👤 Yanhong Liu

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3182
Articles
1983
Name variants
Also published as: A Liu, Ai Liu, Ai-Guo Liu, Aidong Liu, Aiguo Liu, Aihua Liu, Aijun Liu, Ailing Liu, Aimin Liu, Allen P Liu, Aman Liu, An Liu, An-Qi Liu, Ang-Jun Liu, Anjing Liu, Anjun Liu, Ankang Liu, Anling Liu, Anmin Liu, Annuo Liu, Anshu Liu, Ao Liu, Aoxing Liu, B Liu, Baihui Liu, Baixue Liu, Baiyan Liu, Ban Liu, Bang Liu, Bang-Quan Liu, Bao Liu, Bao-Cheng Liu, Baogang Liu, Baohui Liu, Baolan Liu, Baoli Liu, Baoning Liu, Baoxin Liu, Baoyi Liu, Bei Liu, Beibei Liu, Ben Liu, Bi-Cheng Liu, Bi-Feng Liu, Bihao Liu, Bilin Liu, Bin Liu, Bing Liu, Bing-Wen Liu, Bingcheng Liu, Bingjie Liu, Bingwen Liu, Bingxiao Liu, Bingya Liu, Bingyu Liu, Binjie Liu, Bo Liu, Bo-Gong Liu, Bo-Han Liu, Boao Liu, Bolin Liu, Boling Liu, Boqun Liu, Bowen Liu, Boxiang Liu, Boxin Liu, Boya Liu, Boyang Liu, Brian Y Liu, C Liu, C M Liu, C Q Liu, C-T Liu, C-Y Liu, Caihong Liu, Cailing Liu, Caiyan Liu, Can Liu, Can-Zhao Liu, Catherine H Liu, Chan Liu, Chang Liu, Chang-Bin Liu, Chang-Hai Liu, Chang-Ming Liu, Chang-Pan Liu, Chang-Peng Liu, Changbin Liu, Changjiang Liu, Changliang Liu, Changming Liu, Changqing Liu, Changtie Liu, Changya Liu, Changyun Liu, Chao Liu, Chao-Ming Liu, Chaohong Liu, Chaoqi Liu, Chaoyi Liu, Chelsea Liu, Chen Liu, Chenchen Liu, Chendong Liu, Cheng Liu, Cheng-Li Liu, Cheng-Wu Liu, Cheng-Yong Liu, Cheng-Yun Liu, Chengbo Liu, Chenge Liu, Chengguo Liu, Chenghui Liu, Chengkun Liu, Chenglong Liu, Chengxiang Liu, Chengyao Liu, Chengyun Liu, Chenmiao Liu, Chenming Liu, Chenshu Liu, Chenxing Liu, Chenxu Liu, Chenxuan Liu, Chi Liu, Chia-Chen Liu, Chia-Hung Liu, Chia-Jen Liu, Chia-Yang Liu, Chia-Yu Liu, Chiang Liu, Chin-Chih Liu, Chin-Ching Liu, Chin-San Liu, Ching-Hsuan Liu, Ching-Ti Liu, Chong Liu, Christine S Liu, ChuHao Liu, Chuan Liu, Chuanfeng Liu, Chuanxin Liu, Chuanyang Liu, Chun Liu, Chun-Chi Liu, Chun-Feng Liu, Chun-Lei Liu, Chun-Ming Liu, Chun-Xiao Liu, Chun-Yu Liu, Chunchi Liu, Chundong Liu, Chunfeng Liu, Chung-Cheng Liu, Chung-Ji Liu, Chunhua Liu, Chunlei Liu, Chunliang Liu, Chunling Liu, Chunming Liu, Chunpeng Liu, Chunping Liu, Chunsheng Liu, Chunwei Liu, Chunxiao Liu, Chunyan Liu, Chunying Liu, Chunyu Liu, Cici Liu, Clarissa M Liu, Cong Cong Liu, Cong Liu, Congcong Liu, Cui Liu, Cui-Cui Liu, Cuicui Liu, Cuijie Liu, Cuilan Liu, Cun Liu, Cun-Fei Liu, D Liu, Da Liu, Da-Ren Liu, Daiyun Liu, Dajiang J Liu, Dan Liu, Dan-Ning Liu, Dandan Liu, Danhui Liu, Danping Liu, Dantong Liu, Danyang Liu, Danyong Liu, Daoshen Liu, David Liu, David R Liu, Dawei Liu, Daxu Liu, Dayong Liu, Dazhi Liu, De-Pei Liu, De-Shun Liu, Dechao Liu, Dehui Liu, Deliang Liu, Deng-Xiang Liu, Depei Liu, Deping Liu, Derek Liu, Deruo Liu, Desheng Liu, Dewu Liu, Dexi Liu, Deyao Liu, Deying Liu, Dezhen Liu, Di Liu, Didi Liu, Ding-Ming Liu, Dingding Liu, Dinglu Liu, Dingxiang Liu, Dong Liu, Dong-Yun Liu, Dongang Liu, Dongbo Liu, Dongfang Liu, Donghui Liu, Dongjuan Liu, Dongliang Liu, Dongmei Liu, Dongming Liu, Dongping Liu, Dongxian Liu, Dongxue Liu, Dongyan Liu, Dongyang Liu, Dongyao Liu, Dongzhou Liu, Dudu Liu, Dunjiang Liu, Edison Tak-Bun Liu, En-Qi Liu, Enbin Liu, Enlong Liu, Enqi Liu, Erdong Liu, Erfeng Liu, Erxiong Liu, F Liu, F Z Liu, Fan Liu, Fan-Jie Liu, Fang Liu, Fang-Zhou Liu, Fangli Liu, Fangmei Liu, Fangping Liu, Fangqi Liu, Fangzhou Liu, Fani Liu, Fayu Liu, Fei Liu, Feifan Liu, Feilong Liu, Feiyan Liu, Feiyang Liu, Feiye Liu, Fen Liu, Fendou Liu, Feng Liu, Feng-Ying Liu, Fengbin Liu, Fengchao Liu, Fengen Liu, Fengguo Liu, Fengjiao Liu, Fengjie Liu, Fengjuan Liu, Fengqiong Liu, Fengsong Liu, Fonda Liu, Foqiu Liu, Fu-Jun Liu, Fu-Tong Liu, Fubao Liu, Fuhao Liu, Fuhong Liu, Fujun Liu, Gan Liu, Gang Liu, Gangli Liu, Ganqiang Liu, Gaohua Liu, Ge Liu, Ge-Li Liu, Gen Sheng Liu, Geng Liu, Geng-Hao Liu, Geoffrey Liu, George E Liu, George Liu, Geroge Liu, Gexiu Liu, Gongguan Liu, Guang Liu, Guangbin Liu, Guangfan Liu, Guanghao Liu, Guangliang Liu, Guangqin Liu, Guangwei Liu, Guangxu Liu, Guannan Liu, Guantong Liu, Gui Yao Liu, Gui-Fen Liu, Gui-Jing Liu, Gui-Rong Liu, Guibo Liu, Guidong Liu, Guihong Liu, Guiju Liu, Guili Liu, Guiqiong Liu, Guiquan Liu, Guisheng Liu, Guiyou Liu, Guiyuan Liu, Guning Liu, Guo-Liang Liu, Guochang Liu, Guodong Liu, Guohao Liu, Guojun Liu, Guoke Liu, Guoliang Liu, Guopin Liu, Guoqiang Liu, Guoqing Liu, Guoquan Liu, Guowen Liu, Guoyong Liu, H Liu, Hai Feng Liu, Hai-Jing Liu, Hai-Xia Liu, Hai-Yan Liu, Haibin Liu, Haichao Liu, Haifei Liu, Haifeng Liu, Hailan Liu, Hailin Liu, Hailing Liu, Haitao Liu, Haiyan Liu, Haiyang Liu, Haiying Liu, Haizhao Liu, Han Liu, Han-Fu Liu, Han-Qi Liu, Hancong Liu, Hang Liu, Hanhan Liu, Hanjiao Liu, Hanjie Liu, Hanmin Liu, Hanqing Liu, Hanxiang Liu, Hanyuan Liu, Hao Liu, Haobin Liu, Haodong Liu, Haogang Liu, Haojie Liu, Haokun Liu, Haoling Liu, Haowei Liu, Haowen Liu, Haoyue Liu, He-Kun Liu, Hehe Liu, Hekun Liu, Heliang Liu, Heng Liu, Hengan Liu, Hengru Liu, Hengtong Liu, Heyi Liu, Hong Juan Liu, Hong Liu, Hong Wei Liu, Hong-Bin Liu, Hong-Li Liu, Hong-Liang Liu, Hong-Tao Liu, Hong-Xiang Liu, Hong-Ying Liu, Hongbin Liu, Hongbing Liu, Hongfa Liu, Honghan Liu, Honghe Liu, Hongjian Liu, Hongjie Liu, Hongjun Liu, Hongli Liu, Hongliang Liu, Hongmei Liu, Hongqun Liu, Hongtao Liu, Hongwei Liu, Hongxiang Liu, Hongxing Liu, Hongyan Liu, Hongyang Liu, Hongyao Liu, Hongyu Liu, Hongyuan Liu, Houbao Liu, Hsiao-Ching Liu, Hsiao-Sheng Liu, Hsiaowei Liu, Hsu-Hsiang Liu, Hu Liu, Hua Liu, Hua-Cheng Liu, Hua-Ge Liu, Huadong Liu, Huaizheng Liu, Huan Liu, Huan-Yu Liu, Huanhuan Liu, Huanliang Liu, Huanyi Liu, Huatao Liu, Huawei Liu, Huayang Liu, Huazhen Liu, Hui Liu, Hui-Chao Liu, Hui-Fang Liu, Hui-Guo Liu, Hui-Hui Liu, Hui-Xin Liu, Hui-Ying Liu, Huibin Liu, Huidi Liu, Huihua Liu, Huihui Liu, Huijuan Liu, Huijun Liu, Huikun Liu, Huiling Liu, Huimao Liu, Huimin Liu, Huiming Liu, Huina Liu, Huiping Liu, Huiqing Liu, Huisheng Liu, Huiying Liu, Huiyu Liu, Hulin Liu, J Liu, J R Liu, J W Liu, J X Liu, J Z Liu, James K C Liu, Jamie Liu, Jay Liu, Ji Liu, Ji-Kai Liu, Ji-Long Liu, Ji-Xing Liu, Ji-Xuan Liu, Ji-Yun Liu, Jia Liu, Jia-Cheng Liu, Jia-Jun Liu, Jia-Qian Liu, Jia-Yao Liu, JiaXi Liu, Jiabin Liu, Jiachen