👤 Xiaojun Liu

🔍 Search 📋 Browse 🏷️ Tags ❤️ Favourites ➕ Add 🧬 Extraction
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, 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, Yanhong 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

Pitolisant Inhibits Alcohol Drinking and Improves Withdrawal Negative Affect Through Lateral Habenula Histaminergic Signaling in Mice.

Yan Zhao, Yixin Fu, Tianhao Liu +11 more · 2026 · CNS neuroscience & therapeutics · Wiley · added 2026-04-24
Alcohol use disorder (AUD) is a chronic condition marked by compulsive drinking and withdrawal-related negative affect. Histamine (HA) signaling, particularly via the histamine H3 receptor (H3R), may Show more
Alcohol use disorder (AUD) is a chronic condition marked by compulsive drinking and withdrawal-related negative affect. Histamine (HA) signaling, particularly via the histamine H3 receptor (H3R), may modulate alcohol-related behaviors. We investigated the effects of pitolisant, an FDA-approved H3R antagonist, on ethanol (EtOH)-related behaviors in mice. Adult male C57BL/6J mice underwent acute or chronic (2 or > 8 weeks) intermittent alcohol exposure. Pitolisant pretreatment was administered, and then pharmacological behavior, histologic, and molecular assays were conducted. Pitolisant administration reduced acute EtOH-induced locomotor activation, conditioned place preference, and sedative effects, and also curtailed EtOH intake. It alleviated anxiety and depression-like behavior during 24-h withdrawal (Post-EtOH). Mechanistically, the Post-EtOH condition was featured by complicated brain cFos expression mapping, including elevated cFos, [HA] and [glutamine]/[glutamate] ratio in the lateral habenula (LHb). However, systemic pitolisant treatment significantly increased [norepinephrine]/[normetanephrine] ratio, and restored the diminished phosphorylated CREB and BDNF levels in the LHb. Intra-LHb H2R antagonist cimetidine infusion partly blocked the pitolisant therapeutic effect on alcohol-related behavior. These findings highlight the HAergic system as a critical regulator of alcohol-related behaviors. The LHb HA signaling and norepinephrine neurotransmission might underlie pitolisant's potential novel therapeutic strategy for AUD. Show less
📄 PDF DOI: 10.1002/cns.70732
BDNF

Decreased adipokine CTRP4 in CAD patients: CTRP4 attenuates atherosclerosis via inhibition of RAGE and TLR4.

Xinyi Shu, Feifei Li, Jiawei Chen +15 more · 2026 · Clinical and translational medicine · Wiley · added 2026-04-24
C1q/TNF-related proteins (CTRPs) belong to the adipokine family. Here, we aimed to assess the relation of CTRP4 levels in serum and perivascular adipose tissue (PVAT) with coronary artery disease (CAD Show more
C1q/TNF-related proteins (CTRPs) belong to the adipokine family. Here, we aimed to assess the relation of CTRP4 levels in serum and perivascular adipose tissue (PVAT) with coronary artery disease (CAD), and investigate the effect of CTRP4 on atherosclerosis and the underlying mechanisms. CTRP4 levels were examined in serum and epicardial adipose tissue (a major PVAT) from patients with CAD. Atherosclerotic lesions were analysed in CTRP4 CTRP4 levels were lower in serum and epicardial adipose tissue of patients with CAD compared to non-CAD controls. CTRP4 knockout promoted atherosclerosis in ApoE Decreased CTRP4 levels in serum and epicardial adipose tissue are associated with CAD in patients. CTRP4 deficiency promotes the development of atherosclerosis in ApoE Show less
📄 PDF DOI: 10.1002/ctm2.70624
APOE

Vascular smooth muscle cell RNA-binding protein U2AF2 induces copper death by regulating C1qbp expression, delaying development of atherosclerosise.

Yang Yang, Hongxu Chen, Qijun Yu +5 more · 2026 · Biological research · BioMed Central · added 2026-04-24
Atherosclerosis (AS) is the main pathological basis of atherosclerosis-related cardiovascular and cerebrovascular diseases. The phenotypic conversion and death mechanisms of vascular smooth muscle cel Show more
Atherosclerosis (AS) is the main pathological basis of atherosclerosis-related cardiovascular and cerebrovascular diseases. The phenotypic conversion and death mechanisms of vascular smooth muscle cells (VSMCs) are crucial during its development. This study reveals the molecular mechanisms of the C1qbp-DLAT axis and the U2AF2 (U2 Small Nuclear RNA Auxiliary Factor 2)-NEAT1 network in regulating cuproptosis in AS. In this study, an ApoE The study revealed elevated copper ion levels and dysregulated cuproptosis-related genes in an AS model. U2AF2 stabilized C1qbp mRNA, enhancing C1qbp protein expression, which promoted DLAT oligomerization to regulate cuproptosis. LncRNA NEAT1 facilitated this process by scaffolding U2AF2-C1qbp mRNA interaction. Targeted inhibition of U2AF2 significantly improved AS pathological characteristics, reduced lipid deposition, collagen deposition and macrophage infiltration within the plaque, increased smooth muscle cell content and lowered serum levels of total cholesterol (TC), total triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C). This study revealed the role of the U2AF2-C1qbp-copper death regulatory axis in the development of AS, providing new targets and a theoretical basis for the treatment of AS. Targeted inhibition of U2AF2 may become an effective strategy to delay progression of AS. Show less
📄 PDF DOI: 10.1186/s40659-026-00672-3
APOE

SAMHD1 drives immunosuppression in non-small cell lung cancer by promoting macrophage infiltration and restricting oncolytic adenovirus replication.

