👤 Feiyue Chen

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2981
Articles
1996
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Also published as: Wen-Chau Chen, Jingzhao Chen, Dexi Chen, Haifeng Chen, Chung-Jen Chen, Bo-Jun Chen, Gao-Feng Chen, Changyan Chen, Weiwei Chen, Fenghua Chen, Xiaojiang S Chen, Xiu-Juan Chen, Jung-Sheng Chen, Xiao-Ying Chen, Chong Chen, Junyang Chen, YiPing Chen, Xiaohan Chen, Li-Zhen Chen, Jiujiu Chen, Shin-Wen Chen, Guangping Chen, Dapeng Chen, Ximei Chen, Renwei Chen, Jianfei Chen, Yulu Chen, Yu-Chi Chen, Jia-De Chen, Rongfang Chen, She Chen, Zetian Chen, Tianran Chen, Emily Chen, Baoxiang Chen, Ya-Chun Chen, Dongxue Chen, Wei-xian Chen, Danmei Chen, Ceshi Chen, Junling Chen, Xia Chen, Daoyuan Chen, Yongbin Chen, Chi-Yu Chen, Dian Chen, Xiuxiu Chen, Bo-Fang Chen, Fangyuan Chen, Jin-An Chen, Xiaojuan Chen, Zhuohui Chen, Junqi Chen, Lina Chen, Fangfang Chen, Hanwen Chen, Yilei Chen, Po-Han Chen, Xiaoxiang Chen, Jimei Chen, Guochong Chen, Yanyun Chen, Yifei Chen, Cheng-Yu Chen, Zi-Jiang Chen, Jiayuan Chen, Miaoran Chen, Junshi Chen, Yu-Ying Chen, Pengxiang Chen, Hui-Ru Chen, Yupeng Chen, Ida Y-D Chen, Xiaofeng Chen, Qiqi Chen, Shengnan Chen, Mao-Yuan Chen, Lizhu Chen, Weichan Chen, Xiang-Bin Chen, Hanxi Chen, Sulian Chen, Zoe Chen, Minghong Chen, Chi Chen, Yananlan Chen, Yanzhu Chen, Shiyi Chen, Ze-Xu Chen, Zhiheng Chen, Jia-Mei Chen, Shuqin Chen, Yi-Hau Chen, Danni Chen, Donglong Chen, Xiaomeng Chen, Yidong Chen, Keyu Chen, Hao Chen, Junmin Chen, Wenlong Chen, Yufei Chen, Wanbiao Chen, Mo Chen, Youjia Chen, Xin-Jie Chen, Lanlan Chen, Huapu Chen, Shuaiyin Chen, Jing-Hsien Chen, Hengsheng Chen, Bing-Bing Chen, Fa-Xi Chen, Zhiqiang Chen, Ming-Huang Chen, Liangkai Chen, Li-Jhen Chen, Zhi-Hao Chen, Yinzhu Chen, Guanghong Chen, Gaozhi Chen, Jiakang Chen, Yongke Chen, Guangquan Chen, Li-Hsien Chen, Yiduo Chen, Zongnan Chen, Jing Chen, Meilan Chen, Jin-Shuen Chen, Huanxiong Chen, Yann-Jang Chen, Guozhong Chen, Yu-Bing Chen, Xiaobin Chen, Catherine Qing Chen, Youhu Chen, Hui Mei Chen, L F Chen, Haiyang Chen, Ruilin Chen, Peng Chen, Kailang Chen, Chao Chen, Suipeng Chen, Zemin Chen, Jianlin Chen, Shang-Chih Chen, Yen-Hsieh Chen, Jia-Lin Chen, Chaojin Chen, Minglang Chen, Xiatian Chen, Zeyu Chen, Kang Chen, Mei-Chi Chen, Jihai Chen, Pei Chen, Defang Chen, Zhao Chen, Tianrui Chen, Tingtao Chen, Caressa Chen, Jiwei Chen, Xuerong Chen, Yizhi Chen, XueShu Chen, Mingyue Chen, Huichao Chen, Chun-Chi Chen, Xiaomin Chen, Hetian Chen, Yuxing Chen, Jie-Hua Chen, Chuck T Chen, Yuanjia Chen, Hong Chen, Jianxiong Chen, S Chen, D M Chen, Jiao-Jiao Chen, Gongbo Chen, Xufeng Chen, Xiao-Jun Chen, Harn-Shen Chen, Qiu Jing Chen, Tai-Heng Chen, Pei-Lung Chen, Kaifu Chen, Huang-Pin Chen, Tse-Wei Chen, Yanrong Chen, Xianfeng Chen, Chung-Yung Chen, Yuelei Chen, Qili Chen, Guanren Chen, TsungYen Chen, Yu-Si Chen, Junsheng Chen, Min-Jie Chen, Xin-Ming Chen, Jiabing Chen, Sili Chen, Qinying Chen, Yue Chen, Lin Chen, Xiaoli Chen, Zhuo Chen, Aoshuang Chen, Junyu Chen, Chunji Chen, Yian Chen, Shanchun Chen, Shuen-Ei Chen, Canrong Chen, Shih-Jen Chen, Yaowu Chen, Han Chen, Yih-Chieh Chen, Wei-Cong Chen, Yanfen Chen, Tao Chen, Huangtao Chen, Jingyi Chen, Sheng Chen, Jing-Wen Chen, Gao Chen, Lei-Lei Chen, Kecai Chen, Yao-Shen Chen, Haiyu Chen, W Chen, Xiaona Chen, Cheng-Sheng Chen, X R Chen, Shuangfeng Chen, Jingyuan Chen, Xinyuan Chen, Huanhuan Chen, Mengling Chen, Liang-Kung Chen, Ming-Huei Chen, Hongshan Chen, Cuncun Chen, Qingchao Chen, Yanzi Chen, Lingli Chen, Shiqian Chen, Liangwan Chen, Lexia Chen, Wei-Ting Chen, Zhencong Chen, Tzy-Yen Chen, Mingcong Chen, Honglei Chen, Yuyan Chen, Huachen Chen, Yu Chen, Li-Juan Chen, Aozhou Chen, Xinlin Chen, Wai Chen, Dake Chen, Bo-Sheng Chen, Meilin Chen, Kequan Chen, Hong Yang Chen, Yan Chen, Bowei Chen, Silian Chen, Jian Chen, Yongmei Chen, Ling Chen, Jinbo Chen, Yingxi Chen, Ge Chen, Max Jl Chen, C Z Chen, Weitao Chen, Xiaole L Chen, Yonglu Chen, Shih-Pin Chen, Jiani Chen, Huiru Chen, San-Yuan Chen, Bing Chen, Xiao-ping Chen, Shuchun Chen, Zhaolin Chen, Qianxue Chen, Xiaoyang Chen, Bowang Chen, Yinghui Chen, Ting-Ting Chen, Xiao-Yang Chen, Chi-Yuan Chen, Zhi-zhe Chen, Ting-Tao Chen, Xiaoyun Chen, Min-Hsuan Chen, Kuan-Ting Chen, Yongheng Chen, Wenhao Chen, Shengyu Chen, Kai Chen, Yueh-Peng Chen, Guangju Chen, Minghua Chen, Hong-Sheng Chen, Qingmei Chen, Song-Mei Chen, Limei Chen, Yuqi Chen, Yuyang Chen, Yang-Ching Chen, Yu-Gen Chen, Peizhan Chen, Rucheng Chen, Jin-Xia Chen, Szu-Chieh Chen, Xiaojun Chen, Jialing Chen, Heni Chen, Yi Feng Chen, Sen Chen, Alice Ye A Chen, Wen Chen, Han-Chun Chen, Dawei Chen, Fangli Chen, Ai-Qun Chen, Zhaojun Chen, Gong Chen, Yishan Chen, Zhijing Chen, Qiuxuan Chen, Miao-Der Chen, Fengwu Chen, Weijie Chen, Weixin Chen, Mei-Ling Chen, Hung-Po Chen, Rui-Pei Chen, Nian-Ping Chen, Tielin Chen, Canyu Chen, Xiaotao Chen, Nan Chen, C Chen, Juanjuan Chen, Xinan Chen, Jiaping Chen, Xiao-Lin Chen, Jianping Chen, Yayun Chen, Le Qi Chen, Jen-Sue Chen, Mechi Chen, Miao-Yu Chen, Zhou Chen, Szu-Han Chen, Zhen Bouman Chen, Baihua Chen, Qingao Chen, Shao-Ke Chen, Feng Chen, Jiawen Chen, Lianmin Chen, Sifeng Chen, Mengxia Chen, Xueli Chen, Can Chen, Yibo Chen, Zinan Chen, Lei-Chin Chen, Carol Chen, Yanlin Chen, Zihang Chen, Zaozao Chen, Haiqin Chen, Lu Hua Chen, Zhiyuan Chen, Meiyu Chen, Du-Qun Chen, Keying Chen, Naifei Chen, Peixian Chen, Jin-Ran Chen, Yijun Chen, Yulin Chen, Fumei Chen, Zhanfei Chen, Zhe-Yu Chen, Xin-Qi Chen, Valerie Chen, Ru Chen, Mengqing Chen, Runsheng Chen, Tong Chen, Tan-Zhou Chen, Suet Nee Chen, Cuicui Chen, Yifan Chen, Tian Chen, XiangFan Chen, Lingyi Chen, Hsiao-Yun Chen, Kenneth L Chen, Ni Chen, Huishan Chen, Fang-Yu Chen, Ken Chen, Yongshen Chen, Qiong Chen, Mingfeng Chen, Shoudeng Chen, Qiao Chen, Qian Chen, Yuebing Chen, Xuehua Chen, Chang-Lan Chen, Min-Hu Chen, Hongbin Chen, Jingming Chen, Qing Chen, Yu-Fan Chen, Hao-Zhu Chen, Yunjia Chen, Zhongjian Chen, Mingyi Chen, Qianping Chen, Huaxin Chen, Dong-Mei Chen, Peize Chen, Leijie Chen, Ming-Yu Chen, Jiaxuan Chen, Xiao-chun Chen, Wei-Min Chen, Ruisen Chen, Xuanwei Chen, Guiquan Chen, Minyan Chen, Feng-Ling Chen, Yili Chen, Alvin Chen, Xiaodong Chen, Bohong Chen, Chih-Ping Chen, Xuanjing Chen, Shuhui Chen, Ming-Hong Chen, Tzu-Yu Chen, Brian Chen, Bowen Chen, Kai-En Chen, Szu-Chia Chen, Guangchun Chen, Fang Chen, Chuyu Chen, Haotian Chen, Xiaoting Chen, Shaoliang Chen, Chun-Houh Chen, Shali Chen, Yu-Cheng Chen, Zhijun Chen, B Chen, Yuan Chen, Zhanglin Chen, Chaoran Chen, Xing-Long Chen, Zhinan Chen, Yu-Hui Chen, Yuquan Chen, Andrew Chen, Fengming Chen, Guangyong Chen, Jun Chen, Wenshuo Chen, Yi-Guang Chen, Jing-Yuan Chen, Kuangyang Chen, Mingyang Chen, Shaofei Chen, Weicong Chen, Gonghai Chen, Di-Long Chen, Limin Chen, Jishun Chen, Yunfei Chen, Caihong Chen, Tongsheng Chen, Ligang Chen, Wenqin Chen, Shiyu Chen, Xiaoyong Chen, Christina Y Chen, Yushan Chen, Ginny I Chen, Guo-Jun Chen, Xianzhen Chen, Wanling Chen, Kuan-Jen Chen, Maorong Chen, Kaijian Chen, Erqu Chen, Shen Chen, Quan Chen, Zian Chen, Yi-Lin Chen, Juei-Suei Chen, Yi-Ting Chen, Huaiyong Chen, Minjian Chen, Qianzhi Chen, Jiahao Chen, Xikun Chen, Juan-Juan Chen, Xiaobo Chen, Tianzhen Chen, Ziming Chen, Qianbo Chen, Jindong Chen, Jiu-Chiuan Chen, Yinwei Chen, Carl Pc Chen, Li-Hsin Chen, Jenny Chen, Ruoyan Chen, Yanqiu Chen, Yen-Fu Chen, Haiyan Chen, Zhebin Chen, Si Chen, Jian-Qiao Chen, Yang-Yang Chen, Ningning Chen, Zhifeng Chen, Zhenyi Chen, Hangang Chen, Zihe Chen, Mengdi Chen, Zhichuan Chen, Xu Chen, Huixi Chen, Weitian Chen, Bao-Sheng Chen, Tien-Hsing Chen, Junchen Chen, Yan-yan Chen, Xiangning Chen, Sijia Chen, Xinyan Chen, Kuan-Yu Chen, Qunxiang Chen, Guangliang Chen, Bing-Huei Chen, Fei Xavier Chen, Zhangcheng Chen, Qianming Chen, Xianze Chen, Yanhua Chen, Qinghao Chen, Yanting Chen, Sijuan Chen, Chen-Mei Chen, Qiankun Chen, Jianan Chen, Rong Chen, Xiankai Chen, Kaina Chen, Gui-Hai Chen, Y-D Ida Chen, Quanjiao Chen, Shuang Chen, Lichang Chen, Xinyi Chen, Yong-Jun Chen, Zhaoli Chen, Chunnuan Chen, Jui-Chang Chen, Zhiang Chen, Weirui Chen, Zhenguo Chen, Jennifer F Chen, Zhiguo Chen, Kunmei Chen, Huan-Xin Chen, Mengyan Chen, Dongrong Chen, Siyue Chen, Xianyue Chen, Chien-Lun Chen, YiChung Chen, Guang Chen, Quanwei Chen, Zongming E Chen, Ting-Huan Chen, Michael C Chen, Jinli Chen, Beth L Chen, Yuh-Lien Chen, Peihong Chen, Qiaoling Chen, Jiale Chen, Shufeng Chen, Xiaowan Chen, Xian-Kai Chen, Ling-Yan Chen, Yen-Ling Chen, Guiying Chen, Guangyi Chen, Yuling Chen, Xiangqiu Chen, Haiquan Chen, Cuie Chen, Gui-Lai Chen, R Chen, Heng-Yu Chen, Yongxun Chen, Fuxiang Chen, Mingmei Chen, Hua-Pu Chen, Yulong Chen, Zhitao Chen, Guohua Chen, Cheng-Yi Chen, Hongxu Chen, Yuanhao Chen, Qichen Chen, Hualin Chen, Guo-Rong Chen, Rongsheng Chen, Xuesong Chen, Wei-Fei Chen, Bao-Bao Chen, Anqi Chen, Yi-Han Chen, Ying-Jung Chen, Jinhuang Chen, Guochao Chen, Lei Chen, S N Chen, Songfeng Chen, Chenyang Chen, Xing Chen, Letian Chen, Meng Xuan Chen, Xiang-Mei Chen, Xiaoyan Chen, Yi-Heng Chen, D F Chen, Bang Chen, Jiaxu Chen, Wei Chen, Sihui Chen, Shu-Hua Chen, I-M