plasma triglyceride and total cholesterol levels. This was mechanistically explained by an inhibition of de novo lipogenesis in the liver, increased synthesis of bile acids from cholesterol, and down-regulated apolipoprotein B synthesis, which resulted in decreased cholesterol secretion in very low-density lipoprotein particles. As a consequence, IC7Fc treatment considerably reduced atherosclerotic lesion formation and vascular inflammation compared with current antihyperlipidemic therapy. In conclusion, IC7Fc is a promising pharmacological treatment for cardiometabolic diseases targeting hyperlipidemia and inflammation. Show less
📄 PDF DOI: 10.1126/sciadv.adx3794
CETP

APOE

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

Interleukin-27 is a multitarget regulator of fibroblast remodeling in thyroid-associated ophthalmopathy.

Pengbo Zhang, Xiaofang Wang, Nanji Lu +3 more · 2025 · iScience · Elsevier · added 2026-04-24
Thyroid-associated ophthalmopathy (TAO) is characterized by inflammation and tissue remodeling, including fibrosis and adipogenesis. Here, we identify interleukin-27 (IL-27) as a negative feedback imm Show more
Thyroid-associated ophthalmopathy (TAO) is characterized by inflammation and tissue remodeling, including fibrosis and adipogenesis. Here, we identify interleukin-27 (IL-27) as a negative feedback immunomodulator in TAO. Serum IL-27α levels were significantly elevated in patients with TAO compared with healthy and inflammatory disease controls. In orbital fibroblasts (OFs), exogenous IL-27 suppressed IL-1β-induced proinflammatory cytokines and reduced hypoxia-induced NLRP3 inflammasome activation. IL-27 also attenuated TGF-β-driven fibrosis via p38 MAPK signaling in CD90 Show less
📄 PDF DOI: 10.1016/j.isci.2025.113982
IL27

ChREBP mediates metabolic remodeling in FBP1-deficient liver.

Chen-Ma Wang, Qiu-Fang Bai, Ya-Jin Liu +9 more · 2025 · American journal of physiology. Cell physiology · added 2026-04-24
The deficiency of fructose-1,6-bisphosphatase 1 (FBP1), a key enzyme of gluconeogenesis, causes fatty liver. However, its underlying mechanism and physiological significance are not fully understood. Show more
The deficiency of fructose-1,6-bisphosphatase 1 (FBP1), a key enzyme of gluconeogenesis, causes fatty liver. However, its underlying mechanism and physiological significance are not fully understood. Here we demonstrate that carbohydrate response element-binding protein (ChREBP) mediates lipid metabolic remodeling and promotes progressive triglyceride accumulation against metabolic injury in adult FBP1-deficient liver. Inducible liver-specific deletion of Fbp1 gene caused progressive hepatomegaly and hepatic steatosis, with a marked increase in hepatic de novo lipogenesis (DNL) as well as a decrease in plasma β-hydroxybutyrate levels. Notably, FBP1 deficiency resulted in a persistent activation of ChREBP and its target genes involved in glycolysis, lipogenesis, and fatty acid oxidation, even under fasting conditions. Furthermore, liver-specific ChREBP disruption could markedly restore the phenotypes of enhanced DNL and triglyceride accumulation in FBP1-deficient liver but exacerbated its hepatomegaly and liver injury, which was associated with remarkable energy deficit, impaired mammalian target of rapamycin (mTOR) activation, and increased oxidative stress. Furthermore, metabolomics analysis revealed a robust elevation of phosphoenolpyruvate, phosphoglycerates, phospholipids, and ceramides caused by ChREBP deletion in FBP1-deficient liver. Put together, these results suggest that overactivation of ChREBP pathway mediates liver metabolic remodeling in the absence of FBP1, which contributes to the pathogenesis of progressive hepatic steatosis and provides a protection against liver injury. Thus, our findings point to a beneficial role of ChREBP in metabolic remodeling in the context of excessive gluconeogenic intermediates. Show less
no PDF DOI: 10.1152/ajpcell.00875.2024
MLXIPL

NSP6 regulates calcium overload-induced autophagic cell death and is regulated by KLHL22-mediated ubiquitination.