Shichuan Hu, Jian Xu, Zhiwu Wang +7 more · 2026 · Journal for immunotherapy of cancer · added 2026-04-24
Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and the leading cause of cancer-related deaths. Immune checkpoint inhibitors (ICIs) of programmed death-1 (PD-1)/programmed de Show more
Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and the leading cause of cancer-related deaths. Immune checkpoint inhibitors (ICIs) of programmed death-1 (PD-1)/programmed death ligand-1 signaling induce tumor regression in some patients with NSCLC, but most patients with NSCLC exhibit resistance to ICIs therapy. NSCLC shapes the potent tumor immunosuppressive microenvironment (TIME) that underlies tumor immune tolerance and acquired resistance. Therefore, elucidating the cellular and molecular mechanisms by which NSCLC establishes and sustains the TIME is essential for developing novel strategies to overcome immune resistance and enhance the clinical benefit of ICIs. The correlation between sterile alpha motif domain and histidine-aspartate domain-containing protein 1 (SAMHD1) expression and ICIs was analyzed via immunohistochemistry. Cell migration assay was performed to assess the effect of SAMHD1 on macrophage recruitment. Multicolor flow cytometry was performed to analyze the effect of SAMHD1 knockdown on the tumor microenvironment. SAMHD1 regulation of the dual specificity phosphatase 6-extracellular regulated protein kinases 1/2 (DUSP6-ERK1/2) pathway was verified by RNA sequencing and western blotting. Here, we identify the SAMHD1 as a potential therapeutic target and a major determinant of poor response to ICIs in patients with NSCLC. Tumors with high SAMHD1 expression show resistance to anti-PD-1 antibody (αPD-1) treatment, whereas tumors with low SAMHD1 expression are highly sensitive. SAMHD1-dependent resistance to αPD-1 is characterized by increased tumor-associated macrophages (TAMs) infiltration and reduced CD8+T cell numbers. Mechanistically, SAMHD1 regulates the expression of macrophage-associated chemokines by influencing the activation of the DUSP6-ERK1/2 pathway, which contributes to TAMs aggregation within NSCLC tumors to shape an immunosuppressive microenvironment. The HIV accessory protein viral protein-x (VPX) specifically degrades SAMHD1 to promote HIV replication. Similarly, the vpx-engineered oncolytic adenovirus (oAd-vpx) targets SAMDH1 degradation to enhance oncolytic adenovirus replication and weaken the hostile immune microenvironment shaped by TAMs, thereby triggering a CD8+T-cell-dependent antitumor immune response. The combination of oAd-vpx and αPD-1 inhibits tumor growth and enhances sensitivity to ICIs in both mouse and human NSCLC. This research identifies a key mechanism of SAMHD1-driven immunosuppression and highlights its important role in oncolytic adenovirus therapy. This study provides a theoretical basis for targeting SAMHD1 as a drug therapy strategy in patients with NSCLC. Show less
📄 PDF DOI: 10.1136/jitc-2025-013550
DUSP6

IL-27 signaling mediates skin inflammation in experimental psoriasis and atopic dermatitis.

Zeyu Chen, Lian Cui, Zhiyi Lan +14 more · 2026 · Cell & bioscience · BioMed Central · added 2026-04-24
Psoriasis and atopic dermatitis (AD) are two prevalent inflammatory skin disorders, each characterized by distinct adaptive immune responses. However, recent evidence suggests that these diseases may Show more
Psoriasis and atopic dermatitis (AD) are two prevalent inflammatory skin disorders, each characterized by distinct adaptive immune responses. However, recent evidence suggests that these diseases may share overlapping immune mechanisms, especially concerning keratinocyte function. The specific cytokines that coordinate these inflammatory pathways remain largely undefined. The expression of IL-27 and its receptor was analyzed using data derived from GEO datasets. Imiquimod-induced psoriasis-like and MC903-induced AD-like skin inflammation models were established in wild-type and Il27ra knockout littermates. Skin inflammation was evaluated using clinical scoring, histology, and immunostaining. Flow cytometry was employed to characterize immune cell populations in skin. Expression of relevant cytokines and signaling molecules was assessed using quantitative PCR, bulk RNA sequencing, and Western blotting. We found significantly elevated expression of the IL-27 receptor in the lesional skin of patients with psoriasis or AD. IL-27 receptor-deficient mice exhibited markedly reduced skin inflammation in both psoriasis-like and AD-like murine models. Mechanistic investigations revealed that IL-27 induces tumor necrosis factor-α production via signal transducer and activator of transcription 1 activation in keratinocytes, thereby potentiating inflammatory responses. Our findings identify IL-27 signaling in keratinocytes as a pivotal regulator of skin inflammation in both psoriasis and AD. This highlights IL-27 as a promising therapeutic target for inflammatory skin diseases. Show less
📄 PDF DOI: 10.1186/s13578-025-01527-2
IL27

Sex differences in the association of vascular risk and APOE Genotype with cognitive decline and dementia: evidence from a U.S. longitudinal study.

Longjian Liu, Jintong Hou, Saishi Cui +7 more · 2026 · Lancet regional health. Americas · Elsevier · added 2026-04-24
Sex differences in the association between vascular factors and cognitive outcomes remain unclear. We aimed to investigate the associations of blood pressure metrics (hypertension, systolic blood pres Show more
Sex differences in the association between vascular factors and cognitive outcomes remain unclear. We aimed to investigate the associations of blood pressure metrics (hypertension, systolic blood pressure [SBP), pulse pressure, ankle and brachial pressures, and ankle to brachial pressure index [ABI]) with the risk of cognitive decline and dementia. We conducted a population-based longitudinal analysis using data from the Atherosclerosis Risk in Communities (ARIC) study (begun in 1987-1989) in the United States. We analyzed a total of 12,268 participants aged 45-64 years who had validated exposure measurements, cognitive function tests (first administrated 1990-1992), and followed up for incidence of dementia through December 2019. Cognitive function was assessed using the Digit Symbol Substitution Test, the Delayed Word Recall Test, and the Word Fluency Test. Dementia cases were identified through a standardized clinical evaluation process, mostly adjudicated by expert reviewers. We performed sex-stratified analyses to examine the associations of blood pressure metrics and APOE ε4 allele with the risk of cognitive decline and dementia. Over a median follow-up of 26.4 years, 2698 participants developed dementia. Women aged 55-64 had a significantly higher incidence of dementia than men aged 55-64 (14.8 vs. 11.8 per 1000 person-years; p < These findings highlight notable sex differences in the association between vascular factors and cognitive decline and dementia risk. Women appear more vulnerable to both genetic and vascular risk factors, emphasizing the need for sex-specific approaches in research, prevention, and intervention strategies for cognitive impairment. NIH. Show less
📄 PDF DOI: 10.1016/j.lana.2025.101346
APOE

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

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

Identification of Blood Pressure-Associated Metabolites by Integrating Metabolomic and Genetic Analysis.