Chen, Xuxin Chen, Zhangxin Chen, Jin Chen, Yin-Huai Chen, Wuyan Chen, Bingqing Chen, Bao-Fu Chen, Zhen-Hua Chen, Dan Chen, Zhe-Sheng Chen, Ranyun Chen, Wanyin Chen, Xueyan Chen, Xiaoyu Chen, Tai-Tzung Chen, Xiaofang Chen, Yongxing Chen, Yanghui Chen, Hekai Chen, Yuanwei Chen, Liang Chen, Hui-Jye Chen, Chengchun Chen, Han-Bin Chen, Shuaijie Chen, Yibing Chen, Kehui Chen, Shuhai Chen, Xueling Chen, Ying-Jie Chen, Qingxing Chen, Fang-Zhi Chen, Mei-Hua Chen, Yutong Chen, Lixian Chen, Alex Chen, Qiuhong Chen, Qiuxia Chen, Liping Chen, Hou-Tsung Chen, Zhanghua Chen, Chun-Fa Chen, Chian-Feng Chen, Benjamin P C Chen, Yewei Chen, Mu-Hong Chen, Jianshan Chen, Xiaguang Chen, Meiling Chen, Heng Chen, Ying-Hsiang Chen, Longyun Chen, Dengpeng Chen, Jichong Chen, Shixuan Chen, Liaobin Chen, Everett H Chen, ZhuoYu Chen, Qihui Chen, Zhiyong Chen, Nuan Chen, Hongmei Chen, Guiqian Chen, Yan Q Chen, Fengling Chen, Hung-Chang Chen, Zhenghong Chen, Chengsheng Chen, Hegang Chen, Huei-Yan Chen, Liutao Chen, Meng-Lin Chen, Xi Chen, Qing-Juan Chen, Linna Chen, Xiaojing Chen, Lang Chen, Gengsheng Chen, Fengrong Chen, Weilun Chen, Shi Chen, Wan-Yi Chen, On Chen, Yufeng Chen, Benjamin Chen, Hui-Zhao Chen, Bo-Rui Chen, Kangyong Chen, Ruixiang Chen, Weiyong Chen, Ning-Hung Chen, Meng-Ping Chen, Huimei Chen, Ying Chen, Kang-Hua Chen, Pei-zhan Chen, Liujun Chen, Hanqing Chen, Chengchuan Chen, Guojun Chen, Yongfa Chen, Li Chen, Mingling Chen, Jacinda Chen, Jinlun Chen, Kun Chen, Yi Chen, Chiung Mei Chen, Shaotao Chen, Tianhong Chen, Chanjuan Chen, Yuhao Chen, Huizhi Chen, Chung-Hsing Chen, Qiuchi Chen, Haoting Chen, Luzhu Chen, Huanhua Chen, Long Chen, Jiang-hua Chen, Kai-Yang Chen, Jing-Zhou Chen, Yong-Syuan Chen, Lifang Chen, Ruonan Chen, Meimei Chen, Qingchuan Chen, Liugui Chen, Shaokun Chen, Yi-Yung Chen, Jintian Chen, Xuhui Chen, Dongyan Chen, Huei-Rong Chen, Xianmei Chen, Jinyan Chen, Yuxi Chen, Qingqing Chen, Weibo Chen, Qiwei Chen, Mingxia Chen, Hongmin Chen, Jiahui Chen, Yen-Jen Chen, Zihan Chen, Guozhou Chen, Fei Chen, Zhiting Chen, Denghui Chen, Gary Chen, Hongli Chen, Jack Chen, Zhigang Chen, Lie Chen, Siyuan Chen, Haojie Chen, Qing-Wei Chen, Maochong Chen, Mei-Jie Chen, Haining Chen, Xing-Zhen Chen, Weiqing Chen, Huanchun Chen, C-Y Chen, Tzu-An Chen, Jen-Hau Chen, Xiaojie Chen, Dongquan Chen, Gao B Chen, Daijie Chen, Zixi Chen, Lingfeng Chen, Jiayi Chen, Zan Chen, Shuming Chen, Mei-Hsiu Chen, Xueqin Chen, Huan Chen, Xiaoqing Chen, Hui-Xiong Chen, Ruoying Chen, Deying Chen, Huixian Chen, Zhezhe Chen, Lu Chen, Xiaolong Chen, Si-Yue Chen, Xinwei Chen, Wentao Chen, Yucheng Chen, Jiajing Chen, Allen Menglin Chen, Chixiang Chen, Shiqun Chen, Wenwu Chen, Chin-Chuan Chen, Ningbo Chen, Hsin-Hung Chen, Shenglan Chen, Jia-Feng Chen, Changya Chen, ZhaoHui Chen, Guo Chen, Juhai Chen, Xiao-Quan Chen, Cuimin Chen, Yongshuo Chen, Sai Chen, Fengyang Chen, Siteng Chen, Hualan Chen, Lian Chen, Yuan-Hua Chen, Minjie Chen, Shiyan Chen, Z Chen, Zhengzhi Chen, Jonathan Chen, H Chen, You-Yue Chen, Shu-Gang Chen, Hsuan-Yu Chen, Hongyue Chen, Weiyi Chen, Jiaqi Chen, Chengde Chen, Shufang Chen, Ze-Hui Chen, Xiuping Chen, Zhuojia Chen, Zhouji Chen, Lidian Chen, Yilan Chen, Kuan-Ling Chen, Alon Chen, Zi-Yue Chen, Hongmou Chen, Fang-Zhou Chen, Jianzhou Chen, Wenbiao Chen, Yujie Chen, Zhijian Chen, Zhouqing Chen, Xiuhui Chen, Qingguang Chen, Hanbei Chen, Qianyu Chen, Mengping Chen, Yongqi Chen, Sheng-Yi Chen, Siqi Chen, Yelin Chen, Shirui Chen, Yuan-Tsong Chen, Dongyin Chen, Lingxue Chen, Long-Jiang Chen, Yunshun Chen, Yahong Chen, Yaosheng Chen, Zhonghua Chen, Jingyao Chen, Pei-Yin Chen, Fusheng Chen, Xiaokai Chen, Shuting Chen, Miao-Hsueh Chen, Y-D I Chen, Zijie Chen, Haozhu Chen, Haodong Chen, Xiong Chen, Wenxi Chen, Feng-Jung Chen, Shangwu Chen, Zhiping Chen, Zhang-Yuan Chen, Wentong Chen, Ou Chen, Ruiming Chen, Xiyu Chen, Shuqiu Chen, Xiaoling Chen, Ruimin Chen, Hsiao-Wang Chen, Dongli Chen, Haibo Chen, Yiyun Chen, Luming Chen, Wenting Chen, Chongyang Chen, Qingqiu Chen, Wen-Pin Chen, Yuhui Chen, Lingxia Chen, Jun-Long Chen, Xingyu Chen, Haotai Chen, Bang-dang Chen, Qiuwen Chen, Rui Chen, K C Chen, Zhixuan Chen, Gaoyu Chen, Yitong Chen, Tzu-Ju Chen, Jingqing Chen, Huiqun Chen, Runsen Chen, Michelle Chen, Hanyong Chen, Xiaolin Chen, Ke Chen, Yangchao Chen, Y D I Chen, Jinghua Chen, Jia Wei Chen, Man-Hua Chen, H T Chen, Zheyi Chen, Lihong Chen, Guangyao Chen, Rujun Chen, Ming-Fong Chen, Haiyun Chen, Dexiong Chen, Huiqin Chen, Ching Kit Chen, En-Qiang Chen, Wanjia Chen, Xiangliu Chen, Meiting Chen, Szu-Chi Chen, Yii-der Ida Chen, Jian-Hua Chen, Yanjie Chen, Yingying Chen, Paul Chih-Hsueh Chen, Si-Ru Chen, Mingxing Chen, Rui-Zhen Chen, Changjie Chen, Qu Chen, Yintong Chen, Jingde Chen, Mao Chen, Xinghai Chen, Mei-Chih Chen, Xueqing Chen, Chun-An Chen, Cheng Chen, Ruijing Chen, Huayu Chen, Yunqin Chen, Yan-Gui Chen, Ruibing Chen, Size Chen, Qi-An Chen, Yuan-Zhen Chen, J Chen, Heye Chen, T Chen, Junpeng Chen, Tan-Huan Chen, Shuaijun Chen, Hao Yu Chen, Fahui Chen, Lan Chen, Dong-Yi Chen, Xianqiang Chen, Shi-Sheng Chen, Qiao-Yi Chen, Pei-Chen Chen, Xueying Chen, Yi-Wen Chen, Guohong Chen, Zhiwei Chen, Zuolong Chen, Erfei Chen, Yuqing Chen, Zhenyue Chen, Qiongyun Chen, Jianghua Chen, Yingji Chen, Xiuli Chen, Xiaowei Chen, Hengyu Chen, Sheng-Xi Chen, Haiyi Chen, Shao-Peng Chen, Yi-Ru Chen, Zhaoran Chen, Xiuyan Chen, Jinsong Chen, Sunny Chen, Xiaolan Chen, S-D Chen, Ruofan Chen, Qiujing Chen, Yun Chen, Wei-Cheng Chen, Chun-Wei Chen, Liechun Chen, Lulu Chen, Hsiu-Wen Chen, Yanping Chen, Jiayao Chen, Xuejiao Chen, Guan-Wei Chen, Yusi Chen, Yijiang Chen, Chi-Hua Chen, Qixian Chen, Ziqing Chen, Peiyou Chen, Chunhai Chen, Zheren Chen, Qiuyun Chen, Xiaorong Chen, Chaoqun Chen, Dan-Dan Chen, Xuechun Chen, Yafang Chen, Mystie X Chen, Jina Chen, Wei-Kai Chen, Yule Chen, Bo Chen, Kaili Chen, Junqin Chen, Jia Min Chen, Chen Chen, Guoliang Chen, Xiaonan Chen, Guangjie Chen, Xiao Chen, Jeanne Chen, Danyang Chen, Minjiang Chen, Jiyuan Chen, Zheng-Zhen Chen, Shou-Tung Chen, Ouyang Chen, Xiu Chen, H Q Chen, Peiyu Chen, Yuh-Min Chen, Youmeng Chen, Shuoni Chen, Peiqin Chen, Xinji Chen, Chih-Ta Chen, Shang-Hung Chen, Robert Chen, Suet N Chen, Yun-Tzu Chen, Suming Chen, Ye Chen, Yao Chen, Yi-Fei Chen, Ruixue Chen, Tianhang Chen, Suning Chen, Jingnan Chen, Xiaohong Chen, Kun-Chieh Chen, Tuantuan Chen, Mei Chen, He-Ping Chen, Zhi Bin Chen, Yuewu Chen, Mengying Chen, Po-See Chen, Xue Chen, Jian-Jun Chen, Xiyao Chen, Jeremy J W Chen, Jiemei Chen, Daiwen Chen, Christina Yingxian Chen, Qinian Chen, Chih-Wei Chen, Wensheng Chen, Yingcong Chen, Zhishi Chen, Duo Chen, Jiansu Chen, Keping Chen, Min Chen, Yi-Hui Chen, Yun-Ju Chen, Gaoyang Chen, Renjin Chen, Kui Chen, Shuai-Ming Chen, Hui-Fen Chen, Zi-Yun Chen, Shao-Yu Chen, Meiyang Chen, Jiahua Chen, Zongyou Chen, Yen-Rong Chen, Huaping Chen, Yu-Xin Chen, Bohe Chen, Kehua Chen, Zilin Chen, Zhang-Liang Chen, Ziqi Chen, Yinglian Chen, Hui-Wen Chen, Peipei Chen, Baolin Chen, Zugen Chen, Kangzhen Chen, Yanhan Chen, Sung-Fang Chen, Zheping Chen, Zixuan Chen, Jiajia Chen, Yuanjian Chen, Lili Chen, Xiangli Chen, Ban Chen, Yuewen Chen, X Chen, Yan-Qiong Chen, Chider Chen, Yung-Hsiang Chen, Hanlin Chen, Xiangjun Chen, Haibing Chen, Le Chen, Xuan Chen, Xue-Ying Chen, Zexiao Chen, Chen-Yu Chen, Zhe-Ling Chen, Fan Chen, Hsin-Yi Chen, Feilong Chen, Zilong Chen, Yi-Jen Chen, Zhiyun Chen, Ning Chen, Wenxu Chen, Chuanbing Chen, Yaxi Chen, Yi-Hong Chen, Eleanor Y Chen, Yuexin Chen, Kexin Chen, Shoujun Chen, Yen-Ju Chen, Yu-Chuan Chen, Yen-Teen Chen, Bao-Ying Chen, Xiaopeng Chen, Danli Chen, Katharine Y Chen, Jingli Chen, Qianyi Chen, Zihua Chen, Ya-xi Chen, Xuanxu Chen, Chung-Hung Chen, Yajie Chen, Cindi Chen, Hua Chen, Shuliang Chen, Elizabeth H Chen, Gen-Der Chen, Bingyu Chen, Keyang Chen, Siyu S Chen, Xinpu Chen, Yau-Hung Chen, Hsueh-Fen Chen, Han-Hsiang Chen, Wei Ning Chen, Guopu Chen, Zhujun Chen, Yurong Chen, Yuxian Chen, Wanjun Chen, Qiu-Jing Chen, Qifang Chen, Yuhan Chen, Jingshen Chen, Zhongliang Chen, Ching-Hsuan Chen, Zhaoyao Chen, Yongning Chen, Marcus Y Chen, Ping Chen, Junfei Chen, Yung-Wu Chen, Xueting Chen, Yingchun Chen, Wan-Yan Chen, Yuxin Chen, Yisheng Chen, Chun-Yuan Chen, Yulian Chen, Yan-Jun Chen, Guoxun Chen, Ding Chen, Yu-Fen Chen, Jason A Chen, Shuyi Chen, Cuilan Chen, Ruijuan Chen, Kevin Chen, Xuanmao Chen, Shen-Ming Chen, Ya-Nan Chen, Sean Chen, Zhaowei Chen, Xixi Chen, Yu-Chia Chen, Xuemin Chen, Binlong Chen, Weina Chen, Xuemei Chen, Di Chen, P P Chen, Yubin Chen, Chunhua Chen, Li-Chieh Chen, Ping-Chung Chen, Zhihao Chen, Xinyang Chen, Chan Chen, Yan Jie Chen, Shi-Qing Chen, Ivy Xiaoying Chen, Ying-Cheng Chen, Jia-Shun Chen, Shao-Wei Chen, Aiping Chen, Dexiang Chen, Qianfen Chen, Hongyu Chen, Wei-Kung Chen, Danlei Chen, Hongen Chen, Shipeng Chen, Jake Y Chen, Dongsheng Chen, Chien-Ting Chen, Shouzhen Chen, Hehe Chen, Yu-Tung Chen, Yilin Chen, Joy J Chen, Zhong Chen, Zhenfeng Chen, Zhongzhu Chen, Feiyang Chen, Xingxing Chen, Keyan Chen, Huimin Chen, Guanyu Chen, D. Chen, Dianke Chen, Zhigeng Chen, Sien-Tsong Chen, Yii-Der Chen, Chi-Yun Chen, Beidong