👤 Ziguo 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, Yuhui Zhang, Yujia Zhang, Yujiao Zhang, Yujie Zhang, Yujin Zhang, Yujing Zhang, Yujuan Zhang, Yuke Zhang, Yukun Zhang, Yulin Zhang, Yuling Zhang, Yulong Zhang, Yumei Zhang, Yumeng Zhang, Yumin Zhang, Yun Zhang, Yun-Feng Zhang, Yun-Lin Zhang, Yun-Mei Zhang, Yun-Sheng Zhang, Yun-Xiang Zhang, Yunfan Zhang, Yunfei Zhang, Yunfeng Zhang, Yunhai Zhang, Yunhang Zhang, Yunhe Zhang, Yunhui Zhang, Yuning Zhang, Yunjia Zhang, Yunli Zhang, Yunmei Zhang, Yunpeng Zhang, Yunqi Zhang, Yunqiang Zhang, Yunqing Zhang, Yunsheng Zhang, Yunxia Zhang, Yupei Zhang, Yupeng Zhang, Yuping Zhang, Yuqi Zhang, Yuqing Zhang, Yurou Zhang, Yuru Zhang, Yusen Zhang, Yushan Zhang, Yutian Zhang, Yuting Zhang, Yutong Zhang, Yuwei Zhang, Yuxi Zhang, Yuxia Zhang, Yuxin Zhang, Yuxuan Zhang, Yuyan Zhang, Yuyanan Zhang, Yuyang Zhang, Yuying Zhang, Yuyu Zhang, Yuyuan Zhang, Yuzhe Zhang, Yuzhi Zhang, Yuzhou Zhang, Yuzhu Zhang, Yvonne Zhang, Z Zhang, Z-K Zhang, Zai-Rong Zhang, Zaifeng Zhang, Zaijun Zhang, Zaiqi Zhang, Zebang Zhang, Zekun Zhang, Zemin Zhang, Zeming Zhang, Zeng Zhang, Zengdi Zhang, Zengfu Zhang, Zenglei Zhang, Zengli Zhang, Zengqiang Zhang, Zengrong Zhang, Zengtie Zhang, Zepeng Zhang, Zewei Zhang, Zewen Zhang, Zeyan Zhang, Zeyuan Zhang, Zhan-Xiong Zhang, Zhangjin Zhang, Zhanhao Zhang, Zhanjie Zhang, Zhanjun Zhang, Zhanming Zhang, Zhanyi Zhang, Zhao Zhang, Zhao-Huan Zhang, Zhao-Ming Zhang, Zhaobo Zhang, Zhaocong Zhang, Zhaofeng Zhang, Zhaohua Zhang, Zhaohuai Zhang, Zhaohuan Zhang, Zhaohui Zhang, Zhaomin Zhang, Zhaoping Zhang, Zhaoqi Zhang, Zhaotian Zhang, Zhaoxue Zhang, Zhe Zhang, Zhehua Zhang, Zhemei Zhang, Zhen Zhang, Zhen-Dong Zhang, Zhen-Jie Zhang, Zhen-Shan Zhang, Zhen-Tao Zhang, Zhen-lin Zhang, Zhenfeng Zhang, Zheng Zhang, Zhengbin Zhang, Zhengfen Zhang, Zhenglang Zhang, Zhengliang Zhang, Zhengxiang Zhang, Zhengxing Zhang, Zhengyu Zhang, Zhengyun Zhang, Zhenhao Zhang, Zhenhua Zhang, Zhenlin Zhang, Zhenqiang Zhang, Zhentao Zhang, Zhenyang Zhang, Zhenyu Zhang, Zhenzhen Zhang, Zhenzhu Zhang, Zhewei Zhang, Zhewen Zhang, Zheyuan Zhang, Zhezhe Zhang, Zhi Zhang, Zhi-Chang Zhang, Zhi-Jie Zhang, Zhi-Jun Zhang, Zhi-Peng Zhang, Zhi-Qing Zhang, Zhi-Shuai Zhang, Zhi-Shuo Zhang, Zhi-Xin Zhang, Zhibo Zhang, Zhicheng Zhang, Zhicong Zhang, Zhifei Zhang, Zhigang Zhang, Zhiguo Zhang, Zhihan Zhang, Zhihao Zhang, Zhihong Zhang, Zhihua Zhang, Zhihui Zhang, Zhijian Zhang, Zhijiao Zhang, Zhijing Zhang, Zhijun Zhang, Zhikun Zhang, Zhimin Zhang, Zhiming Zhang, Zhiping Zhang, Zhiqian Zhang, Zhiqiang Zhang, Zhiqiao Zhang, Zhiru Zhang, Zhishang Zhang, Zhishuai Zhang, Zhiwang Zhang, Zhiwen Zhang, Zhixia Zhang, Zhixin Zhang, Zhiyan Zhang, Zhiyao Zhang, Zhiye Zhang, Zhiyi Zhang, Zhiyong Zhang, Zhiyu Zhang, Zhiyuan Zhang, Zhiyun Zhang, Zhizhong Zhang, Zhong Zhang, Zhong-Bai Zhang, Zhong-Yi Zhang, Zhong-Yin Zhang, Zhong-Yuan Zhang, Zhongheng Zhang, Zhongjie Zhang, Zhonglin Zhang, Zhongqi Zhang, Zhongwei Zhang, Zhongxin Zhang, Zhongxu Zhang, Zhongyang Zhang, Zhongyi Zhang, Zhou Zhang, Zhu Zhang, Zhu-Qin Zhang, Zhuang Zhang, Zhuo Zhang, Zhuo-Ya Zhang, Zhuohua Zhang, Zhuojun Zhang, Zhuorong Zhang, Zhuoya Zhang, Zhuqin Zhang, Zhuqing Zhang, Zhuzhen Zhang, Zi-Feng Zhang, Zi-Jian Zhang, Zian Zhang, Zicheng Zhang, Ziding Zhang, 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

Multi-omics analysis unraveling stemness features associated with oncogenic dedifferentiation in 12 cancers.

Jun Cheng, Jiafan Cao, Yalan Yang +16 more · 2025 · Cancer letters · Elsevier · added 2026-04-24
Tumorigenesis is typically accompanied by cellular dedifferentiation and the acquisition of stem cell-like attributes. However, few studies have comprehensively evaluated the putative relationships be Show more
Tumorigenesis is typically accompanied by cellular dedifferentiation and the acquisition of stem cell-like attributes. However, few studies have comprehensively evaluated the putative relationships between these characteristics and various cancers. Here, we integrated gene expression and DNA methylation quantitative trait loci (cis-eQTL and cis-mQTL) data from the blood to perform multi-omics Mendelian randomization analysis. Our analyses revealed 967 stem cell-associated genes (P < 0.05) and 11,262 methylation sites (P < 0.01) significantly related to 12 cancers. SMAD7 (cg14321542) in colon cancer, IGF2 (cg13508136) in prostate cancer, and FADS1 (cg07005513) in rectal cancer were prioritized as candidate causal genes and regulatory elements. Notably, using cis-eQTL data from the corresponding tissue sites, we detected 16 stem cell-associated genes dramatically causally associated with six cancers (FDR<0.2). The gene THBS3 was particularly common in both blood and stomach tissues and exhibited prognostic significance. Furthermore, it was markedly associated with one microbial metabolic pathway and four immunophenotypes. Functional validation using the ECC12 gastric cancer cell line revealed that the inhibition of its expression could accelerate oxidative phosphorylation and reactive oxygen species production, reduce clonal proliferation ability, and promote the apoptosis of stomach tumor cells. Additionally, based on spatial transcriptomic data from gastrointestinal cancers, the results demonstrated the clusters enriched with the most stem cell-associated genes exhibited significantly enhanced tumor-promoting potency, and the THBS3-expressing cells displayed suppressed oxidative phosphorylation. Overall, this study enhances our understanding of tumorigenic mechanisms and aids in the identification of therapeutic targets. Show less
no PDF DOI: 10.1016/j.canlet.2025.217816
FADS1

Single-cell transcriptomic profiling reveals liver fibrosis in colorectal cancer liver metastasis.