Yuanjiao Liu, Chunxiao Cheng, Xiong-Fei Pan +3 more · 2026 · MedComm · Wiley · added 2026-04-24
This study aimed to identify blood pressure-associated metabolites and explore their underlying pathways using multiomics data from 1188 Chinese participants. Serum metabolite levels were profiled usi Show more
This study aimed to identify blood pressure-associated metabolites and explore their underlying pathways using multiomics data from 1188 Chinese participants. Serum metabolite levels were profiled using untargeted and widely targeted metabolomic technologies. The associations of metabolites as well as ratios with blood pressure were assessed using generalized linear models (GLM). Targeted metabolomics was used to replicate a subset of metabolites. Genome-wide association studies (GWAS) were performed on all metabolites identified. Potential causality was examined using two-sample Mendelian randomization (MR) analyses, with partial validation against GWAS results from an independent cohort. This study identified 10 blood pressure-associated metabolites supported by GLM and MR analyses. Cortisol demonstrated the strongest association with blood pressure, with l-glutamic acid and its ratios identified as key drivers. Multiomics integration revealed that a genetic variant near the omega-3 metabolism genes ( Show less
📄 PDF DOI: 10.1002/mco2.70718
FADS1

Effects of GABAAR modulators CL218872 and MRK-016 on neural repair and synaptic plasticity in mice with Intracerebral hemorrhage.

Tingting Chen, Hongxia He, Fei Huang +3 more · 2026 · PloS one · PLOS · added 2026-04-24
Intracerebral hemorrhage (ICH) is a devastating condition characterized by rapid onset, high rates of disability and mortality, and prolonged recovery. Dysregulated γ-aminobutyric acid type A receptor Show more
Intracerebral hemorrhage (ICH) is a devastating condition characterized by rapid onset, high rates of disability and mortality, and prolonged recovery. Dysregulated γ-aminobutyric acid type A receptor (GABAAR) signaling contributes to ICH-induced neurotoxicity, presenting a promising therapeutic target. To assess the neurorestorative effects of the GABAAR α1-selective partial positive allosteric modulator (PAM) CL218872 and the α5-selective negative allosteric modulator (NAM) MRK-016 on synaptic plasticity and neural repair following ICH. An ICH mouse model was constructed using collagenase IV, and ICH mice were administered the GABAAR modulators CL218872 or MRK-016. Differences in inflammation and neurological deficit score were compared between different groups of mice. Morphologic and functional changes in mouse neuronal cells were next determined by Nissl and Golgi-Cox staining. Synaptic structural changes in ICH mice were visualized by transmission electron microscopy, and changes in synaptic plasticity-related molecules were quantified to assess the effects of GABAAR modulators on synapses in ICH mice. Treatment with CL218872 resulted in a reduction in hemorrhage and improved neurobehavioral outcomes in ICH mice. Additionally, CL218872 mitigated inflammation by downregulating phospho-p65, IL-6 and TNF-α expression. Histological analysis revealed an increase in neuronal density, preservation of cell morphology, and enhanced synaptic connectivity following CL218872 treatment. Furthermore, synaptic structure was restored, and there was an upregulation of brain-derived neurotrophic factor (BDNF), growth-associated protein-43 (GAP-43), postsynaptic density protein 95 (PSD-95), and synaptophysin in ICH mice. However, treatment with MRK-016 yielded the opposite result. The GABAAR α1-selective PAM CL218872 exerts neuroprotective and neurorestorative effects in ICH, suggesting its therapeutic potential for ICH management. Show less
📄 PDF DOI: 10.1371/journal.pone.0345025
BDNF

Predictive lipidaemic and clinical factors for PVR formation after RRD surgery in nondiabetic patients.

Yan Jiang, Tian Niu, Guo-Hui Lan +2 more · 2026 · International journal of ophthalmology · added 2026-04-24
To investigate the potential impact of lipidaemic and clinical factors on the development of proliferative vitreoretinopathy (PVR) following uncomplicated primary rhegmatogenous retinal detachment (RR Show more
To investigate the potential impact of lipidaemic and clinical factors on the development of proliferative vitreoretinopathy (PVR) following uncomplicated primary rhegmatogenous retinal detachment (RRD) surgery in nondiabetic individuals. This was a retrospective, single-center, case-control study of consecutive patients who underwent primary RRD surgery. The study group comprised 145 patients who developed PVR within 3y of follow-up, while the control group comprised 161 patients with RRD who did not develop PVR. Cox regression analysis was utilized to identify independent associations between various risk markers and the occurrence of PVR. The mean age of patients was 52.31y (SD=13.29), and 54.25% ( Apart from macular involvement and smoking, the lipidaemic factors ApoA1 and ApoE are risk factors of PVR after primary RRD surgery. Show less
no PDF DOI: 10.18240/ijo.2026.04.12
APOE

Paeonol alleviates atherosclerosis by inhibiting CD8

Yulong Yang, Ting Zhang, Lishun Dong +4 more · 2026 · Journal of ethnopharmacology · Elsevier · added 2026-04-24
Moutan Cortex, a traditional Chinese medicine, has been used to treat cardiovascular diseases. Paeonol (Pae), a key bioactive compound, is responsible for its anti-atherosclerotic effects. Although CD Show more
Moutan Cortex, a traditional Chinese medicine, has been used to treat cardiovascular diseases. Paeonol (Pae), a key bioactive compound, is responsible for its anti-atherosclerotic effects. Although CD8 We investigated whether Pae inhibits atherosclerosis by targeting the spleen tyrosine kinase (SYK)/nuclear factor of activated T-cells c1 (NFATc1) pathway, thereby reducing CD8 High-fat diet-fed apolipoprotein E-deficient (ApoE Pae attenuated plaque formation and T-cell activation in ApoE SYK in CD8 Show less
no PDF DOI: 10.1016/j.jep.2026.121462
APOE

Alzheimer's Disease Risk Factor APOE4 Exerts Dimorphic Effects on Female Bone.

Charles A Schurman, Gurcharan Kaur, Serra Kaya +13 more · 2026 · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Wiley · added 2026-04-24
Individuals with Alzheimer's disease (AD) are at an increased risk of bone fracture, while osteoporosis in women is one of the earliest predictors of AD. Yet the mechanisms linking cognitive decline a Show more
Individuals with Alzheimer's disease (AD) are at an increased risk of bone fracture, while osteoporosis in women is one of the earliest predictors of AD. Yet the mechanisms linking cognitive decline and skeletal deterioration remain poorly defined. Proteomic analysis of cortical bone from aged 21-month-old mice revealed strong enrichment of neurodegeneration-associated proteins, including apolipoprotein E (Apoe) and amyloid precursor protein. Apoe localized specifically to osteocytes, with expression in aged female bone nearly twice that of young 4-month-old male bone. Because human APOE alleles confer different age-related AD risks, we examined their roles in bone using humanized APOE2, APOE3, and APOE4 knock-in mice and analyzed bone and hippocampus from the same animals. APOE4 produced marked sex-specific effects on the bone transcriptome and proteome compared with APOE2 or APOE3. Strikingly, APOE4-associated proteomic disruptions were stronger in female bone than in the hippocampus. Functionally, APOE4 caused bone fragility in females without altering cortical structure. These deficits stemmed from impaired osteocyte perilacunocanalicular remodeling. Our findings identify APOE4 as a molecular driver of early osteocyte dysfunction and reduced bone quality, disproportionately affecting females. These findings highlight osteocytes as potential targets for early diagnosis of age-related cognitive impairment and treatment for bone fragility, in females. Show less
no PDF DOI: 10.1002/advs.202523511
APOE

Bidirectional association between immune-mediated diseases and major depressive disorder: evidence from cohort, genome-wide pleiotropic, and experimental studies.

