👤 Yongxing 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, Yongyan Zhang, Yongyun Zhang, You-Zhi Zhang, Youjin Zhang, Youmin Zhang, Youti Zhang, Youwen Zhang, Youyi Zhang, Youying Zhang, Youzhong Zhang, Yu Chen Zhang, Yu Zhang, Yu-Bo Zhang, Yu-Chi Zhang, Yu-Fei Zhang, Yu-Hui Zhang, Yu-Jie Zhang, Yu-Jing Zhang, Yu-Qi Zhang, Yu-Qiu Zhang, Yu-Yu Zhang, Yu-Zhe Zhang, YuHang Zhang, YuHong Zhang, Yuan Zhang, Yuan-Wei Zhang, Yuan-Yuan Zhang, Yuanchao Zhang, Yuanhao Zhang, Yuanhui Zhang, Yuanping Zhang, Yuanqiang Zhang, Yuanqing Zhang, Yuansheng Zhang, Yuanxi Zhang, Yuanxiang Zhang, Yuanyi Zhang, Yuanyuan Zhang, Yuanzhen Zhang, Yuanzhuang Zhang, Yubin Zhang, Yucai Zhang, Yuchao Zhang, Yuchen Zhang, Yuchi Zhang, Yue Zhang, Yue-Bo Zhang, Yue-Ming Zhang, Yuebin Zhang, Yuebo Zhang, Yuehong Zhang, Yuehua Zhang, Yuejuan Zhang, Yuemei Zhang, Yueqi Zhang, Yueru Zhang, Yuetong Zhang, Yufang Zhang, Yufeng Zhang, Yuhan Zhang, Yuhao Zhang, Yuheng Zhang, Yuhua Zhang, Yuhui Zhang, Yujia Zhang, Yujiao Zhang, Yujie Zhang, Yujin Zhang, Yujing Zhang, Yujuan Zhang, Yuke Zhang, Yukun Zhang, Yulin Zhang, Yuling Zhang, Yulong Zhang, Yumei Zhang, Yumeng Zhang, Yumin Zhang, Yun Zhang, Yun-Feng Zhang, Yun-Lin Zhang, Yun-Mei Zhang, Yun-Sheng Zhang, Yun-Xiang Zhang, Yunfan Zhang, Yunfei Zhang, Yunfeng Zhang, Yunhai Zhang, Yunhang Zhang, Yunhe Zhang, Yunhui Zhang, Yuning Zhang, Yunjia Zhang, Yunli Zhang, Yunmei Zhang, Yunpeng Zhang, Yunqi Zhang, Yunqiang Zhang, Yunqing Zhang, Yunsheng Zhang, Yunxia Zhang, Yupei Zhang, Yupeng Zhang, Yuping Zhang, Yuqi Zhang, Yuqing Zhang, Yurou Zhang, Yuru Zhang, Yusen Zhang, Yushan Zhang, Yutian Zhang, Yuting Zhang, Yutong Zhang, Yuwei Zhang, Yuxi Zhang, Yuxia Zhang, Yuxin Zhang, Yuxuan Zhang, Yuyan Zhang, Yuyanan Zhang, Yuyang Zhang, Yuying Zhang, Yuyu Zhang, Yuyuan Zhang, Yuzhe Zhang, Yuzhi Zhang, Yuzhou Zhang, Yuzhu Zhang, Yvonne Zhang, Z Zhang, Z-K Zhang, Zai-Rong Zhang, Zaifeng Zhang, Zaijun Zhang, Zaiqi Zhang, Zebang Zhang, Zekun Zhang, Zemin Zhang, Zeming Zhang, Zeng Zhang, Zengdi Zhang, Zengfu Zhang, Zenglei Zhang, Zengli Zhang, Zengqiang Zhang, Zengrong Zhang, Zengtie Zhang, Zepeng Zhang, Zewei Zhang, Zewen Zhang, Zeyan Zhang, Zeyuan Zhang, Zhan-Xiong Zhang, Zhangjin Zhang, Zhanhao Zhang, Zhanjie Zhang, Zhanjun Zhang, Zhanming Zhang, Zhanyi Zhang, Zhao Zhang, Zhao-Huan Zhang, Zhao-Ming Zhang, Zhaobo Zhang, Zhaocong Zhang, Zhaofeng Zhang, Zhaohua Zhang, Zhaohuai Zhang, Zhaohuan Zhang, Zhaohui Zhang, Zhaomin Zhang, Zhaoping Zhang, Zhaoqi Zhang, Zhaotian Zhang, Zhaoxue Zhang, Zhe Zhang, Zhehua Zhang, Zhemei Zhang, Zhen Zhang, Zhen-Dong Zhang, Zhen-Jie Zhang, Zhen-Shan Zhang, Zhen-Tao Zhang, Zhen-lin Zhang, Zhenfeng Zhang, Zheng Zhang, Zhengbin Zhang, Zhengfen Zhang, Zhenglang Zhang, Zhengliang Zhang, Zhengxiang Zhang, Zhengxing Zhang, Zhengyu Zhang, Zhengyun Zhang, Zhenhao Zhang, Zhenhua Zhang, Zhenlin Zhang, Zhenqiang Zhang, Zhentao Zhang, Zhenyang Zhang, Zhenyu Zhang, Zhenzhen Zhang, Zhenzhu Zhang, Zhewei Zhang, Zhewen Zhang, Zheyuan Zhang, Zhezhe Zhang, Zhi Zhang, Zhi-Chang Zhang, Zhi-Jie Zhang, Zhi-Jun Zhang, Zhi-Peng Zhang, Zhi-Qing Zhang, Zhi-Shuai Zhang, Zhi-Shuo Zhang, Zhi-Xin Zhang, Zhibo Zhang, Zhicheng Zhang, Zhicong Zhang, Zhifei Zhang, Zhigang Zhang, Zhiguo Zhang, Zhihan Zhang, Zhihao Zhang, Zhihong Zhang, Zhihua Zhang, Zhihui Zhang, Zhijian Zhang, Zhijiao Zhang, Zhijing Zhang, Zhijun Zhang, Zhikun Zhang, Zhimin Zhang, Zhiming Zhang, Zhiping Zhang, Zhiqian Zhang, Zhiqiang Zhang, Zhiqiao Zhang, Zhiru Zhang, Zhishang Zhang, Zhishuai Zhang, Zhiwang Zhang, Zhiwen Zhang, Zhixia Zhang, Zhixin Zhang, Zhiyan Zhang, Zhiyao Zhang, Zhiye Zhang, Zhiyi Zhang, Zhiyong Zhang, Zhiyu Zhang, Zhiyuan Zhang, Zhiyun Zhang, Zhizhong Zhang, Zhong Zhang, Zhong-Bai Zhang, Zhong-Yi Zhang, Zhong-Yin Zhang, Zhong-Yuan Zhang, Zhongheng Zhang, Zhongjie Zhang, Zhonglin Zhang, Zhongqi Zhang, Zhongwei Zhang, Zhongxin Zhang, Zhongxu Zhang, Zhongyang Zhang, Zhongyi Zhang, Zhou Zhang, Zhu Zhang, Zhu-Qin Zhang, Zhuang Zhang, Zhuo Zhang, Zhuo-Ya Zhang, Zhuohua Zhang, Zhuojun Zhang, Zhuorong Zhang, Zhuoya Zhang, Zhuqin Zhang, Zhuqing Zhang, Zhuzhen Zhang, Zi-Feng Zhang, Zi-Jian Zhang, Zian Zhang, Zicheng Zhang, Ziding Zhang, Ziguo Zhang, Zihan Zhang, Ziheng Zhang, Zijian Zhang, Zijiao Zhang, Zijing Zhang, Zikai Zhang, Zilong Zhang, Zilu Zhang, Ziping Zhang, Ziqi Zhang, Zishuo Zhang, Zixiong Zhang, Zixu Zhang, Zixuan Zhang, Ziyang Zhang, Ziyi Zhang, Ziyin Zhang, Ziyu Zhang, Ziyue Zhang, Zizhen Zhang, Zongping Zhang, Zongquan Zhang, Zongwang Zhang, Zongxiang Zhang, Zu-Xuan Zhang, Zufa Zhang, Zuoyi Zhang
articles

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

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

SIRT6 Ameliorates Atherosclerosis by Inhibiting M1 Macrophage Polarisation Through Deacetylated-TLR4.