Yiqiao Deng, Chengyao Guo, Xiaomeng Liu +14 more · 2025 · Experimental & molecular medicine · Nature · added 2026-04-24
Tumor fibrosis is recognized as a malignant hallmark in various solid tumors; however, the clinical importance and associated molecular characteristics of tumor fibrosis in liver metastases (LM) from Show more
Tumor fibrosis is recognized as a malignant hallmark in various solid tumors; however, the clinical importance and associated molecular characteristics of tumor fibrosis in liver metastases (LM) from colorectal cancer (CRLM) remain poorly understood. Here we show that patients with CRLM whose liver metastases (LM) exhibited tumor fibrosis (Fibrosis+ LM) had significantly worse progression-free survival (P = 0.025) and overall survival (P = 0.008). Single-cell RNA sequencing revealed that the tumor microenvironment of the Fibrosis+ LM was characterized by T cells with an exhausted phenotype, macrophages displaying a profibrotic and suppressive phenotype and fibrosis-promoting fibroblasts. Further investigation highlighted the pivotal role of VCAN_eCAF in remodeling the tumor fibrosis in the tumor microenvironment of Fibrosis+ LM, emphasizing potential targetable interactions such as FGF23 or FGF3-FGFR1. Validation through multiplex immunohistochemistry/immunofluorescence and spatial transcriptomics supported these findings. Here we present a comprehensive single-cell atlas of tumor fibrosis in LM, revealing the intricate multicellular environment and molecular features associated with it. These insights deepen our understanding of tumor fibrosis mechanisms and inform improved clinical diagnosis and treatment strategies. Show less
📄 PDF DOI: 10.1038/s12276-025-01573-3
FGFR1

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

Explainable machine learning model for classifying atherosclerotic cardiovascular disease in patients with metabolic dysfunction-associated steatotic liver disease.

Zhengliang Li, Xiaokai Chen, Linlin Ren +4 more · 2025 · Frontiers in endocrinology · Frontiers · added 2026-04-24
Cardiovascular disease (CVD) is the leading cause of mortality in patients with metabolic dysfunction-associated steatotic liver disease (MASLD), yet traditional risk predictors remain limited in clin Show more
Cardiovascular disease (CVD) is the leading cause of mortality in patients with metabolic dysfunction-associated steatotic liver disease (MASLD), yet traditional risk predictors remain limited in clinical practice. To develop machine learning (ML) models for classifying prevalent atherosclerotic cardiovascular disease (ASCVD) risk in MASLD patients, and to enhance model interpretability using SHapley Additive exPlanations (SHAP). Methods: This retrospective study included 590 MASLD patients diagnosed at the Affiliated Hospital of Qingdao University between December 2019 and December 2024. Patients were randomly divided into a training set (n=413) and a validation set (n=177), and further stratified based on ASCVD status. Least absolute shrinkage and selection operator (LASSO) regression was used for feature selection. Six ML models were developed and evaluated using sensitivity, specificity, accuracy, area under the receiver operating characteristic curve (AUC), and F1 score. SHAP analysis was performed to interpret feature contributions. ASCVD was present in 434 of 590 patients (73.6%). The Gradient Boosting (GB) model achieved the best performance, with AUCs of 0.918 (95% CI: 0.890-0.944) in the training set and 0.817 (95% CI: 0.739-0.883) in the validation set. SHAP analysis identified the top predictors as the Cholesterol-HDL-Glucose (CHG) index, Castelli Risk Index II (CRI-II), lipoprotein(a) [Lp(a)], serum creatinine (Scr), and uric acid (UA). The GB model demonstrated strong high accuracy in identifying existing ASCVD in MASLD patients and may serve as a useful tool for early risk stratification in clinical settings. Show less
📄 PDF DOI: 10.3389/fendo.2025.1684558
LPA

Integration of Fatty Acid-Targeted Metabolome and Transcriptomics Reveals the Mechanism of Chronic Environmental Microcystin-LR-Induced Hepatic Steatosis.

Sisi Yan, Ying Liu, Yin Zhang +8 more · 2025 · Journal of agricultural and food chemistry · ACS Publications · added 2026-04-24
Microcystin-LR (MC-LR) is a toxin that causes hepatic steatosis. Our previous study found that exposure to 60 μg/L MC-LR for 9 months resulted in liver lipid accumulation, but the underlying mechanism Show more
Microcystin-LR (MC-LR) is a toxin that causes hepatic steatosis. Our previous study found that exposure to 60 μg/L MC-LR for 9 months resulted in liver lipid accumulation, but the underlying mechanisms remain elusive. Herein, for the first time, fatty acid-targeted metabolome and RNA-seq were combined to probe the effect and mechanism of chronic (12-month) MC-LR treatment on mice lipid metabolism at environmental-related levels (1, 60, and 120 μg/L). It was found that MC-LR dose-dependently raised serum and liver lipid levels. The total cholesterol (TC) levels in the liver were significantly increased following treatment with 1 μg/L MC-LR (equivalent to 0.004 μ/L in human). Treatment with 60 and 120 μg/L MC-LR significantly elevated TC and triglyceride (TG) levels in both serum and liver. Serum fatty acid-targeted metabolome analysis demonstrated that exposure to 1, 60, and 120 μg/L MC-LR caused significant alterations in the fatty acid profile. Chronic 1, 60, and 120 μg/L MC-LR treatment significantly increased serum polyunsaturated fatty acids (PUFAs), including conjugated linoleic acid and eicosapentaenoic acid, which positively correlated with serum or liver TG levels. Chronic exposure to 120 μg/L MC-LR led to a significant decrease in the accumulation of saturated fatty acids, including citramalic acid, pentadecanoic acid, and docosanoic acid, which were negatively correlated with serum or liver lipid levels. These findings suggested that 1 μg/L MC-LR exposure caused mild lipid metabolism disruption, while 60 and 120 μg/L MC-LR treatment resulted in pronounced hepatic steatosis in mice. Transcriptome analysis revealed that chronic environmental MC-LR treatment regulated the expression of genes involved in the phosphatidylinositol 3-kinase (PI3K) complex and fatty acid metabolism. Western blotting and RT-qPCR confirmed that chronic environmental MC-LR exposure activated the PI3K/AKT/mTOR signaling pathway, the downstream of Show less
no PDF DOI: 10.1021/acs.jafc.4c07085
FADS3

Case Report: Combined PD-1 and tyrosine kinase blockade stabilizes refractory pancreatic cancer guided by the spatial structure of tumor immune microenvironment.