Xingyu Tao, Yanan Wang, Jiangbo Jin +10 more · 2025 · Journal of advanced research · Elsevier · added 2026-04-24
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a substantial global threat. SARS-CoV-2 nonstructural proteins (NSPs) are essential for impeding the host replication mechanism while Show more
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a substantial global threat. SARS-CoV-2 nonstructural proteins (NSPs) are essential for impeding the host replication mechanism while also assisting in the production and organization of new viral components. However, NSPs are not incorporated into viral particles, and their subsequent fate within host cells remains poorly understood. Additionally, their role in viral pathogenesis requires further investigation. This study aimed to discover the ultimate fate of NSP6 in host cells and to elucidate its role in viral pathogenesis. We investigated the effects of NSP6 on cell death and explored the underlying mechanism; moreover, we examined the degradation mechanism of NSP6 in human cells, along with analysing its correlation with coronavirus disease 2019 (COVID-19) severity in patient peripheral blood mononuclear cells (PBMCs). NSP6 was demonstrated to induce cell death. Specifically, NSP6 interacted with EI24 autophagy-associated transmembrane protein (EI24) to increase intracellular Ca This study reveals that KLHL22-mediated ubiquitination controls NSP6 stability and that NSP6 induces autophagic cell death via calcium overload, highlighting its cytotoxic role and suggesting therapeutic strategies that target calcium signaling or promote NSP6 degradation as potential interventions against COVID-19. Show less
no PDF DOI: 10.1016/j.jare.2025.05.031
PIK3C3

A Multi-Task Self-Supervised Strategy for Predicting Molecular Properties and FGFR1 Inhibitors.

Xin Yang, Yang Wang, Ye Lin +4 more · 2025 · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Wiley · added 2026-04-24
Studying the molecular properties of drugs and their interactions with human targets aids in better understanding the clinical performance of drugs and guides drug development. In computer-aided drug Show more
Studying the molecular properties of drugs and their interactions with human targets aids in better understanding the clinical performance of drugs and guides drug development. In computer-aided drug discovery, it is crucial to utilize effective molecular feature representations for predicting molecular properties and designing ligands with high binding affinity to targets. However, designing an effective multi-task and self-supervised strategy remains a significant challenge for the pretraining framework. In this study, a multi-task self-supervised deep learning framework is proposed, MTSSMol, which utilizes ≈10 million unlabeled drug-like molecules for pretraining to identify potential inhibitors of fibroblast growth factor receptor 1 (FGFR1). During the pretraining of MTSSMol, molecular representations are learned through a graph neural networks (GNNs) encoder. A multi-task self-supervised pretraining strategy is proposed to fully capture the structural and chemical knowledge of molecules. Extensive computational tests on 27 datasets demonstrate that MTSSMol exhibits exceptional performance in predicting molecular properties across different domains. Moreover, MTSSMol's capability is validated to identify potential inhibitors of FGFR1 through molecular docking using RoseTTAFold All-Atom (RFAA) and molecular dynamics simulations. Overall, MTSSMol provides an effective algorithmic framework for enhancing molecular representation learning and identifying potential drug candidates, offering a valuable tool to accelerate drug discovery processes. All of the codes are freely available online at https:// github.com/zhaoqi106/MTSSMol. Show less
📄 PDF DOI: 10.1002/advs.202412987
FGFR1

Precision engineering of anti-atherosclerotic herbal nanomedicine: from machine learning-aided active components screening to optimized metal-phenolic network codelivery.