Jian Huang, Huiming Yi, Yanhui Wu +2 more · 2026 · Immunology · Blackwell Publishing · added 2026-04-24
Atherosclerosis serves as the fundamental pathological process underlying numerous cardiovascular disorders, and the change of macrophage polarisation is the key to regulate the inflammatory response Show more
Atherosclerosis serves as the fundamental pathological process underlying numerous cardiovascular disorders, and the change of macrophage polarisation is the key to regulate the inflammatory response of AS. SIRT6 plays a protective effect in AS, but whether it regulates macrophage polarisation in AS remains uncertain. We aimed to characterise the mechanistic role of SIRT6 in atherosclerosis development mediated by macrophage polarisation. ApoE Show less
no PDF DOI: 10.1111/imm.70129
APOE

Cell surface nucleolin promotes endothelial cell pyroptosis in atherosclerosis through RASSF2.

Li Fang, Zhijie Shen, Dan Huang +4 more · 2026 · Atherosclerosis · Elsevier · added 2026-04-24
Increasing evidence indicates that modulating pyroptosis in endothelial cells (ECs) can alleviate atherosclerosis (AS) progression; however, despite reports that nucleolin (NCL) regulates vascular smo Show more
Increasing evidence indicates that modulating pyroptosis in endothelial cells (ECs) can alleviate atherosclerosis (AS) progression; however, despite reports that nucleolin (NCL) regulates vascular smooth muscle cell proliferation in AS, the potential mechanism by which cell surface NCL mediates pyroptosis in ECs during AS remains poorly understood. AS was induced in ApoE AS model mice developed severe aortic lesions accompanied by pronounced EC pyroptosis and inflammation, together with elevated NCL expression in ECs of the aortic root. Both inhibition of NLRP3 and NCL knockdown alleviated atherosclerotic lesion severity in ApoE This study demonstrates that, in AS, NCL exacerbates EC pyroptosis and promotes disease progression by facilitating nuclear transport of RASSF2. This study defines the mechanistic roles of NCL in AS, thereby identifying a new molecular pathway and suggesting potential therapeutic targets. Show less
no PDF DOI: 10.1016/j.atherosclerosis.2026.120715
APOE

Dual Roles of MAPK-Mediated C/EBPβ Phosphorylation in Promoting Maturation and Suppressing EMT During Hepatocyte Differentiation from hESCs.

Shoupei Liu, Xiangting Cao, Haibin Wu +7 more · 2026 · Stem cells (Dayton, Ohio) · Oxford University Press · added 2026-04-24
Human embryonic stem cell (hESC)-derived hepatocytes (hEHs) display functional deficits, particularly impaired albumin secretion and ammonia metabolism, compared to primary human hepatocytes (PHHs). H Show more
Human embryonic stem cell (hESC)-derived hepatocytes (hEHs) display functional deficits, particularly impaired albumin secretion and ammonia metabolism, compared to primary human hepatocytes (PHHs). Here, we investigated the regulatory role of CCAAT/enhancer-binding protein beta (C/EBPβ) in hepatocyte maturation. Forced C/EBPβ expression enhanced hepatocyte functionality and upregulated hepatocyte-specific genes, while suppressing epithelial-mesenchymal transition (EMT) via downregulating canonical EMT markers. Mechanistically, CUT&Tag and luciferase reporter assays confirmed C/EBPβ directly binds to the promoter regions of CDH1 (E-cadherin) and CPS1 (carbamoyl phosphate synthetase 1). Co-immunoprecipitation identified an interaction between C/EBPβ and the MAPK pathway. RNA interference combined with Western blot analysis revealed that MAPK1-mediated phosphorylation of C/EBPβ at Thr-235 augmented its transactivation activity, accelerating hepatocyte maturation. Our findings establish C/EBPβ as a master regulator that coordinates transcriptional networks and post-translational modifications during hEHs maturation, providing novel insights for generating mature hepatocytes for disease modeling and regenerative medicine applications. The transcriptional activity of C/EBPβ is regulated by MAPK1 protein within the ERK/MAPK signaling pathway. MAPK1 moves from the cytoplasm into the nucleus and transfers phosphate groups to C/EBPβ. This process reverses the "self-inhibition" state of C/EBPβ and enhances its transcriptional activity on downstream target genes. Show less
no PDF DOI: 10.1093/stmcls/sxag016
CPS1

Dynamic evaluation of blood marker changes induced by acute binge drinking in healthy individuals: a randomized controlled trial.

Jiaomei Li, Kaixin Pan, Yuxuan Zhang +8 more · 2026 · Scientific reports · Nature · added 2026-04-24
Acute alcohol consumption is known to exert widespread physiological effects, yet the immediate impacts on metabolic biomarkers remain incompletely understood. The present randomized controlled trial Show more
Acute alcohol consumption is known to exert widespread physiological effects, yet the immediate impacts on metabolic biomarkers remain incompletely understood. The present randomized controlled trial was conducted to investigate the acute effects of a single episode of alcohol ingestion on various biomarkers in healthy individuals. A total of 45 male participants were recruited and randomized into an alcohol group (n = 40) and a control group (n = 5) at an 8:1 ratio. Volunteers in the alcohol group ingested 40% Absolut vodka within 15 min. Blood pressure, heart rate, and blood oxygen saturation were measured at 0 h, 1 h, 3 h, 5 h, 12 h, and 24 h. Venous blood samples were drawn at 0 h, 1 h, 5 h, 12 h, and 24 h after alcohol intake. Our results showed that levels of liver function markers, including α-fucosidase (AFU), albumin (ALB), and alkaline phosphatase (ALP), were significantly increased in the alcohol group compared to the control group. The 24-h area under curve (AUC) of AFU, ALB, and ALP were significantly higher in the alcohol group. The liver fibrosis maker collagen type Ⅳ (Ⅳ-C) tended to be higher at 1 h and 12 h in the alcohol group compared to the control group. Lipid levels, including triglycerides (TG), apolipoprotein A1 (APOA1), and the APOA1/APOB, were significantly elevated after alcohol ingestion, particularly at 5 h and 12 h. The 24 h-AUC of TG, APOA1, and APOA1/APOB were higher in the alcohol group than in the control group. Additionally, cardiac function indicators, including heart rate, systolic blood pressure (SBP), and diastolic blood pressure (DBP), were significantly elevated in the alcohol group. SBP and DBP remained higher 24 h after alcohol ingestion compared to the control group. This study demonstrated that even a single episode of binge drinking could induce significant alterations of biomarkers related to liver function, cardiac function, and lipid profiles. These findings provided valuable insights into the short-term impact of alcohol on health and highlighted the importance of further research to explore the long-term implications of repeated acute alcohol exposure. Given the very small control group, these results should be interpreted as preliminary and confirmed in larger, more balanced randomized trials. The online version contains supplementary material available at 10.1038/s41598-026-40028-1. Show less
📄 PDF DOI: 10.1038/s41598-026-40028-1
APOB

Expression of BDNF-TrkB-AKT1 pathway components and apoptosis-related factors across yak brain regions at low and high altitudes.