Heqi Yang, Yuhang Ma, Chenyan Zhang +4 more · 2025 · Frontiers in immunology · Frontiers · added 2026-04-24
Pancreatic cancer is characterized by a poor prognosis and limited responsiveness to conventional therapies, presenting a substantial therapeutic challenge. Although chemotherapy remains the cornersto Show more
Pancreatic cancer is characterized by a poor prognosis and limited responsiveness to conventional therapies, presenting a substantial therapeutic challenge. Although chemotherapy remains the cornerstone of systemic treatment, options become scarce once frontline therapies fail. While targeted therapies and immunotherapies have emerged as potential alternatives, their efficacy in pancreatic cancer is not well established. As research advances, exploring the tumor immune microenvironment (TiME) of pancreatic cancer is crucial and holds significant potential for developing novel treatment strategies.We report a case of a pancreatic cancer patient who, after the failure of frontline and second-line treatments, was treated with a pioneering combination of targeted therapy and immunotherapy to modulate the unique TiME. The targeted agent, surufatinib, is a tyrosine kinase inhibitor (TKI) that targets vascular endothelial growth factor receptor (VEGFR) 1-3, fibroblast growth factor receptor 1 (FGFR1), and colony-stimulating factor 1 receptor (CSF-1R). The immunotherapy agent, toripalimab, is an immune checkpoint inhibitor targeting programmed cell death protein 1 (PD-1). Remarkably, the patient benefitted from this regimen, exhibiting stable disease, improved clinical symptoms, and prolonged progression-free survival. This case highlights the potential of personalized therapy in treating pancreatic cancer, particularly in patients with distinctive features of the TiME that may predict favorable responses to immunotherapy. Personalized strategies that consider the spatial structure and composition of the TiME may offer a promising avenue for achieving long-term progression-free survival in patients with pancreatic cancer. Show less
📄 PDF DOI: 10.3389/fimmu.2025.1547388
FGFR1

Dexmedetomidine and dezocine targets (NR1H3 and ADRB1) are potential prognostic biomarkers for breast cancer.

Shaochun Zhang, Fang Yuan, Jing Ke · 2025 · Discover oncology · Springer · added 2026-04-24
Breast cancer (BRCA) is a prevalent malignant tumor among women, and the use of anesthetic drugs during surgical resection may influence tumor biology and patient prognosis. This study aimed to identi Show more
Breast cancer (BRCA) is a prevalent malignant tumor among women, and the use of anesthetic drugs during surgical resection may influence tumor biology and patient prognosis. This study aimed to identify prognostic biomarkers associated with dexmedetomidine and dezocine (DD) in BRCA patients. Through Mendelian Randomization analysis, we screened four DD targets that had a causal relationship with BRCA. Subsequently, utilizing TCGA-BRCA data, univariate and Lasso Cox analyses revealed two significant prognostic biomarkers (NR1H3 and ADRB1) associated with BRCA patient prognosis, leading to the successful construction and validation of a prognostic risk model. Kaplan-Meier survival curves indicated that patients with higher NR1H3 and ADRB1 expression had longer overall survival (OS). Immunoinfiltration analysis showed that high-risk group patients exhibited increased infiltration levels of CD56 bright natural killer cells, CD56 dim natural killer cells, eosinophils, and plasmacytoid dendritic cells. Conversely, activated B cells and immature B cells demonstrated greater infiltration in the low-risk group. Correlation analysis revealed significant associations between prognostic biomarkers and various immune cells, including CD56 bright natural killer cells, CD56 dim natural killer cells, and activated CD8 T cells. NR1H3 was highly positively correlated with immune checkpoints such as TIGIT, PDCD1, CD274, CTLA4, LAG3, and HAVCR2 (|cor|≥0.3, The online version contains supplementary material available at 10.1007/s12672-025-03694-7. Show less
no PDF DOI: 10.1007/s12672-025-03694-7
NR1H3

Multi-omics integrated analysis identifies causal risk factors and therapeutic targets for diabetic retinopathy.

Jing Xu, Shuntai Chen, Mei Sun +5 more · 2025 · Journal of translational medicine · BioMed Central · added 2026-04-24
Diabetic retinopathy (DR) is the main cause of blindness worldwide, and its prevalence rate is constantly rising. More in-depth exploration of its risk factors and pathogenic mechanisms is needed. Thi Show more
Diabetic retinopathy (DR) is the main cause of blindness worldwide, and its prevalence rate is constantly rising. More in-depth exploration of its risk factors and pathogenic mechanisms is needed. This study systematically identified potential therapeutic targets for DR by evaluating causal effects of 16,989 genes and 2,923 proteins on DR/subtypes via two-sample Mendelian randomization (MR), validated with colocalization/Summary-data-based Mendelian randomization (SMR). National Health and Nutrition Examination Survey (NHANES) 1999-2010 cross-sectional data (weighted logistic/Restricted cubic spline (RCS)) pinpointed key risk factors; MR explored their links to DR subtypes. Bioinformatics (bulk and single-cell transcriptomics) analyzed molecular mechanisms of shared targets (gene expression, immune infiltration, pathway enrichment). Machine learning selected key targets for models. Finally, two-step mediation MR examined how targets regulate DR via risk factors. This study identified 64 core targets with causal links to DR. Subtype analysis revealed 2,128 causal genes and subtype-specific targets (e.g. 52 for background DR, 66 for proliferative DR). SMR validated these findings. NHANES data highlighted body mass index (BMI), stroke, hypertension (HBP), and C-reactive protein (CRP) as key DR risk factors, confirmed by MR. Transcriptomics identified 29 differentially expressed genes associated with both risk factors and DR, linked to immune cell regulation. Machine learning selected core targets (LY9, WWP2, etc.) and built a nomogram for DR risk prediction. Functional enrichment showed these targets enriched in chemokine/cytokine and immune-inflammatory pathways. Two-step mediation MR further revealed LY9, ARHGAP1, and WWP2 influence DR subtypes via regulating BMI, CRP, and HBP. This study systematically elucidates the key risk factors, potential molecular mechanisms, and core regulatory targets of DR through multi-omics integration, causal inference, and bioinformatics approaches. The results indicate that inflammation, immune dysregulation, and metabolic disorders play crucial roles in the pathogenesis of DR. Key genes such as LY9, ARHGAP1, and WWP2 could serve as potential intervention targets, offering theoretical foundations and strategic support for early warning and precision treatment of DR. Show less
no PDF DOI: 10.1186/s12967-025-07353-x
WWP2

Sex hormones, blood metabolites and proteins mediating the causal associations between gut microbiota and prostatic diseases: evidences from Mendelian randomization study.

Tianrui Liu, Feixiang Yang, Zhige Wang +7 more · 2025 · Prostate international · Elsevier · added 2026-04-24
The causal relationships between the gut microbiota and prostate cancer, prostatitis, and benign prostatic hyperplasia remain uncertain. We intend to identify the causal connections between the gut mi Show more
The causal relationships between the gut microbiota and prostate cancer, prostatitis, and benign prostatic hyperplasia remain uncertain. We intend to identify the causal connections between the gut microbiota and prostatic diseases and investigate the potential mechanisms involved. A two-sample Mendelian randomization (MR) analysis was conducted to elucidate the impact of 196 gut microbiota on prostatic diseases risk. Reverse MR, linkage disequilibrium regression score (LDSC), and colocalization analyses were performed to strengthen causal evidence. Phenome-wide MR (Phe-MR) analysis was used to evaluate the potential side effects of targeting the detected gut microbiota. We designed a two-step MR study to assess the mediating effects of sex hormones, blood metabolites, and proteins. According to the MR analyses, 31 bacterial taxa were causally associated with prostatic diseases, of which 23 types were newly identified. In addition, Our study represents the first comprehensive exploration of the causal effects of the gut microbiota on prostatic diseases and reveals the mediating effects of sex hormones and blood metabolites on the "gut-prostate axis." Show less
📄 PDF DOI: 10.1016/j.prnil.2024.11.004
FGFR1

Whole-Genome Resequencing Provides Novel Insights Into the Genetic Diversity, Population Structure, and Patterns of Runs of Homozygosity in Mud Crab (

Xiyi Zhou, Min Ouyang, Yin Zhang +3 more · 2025 · Evolutionary applications · Blackwell Publishing · added 2026-04-24
Mud crab (
no PDF DOI: 10.1111/eva.70153
UNC79

Naringin Mitigates PEDV-Induced Intestinal Damage in Suckling Piglets by Modulating Inflammatory, Antiviral, and Metabolic and Transport Pathways.