Yao Chen, Meiting Lu, Lu Zhang +9 more · 2025 · Drug delivery and translational research · Springer · added 2026-04-24
Atherosclerosis (AS), a chronic inflammatory disease linked to oxidative stress and lipid imbalance, remains a major cardiovascular threat. Traditional herbs Salvia miltiorrhiza and Carthamus tinctori Show more
Atherosclerosis (AS), a chronic inflammatory disease linked to oxidative stress and lipid imbalance, remains a major cardiovascular threat. Traditional herbs Salvia miltiorrhiza and Carthamus tinctorius exhibit multi-target anti-AS potential, yet their compositional complexity limits clinical translation. This study aimed to systematically identify core anti-AS components from these herbs and enhance their anti-AS efficacy via machine learning-aided screening and nanotechnology-driven codelivery. We initially pioneered a machine learning-aided hybrid strategy integrating network pharmacology and quantitative activity relationship (QSAR) modeling to identify four core anti-AS polyphenols (i.e., salvianic acid A, salvianolic acid B, protocatechuic acid, and hydroxysafflor yellow A). Subsequently, a quaternary metal-phenolic network (SSPH-MPN) was engineered for plaque-targeted codelivery, optimized via the median-effect principle for achieving a synergistic effect based on ROS scavenging efficacy. The optimized SSPH-MPN was characterized by a series of studies, including molecular dynamics simulations, UV, DLS, TEM, FTIR, XPS, and ICP-MS. The anti-AS effect of the optimized SSPH-MPN was evaluated by monitoring oxidative status (ROS levels, antioxidant enzymes SOD, GSH-Px, MDA, T-AOC), inflammatory markers (IL-1β, IL-6, TNF-α), lipid metabolism (DiI-oxLDL uptake, cholesterol efflux, blood lipid levels, lipid accumulation), and plaque areas. The results demonstrated that the optimized SSPH-MPN showed great efficiency in inhibiting lipid uptake and accumulation, and mediating cholesterol efflux in RAW 264.7 cells, and exhibited improved lipid metabolism, attenuated oxidative stress and inflammation, thus acquired diminished plaque area in apoE Show less
📄 PDF DOI: 10.1007/s13346-025-02023-3
APOE

Bidirectional causal associations between plasma metabolites and bipolar disorder.

Qian Zhao, Ancha Baranova, Dongming Liu +2 more · 2025 · Molecular psychiatry · Nature · added 2026-04-24
Altered levels of human plasma metabolites have been implicated in the etiology of bipolar disorder (BD). However, the causality between metabolites and the disease was not well described. We performe Show more
Altered levels of human plasma metabolites have been implicated in the etiology of bipolar disorder (BD). However, the causality between metabolites and the disease was not well described. We performed a bidirectional metabolome-wide Mendelian randomization (MR) analysis to evaluate the potential causal relationships between 871 plasma metabolites and BD. We used DrugBank and ChEMBL to evaluate whether related metabolites are potential therapeutic targets. Finally, Bayesian colocalization analysis was performed to identify shared genomic loci BD and identified metabolites. Our MR results showed that six metabolites were significantly associated with a reduced risk of BD, including arachidonate (20:4n6) (OR: 0.90, 95% CI: 0.84-0.95) and sphingomyelin (d18:2/24:1, d18:1/24:2) (OR: 0.92, 95% CI: 0.87-0.96), while five metabolites were significantly associated with an increased risk of BD, including 1-palmitoyl-2-linoleoyl-GPE (16:0/18:2) (OR: 1.09, 95% CI: 1.05-1.13). However, our reverse MR analysis showed that BD was not associated with the levels of any metabolite. Additionally, the leave-one-out analysis revealed SNPs within chromosome 11 loci harboring MYRF, FADS1, and FADS2 as ones with the potential to influence partial causal effects. Druggability evaluation showed that 10 of the BD-related metabolites, such as sphingomyelin and cytidine, have been targeted by pharmacologic intervention. Colocalization analysis highlighted one colocalized region (chromosome 11q12) shared by 11 metabolites and BD and pointed to some genes as possible players, including FADS1, FADS2, FADS3, and SYT7. Our study supported a causal role of plasma metabolites in the susceptibility to BD, and the identified metabolites may provide a new avenue for the prevention and treatment of BD. Show less
📄 PDF DOI: 10.1038/s41380-025-02977-3
FADS1

Sparstolonin B and Curcumin alleviate atherogenesis by modulating T helper 17-stromal cell interactions associated with interleukin-17 receptor A (IL-17RA) - transforming growth factor-β-activated kinase 1 (TAK1) - nuclear factor-kappa B (NF-κB) signaling.