Qian ZHANG, Yan Cui, Junfeng He +3 more · 2026 · Folia histochemica et cytobiologica · added 2026-04-24
This study investigated the expression of brain-derived neurotrophic factor (BDNF) signaling components (BDNF-TrkB-AKT1) and apoptosis-related factors (Bcl-2 and Bax) in yak brain regions at different Show more
This study investigated the expression of brain-derived neurotrophic factor (BDNF) signaling components (BDNF-TrkB-AKT1) and apoptosis-related factors (Bcl-2 and Bax) in yak brain regions at different altitudes. The cerebral cortex, cerebellum, hippocampus, thalamus, and medulla oblongata were collected from 3-year-old yaks living at low and high altitudes. The relative mRNA expression of BDNF, TrkB, AKT1, Bcl-2, and Bax was assessed by qRT-PCR. Protein abundance and cellular localization of BDNF, TrkB, AKT1, Bcl-2, and Bax were evaluated by Western blotting and immunohistochemistry, with immunoreactivity quantified by optical density analysis. Within each altitude group, BDNF, TrkB, AKT1, and Bcl-2 mRNA expression and the corresponding protein levels (BDNF, TrkB, AKT1, and Bcl-2) were significantly higher in the cerebral cortex and hippocampus than in the cerebellum, thalamus, and medulla oblongata (P < 0.05). In contrast, Bax mRNA and Bax protein levels did not differ significantly among the five regions. Compared with low-altitude yaks, high-altitude yaks showed significantly higher BDNF, TrkB, AKT1, and Bcl-2 mRNA expression and higher BDNF, TrkB, AKT1, and Bcl-2 protein levels in brain tissues (P < 0.05), whereas Bax protein expression did not differ between altitude groups. Immunohistochemistry revealed immunoreactivity for BDNF, TrkB, AKT1, Bcl-2, and Bax in both altitude groups, with prominent labeling in cortical pyramidal neurons and across the pyramidal cell layer in the hippocampal CA region. Immunoreactivity was also detected in large neurons of the thalamus and medulla oblongata. In the cerebellum, labeling was strongest in Purkinje cells, with weaker signals in the granule cell layer and molecular layer. BDNF-TrkB-AKT1 pathway components and Bcl-2 showed relatively higher expression in the cerebral cortex and hippocampus within each altitude group, whereas Bax expression did not vary across regions. These patterns are consistent with an association between BDNF-TrkB-AKT1 signaling and increased Bcl-2 expression without a corresponding increase in Bax, which may support neuronal adaptation in the cerebral cortex and hippocampus. Elevated expression of BDNF, TrkB, AKT1, and Bcl-2 at high altitude suggests enhanced adaptation to hypoxia in high-altitude yaks; the underlying mechanisms require further investigation. Show less
📄 PDF DOI: 10.5603/fhc.110409
BDNF akt1 apoptosis bax bcl-2 bdnf brain-derived neurotrophic factor trkb

BDNF genetic variants modulate the impact of childhood trauma on symptom dimensions in first-episode schizophrenia.

Junjiao Ping, Yong Wu, Jiali Luo +3 more · 2026 · Frontiers in psychiatry · Frontiers · added 2026-04-24
Gene-environment interactions play a critical role in shaping phenotypic heterogeneity in complex psychiatric disorders. Brain-derived neurotrophic factor (BDNF) is a key genetic regulator of stress-s Show more
Gene-environment interactions play a critical role in shaping phenotypic heterogeneity in complex psychiatric disorders. Brain-derived neurotrophic factor (BDNF) is a key genetic regulator of stress-sensitive neuroplasticity. Yet, how We conducted a case-control study including 93 patients with first-episode schizophrenia (SZ) and 64 healthy controls. Childhood trauma exposure was assessed using the Childhood Trauma Questionnaire (CTQ), and symptom dimensions were evaluated with the Positive and Negative Syndrome Scale (PANSS). Three Patients with SZ exhibited significantly higher CTQ scores across all trauma subtypes compared with controls (all These findings demonstrate that Show less
📄 PDF DOI: 10.3389/fpsyt.2026.1790184
BDNF

Phase 1 dose-escalation trial of sub-endometrial injection of human embryonic stem cells-derived immunity-and-matrix-regulatory cells to promote endometrial angiogenesis in refractory intrauterine adhesion.

Qiang Li, Zhiqi Liao, Xinyao Hu +26 more · 2026 · Molecular therapy : the journal of the American Society of Gene Therapy · Elsevier · added 2026-04-24
Clinical application of mesenchymal stem cells for endometrial repair has been hampered by variability in cell quality, large-scale production, and uncertainty regarding the optimal delivery route. In Show more
Clinical application of mesenchymal stem cells for endometrial repair has been hampered by variability in cell quality, large-scale production, and uncertainty regarding the optimal delivery route. In this study, we investigated the therapeutic potential of clinical-grade human embryonic stem cell-derived immunity-and-matrix-regulatory cells (IMRCs) for treating refractory moderate-to-severe intrauterine adhesion (IUA). In a rabbit IUA model, sub-endometrial injection of IMRCs significantly reduced fibrosis and enhanced endometrial angiogenesis, outperforming uterine perfusion. Transcriptomic analysis revealed distinct pro-angiogenic gene expression profiles between the two delivery routes. In vitro, IMRCs co-cultured with endometrial stromal cells (ESCs) markedly enhanced angiogenic potential compared to either cell type alone. Protein array analysis of the co-culture supernatant showed elevated levels of angiogenic factors, with functional assays confirming that inhibition of ANGPTL4, a non-canonical pro-angiogenic mediator, impaired angiogenesis. In a first-in-human, single-center, phase 1 dose-escalation trial involving 18 patients with refractory IUA, high-dose sub-endometrial IMRC injection promoted angiogenesis, reduced uterine scarring, and improved pregnancy outcomes, with no safety concerns observed over 3 years of follow-up. These findings highlight the translational promise of IMRCs as a novel therapeutic strategy for endometrial regeneration in severe IUA. Show less
📄 PDF DOI: 10.1016/j.ymthe.2025.09.035
ANGPTL4

Rab35 drives the malignant progression of endometrial carcinoma by regulating the nuclear translocation of β-catenin.

Eryan Yang, Yindan Wang, Wenxin Mao +8 more · 2026 · Experimental cell research · Elsevier · added 2026-04-24
Endometrial carcinoma (EC) is a common malignancy of the female reproductive system. Rab35 is widely recognized as an oncogenic driver and has been implicated in the progression of various malignant t Show more
Endometrial carcinoma (EC) is a common malignancy of the female reproductive system. Rab35 is widely recognized as an oncogenic driver and has been implicated in the progression of various malignant tumors. However, its regulatory mechanism and pathobiological roles in EC remain unclear. Rab35 expression in EC was systematically profiled via integrative analysis of clinical endometrial specimens and multi-omics databases (CPTAC and GEO). The association between clinical prognosis and Rab35 expression was examined using Kaplan-Meier analysis. Mechanistic investigations included transwell assays, western blotting, and immunofluorescence in Rab35-overexpressing and CRISPR/Cas9-mediated Rab35-knockout EC cells. A mouse xenograft tumor model was established to confirm the effects of Rab35 in vivo. The Rab35 content increased gradually from normal endometrium to atypical hyperplastic endometrium to EC. Moreover, the findings indicated that elevated Rab35 expression was significantly associated with advanced disease characteristics and poor overall survival in patients with EC. In addition, Rab35 enhanced the migratory and invasive nature of EC cells. The expression of Rab35 was inversely linked to that of the β-catenin destruction complex-related proteins Axin-1 and GSK3β, leading to the increased nuclear translocation of β-catenin in EC cells. Animal experiments further verified that Rab35 augmented EC progression by regulating the nuclear translocation of β-catenin. The study revealed that high expression of Rab35 was strongly correlated with EC progression and a poor clinical outcome. Furthermore, Rab35 promoted EC cell metastasis by accelerating the nuclear translocation of β-catenin. These findings suggest that Rab35 serves as a valuable biomarker and therapeutic target for EC. Show less
no PDF DOI: 10.1016/j.yexcr.2026.114950
AXIN1

A case of late-onset carbamoyl phosphate synthetase 1 deficiency: diagnostic challenges and management in a low-resource setting.