Yanyan Zhang, Muzi Li, Zongyun Li +6 more · 2025 · Biomolecules · MDPI · added 2026-04-24
This study evaluated the protective effects of naringin (NG) against intestinal injury in 7-day-old piglets infected with porcine epidemic diarrhea virus (PEDV). Eighteen piglets (Duroc × Landrace × L Show more
This study evaluated the protective effects of naringin (NG) against intestinal injury in 7-day-old piglets infected with porcine epidemic diarrhea virus (PEDV). Eighteen piglets (Duroc × Landrace × Large, body weight = 2.58 ± 0.05 kg) were divided into three treatment groups based on similar body weights and equal numbers of males and females: the blank control group (CON group), the PEDV infection group (PEDV group), and the NG intervention + PEDV infection group (NG + PEDV group) ( Show less
📄 PDF DOI: 10.3390/biom16010048
APOA4

Multifunctional natural chlorogenic acid based nanocarrier for Alzheimer's disease treatment.

Chenchen Wang, Xiaolei Song, Xiaowan Zhang +4 more · 2025 · Materials today. Bio · Elsevier · added 2026-04-24
Alzheimer's disease (AD) presents significant challenges due to its intricate pathogenic mechanisms and the limited efficacy of single-target therapies. In this study, we investigated the potential of Show more
Alzheimer's disease (AD) presents significant challenges due to its intricate pathogenic mechanisms and the limited efficacy of single-target therapies. In this study, we investigated the potential of chlorogenic acid (CHA), a multifunctional natural active compound, in AD therapy by developing a trifunctional nanocarrier (MC-H/R/si). CHA was effectively conjugated with iron-based metal-organic frameworks (MIL/Fe-100) through chelation interaction. The resulting nanocomplex (MC) not only enhances the bioavailability of CHA but also facilitates a synergistic antioxidant effect between CHA and MIL/Fe-100. Importantly, CHA can chelate Zn Show less
📄 PDF DOI: 10.1016/j.mtbio.2025.101841
BACE1

Unraveling the causal links and mediation effects of lipid metabolites and inflammatory factors on gallstone disease risk.

Xuan Bai, Dingzi Zhou, Jing Luo +14 more · 2025 · Medicine · added 2026-04-24
Lipid metabolism abnormalities and inflammation have been implicated in gallstone disease (GSD) development, but the causal relationships and potential mediation effects among lipid metabolites, infla Show more
Lipid metabolism abnormalities and inflammation have been implicated in gallstone disease (GSD) development, but the causal relationships and potential mediation effects among lipid metabolites, inflammatory factors, and GSD remain unclear. The aim of this study is to explore the causal relationships among these 3 factors. This study employed 2-sample Mendelian Randomization (TSMR) and 2-step MR to investigate the causal relationships and potential mediation effects among 91 inflammatory factors, 6 lipid metabolism-related molecules (HDL-C, LDL-C, TG, total cholesterol, ApoA1, and ApoB), and GSD. We opted for 4 distinct MR analysis methods including inverse variance weighted method, weighted median method, MR-Egger regression method and MR-PRESSO analysis. Sensitivity analyses included MR-Egger intercept tests, Cochran's Q statistic, Steiger tests, and leave-one-out analyses. Product of coefficients method was used to estimate mediation proportion. TSMR analysis revealed that every 1-unit increase in low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), apolipoprotein A1 (ApoA1), and apolipoprotein B (ApoB), the risk of GSD decreased by 16.5%, 10.2%, 8.4%, and 13.1%, respectively. Inflammatory factors such as Natural killer cell receptor 2B4 (CD244), Macrophage colony-stimulating factor 1 (CSF-1), and interleukin-18 receptor 1 (IL-18R1) were identified as risk factors for GSD, while Fibroblast growth factor 19 levels (FGF19), Interleukin-1-alpha levels (IL-1α), and Interleukin-8 levels (IL-8) were found to be protective. Mediation analysis through 2-step MR identified potential pathways involving ApoA1--IL-8--GSD (P = .084) and IL-1α--ApoB--GSD (P = .117). This study provides robust evidence of causal links between specific lipid metabolites and GSD, as well as suggestive causal associations for several inflammatory factors. However, mediation analysis did not support significant roles for lipids or inflammatory factors as mediators in GSD pathogenesis. Future research could be further pursued in areas such as drug target intervention and mechanistic studies. Show less
no PDF DOI: 10.1097/MD.0000000000044704
APOB

Development and validation of a hypoxia-immune-based microenvironment gene signature for predicting survival in non-small cell lung cancer.

Xiangwu Zhang, Rongxian Zhou, Guangqiang Zhao +5 more · 2025 · Discover oncology · Springer · added 2026-04-24
This study aims to establish a hypoxia-immune-related gene signature within the tumor microenvironment (TME) to reliably predict prognosis in non-small cell lung cancer (NSCLC). Transcriptomic profile Show more
This study aims to establish a hypoxia-immune-related gene signature within the tumor microenvironment (TME) to reliably predict prognosis in non-small cell lung cancer (NSCLC). Transcriptomic profiles and clinical data of lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases (GSE74777, GSE68465). Hypoxia- and immune-related genes were curated from MSigDB, ImmPort, and INATDB. Prognostic genes were identified via Cox and LASSO regression analyses, and a risk model was constructed. Model validity was assessed through Kaplan-Meier survival analysis, receiver operating characteristic (ROC) curves, and external validation. An eight-gene prognostic signature (AKAP12, MT2A, SERPINE1, CD1E, CD79A, CXCL13, XCL2, ANGPTL4) was established. The model demonstrated significant predictive accuracy for NSCLC survival (AUC: 0.643/0.649/0.620 at 1/3/5 years in TCGA cohort). Patients with high immune activity exhibited superior survival outcomes compared to those with low-immune counterparts (log-rank P < 0.001). Multivariate Cox regression confirmed the risk score as an independent prognostic factor (HR = 1.82, 95% CI: 1.44-2.30, P < 0.001). The hypoxia-immune microenvironment signature serves as a robust prognostic classifier for NSCLC, providing a quantitative framework for personalized risk stratification and clinical decision support. Show less
📄 PDF DOI: 10.1007/s12672-025-03319-z
ANGPTL4

Serum-derived exosome proteomics unveils the distinct and adjustable nature of the dampness constitution in traditional Chinese medicine.