Guofu Zhong, Qingqing Liu, Qing Zhang +11 more · 2025 · Phytomedicine : international journal of phytotherapy and phytopharmacology · Elsevier · added 2026-04-24
Sparstolonin B (SSNB) and Curcumin (Cur), from a pair of compatible herbs, were previously identified as anti-inflammation and T helper 17 (Th17) modulation reagents. However, their compatible roles i Show more
Sparstolonin B (SSNB) and Curcumin (Cur), from a pair of compatible herbs, were previously identified as anti-inflammation and T helper 17 (Th17) modulation reagents. However, their compatible roles in atherosclerosis (AS) and underlying mechanisms remain uninvestigated. In vivo, the apoE The gene-disease interaction and hub gene network reveals Th17-associated genes in the pathogenesis of atherosclerosis. In vitro, SSNB and Cur reduced oxLDL-induced BMDC activation by downregulating CD36. SSNB showed stronger inhibition to inflammatory activation of DC, while Cur more intensively suppressed co-stimulatory molecules. For the Th17/Treg bias in co-culture of BMDC and CD4 Our findings reveal, for the first time, that SSNB and Cur alleviate AS by modulating Th17-stromal cell interactions, with the IL-17RA-TAK1-NF-κB pathway as a related mediator. Notably, SSNB and Cur exhibit distinct anti-atherogenic roles. SSNB primarily targets TLR4/CD36 to inhibit DC activation, Th17 differentiation, VSMC inflammation and mainly inhibited TAK1 phosphorylation, while Cur more significant inhibited macrophage inflammation, and more directly inhibited NF-κB P65 phosphorylation. This study will be valuable for developing novel and precise adjuvant therapies for AS. Show less
no PDF DOI: 10.1016/j.phymed.2025.157578
APOE

Ferroptosis-related hub genes and immune cell dynamics as diagnostic biomarkers in age-related macular degeneration.

Jinquan Chen, Zhao Long, Dandan Shi +2 more · 2025 · European journal of medical research · BioMed Central · added 2026-04-24
Age-related Macular Degeneration (AMD) is widely acknowledged as a principal cause of vision loss in the elderly. Currently, the therapeutic interventions available in clinical practice fail to achiev Show more
Age-related Macular Degeneration (AMD) is widely acknowledged as a principal cause of vision loss in the elderly. Currently, the therapeutic interventions available in clinical practice fail to achieve satisfactory outcomes. Therefore, it is imperative that we approach the progress of AMD from novel perspectives in order to explore new therapeutic strategies. We obtained transcriptomic data from the macular and the peripheral retina from patients with AMD and a control group from the Gene Expression Omnibus (GEO) database. Through Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, we identified differentially expressed genes (DEGs) that were significantly enriched in functions associated with ferroptosis. Subsequent application of machine learning techniques enabled the identification of key hub genes, whose diagnostic potential was further validated. Additionally, the expression of these hub genes was corroborated in both animal and cellular models. Finally, we performed a functional enrichment analysis of these hub genes. In the macula of patients with AMD, 452 DEGs were identified, while in the peripheral retina, 222 DEGs were discovered. Within the macula, 19 genes were associated with ferroptosis, compared to 3 in the peripheral retina. Consequently, the macular was selected as the primary focus of the study. Subsequent screening of these 19 genes using LASSO regression, Support Vector Machine (SVM), and Random Forest algorithms identified four hub genes: FADS1, TFAP2A, AKR1C3, and TTPA. Consequently, we utilized cigarette smoke extract (CSE) to either stimulate retinal pigment epithelial (RPE) cells in vitro or administer it via intravitreal injection, thereby establishing in vitro and in vivo models of AMD. Results from RT-PCR and Western blot analyses revealed an upregulation of FADS1, AKR1C3, and TTPA, while TFAP2A exhibited decreased expression. Finally, we investigated the infiltration of immune cells within the macular and performed a functional enrichment analysis of the hub genes. We identified four key ferroptosis-related genes (FRGs)-FADS1, AKR1C3, TFAP2A, and TTPA-that possess diagnostic relevance for AMD and correlate with immune cell infiltration. Moreover, significant changes in both mRNA and protein expression levels of these genes have been observed in in vitro experiments and mice models. Show less
📄 PDF DOI: 10.1186/s40001-025-03044-x
FADS1