Liu, Jiahao Liu, Jiahua Liu, Jiahui Liu, Jiajie Liu, Jiajuan Liu, Jiakun Liu, Jiali Liu, Jialin Liu, Jiamin Liu, Jiaming Liu, Jian Liu, Jian-Jun Liu, Jian-Kun Liu, Jian-hong Liu, Jian-shu Liu, Jianan Liu, Jianbin Liu, Jianbo Liu, Jiandong Liu, Jianfang Liu, Jianfeng Liu, Jiang Liu, Jiangang Liu, Jiangbin Liu, Jianghong Liu, Jianghua Liu, Jiangjiang Liu, Jiangjin Liu, Jiangling Liu, Jiangxin Liu, Jiangyan Liu, Jianhua Liu, Jianhui Liu, Jiani Liu, Jianing Liu, Jianjiang Liu, Jianjun Liu, Jiankang Liu, Jiankun Liu, Jianlei Liu, Jianmei Liu, Jianmin Liu, Jiannan Liu, Jianping Liu, Jiantao Liu, Jianwei Liu, Jianxi Liu, Jianxin Liu, Jianyong Liu, Jianyu Liu, Jianyun Liu, Jiao Liu, Jiaojiao Liu, Jiaoyang Liu, Jiaqi Liu, Jiaqing Liu, Jiawen Liu, Jiaxian Liu, Jiaxiang Liu, Jiaxin Liu, Jiayan Liu, Jiayi Liu, Jiayin Liu, Jiaying Liu, Jiayu Liu, Jiayun Liu, Jiazhe Liu, Jiazheng Liu, Jiazhuo Liu, Jidan Liu, Jie Liu, Jie-Qing Liu, Jierong Liu, Jiewei Liu, Jiewen Liu, Jieying Liu, Jieyu Liu, Jihe Liu, Jiheng Liu, Jin Liu, Jin-Juan Liu, Jin-Qing Liu, Jinbao Liu, Jinbo Liu, Jincheng Liu, Jindi Liu, Jinfeng Liu, Jing Liu, Jing Min Liu, Jing-Crystal Liu, Jing-Hua Liu, Jing-Ying Liu, Jing-Yu Liu, Jingbo Liu, Jingchong Liu, Jingfang Liu, Jingfeng Liu, Jingfu Liu, Jinghui Liu, Jingjie Liu, Jingjing Liu, Jingmeng Liu, Jingmin Liu, Jingqi Liu, Jingquan Liu, Jingqun Liu, Jingsheng Liu, Jingwei Liu, Jingwen Liu, Jingxing Liu, Jingyi Liu, Jingying Liu, Jingyun Liu, Jingzhong Liu, Jinjie Liu, Jinlian Liu, Jinlong Liu, Jinman Liu, Jinpei Liu, Jinpeng Liu, Jinping Liu, Jinqin Liu, Jinrong Liu, Jinsheng Liu, Jinsong Liu, Jinsuo Liu, Jinxiang Liu, Jinxin Liu, Jinxing Liu, Jinyue Liu, Jinze Liu, Jinzhao Liu, Jinzhi Liu, Jiong Liu, Jishan Liu, Jitao Liu, Jiwei Liu, Jixin Liu, Jonathan Liu, Joyce F Liu, Joyce Liu, Ju Liu, Ju-Fang Liu, Juan Liu, Juanjuan Liu, Juanxi Liu, Jue Liu, Jui-Tung Liu, Jun Liu, Jun O Liu, Jun Ting Liu, Jun Yi Liu, Jun-Jen Liu, Jun-Yan Liu, Jun-Yi Liu, Junbao Liu, Junchao Liu, Junfen Liu, Junhui Liu, Junjiang Liu, Junjie Liu, Junjin Liu, Junjun Liu, Junlin Liu, Junling Liu, Junnian Liu, Junpeng Liu, Junqi Liu, Junrong Liu, Juntao Liu, Juntian Liu, Junwen Liu, Junwu Liu, Junxi Liu, Junyan Liu, Junye Liu, Junying Liu, Junyu Liu, Juyao Liu, Kai Liu, Kai-Zheng Liu, Kaidong Liu, Kaijing Liu, Kaikun Liu, Kaiqi Liu, Kaisheng Liu, Kaitai Liu, Kaiwen Liu, Kang Liu, Kang-le Liu, Kangdong Liu, Kangwei Liu, Kathleen D Liu, Ke Liu, Ke-Tong Liu, Kechun Liu, Kehui Liu, Kejia Liu, Keng-Hau Liu, Keqiang Liu, Kexin Liu, Kiang Liu, Kuangyi Liu, Kun Liu, Kun-Cheng Liu, Kwei-Yan Liu, L L Liu, L Liu, L W Liu, Lan Liu, Lan-Xiang Liu, Lang Liu, Lanhao Liu, Le Liu, Lebin Liu, Lei Liu, Lele Liu, Leping Liu, Li Liu, Li-Fang Liu, Li-Min Liu, Li-Rong Liu, Li-Wen Liu, Li-Xuan Liu, Li-Ying Liu, Li-ping Liu, Lian Liu, Lianfei Liu, Liang Liu, Liang-Chen Liu, Liang-Feng Liu, Liangguo Liu, Liangji Liu, Liangjia Liu, Liangliang Liu, Liangyu Liu, Lianxin Liu, Lianyong Liu, Libin Liu, Lichao Liu, Lichun Liu, Lidong Liu, Liegang Liu, Lifang Liu, Ligang Liu, Lihua Liu, Lijuan Liu, Lijun Liu, Lili Liu, Liling Liu, Limin Liu, Liming Liu, Lin Liu, Lina Liu, Ling Liu, Ling-Yun Liu, Ling-Zhi Liu, Lingfei Liu, Lingjiao Liu, Lingjuan Liu, Linglong Liu, Lingyan Liu, Lining Liu, Linlin Liu, Linqing Liu, Linwen Liu, Liping Liu, Liqing Liu, Liqiong Liu, Liqun Liu, Lirong Liu, Liru Liu, Liu Liu, Liumei Liu, Liusheng Liu, Liwen Liu, Lixia Liu, Lixian Liu, Lixiao Liu, Liying Liu, Liyue Liu, Lizhen Liu, Long Liu, Longfei Liu, Longjian Liu, Longqian Liu, Longyang Liu, Longzhou Liu, Lu Liu, Luhong Liu, Lulu Liu, Luming Liu, Lunxu Liu, Luping Liu, Lushan Liu, Lv Liu, M L Liu, M Liu, Man Liu, Man-Ru Liu, Manjiao Liu, Manqi Liu, Manran Liu, Maolin Liu, Mei Liu, Mei-mei Liu, Meicen Liu, Meifang Liu, Meijiao Liu, Meijing Liu, Meijuan Liu, Meijun Liu, Meiling Liu, Meimei Liu, Meixin Liu, Meiyan Liu, Meng Han Liu, Meng Liu, Meng-Hui Liu, Meng-Meng Liu, Meng-Yue Liu, Mengduan Liu, Mengfan Liu, Mengfei Liu, Menggang Liu, Menghan Liu, Menghua Liu, Menghui Liu, Mengjia Liu, Mengjiao Liu, Mengke Liu, Menglin Liu, Mengling Liu, Mengmei Liu, Mengqi Liu, Mengqian Liu, Mengxi Liu, Mengxue Liu, Mengyang Liu, Mengying Liu, Mengyu Liu, Mengyuan Liu, Mengzhen Liu, Mi Liu, Mi-Hua Liu, Mi-Min Liu, Miao Liu, Miaoliang Liu, Min Liu, Minda Liu, Minetta C Liu, Ming Liu, Ming-Jiang Liu, Ming-Qi Liu, Mingcheng Liu, Mingchun Liu, Mingfan Liu, Minghui Liu, Mingjiang Liu, Mingjing Liu, Mingjun Liu, Mingli Liu, Mingming Liu, Mingna Liu, Mingqin Liu, Mingrui Liu, Mingsen Liu, Mingsong Liu, Mingxiao Liu, Mingxing Liu, Mingxu Liu, Mingyang Liu, Mingyao Liu, Mingying Liu, Mingyu Liu, Minhao Liu, Minxia Liu, Mo-Nan Liu, Modan Liu, Mouze Liu, Muqiu Liu, Musang Liu, N A Liu, N Liu, Na Liu, Na-Nv Liu, Na-Wei Liu, Nai-feng Liu, Naihua Liu, Naili Liu, Nan Liu, Nan-Song Liu, Nana Liu, Nannan Liu, Nanxi Liu, Ni Liu, Nian Liu, Ning Liu, Ning'ang Liu, Ningning Liu, Niya Liu, Ou Liu, Ouxuan Liu, P C Liu, Pan Liu, Panhong Liu, Panting Liu, Paul Liu, Pei Liu, Pei-Ning Liu, Peijian Liu, Peijie Liu, Peijun Liu, Peilong Liu, Peiqi Liu, Peiqing Liu, Peiwei Liu, Peixi Liu, Peiyao Liu, Peizhong Liu, Peng Liu, Pengcheng Liu, Pengfei Liu, Penghong Liu, Pengli Liu, Pengtao Liu, Pengyu Liu, Pengyuan Liu, Pentao Liu, Peter S Liu, Piaopiao Liu, Pinduo Liu, Ping Liu, Ping-Yen Liu, Pinghuai Liu, Pingping Liu, Pingsheng Liu, Q Liu, Qi Liu, Qi-Xian Liu, Qian Liu, Qian-Wen Liu, Qiang Liu, Qiang-Yuan Liu, Qiangyun Liu, Qianjin Liu, Qianqi Liu, Qianshuo Liu, Qianwei Liu, Qiao-Hong Liu, Qiaofeng Liu, Qiaoyan Liu, Qiaozhen Liu, Qiji Liu, Qiming Liu, Qin Liu, Qinfang Liu, Qing Liu, Qing-Huai Liu, Qing-Rong Liu, Qingbin Liu, Qingbo Liu, Qingguang Liu, Qingguo Liu, Qinghao Liu, Qinghong Liu, Qinghua Liu, Qinghuai Liu, Qinghuan Liu, Qinglei Liu, Qingping Liu, Qingqing Liu, Qingquan Liu, Qingsong Liu, Qingxia Liu, Qingxiang Liu, Qingyang Liu, Qingyou Liu, Qingyun Liu, Qingzhuo Liu, Qinqin Liu, Qiong Liu, Qiu-Ping Liu, Qiulei Liu, Qiuli Liu, Qiulu Liu, Qiushi Liu, Qiuxu Liu, Qiuyu Liu, Qiuyue Liu, Qiwei Liu, Qiyao Liu, Qiye Liu, Qizhan Liu, Quan Liu, Quan-Jun Liu, Quanxin Liu, Quanying Liu, Quanzhong Liu, Quentin Liu, Qun Liu, Qunlong