Xiaopu Cui, Sixian Guo, Yu Zhang +5 more · 2026 · Clinical biochemistry · Elsevier · added 2026-04-24
This study aimed to analyze the clinical features, genetic basis, and management of late-onset carbamoyl phosphate synthetase 1 deficiency (CPS1D) through a pediatric case report and literature review Show more
This study aimed to analyze the clinical features, genetic basis, and management of late-onset carbamoyl phosphate synthetase 1 deficiency (CPS1D) through a pediatric case report and literature review, highlighting diagnostic challenges and therapeutic strategies. We present a 19-year-old female with recurrent neurological symptoms since age 8. She underwent comprehensive metabolic screening, neuroimaging, and whole-exome sequencing of theCPS1gene. Identified variants were assessed for pathogenicity using multiple orthogonalin silicoprediction tools. The patient's initial hyperammonemic crisis at age 8 was misdiagnosed as encephalitis. Workup at age 13 confirmed hyperammonemia (peak 168 µmol/L), hypocitrullinemia, and elevated glutamine. Genetic analysis identified compound heterozygousCPS1variants: a novel c.1058 T > C (p.F353S) and known pathogenic c.1145C > T (p.P382L). A self-selected low-protein diet controlled acute crises but led to severe growth failure (height 145 cm, weight 30 kg). Late-onset CPS1D's nonspecific neurological symptoms often lead to misdiagnosis. Diagnosis requires a high index of suspicion, integrating metabolic profiling with genetic confirmation. This case expands the pathogenic genotypic spectrum of CPS1D. It crucially highlights that while dietary management is life-saving, it requires expert multidisciplinary oversight to prevent devastating consequences like growth failure, especially in resource-limited settings. Routine ammonia testing in unexplained encephalopathy is paramount. Show less
no PDF DOI: 10.1016/j.clinbiochem.2025.111041
CPS1

Lysophosphatidic acid-induced Arf6-driven macropinocytosis of CD147

Luomeng Qian, Zhiguang Fu, Ping Chen +11 more · 2026 · International journal of biological sciences · added 2026-04-24
📄 PDF DOI: 10.7150/ijbs.125483
LPA

Low shear stress promotes atherosclerosis by inducing endothelial ferroptosis via the P53/xCT pathway.

Jia-Wei Hu, Ya-Peng Chen, Ai-Qun Chen +8 more · 2026 · Experimental cell research · Elsevier · added 2026-04-24
Atherosclerotic lesions commonly develop in curved or bifurcated arteries, where blood flow exhibits characteristics of low shear stress (LSS). Subjected to LSS continually, endothelial cells (ECs) ad Show more
Atherosclerotic lesions commonly develop in curved or bifurcated arteries, where blood flow exhibits characteristics of low shear stress (LSS). Subjected to LSS continually, endothelial cells (ECs) adopt a pro-atherosclerotic phenotype. Ferroptosis is a recently identified form of controlled cell demise prompted by iron-dependent buildup of cellular reactive oxygen species (ROS), which has been associated with diverse cardiovascular diseases, particularly atherosclerosis (AS). P53 is a broadly acting tumor suppressor that can be activated by diverse stimuli and mediates multiple biological outcomes, including cell cycle arrest, DNA repair, apoptosis, and ferroptosis. However, it remains unknown whether LSS promotes the development of AS by inducing P53-dependent ferroptosis in endothelial cells. In our experiments, we induced LSS by partial ligation of the right common carotid artery in high-fat diet-fed (HFD) male ApoE Our findings demonstrated that LSS induced endothelial ferroptosis, which in turn accelerated AS development both in vivo and in vitro. This effect was partially counteracted by both the ferroptosis inhibitor Fer-1 and endothelium-specific glutathione peroxidase 4 (GPX4) overexpression in ApoE Our experiments suggested that LSS promotes atherosclerosis by inducing endothelial ferroptosis through the P53/xCT signaling pathway. Show less
no PDF DOI: 10.1016/j.yexcr.2026.114901
APOE

Mechanistic study on nonylphenol-induced depressive-like behavior: PINK1/parkin-mediated mitophagy regulates synaptic remodeling in neurons.

Huawen Yu, Jie Yu, Xiao Yang +7 more · 2026 · Ecotoxicology and environmental safety · Elsevier · added 2026-04-24
To investigate the role of PINK1/Parkin-mediated mitophagy in regulating synaptic remodeling of neuronal cells in depression-like behaviors induced by nonylphenol (NP). In vitro experiments: HT-22 neu Show more
To investigate the role of PINK1/Parkin-mediated mitophagy in regulating synaptic remodeling of neuronal cells in depression-like behaviors induced by nonylphenol (NP). In vitro experiments: HT-22 neuronal cells were exposed to NP, and mitophagy and Parkin expression were inhibited using specific inhibitors. The cells were categorized into the following groups: (1) control (C) and low-dose NP group (L: 2.5 µM), medium-dose NP group (M: 50 µM), and high-dose NP groups (H: 100 µM); (2) control (C), NP (100 µM), Mdivi-1 (5 µM), and Mdivi-1 + NP (5 µM Mdivi-1 +100 µM NP) groups; (3) control (C), NP (100 µM), AC220 (2 nM), and AC220 + NP (2 nM AC220 +100 µM NP) groups. In vivo experiments: a total of 48 mice, including 24 C57BL/6 wild-type mice and 24 PKRK2 gene-knockout mice, were randomly assigned to the following four groups: control (C), NP (100 mg/kg/day), PKRK2-knockout (KO), and PKRK2-knockout + NP (100 mg/kg/day, KH) groups, with 12 mice in each group. In vitro: With increasing NP concentration, the ATP content reduced and the expressions of synaptic remodeling-related proteins (i.e., PSD-95, BDNF, SYN) decreased. In contrast, the expressions of mitophagy-related proteins and those involved in the PINK1/Parkin-signaling pathway (such as p62, Beclin1, PINK1, Parkin) increased (P < 0.05). Inhibition of mitophagy with Mdivi-1 alleviated the NP-induced changes in synaptic, mitophagy-related, and PINK1/Parkin pathway-related proteins. Similarly, the inhibition of Parkin with AC220 mitigated NP-induced effects on synaptic, mitophagy-related, and PINK1/Parkin-signaling pathway-related proteins and mRNA expression. In vivo: PKRK2 gene-knockout mice exhibited improved NP-induced depression-like behaviors and decreased NP-induced synaptic morphology and mitochondrial ultrastructure changes. Moreover, the gene knockout alleviated the downregulation of synaptic remodeling-related proteins and inhibited the PINK1/Parkin-signaling pathway-mediated mitophagy activated by NP. Mitophagy inhibition or PKRK2 knockout can alleviate NP-induced downregulation of synaptic remodeling-related proteins, protect synaptic morphology and ultrastructure, and improve NP-induced depression-like behaviors. Show less
no PDF DOI: 10.1016/j.ecoenv.2026.120149
BDNF depression mitophagy neuronal cells neuroscience parkin pink1 synaptic remodeling

Joint control of low-density lipoprotein cholesterol, lipoprotein(a), and high-sensitivity C-reactive protein in relation to risk of cardiovascular disease in adults with steatotic liver disease.