Xiaohua Chen, Huan Liu, Yurong Liu +16 more · 2026 · Molecular psychiatry · Nature · added 2026-04-24
Although immune-mediated diseases (IMDs) and major depressive disorder (MDD) commonly co-occur, the bidirectional relationship between them remains to be fully elucidated. Using data from the prospect Show more
Although immune-mediated diseases (IMDs) and major depressive disorder (MDD) commonly co-occur, the bidirectional relationship between them remains to be fully elucidated. Using data from the prospective UK Biobank cohort, we evaluated the bidirectional associations by time-varying Cox proportional hazards regression models and assessed shared genetic architecture using genome-wide association study summary statistics. Additionally, we employed collagen-induced arthritis (CIA) and chronic social defeat stress (CSDS) mouse models to investigate the relationship between rheumatoid arthritis (RA) and depression. Over 5,226,841 person-years of follow-up, 23,534 incident MDD cases were identified. The presence of any IMD was associated with higher MDD risk (hazard ratio [HR]: 1.95; 95% CI: 1.89-2.01). Conversely, 59,742 incident cases of IMD were documented. MDD was associated with increased IMD risk (HR: 1.47; 95% CI: 1.40-1.54). We observed significant global genetic correlations between IMDs and MDD (r Show less
📄 PDF DOI: 10.1038/s41380-026-03459-w
BDNF

Multiscale Mechanisms of Exercise-Induced Neuroplasticity: From Molecular Pathways to Network Dynamics and Behavioral Adaptation.

Xue Wang, Jun Zhang, Xiaoyu Wang +7 more · 2026 · Brain sciences · MDPI · added 2026-04-24
Exercise as a non-pharmacological measure is important to increase the brain plasticity hence improving cognitive performance as well as mental health. This narrative review describes in depth the hie Show more
Exercise as a non-pharmacological measure is important to increase the brain plasticity hence improving cognitive performance as well as mental health. This narrative review describes in depth the hierarchical multiscale processes of neuroplasticity to exercise, including the presence of neurotrophic factor regulation, cellular metabolic adaptations and neurotransmitter remodeling, up to the structure and functional reorganization of brain networks as seen through neuroimaging, and concluding with adaptive cognitive and behavioral outcomes. We further investigate the role of personal variations in genetic time and social environments in moderating the neuroplasticity of exercise. Furthermore, the review identifies the importance of combining multimodal visualization methods with computational models in generating accurate workout prescriptions and their potential of translation into clinical and educational practice. Lastly, the research problems and "grand challenges" are addressed, with a focus on the importance of exercise as a pleiotropic behavior-intervention and its general implications to the area of promoting brain health. Show less
📄 PDF DOI: 10.3390/brainsci16030294
BDNF

Brusatol derivative ameliorates rheumatoid arthritis and atherosclerosis with associated suppression of mitochondrial fission.

Ruicong Ma, Jiaqing Liu, Siwen Yang +8 more · 2026 · Phytomedicine : international journal of phytotherapy and phytopharmacology · Elsevier · added 2026-04-24
Brusatol (BRU), a major bioactive quassinoid isolated from Brucea javanica, has shown potential in the treatment of inflammatory diseases. As mitochondrial dysfunction has been implicated in chronic i Show more
Brusatol (BRU), a major bioactive quassinoid isolated from Brucea javanica, has shown potential in the treatment of inflammatory diseases. As mitochondrial dysfunction has been implicated in chronic inflammatory disorders, modulation of mitochondrial homeostasis may offer a potential approach for the treatment of rheumatoid arthritis (RA) and atherosclerosis (AS). To develop a novel BRU derivative through rational modification at the C11‑hydroxyl group and to compare the therapeutic effects of BRU and its derivative BRUD in experimental models of RA and AS, with particular focus on mitochondrial regulation and Drp1-associated signaling. This study combined in vivo and in vitro experiments to evaluate the pharmacological effects of BRU and BRUD and investigate the underlying mechanisms. The chemical constituents of BRU and BRUD were confirmed by HPLC and NMR spectroscopy ( In vivo studies demonstrated that both compounds ameliorated joint damage in CIA rats and reduced atherosclerotic lesion burden in ApoE These findings suggest that BRUD exhibits improved activity compared with BRU in RA and AS models, with protective effects associated with modulation of mitochondrial dysfunction, supporting its further evaluation as a lead compound. Show less
no PDF DOI: 10.1016/j.phymed.2026.158171
APOE

FOXF2 regulates pericyte-endothelial signaling required for vascular homeostasis after neonatal hyperoxic lung injury.

Fei Sun, Yuchen Zhao, Jonathan Do +8 more · 2026 · Nature communications · Nature · added 2026-04-24
Pulmonary vascular development is essential for alveolarization, and disruption of this process contributes to pathogenesis of bronchopulmonary dysplasia (BPD). Proper vascular development requires an Show more
Pulmonary vascular development is essential for alveolarization, and disruption of this process contributes to pathogenesis of bronchopulmonary dysplasia (BPD). Proper vascular development requires an orchestration of many cell types within the lung. However, the transcriptional mechanisms by which pericytes support the endothelium in the postnatal lung remain poorly understood. Herein, we identify FOXF2 as a critical transcription factor that governs pericyte maturation and function during postnatal lung development and regeneration. FOXF2 expression in pericytes increases postnatally and is selectively downregulated after neonatal hyperoxic injury. Pdgfrb-CreER mediated Foxf2 deletion in pericytes leads to pericyte hyperplasia, impaired migration, and reduced expression of angiogenic factors such as ANGPTL4. Transcriptomic and genomic studies demonstrate that FOXF2 maintains chromatin accessibility at pro-angiogenic loci and modulates paracrine signaling essential for endothelial regeneration. Loss of FOXF2 disrupts pericyte-endothelial crosstalk, leading to impaired angiogenesis and alveolarization as well as increased vascular permeability after neonatal lung injury. Altogether, FOXF2 acts as a key transcriptional regulator of the pericyte-driven vascular niche in the neonatal lung, highlighting the pathogenic role of pericyte dysfunction in BPD. Show less
📄 PDF DOI: 10.1038/s41467-026-69525-7
ANGPTL4

In vivo epigenome editing reduces circulating lipids and attenuates atherosclerosis in mice.