Liu, Qunpeng Liu, R F Liu, R Liu, R Y Liu, Ran Liu, Rangru Liu, Ranran Liu, Ren Liu, Renling Liu, Ri Liu, Rong Liu, Rong-Zong Liu, Rongfei Liu, Ronghua Liu, Rongxia Liu, Rongxun Liu, Rui Liu, Rui-Jie Liu, Rui-Tian Liu, Rui-Xuan Liu, Ruichen Liu, Ruihua Liu, Ruijie Liu, Ruijuan Liu, Ruilong Liu, Ruiping Liu, Ruiqi Liu, Ruitong Liu, Ruixia Liu, Ruiyi Liu, Ruizao Liu, Runjia Liu, Runjie Liu, Runni Liu, Runping Liu, Ruochen Liu, Ruotian Liu, Ruowen Liu, Ruoyang Liu, Ruyi Liu, Ruyue Liu, S Liu, Saiji Liu, Sasa Liu, Sen Liu, Senchen Liu, Senqi Liu, Sha Liu, Shan Liu, Shan-Shan Liu, Shandong Liu, Shang-Feng Liu, Shang-Xin Liu, Shangjing Liu, Shangxin Liu, Shangyu Liu, Shangyuan Liu, Shangyun Liu, Shanhui Liu, Shanling Liu, Shanshan Liu, Shao-Bin Liu, Shao-Jun Liu, Shao-Yuan Liu, Shaobo Liu, Shaocheng Liu, Shaohua Liu, Shaojun Liu, Shaoqing Liu, Shaowei Liu, Shaoying Liu, Shaoyou Liu, Shaoyu Liu, Shaozhen Liu, Shasha Liu, Sheng Liu, Shengbin Liu, Shengjun Liu, Shengnan Liu, Shengyang Liu, Shengzhi Liu, Shengzhuo Liu, Shenhai Liu, Shenping Liu, Shi Liu, Shi-Lian Liu, Shi-Wei Liu, Shi-Yong Liu, Shi-guo Liu, ShiWei Liu, Shih-Ping Liu, Shijia Liu, Shijian Liu, Shijie Liu, Shijun Liu, Shikai Liu, Shikun Liu, Shilin Liu, Shing-Hwa Liu, Shiping Liu, Shiqian Liu, Shiquan Liu, Shiru Liu, Shixi Liu, Shiyan Liu, Shiyang Liu, Shiying Liu, Shiyu Liu, Shiyuan Liu, Shou-Sheng Liu, Shouguo Liu, Shoupei Liu, Shouxin Liu, Shouyang Liu, Shu Liu, Shu-Chen Liu, Shu-Jing Liu, Shu-Lin Liu, Shu-Qiang Liu, Shu-Qin Liu, Shuai Liu, Shuaishuai Liu, Shuang Liu, Shuangli Liu, Shuangzhu Liu, Shuhong Liu, Shuhua Liu, Shui-Bing Liu, Shujie Liu, Shujing Liu, Shujun Liu, Shulin Liu, Shuling Liu, Shumin Liu, Shun-Mei Liu, Shunfang Liu, Shuning Liu, Shunming Liu, Shuqian Liu, Shuqing Liu, Shuwen Liu, Shuxi Liu, Shuxian Liu, Shuya Liu, Shuyan Liu, Shuyu Liu, Si-Jin Liu, Si-Xu Liu, Si-Yan Liu, Si-jun Liu, Sicheng Liu, Sidan Liu, Side Liu, Sihao Liu, Sijing Liu, Sijun Liu, Silvia Liu, Simin Liu, Sipu Liu, Siqi Liu, Siqin Liu, Siru Liu, Sirui Liu, Sisi Liu, Sitian Liu, Siwen Liu, Sixi Liu, Sixin Liu, Sixiu Liu, Sixu Liu, Siyao Liu, Siyi Liu, Siyu Liu, Siyuan Liu, Song Liu, Song-Fang Liu, Song-Mei Liu, Song-Ping Liu, Songfang Liu, Songhui Liu, Songqin Liu, Songsong Liu, Songyi Liu, Su Liu, Su-Yun Liu, Sudong Liu, Suhuan Liu, Sui-Feng Liu, Suling Liu, Suosi Liu, Sushuang Liu, Susu Liu, Szu-Heng Liu, T H Liu, T Liu, Ta-Chih Liu, Taihang Liu, Taixiang Liu, Tang Liu, Tao Liu, Taoli Liu, Taotao Liu, Te Liu, Teng Liu, Tengfei Liu, Tengli Liu, Teresa T Liu, Tian Liu, Tian Shu Liu, Tianhao Liu, Tianhu Liu, Tianjia Liu, Tianjiao Liu, Tianlai Liu, Tianlang Liu, Tianlong Liu, Tianqiang Liu, Tianrui Liu, Tianshu Liu, Tiantian Liu, Tianyao Liu, Tianyi Liu, Tianyu Liu, Tianze Liu, Tiemin Liu, Tina Liu, Ting Liu, Ting-Li Liu, Ting-Ting Liu, Ting-Yuan Liu, Tingjiao Liu, Tingting Liu, Tong Liu, Tonglin Liu, Tongtong Liu, Tongyan Liu, Tongyu Liu, Tongyun Liu, Tongzheng Liu, Tsang-Wu Liu, Tsung-Yun Liu, Vincent W S Liu, W Liu, W-Y Liu, Wan Liu, Wan-Chun Liu, Wan-Di Liu, Wan-Guo Liu, Wan-Ying Liu, Wang Liu, Wangrui Liu, Wanguo Liu, Wangyang Liu, Wanjun Liu, Wanli Liu, Wanlu Liu, Wanqi Liu, Wanqing Liu, Wanting Liu, Wei Liu, Wei-Chieh Liu, Wei-Hsuan Liu, Wei-Hua Liu, Weida Liu, Weifang Liu, Weifeng Liu, Weiguo Liu, Weihai Liu, Weihong Liu, Weijian Liu, Weijie Liu, Weijun Liu, Weilin Liu, Weimin Liu, Weiming Liu, Weina Liu, Weiqin Liu, Weiqing Liu, Weiren Liu, Weisheng Liu, Weishuo Liu, Weiwei Liu, Weiyang Liu, Wen Liu, Wen Yuan Liu, Wen-Chun Liu, Wen-Di Liu, Wen-Fang Liu, Wen-Jie Liu, Wen-Jing Liu, Wen-Qiang Liu, Wen-Tao Liu, Wen-ling Liu, Wenbang Liu, Wenbin Liu, Wenbo Liu, Wenchao Liu, Wenen Liu, Wenfeng Liu, Wenhan Liu, Wenhao Liu, Wenhua Liu, Wenjie Liu, Wenjing Liu, Wenlang Liu, Wenli Liu, Wenling Liu, Wenlong Liu, Wenna Liu, Wenping Liu, Wenqi Liu, Wenrui Liu, Wensheng Liu, Wentao Liu, Wenwu Liu, Wenxiang Liu, Wenxuan Liu, Wenya Liu, Wenyan Liu, Wenyi Liu, Wenzhong Liu, Wu Liu, Wuping Liu, Wuyang Liu, X C Liu, X Liu, X P Liu, X-D Liu, Xi Liu, Xi-Yu Liu, Xia Liu, Xia-Meng Liu, Xialin Liu, Xian Liu, Xianbao Liu, Xianchen Liu, Xianda Liu, Xiang Liu, Xiang-Qian Liu, Xiang-Yu Liu, Xiangchen Liu, Xiangfei Liu, Xianglan Liu, Xiangli Liu, Xiangliang Liu, Xianglu Liu, Xiangning Liu, Xiangping Liu, Xiangsheng Liu, Xiangtao Liu, Xiangting Liu, Xiangxiang Liu, Xiangxuan Liu, Xiangyong Liu, Xiangyu Liu, Xiangyun Liu, Xianli Liu, Xianling Liu, Xiansheng Liu, Xianyang Liu, Xiao Dong Liu, Xiao Liu, Xiao Yan Liu, Xiao-Cheng Liu, Xiao-Dan Liu, Xiao-Gang Liu, Xiao-Guang Liu, Xiao-Huan Liu, Xiao-Jiao Liu, Xiao-Li Liu, Xiao-Ling Liu, Xiao-Ning Liu, Xiao-Qiu Liu, Xiao-Qun Liu, Xiao-Rong Liu, Xiao-Song Liu, Xiao-Xiao Liu, Xiao-lan Liu, Xiaoan Liu, Xiaobai Liu, Xiaobei Liu, Xiaobing Liu, Xiaocen Liu, Xiaochuan Liu, Xiaocong Liu, Xiaodan Liu, Xiaoding Liu, Xiaodong Liu, Xiaofan Liu, Xiaofang Liu, Xiaofei Liu, Xiaogang Liu, Xiaoguang Liu, Xiaoguang Margaret Liu, Xiaohan Liu, Xiaoheng Liu, Xiaohong Liu, Xiaohua Liu, Xiaohuan Liu, Xiaohui Liu, Xiaojie Liu, Xiaojing Liu, Xiaoju Liu, Xiaojun Liu, Xiaole Shirley Liu, Xiaolei Liu, Xiaoli Liu, Xiaolin Liu, Xiaoling Liu, Xiaoman Liu, Xiaomei Liu, Xiaomeng Liu, Xiaomin Liu, Xiaoming Liu, Xiaona Liu, Xiaonan Liu, Xiaopeng Liu, Xiaoping Liu, Xiaoqian Liu, Xiaoqiang Liu, Xiaoqin Liu, Xiaoqing Liu, Xiaoran Liu, Xiaosong Liu, Xiaotian Liu, Xiaoting Liu, Xiaowei Liu, Xiaoxi Liu, Xiaoxia Liu, Xiaoxiao Liu, Xiaoxu Liu, Xiaoxue Liu, Xiaoya Liu, Xiaoyan Liu, Xiaoyang Liu, Xiaoye Liu, Xiaoying Liu, Xiaoyong Liu, Xiaoyu Liu, Xiawen Liu, Xibao Liu, Xibing Liu, Xie-hong Liu, Xiehe Liu, Xiguang Liu, Xijun Liu, Xili Liu, Xin Liu, Xin-Hua Liu, Xin-Yan Liu, Xinbo Liu, Xinchang Liu, Xing Liu, Xing-De Liu, Xing-Li Liu, Xing-Yang Liu, Xingbang Liu, Xingde Liu, Xinghua Liu, Xinghui Liu, Xingjing Liu, Xinglei Liu, Xingli Liu, Xinglong Liu, Xinguo Liu, Xingxiang Liu, Xingyi Liu, Xingyu Liu, Xinhua Liu, Xinjun Liu, Xinlei Liu, Xinli Liu, Xinmei Liu, Xinmin Liu, Xinran Liu, Xinru Liu, Xinrui Liu, Xintong Liu, Xinxin Liu, Xinyao Liu, Xinyi Liu, Xinying Liu, Xinyong Liu, Xinyu Liu, Xinyue Liu, Xiong Liu, Xiqiang Liu, Xiru Liu, Xishan Liu, Xiu Liu, Xiufen