Wenhui Wu, Chengcheng Wang, Tao Zhang +12 more · 2025 · Journal of ethnopharmacology · Elsevier · added 2026-04-24
In Traditional Chinese Medicine (TCM), dampness is a pathogenic factor arising from impaired production and transportation of bodily fluids. While Fuling Zexie decoction (FLZXD) has demonstrated thera Show more
In Traditional Chinese Medicine (TCM), dampness is a pathogenic factor arising from impaired production and transportation of bodily fluids. While Fuling Zexie decoction (FLZXD) has demonstrated therapeutic efficacy in dampness constitution (DC) treatment, the material basis underlying its constitutional modulatory effects remains unclear. This study proposes objective indicators for the differentiation and therapeutic evaluation of DC and elucidates the material basis of FLZXD in DC treatment. Serum exosome proteomic profiling was conducted across two independent cohorts to identify DC-related indicators and assess the therapeutic efficacy of FLZXD in DC-associated hyperlipidemia (DC-hyperlipidemia). The bioactive compounds of FLZXD were prioritized through a comprehensive analysis of patent documentation and network pharmacology, with subsequent validation of DC-related targets using enzyme-linked immunosorbent assay (ELISA). Proteomic analysis of serum exosomes revealed signatures that differentiate individuals with a balanced constitution (BC) from those with DC. The differentially expressed proteins (DEPs) were enriched predominantly in pathways related to the complement cascade and cardiovascular diseases. FLZXD demonstrated therapeutic efficacy against DC-hyperlipidemia, as evidenced by the reversal of DEPs expression following treatment, which was supported by the patentable findings and network pharmacology analysis. Through experimental validation and pharmacological evidence, the active herbs of FLZXD (Fuling, Zexie and Baizhu, collectively referred to as FZB) were identified, and a total of 73 putative therapeutic targets involved in the dampness-resolving effects of FZB were revealed. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment further confirmed that FLZXD exerts its anti-dampness effects primarily through regulation of the complement and coagulation cascades. Among eight candidate indicators specifically associated with DC, four proteins were validated via ELISA, indicating potential utility for the differentiation of DC. The sensitivity (%), specificity (%), fold change (FC), p-value, and area under the curve (AUC) for each indicator were as follows: apolipoprotein B-100 (APOB) (100.00, 80.00, 0.63, 0.0051, 0.94), complement factor H-related protein 1 (CFHR1) (90.00, 100.00, 0.55, 0.0001, 0.98), alpha-1-acid glycoprotein 1 (ORM1) (100.00, 80.00, 0.71, 0.0043, 0.92), and pigment epithelium-derived factor (SERPINF1) (90.00, 70.00, 0.66, 0.0002, 0.87). The integrative approach, combining proteomic profiling, network pharmacology analysis, and clinical validation, establishes an integrative approach for research on TCM constitutions. This approach provides (1) molecular insights into the differentiation of DC, (2) a foundation for mechanism-based, targeted therapeutic strategies, and (3) enhanced patient stratification to support personalized treatment approaches. Show less
no PDF DOI: 10.1016/j.jep.2025.120353
APOB

The expression and clinical significance of IL-27 and Foxp3 in oral squamous cell carcinoma.

Mengna Wu, Jiajun Fang, Tonghan Zhang · 2025 · BMC cancer · BioMed Central · added 2026-04-24
This study aimed to investigate the expression and clinical significance of interleukin-27 (IL-27) and forkhead box P3 (Foxp3) in oral squamous cell carcinoma (OSCC) tissues, analyze their co-expressi Show more
This study aimed to investigate the expression and clinical significance of interleukin-27 (IL-27) and forkhead box P3 (Foxp3) in oral squamous cell carcinoma (OSCC) tissues, analyze their co-expression correlations, and explore their potential as prognostic biomarkers and therapeutic targets for OSCC. Immunohistochemistry (IHC) was used to detect the expression of the two subunits of IL-27, IL-27p28 and Epstein-Barr virus-induced gene 3 (EBI3), and Foxp3 in OSCC tissues and normal tissues. Chi-square test was used to analyze the correlation between the expression of the three in OSCC tissues and the clinical pathological parameters of patients. The IHC results showed that the expressions of IL-27p28, EBI3 and Foxp3 proteins in OSCC tissues were all higher than those in normal control tissues( The expression levels of IL-27p28, EBI3 and Foxp3 in OSCC tissues are significantly upregulated, indicating that the three play important roles in the occurrence and development of OSCC tumors. Furthermore, its high expression is associated with various clinicopathological characteristics of OSCC patients and can be used as a potential indicator for evaluating the prognosis of OSCC patients. Show less
📄 PDF DOI: 10.1186/s12885-025-14597-9
IL27

A new perspective on cognitive impairment in major depressive disorder: Changes in gut microbiota and their inflammatory regulatory mechanisms.

Xiaodong Song, Qilin Zhong, Rongxu Zhang +10 more · 2025 · Journal of affective disorders · Elsevier · added 2026-04-24
Cognitive impairments in major depressive disorder (MDD) affect patients' social functioning, with underlying mechanisms involving gut microbiota and inflammatory factors remaining unclear. The study Show more
Cognitive impairments in major depressive disorder (MDD) affect patients' social functioning, with underlying mechanisms involving gut microbiota and inflammatory factors remaining unclear. The study analyzed cognitive function, gut microbiota changes, and inflammatory factor levels in 39 unmedicated MDD patients and 41 healthy controls, employing correlation and moderation effect analysis. MDD patients scored lower than controls in cognitive functions like information processing speed, attention/vigilance, verbal learning, visual learning and social cognition. They showed reduced gut microbiota diversity and increased levels of inflammatory markers (TNF-α, IL-1, IL-6, IL-17, IL-27, IL-33). Sellimonas abundance correlated negatively with attention/vigilance, moderated by TNF-α, IL-27, and IL-33. This relationship was stronger at lower inflammation levels. MDD patients exhibit multi-domain cognitive dysfunction alongside pro-inflammatory states and disrupted gut microbiota. The abundance of Sellimonas significantly predicts attention/vigilance deficits. Inflammatory factors modulate the impact of gut microbiota on cognitive function, suggesting chronic low-grade inflammation as a key risk factor for cognitive impairment in MDD. Show less
no PDF DOI: 10.1016/j.jad.2025.119648
IL27

Novel genes involved in vascular dysfunction of the middle temporal gyrus in Alzheimer's disease: transcriptomics combined with machine learning analysis.

Meiling Wang, Aojie He, Yubing Kang +5 more · 2025 · Neural regeneration research · added 2026-04-24
JOURNAL/nrgr/04.03/01300535-202512000-00030/figure1/v/2025-01-31T122243Z/r/image-tiff Studies have shown that vascular dysfunction is closely related to the pathogenesis of Alzheimer's disease. The mi Show more
JOURNAL/nrgr/04.03/01300535-202512000-00030/figure1/v/2025-01-31T122243Z/r/image-tiff Studies have shown that vascular dysfunction is closely related to the pathogenesis of Alzheimer's disease. The middle temporal gyrus region of the brain is susceptible to pronounced impairment in Alzheimer's disease. Identification of the molecules involved in vascular aberrance of the middle temporal gyrus would support elucidation of the mechanisms underlying Alzheimer's disease and discovery of novel targets for intervention. We carried out single-cell transcriptomic analysis of the middle temporal gyrus in the brains of patients with Alzheimer's disease and healthy controls, revealing obvious changes in vascular function. CellChat analysis of intercellular communication in the middle temporal gyrus showed that the number of cell interactions in this region was decreased in Alzheimer's disease patients, with altered intercellular communication of endothelial cells and pericytes being the most prominent. Differentially expressed genes were also identified. Using the CellChat results, AUCell evaluation of the pathway activity of specific cells showed that the obvious changes in vascular function in the middle temporal gyrus in Alzheimer's disease were directly related to changes in the vascular endothelial growth factor (VEGF)A-VEGF receptor (VEGFR) 2 pathway. AUCell analysis identified subtypes of endothelial cells and pericytes directly related to VEGFA-VEGFR2 pathway activity. Two subtypes of middle temporal gyrus cells showed significant alteration in AD: endothelial cells with high expression of Erb-B2 receptor tyrosine kinase 4 (ERBB4 high ) and pericytes with high expression of angiopoietin-like 4 (ANGPTL4 high ). Finally, combining bulk RNA sequencing data and two machine learning algorithms (least absolute shrinkage and selection operator and random forest), four characteristic Alzheimer's disease feature genes were identified: somatostatin ( SST ), protein tyrosine phosphatase non-receptor type 3 ( PTPN3 ), glutinase ( GL3 ), and tropomyosin 3 ( PTM3 ). These genes were downregulated in the middle temporal gyrus of patients with Alzheimer's disease and may be used to target the VEGF pathway. Alzheimer's disease mouse models demonstrated consistent altered expression of these genes in the middle temporal gyrus. In conclusion, this study detected changes in intercellular communication between endothelial cells and pericytes in the middle temporal gyrus and identified four novel feature genes related to middle temporal gyrus and vascular functioning in patients with Alzheimer's disease. These findings contribute to a deeper understanding of the molecular mechanisms underlying Alzheimer's disease and present novel treatment targets. Show less
📄 PDF DOI: 10.4103/NRR.NRR-D-23-02004
ANGPTL4