Shunming Zhang, Yan Borné, Le Ma +2 more · 2026 · Nutrition, metabolism, and cardiovascular diseases : NMCD · Elsevier · added 2026-04-24
We examined whether the excess cardiovascular disease (CVD) risk among adults with steatotic liver disease (SLD) subtypes could be reduced or eliminated through joint control of low-density lipoprotei Show more
We examined whether the excess cardiovascular disease (CVD) risk among adults with steatotic liver disease (SLD) subtypes could be reduced or eliminated through joint control of low-density lipoprotein cholesterol (LDL-C), lipoprotein(a) [Lp(a)], and high-sensitivity C-reactive protein (hs-CRP). This prospective cohort study included 291,995 participants from the UK Biobank, comprising 77,187 with metabolic dysfunction-associated steatotic liver disease (MASLD), 22,190 with metabolic dysfunction and alcohol-associated liver disease (MetALD), 5474 with alcohol-associated liver disease (ALD), and 187,144 without SLD. Cox proportional hazards models were used to assess CVD risk associated with numbers of LDL-C, Lp(a), and hs-CRP controlled within the target range. During 12 years of median follow-up, 24,251 CVD events were documented, with 19,661 coronary heart disease and 5600 stroke. Among individuals with various SLD subtypes, those with all three factors controlled had the lowest risks of CVD, with HRs (95% CIs) of 0.65 (0.58, 0.72) in MASLD, 0.61 (0.49, 0.76) in MetALD, and 0.57 (0.35, 0.93) in ALD when comparing to zero-factor control. In addition, among individuals with SLD subtypes achieving all three factors within target ranges, the HRs (95% CIs) of CVD were 0.97 (0.88, 1.07) in MASLD, 0.90 (0.75, 1.08) in MetALD, and 0.63 (0.42, 0.95) in ALD, as compared with non-SLD controls. Similar association patterns were observed for coronary heart disease and stroke. Participants with various SLD subtypes who had optimally controlled LDL-C, Lp(a), and hs-CRP showed no excess or even lower risk of CVD as compared with the general population. Not available. Show less
no PDF DOI: 10.1016/j.numecd.2026.104722
LPA

Suppression of dual-specificity phosphatase 6 protects against liver fibrosis via targeting CYP2E1-mediated ferroptosis.

Can Jiang, Xiaoli Tang, Ziyang Xu +5 more · 2026 · International journal of biological macromolecules · Elsevier · added 2026-04-24
DUSP6, a dual-specificity phosphatase, has become a focal point in understanding the pathogenesis of various liver disorders. This study aims to investigate the role of DUSP6 in liver fibrosis and exp Show more
DUSP6, a dual-specificity phosphatase, has become a focal point in understanding the pathogenesis of various liver disorders. This study aims to investigate the role of DUSP6 in liver fibrosis and explore the underlying mechanism. Using a CCL4-induced mouse model, the consistent upregulation of DUSP6 expression was observed. Notably, when Dusp6 was knocked down, liver fibrosis showed significant improvement, revealing a protective effect intricately linked to the ERK pathway. This was accompanied by an increase in ferroptosis-related proteins SLC7A11 and GPX4, underscoring the role of ferroptosis, an iron-dependent form of regulated cell death, in this process. Transcriptomic analysis further revealed a crucial downregulation of Cyp2e1 following Dusp6 knockdown. In vitro, DUSP6 knockdown not only promoted ERK phosphorylation but also suppressed CYP2E1 expression, enhancing cell proliferation, bolstering hepatocyte resistance to ferroptosis, and alleviating hepatocyte injury. Importantly, inhibiting CYP2E1 in mouse models of liver fibrosis effectively slowed the progression. These findings illuminate a critical regulatory mechanism that DUSP6 regulates liver fibrosis via targeting ferroptosis, offering new a direction for therapeutic strategies in liver disease. Show less
no PDF DOI: 10.1016/j.ijbiomac.2025.149856
DUSP6

Integrated multi-Omics and network toxicology elucidate the multi-target mechanisms of environmental hormones in driving hepatocellular carcinoma.

Rong Huang, Jinyue Ma, Jiaxin Yao +8 more · 2026 · Ecotoxicology and environmental safety · Elsevier · added 2026-04-24
Hepatocellular carcinoma (HCC) is a major malignancy with rising global incidence and mortality. Clinical treatment is limited by molecular heterogeneity and drug resistance. In recent years, endocrin Show more
Hepatocellular carcinoma (HCC) is a major malignancy with rising global incidence and mortality. Clinical treatment is limited by molecular heterogeneity and drug resistance. In recent years, endocrine-disrupting chemicals (EDCs) have attracted attention as emerging risk factors, but systematic pathogenic evidence for their roles in HCC initiation and progression remains insufficient. First, we predicted potential targets of EDCs using SwissTargetPrediction, STITCH, and ChEMBL, and intersected them with differentially expressed genes and key module genes from WGCNA in the GEO database to screen candidate key genes. Second, based on these candidates, we constructed diagnostic models using 14 machine-learning algorithms and evaluated feature importance via the SHAP framework to identify key biomarkers and their functional contributions. Molecular docking and molecular dynamics simulations were used to validate interaction mechanisms between EDCs and key target proteins. We then built a multivariable Cox proportional hazards model in the TCGA-LIHC cohort and performed stratified survival analysis, somatic mutation profiling, and immune evasion characterization. Subsequently, we evaluated the tumor immune microenvironment using CIBERSORT and ssGSEA, and integrated single-cell transcriptomic data to resolve cell-subtype heterogeneity, target expression distributions, and cell-cell communication. Meanwhile, we integrated the GDSC drug-sensitivity database to evaluate associations between risk scores and drug response, and conducted pan-cancer analyses to examine cross-cancer applicability. We identified 18 genes jointly associated with EDCs and HCC, significantly enriched in AMPK, p53, and FoxO signaling pathways and cell cycle-related pathways. Among models built with 14 machine-learning algorithms, CatBoost showed the best discriminative performance and identified CCNB2 and AKR1C3 as core driver genes. Docking and dynamics simulations indicated strong binding affinities and stable binding conformations between EDCs and target proteins including CCNB1 (-8.9 kcal/mol), AKR1C3 (-8.4 kcal/mol), and FADS1 (-8.5 kcal/mol). A multivariable Cox risk model based on nine key genes served as an independent prognostic predictor for HCC (HR = 1.746, 95% CI: 1.477-2.064, P < 0.001). The nomogram achieved AUCs of 0.836, 0.810, and 0.788 at 1, 3, and 5 years, respectively, indicating good predictive performance. The high-risk group was significantly associated with high tumor mutational burden (TMB), TP53 mutations, and low immune evasion scores. Regarding the tumor immune microenvironment, CIBERSORT and ssGSEA analyses showed marked enrichment of Tregs and M0 macrophages, while most effector immune cells and functions were suppressed. Single-cell transcriptomics further showed enrichment of endothelial cells, fibroblasts, hepatocytes, and macrophages in HCC tissues, with notable reductions in T cells, B cells, NK cells, and neutrophils, indicating an immunosuppressive microenvironment with stromal remodeling. Cell-cell communication analysis indicated that the MIF-CD74 receptor axis is central in immune-cell interactions. Drug-sensitivity analysis suggested that the high-risk group was more sensitive to GDC0810, BPD-00008900, and Fulvestrant, indicating potential beneficiary populations. Pan-cancer analysis showed that the risk model also had diagnostic and prognostic value in LUAD, KIRP, KIRC, and KICH, suggesting cross-cancer generalizability. This study systematically reveals that EDCs promote HCC initiation and progression by perturbing cell cycle, metabolic, and immune homeostasis through multi-target, multi-pathway mechanisms. The nine-gene risk model demonstrates superior performance in HCC diagnosis and prognosis and shows potential clinical translational value in drug-sensitivity prediction and pan-cancer analyses. This work provides a new perspective at the intersection of environmental toxicology and precision oncology and informs individualized therapeutic strategies. Show less
no PDF DOI: 10.1016/j.ecoenv.2025.119519
FADS1

Methamphetamine regulates microglial polarization and glycolytic activity to promote Parkinson's disease through the LIPH/LPA/PI3K/AKT signaling axis.