Chen, Wu-Xian Chen, Zhihang Chen, Yuanqi Chen, Jianhua Chen, Xian Chen, Xiangding Chen, Jingteng Chen, Shuaiyu Chen, Xue-Mei Chen, Yu-Han Chen, Hongqiao Chen, Weili Chen, Yunzhu Chen, Guo-qing Chen, Miao Chen, Zhi Chen, Junhui Chen, Jing-Xian Chen, Zhiquan Chen, Shuhuang Chen, Shaokang Chen, Irwin Chen, Xiang Chen, Chuo Chen, Siting Chen, Keyuan Chen, Xia-Fei Chen, Zhihai Chen, Yuanyu Chen, Po-Sheng Chen, Qingjiang Chen, Yi-Bing Chen, Rongrong Chen, Katherine C Chen, Shaoxing Chen, Lifen Chen, Luyi Chen, Sisi Chen, Ning-Bo Chen, Yihong Chen, Guanjie Chen, Li-Hua Chen, Xiao-Hui Chen, Ting Chen, Chun-Han Chen, Xuzhuo Chen, Junming Chen, Zheng Chen, Wen-Jie Chen, Bingdi Chen, Jiang Ye Chen, Yanbin Chen, Duoting Chen, Shunyou Chen, Shaohua Chen, Jien-Jiun Chen, Jiaohua Chen, Shaoze Chen, Yifang Chen, Chiqi Chen, Yen-Hao Chen, Rui-Fang Chen, Hung-Sheng Chen, Kuey Chu Chen, Y S Chen, Xijun Chen, Chaoyue Chen, Heng-Sheng Chen, Lianfeng Chen, Yen-Ching Chen, Yuhong Chen, Yixin Chen, Yuanli Chen, Cancan Chen, Yanming Chen, Yajun Chen, Chaoping Chen, F-K Chen, Menglan Chen, Zi-Yang Chen, Yongfang Chen, Hsin-Hong Chen, Hongyan Chen, Chao-Wei Chen, Jijun Chen, Xiaochun Chen, Yazhuo Chen, Zhixin Chen, YongPing Chen, Jui-Yu Chen, Mian-Mian Chen, Liqiang Chen, Y P Chen, D-F Chen, Jinhao Chen, Yanyan Chen, Chang-Zheng Chen, Shao-long Chen, Guoshun Chen, Lo-Yun Chen, Yen-Lin Chen, Bingqian Chen, Dafang Chen, Yi-Chung Chen, Liming Chen, Qiuli Chen, Shuying Chen, Chih-Mei Chen, Renyu Chen, Wei-Hao Chen, Lihua Chen, Hang Chen, Hai-Ning Chen, Hu Chen, Yu-Fu Chen, Yalan Chen, Wan-Tzu Chen, Benjamin Jieming Chen, Yingting Chen, Jiacai Chen, Ning-Yuan Chen, Shuo-Bin Chen, Yu-Ling Chen, Jian-Kang Chen, Hengsan Chen, Yu-Ting Chen, Y Chen, Qingjie Chen, Jiong Chen, Chaoyi Chen, Yunlin Chen, Gang Chen, Hui-Chun Chen, Li-Tzong Chen, Zhangliang Chen, Qiangpu Chen, Xianbo Chen, Jinxuan Chen, Hebing Chen, Ran Chen, Zhehui Chen, Carol X-Q Chen, Yuping Chen, Xiangyu Chen, Xinyu Chen, Qianyun Chen, Junyi Chen, B-S Chen, Zhesheng Chen, Man Chen, Dali Chen, Danyu Chen, Huijiao Chen, Naisong Chen, Qitong Chen, Chueh-Tan Chen, Kai-Ming Chen, Jiarou Chen, Huang Chen, Chunjie Chen, Weiping Chen, Po-Min Chen, Guang-Chao Chen, Danxia Chen, Youran Chen, Chuanzhi Chen, Peng-Cheng Chen, Wen-Tsung Chen, Linxi Chen, Si-guo Chen, Zike Chen, Zhiyu Chen, Wanting Chen, Jiangxia Chen, Wenhua Chen, Roufen Chen, Shi-You Chen, Fang-Pei Chen, Chu Chen, Feifeng Chen, Chunlin Chen, Yunwei Chen, Wenbing Chen, Xuejun Chen, Meizhen Chen, Li Jia Chen, Tianhua Chen, Xiangmei Chen, Kewei Chen, Yuh-Ling Chen, Dejuan Chen, Jiyan Chen, Xinzhuo Chen, Yue-Lai Chen, Hsiao-Jou Cortina Chen, Weiqin Chen, Huey-Miin Chen, Elizabeth Suchi Chen, Kai-Ting Chen, Lizhen Chen, Xiaowen Chen, Chien-Yu Chen, Lingjun Chen, Gonglie Chen, Jiao Chen, Zhuo-Yuan Chen, Wei-Peng Chen, Xiangna Chen, Jiade Chen, Lanmei Chen, Siyu Chen, Kunpeng Chen, Hung-Chi Chen, Jia Chen, Shuwen Chen, Siqin Chen, Zhenlei Chen, Wen-Yi Chen, Si-Yuan Chen, Yidan Chen, Tianfeng Chen, Fu Chen, Leqi Chen, Jiamiao Chen, Shasha Chen, Qingyi Chen, Ben-Kuen Chen, Haitao Chen, Qi Chen, Yihao Chen, Yunfeng Chen, Elizabeth S Chen, Yiming Chen, Youwei Chen, Lichun Chen, Yanfei Chen, Hongxing Chen, Muh-Shy Chen, Yingyu Chen, Weihong Chen, Ming Chen, Kelin Chen, Duan-Yu Chen, Shi-Yi Chen, Shih-Yu Chen, Yanling Chen, Shuanghui Chen, Ya Chen, Yusheng Chen, Yuting Chen, Shiming Chen, Xinqiao Chen, Hongbo Chen, Mien-Cheng Chen, Jiacheng Chen, Herbert Chen, Ji-ling Chen, Sun Chen, Chen-Sheng Chen, Na Chen, Chih-Yi Chen, Wenfang Chen, Yii-Der I Chen, Qinghua Chen, Shuai Chen, Hsi-Hsien Chen, F Chen, Guo-Chong Chen, Zhe Chen, Beijian Chen, Roger Chen, You-Ming Chen, Hongzhi Chen, Zhen-Yu Chen, Xianxiong Chen, Chang Chen, Chujie Chen, Chuannan Chen, Kan Chen, Lu-Biao Chen, Yupei Chen, Qiu-Sheng Chen, Shangduo Chen, Yuan-Yuan Chen, Yundai Chen, Binzhen Chen, Cai-Long Chen, Yen-Chen Chen, Xue-Xin Chen, Yanru Chen, Chunxiu Chen, Yifa Chen, Xingdong Chen, Ruey-Hwa Chen, Shangzhong Chen, Ching-Wen Chen, Danna Chen, Jingjing Chen, Yafei Chen, Dandan Chen, Pei-Yi Chen, Shan Chen, Guanghao Chen, Longqing Chen, Yen-Cheng Chen, Zhanjuan Chen, Jinguo Chen, Zhongxiu Chen, Rui-Min Chen, Shunde Chen, Xun Chen, Jianmin Chen, Linyi Chen, Ying-Ying Chen, Chien-Hsiun Chen, Li-Nan Chen, Yu-Ming Chen, Qianqian Chen, Xue-Yan Chen, Shengdi Chen, Huali Chen, Xinyue Chen, Ching-Yi Chen, Honghai Chen, Baosheng Chen, Pingguo Chen, Yike Chen, Yuxiang Chen, Qing-Hui Chen, Yuanwen Chen, Yongming Chen, Zongzheng Chen, Ruiying Chen, Huafei Chen, Tingen Chen, Zhouliang Chen, Shih-Yin Chen, Shanyuan Chen, Yiyin Chen, Feiyu Chen, Zitao Chen, Constance Chen, Zhoulong Chen, Haide Chen, Jiang Chen, Ray-Jade Chen, Shiuhwei Chen, Chih-Chieh Chen, Chaochao Chen, Lijuan Chen, Qianling Chen, Jian-Min Chen, Xihui Chen, Yuli Chen, Wu-Jun Chen, Diyun Chen, Alice P Chen, Jingxuan Chen, Chiung-Mei Chen, Shibo Chen, M L Chen, Lena W Chen, Xiujuan Chen, Christopher S Chen, Yeh Chen, Xingyong Chen, Feixue Chen, Boyu Chen, Weixian Chen, Tingting Chen, Bosong Chen, Junjie Chen, Han-Min Chen, Szu-Yun Chen, Qingliang Chen, Huatao Chen, Bin Chen, L B Chen, Xuanyi Chen, Chun Chen, Dong Chen, Yinjuan Chen, Jiejian Chen, Lu-Zhu Chen, Alex F Chen, Pei-Chun Chen, Chien-Jen Chen, Y M Chen, Xiao-Chen Chen, Tania Chen, Yang Chen, Yangxin Chen, Mark I-Cheng Chen, Haiming Chen, Shuo Chen, Yong Chen, Hsiao-Tan Chen, Erzhen Chen, Jiaye Chen, Fangyan Chen, Guanzheng Chen, Haoyun Chen, Jiongyu Chen, Baofeng Chen, Yuqin Chen, Juan Chen, Haobo Chen, Shuhong Chen, Fu-Shou Chen, Wei-Yu Chen, Haw-Wen Chen, Feifan Chen, Deqian Chen, Linlin Chen, Xiaoshan Chen, Hui Chen, Wenwen Chen, Yanli Chen, Yuexuan Chen, Xiaoyin Chen, Yen-Chang Chen, Tiantian Chen, Ruiai Chen, Alice Y Chen, Jinglin Chen, Zifan Chen, Wantao Chen, Shanshan Chen, Jianjun Chen, Xiaoyuan Chen, Xuefei Chen, Runfeng Chen, Weisan Chen, Guangnan Chen, Junpan Chen, An Chen, Lankai Chen, Yiding Chen, Tianpeng Chen, Ya-Ting Chen, Lijin Chen, Ching-Yu Chen, Y Eugene Chen, Guanglong Chen, Rongyuan Chen, Yali Chen, Yanan Chen, Liyun Chen, Shuai-Bing Chen, Zhixue Chen, Xiaolu Chen, Xiao-he Chen, Hongxiang Chen, Bing-Feng Chen, Gary K Chen, Xiaohui Chen, Jin-Wu Chen, Qiuxiang Chen, Huaqiu Chen, X Steven Chen, Xiaoqian Chen, Chao-Jung Chen, Zhengjun Chen, Yong-Ping Chen, Zhelin Chen, Xuancai Chen, Yi-Hsuan Chen, Daiyu Chen, Gui Mei Chen, Hongqi Chen, Zhizhong Chen, Mengting Chen, Guofang Chen, Jian-Guo Chen, Hou-Zao Chen, Yuyao Chen, Lixia Chen, Yu-Yang Chen, Zhengling Chen, Qinfen Chen, Jiajun Chen, Xue-Qing Chen, Shenghui Chen, Yii-Derr Chen, Linbo Chen, Yanjing Chen, S Pl Chen, Chi-Long Chen, Jiawei Chen, Rong-Hua Chen, Shu-Fen Chen, Yu-San Chen, Ying-Lan Chen, Xiaofen Chen, Weican Chen, Xin Chen, Yumei Chen, Ruohong Chen, You-Xin Chen, Tse-Ching Chen, Xiancheng Chen, Yu-Pei Chen, Weihao Chen, Baojiu Chen, Haimin Chen, Zhihong Chen, Jion Chen, Yi-Chun Chen, Ping-Kun Chen, Wan Jun Chen, Willian Tzu-Liang Chen, Qingshi Chen, Ren-Hui Chen, Weihua Chen, Hanjing Chen, Guihao Chen, Xiao-Qing Chen, Po-Yu Chen, Liangsheng Chen, Fred K Chen, Haiying Chen, Tzu-Chieh Chen, Wei J Chen, Zhen Chen, Shu Chen, Jie Chen, Chung-Hao Chen, Zi-Qing Chen, Yu-Xia Chen, Weijia Chen, Ming-Han Chen, Yaodong Chen, Yong-Zhong Chen, Jinquan Chen, Haijiao Chen, Tom Wei-Wu Chen, Jingzhou Chen, Ya-Peng Chen, Shiwei Chen, Xiqun Chen, Yingjie Chen, Wenjun Chen, Linjie Chen, Hung-Chun Chen, Xiaoping Chen, Haoran Chen, Qiang Chen, Sy-Jou Chen, Y U Chen, Weineng Chen, Li-hong Chen, Cheng-Fong Chen, Yajing Chen, Song Chen, Qiaoli Chen, Yiru Chen, Guang-Yu Chen, Zhi-bin Chen, Deyu Chen, C Y Chen, Junhong Chen, Yonghui Chen, Chaoli Chen, Syue-Ting Chen, Sufang Chen, I-Chun Chen, Shangsi Chen, Xiao-Wei Chen, Qinsheng Chen, Zhao-Xia Chen, Yun-Yu Chen, Chi-Chien Chen, Wenxing Chen, Meng Chen, Zixin Chen, Jianhui Chen, Yuanyuan Chen, Jiamin Chen, Wei-Wei Chen, Xingyi Chen, Yen-Ni Chen, Danxiang Chen, Po-Ju Chen, Mei-Ru Chen, Ziying Chen, E S Chen, Tailai Chen, Qingyang Chen, Miaomiao Chen, Shuntai Chen, Wei-Lun Chen, Xuanli Chen, Zhengwei Chen, Fengju Chen, Chengwei Chen, Xujia Chen, Faye H Chen, Xiaoxiao Chen, Shengpan Chen, Shin-Yu Chen, Shiyao Chen, Yuan-Shen Chen, Shengzhi Chen, Shaohong Chen, Ching-Jung Chen, Zihao Chen, Kaiquan Chen, Duo-Xue Chen, Xiaochang Chen, Siping Chen, Rongfeng Chen, Jiali Chen, Hsin-Han Chen, Xiaohua Chen, Delong Chen, Wenjie Chen, Huijia Chen, Yunn-Yi Chen, Siyi Chen, Zhengming Chen, Chu-Huang Chen, Zhuchu Chen, Yuanbin Chen, Jinyong Chen, Yunzhong Chen, Pan Chen, Bihong T Chen, Yunyun Chen, Shujuan Chen, M Chen, Mulan Chen, Jiaren Chen, Zechuan Chen, Jian-Qing Chen, Wei-Hui Chen, Lifeng Chen, Geng Chen, Yan-Ming Chen, Zhijian J Chen, Honghui Chen, Wenfan Chen, Zhongbo Chen, Rouxi Chen, Ye-Guang Chen, Zhimin Chen, Tzu-Ting Chen, Xiaolei Chen, Ziyuan Chen, Shilan Chen, Ruiqi Chen, Xiameng Chen, Huijie Chen, Jiankui Chen, Yuhang Chen, Jianzhong Chen, Wen-Qi Chen, Fa Chen, Shu-Jen Chen, Li-Mien Chen, Xing-Lin Chen, Xuxiang Chen, Erbao Chen, Jiaqing Chen, Hsiang-Wen Chen, Jiaxin Chen
articles