Liu, Xiufeng Liu, Xiuheng Liu, Xiuling Liu, Xiumei Liu, Xiuqin Liu, Xiyong Liu, Xu Liu, Xu-Dong Liu, Xu-Hui Liu, Xuan Liu, Xuanlin Liu, Xuanyu Liu, Xuanzhu Liu, Xue Liu, Xue-Lian Liu, Xue-Min Liu, Xue-Qing Liu, Xue-Zheng Liu, Xuefang Liu, Xuejing Liu, Xuekui Liu, Xuelan Liu, Xueling Liu, Xuemei Liu, Xuemeng Liu, Xuemin Liu, Xueping Liu, Xueqin Liu, Xueqing Liu, Xueru Liu, Xuesen Liu, Xueshibojie Liu, Xuesong Liu, Xueting Liu, Xuewei Liu, Xuewen Liu, Xuexiu Liu, Xueying Liu, Xueyuan Liu, Xuezhen Liu, Xuezheng Liu, Xuezhi Liu, Xufeng Liu, Xuguang Liu, Xujie Liu, Xulin Liu, Xuming Liu, Xunhua Liu, Xunyue Liu, Xuxia Liu, Xuxu Liu, Xuyi Liu, Xuying Liu, Y H Liu, Y L Liu, Y Liu, Y Y Liu, Ya Liu, Ya-Jin Liu, Ya-Kun Liu, Ya-Wei Liu, Yadong Liu, Yafei Liu, Yajing Liu, Yajuan Liu, Yaling Liu, Yalu Liu, Yan Liu, Yan-Li Liu, Yanan Liu, Yanchao Liu, Yanchen Liu, Yandong Liu, Yanfei Liu, Yanfen Liu, Yanfeng Liu, Yang Liu, Yange Liu, Yangfan Liu, Yangfan P Liu, Yangjun Liu, Yangkai Liu, Yangruiyu Liu, Yangyang Liu, Yanhua Liu, Yanhui Liu, Yanjie Liu, Yanju Liu, Yanjun Liu, Yankuo Liu, Yanli Liu, Yanliang Liu, Yanling Liu, Yanman Liu, Yanmin Liu, Yanping Liu, Yanqing Liu, Yanqiu Liu, Yanquan Liu, Yanru Liu, Yansheng Liu, Yansong Liu, Yanting Liu, Yanwu Liu, Yanxiao Liu, Yanyan Liu, Yanyao Liu, Yanying Liu, Yanyun Liu, Yao Liu, Yao-Hui Liu, Yaobo Liu, Yaoquan Liu, Yaou Liu, Yaowen Liu, Yaoyao Liu, Yaozhong Liu, Yaping Liu, Yaqiong Liu, Yarong Liu, Yaru Liu, Yating Liu, Yaxin Liu, Ye Liu, Ye-Dan Liu, Yehai Liu, Yen-Chen Liu, Yen-Chun Liu, Yen-Nien Liu, Yeqing Liu, Yi Liu, Yi-Chang Liu, Yi-Chien Liu, Yi-Han Liu, Yi-Hung Liu, Yi-Jia Liu, Yi-Ling Liu, Yi-Meng Liu, Yi-Ming Liu, Yi-Yun Liu, Yi-Zhang Liu, YiRan Liu, Yibin Liu, Yibing Liu, Yicun Liu, Yidan Liu, Yidong Liu, Yifan Liu, Yifu Liu, Yihao Liu, Yiheng Liu, Yihui Liu, Yijing Liu, Yilei Liu, Yili Liu, Yilin Liu, Yimei Liu, Yiming Liu, Yin Liu, Yin-Ping Liu, Yinchu Liu, Yinfang Liu, Ying Liu, Ying Poi Liu, Yingchun Liu, Yinghua Liu, Yinghuan Liu, Yinghui Liu, Yingjun Liu, Yingli Liu, Yingwei Liu, Yingxia Liu, Yingyan Liu, Yingyi Liu, Yingying Liu, Yingzi Liu, Yinhe Liu, Yinhui Liu, Yining Liu, Yinjiang Liu, Yinping Liu, Yinuo Liu, Yiping Liu, Yiqing Liu, Yitian Liu, Yiting Liu, Yitong Liu, Yiwei Liu, Yiwen Liu, Yixiang Liu, Yixiao Liu, Yixuan Liu, Yiyang Liu, Yiyi Liu, Yiyuan Liu, Yiyun Liu, Yizhi Liu, Yizhuo Liu, Yong Liu, Yong Mei Liu, Yong-Chao Liu, Yong-Hong Liu, Yong-Jian Liu, Yong-Jun Liu, Yong-Tai Liu, Yong-da Liu, Yongchao Liu, Yonggang Liu, Yonggao Liu, Yonghong Liu, Yonghua Liu, Yongjian Liu, Yongjie Liu, Yongjun Liu, Yongli Liu, Yongmei Liu, Yongming Liu, Yongqiang Liu, Yongshuo Liu, Yongtai Liu, Yongtao Liu, Yongtong Liu, Yongxiao Liu, Yongyue Liu, You Liu, You-ping Liu, Youan Liu, Youbin Liu, Youdong Liu, Youhan Liu, Youlian Liu, Youwen Liu, Yu Liu, Yu Xuan Liu, Yu-Chen Liu, Yu-Ching Liu, Yu-Hui Liu, Yu-Li Liu, Yu-Lin Liu, Yu-Peng Liu, Yu-Wei Liu, Yu-Zhang Liu, YuHeng Liu, Yuan Liu, Yuan-Bo Liu, Yuan-Jie Liu, Yuan-Tao Liu, YuanHua Liu, Yuanchu Liu, Yuanfa Liu, Yuanhang Liu, Yuanhui Liu, Yuanjia Liu, Yuanjiao Liu, Yuanjun Liu, Yuanliang Liu, Yuantao Liu, Yuantong Liu, Yuanxiang Liu, Yuanxin Liu, Yuanxing Liu, Yuanying Liu, Yuanyuan Liu, Yubin Liu, Yuchen Liu, Yue Liu, Yuecheng Liu, Yuefang Liu, Yuehong Liu, Yueli Liu, Yueping Liu, Yuetong Liu, Yuexi Liu, Yuexin Liu, Yuexing Liu, Yueyang Liu, Yueyun Liu, Yufan Liu, Yufei Liu, Yufeng Liu, Yuhao Liu, Yuhe Liu, Yujia Liu, Yujiang Liu, Yujie Liu, Yujun Liu, Yulan Liu, Yuling Liu, Yulong Liu, Yumei Liu, Yumiao Liu, Yun Liu, Yun-Cai Liu, Yun-Qiang Liu, Yun-Ru Liu, Yun-Zi Liu, Yunfen Liu, Yunfeng Liu, Yuning Liu, Yunjie Liu, Yunlong Liu, Yunqi Liu, Yunqiang Liu, Yuntao Liu, Yunuan Liu, Yunuo Liu, Yunxia Liu, Yunyun Liu, Yuping Liu, Yupu Liu, Yuqi Liu, Yuqiang Liu, Yuqing Liu, Yurong Liu, Yuru Liu, Yusen Liu, Yutao Liu, Yutian Liu, Yuting Liu, Yutong Liu, Yuwei Liu, Yuxi Liu, Yuxia Liu, Yuxiang Liu, Yuxin Liu, Yuxuan Liu, Yuyan Liu, Yuyi Liu, Yuyu Liu, Yuyuan Liu, Yuzhen Liu, Yv-Xuan Liu, Z H Liu, Z Q Liu, Z Z Liu, Zaiqiang Liu, Zan Liu, Zaoqu Liu, Ze Liu, Zefeng Liu, Zekun Liu, Zeming Liu, Zengfu Liu, Zeyu Liu, Zezhou Liu, Zhangyu Liu, Zhangyuan Liu, Zhansheng Liu, Zhao Liu, Zhaoguo Liu, Zhaoli Liu, Zhaorui Liu, Zhaotian Liu, Zhaoxiang Liu, Zhaoxun Liu, Zhaoyang Liu, Zhe Liu, Zhekai Liu, Zheliang Liu, Zhen Liu, Zhen-Lin Liu, Zhendong Liu, Zhenfang Liu, Zhenfeng Liu, Zheng Liu, Zheng-Hong Liu, Zheng-Yu Liu, ZhengYi Liu, Zhengbing Liu, Zhengchuang Liu, Zhengdong Liu, Zhenghao Liu, Zhengkun Liu, Zhengtang Liu, Zhengting Liu, Zhenguo Liu, Zhengxia Liu, Zhengye Liu, Zhenhai Liu, Zhenhao Liu, Zhenhua Liu, Zhenjiang Liu, Zhenjiao Liu, Zhenjie Liu, Zhenkui Liu, Zhenlei Liu, Zhenmi Liu, Zhenming Liu, Zhenna Liu, Zhenqian Liu, Zhenqiu Liu, Zhenwei Liu, Zhenxing Liu, Zhenxiu Liu, Zhenzhen Liu, Zhenzhu Liu, Zhi Liu, Zhi Y Liu, Zhi-Fen Liu, Zhi-Guo Liu, Zhi-Jie Liu, Zhi-Kai Liu, Zhi-Ping Liu, Zhi-Ren Liu, Zhi-Wen Liu, Zhi-Ying Liu, Zhicheng Liu, Zhifang Liu, Zhigang Liu, Zhiguo Liu, Zhihan Liu, Zhihao Liu, Zhihong Liu, Zhihua Liu, Zhihui Liu, Zhijia Liu, Zhijie Liu, Zhikui Liu, Zhili Liu, Zhiming Liu, Zhipeng Liu, Zhiping Liu, Zhiqian Liu, Zhiqiang Liu, Zhiru Liu, Zhirui Liu, Zhishuo Liu, Zhitao Liu, Zhiteng Liu, Zhiwei Liu, Zhixiang Liu, Zhixue Liu, Zhiyan Liu, Zhiying Liu, Zhiyong Liu, Zhiyuan Liu, Zhong Liu, Zhong Wu Liu, Zhong-Hua Liu, Zhong-Min Liu, Zhong-Qiu Liu, Zhong-Wu Liu, Zhong-Ying Liu, Zhongchun Liu, Zhongguo Liu, Zhonghua Liu, Zhongjian Liu, Zhongjuan Liu, Zhongmin Liu, Zhongqi Liu, Zhongqiu Liu, Zhongwei Liu, Zhongyu Liu, Zhongyue Liu, Zhongzhong Liu, Zhou Liu, Zhou-di Liu, Zhu Liu, Zhuangjun Liu, Zhuanhua Liu, Zhuo Liu, Zhuoyuan Liu, Zi Hao Liu, Zi-Hao Liu, Zi-Lun Liu, Zi-Ye Liu, Zi-wen Liu, Zichuan Liu, Zihang Liu, Zihao Liu, Zihe Liu, Ziheng Liu, Zijia Liu, Zijian Liu, Zijing J Liu, Zimeng Liu, Ziqian Liu, Ziqin Liu, Ziteng Liu, Zitian Liu, Ziwei Liu, Zixi Liu, Zixuan Liu, Ziyang Liu, Ziying Liu, Ziyou Liu, Ziyuan Liu, Ziyue Liu, Zong-Chao Liu, Zong-Yuan Liu, Zonghua Liu, Zongjun Liu, Zongtao Liu, Zongxiang Liu, Zu-Guo Liu, Zuguo Liu, Zuohua Liu, Zuojin Liu, Zuolu Liu, Zuyi Liu, Zuyun Liu
articles