Yanghong Zou, Chunhai Zhang, Hui Bian +5 more · 2026 · International immunopharmacology · Elsevier · added 2026-04-24
The abuse of methamphetamine (METH) is associated with an increased risk of Parkinson's disease (PD), whereas microglial polarization and glucose metabolism disorders are closely related to the progre Show more
The abuse of methamphetamine (METH) is associated with an increased risk of Parkinson's disease (PD), whereas microglial polarization and glucose metabolism disorders are closely related to the progression of PD. This study aimed to investigate the specific molecular mechanism underlying the promotion of PD progression by METH through the regulation of microglial polarization and glycolysis. METH-induced C57BL/6 mice and BV2 cells were used to construct PD-like neurotoxicity animal and cell models for experimental investigation. Behavioral tests, immunohistochemistry and Nissl staining were used to assess the behavioral ability and neuronal damage of the animals. The levels of related proteins, inflammatory cytokines and glycolysis were detected using immunofluorescence, ELISA, Western blotting, and CCK-8 assays. METH treatment significantly promoted behavioral disorders in PD mice, reduced the number of TH-positive neurons, and aggravated neuronal damage in the substantia nigra (SN). In addition, METH decreased the M2 marker proteins Arg-1 and CD206 and increased the M1 marker proteins iNOS and CD86; the proinflammatory cytokines TNF-α, IL-β, and IL-6; and glucose uptake, glucose consumption and lactic acid production, thus promoting M1 polarization and glycolytic activity in BV2 cells. In terms of the underlying molecular mechanism, METH treatment significantly increased the level of LPA. METH promotes LPA expression via upregulation of LIPH expression, and activates the PI3K/AKT pathway. Knockdown of LIPH or treatment with BrP-LPA reduces the ability of METH to promote M1 microglial polarization and glycolytic activity. Furthermore, the addition of the PI3K/AKT signaling pathway activator 740 YP weakened the inhibitory effect of BrP-LPA on the above process. METH may promote M1 polarization and glycolytic activity in microglia by activating LIPH/LPA/PI3K/AKT signaling, thus promoting the progression of PD. Show less
no PDF DOI: 10.1016/j.intimp.2026.116306
LPA

Molecular characterization of humanized APOE mouse models reveals source and genotype dependent differences.

Na Wang, Gefei Yu, Zhen Wang +21 more · 2026 · Molecular neurodegeneration · BioMed Central · added 2026-04-24
no PDF DOI: 10.1186/s13024-026-00940-6
APOE

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

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

IRF6 induces endothelial dysfunction through the transcriptional activation of NDRG1 and aggravates low shear stress-mediated atherosclerosis.

Yong Chen, Yanchao Zhang, Shen Rui +3 more · 2026 · iScience · Elsevier · added 2026-04-24
Atherosclerosis (AS), a chronic inflammatory disorder initiated by vascular endothelial dysfunction (ED), is prominently triggered by hemodynamic low-shear stress (LSS). Interferon regulatory factor 6 Show more
Atherosclerosis (AS), a chronic inflammatory disorder initiated by vascular endothelial dysfunction (ED), is prominently triggered by hemodynamic low-shear stress (LSS). Interferon regulatory factor 6 (IRF6) is a transcription factor that regulates the inflammatory response following injury. In this work, the LSS-induced AS model was induced by the partial ligation of the left carotid artery in high-fat diet-fed ApoE Show less
📄 PDF DOI: 10.1016/j.isci.2026.115127
APOE

New co-drugs of O-demethylvenlafaxine and NSAIDs exert antidepressant effects by alleviating inflammation, oxidative stress, and increasing neurotransmitter.

Yangyang Song, Jie Song, Shuxian Liu +6 more · 2026 · International immunopharmacology · Elsevier · added 2026-04-24
Depression and anxiety disorders are highly comorbid, yet their complex pathogenesis often limits the efficacy of monotherapy. Growing evidence implicates neuroinflammation in their pathogenesis. Co-d Show more
Depression and anxiety disorders are highly comorbid, yet their complex pathogenesis often limits the efficacy of monotherapy. Growing evidence implicates neuroinflammation in their pathogenesis. Co-drugs that linked two active molecules into a single compound and released the drugs after administration, which offering improved efficacy and tolerability than individual drug mixtures or monotherapy. In this work, five new co-drugs ODV-NSAIDs were synthesized from O-desmethylvenlafaxine (ODV) with non-steroidal anti-inflammatory drugs (NSAIDs) to achieve synergistic antidepression and anxiolytic effects. In vitro stability studies exhibited that these co-drugs can be metabolized into two single drugs within 60 min in simulated intestinal fluid. In both acute and chronic LPS-induced models, co-drug ODV-NAP significantly ameliorated depressive-like behaviors, evidenced by increased sucrose preference, reduced immobility in the tail suspension test (TST) and forced swim test (FST), and enhanced locomotion in the open field test (OFT). Furthermore, ODV-NAP decreased brain levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and malondialdehyde (MDA), while elevating serotonin (5-HT), norepinephrine (NE), and superoxide dismutase (SOD) activity. Nissl staining confirmed ODV-NAP significantly attenuated hippocampal neuronal damage. Moreover, western blotting revealed ODV-NAP inhibited the TLR4/NF-κB signaling pathway and upregulated BDNF and p-TrkB protein expression. ODV-NAP also inhibited LPS-induced p65 nuclear translocation in BV-2 microglia in vitro, and caused no toxicity in histology. Thus, co-drug ODV-NAP represented a promising novel candidate for treating depression and anxiety. Show less
no PDF DOI: 10.1016/j.intimp.2026.116456
BDNF anxiety disorders depression inflammation neuroinflammation neurotransmitter oxidative stress

Stevia rebaudiana Bertoni root polysaccharide ameliorate high-fat-diet-induced atherosclerosis in ApoE-knock out mice: potential role of inflammation regulation.

Chunyan Liu, Guangdong Hu, Haoyu Zhang +5 more · 2026 · Natural product research · Taylor & Francis · added 2026-04-24
Atherosclerosis (AS) is a prevalent typical chronic inflammation disease characterised by lipid deposition, immune cell infiltration and inflammatory response in the arterial intima. The long-term tre Show more
Atherosclerosis (AS) is a prevalent typical chronic inflammation disease characterised by lipid deposition, immune cell infiltration and inflammatory response in the arterial intima. The long-term treatments of the existing drugs suffered safety concerns. Show less
no PDF DOI: 10.1080/14786419.2026.2613756
APOE

A mechanistic study of mitochondria-targeted PCSK9 liposomes attenuate oxidative damage in carotid artery plaques.