Chronic sleep deprivation induces depression- and Alzheimer's disease-like changes in adult and ageing wild-type and Fat-1 transgenic mice.

Nasar Ullah Khan Niazi, Zhiyou Yang, Yongping Zhang +1 more · 2025 · Prostaglandins, leukotrienes, and essential fatty acids · Elsevier · added 2026-04-24
Sleep disorders show comorbidity with depression and Alzheimer's disease (AD), especially in ageing. However, the neuroimmunological role of sleep deprivation (SD) as possible inducer to these conditi Show more
Sleep disorders show comorbidity with depression and Alzheimer's disease (AD), especially in ageing. However, the neuroimmunological role of sleep deprivation (SD) as possible inducer to these conditions remains unknown. Omega-3 fatty acids (n-3 FAs) can improve depression and AD through anti-inflammation, up-regulating neurotrophins and normalizing neurotransmitters, while their therapeutic effects on sleep deprivation (SD)-induced changes in different ages requires investigation. Adult and old Fat-1 (converting n-6 to n-3 FAs) and wild-type (WT) mice were subjected to chronic SD. After behavioral evaluation, brain FAs, monoamine neurotransmitters, circadian-gene expression, TLR-4 signaling-pathway, glial polarization, cytokine profile, and AD-related markers were analyzed using GC-MS, HPLC, qPCR, ELISA and western-blotting. Furthermore, bioinformatic analysis evaluated SD-related networking with depression and AD. SD induced anxiety, anhedonia, despair, and memory impairments. The n-3:n-6 ratio, BMAL-1 gene expression, and melatonin concentration were decreased, whereas corticosterone, TLR-4, GSK3β, and NFκB concentrations increased in SD groups compared to the controls. Increased IBA-1 protein expression and proinflammatory IL-1β, TNF-α, and IL-6 concentrations were associated with decreased monoamine neuro-transmitter levels in SD groups. APP, BACE-1, RAGE and APPβ concentrations were increased, whereas LRP-1 and APPα concentrations and the APPα/APPβ ratio were decreased in SD groups than controls. These changes were more pronounced in old WT and Fat-1 animals than adults. However, compared to WT-SD, these changes were significantly ameliorated in Fat-1-SD mice, but recovery was less pronounced in old Fat-1. SD-induced neuroinflammation and impaired APP processing may contribute to behavioral impairments, which exacerbated with age. Although n-3 FAs significantly ameliorated SD-induced adverse behavioral and neuroimmunological changes, this therapeutic effect was markedly reduced in old animals. Show less
no PDF DOI: 10.1016/j.plefa.2025.102699
BACE1

Knockdown of PLK1 suppresses malignant phenotypes and tumor growth in bladder cancer via activating Hippo pathway.

Yue Yang, Yunhan Wang, Zhou Zheng +2 more · 2025 · General physiology and biophysics · added 2026-04-24
Bladder cancer (BLCA) is a prevalent urological malignancy. We aim to identify novel biomarkers for BLCA and elucidate the specific regulatory mechanisms of polo-like kinase 1 (PLK1). Using differenti Show more
Bladder cancer (BLCA) is a prevalent urological malignancy. We aim to identify novel biomarkers for BLCA and elucidate the specific regulatory mechanisms of polo-like kinase 1 (PLK1). Using differentially expressed genes (DEGs) screened from GSE38264 and GSE130598 datasets, we constructed protein-protein interaction networks to identify hub genes, whose expression was validated using reverse transcription-quantitative polymerase chain reaction. The malignant phenotype of BLCA cells was assessed by Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine, Transwell, and wound-healing assays. Hematoxylin-eosin and immunohistochemical staining were employed to evaluate BLCA development in mouse xenograft models. The protein expression was detected by Western blot. PLK1, AURKA, AURKB, CDK1, ERBB2, ERBB3, FGFR1, FYN, ABL1, and PRKDC were hub genes with predictive value for BLCA. Among them, PLK1 was selected as a key target of BLCA. PLK1 knockdown inhibited the viability, proliferation, migration, and invasion of BLCA cells. In vivo, PLK1 knockdown inhibited tumor growth. Silencing PLK1 activated the Hippo pathway in BLCA cells and tumor tissues. The Hippo pathway inhibitor reversed the inhibitory effects of PLK1 silencing on malignant phenotype of BLCA cells. PLK1 knockdown exerts an inhibitory effect on BLCA via activating the Hippo pathway, which presents promising therapeutic strategies for BLCA. Show less
no PDF DOI: 10.4149/gpb_2025015
FGFR1

A novel splicing variant of CNTRL::FGFR1 in myeloid/lymphoid neoplasm with eosinophilia and rearrangement of FGFR1.

Xianqi Feng, Xueting Bai, Hong Zhang +7 more · 2025 · Journal of hematopathology · Springer · added 2026-04-24
Background Myeloid/lymphoid neoplasm with eosinophilia and rearrangement of FGFR1(MLN-FGFR1), also referred to as 8p11 myeloproliferative syndrome (EMS), arises from aberrant FGFR1 gene rearrangement Show more
Background Myeloid/lymphoid neoplasm with eosinophilia and rearrangement of FGFR1(MLN-FGFR1), also referred to as 8p11 myeloproliferative syndrome (EMS), arises from aberrant FGFR1 gene rearrangement in bone marrow hematopoietic stem cells, resulting in the transformation of myeloid/lymphoid cells into neoplastic growths. The clinical and laboratory features of affected individuals are influenced by the specific partner genes. Purpose This article aims to report a case of MLN-FGFR1 involving a novel CNTRL::FGFR1 splicing variant and to discuss its clinicopathological characteristics and treatment challenges. Methods/Results We report a case of MLN-FGFR1 in a 35-year-old male patient presenting with leukocytosis, lymphadenopathy, hepatosplenomegaly, and a mixed population of B lymphoblasts, T lymphoblasts, and monoblasts in the bone marrow and lymph nodes. Comprehensive molecular profiling, including chromosomal karyotyping, fluorescence in situ hybridization (FISH), targeted transcriptome sequencing, reverse transcription polymerase chain reaction (RT-PCR), and Sanger sequencing, identified a novel splicing variant of the CNTRL::FGFR1 fusion, resulting from a t(8;9)(p11;q33) translocation. This novel splicing variant involves an in-frame fusion between exon 38 of CNTRL and exon 11 of FGFR1, retaining the kinase domain of FGFR1 and leading to its constitutive activation. Despite multiple treatment regimens, the patient failed to achieve complete remission (CR). Conclusion The findings highlight the urgent need for targeted therapies, such as FGFR inhibitors, to improve outcomes in patients with FGFR1-rearranged malignancies. Show less
📄 PDF DOI: 10.1007/s12308-025-00670-6
FGFR1

Screening and experimental validation of modified Gandou Decoction-targeted inhibitors for alleviating AD components via network pharmacology, machine learning, and molecular dynamics simulation.