Effect of Genetic Polymorphism Including NUP153 and SVEP1 on the Pharmacokinetics and Pharmacodynamics of Ticagrelor in Healthy Chinese Subjects.

Qian Xiang, Zhiyan Liu, Guangyan Mu +10 more · 2022 · Clinical drug investigation · Springer · added 2026-04-24
The search for potential gene loci that affect the pharmacodynamics and pharmacokinetics of ticagrelor is a matter of broad clinical interest. The objective of this study was to investigate the effect Show more
The search for potential gene loci that affect the pharmacodynamics and pharmacokinetics of ticagrelor is a matter of broad clinical interest. The objective of this study was to investigate the effect of genetic polymorphisms on the pharmacokinetics and pharmacodynamics of ticagrelor in healthy Chinese subjects. This is a multi-center study in China, including three hospitals from Beijing, Nanchang, and Changsha. Healthy Chinese subjects aged 18-45 years with unknown genotypes were included. All subjects received a single oral dose of 90 mg of ticagrelor. Platelet aggregation and the area under the concentration-time curve for ticagrelor and its major active metabolite in plasma samples were assessed. Genome-wide association studies and candidate gene association analysis related to ticagrelor were performed. One hundred and seventy-five native Chinese subjects were enrolled and completed the study. According to the p value, the threshold of ticagrelor population was 6.57 × 10 Genetic variation affects the pharmacokinetics and pharmacodynamics of ticagrelor in healthy individuals. The detection of NUP153, SVEP1 gene variation will be helpful for pharmacodynamic prediction and evaluation, and the regulation of these genes may be the target of new drug development. Further studies are required to confirm the results and explore whether these single-nucleotide polymorphisms are associated only with platelet activity or also with cardiovascular events and all-cause mortality. NCT03161002. Show less
no PDF DOI: 10.1007/s40261-022-01154-6
CETP

Association of serum C1Q/TNF-related protein 4 levels with carotid atherosclerosis in subjects with type 2 diabetes mellitus: A cross-sectional study.

Zheng Liu, Junxia Han, Ye Wang +3 more · 2022 · Clinica chimica acta; international journal of clinical chemistry · Elsevier · added 2026-04-24
Carotid atherosclerosis (CAS) is a common manifestation of macroangiopathy in type 2 diabetes mellitus (T2DM). C1Q/TNF-related protein 4 (CTRP4) was found to be involved in regulation of food intake b Show more
Carotid atherosclerosis (CAS) is a common manifestation of macroangiopathy in type 2 diabetes mellitus (T2DM). C1Q/TNF-related protein 4 (CTRP4) was found to be involved in regulation of food intake behaviors and glucolipid metabolism, which were also key factors in the development of CAS. However, the relationship between serum CTRP4 and CAS in T2DM remains unclear. A total of 111 participants with T2DM were enrolled in the study and were divided into 2 groups (T2DM group and T2DM + CAS group) according to the result of carotid ultrasound examinations. Serum CTRP4 levels were measured by enzyme linked immunosorbent assay (ELISA). Trend χ Serum CTRP4 concentrations in T2DM + CAS group were significantly lower compared with those in T2DM group [7.98 (5.53) vs. 11.29 (7.36) ng/ml, P < 0.01]. The risk of CAS in T2DM decreased with the increasing of CTRP4 quartiles (P for trend < 0.01). Binary stepwise logistic regression suggested that serum CTRP4 might be an independent influence factor for CAS in patients with T2DM (P < 0.01) and high concentrations of serum CTRP4 were related to low risk of CAS in T2DM. The concentrations of serum CTRP4 are lower in T2DM patients with CAS compared to those without CAS. Serum CTRP4 levels are negatively related to the risk of CAS in T2DM. Show less
no PDF DOI: 10.1016/j.cca.2022.04.1004
C1QTNF4

Exostosin glycosyltransferase 1 reduces porcine reproductive and respiratory syndrome virus infection through proteasomal degradation of nsp3 and nsp5.

Xiaoxiao Zhang, Wenjuan Dong, Xun Wang +6 more · 2022 · The Journal of biological chemistry · Elsevier · added 2026-04-24
Porcine reproductive and respiratory syndrome virus (PRRSV) continues to be a serious threat to the swine industry worldwide. Exostosin glycosyltransferase 1 (EXT1), an enzyme involved in the biosynth Show more
Porcine reproductive and respiratory syndrome virus (PRRSV) continues to be a serious threat to the swine industry worldwide. Exostosin glycosyltransferase 1 (EXT1), an enzyme involved in the biosynthesis of heparin sulfate, has also been reported to be a host factor essential for a wide variety of pathogens. However, the role of EXT1 in PRRSV infection remains uncharted. Here, we identified that PRRSV infection caused an increase of EXT1 expression. EXT1 knockdown promoted virus infection, whereas its overexpression inhibited virus infection, suggesting an inhibitory function of EXT1 to PRRSV infection. We found that EXT1 had no effects on the attachment, internalization, or release of PRRSV but did restrict viral RNA replication. EXT1 was determined to interact with viral nonstructural protein 3 (nsp3) and nsp5 via its N-terminal cytoplasmic tail and to enhance K48-linked polyubiquitination of these two nsps to promote their degradation. Furthermore, the C-terminal glycosyltransferase activity domain of EXT1 was necessary for nsp3 and nsp5 degradation. We also found that EXT2, a EXT1 homolog, interacted with EXT1 and inhibited PRRSV infection. Similarly, EXT1 effectively restricted porcine epidemic diarrhea virus and porcine enteric alphacoronavirus infection in Vero cells. Taken together, this study reveals that EXT1 may serve as a broad-spectrum host restriction factor and suggests a molecular basis for the potential development of therapeutics against PRRSV infection. Show less
📄 PDF DOI: 10.1016/j.jbc.2021.101548
EXT1

Characterization of coagulation-related gene signature to predict prognosis and tumor immune microenvironment in skin cutaneous melanoma.

Binyu Song, Hao Chi, Gaoge Peng +11 more · 2022 · Frontiers in oncology · Frontiers · added 2026-04-24
Skin cutaneous melanoma (SKCM) is an extremely metastatic form of skin cancer. However, there are few valuable molecular biomarkers, and accurate diagnosis is still a challenge. Hypercoagulable state Show more
Skin cutaneous melanoma (SKCM) is an extremely metastatic form of skin cancer. However, there are few valuable molecular biomarkers, and accurate diagnosis is still a challenge. Hypercoagulable state encourages the infiltration and development of tumor cells and is significantly associated with poor prognosis in cancer patients. However, the use of a coagulation-related gene (CRG) signature for prognosis in SKCM, on the other hand, has yet to be determined. We used data from The Cancer Genome Atlas (TCGA) and Genotype Tissue Expression (GTEx) databases to identify differentially expressed CRGs, then designed a prognostic model by using the LASSO algorithm, univariate and multivariate Cox regression analysis, and constructed a nomogram which was evaluated by calibration curves. Moreover, the Gene Expression Omnibus (GEO), GSE54467 was used as an independent validation. The correlation between risk score and clinicopathological characteristics, tumor microenvironment (TME), and immunotherapy was further analyzed. To develop a prognostic model, seven CRGs in SKCM patients related to overall survival (OS) were selected: ANG, C1QA, CFB, DUSP6, KLKB1, MMP7, and RABIF. According to the Kaplan-Meier survival analysis, an increased OS was observed in the low-risk group than in the high-risk group (P<0.05). Immunotherapy was much more beneficial in the low-risk group, as per immune infiltration, functional enrichment, and immunotherapy analysis. The prognosis of SKCM patients may now be predicted with the use of a CRG prognostic model, thus guiding the development of treatment plans for SKCM patients and promoting OS rates. Show less
📄 PDF DOI: 10.3389/fonc.2022.975255
DUSP6

IL-27 Signaling Promotes Th1 Responses and Is Required to Inhibit Fungal Growth in the Lung during Repeated Exposure to

Ashley B Strickland, Donglei Sun, Peng Sun +3 more · 2022 · ImmunoHorizons · added 2026-04-24
no PDF DOI: 10.4049/immunohorizons.2100117
IL27

Case Report: Successful Management of a 29-Day-Old Infant With Severe Hyperlipidemia From a Novel Homozygous Variant of

Shu Liu, Zhiqing Wang, Xianhua Zheng +7 more · 2022 · Frontiers in pediatrics · Frontiers · added 2026-04-24
Severe hyperlipidemia is characterized by markedly elevated blood triglyceride levels and severe early-onset cardiovascular diseases, pancreatitis, pancreatic necrosis or persistent multiple organ fai Show more
Severe hyperlipidemia is characterized by markedly elevated blood triglyceride levels and severe early-onset cardiovascular diseases, pancreatitis, pancreatic necrosis or persistent multiple organ failure if left untreated. It is a rare autosomal recessive metabolic disorder originated from the variants of lipoprotein lipase gene, and previous studies have demonstrated that most cases with severe hyperlipidemia are closely related to the variants of some key genes for lipolysis, such as The 29-day-old infant was diagnosed with severe hyperlipidemia, registering a plasma triglyceride level as high as 25.46 mmol/L. Whole exome sequencing was conducted to explore the possible pathogenic gene variants for this patient. The infant was put on a low-fat diet combined with pharmacological therapy, which was successful in restraining the level of serum triglyceride and total cholesterol to a low to medium range during the follow-ups. The patient was found to be a rare novel homozygous duplication variant-c.45₄₈dupGCGG (Pro17Alafs Our study expands on the spectrum of Show less
📄 PDF DOI: 10.3389/fped.2022.792574
APOA5

Interleukin‑27 ameliorates allergic asthma by alleviating the lung Th2 inflammatory environment.