Brexpiprazole inhibits EMT and migration of colorectal cancer cells by downregulating the SREBP1/SNAI1 signaling pathway.

Xiaojie Liu, Jingyi He, Ao Ma +5 more · 2025 · Frontiers in oncology · Frontiers · added 2026-04-24
To investigate the role and mechanism of the SREBP1/SNAI1 signalling pathway in the effect of brexpiprazole on the EMT and metastasis of CRC. The effects of different concentrations of brexpiprazole o Show more
To investigate the role and mechanism of the SREBP1/SNAI1 signalling pathway in the effect of brexpiprazole on the EMT and metastasis of CRC. The effects of different concentrations of brexpiprazole on cell migration, cell invasion and protein expression Brexpiprazole significantly inhibited the migration and invasion of CRC cells; downregulated the expression of SREBP1(m), SNAI1 and MMP9; upregulated the expression of E-Cad and ZO1; and decreased the levels of secreted ICAM-1 and VEGF in the supernatant of CRC cells. Western blotting and dual-luciferase assays revealed that SREBP1 could directly regulate the expression of SANI1. On the other hand, Brexpiprazole inhibits the migration, invasion and metastasis of CRC cells by inhibiting the SREBP1/SNAI1 signalling pathway and downregulating the expression of EMT-related factors. Show less
no PDF DOI: 10.3389/fonc.2025.1734678
SNAI1

Tryptophan regulates food intake in growing pigs by modulating hypothalamic AMPK-mTOR signalling pathway.

Juexin Fan, Yuezhou Yao, Leli Wang +5 more · 2025 · The British journal of nutrition · added 2026-04-24
Tryptophan (Trp) is an essential amino acid acting as a key nutrition factor regulating animal growth and development. But how Trp modulates food intake in pigs is still not well known. Here, we inves Show more
Tryptophan (Trp) is an essential amino acid acting as a key nutrition factor regulating animal growth and development. But how Trp modulates food intake in pigs is still not well known. Here, we investigated the effect of dietary supplementation of Trp with different levels on food intake of growing pigs. The data showed that dietary Trp supplementation with the standardised ileal digestibility (SID) Trp to lysine (Lys) ratio at both 0·18 and 0·20 significantly increased the food intake by activating the expression of orexigenic gene agouti-related peptide (AgRP) and inhibiting the expression of anorexigenic gene pro-opiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART) and melanocortin receptor 4 (MC4R) in the hypothalamus. Meanwhile, the level of anorexigenic hormones appetite-regulating peptide YY (PYY) in the duodenum and serum and leptin receptor in the duodenum were also significantly decreased. Importantly, both the kynurenine and serotonin metabolic pathways were activated upon dietary Trp supplementation to downregulate MC4R expression in the hypothalamus. Further mechanistic studies revealed that the reduced MC4R expression activated the hypothalamic AMP-activated protein kinase (AMPK) pathway, which in turn inhibited the mammalian target of rapamycin (mTOR)/S6 kinase 1 (S6K1) activity to stimulate food intake. Together, our study unravels the orexigenic effect of dietary Trp supplementation in pigs and expands its potential application in developing nutrition intervention strategy in pig production. Show less
no PDF DOI: 10.1017/S0007114524003210
MC4R

Optimization of row-ratios in mechanized hybrid rice seed production: a study on pollen dispersal and seed-setting characteristics at two ecological sites.