Wei Wang, Yingjie Zhang, Lin Chen +10 more · 2026 · Journal of genetics and genomics = Yi chuan xue bao · Elsevier · added 2026-04-24
Atherosclerotic cardiovascular disease remains the leading cause of global mortality, with hypercholesterolemia serving as a critical driver of atherogenesis. Although current lipid-lowering therapies Show more
Atherosclerotic cardiovascular disease remains the leading cause of global mortality, with hypercholesterolemia serving as a critical driver of atherogenesis. Although current lipid-lowering therapies substantially improve circulating lipid profiles, strategies that provide more durable, safe, and efficient control of lipid metabolism are still needed. Epigenome editing offers a promising approach for long-lasting repression of disease-modifying genes without altering the underlying DNA sequence. Here, we develop CRISPRoff platforms delivered by adeno-associated virus or lipid nanoparticle to epigenetically silence hepatic Hmgcr or Pcsk9 in vivo. In both C57BL/6J wild-type and ApoE Show less
no PDF DOI: 10.1016/j.jgg.2026.04.004
APOE

Cerebral FURIN deficiency impairs astrocytic lipophagy through ITGAV maturation.

Xiao-Yong Xie, Lu Wang, Shi-Qi Xie +14 more · 2026 · Autophagy · Taylor & Francis · added 2026-04-24
FURIN cleaves a subset of proproteins into functional mature fragments. Evidence suggests that FURIN is involved in brain development and the associated diseases, whereas the potential mechanisms rema Show more
FURIN cleaves a subset of proproteins into functional mature fragments. Evidence suggests that FURIN is involved in brain development and the associated diseases, whereas the potential mechanisms remain incompletely understood. Here, we report that cerebral FURIN-deficient mice exhibit cognitive decline and neurodegeneration. Lipid droplets (LDs) that are preferentially accumulated in astrocytes correlate with an increase of the LD markers PLIN2 and PLIN3, and conversely a decreased level of autophagic proteins including ATG5, BECN1 and MAP1LC3/LC3 as well as LAMP1. Accordingly, silencing of Show less
no PDF DOI: 10.1080/15548627.2025.2601039
BACE1

Dapagliflozin Attenuates Atherosclerosis Under Chronic Stress by Maintaining AKT/FoxO1 Pathway Through Downregulation of REDD1.

Jianyi Li, Luyao Zhang, Jiapei Xu +7 more · 2026 · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · added 2026-04-24
Chronic stress is associated with inflammatory activation and oxidative stress responses leading to endothelial dysfunction, which promotes the development of atherosclerosis (AS). SGLT2 inhibitors, s Show more
Chronic stress is associated with inflammatory activation and oxidative stress responses leading to endothelial dysfunction, which promotes the development of atherosclerosis (AS). SGLT2 inhibitors, such as Dapagliflozin (DAPA), exhibit a protective effect against cardiovascular diseases. However, the effects and mechanisms of DAPA on chronic stress-induced AS are largely unknown. The aim of this study was to determine whether DAPA confers a protective effect against chronic stress-induced AS and to elucidate its further molecular mechanisms. The combined high-fat diet-fed and chronic unpredictable mild stress in ApoE-/- mice and lipopolysaccharides- and corticosterone-induced human umbilical vein endothelial cells (HUVECs) were employed to evaluate the antiatherosclerotic effect of DAPA under chronic stress in vivo and in vitro. Histological staining, western blot analysis, siRNA transfection, reactive oxygen species (ROS) staining, and apoptosis assessment were used to investigate the potential mechanisms of DAPA against AS under chronic stress. The results indicate that DAPA significantly improved plaque size and increased plaque stability in the aorta under chronic stress and reduced inflammation and oxidative stress and inhibited apoptosis in the aorta and HUVECs. Chronic stress upregulated regulated in development and DNA damage response 1 (REDD1) expression, which exacerbated cellular inflammation, oxidative stress, and apoptosis levels, leading to endothelial dysfunction. In contrast, DAPA downregulated REDD1 expression and activated the AKT/FoxO1 pathway. In addition, p53 was a transcriptional regulator of REDD1 under chronic stress. More importantly, p53 agonists prevented DAPA from downregulating REDD1 and inhibited AKT/FoxO1 activation, thereby exacerbating chronic stress-induced endothelial dysfunction. These results suggest that DAPA effectively attenuates chronic stress-induced endothelial dysfunction and AS by downregulating REDD1 to activate the AKT/FoxO1 pathway. Show less
no PDF DOI: 10.1096/fj.202502868R
APOE

Potential profile and influencing factors of feedback-seeking behavior among nursing interns during the early stages of internships: a multicenter cross-sectional study.

Chuqin Xiong, Shuge Wang, Peiran Guo +6 more · 2026 · Frontiers in medicine · Frontiers · added 2026-04-24
Nursing interns often face maladjustment during the early stages of clinical practice, which not only directly affects their physical and mental health as well as work efficiency but also significantl Show more
Nursing interns often face maladjustment during the early stages of clinical practice, which not only directly affects their physical and mental health as well as work efficiency but also significantly inhibits their proactive feedback-seeking behavior (FSB). As an active self-regulation strategy, FSB can enhance interns' work initiative and promote role transition. However, existing research has yet to thoroughly investigate the potential heterogeneity and categorical characteristics of FSB within this population, and the role of psychological resources such as career adaptability in shaping these patterns requires further investigation. To investigate the status of FSB in early-stage nursing interns, identify latent subgroups via latent profile analysis (LPA), and analyze associated factors, thereby providing evidence for targeted clinical educational interventions. Multicenter cross-sectional research. This study employed a multistage stratified cluster sampling to survey 1,308 early-stage nursing interns from nine universities in Hubei, China, between June and September 2024. Data were collected using a demographic questionnaire, Feedback-Seeking Behavior Scale, and Career Adapt-Abilities Scale. LPA was employed to delineate FSB profiles and multivariate logistic regression analysis to examine the associated predictors. A total of 1,370 questionnaires were distributed, with 1,308 valid responses, yielding an effective response rate of 95.47%. The mean score on the feedback-seeking behavior scale was 5.06 ± 1.08. LPA identified three distinct feedback-seeking profiles: low (20.87%), moderate (38.3%), and high (40.83%). Education level, student cadre experience, internship hospital type, and career adaptability were significant predictors of profile membership ( FSB among early-stage nursing interns exhibited heterogeneity. Nursing educators and managers should implement tiered interventions: for the low and moderate feedback-seeking groups, career guidance and feedback awareness cultivation should be strengthened; for the high feedback-seeking group, peer modeling should be encouraged. This strategy can enhance proactive FSB, supports role transition and professional identity, and promotes long-term nursing workforce stability. Show less
📄 PDF DOI: 10.3389/fmed.2026.1664329
LPA