Jiameng Lu, Xiaoqing Ji, Lixia Wang +8 more · 2022 · International journal of molecular medicine · added 2026-04-24
Interleukin (IL)‑27 can inhibit the differentiation of Th2 cells and plays a role in the development of asthma. However, whether the therapeutic administration of IL‑27 in a mouse model of asthma can Show more
Interleukin (IL)‑27 can inhibit the differentiation of Th2 cells and plays a role in the development of asthma. However, whether the therapeutic administration of IL‑27 in a mouse model of asthma can inhibit allergic responses remains a matter of debate. Additionally, the mechanisms through which IL‑27 ameliorates inflammatory responses in asthma are not yet fully understood. Thus, the aim of the present study was to examine the effects of IL‑27 on asthma using a mouse model and to elucidate the underlying mechanisms. For this purpose, mice received an intranasal administration of IL‑27 and the total and differential cell counts, levels of cytokines and type 1 regulatory T (Tr1) cells in the lungs were detected. The protein and mRNA levels of signal transducer and activator of transcription (STAT)1 and STAT3 were analyzed and airway remodeling was assessed. The results indicated that IL‑27 did not ameliorate airway inflammation, airway hyperresponsiveness, and airway remolding when administrated therapeutically. Preventatively, the administration of IL‑27 decreased the concentrations of Th2 cytokines and increased the number of Tr1 cells. The protein and mRNA levels of STAT1 and STAT3 were increased. Taken together, these findings demonstrate that the prophylactic administration of IL‑27 ameliorates asthma by alleviating the lung Th2 inflammatory environment through the restoration of both the STAT1 and STAT3 pathways. IL‑27 may thus prove to be useful as a novel agent for the prevention of asthma. Show less
📄 PDF DOI: 10.3892/ijmm.2022.5142
IL27

Moringa Oleifera Alleviates Aβ Burden and Improves Synaptic Plasticity and Cognitive Impairments in APP/PS1 Mice.

Yacoubou Abdoul Razak Mahaman, Jun Feng, Fang Huang +7 more · 2022 · Nutrients · MDPI · added 2026-04-24
Alzheimer's disease is a global public health problem and the most common form of dementia. Due to the failure of many single therapies targeting the two hallmarks, Aβ and Tau, and the multifactorial Show more
Alzheimer's disease is a global public health problem and the most common form of dementia. Due to the failure of many single therapies targeting the two hallmarks, Aβ and Tau, and the multifactorial etiology of AD, there is now more and more interest in nutraceutical agents with multiple effects such as Show less
📄 PDF DOI: 10.3390/nu14204284
BACE1

HBeAg Is Indispensable for Inducing Liver Sinusoidal Endothelial Cell Activation by Hepatitis B Virus.

Xiaohong Xie, Jinzhuo Luo, Dan Zhu +8 more · 2022 · Frontiers in cellular and infection microbiology · Frontiers · added 2026-04-24
Liver sinusoidal endothelial cells (LSECs) serve as sentinel cells to detect microbial infection and actively contribute to regulating immune responses for surveillance against intrahepatic pathogens. Show more
Liver sinusoidal endothelial cells (LSECs) serve as sentinel cells to detect microbial infection and actively contribute to regulating immune responses for surveillance against intrahepatic pathogens. We recently reported that hepatitis B e antigen (HBeAg) stimulation could induce LSEC maturation and abrogate LSEC-mediated T cell suppression in a TNF-α and IL27 dependent manner. However, it remains unclear how HBeAg deficiency during HBV infection influences LSEC immunoregulation function and intrahepatic HBV-specific CD8 T cell responses. The function of LSECs in regulating effector T cell response, intrahepatic HBV-specific CD8 T cell responses and HBV viremia were characterized in both HBeAg-deficient and -competent HBV hydrodynamic injection (HDI) mouse models. LSECs isolated from HBeAg-deficient HBV HDI mice showed a reduced capacity to promote T cell immunity Our study underlines that HBeAg is indispensable for HBV-induced LSEC maturation to trigger intrahepatic HBV-specific T cell activation, and provides a new mechanism to elucidate the intrahepatic immune microenvironment regulation upon HBV exposure. Show less
📄 PDF DOI: 10.3389/fcimb.2022.797915
IL27

Identification of shared loci associated with both Crohn's disease and leprosy in East Asians.

Seulgi Jung, Dohoon Park, Ho-Su Lee +12 more · 2022 · Human molecular genetics · Oxford University Press · added 2026-04-24
Genome-wide association studies (GWAS) of Crohn's disease (CD) in European and leprosy in Chinese population have shown that CD and leprosy share genetic risk loci. As these shared loci were identifie Show more
Genome-wide association studies (GWAS) of Crohn's disease (CD) in European and leprosy in Chinese population have shown that CD and leprosy share genetic risk loci. As these shared loci were identified through cross-comparisons across different ethnic populations, we hypothesized that meta-analysis of GWAS on CD and leprosy in East Asian populations would increase power to identify additional shared loci. We performed a cross-disease meta-analysis of GWAS data from CD (1621 cases and 4419 controls) and leprosy (2901 cases 3801 controls) followed by replication in additional datasets comprising 738 CD cases and 488 controls and 842 leprosy cases and 925 controls. We identified one novel locus at 7p22.3, rs77992257 in intron 2 of ADAP1, shared between CD and leprosy with genome-wide significance (P = 3.80 × 10-11) and confirmed 10 previously established loci in both diseases: IL23R, IL18RAP, IL12B, RIPK2, TNFSF15, ZNF365-EGR2, CCDC88B, LACC1, IL27, NOD2. Phenotype variance explained by the polygenic risk scores derived from Chinese leprosy data explained up to 5.28% of variance of Korean CD, supporting similar genetic structures between the two diseases. Although CD and leprosy shared a substantial number of genetic susceptibility loci in East Asians, the majority of shared susceptibility loci showed allelic effects in the opposite direction. Investigation of the genetic correlation using cross-trait linkage disequilibrium score regression also showed a negative genetic correlation between CD and leprosy (rg [SE] = -0.40[0.13], P = 2.6 × 10-3). These observations implicate the possibility that CD might be caused by hyper-sensitive reactions toward pathogenic stimuli. Show less
no PDF DOI: 10.1093/hmg/ddac101
IL27

Genetic parameters estimation and genome-wide association studies for internal organ traits in an F

Yudong Li, Xin Liu, Xue Bai +12 more · 2022 · Journal of animal breeding and genetics = Zeitschrift fur Tierzuchtung und Zuchtungsbiologie · Blackwell Publishing · added 2026-04-24
Chicken internal organs are indispensable parts of the body, but their genetic architectures have not been commonly understood. Herein, we estimated the genetic parameters for heart weight (HW), liver Show more
Chicken internal organs are indispensable parts of the body, but their genetic architectures have not been commonly understood. Herein, we estimated the genetic parameters for heart weight (HW), liver weight (LW), spleen weight (SpW), testis weight (TW), glandular stomach weight (GSW), muscular stomach weight (MSW) and identified single nucleotide polymorphisms (SNPs) and potential candidate genes associated with internal organ weights in an F Show less
no PDF DOI: 10.1111/jbg.12674
KANSL1

Cadmium perturbed lipid profile and induced liver dysfunction in mice through phosphatidylcholine remodeling and promoting arachidonic acid synthesis and metabolism.

Jie Gu, Anqi Kong, Chuanzhi Guo +6 more · 2022 · Ecotoxicology and environmental safety · Elsevier · added 2026-04-24
Cadmium ion (Cd
no PDF DOI: 10.1016/j.ecoenv.2022.114254
FADS1

Multi-omics integration reveals a six-malignant cell maker gene signature for predicting prognosis in high-risk neuroblastoma.

Zijun Yan, Qiming Liu, Ziyang Cao +4 more · 2022 · Frontiers in neuroinformatics · Frontiers · added 2026-04-24
Neuroblastoma is the most common extracranial solid tumor of childhood, arising from the sympathetic nervous system. High-risk neuroblastoma (HRNB) remains a major therapeutic challenge with low survi Show more
Neuroblastoma is the most common extracranial solid tumor of childhood, arising from the sympathetic nervous system. High-risk neuroblastoma (HRNB) remains a major therapeutic challenge with low survival rates despite the intensification of therapy. This study aimed to develop a malignant-cell marker gene signature (MMGS) that might serve as a prognostic indicator in HRNB patients. Multi-omics datasets, including mRNA expression (single-cell and bulk), DNA methylation, and clinical information of HRNB patients, were used to identify prognostic malignant cell marker genes. MMGS was established by univariate Cox analysis, LASSO, and stepwise multivariable Cox regression analysis. Kaplan-Meier (KM) curve and time-dependent receiver operating characteristic curve (tROC) were used to evaluate the prognostic value and performance of MMGS, respectively. MMGS further verified its reliability and accuracy in the independent validation set. Finally, the characteristics of functional enrichment, tumor immune features, and inflammatory activity between different MMGS risk groups were also investigated. We constructed a prognostic model consisting of six malignant cell maker genes (MAPT, C1QTNF4, MEG3, NPW, RAMP1, and CDT1), which stratified patients into ultra-high-risk (UHR) and common-high-risk (CHR) group. Patients in the UHR group had significantly worse overall survival (OS) than those in the CHR group. MMGS was verified as an independent predictor for the OS of HRNB patients. The area under the curve (AUC) values of MMGS at 1-, 3-, and 5-year were 0.78, 0.693, and 0.618, respectively. Notably, functional enrichment, tumor immune features, and inflammatory activity analyses preliminarily indicated that the poor prognosis in the UHR group might result from the dysregulation of the metabolic process and immunosuppressive microenvironment. This study established a novel six-malignant cell maker gene prognostic model that can be used to predict the prognosis of HRNB patients, which may provide new insight for the treatment and personalized monitoring of HRNB patients. Show less
📄 PDF DOI: 10.3389/fninf.2022.1034793
C1QTNF4

Novel small molecular compound 2JY-OBZ4 alleviates AD pathology in cell models via regulating multiple targets.