Shixin Ye, Shun Zhang, Liangdong Zhang +4 more · 2025 · Frontiers in pharmacology · Frontiers · added 2026-04-24
Alzheimer's disease (AD) is a neurodegenerative disease characterized by abnormal accumulation of β-amyloid (Aβ) and hyperphosphorylation of the Tau protein. Currently, there is a lack of effective an Show more
Alzheimer's disease (AD) is a neurodegenerative disease characterized by abnormal accumulation of β-amyloid (Aβ) and hyperphosphorylation of the Tau protein. Currently, there is a lack of effective and safe therapeutic approaches. In Traditional Chinese medicine (TCM), Gandou Decoction has shown significant efficacy in improving cognitive decline and dementia-related symptoms, but its specific mechanism remains unclear. This study systematically analyzed the active components and anti-AD mechanism of Modified Gandou Decoction (MGD) by integrating network pharmacology, machine learning, molecular docking, molecular dynamics (MD) simulation, and A total of 21 potential active molecules of MGD and 68 intersection targets were screened out. Among them, 8 core targets (EIF2AK2, PPARG, BACE1, ESR1, GSK3B, ACE, CASP3, MAPK14) were confirmed to be significantly associated with AD pathology by gene expression difference analysis (P ≤ 0.05). KEGG enrichment analysis showed that MGD mainly intervenes in the amyloid production pathway, the MAPK pathway, and the IL-17 pathway. Molecular docking demonstrated that the majority of the 21 potential active compounds exhibited strong binding affinities to the 8 core targets. Moreover, some potential active molecules exhibited better binding energy and similar binding modes compared with known inhibitors when binding to the corresponding target proteins. Molecular dynamics simulation showed that Alisol B, a potential active component of MGD, could stably bind to BACE1, EIF2AK2, and CASP3. MGD exerts its anti-AD effect through its potential active component Alisol B, which binds to target proteins BACE1, EIF2AK2, and CASP3, and synergistically inhibits Aβ production, Tau phosphorylation, and neuroinflammatory processes through multiple pathways. This study provides a foundation for developing MGD-derived natural products for AD treatment, although the precise mechanisms require further experimental validation. Show less
📄 PDF DOI: 10.3389/fphar.2025.1685866
BACE1

Endothelial adenosine receptor 2A loss alleviates diabetic vascular calcification by blocking CREB1-SNAI1-driven EndMT.

Yaqi Zhou, Dingwei Zhao, Qian Ma +11 more · 2025 · Pharmacological research · Elsevier · added 2026-04-24
Vascular calcification (VC), a common complication associated with diabetes mellitus (DM), substantially increases the risk of cardiovascular diseases and is associated with elevated mortality in indi Show more
Vascular calcification (VC), a common complication associated with diabetes mellitus (DM), substantially increases the risk of cardiovascular diseases and is associated with elevated mortality in individuals with DM. Endothelial-to-mesenchymal transition (EndMT) imparts phenotypic plasticity to vascular endothelial cells (VECs), granting them the potential for osteogenic differentiation, which is a crucial mechanism in regulating VC. Notably, adenosine-ADORA2A-mediated endothelial dysfunction plays a pivotal regulatory role in cardiovascular diseases. However, the specific role of endothelial ADORA2A in diabetic VC remains to be elucidated. In this study, we found that ADORA2A was upregulated in the endothelium of diabetic mice and cultured human aortic endothelial cells (HAECs) with high glucose treatment. Deletion of endothelial Adora2a or pharmacologic inhibition of ADORA2A with KW6002 attenuated EndMT, osteogenic differentiation, and calcium deposit in diabetic aortas of Ins2 Show less
no PDF DOI: 10.1016/j.phrs.2025.107981
SNAI1

Unveiling the genetic overlap and causal links between gastroesophageal reflux disease and asthma.

Yajie Zhang, Yang Li, Wentao Huang +7 more · 2025 · International journal of surgery (London, England) · added 2026-04-24
Gastroesophageal reflux disease (GERD) and asthma are commonly co-occurring conditions, with shared genetic factors identified. However, the specific loci and the influence of common genetic architect Show more
Gastroesophageal reflux disease (GERD) and asthma are commonly co-occurring conditions, with shared genetic factors identified. However, the specific loci and the influence of common genetic architecture remain undefined. We obtained genome-wide association study (GWAS) summary statistics for GERD (71 522 cases and 261 079 controls) and asthma (56 167 cases and 352 255 controls). Using linkage disequilibrium score regression (LDSC), we assessed genetic correlations between GERD and asthma. Bidirectional Mendelian randomization (MR) was performed to investigate potential causal relationships, followed by cross-trait GWAS meta-analysis and colocalization analysis to identify shared risk loci. Additionally, summary-data-based MR and transcriptome-wide association study were conducted to pinpoint common functional genes. Finally, we analyzed gene expression profiles in both healthy individuals and GERD patients using esophageal single-cell RNA sequencing (scRNA-seq) data. We identified a significant genetic correlation between GERD and asthma ( rg  = 0.37, P = 6.19 × 10 -38 ) and a significant causal effect of GERD on asthma [odds ratio (OR) = 1.22, P = 1.54 × 10 -5 ]. Cross-trait meta-analyses revealed 56 shared risk loci between GERD and asthma, including 51 loci that were newly identified. Three loci (rs61937247, rs7960225, and rs769670) exhibited evidence of colocalization. Gene-level analyses pinpointed three novel shared genes ( RBM6, SUOX , and MPHOSPH9 ) between GERD and asthma. scRNA-seq analysis uncovered heightened expression of these genes in immune cells of patients diagnosed with GERD. Our study has discovered novel shared genetic loci and candidate genes between GERD and asthma, providing further insights into the genetic susceptibility of comorbidity and potential mechanisms of the two diseases. Show less
no PDF DOI: 10.1097/JS9.0000000000003283
RBM6

Targeting polyunsaturated fatty acids desaturase FADS1 inhibits renal cancer growth via ATF3-mediated ER stress response.

Gioia Heravi, Zhenjie Liu, Mackenzie Herroon +11 more · 2025 · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · Elsevier · added 2026-04-24
Fatty Acid Desaturase 1 (FADS1) is a rate-limiting enzyme controlling the bioproduction of long-chain polyunsaturated fatty acids (PUFAs). Increasing studies suggest that FADS1 is a potential cancer t Show more
Fatty Acid Desaturase 1 (FADS1) is a rate-limiting enzyme controlling the bioproduction of long-chain polyunsaturated fatty acids (PUFAs). Increasing studies suggest that FADS1 is a potential cancer target. Our previous research has demonstrated the significant role of FADS1 in cancer biology and patient survival, especially in kidney cancers. We aim to explore the underlying mechanism in this study. We found that pharmacological inhibition or knockdown of the expression of FADS1 significantly reduced the intracellular conversion of long-chain PUFAs, effectively inhibits renal cancer cell proliferation, and induces cell cycle arrest. The stable knockdown of FADS1 also significantly inhibits tumor formation in vivo. Mechanistically, we showed that while FADS1 inhibition induces endoplasmic reticulum (ER) stress, FADS1 expression is augmented by ER-stress inducer, suggesting a necessary role of PUFA production in response to ER stress. FADS1-inhibition sensitized cellular response to ER stress inducers, leading to cell apoptosis. Also, FADS1 inhibition-induced ER stress leads to activation of the PERK/eIF2α/ATF4/ATF3 pathway. Inhibiting PERK or knockdown of ATF3 rescued FADS1 inhibition-induced ER stress and cell growth suppression, while ATF3-overexpression aggravates the FADS1 inhibition-induced cell growth suppression and leads to cell death. Metabolomic analysis revealed that FADS1 inhibition results in decreased level of UPD-N-Acetylglucosamine, a critical mediator of the unfolded protein response, as well as impaired biosynthesis of nucleotides, possibly accounting for the cell cycle arrest. Our findings suggest that PUFA desaturation is crucial for rescuing cancer cells from persistent ER stress, supporting FADS1 as a new therapeutic target. Show less
📄 PDF DOI: 10.1016/j.biopha.2025.118006
FADS1

SULF1's Role in Endothelial Senescence and Atherosclerosis: Insights from Single-Cell and Bulk Transcriptomics.