Effect and mechanism of compound Nujia honey paste on chronic unpredictable mild stress (CUMS) depression rats based on network pharmacology analysis.

Shaowei Fu, Mahinur Bakri, Xueying Lu +3 more · 2026 · Journal of ethnopharmacology · Elsevier · added 2026-04-24
Compound Nujia honey paste (Nujia), a classic formulation from Traditional Uyghur Medicine, has been historically used for depression treatment and is listed in the Catalog of Ancient Classical Famous Show more
Compound Nujia honey paste (Nujia), a classic formulation from Traditional Uyghur Medicine, has been historically used for depression treatment and is listed in the Catalog of Ancient Classical Famous Formulas issued by the National Administration of Traditional Chinese Medicine and the National Medical Products Administration. Clarifying its pharmacodynamic material basis is essential for understanding its efficacy, yet this remains incompletely characterized. This study aimed to systematically elucidate Nujia's antidepressant efficacy and mechanisms by combining chemical analysis, computational prediction, and experimental validation in a CUMS rat model, providing a comprehensive approach to understanding its action. This study employed LC/MS to analyze the chemical constituents and blood-absorbed compounds of Nujia. This was combined with network pharmacology and molecular docking to predict and verify its potential antidepressant targets and signaling pathways. Using behavioral tests, ELISA, histopathology, Western blot, and qRT-PCR in a CUMS rat model, the research thoroughly evaluated Nujia's therapeutic effects and mechanisms, fostering trust in the findings. In this study, LC/MS analysis identified 124 chemical constituents from Nujia, and further analysis determined 26 blood-absorbed compounds (including 10 prototype compounds). Network pharmacology analysis revealed that its potential antidepressant effects are closely associated with core targets such as AKT1 and TNF, a prediction subsequently verified by molecular docking results. In the CUMS-induced rat model of depression, intervention with Nujia significantly ameliorated depression-like behaviors in the animals and alleviated neuropathological damage in the hippocampus and prefrontal cortex. Mechanistic investigations revealed that Nujia upregulated the levels of monoamine neurotransmitters (5-HT, DA, NE) and neurotrophic factors (BDNF, NGF) in serum, while downregulating the expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-18). Further molecular experiments confirmed that Nujia likely mitigates neuroinflammation by inhibiting the TNF-α/NF-κB signaling pathway, and inhibits neuronal apoptosis by activating the PI3K/AKT signaling pathway and its downstream anti-apoptotic proteins. Furthermore, Nujia significantly upregulated the expression of key synaptic plasticity proteins (SYP, GAP43, and PSD95) in hippocampal tissue, thereby enhancing synaptic structure and function. These findings underscore the complex, multi-target mechanisms underlying Nujia's antidepressant effects, encouraging further exploration of its therapeutic potential. This study systematically elucidates that Nujia achieves its antidepressant therapeutic effects by mediating multi-pathway synergistic actions, including but not limited to the TNF-α/NF-κB and PI3K/AKT signaling pathways, to ameliorate neuroinflammation, attenuate apoptosis, and enhance synaptic plasticity. Show less
no PDF DOI: 10.1016/j.jep.2026.121518
BDNF chronic unpredictable mild stress cums depression network pharmacology pharmacology stress traditional chinese medicine

Relationship between amyloid burden, cholinergic integrity, and cognitive function.

Li-Hua Lee, Chia-Ju Chou, Yao-Chia Shih +4 more · 2026 · Journal of Alzheimer's disease : JAD · SAGE Publications · added 2026-04-24
BackgroundAmyloid accumulation and degeneration of the cholinergic white matter pathways are key factors in early Alzheimer's disease pathogenesis and progression. However, the relationship between th Show more
BackgroundAmyloid accumulation and degeneration of the cholinergic white matter pathways are key factors in early Alzheimer's disease pathogenesis and progression. However, the relationship between them remains unclear.ObjectiveTo investigate the association between amyloid accumulation, the integrity of cholinergic white matter pathways, and cognitive performance.MethodsThis cross-sectional study recruited 109 individuals, including 37 controls with normal cognition and 72 patients with early Alzheimer's disease. All participants underwent neuropsychological testing: the Mini-Mental Status Examination (MMSE), Clinical Dementia Rating scale with sum of box (CDR-SB), and verbal fluency tests. Cholinergic white matter integrity and amyloid burden were assessed through diffusion tensor imaging study (DTI) and amyloid positron emission tomography (PET). Stepwise linear regression analyses were performed. Partial correlations between amyloid burden and cholinergic integrity were also evaluated according to apolipoprotein E4 ( Show less
no PDF DOI: 10.1177/13872877251406620
APOE

Latent Physical Activity Patterns and Their Related Factors in Breast Cancer Patients During Chemotherapy Intervals.