Liwei Zhang, Guanyu Chen, Yuhai Bai +1 more · 2026 · Journal of liposome research · Taylor & Francis · added 2026-04-24
Atherosclerotic plaque instability is a direct cause of cardiovascular and cerebrovascular events. In this study, a mitochondria-targeted liposome (LIP), modified with triphenylphosphonium (TPP) to en Show more
Atherosclerotic plaque instability is a direct cause of cardiovascular and cerebrovascular events. In this study, a mitochondria-targeted liposome (LIP), modified with triphenylphosphonium (TPP) to enable specific mitochondrial delivery, was innovatively constructed to encapsulate a PCSK9 inhibitor (TPP-LIP@PCSK9). The aim was to explore a novel strategy for stabilizing plaques by restoring mitochondrial function in endothelial cells. Characterization results showed that TPP-LIP@PCSK9 possesses favorable nano-characteristics, and its targeting capability was confirmed through mitochondrial co-localization experiments. In an Apoe Show less
no PDF DOI: 10.1080/08982104.2026.2651190
APOE

Endothelial versus global METRNL reveals importance of endothelial METRNL against atherosclerosis via mitochondrial homeostasis.

Dao-Xin Wang, Pin Wang, Zhu-Wei Miao +8 more · 2026 · Pharmacological research · Elsevier · added 2026-04-24
We recently showed that METRNL (Meteorin-like) protects against atherosclerosis. However, the mechanism for METRNL in atherosclerosis is largely unclear. This study aimed to demonstrate the relative i Show more
We recently showed that METRNL (Meteorin-like) protects against atherosclerosis. However, the mechanism for METRNL in atherosclerosis is largely unclear. This study aimed to demonstrate the relative importance of endothelial METRNL in atherosclerosis by comparing the effects of whole-body METRNL deficiency to endothelial-specific deficiency, and to show the subcellular distribution of endothelial METRNL and its role in mitochondrial homeostasis against atherosclerosis. Our study demonstrated that a deficiency in either endothelial or global METRNL exacerbated atherosclerosis to a similar degree in both spontaneous (age-related) and high fat diet-induced atherosclerosis, suggesting that endothelial METRNL is pivotal in the progression of atherosclerosis due to METRNL deficiency. Endothelial METRNL was diffusely distributed in the cytoplasm with subcellular localization to mitochondria, nucleus, endoplasmic reticulum, and Golgi apparatus (especially enriched in mitochondria and nucleus). In both an in vivo apolipoprotein E-deficient (ApoE Show less
no PDF DOI: 10.1016/j.phrs.2026.108123
APOE

LILRB4 shapes an immunosuppressive microenvironment to drive cervical cancer progression through tumor-infiltrating myeloid cell expansion and CD8

Yue Zhang, Yan Gao, Xin Guan +2 more · 2026 · Cellular and molecular life sciences : CMLS · Springer · added 2026-04-24
Cervical cancer (CC) is the most common gynecological malignancy and is strongly linked to human papillomavirus (HPV) infection. Currently, immune checkpoint blockade therapy has shown limited clinica Show more
Cervical cancer (CC) is the most common gynecological malignancy and is strongly linked to human papillomavirus (HPV) infection. Currently, immune checkpoint blockade therapy has shown limited clinical benefits for CC, highlighting the need to find more effective therapeutic targets. LILRB4, a member of the leukocyte immunoglobulin-like receptor superfamily, is considered a key mediator of cancer immunosuppression. However, its role in the CC immune microenvironment remains unclear. Here, LILRB4 expression was upregulated in CC tissues, and high expression levels were positively associated with advanced disease and immunosuppressive genes in tumors. In an immunocompetent mouse model, LILRB4 expression in CC tumors increased with tumor growth, whereas blocking LILRB4 reduced tumor growth. Flow cytometry analysis revealed that blockade of LILRB4 reduced CD8 Show less
📄 PDF DOI: 10.1007/s00018-026-06121-4
APOE

Polyphenol consumption and neurodegeneration risk: a systematic meta-analysis of randomized controlled trials bridging nutrition and cognitive health.

Xiaomei Wang, Jiao Yang, Jiayuan Zhang +3 more · 2026 · Food & function · Royal Society of Chemistry · added 2026-04-24
Given the potential of polyphenols to mitigate neurodegenerative diseases (NDDs), this meta-analysis investigated whether clinical evidence supports the use of polyphenols for neuroprotection and as n Show more
Given the potential of polyphenols to mitigate neurodegenerative diseases (NDDs), this meta-analysis investigated whether clinical evidence supports the use of polyphenols for neuroprotection and as nutritional strategies in NDDs. We analyzed different polyphenol types across seven NDDs, 13 studies involving 849 participants were included. Prespecified outcomes comprised global cognition (Mini-Mental State Examination, MMSE), domain-specific cognition (Alzheimer's Disease Cooperative Study-Cognitive Subscale, ADCS-Cog), activities of daily living (Alzheimer's Disease Cooperative Study-Activities of Daily Living, ADCS-ADL), neuropsychiatric symptoms (Neuropsychiatric Inventory, NPI), and selected biomarkers (plasma amyloid-β40 and brain-derived neurotrophic factor, BDNF). Reporting followed PRISMA 2020 guidelines, methods conformed to the Cochrane Handbook, and certainty of evidence was assessed using GRADE. Overall, polyphenol supplementation was associated with improved global cognition (pooled MD in MMSE = 2.06; 95% CI 0.62-3.49). In subgroup analyses, flavonoids were associated with a modest but significant improvement in MMSE scores, whereas stilbenes produced a significant benefit in daily functioning (ADCS-ADL) without clear gains in MMSE or ADCS-Cog and no consistent effects on NPI. Anthocyanidins, phenolic acids, and lignans did not significantly affect cognitive outcomes (MMSE or ADCS-Cog), and polyphenol subclasses did not yield robust or consistent changes in NPI or biomarker endpoints (Aβ40 and BDNF). Specific polyphenol subclasses therefore appear to confer selective cognitive and functional benefits, with stilbenes primarily supporting functional outcomes and flavonoids potentially enhancing global cognition. Show less
no PDF DOI: 10.1039/d5fo05135e
BDNF cognitive health neurodegeneration neurodegenerative diseases neuroprotection nutrition polyphenols randomized controlled trials

Identifying High-Performance Advanced Practice Profile of Specialist Nurses in Mainland China: A Mixed-Methods Sequential Explanatory Study.

Wenjuan Zhao, Jie Zhong, Xiaobin Lai +3 more · 2026 · Journal of nursing management · added 2026-04-24
Identifying high-performing advanced practice nursing roles and understanding the factors that contribute to their effectiveness are critical for advancing professional development, optimizing workfor Show more
Identifying high-performing advanced practice nursing roles and understanding the factors that contribute to their effectiveness are critical for advancing professional development, optimizing workforce deployment, and ensuring long-term sustainability in nursing. This study aimed to (1) identify distinct latent profiles of advanced practice nursing among specialist nurses in mainland China, (2) quantitatively examine the individual and contextual factors associated with high performance, as characterized by these profiles, and (3) qualitatively confirm the significant factors using explanatory semistructured interviews in the high-performance groups. A mixed-methods sequential explanatory design was used, in which quantitative data were collected first and subsequently explained through qualitative interviews. Certified specialist nurses from 16 hospitals across urban and rural areas of Shanghai were included. Latent profile analysis (LPA) was conducted using the five domains from the Advanced Practice Role Delineation tool as manifest indicators to classify nurses into distinct performance profiles. Multinomial logistic regression was used to examine potential determinants (e.g., job position) of group membership. Additionally, a backpropagation neural network (BPNN) was developed to rank the importance of contributing factors. Specialist nurses identified as high performers in the quantitative phase were purposively sampled for explanatory semistructured qualitative interviews. Three latent profiles emerged: high performance (26.1%), moderate performance (46.3%), and low performance (27.6%). Compared to APNs, staff nurses had significantly lower odds of belonging to the high-performance group ( Identifying the profiles of advanced practice nursing roles provides valuable insights for optimizing APN performance and informing targeted management and policy strategies. High-performing specialist nurses are positioned at the nexus of individual capability, interdisciplinary collaboration, and institutional support. Show less
📄 PDF DOI: 10.1155/jonm/3528145
LPA

Exploring the Hypoglycemic Activity and Mechanism of Polyphenols From Highland Barley Through Lactobacillus acidophilus Fermentation.