Meng-Ting Jiang, Shi-Lei Wan, Xiang-Yu Shen +4 more · 2025 · Journal of inflammation research · added 2026-04-24
Endothelial cells (ECs) senescence has emerged as a critical factor in the pathogenesis of atherosclerosis, contributing to vascular aging and plaque formation. However, the molecular mechanisms under Show more
Endothelial cells (ECs) senescence has emerged as a critical factor in the pathogenesis of atherosclerosis, contributing to vascular aging and plaque formation. However, the molecular mechanisms underlying endothelial senescence in atherosclerosis remain poorly understood. Single-cell RNA sequencing (scRNA-seq) data from atherosclerotic core plaques and adjacent normal tissues were analyzed using the Seurat package to identify cell subpopulations and senescence markers. RNA-seq data from early and late atherosclerotic plaques were used for differential gene expression analysis. Subsequently, the candidate gene was identified and validated in the atherosclerotic plaques of Single-cell analysis revealed elevated levels of senescence markers in ECs within atherosclerotic plaques. Combined with bulk RNA-seq analysis, This study highlights the critical role of endothelial senescence in atherosclerosis and identifies Show less
📄 PDF DOI: 10.2147/JIR.S544852
APOE

Identification of potential anti aging drugs and targets in chronic kidney disease.

Qian ZHANG, Bing Bai, Lidan Ran +1 more · 2025 · Scientific reports · Nature · added 2026-04-24
Chronic kidney disease (CKD) is highly prevalent, incurable, and lacks effective treatments. Aging is closely linked to various kidney diseases. In this study, we combined CKD and aging using bioinfor Show more
Chronic kidney disease (CKD) is highly prevalent, incurable, and lacks effective treatments. Aging is closely linked to various kidney diseases. In this study, we combined CKD and aging using bioinformatics approaches to identify potential anti aging drugs and therapeutic targets for CKD. We analyzed datasets GSE37171 and GSE66494 from the GEO database, identifying 317 differentially expressed genes (DEGs). By intersecting these DEGs with aging related genes, we identified 23 aging associated differential genes (ARDEGs). A protein-protein interaction (PPI) network was constructed using the STRING database, and the top 10 hub ARDEGs were identified using Cytoscape software. Potential anti aging drugs, including Cinnamaldehyde, were identified through the ceRNA and transcription factor regulatory networks, as well as the DGldb database. Among the key regulatory genes identified in CKD patient samples were SOD2, FGF21, FOS, RELA, DDIT4, BMI1, DUSP6, LGALS3, CXCR2, and CEBPB. Cinnamaldehyde and other drugs were found to target aging associated pathways, suggesting their potential to delay CKD progression through modulating these pathways. Finally, we verified the low-expression of DDIT4 and DUSP6, the two targets of Cinnamaldehyde, in unilateral ureteral obstruction (UUO) animal model. Additionally, Cinnamaldehyde was shown to reduce the expression of fibrosis markers such as fibronectin (FN) and α-smooth muscle actin (α-SMA) in HK2 cells under TGF-β1 stimulation. This study provides a foundational understanding of aging related molecular targets in CKD and offers new directions for developing anti aging therapies to treat CKD. Show less
📄 PDF DOI: 10.1038/s41598-025-96985-6
DUSP6

Association between the ApoB/ApoA1 ratio and both the severity and mortality of metabolic dysfunction-associated fatty liver disease.

Chao Fu, Yan Gong, Xiangyang Gao +8 more · 2025 · BMC gastroenterology · BioMed Central · added 2026-04-24
📄 PDF DOI: 10.1186/s12876-025-04130-4
APOB

Dual-specificity phosphatases: Potential targets for cognitive impairment induced by chronic kidney disease.

Lishang Liao, Qiongdan Hu, Yong Zhang +5 more · 2025 · International immunopharmacology · Elsevier · added 2026-04-24
The aim of this review is to systematically explore the critical role of dual-specific phosphatases (DUSPs) in CKD-associated cognitive impairment and their therapeutic potential. Chronic kidney disea Show more
The aim of this review is to systematically explore the critical role of dual-specific phosphatases (DUSPs) in CKD-associated cognitive impairment and their therapeutic potential. Chronic kidney disease (CKD) is a global health burden, and the cognitive impairment it induces seriously affects patients' quality of life. Studies have shown that DUSPs are involved in pathological processes such as inflammation, oxidative stress, fibrosis, and neuronal apoptosis through the regulation of signaling pathways such as MAPK, which in turn affects the cognitive function of CKD patients. Specifically, downregulation of DUSP1 and DUSP6 expression in brain tissues of CKD patients is associated with cognitive impairment, whereas upregulation of DUSP8 and DUSP16 exacerbates cognitive deficits by promoting neuroinflammation. In addition, uremic toxins (e.g., indolephenol sulfate) can further deteriorate cognitive function by altering the activity of DUSPs and interfering with central nervous system signaling. Although there are currently no clinical drugs targeting DUSPs, small molecule inhibitors, gene modulation techniques, and natural compounds have demonstrated the potential to improve cognitive function by modulating DUSPs. Future studies need to focus on optimizing the specificity and selectivity of DUSPs inhibitors and conducting rigorous clinical validation. In-depth elucidation of the mechanism of action of DUSPs in the renal-brain axis will provide an important theoretical basis for the development of novel intervention strategies for CKD-associated cognitive impairment. Show less
no PDF DOI: 10.1016/j.intimp.2025.114883
DUSP6

Feasibility Evaluation of Dried Whole Egg Powder Application in Tadpole (

Quan Li, Chuang Shao, Yi Hu +2 more · 2025 · Animals : an open access journal from MDPI · MDPI · added 2026-04-24
At present, studies on tadpole nutrition and metabolism are scarce. This study aimed at comparing the influence of two protein sources, fishmeal (FM) and dried whole egg powder (DWEP), on tadpoles fro Show more
At present, studies on tadpole nutrition and metabolism are scarce. This study aimed at comparing the influence of two protein sources, fishmeal (FM) and dried whole egg powder (DWEP), on tadpoles from the perspective of growth, the metamorphosis rate, lipid metabolism, antioxidant properties and the intestinal flora. In this experiment, the control diet was set to contain no FM or DWEP. Based on the control diet, 5% and 10% FM or DWEP were included, respectively. The results of the experiment indicated that FM or DWEP inclusion significantly enhanced the growth performance and metamorphosis rate ( Show less
📄 PDF DOI: 10.3390/ani15040584
LPL