Ziyu Li, Guangyi Chen, Wei Li +10 more · 2025 · Frontiers in plant science · Frontiers · added 2026-04-24
To explore the optimal row-ratio in mechanized hybrid rice seed production, a field experiment was conducted in 2024 at Qionglai and Mianzhu using 'Tiantai A' × 'Taihui 808'. Three row-ratio treatment Show more
To explore the optimal row-ratio in mechanized hybrid rice seed production, a field experiment was conducted in 2024 at Qionglai and Mianzhu using 'Tiantai A' × 'Taihui 808'. Three row-ratio treatments (H1: 18:6, H2: 24:6, and H3: 30:6) were tested using agricultural unmanned aerial vehicles (AUAVs) for pollination assistance. The results showed that row-ratio had little effect on sterile line flowering dynamics. The index of flowers meeting (IFM) was 0.71-0.72 at Qionglai and 0.81-0.86 at Mianzhu, with 11 to 12 days of flowering duration. As the row-ratio increased, total pollen quantity in the panicle layer and grain filling rate (GFR) decreased, while grain infection rate (GIR) increased. The responses of grain blighted rate (GBR), grain empty rate (GER), and fertilization success rate (FSR) to row-ratio varied between sites. Pollen density and GFR followed the pattern of near region (NR) > central region (CR) > far region (FR). Within the panicle, pollen density was generally highest in the upper panicle layer (UPL), followed by the middle (MPL) and lower (LPL) layers, with partial exceptions observed in the H2 and H3 treatments at Mianzhu. The vertical distribution of GFR varied by site: at Qionglai, it was apical parts of panicle (APP) > median parts (MPP) > basal parts (BPP), whereas at Mianzhu the order was MPP > APP > BPP. With wider row-ratios, yield per unit area (YUA) and GFR declined (H1 > H2 > H3), while 1,000-grain weight increased or decreased and then increased. Under H1, yields reached 2,107.50 kg ha Show less
📄 PDF DOI: 10.3389/fpls.2025.1704773
LPL

Sodium butyrate modulates ocular surface microbiome and attenuates inflammation of meibomian gland dysfunction in ApoE

Qiankun Chen, Leying Wang, Yuan Wei +8 more · 2025 · Microbiome · BioMed Central · added 2026-04-24
The ocular surface microbiome (OSM) in patients with meibomian gland dysfunction (MGD) differs from that of healthy individuals. However, the precise role of OSM in MGD remains unknown. Therefore, we Show more
The ocular surface microbiome (OSM) in patients with meibomian gland dysfunction (MGD) differs from that of healthy individuals. However, the precise role of OSM in MGD remains unknown. Therefore, we aimed to investigate the mechanism of OSM in the inflammation of MGD and the effects of topical sodium butyrate (SB) treatment in ApoE ApoE Five-month-old ApoE ApoE Show less
📄 PDF DOI: 10.1186/s40168-025-02294-5
APOE

Associations of perceived teacher-student relationship and friendship quality with adolescents' interest in physical education: a latent profile analysis.

Xinyi Chen, Wenying Huang, Chang Hu · 2025 · Frontiers in sports and active living · Frontiers · added 2026-04-24
This study employed a person-centered Latent Profile Analysis (LPA) to explore adolescents' perceived teacher-student and friendship relationships in the school environment and to examine their associ Show more
This study employed a person-centered Latent Profile Analysis (LPA) to explore adolescents' perceived teacher-student and friendship relationships in the school environment and to examine their association with interest in physical education. A survey was conducted among 3,613 adolescents using the Teacher-Student Relationship Scale, the Friendship Quality Scale, and the Interest in Physical Education Scale. LPA was applied to identify relationship quality profiles, and multinomial logistic regression was used to examine gender differences and associations with interest in physical education. Three profiles emerged from the LPA: the Low Relationship Quality profile (23%, Adolescents exhibit heterogeneous experiences of teacher-student and friendship relationship quality, which were significantly associated with differences in interest in physical education. By applying a person-centered approach, the study extends prior research by showing that teacher-student and friendship contexts are linked to adolescents' interest in physical education, underscoring the importance of considering interest as a distinct outcome in relational research. Show less
📄 PDF DOI: 10.3389/fspor.2025.1677083
LPA

Ancestral Variation in Lp(a): Epidemiology, Isoform Diversity, and Testing.

Priyansh Shah, Sara King, Sophia Trabanino +3 more · 2025 · Current atherosclerosis reports · Springer · added 2026-04-24
This review aims to explore the epidemiology of lipoprotein(a) [Lp(a)] by its structural and genetic make-up variation amongst ancestry groups. Lipoprotein(a) [Lp(a)] is a genetically determined lipop Show more
This review aims to explore the epidemiology of lipoprotein(a) [Lp(a)] by its structural and genetic make-up variation amongst ancestry groups. Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein particle, causally implicated in atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis (CAVS). Given its genetic basis, studies have shown marked ancestry-related differences in different races and ethnicities. Lp(a) plasma concentrations vary by more than 100-fold among individuals, primarily due to LPA gene polymorphisms and the number of kringle-IV type 2 (KIV2) repeats, which define apolipoprotein(a) [apo(a)] isoform size. Individuals of African descent have the highest median concentrations, followed by South Asians, with Hispanics/Latinos and East Asians having lower levels. Admixed populations display heterogeneity reflecting genetic ancestry. Despite differences in absolute levels, the relative ASCVD risk per unit increase in Lp(a) is consistent across groups, highlighting the universal atherogenicity of elevated Lp(a). Small apo(a) isoforms are associated with higher Lp(a) concentrations and risk, though isoform size is mainly a surrogate for Lp(a) burden. Despite a strong genetic basis and disproportionate burden in some populations, ancestry-specific testing guidelines are limited and testing rates remain low. Therapies targeting LPA transcription are in development, with outcome trials underway. Integrating ancestry-informed perspectives with universal risk principles is essential for equitable prevention and treatment. Routine, one-time Lp(a) testing enables cost-effective early risk stratification as Lp(a)-directed therapies emerge. Show less
📄 PDF DOI: 10.1007/s11883-025-01365-0
LPA

The spectrum and prognosis of Sjögren's syndrome with membranous nephropathy.

Dan-Dan Qiu, Zhi Li, Jing-Jing Wang +7 more · 2025 · Clinical kidney journal · Oxford University Press · added 2026-04-24
This study aims to investigate the spectrum and prognosis of membranous nephropathy (MN) in patients with Sjögren's syndrome (SS). SS patients with biopsy-proven kidney involvement who were diagnosed Show more
This study aims to investigate the spectrum and prognosis of membranous nephropathy (MN) in patients with Sjögren's syndrome (SS). SS patients with biopsy-proven kidney involvement who were diagnosed at our center between April 2007 and February 2024 were retrospectively reviewed and analyzed. A total of 290 SS patients with kidney involvement were enrolled. The frequency of MN increased from 16.28% during the 2007-2010 period to 44.05% during the 2021-2024 period. After 2016, MN became the most common renal pathologic type, surpassing tubulointerstitial nephritis. PLA2R antibody or antigen was detected in 74 SS-MN patients, in whom 37 (50%) showed a negative result. Within the PLA2R-negative group, five out of 15 showed positivity for EXT1/EXT2 antigen and one out of eight for THSD7A antigen. Sixty-one SS patients with MN were followed up for >6 months, and 44 (72.13%) of them achieved renal complete remission (CR). Compared with PLA2R-negative patients, PLA2R-positive patients spent a longer time to achieve CR (1.46 ± 1.16 vs. 0.74 ± 0.47 years, MN has become the predominant renal pathologic type in SS. PLA2R-positivity testing followed by EXT1/EXT2 and THSD7A testing is recommended for SS-MN patients. Although most patients can achieve renal CR, the prognosis is usually poor in PLA2R-positive SS-MN patients. Show less
📄 PDF DOI: 10.1093/ckj/sfae384
EXT1

Endothelial cells-derived SEMA3G suppresses glioblastoma stem cells by inducing c-Myc degradation.

Peng-Xiang Min, Li-Li Feng, Yi-Xuan Zhang +12 more · 2025 · Cell death and differentiation · Nature · added 2026-04-24
The poor prognosis of glioblastoma (GBM) patients is attributed mainly to abundant neovascularization and presence of glioblastoma stem cells (GSCs). GSCs are preferentially localized to the perivascu Show more
The poor prognosis of glioblastoma (GBM) patients is attributed mainly to abundant neovascularization and presence of glioblastoma stem cells (GSCs). GSCs are preferentially localized to the perivascular niche to maintain stemness. However, the effect of abnormal communication between endothelial cells (ECs) and GSCs on GBM progression remains unknown. Here, we reveal that ECs-derived SEMA3G, which is aberrantly expressed in GBM patients, impairs GSCs by inducing c-Myc degradation. SEMA3G activates NRP2/PLXNA1 in a paracrine manner, subsequently inducing the inactivation of Cdc42 and dissociation of Cdc42 and WWP2 in GSCs. Once released, WWP2 interacts with c-Myc and mediates c-Myc degradation via ubiquitination. Genetic deletion of Sema3G in ECs accelerates GBM growth, whereas SEMA3G overexpression or recombinant SEMA3G protein prolongs the survival of GBM bearing mice. These findings illustrate that ECs play an intrinsic inhibitory role in GSCs stemness via the SMEA3G-c-Myc distal regulation paradigm. Targeting SEMA3G signaling may have promising therapeutic benefits for GBM patients. Show less
no PDF DOI: 10.1038/s41418-025-01534-3
WWP2

Establishing an algorithm for molecular genetic diagnostics in Chinese children with brachydactyly type E.

Xueqian Wang, Shengzhuang Guan, Yiqing Gao +13 more · 2025 · Frontiers in endocrinology · Frontiers · added 2026-04-24
Brachydactyly type E (BDE) is characterized by variable shortening of metacarpals or metatarsals, often involving phalanges. It may occur as an isolated anomaly or as part of congenital syndromes. Wit Show more
Brachydactyly type E (BDE) is characterized by variable shortening of metacarpals or metatarsals, often involving phalanges. It may occur as an isolated anomaly or as part of congenital syndromes. With advancements in molecular diagnostic technologies, how genetic testing enhances the precise diagnosis of BDE remains unclear. Our aims were to establish an algorithm for molecular genetic diagnostics in Chinese children with BDE and to explore the phenotype-genotype correlations of Chinese patients with BDE. We reviewed left-hand wrist X-rays from children visiting Children's Hospital of Soochow University (Jun 2021-Dec 2023). From 60,650 films, 135 BDE cases were identified, and their comprehensive phenotypes were collected. Whole-exome sequencing (WES) with copy number variation (CNV) analysis was performed on 60 patients and their parents. Sanger sequencing was used to validate single nucleotide variants (SNV) and indels. Causative variants were found in 19 patients. SNVs and indels affecting 10 genes were identified in 15 patients, and CNVs in four. Through comprehensive evaluation of genotype-phenotype correlations, we propose a diagnostic algorithm for precise molecular diagnosis in Chinese children with BDE. Show less
📄 PDF DOI: 10.3389/fendo.2025.1571136
EXT1

LMOD1 Exerts a Tumor-Suppressive Role in Breast Cancer by Restraining the JAK2/STAT3 Pathway.

Xiansong Fang, Xiaoyun Wen, Ya Hou +3 more · 2025 · Journal of biochemical and molecular toxicology · Wiley · added 2026-04-24
Breast cancer has seriously affected women's physical and mental health. This investigation aims at screening differentially expressed genes (DEGs) in breast cancer and illuminating the potential biol Show more
Breast cancer has seriously affected women's physical and mental health. This investigation aims at screening differentially expressed genes (DEGs) in breast cancer and illuminating the potential biological functions of Leiomodin 1 (LMOD1) and its behind mechanisms against breast cancer. The common DEGs (co-DEGs) between the GSE22820 and GSE29431 data sets and pivotal genes were screened out using bioinformatics methods. The biological roles of LMOD1 overexpression on malignant phenotypes were validated by functional assays and the impact on fatty acid synthesis was also elucidated in breast cancer cell lines. Additionally, colivelin, a STAT3 activator, was applied for further investigating the role of LMOD1 on the JAK2/STAT3 pathway in vitro. A total of 208 co-DEGs and 5 focal genes were screened through bioinformatics analysis, and 5 focal genes were downregulated in breast cancer cell lines. LMOD1 overexpression retarded proliferative, migratory, invasive capabilities of breast cancer cells. LMOD1 overexpression suppressed fatty acid synthesis. Furthermore, the inhibitory effects on malignant phenotypes of breast cancer cells with LMOD1 overexpression were partially abolished after colivelin treatment. Additionally, LMOD1 could impede fatty acid synthesis in breast cancer cells. Our study highlighted LMOD1 exerted as a tumor-suppressive role in breast cancer, which was correlated with restraining the JAK2/STAT3 pathway activation. Show less
no PDF DOI: 10.1002/jbt.70092
LMOD1

Risk factors for heart failure within one year after percutaneous coronary intervention in patients with acute coronary syndrome: development of a predictive model.