Mengyao Zhu, Xu Guo, Yingying Chen +6 more · 2026 · Journal of food science · Blackwell Publishing · added 2026-04-24
The polyphenols in grains are highly active, but some polyphenols in highland barley are in a bound form and have extremely low bioavailability. Fermentation by lactic acid bacteria (LAB) is capable o Show more
The polyphenols in grains are highly active, but some polyphenols in highland barley are in a bound form and have extremely low bioavailability. Fermentation by lactic acid bacteria (LAB) is capable of altering the functionality of foods. This research investigated the effects of fermentation with different LAB, such as Lactobacillus acidophilus (LAC), Lactobacillus casei (LCA), Lactobacillus rhamnosus (LRH), Lactobacillus plantarum (LPL), and Lactobacillus bulgaricus (LBU), on the hypoglycemic activity and mechanism of polyphenols in highland barley. The hypoglycemic activity of the fermentation products was measured by in vitro antioxidant, enzyme activity, and glucose consumption experiments. Untargeted metabolomic analysis used UHPLC-Q Exactive HF-X/MS to reveal distinct metabolic profiles among the fermented groups. Molecular docking and western blot experiments were conducted to elucidate the mechanism underlying the hypoglycemic effect of fermentation products. Polyphenolic antioxidant activity in highland barley and its inhibitory activities against α-glucosidase and α-amylase were increased after LAC fermentation. Furthermore, the fermented extracts improved glucose consumption in HepG2 cells. The content determination and metabolomic analysis showed that fermented highland barley polyphenols were increased, and 113 differential phenolic metabolites were identified and annotated, among which 44 exhibited a significant upregulation compared with raw highland barley polyphenols. At the molecular level, the polyphenol extract upregulated PI3K and phosphorylated Akt expression in HepG2 cells. Overall, the results indicate that fermentation by LAC biotransformed highland barley polyphenols into smaller molecules with improved hypoglycemic activities, thereby enhancing their bioavailability. Show less
no PDF DOI: 10.1111/1750-3841.71061
LPL

TRIM21 as a Context-Dependent Regulator in Hepatocellular Carcinoma: Integrating Etiological Landscapes (HBV/NASH) with Core Tumor Progression Mechanisms.

Jiatong Sun, Zixuan Gao, Yuanhao Li +5 more · 2026 · Journal of hepatocellular carcinoma · added 2026-04-24
Tripartite motif-containing protein 21 (TRIM21), an E3 ubiquitin ligase of the TRIM superfamily, modulates critical cellular processes including ubiquitination, autophagy, and oxidative stress respons Show more
Tripartite motif-containing protein 21 (TRIM21), an E3 ubiquitin ligase of the TRIM superfamily, modulates critical cellular processes including ubiquitination, autophagy, and oxidative stress response. Accumulating evidence highlights its context-dependent regulatory roles in hepatocellular carcinoma (HCC)-the most prevalent primary liver malignancy with high mortality and limited therapeutic efficacy. This review systematically summarizes the core mechanisms by which TRIM21 orchestrates HCC progression: ① Autophagy regulation: TRIM21 modulates HCC autophagy via multiple axes, including CCR4-NOT complex (TNKS1BP1/CNOT4)-mediated substrate ubiquitination, ATG14-dependent autophagosome initiation, and RETREG1-driven reticulophagy, with context-dependent effects on tumor proliferation. ② Drug resistance: TRIM21 enhances oxaliplatin sensitivity by ubiquitinating and degrading G6PD (the rate-limiting enzyme of the pentose phosphate pathway), while its role in sorafenib resistance involves dual pathways-the MST1/YAP axis and the ApoE/cholesterol/PI3K-AKT cascade. ③ Metastasis suppression: TRIM21 restricts HCC invasion and metastasis by ubiquitinating key oncoproteins, preserving epithelial integrity and inhibiting mesenchymal transition. ④ Reactive oxygen species (ROS) balance: TRIM21 regulates oxidative stress in HCC via the SQSTM1/p62-Keap1-NRF2 axis, coordinating with HIF1α to modulate antioxidant responses and tumor cell survival. Additionally, we discuss the regulatory significance of TRIM21 in HCC associated with hepatitis B virus (HBV) infection (via HBx/DNA polymerase ubiquitination) and nonalcoholic steatohepatitis (NASH) (via suppressing lipogenic enzymes to reduce steatosis-driven carcinogenesis). This review provides a theoretical basis for TRIM21 as a potential diagnostic marker and therapeutic target for HCC. Show less
📄 PDF DOI: 10.2147/JHC.S575307
APOE

The KANSL1-ARL17A fusion gene generates oncogenic chKANSARL and F-circKA RNAs that synergistically drive lung cancer progression via a novel F-circKA/miR-6860/chKANSARL axis.

Xinchao Guan, Tao Liu, Sili Chen +4 more · 2026 · The Journal of biological chemistry · Elsevier · added 2026-04-24
Fusion genes are pivotal drivers of tumorigenesis, often generating oncogenic chimeric RNAs and fusion circular RNAs. However, the mechanisms by which these transcripts synergistically contribute to c Show more
Fusion genes are pivotal drivers of tumorigenesis, often generating oncogenic chimeric RNAs and fusion circular RNAs. However, the mechanisms by which these transcripts synergistically contribute to cancer progression remain poorly understood. Here, we identified a lung cancer-specific chimeric RNA KANSL1-ARL17A (chKANSARL) and its circular variant fusion circular RNA KANSL1-ARL17 A (F-circKA), both derived from the fusion gene KANSARL. Functional assays revealed that overexpression of either chKANSARL or F-circKA significantly enhanced lung cancer cell proliferation, migration, and invasion, while their knockdown suppressed these malignant phenotypes. In vivo experiments demonstrated that chKANSARL overexpression accelerated tumor growth in immunodeficient mice. Notably, coexpression experiments uncovered a synergistic regulatory interaction between F-circKA and chKANSARL, amplifying oncogenic effects. Mechanistically, miRNA sequencing and dual-luciferase assays revealed that F-circKA acts as a molecular sponge for miR-6860, thereby derepressing chKANSARL expression. Rescue experiments further validated this regulatory axis, wherein miR-6860 inhibition reversed the tumor-suppressive effects of F-circKA knockdown. Collectively, our study identifies and characterizes a novel F-circKA/miR-6860/chKANSARL regulatory axis, revealing how dual transcriptional outputs from the KANSARL fusion gene can synergistically drive lung cancer progression. These findings highlight a previously unrecognized layer of cooperative regulation between linear and circular fusion RNAs in oncogenesis and provide a new framework for understanding fusion gene-mediated tumorigenesis. Show less
📄 PDF DOI: 10.1016/j.jbc.2026.111170
KANSL1