Qian Guo, Gang Wu, Fang Huang +7 more · 2022 · Aging · Impact Journals · added 2026-04-24
Alzheimer's disease (AD) is the most common form of neurodegenerative dementia, characterized by cognitive deficits and memory dysfunction, which is clinically incurable so far. Novel small molecular Show more
Alzheimer's disease (AD) is the most common form of neurodegenerative dementia, characterized by cognitive deficits and memory dysfunction, which is clinically incurable so far. Novel small molecular compound 2JY-OBZ4 is one of structural analogue of Huperzine A (Hup-A), an anti-AD drug in China. In our previous work, 2JY-OBZ4 exhibited potent effects on tau hyperphosphorylation, Aβ production and acetylcholinesterase (AChE) activity. However, 2JY-OBZ4's anti-AD effects and the underlying molecular mechanisms remain unclear. We here reported that 2JY-OBZ4 resisted tau hyperphosphorylation at Thr181 and Ser396 sites in HEK293-hTau cells transfected with GSK-3β, decreased tau phosphorylation via upregulating the activity of PP2A in HEK293-hTau cells and reduced Aβ production through regulating protein levels of APP cleavage enzymes in N2a-hAPP cells. Meanwhile, we found that 2JY-OBZ4 had no adverse effects on cell viability of mice primary neuron even at high concentration, and ameliorated synaptic loss induced by human oligomeric Aβ42. 2JY-OBZ4 had moderate AChE inhibitory activity with the half maximal inhibitory concentration (IC50) to be 39.48 μg/ml Show less
📄 PDF DOI: 10.18632/aging.204336
BACE1

IL-17D affects the chemokines and chemokine receptors of intestinal epithelial cells under hyperoxia.

Tianming Li, Yanping Liu, Xuefei Yu +3 more · 2022 · International immunopharmacology · Elsevier · added 2026-04-24
IL-17D is a new member of the IL-17 family. Currently, it is believed that IL-17D can directly act on immune cells or may indirectly modulate immune responses by regulating cytokine expression. Herein Show more
IL-17D is a new member of the IL-17 family. Currently, it is believed that IL-17D can directly act on immune cells or may indirectly modulate immune responses by regulating cytokine expression. Herein, we hypothesized that IL-17D regulates the expression of chemokines in intestinal epithelial cells, in turn modulating the immune response within intestinal mucosa under hyperoxia. To explore this notion, newborn rats were divided into a hyperoxia group (85 % O Show less
no PDF DOI: 10.1016/j.intimp.2022.109386
IL27

ZC3H4 regulates infiltrating monocytes, attenuating pulmonary fibrosis through IL-10.

Yaping Liu, Xinxin Zhang, Jing Wang +8 more · 2022 · Respiratory research · BioMed Central · added 2026-04-24
Silicosis is a pulmonary fibrosis-associated disease caused by the inhalation of large amounts of free silicon dioxide (SiO
no PDF DOI: 10.1186/s12931-022-02134-2
ZC3H4

Design, Synthesis, and Biological Evaluation of Notopterol Derivatives as Triple Inhibitors of AChE/BACE1/GSK3β for the Treatment of Alzheimer's Disease.

Nan Wang, Wenjie Liu, Lijun Zhou +11 more · 2022 · ACS omega · ACS Publications · added 2026-04-24
The pathogenesis of Alzheimer's disease (AD) is very complex, and there are many hypotheses. Therefore, the development of a multi-target-directed-ligand may be an effective therapeutic strategy. Our Show more
The pathogenesis of Alzheimer's disease (AD) is very complex, and there are many hypotheses. Therefore, the development of a multi-target-directed-ligand may be an effective therapeutic strategy. Our previous study showed that notopterol (a natural product from Show less
📄 PDF DOI: 10.1021/acsomega.2c03368
BACE1

Plasma Proteome Profiling of Patients With In-stent Restenosis by Tandem Mass Tag-Based Quantitative Proteomics Approach.

Jingyuan Hou, Qiaoting Deng, Sudong Liu +4 more · 2022 · Frontiers in cardiovascular medicine · Frontiers · added 2026-04-24
Despite the widespread application of new drug-eluting stents, a considerable portion of patients experience in-stent restenosis (ISR). To date, the pathophysiologic mechanisms of ISR remain poorly un Show more
Despite the widespread application of new drug-eluting stents, a considerable portion of patients experience in-stent restenosis (ISR). To date, the pathophysiologic mechanisms of ISR remain poorly understood. In this study, we collected plasma samples from ISR patients ( A total of 1,696 proteins were identified, of which 278 differed in protein abundance between non-ISR and HCs, 497 between ISR and HCs, and 387 between ISR and non-ISR, respectively. Bioinformatic analyses, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and PPI, further demonstrated that differentially abundant proteins between ISR and non-ISR are involved in several crucial biological processes and signaling pathways, such as focal adhesion, platelet activation, Rap1 signaling, regulation of actin cytoskeleton, and cholesterol metabolism. Among the identified differentially abundant proteins in ISR, 170 were increased in abundance relative to both non-ISR patients and HCs. Some of these proteins were identified to have critical functions for atherosclerosis development and might be involved in ISR pathology. Among these proteins, 3 proteins with increased abundance including fetuin-B, apolipoprotein C-III (APOC3), and cholesteryl ester transfer protein (CETP) were confirmed by ELISA. This is the first study provided a comprehensive proteomic profile to understand ISR pathology, which may help identify early diagnostic biomarkers and therapeutic targets. Show less
📄 PDF DOI: 10.3389/fcvm.2022.793405
APOC3

Hyperuricemia induces liver injury by upregulating HIF-1α and inhibiting arginine biosynthesis pathway in mouse liver and human L02 hepatocytes.

Lei Huang, Xinyu He, Wen Peng +11 more · 2022 · Biochemical and biophysical research communications · Elsevier · added 2026-04-24
The molecular mechanisms of uric acid (UA)-induced liver injury has not been clearly elucidated. In this study, we aimed to investigate the effect and action mechanisms of UA in liver injury. We analy Show more
The molecular mechanisms of uric acid (UA)-induced liver injury has not been clearly elucidated. In this study, we aimed to investigate the effect and action mechanisms of UA in liver injury. We analyzed the damaging effect of UA on mouse liver and L02 cells and subsequently performed metabolomics studies on L02 cells to identify abnormal metabolic pathways. Finally, we verified transcription factors that regulate related metabolic enzymes. UA directly activated the hepatic NLRP3 inflammasome and Bax apoptosis pathway invivo and invitro. Related metabolites in the arginine biosynthesis pathway (or urea cycle), l-arginine and l-argininosuccinate were decreased, and ammonia was increased in UA-stimulated L02 cells, which was mediated by carbamoyl phosphate synthase 1 (CPS1), argininosuccinate synthase (ASS) and argininosuccinate lyase (ASL) downregulation. UA upregulated hypoxia inducible factor-1alpha (HIF-1α) invivo and invitro, and HIF-1α inhibition alleviated the UA-induced ASS downregulation and hepatocyte injury. In conclusion, UA upregulates HIF-1α and inhibits urea cycle enzymes (UCEs). This leads to liver injury, with evidence of hepatocyte inflammation, apoptosis and oxidative stress. Show less
no PDF DOI: 10.1016/j.bbrc.2022.05.096
CPS1

Interferon-

Peng Xiong, Tonglin Liu, Yu Chen +4 more · 2022 · Disease markers · added 2026-04-24
The initiation and progression of allergic asthma (AA) are associated with complex interactions between inflammation and immune response. Herein, we report the specific mechanisms underlying the molec Show more
The initiation and progression of allergic asthma (AA) are associated with complex interactions between inflammation and immune response. Herein, we report the specific mechanisms underlying the molecular action of interferon (IFN)- Show less
📄 PDF DOI: 10.1155/2022/1542112
IL27

Transcriptomics and Metabolomics Identify Drug Resistance of Dormant Cell in Colorectal Cancer.

Lang Xie, Renli Huang, Hongyun Huang +2 more · 2022 · Frontiers in pharmacology · Frontiers · added 2026-04-24
📄 PDF DOI: 10.3389/fphar.2022.879751
LMOD1

[Activation of Notch signaling in bone marrow stromal cells promotes osteogenesis in mice in vitro].

Xinyu Liu, Cen Luo, Xiaolin Tu · 2022 · Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology · added 2026-04-24
Objective To investigate the osteogenic differentiation of bone marrow stromal cells (BMSC) with Notch signaling activation in vitro. Methods The BMSC derived from Notch1-NICD
no PDF
HEY2

Ferroptosis and Autophagy-Related Genes in the Pathogenesis of Ischemic Cardiomyopathy.

Yue Zheng, Wenqing Gao, Qiang Zhang +4 more · 2022 · Frontiers in cardiovascular medicine · Frontiers · added 2026-04-24
Obesity plays an important role in type 2 diabetes mellitus (T2DM) and myocardial infarction (MI). Ferroptosis and ferritinophagy are related to metabolic pathways, such as fatty acid metabolism and m Show more
Obesity plays an important role in type 2 diabetes mellitus (T2DM) and myocardial infarction (MI). Ferroptosis and ferritinophagy are related to metabolic pathways, such as fatty acid metabolism and mitochondrial respiration. We aimed to investigate the ferroptosis- and autophagy-related differentially expressed genes (DEGs) that might be potential targets for MI progression. GSE116250 was analyzed to obtain DEGs. A Venn diagram was used to obtain the overlapping ferroptosis- and autophagy-related DEGs. The enrichment pathway analysis was performed and the hub genes were obtained. Pivotal miRNAs, transcription factors, and drugs with the hub genes interactions were also predicted. The MI mice model was constructed, and qPCR analysis and single-cell sequencing were used to validate the hub genes. Utilizing the limma package and the Venn diagram, 26 ferroptosis-related and 29 autophagy-related DEGs were obtained. The list of ferroptosis-related DEGs was analyzed, which were involved in the cellular response to a toxic substance, cellular oxidant detoxification, and the IL-17 signaling pathway. The list of autophagy-related DEGs was involved in the regulation of autophagy, the regulation of JAK-STAT signaling pathway, and the regulation of MAPK cascade. In the protein-protein interaction network, the hub DEGs, such as IL-6, PTGS2, JUN, NQO1, NOS3, LEPR, NAMPT, CDKN2A, CDKN1A, and Snai1, were obtained. After validation using qPCR analysis in the MI mice model and single-cell sequencing, the 10 hub genes can be the potential targets for MI deterioration. The screened hub genes, IL-6, PTGS2, JUN, NQO1, NOS3, LEPR, NAMPT, CDKN2A, CDKN1A, and Snai1, may be therapeutic targets for patients with MI and may prevent adverse cardiovascular events. Show less
no PDF DOI: 10.3389/fcvm.2022.906753
SNAI1

A Time-course Transcriptional Kinetics of Genes in Behavior, Cortisol Synthesis and Neurodevelopment in Zebrafish Larvae Exposed to Imidacloprid and Thiamethoxam.