Lin Chen, Mingzhu Xu, Yan Zhu +1 more · 2025 · American journal of translational research · added 2026-04-24
To identify risk factors for heart failure (HF) within one year after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) and to develop a predictive nomogram model Show more
To identify risk factors for heart failure (HF) within one year after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) and to develop a predictive nomogram model. A retrospective analysis was performed on 492 patients with ACS treated at Suzhou Municipal Hospital between January 2020 and October 2023. Patients were divided into the HF group and the non-HF group according to the occurrence of HF within one year after PCI. 70% of the cases were randomly assigned to the training set and 30% to the validation set. Univariate and multivariate logistic regression analyses were conducted to screen independent predictors, and a nomogram model was subsequently established. Model performance was evaluated using receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA). Among the 492 patients, the incidence of HF within one year after PCI was 26.42% (n = 130). Logistic regression identified type 2 diabetes mellitus (T2DM), left ventricular ejection fraction (LVEF), lipoprotein(a) [LP(a)], B-type natriuretic peptide (BNP), and high-sensitivity C-reactive protein (Hs-CRP) as independent predictors of HF, with odds ratios of 5.756, 0.904, 1.427, 1.012, and 1.666, respectively (all P < 0.05). The model demonstrated excellent discrimination, with areas under the ROC curve of 0.946 in the training set and 0.958 in the validation set. DCA indicated that the model provided greater net clinical benefit than the "treat-all" or "treat-none" strategies, and its predictive performance surpassed that of each individual factor (P < 0.05). The nomogram model incorporating T2DM, LVEF, LP(a), BNP and Hs-CRP provides an effective tool for predicting HF risk within one year after PCI in patients with ACS, offering valuable guidance for early clinical identification and risk stratification of high-risk individuals. Show less
no PDF DOI: 10.62347/DTOE6334
LPA

Nf2/FGFR1/AKT axis directs cranial neural crest-derived skull morphogenesis via collagen synthesis and trafficking.

Yuping Huang, Junguang Liao, Panpan Shen +7 more · 2025 · JCI insight · added 2026-04-24
Cranial neural crest cells (CNCs) play a critical role in craniofacial bone morphogenesis, engaging in intricate interactions with various molecular signals to ensure proper development, yet the molec Show more
Cranial neural crest cells (CNCs) play a critical role in craniofacial bone morphogenesis, engaging in intricate interactions with various molecular signals to ensure proper development, yet the molecular scaffolds coordinating these processes remain incompletely defined. Here, we identify neurofibromin 2 (Nf2) as a critical regulator to direct CNC-derived skull morphogenesis. Genetic ablation of Nf2 in murine CNCs causes severe craniofacial anomalies, featuring declined proliferation and increased apoptosis in osteoprogenitors, impaired type I collagen biosynthesis and trafficking, and aberrant osteogenic mineralization. Mechanistically, we uncover that Nf2 serves as a molecular linker that individually interacts with FGF receptor 1 (FGFR1) and Akt through spatially segregated phosphor-sites, and structural modeling and mutagenesis identified Ser10 and Thr230 as essential residues, with Thr230 mutation selectively ablating Akt binding while preserving FGFR1 association. Strikingly, Akt inhibition phenocopied Nf2 deficiency, reducing collagen production and Nf2 phosphorylation, whereas phospho-mimetic Nf2 (T230D) rescued CNC-derived osteogenic defects in Nf2-mutant animals. Our findings underscore the physiological significance of Nf2 as a phosphorylation-operated scaffold licensing the FGFR1/AKT axis to regulate collagen type I biogenesis and trafficking, ensuring normal CNC-derived osteogenesis and craniofacial bone development, thus exposing the Nf2/FGFR1/AKT signaling axis as a therapeutic target and promising advancements in treatment of craniofacial anomalies. Show less
📄 PDF DOI: 10.1172/jci.insight.191112
FGFR1

FBXL14 inhibits foam cell formation and atherosclerosis plaque progression by activating the NRF2 signal axis through ubiquitination of DUSP6.

Wenjie Luo, Yubin Chen, Cheng Fang +2 more · 2025 · Journal of receptor and signal transduction research · Taylor & Francis · added 2026-04-24
Atherosclerosis is characterized by persistent inflammatory condition, leading to various cardiovascular complications. Foam cell formation, resulting from macrophage uptake of oxidized low-density li Show more
Atherosclerosis is characterized by persistent inflammatory condition, leading to various cardiovascular complications. Foam cell formation, resulting from macrophage uptake of oxidized low-density lipoprotein (ox-LDL), contributes significantly to atherosclerosis progression. This study was designed to investigate the involvement of bispecific phosphatase-6 (DUSP6) and its potential regulatory mechanisms in foam cell formation and atherosclerosis. We employed THP-1 cells to induce foam cell formation. The lipid droplet accumulation, cholesterol content, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels were evaluated using Oil Red O staining, cholesterol assay, ELISA, and qRT-PCR techniques. We investigated DUSP6 ubiquitination via immunoprecipitation and western blot (WB) analysis. A bioinformatics approach identified FBXL14 as a potential E3 ligase involved in DUSP6 ubiquitination, further confirmed by siRNA and overexpression experiments. The impact of FBXL14 on the NRF2 signaling pathway was assessed using WB analysis. DUSP6 interference suppressed foam cell formation and inflammatory factor secretion. Upon ox-LDL treatment, DUSP6 underwent deubiquitylation, with FBXL14 emerging as the candidate E3 ligase. FBXL14 overexpression induced DUSP6 ubiquitination, leading to the NRF2 signaling pathway activation. It counteracted with DUSP6 overexpression on foam cell formation and inflammation. In ApoE-/- mice, sh-DUSP6 adenovirus injection mitigated atherosclerotic lesion progression and improved the lipid profile, with increased the proteins expression of NQO1, HO-1, and NRF2 in aortic tissue. DUSP6 and FBXL14 play vital roles in modulating foam cell formation and inflammatory responses in atherosclerosis. Targeting these molecules could offer therapeutic potential in attenuating atherosclerosis-related complications. Not applicable. Show less
no PDF DOI: 10.1080/10799893.2025.2466689
DUSP6

Identification of Aging-Related Hub Genes (ATP11B, RBBP7, DOCK10, and NUP160) as Potential Biomarkers and Therapeutic Targets in Sepsis.

Xueyi Sun, Shaolei Geng, Zeyuan Wang +1 more · 2025 · Human mutation · added 2026-04-24
Sepsis arises from a dysregulated host response to infection, leading to multiorgan inflammatory injury. Early diagnosis and treatment necessitate the identification of reliable immune biomarkers. Thi Show more
Sepsis arises from a dysregulated host response to infection, leading to multiorgan inflammatory injury. Early diagnosis and treatment necessitate the identification of reliable immune biomarkers. This study investigated the relationship between aging, immunity, and sepsis by analyzing six human aging-related gene sets (656 genes). We identified 16 aging-related differentially expressed genes (DEGs) in sepsis. Among these, ATP11B, RBBP7, DOCK10, and NUP160 demonstrated the strongest connectivity with other genes and exhibited significant predictive power. Functional enrichment analysis (GO and KEGG) revealed distinct signaling pathway profiles between high-risk and low-risk sepsis groups (stratified based on risk scores). These dysregulated pathways, associated with multiple immune cells, were primarily linked to transcriptional dysregulation in cellular processes and cancer-related pathways. Experimental validation assays corroborated the roles of ATP11B and RBBP7. Collectively, our bioinformatic and experimental findings indicate that ATP11B, RBBP7, DOCK10, and NUP160 are implicated in the pathogenesis and progression of sepsis. But their potential for sepsis biomarkers still requires further verification. Show less
no PDF DOI: 10.1155/humu/9789556
NUP160

Exploring Potential Drug Targets in Multiple Cardiovascular Diseases: A Study Based on Proteome-Wide Mendelian Randomization and Colocalization Analysis.

Maoxia Fan, Na Li, Libin Huang +3 more · 2025 · Cardiovascular therapeutics · added 2026-04-24
📄 PDF DOI: 10.1155/cdr/5711316
ANGPTL4

Exploring the Causal Relationships between Lipid Biomarkers and Anti-VEGF Treatment Response in Patients with Neovascular Age-related Macular Degeneration.

Feixiang He, Qifang Chen, Peilin Gu +4 more · 2025 · Ophthalmology science · Elsevier · added 2026-04-24
To identify the connections between lipid biomarkers and the anti-VEGF therapy response in patients with neovascular age-related macular degeneration (nAMD). A bidirectional and multivariable Mendelia Show more
To identify the connections between lipid biomarkers and the anti-VEGF therapy response in patients with neovascular age-related macular degeneration (nAMD). A bidirectional and multivariable Mendelian randomization study. The summary statistics for anti-VEGF nAMD treatment response included a total of 128 responders, 51 nonresponders, and 6 908 005 genetic variants available for analysis. The sample size of lipid biomarkers is 441 016 and 12 321 875 genetic variants available for analysis. Two-sample Mendelian randomization (MR) method was conducted to exhaustively appraise the causalities among 13 lipid biomarkers and the risk of different anti-VEGF treatment responses (including visual acuity [VA] and central retinal thickness [CRT]) for nAMD subtypes. Thirteen lipid biomarkers, VA, and CRT. A positive causal relationship was identified between triglycerides (TGs), apolipoproteins (Apos) E2, ApoE3, total cholesterol (TC), and VA response to anti-VEGF therapy in patients with nAMD, as confirmed by MR-Egger, weighted median, and weighted mode models. The MR-Egger model yielded statistically significant results for TC, ApoA-I, ApoB, and ApoA-V in relation to the CRT response to anti-VEGF treatment in patients with nAMD. In the reverse MR, the MR-Egger model identified significant causal relationships between ApoA-I, low-density lipoprotein cholesterol (LDL-c), ApoE3, and ApoF and the VA response. However, this was not the case in the weighted median and weighted mode models. In the MR-Egger model, ApoB, LDL-c, ApoE3, and ApoM were identified as significantly influencing the CRT response. In the multisample MR analysis, TC, high-density lipoprotein cholesterol, LDL-c, and TG were found to be causally related to VA response, and TC was also identified as being causally related to the CRT response to anti-VEGF therapy in patients with nAMD. This MR study suggests unidirectional causality between TG and ApoE3 and the response to anti-VEGF treatment in patients with nAMD. The author(s) have no proprietary or commercial interest in any materials discussed in this article. Show less
📄 PDF DOI: 10.1016/j.xops.2025.100711
APOB

Elevated BACE1 and IFNγ+ T Cells in Patients with Cognitive Impairment and the 5xFAD Mouse Model.

Yaxi Zhan, Zuolong Chen, Shuxin Zheng +6 more · 2025 · ACS chemical neuroscience · ACS Publications · added 2026-04-24
The dysregulation of T cell differentiation was associated with cognitive impairment. Recently, the peripheric β-secretase (BACE1) has been suggested as a regulator of T cell differentiation, which wa Show more
The dysregulation of T cell differentiation was associated with cognitive impairment. Recently, the peripheric β-secretase (BACE1) has been suggested as a regulator of T cell differentiation, which was increased in both cognitive impairment (CI) and type 2 diabetes mellitus (T2DM) in CI patients. However, the relationship between T cell dysfunction and CI remains unclear. To address this question, we measured T cell subtypes and BACE1 enzyme activity in a clinical cohort and 5xFAD mice. We found that both IFNγ+ Th1 and Tc1 cells were increased in the CI and T2DM-CI groups, which were associated with worsening cognitive function. The elevated IFNγ + Th1 and Tc1 cells were also observed in 8-month-old 5xFAD mice. The elevated BACE1-mediated INSR cleavage was associated with increased IFNγ + Th1 and Tc1 cells. These findings demonstrate the potential role of elevated BACE1 in IFNγ+ T cells and CI. Show less
📄 PDF DOI: 10.1021/acschemneuro.4c00565
BACE1

Joint associations of accelerometer-measured physical activity and cardiovascular-kidney-metabolic syndrome stages with the risks of cancer and all-cause mortality.