Siqi Shi, Guangting Chang, Chunying Xie +3 more · 2026 · Patient preference and adherence · added 2026-04-24
Previous research on breast cancer patients has primarily examined singular behavioral indicators, often overlooking the coexistence and interaction between physical activity and sedentary behavior-pa Show more
Previous research on breast cancer patients has primarily examined singular behavioral indicators, often overlooking the coexistence and interaction between physical activity and sedentary behavior-particularly screen-based sedentary time. This study aims to identify the latent activity pattern categories among breast cancer patients during chemotherapy intervals and explore their associated factors to inform targeted behavioral interventions. A cross-sectional survey was conducted with 292 breast cancer patients undergoing chemotherapy intervals at four general hospitals in Foshan, Guangdong Province. Latent Profile Analysis (LPA) was applied as a person-centered analytic approach to identify distinct activity pattern profiles. Data were collected using a general information questionnaire, the Adult Sedentary Behavior Questionnaire (ASBQ), the Chinese version of the International Physical Activity Questionnaire (IPAQ-SC), the Exercise Self-Efficacy Scale (ESES), the Perceived Social Support Scale (PSSS), and the Hospital Anxiety and Depression Scale (HADS). The activity patterns of breast cancer patients were categorized into three groups: Moderate Activity-Dominant Group (37.33%), Screen-Sedentary High-Risk Group (8.22%), and Activity-Sedentary Coexistence Group (54.45%). Logistic regression analysis showed that, compared to the Moderate Activity-Dominant Group, patients with low exercise self-efficacy and higher anxiety and depression levels were more likely to be classified into the Screen-Sedentary High-Risk Group and Activity-Sedentary Coexistence Group. Higher education levels and being on medical leave were associated with a higher probability of belonging to the Activity-Sedentary Coexistence Group (all Activity patterns in breast cancer patients show significant heterogeneity. Healthcare providers should pay attention to the individual physical activity characteristics of patients and offer personalized physical activity guidance. Tailored interventions that meet the needs of breast cancer patients should be developed to improve health outcomes. Show less
📄 PDF DOI: 10.2147/PPA.S561144
LPA

OGT deficiency in vascular smooth muscle orchestrates foam cell formation and PANoptosis during atherosclerotic progression.

Boao Liu, Huiping Ma, Yunxuan Guo +5 more · 2026 · Atherosclerosis · Elsevier · added 2026-04-24
Vascular smooth muscle cells (VSMCs) contribute to atherosclerotic foam cell formation, but mechanisms regulating their phenotypic switching and programmed cell death remain unclear. O-GlcNAcylation, Show more
Vascular smooth muscle cells (VSMCs) contribute to atherosclerotic foam cell formation, but mechanisms regulating their phenotypic switching and programmed cell death remain unclear. O-GlcNAcylation, a nutrient-sensitive post-translational modification implicated in vascular calcification, lacks defined roles in VSMC foam cell biology. Inducible smooth muscle-specific Ogt knockout mice on an Apoe OGT expression and global O-GlcNAcylation were reduced in VSMCs during atherogenic progression. Ogt deletion in VSMCs promoted foam cell formation with enhanced lipid accumulation but paradoxically reduced atherosclerotic lesion area concurrent with increased intraplaque cell death. Both genetic and pharmacological OGT inhibition recapitulated this duality in vitro, simultaneously accelerating lipid accumulation while triggering PANoptosis, as evidenced by concurrent activation of cleaved caspase-3, phosphorylated MLKL, and cleaved GSDMD. Individual inhibition of apoptosis, necroptosis, or pyroptosis provided only partial rescue. OGT acts as a dual regulator of VSMC fate, attenuating plaque burden through PANoptosis induction while promoting foam cell formation, revealing its complex role in atherosclerosis pathogenesis and suggesting context-dependent therapeutic implications. Show less
no PDF DOI: 10.1016/j.atherosclerosis.2025.120604
APOE

Mechanistic insights into the antidepressant effects of the Angelica sinensis and Ligusticum chuanxiong Herb Pair: Involvement of the PI3K/AKT signaling pathway.

Tong Yi Yang, Xiang Ming Sun, Zhi Wei Xiong +6 more · 2026 · Journal of ethnopharmacology · Elsevier · added 2026-04-24
The Angelica sinensis and Ligusticum chuanxiong Herb Pair (DC) serves as a core pairing in Traditional Chinese Medicine for treating blood stasis and blood deficiency syndromes, which are frequently a Show more
The Angelica sinensis and Ligusticum chuanxiong Herb Pair (DC) serves as a core pairing in Traditional Chinese Medicine for treating blood stasis and blood deficiency syndromes, which are frequently associated with depressive-like symptoms in clinical practice. The antidepressant potential of this combination aligns with its traditional functions of promoting qi circulation, activating blood flow, and alleviating depression. This study aims to investigate the antidepressant effects of DC and its potential mechanisms through a combination of network pharmacology prediction and in vitro and in vivo experimental validation. Network pharmacology screening identified active components and target molecules in DC, constructing a component-target network and validating binding activity through molecular docking. A CUMS-induced rat model of depression was established, with drug efficacy evaluated via behavioral tests (forced swim, sucrose preference, and open field tests) and blood rheology parameters measured. ELISA assay of neurotransmitter and inflammatory factor levels in serum and hippocampal tissue, Observation of histopathological changes in hippocampal tissue using HE and Nissl staining, Western blot and immunofluorescence assays were performed to detect the expression of proteins in the PI3K/AKT pathway. An in vitro inflammatory model was established by inducing BV-2 cells with LPS. The MTT assay was used to screen for the safe concentration of drug-containing serum and observe cell morphology, the Gries method for detecting NO release, ELISA for detecting inflammatory cytokines, Western blot analysis of PI3K/AKT pathway proteins was performed, and pathway inhibition was validated using LY294002. Through network pharmacology analysis, seven major active components of DC and 197 related functional targets for depression treatment were identified, with the majority enriched in the PI3K/AKT signaling pathway. Behavioral studies and in vivo experiments indicate that DC significantly ameliorates depressive-like behaviors in CUMS rats, reduces blood viscosity, increases hippocampal tissue levels of 5-HT, NE, and DA, decreases IL-1β, IL-6, and TNF-α content, and mitigates hippocampal neuronal damage. Western blot and immunofluorescence results indicate that DC can activate the PI3K/AKT pathway, upregulating p-AKT and BDNF expression. In vitro experiments further confirmed that the drug-containing serum could suppress LPS-induced inflammatory responses in BV-2 cells, reducing the release of factors such as NO and IL-1β. This effect was reversible upon treatment with the PI3K inhibitor LY294002. DC exhibits potent antidepressant effects by modulating the PI3K/AKT pathway to enhance neurotransmitter release and reduce inflammatory factor levels. This mechanism protects neurons and alleviates neuroinflammation, thereby exerting antidepressant effects. Show less
no PDF DOI: 10.1016/j.jep.2026.121419
BDNF antidepressant depression herb pair pi3k/akt signaling pathway traditional chinese medicine

Associations of physical activity intensity with the non-high-density lipoprotein to high-density lipoprotein cholesterol ratio and mortality in middle-aged and older adults: New evidence from China.