Jin-Ge Zhang, Dong-Dong Ma, Si-Ying Li +4 more · 2022 · Bulletin of environmental contamination and toxicology · Springer · added 2026-04-24
Agricultural use of neonicotinoid insecticides, neuroactive nitroguanidine compounds, has been detected everywhere in the global, posing significant hazard to nontarget organisms. This work studied th Show more
Agricultural use of neonicotinoid insecticides, neuroactive nitroguanidine compounds, has been detected everywhere in the global, posing significant hazard to nontarget organisms. This work studied the developmental neurotoxicity of zebrafish larvae exposed to imidacloprid (IMI) and thiamethoxam (THM), ranging from 0.05 µg L Show less
no PDF DOI: 10.1007/s00128-022-03645-w
MACF1

Intestinal changes associated with nitrite exposure in Bufo gargarizans larvae: Histological damage, immune response, and microbiota dysbiosis.

Yutian Liu, Hemei Wang, Lifeng Wu +7 more · 2022 · Aquatic toxicology (Amsterdam, Netherlands) · Elsevier · added 2026-04-24
Nitrite is a ubiquitous toxic compound in aquatic ecosystems and has negative effects on aquatic organisms. The intestine and the trillions of microbes that inhabit it, play an integral role in mainta Show more
Nitrite is a ubiquitous toxic compound in aquatic ecosystems and has negative effects on aquatic organisms. The intestine and the trillions of microbes that inhabit it, play an integral role in maintaining digestive and immune functions. However, the effects of nitrite on intestinal health and microflora have been poorly investigated. Therefore, the present study evaluated the response of intestinal histology, immunity, digestive enzyme activities and microbiota to nitrite exposure in Bufo gargarizans tadpoles. The results showed that nitrite caused damage to the intestine and impaired digestive performance. Significant changes in the transcriptional profiles of genes involved in oxidative stress (sod, gpx and hsp), inflammation, and immunity (socs3, il-27, il-1β and il-17d) were observed in the NO Show less
no PDF DOI: 10.1016/j.aquatox.2022.106228
IL27

The c.612A>G mutation of MC4R affects constitutive activity and signaling in domestic goats.

Yinan Yan, Shaxuan Chi, Guiqiong Liu +3 more · 2022 · Animal genetics · Blackwell Publishing · added 2026-04-24
As a key gene for balancing energy and regulating feeding behavior, MC4R is relevant to the growth of ruminants. In this presentation, a highly conserved c.612A>G site in the coding sequence (CDS) of Show more
As a key gene for balancing energy and regulating feeding behavior, MC4R is relevant to the growth of ruminants. In this presentation, a highly conserved c.612A>G site in the coding sequence (CDS) of MC4R has been selected during a selective sweep analysis of 35 Yiling goats and 20 other wild goats. This site mutation results in an amino acid change from Ile to Met. The genotyping analysis of the c.612A>G site revealed that the A allele was the dominant allele in the domestic goat populations, while the wild goat individuals only had the G allele. For a better understanding of the biological significance of this site, we examined the protein localization and signal detection to explain the function of the two MC4R receptors. The results showed that both the M204 and I204 receptors can normally localize on the membrane. When stimulating the M204 type without α-MSH, it was defective at the level of basal cAMP and decreased significantly against the I204 type. In contrast, the signaling capacity of the M204 receptor was also lower than that of I204 under the stimulation of α-MSH. In the ERK1/2 pathway, stimulating MC4R with NDP-α-MSH, both the M204 and I204 receptors had normal pERK1/2 levels. These results indicate that the p.I204M mutation may change the function by damaging the constitutive activity and signaling, and thus may regulate goats' appetite. This study has potential application for rearing domestic goats. Show less
no PDF DOI: 10.1111/age.13214
MC4R

RBPMS2 Is a Myocardial-Enriched Splicing Regulator Required for Cardiac Function.

Alexander A Akerberg, Michael Trembley, Vincent Butty +12 more · 2022 · Circulation research · added 2026-04-24
RBPs (RNA-binding proteins) perform indispensable functions in the post-transcriptional regulation of gene expression. Numerous RBPs have been implicated in cardiac development or physiology based on Show more
RBPs (RNA-binding proteins) perform indispensable functions in the post-transcriptional regulation of gene expression. Numerous RBPs have been implicated in cardiac development or physiology based on gene knockout studies and the identification of pathogenic RBP gene mutations in monogenic heart disorders. The discovery and characterization of additional RBPs performing indispensable functions in the heart will advance basic and translational cardiovascular research. We performed a differential expression screen in zebrafish embryos to identify genes enriched in We identified 1848 genes enriched in the Our study identifies Show less
📄 PDF DOI: 10.1161/CIRCRESAHA.122.321728
MYBPC3

Slug Mediates MRP2 Expression in Non-Small Cell Lung Cancer Cells.

Xieyi Zhang, Wangyang Liu, Kazue Edaki +5 more · 2022 · Biomolecules · MDPI · added 2026-04-24
Transcriptional factors, such as Snail, Slug, and Smuc, that cause epithelial-mesenchymal transition are thought to regulate the expression of Ezrin, Radixin, and Moesin (ERM proteins), which serve as Show more
Transcriptional factors, such as Snail, Slug, and Smuc, that cause epithelial-mesenchymal transition are thought to regulate the expression of Ezrin, Radixin, and Moesin (ERM proteins), which serve as anchors for efflux transporters on the plasma membrane surface. Our previous results using lung cancer clinical samples indicated a correlation between Slug and efflux transporter MRP2. In the current study, we aimed to evaluate the relationships between MRP2, ERM proteins, and Slug in lung cancer cells. HCC827 cells were transfected by Mock and Slug plasmid. Both mRNA expression levels and protein expression levels were measured. Then, the activity of MRP2 was evaluated using CDCF and SN-38 (MRP2 substrates). HCC827 cells transfected with the Slug plasmid showed significantly higher mRNA expression levels of MRP2 than the Mock-transfected cells. However, the mRNA expression levels of ERM proteins did not show a significant difference between Slug-transfected cells and Mock-transfected cells. Protein expression of MRP2 was increased in Slug-transfected cells. The uptake of both CDCF and SN-38 was significantly decreased after transfection with Slug. This change was abrogated by treatment with MK571, an MRP2 inhibitor. The viability of Slug-transfected cells, compared to Mock cells, significantly increased after incubation with SN-38. Thus, Slug may increase the mRNA and protein expression of MRP2 without regulation by ERM proteins in HCC827 cells, thereby enhancing MRP2 activity. Inhibition of Slug may reduce the efficacy of multidrug resistance in lung cancer. Show less
no PDF DOI: 10.3390/biom12060806
SNAI1

Crosstalk between Host Genome and Metabolome among People with HIV in South Africa.

Chang Liu, Zicheng Wang, Qin Hui +14 more · 2022 · Metabolites · MDPI · added 2026-04-24
Genome-wide association studies (GWAS) of circulating metabolites have revealed the role of genetic regulation on the human metabolome. Most previous investigations focused on European ancestry, and f Show more
Genome-wide association studies (GWAS) of circulating metabolites have revealed the role of genetic regulation on the human metabolome. Most previous investigations focused on European ancestry, and few studies have been conducted among populations of African descent living in Africa, where the infectious disease burden is high (e.g., human immunodeficiency virus (HIV)). It is important to understand the genetic associations of the metabolome in diverse at-risk populations including people with HIV (PWH) living in Africa. After a thorough literature review, the reported significant gene−metabolite associations were tested among 490 PWH in South Africa. Linear regression was used to test associations between the candidate metabolites and genetic variants. GWAS of 154 plasma metabolites were performed to identify novel genetic associations. Among the 29 gene−metabolite associations identified in the literature, we replicated 10 in South Africans with HIV. The UGT1A cluster was associated with plasma levels of biliverdin and bilirubin; SLC16A9 and CPS1 were associated with carnitine and creatine, respectively. We also identified 22 genetic associations with metabolites using a genome-wide significance threshold (p-value < 5 × 10−8). In a GWAS of plasma metabolites in South African PWH, we replicated reported genetic associations across ancestries, and identified novel genetic associations using a metabolomics approach. Show less
📄 PDF DOI: 10.3390/metabo12070624
CPS1

Development and Validation of a Hypoxia-related Prognostic Model for Ovarian Cancer.

Linling Xie, Meijun Pan, Zhaoping Zhang +8 more · 2022 · Recent patents on anti-cancer drug discovery · Bentham Science · added 2026-04-24
The high heterogeneity of ovarian cancer (OC) brings great difficulties to its early diagnosis and prognostic forecast. There is an urgent need to establish a prognostic model of OC based on clinicopa Show more
The high heterogeneity of ovarian cancer (OC) brings great difficulties to its early diagnosis and prognostic forecast. There is an urgent need to establish a prognostic model of OC based on clinicopathological features and genomics. We identified hypoxia-related differentially expressed genes (DEGs) between OC tissues from The Cancer Genome Atlas (TCGA) and normal tissues from the Genotype-Tissue Expression (GTEx). LASSO Cox regression analysis was applied for building a prognostic model in the TCGA-GTEx cohorts, and its predictive value was validated in the GEO-OC cohort. Functional enrichment analysis was performed to investigate the underlying mechanisms. By constructing a hypoxia model of the SKOV3 cell line and applying qRT-PCR, we investigated the relationship between hypoxia with two novel genes in the prognostic model (ISG20 and ANGPTL4). Twelve prognostic hypoxia-related DEGs were identified, and nine of them were selected to establish a prognostic model. OC patients were stratified into two risk groups, and the high-risk group showed reduced survival time compared to the low-risk group upon survival analysis. Univariate and multivariate Cox regression analysis demonstrated that the risk score was an independent risk factor for overall survival. The biological function of the identified prognostic hypoxia-related gene signature was involved in immune cell infiltration. Low expression of ISG20 was observed in the CoCl Our findings showed that this hypoxia-related gene signature could serve as a satisfactory prognostic classifier for OC and will be beneficial to the research and development of targeted therapeutic strategies. Show less
no PDF DOI: 10.2174/1574892817666220623154831
ANGPTL4