Jia-Cheng Liu, Rui Yang, Zan-Fei Feng +9 more · 2025 · Journal of the National Cancer Institute · Oxford University Press · added 2026-04-24
Cardiovascular-kidney-metabolic (CKM) syndrome significantly increases cancer and mortality risks, but the combined effects of CKM syndrome and physical activity (PA) on these outcomes remain poorly u Show more
Cardiovascular-kidney-metabolic (CKM) syndrome significantly increases cancer and mortality risks, but the combined effects of CKM syndrome and physical activity (PA) on these outcomes remain poorly understood. This prospective study included 66,650 UK Biobank participants with accelerometry data. CKM syndrome was classified into five stages based on metabolic, kidney, and cardiovascular health. PA was categorized by intensity into light (LPA), moderate (MPA), vigorous (VPA), and moderate-to-vigorous (MVPA) levels, and further divided into tertiles by daily duration. Multivariable Cox models were used to estimate hazard ratios. Over a median follow-up of 8.03 years, 4,301 incident cancer cases and 2,442 deaths occurred. Advancing CKM stages were associated with elevated risks of both cancer incidence and all cause mortality, while increasing PA levels reduced these risks. Significant interactions were observed between CKM syndrome and both MPA and MVPA on cancer and mortality risks (P interaction < 0.05). In participants with the lowest tertile of MPA or MVPA, those in stages 2 and 4 had higher cancer risk, while in the highest tertile, this risk was no longer elevated. For all-cause mortality, in participants with the lowest tertile of MPA or MVPA, CKM stage 3 exhibited higher risks, while those in the highest tertile did not. CKM stage 4 remained associated with higher mortality across all PA intensity levels, but risks decreased with increasing MVPA levels. Higher levels of MPA and MVPA may mitigate the elevated risks of both cancer incidence and all-cause mortality associated with CKM stages 2 to 4. Show less
no PDF DOI: 10.1093/jnci/djaf365
LPA

APP lysine 612 lactylation ameliorates amyloid pathology and memory decline in Alzheimer's disease.

Qiuyun Tian, Junjie Li, Bin Wu +16 more · 2025 · The Journal of clinical investigation · added 2026-04-24
Posttranslational modification (PTM) of the amyloid precursor protein (APP) plays a critical role in Alzheimer's disease (AD). Recent evidence reveals that lactylation modification, as a novel PTM, is Show more
Posttranslational modification (PTM) of the amyloid precursor protein (APP) plays a critical role in Alzheimer's disease (AD). Recent evidence reveals that lactylation modification, as a novel PTM, is implicated in the occurrence and development of AD. However, whether and how APP lactylation contributes to both the pathogenesis and cognitive function in AD remains unknown. Here, we observed a reduction in APP lactylation in AD patients and AD model mice and cells. Proteomic mass spectrometry analysis further identified lysine 612 (APP-K612la) as a crucial site for APP lactylation, influencing APP amyloidogenic processing. A lactyl-mimicking mutant (APPK612T) reduced amyloid-β peptide (Aβ) generation and slowed down cognitive deficits in vivo. Mechanistically, APPK612T appeared to facilitate APP trafficking and metabolism. However, lactylated APP entering the endosome inhibited its binding to BACE1, suppressing subsequent cleavage. Instead, it promoted protein interaction between APP and CD2-associated protein (CD2AP), thereby accelerating the endosomal-lysosomal degradation pathway of APP. In the APP23/PS45 double-transgenic mouse model of AD, APP-Kla was susceptible to L-lactate regulation, which reduced Aβ pathology and repaired spatial learning and memory deficits. Thus, these findings suggest that targeting APP lactylation may be a promising therapeutic strategy for AD in humans. Show less
📄 PDF DOI: 10.1172/JCI184656
BACE1

Mannose Promotes β-Amyloid Pathology by Regulating BACE1 Glycosylation in Alzheimer's Disease.

Chensi Liang, Ziqi Yuan, Shangchen Yang +7 more · 2025 · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Wiley · added 2026-04-24
Hyperglycemia accelerates Alzheimer's disease (AD) progression, yet the role of monosaccharides remains unclear. Here, it is demonstrated that mannose, a hexose, closely correlates with the pathologic Show more
Hyperglycemia accelerates Alzheimer's disease (AD) progression, yet the role of monosaccharides remains unclear. Here, it is demonstrated that mannose, a hexose, closely correlates with the pathological characteristics of AD, as confirmed by measuring mannose levels in the brains and serum of AD mice, as well as in the serum of AD patients. AD mice are given mannose by intra-cerebroventricular injection (ICV) or in drinking water to investigate the effects of mannose on cognition and AD pathological progression. Chronic mannose overload increases β-amyloid (Aβ) burdens and exacerbates cognitive impairments, which are reversed by a mannose-free diet or mannose transporter antagonists. Mechanistically, single-cell RNA sequencing and metabolomics suggested that mannose-mediated N-glycosylation of BACE1 and Nicastrin enhances their protein stability, promoting Aβ production. Additionally, reduced mannose intake decreased BACE1 and Nicastrin stability, ultimately lowering Aβ production and mitigating AD pathology. this results highlight that high-dose mannose consumption may exacerbate AD pathogenesis. Restricting dietary mannose may have therapeutic benefits. Show less
📄 PDF DOI: 10.1002/advs.202409105
BACE1

Absence of the intracellular lipolytic inhibitor G0S2 enhances intravascular triglyceride clearance and abolishes diet-induced hypertriglyceridemia.

Yongbin Chen, Scott M Johnson, Stephanie D Burr +4 more · 2025 · The Journal of clinical investigation · added 2026-04-24
The interplay between intracellular and intravascular lipolysis is crucial for maintaining circulating lipid levels and systemic energy homeostasis. Adipose triglyceride lipase (ATGL) and lipoprotein Show more
The interplay between intracellular and intravascular lipolysis is crucial for maintaining circulating lipid levels and systemic energy homeostasis. Adipose triglyceride lipase (ATGL) and lipoprotein lipase (LPL), the primary triglyceride (TG) lipases responsible for these two spatially separate processes, are highly expressed in adipose tissue. Yet the mechanisms underlying their coordinated regulation remain undetermined. Here, we demonstrate that genetic ablation of G0S2, a specific inhibitory protein of ATGL, completely abolished diet-induced hypertriglyceridemia and significantly attenuated atherogenesis in mice. These effects were attributable to enhanced whole-body TG clearance, not altered hepatic TG secretion. Specifically, G0S2 deletion increased circulating LPL concentration and activity, predominantly through LPL production from white adipose tissue (WAT). Strikingly, transplantation of G0S2-deficient WAT normalized plasma TG levels in mice with hypertriglyceridemia. In conjunction with improved insulin sensitivity and decreased ANGPTL4 expression, the absence of G0S2 enhanced the stability of LPL protein in adipocytes, a phenomenon that could be reversed upon ATGL inhibition. Collectively, these findings highlight the pivotal role of adipocyte G0S2 in regulating both intracellular and intravascular lipolysis, and the possibility of targeting G0S2 as a viable pharmacological approach to reducing levels of circulating TGs. Show less
📄 PDF DOI: 10.1172/JCI181754
ANGPTL4

Two-Coordinate Gold(I) Complex with Rotational Freedom: A Platform Integrating Thermally Activated Delayed Fluorescence, Polymorphism, and Linearly Polarized Luminescence.

Xi Zhang, Xiu-Fang Song, Shan Jiang +5 more · 2025 · Angewandte Chemie (International ed. in English) · Wiley · added 2026-04-24
Two-coordinate coinage metal complexes have been exploited for various applications. Herein, a new donor-metal-acceptor (D-M-A) complex PZI-Au-TOT, using bulky pyrazine-fused N-heterocyclic carbene (P Show more
Two-coordinate coinage metal complexes have been exploited for various applications. Herein, a new donor-metal-acceptor (D-M-A) complex PZI-Au-TOT, using bulky pyrazine-fused N-heterocyclic carbene (PZI) and trioxytriphenylamine (TOT) ligands, was synthesized. PZI-Au-TOT displays decent thermally activated delayed fluorescence (TADF) with a quantum yield of 93 % in doped film. The crystals of PZI-Au-TOT show simultaneous TADF, polymorphism, and linearly polarized luminescence (LPL). The polymorph-dependent emission properties with widely varied peaks from 560 to 655 nm are attributed to different packing modes in terms of isolated monomers, discrete π-π stacked dimers or dimer PLUS. Two well-defined microcrystals of PZI-Au-TOT exhibit linearly polarized thermally activated delayed fluorescence with a degree of polarization up to 0.64. This work demonstrates that the molecular rotational flexibility of D-M-A type complexes endows an integration of multiple functions into one complex through manipulation of supramolecular aggregation. This type of complexes is expected to serve as a versatile platform for the fabrication of crystal materials for advanced photonic applications. Show less
no PDF DOI: 10.1002/anie.202414892
LPL

Potential of CETP inhibition in treating dyslipidemia in systemic lupus erythematosus: Novel and comprehensive evidence from clinical studies and Mendelian randomization.

Yihong Gan, Yilin Zhang, Jingqun Liu +10 more · 2025 · International immunopharmacology · Elsevier · added 2026-04-24
Cardiovascular diseases from abnormal lipid metabolism significantly increase mortality in systemic lupus erythematosus (SLE). The causal link between dyslipidemia and SLE is unclear. Lipid metabolism Show more
Cardiovascular diseases from abnormal lipid metabolism significantly increase mortality in systemic lupus erythematosus (SLE). The causal link between dyslipidemia and SLE is unclear. Lipid metabolism in patients with SLE was evaluated based on clinical data from 511 patients with SLE and 706 healthy individuals. Bidirectional Mendelian randomization (MR) was employed to assess causal links between 179 plasma lipid metabolites, lipid-lowering drug targets, and SLE risk. Genetic instruments from GWAS and eQTL data were used to evaluate CETP and APOA4 effects. Peripheral blood CETP and apolipoprotein levels in SLE patients were validated via ELISA. SLE patients exhibited reduced HDL-C (P < 0.0001), APOA1 (P < 0.0001), and APOA4 (P < 0.0001), alongside elevated triglycerides (TG, P < 0.0001), APOC3, APOD, and APOF. MR identified three lipid metabolites-PC(18:2₂₀:4), TG(56:6), and TG(58:7)-as causal factors for SLE (P < 2.79E-5). CETP inhibition significantly reduced SLE risk via HDL-C modulation (OR = 0.72, P = 3.38E-08) and influenced LDL-C, TG, and apolipoproteins. Clinical validation confirmed elevated CETP and reduced APOA4 in SLE, correlating with disease activity. APOA4 activation showed protective effects, while PCSK9 inhibition lacked relevance. Bidirectional Mendelian randomization analyses confirmed dyslipidemia as a causal antecedent to SLE, with no evidence of reverse causation. A variety of MR analyses and clinical validation indicated that targeting HDL-C regulation offers significant advantages for managing dyslipidemia in patients with SLE, with CETP identified as the optimal pharmacological target. Show less
no PDF DOI: 10.1016/j.intimp.2025.114736
APOA4

Exploration of calcium and amino acids for children with primary cardiomyopathies based on genetic characteristics.

Shirui Jiang, Ailin Zhang, Jiegang Deng +5 more · 2025 · Frontiers in pediatrics · Frontiers · added 2026-04-24
Pediatric primary cardiomyopathies (PCMs) are rare diseases with complex causes and nonspecific treatment. The influence of electrolytes and amino acids (AAs) on cardiomyopathies has not been extensiv Show more
Pediatric primary cardiomyopathies (PCMs) are rare diseases with complex causes and nonspecific treatment. The influence of electrolytes and amino acids (AAs) on cardiomyopathies has not been extensively studied. This study aimed to explore clinical characteristics and the usage of electrolytes and AAs in children with PCMs. Children diagnosed with PCMs who had genetic test reports were included. Relevant information was collected and processed, and clinical characteristics and mutated genes were clarified. Gene databases were searched to explore related electrolytes and AAs in the treatment of PCMs. The effect of calcium was explored in children with DCM. Paired samples T tests and nonparametric Wilcoxon signed-rank tests were performed for comparison between before and after using calcium. In this study, 27 children with gene test results were enrolled to perform gene-related analysis. The median age was 2.5 years old. Mutated genes were collected, including pathogenic, likely pathogenic, uncertain significance, and other mutations. The most frequently mutated genes related to dilated cardiomyopathy (DCM) were For children with DCM, calcium supplements may be beneficial. AAs, including serine, cysteine, and arginine, could be used for supplementary treatment in children with DCM and HCM. Show less
📄 PDF DOI: 10.3389/fped.2025.1631632
MYBPC3

Remote ischemic conditioning slows blood-retinal barrier damage in type 1 diabetic rats.