Fangyu Zhao, Xuemin Peng, Yongbin Zhuang +4 more · 2026 · Experimental gerontology · Elsevier · added 2026-04-24
The non-high-density lipoprotein to high-density lipoprotein cholesterol ratio (NHHR) has emerged as a comprehensive lipid index reflecting the balance between atherogenic and anti-atherogenic lipopro Show more
The non-high-density lipoprotein to high-density lipoprotein cholesterol ratio (NHHR) has emerged as a comprehensive lipid index reflecting the balance between atherogenic and anti-atherogenic lipoproteins. However, evidence on how different intensities and durations of physical activity (PA) influence NHHR remains scarce, particularly in aging populations. Data were obtained from China Health and Retirement Longitudinal Study. PA was self-reported and categorized as high- (HPA), moderate- (MPA), or low-intensity (LPA). Multivariable linear regression models assessed associations between PA and NHHR, with subgroup, sensitivity, and dose-response analyses further exploring robustness. Cox regression and mediation analyses examined the associations of PA and NHHR with 10-year all-cause mortality. Higher levels of total, moderate-, and high-intensity PA were significantly associated with lower NHHR. The results were generally consistent with a graded pattern, with lower NHHR observed at higher activity durations, particularly for moderate-to-vigorous activity. Exploratory mediation analyses suggested that NHHR may partially account for the inverse association between PA and mortality. This study adds large-scale, population-based evidence on the associations between different PA intensities and NHHR. Regular moderate-to-vigorous PA is associated with more favorable lipid profiles and lower mortality risk. These findings highlight NHHR as a valuable biomarker linking physical activity to cardiometabolic health and longevity in middle-aged and older adults. Show less
no PDF DOI: 10.1016/j.exger.2026.113098
LPA

Gut-Brain Metabolic Remodeling Mediates the Neuroprotective Effects of Combined Shrimp and Corn Peptides in Scopolamine-Induced Cognitive Impairment.

Xiaomeng Xu, Ruowen Liu, Enhui Ma +2 more · 2026 · Foods (Basel, Switzerland) · MDPI · added 2026-04-24
(1) Background: Bioactive peptides from marine and plant sources show neuroprotective potential, yet how their combination ratios affect memory regulation via the gut-brain axis remains unclear. This Show more
(1) Background: Bioactive peptides from marine and plant sources show neuroprotective potential, yet how their combination ratios affect memory regulation via the gut-brain axis remains unclear. This study investigated the effects of different ratios of marine peptide QMDDQ (Glutamine-Methionine-Aspartate-Aspartate-Glutamine) and plant peptide AGLPM (Alanine-Glycine-Leucine-Proline-Methionine) on scopolamine-induced memory impairment in mice. (2) Methods: Cognitive function was assessed using the Morris water maze and novel object recognition tests. Nissl staining, microplate-based assays for acetylcholine (ACh) content and acetylcholinesterase (AChE) activity, Western blotting for neurotrophic factors, LC-MS/MS-based intestinal peptide profiling, and HPLC-based brain amino acid analysis were performed. (3) Results: The 1:1 ratio most effectively restored learning and memory, regulated hippocampal cholinergic function, mitigated neuronal damage, and elevated BDNF, NGF, and NTF-3 expression. In the gut, peptides were hydrolyzed into glutamate- and proline-rich fragments, which influenced brain amino acid balance by elevating glutamate and proline levels while reducing NH Show less
📄 PDF DOI: 10.3390/foods15050827
BDNF

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

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

Rs12516 A allele elevates the risk of colorectal cancer via functional CeRNA network of BDNF-AS, miR-4704-5p and BRCA1.

Daxu Liu, Zhijun Fan, Teng Zhang +5 more · 2026 · BMC cancer · BioMed Central · added 2026-04-24
DNA double-strand break repair has emerged as a vital pathway to repair DNA damage seriously related to the risk of colorectal cancer (CRC). To explore valid susceptible biomarkers of CRC via investig Show more
DNA double-strand break repair has emerged as a vital pathway to repair DNA damage seriously related to the risk of colorectal cancer (CRC). To explore valid susceptible biomarkers of CRC via investigating the association of single nucleotide polymorphisms in DSBR genes with CRC risk, seven polymorphisms located in 3'-untranslated regions of DSBR genes including RAD51 rs11852786, RAD51B rs963917, BRCA1 rs12516 and rs8176318, BRCA2 rs15869, XRCC4 rs2035990 and XRCC5 rs2440 were detected and analyzed in a CRC case-control study (cases (202) and also controls (202)). The PolymiRTs and miRSNP database were used to predict the microRNAs that can bind to 3'UTR SNPs. Since long non-coding RNA as a miRNA "sponge" played the role of competing endogenous RNA, DAVID database was used to find the lncRNAs that can bind to the candidate miRNA seed sequences. BRCA1 rs12516 minor A allele was found to be linked with a higher risk of CRC than its major G allele (OR = 2.716, 95%CI: 1.394-5.292, P = 0.003). The stratified analyses demonstrated rs12516 AA genotype with a more elevated risk of CRC in male (OR = 3.089, 95% CI:1.315 ~ 7.255) or age > 50 population (OR = 3.318, 95%CI:1.571 ~ 7.006) than its GG genotype. BRCA1 rs12516 A allele created a novel miR-4704-5p binding target, and there was a negative correlation between miR-4704-5p and BRCA1 expression (r =-0.7199, P = 0.0440). Based on the theory of ceRNA network, it was predicted that lncRNA BDNF-AS can competitively bind to miR-4704-5p, whose expression was exhibited to be negatively correlated with BDNF-AS (r=-0.3481, P = 0.0375). On the contrary, BDNF-AS expression showed a positive correlation with BRCA1 mRNA level in colorectal tissue carrying rs12516 of A allele (adjacent tissue: r = 0.7269, P = 0.0411; cancer tissue: r = 0.7134, P = 0.0469). ROC curve showed both BDNF-AS (AUC = 0.651, P = 0.0277) and miR-4704-5p (AUC = 0.7215, P = 0.0012) can distinguish CRC tissues from their adjacent tissues. BRCA1 rs12516 is characterized as a potential biomarker associated with CRC risk, via a possible functional ceRNA network of BDNF-AS, miR-4704-5p and BRCA1. The interaction of a lower expression of BDNF-AS, a higher expression of miR-4704-5p and rs12516 A allele could together increase the risk of colorectal cancer. Show less
📄 PDF DOI: 10.1186/s12885-025-14692-x
BDNF

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