Xiaohan Xu, Shuaili Xu, Yuan Gao +5 more · 2025 · Brain research · Elsevier · added 2026-04-24
Diabetic retinopathy (DR) is one of the major complications of diabetes and can cause severe visual impairment. Blood-retina barrier (BRB) destruction resulted from chronic hyperglycemia underlines it Show more
Diabetic retinopathy (DR) is one of the major complications of diabetes and can cause severe visual impairment. Blood-retina barrier (BRB) destruction resulted from chronic hyperglycemia underlines its major pathological process. However, current treatments have limited efficacy and may even cause serious complications. Remote ischemic conditioning (RIC), through repeated transient mechanical occlusion of limb blood vessels, has been confirmed to promote blood-brain barrier integrity after stroke, but its role in BRB disruption has not been elucidated. This study aimed to investigate the protective effects of RIC on the BRB in diabetic rats and its potential mechanisms. 48 Sprague-Dawley rats were randomly assigned to the Sham group, Sham + RIC group, diabetes mellitus (DM) group and DM+RIC group. The diabetic model was successfully induced by intraperitoneal injection of streptozotocin. RIC treatment was administered daily and lasted for 9 weeks. In functional analysis, RIC improved the retinal function based on electroretinogram data and reduced the leakage of BRB in diabetic rats. In proteomic analysis, tight junction pathway was enriched after RIC treatment, in which Patj gene was significantly increased. We also found that RIC increased mRNA levels of Patj, claudin-1 and zonula occludens (ZO)-1, protein expression of claudin-1 when compared with diabetic models. In conclusion, RIC slowed BRB damage in diabetic rats, which may be related to the preservation of tight junction proteins. RIC may be a promising protective strategy for the treatment of DR. Show less
no PDF DOI: 10.1016/j.brainres.2024.149253
PATJ

Multi-omics analyses reveal distinct molecular characteristics and transformation mechanisms of stage I-III micropapillary lung adenocarcinoma.

Yang Qu, Xiaoli Feng, Hanlin Chen +9 more · 2025 · The Journal of pathology · Wiley · added 2026-04-24
The micropapillary (MIP) pattern is a high-grade histological subtype of lung adenocarcinoma (LUAD) with poor prognosis. In this study, surgically resected tumor samples from 101 patients with stage I Show more
The micropapillary (MIP) pattern is a high-grade histological subtype of lung adenocarcinoma (LUAD) with poor prognosis. In this study, surgically resected tumor samples from 101 patients with stage I-III MIP-LUAD (MIP ≥30%) were microdissected to separate MIP components from non-MIP components, all of which underwent RNA and DNA whole-exome sequencing (WES). The genomic and transcriptomic landscapes of MIP and non-MIP components within MIP-enriched tumor tissues demonstrated remarkable similarities, notably marked by high epidermal growth factor receptor (EGFR) alteration frequencies. However, when compared to MIP-naïve LUAD tissues, MIP components showed higher chromosomal instability and revealed 18 enriched alterations, encompassing EGFR mutations, EGFR amplifications, and CDKN2A/CDKN2B deletions, which all linked to upregulation of cell proliferation pathways and downregulation of immune pathways. Shared mutations were observed in 97.8% (91/93) of patients with paired DNA WES data for MIP and non-MIP components within the same tissues, suggesting a common origin. The recurrence-free survival analysis identified MACF1, PCLO, ADGRV1, and Fanconi Anemia pathway mutations as negative indicators. In all, we conducted an in-depth analysis of the molecular characteristics and transformation mechanisms of MIP-LUAD, employing microdissection techniques to investigate the genomic and transcriptomic levels within a substantial cohort, providing insights for precision medicine of this aggressive cancer subtype. © 2025 The Pathological Society of Great Britain and Ireland. Show less
no PDF DOI: 10.1002/path.6416
MACF1

Coral calcium hydride promotes peripheral mitochondrial division and reduces AT-II cells damage in ARDS via activation of the Trx2/Myo19/Drp1 pathway.

Qian Li, Yang Ang, Qing-Qing Zhou +15 more · 2025 · Journal of pharmaceutical analysis · Elsevier · added 2026-04-24
Acute respiratory distress syndrome (ARDS) is a common respiratory emergency, but current clinical treatment remains at the level of symptomatic support and there is a lack of effective targeted treat Show more
Acute respiratory distress syndrome (ARDS) is a common respiratory emergency, but current clinical treatment remains at the level of symptomatic support and there is a lack of effective targeted treatment measures. Our previous study confirmed that inhalation of hydrogen gas can reduce the acute lung injury of ARDS, but the application of hydrogen has flammable and explosive safety concerns. Drinking hydrogen-rich liquid or inhaling hydrogen gas has been shown to play an important role in scavenging reactive oxygen species and maintaining mitochondrial quality control balance, thus improving ARDS in patients and animal models. Coral calcium hydrogenation (CCH) is a new solid molecular hydrogen carrier prepared from coral calcium (CC). Whether and how CCH affects acute lung injury in ARDS remains unstudied. In this study, we observed the therapeutic effect of CCH on lipopolysaccharide (LPS) induced acute lung injury in ARDS mice. The survival rate of mice treated with CCH and hydrogen inhalation was found to be comparable, demonstrating a significant improvement compared to the untreated ARDS model group. CCH treatment significantly reduced pulmonary hemorrhage and edema, and improved pulmonary function and local microcirculation in ARDS mice. CCH promoted mitochondrial peripheral division in the early course of ARDS by activating mitochondrial thioredoxin 2 (Trx2), improved lung mitochondrial dysfunction induced by LPS, and reduced oxidative stress damage. The results indicate that CCH is a highly efficient hydrogen-rich agent that can attenuate acute lung injury of ARDS by improving the mitochondrial function through Trx2 activation. Show less
no PDF DOI: 10.1016/j.jpha.2024.101039
MYO19

Tumor Cells-Derived FGF-2 Promotes Lymphangiogenesis as a Prognostic Marker in OSCC.

Jia Kang, Aoming Cheng, Guanzheng Chen +3 more · 2025 · Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · Blackwell Publishing · added 2026-04-24
The "cold" tumor microenvironment of oral squamous cell carcinoma (OSCC), where tumor-associated lymphatic vessels play a critical role in the transport of immune cells, is associated with a poor prog Show more
The "cold" tumor microenvironment of oral squamous cell carcinoma (OSCC), where tumor-associated lymphatic vessels play a critical role in the transport of immune cells, is associated with a poor prognosis. However, the effect of tumor-induced lymphangiogenesis on CD8+ T cell infiltration and its role in the formation of the tumor immune microenvironment remain unclear. We analyzed the prognostic significance of several lymphangiogenesis factors in OSCC with The Cancer Genome Atlas dataset, and confirmed the impact of fibroblast growth factor-2 (FGF-2) on prognosis in tissue specimens. Subsequently, we investigated the effects of FGF-2 on the proliferation, migration, and tube formation capacities of lymphatic endothelial cells, and CD8+ T cell infiltration through in vivo and in vitro experiments. Survival analysis was performed by Kaplan-Meier analysis and log-rank tests. The hazard ratio was calculated by Cox proportional hazards model. Patients with high FGF-2 levels and increased numbers of peritumoral lymphatic vessels were associated with a worse prognosis. Furthermore, we demonstrated that tumor cell-derived FGF-2 promoted lymphangiogenesis by regulating the FGFR1/PTEN/AKT axis and increased the secretion of CXCL9 to recruit and egress CD8+ T cells via neo-lymphatic vessels. PD-166866, an inhibitor of FGFR1, suppressed lymphangiogenesis and the secretion of CXCL9 to increase CD8+ T cell infiltration and inhibit tumor progression. Our data suggest that FGF-2 is a significant prognostic factor that induces lymphangiogenesis and affects intratumoral CD8+ T cells, contributing to the formation of a "cold" tumor microenvironment in OSCC. FGF-2/FGFR1 could serve as an effective target for improving the prognosis of OSCC. Show less
no PDF DOI: 10.1111/jop.70019
FGFR1

Associations between selected genetic variants and lipid profile variability in response to statins in Alzheimer's disease: a prospective observational study.

Fabricio Ferreira de Oliveira, Sandro Soares de Almeida, Elizabeth Suchi Chen +2 more · 2025 · Sao Paulo medical journal = Revista paulista de medicina · added 2026-04-24
Lipid profiles are largely determined by genetic variants, and lipid metabolism plays a crucial role in Alzheimer's disease. To investigate whether lipid profile variability in response to diverse sta Show more
Lipid profiles are largely determined by genetic variants, and lipid metabolism plays a crucial role in Alzheimer's disease. To investigate whether lipid profile variability in response to diverse statins could be affected by cholesterol metabolism-related genetic variants in Alzheimer's disease.. This prospective observational pharmacogenetic study was conducted at the Universidade Federal de São Paulo (Unifesp), Brazil. Consecutive outpatients were prospectively followed for lipid profile variations over one year, estimated by the associations between statin therapy and the following variants: rs2695121 (NR1H2), rs3846662 (HMGCR), rs11669576 (LDLR8), rs5930 (LDLR10), rs5882 and rs708272 (CETP), rs7412 and rs429358 (APOE), and ACE insertion/deletion polymorphism. All polymorphisms in the 189 patients were in Hardy-Weinberg equilibrium. Statins resulted in lower total cholesterol and LDL cholesterol levels, whereas the effects on HDL cholesterol varied according to the statin used. Atorvastatin resulted in lower triglyceride level variations than simvastatin. APOE-ε4 carriers showed a better response to atorvastatin in elevating HDL-cholesterol than APOE-ε4 non-carriers. Carriers of the ACE insertion allele had cumulatively lower total cholesterol and LDL-cholesterol levels, regardless of statin therapy, but lower triglyceride levels when using atorvastatin. Carriers of rs11669576-G had lower total cholesterol and LDL-cholesterol levels when using simvastatin, and lower total cholesterol and triglycerides when using atorvastatin. Concerning CETP haplotypes, carriers of rs5882-A and rs708272-A benefitted the most from statins, which lowered total cholesterol and increased HDL-cholesterol levels, and from atorvastatin lowering triglycerides; however, the effects of atorvastatin lowering total cholesterol and LDL-cholesterol were more pronounced for carriers of rs5882-GG/rs708272-GG. Lipid profile variations may be pharmacogenetically mediated in Alzheimer's disease, thus, confirming their high heritability. Show less
📄 PDF DOI: 10.1590/1516-3180.2024.0160.27112024
CETP

Oxidative modification of G-quadruplex triggers CLIC4-associated mitochondrial dysfunction to promote glioblastoma progression.

Xiaodong Li, Yaning Fu, Yalan Luo +3 more · 2025 · Redox biology · Elsevier · added 2026-04-24
Glioblastoma is the most aggressive form of primary brain tumor, characterized with poor prognosis and resistance to conventional therapies. Increasing evidence points to oxidative stress and redox dy Show more
Glioblastoma is the most aggressive form of primary brain tumor, characterized with poor prognosis and resistance to conventional therapies. Increasing evidence points to oxidative stress and redox dysregulation as important contributors to glioblastoma progression. Previously, chloride intracellular channel protein 4 (CLIC4), a redox-sensitive protein, has been implicated in cancer biology. However, its roles in glioblastoma remain poorly understood. Here, we found that CLIC4 expression is upregulated in glioblastoma tissues and cell lines, and is positively correlated with tumor malignancy and poor survival outcomes in patients with glioblastoma. Gene silencing of CLIC4 significantly reduces glioblastoma cell viability, migration, and proliferation in vitro and suppress tumor growth in vivo. Mechanistically, CLIC4 appears to maintain redox homeostasis by regulating mitochondrial functions, including membrane potential, mass, ROS production, and the activity of complexes III and IV. Moreover, a G-quadruplex (G4) structure located in CLIC4 promoter region is related to CLIC4 upregulation by oxidative stress in glioblastoma. This G4 structure can be readily oxidized to a parallel conformation, thereby enhancing its binding with DHX36 protein to promote gene transcription. Collectively, these findings position CLIC4 as a pivotal modulator of oxidative stress in glioblastoma and a potential target for developing therapeutic approaches for the treatment of glioblastoma. Show less
📄 PDF DOI: 10.1016/j.redox.2025.103917
DHX36