👤 Huichao Chen

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2981
Articles
1996
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Also published as: Ai-Qun Chen, Aiping Chen, Alex Chen, Alex F Chen, Alice P Chen, Alice Y Chen, Alice Ye A Chen, Allen Menglin Chen, Alon Chen, Alvin Chen, An Chen, Andrew Chen, Anqi Chen, Aoshuang Chen, Aozhou Chen, B Chen, B-S Chen, Baihua Chen, Ban Chen, Bang Chen, Bang-dang Chen, Bao-Bao Chen, Bao-Fu Chen, Bao-Sheng Chen, Bao-Ying Chen, Baofeng Chen, Baojiu Chen, Baolin Chen, Baosheng Chen, Baoxiang Chen, Beidong Chen, Beijian Chen, Ben-Kuen Chen, Benjamin Chen, Benjamin Jieming Chen, Benjamin P C Chen, Beth L Chen, Bihong T Chen, Bin Chen, Bing Chen, Bing-Bing Chen, Bing-Feng Chen, Bing-Huei Chen, Bingdi Chen, Bingqian Chen, Bingqing Chen, Bingyu Chen, Binlong Chen, Binzhen Chen, Bo Chen, Bo-Fang Chen, Bo-Jun Chen, Bo-Rui Chen, Bo-Sheng Chen, Bohe Chen, Bohong Chen, Bosong Chen, Bowang Chen, Bowei Chen, Bowen Chen, Boyu Chen, Brian Chen, C Chen, C Y Chen, C Z Chen, C-Y Chen, Cai-Long Chen, Caihong Chen, Can Chen, Cancan Chen, Canrong Chen, Canyu Chen, Caressa Chen, Carl Pc Chen, Carol Chen, Carol X-Q Chen, Catherine Qing Chen, Ceshi Chen, Chan Chen, Chang Chen, Chang-Lan Chen, Chang-Zheng Chen, Changjie Chen, Changya Chen, Changyan Chen, Chanjuan Chen, Chao Chen, Chao-Jung Chen, Chao-Wei Chen, Chaochao Chen, Chaojin Chen, Chaoli Chen, Chaoping Chen, Chaoqun Chen, Chaoran Chen, Chaoyi Chen, Chaoyue Chen, Chen Chen, Chen-Mei Chen, Chen-Sheng Chen, Chen-Yu Chen, Cheng Chen, Cheng-Fong Chen, Cheng-Sheng Chen, Cheng-Yi Chen, Cheng-Yu Chen, Chengchuan Chen, Chengchun Chen, Chengde Chen, Chengsheng Chen, Chengwei Chen, Chenyang Chen, Chi Chen, Chi-Chien Chen, Chi-Hua Chen, Chi-Long Chen, Chi-Yu Chen, Chi-Yuan Chen, Chi-Yun Chen, Chian-Feng Chen, Chider Chen, Chien-Hsiun Chen, Chien-Jen Chen, Chien-Lun Chen, Chien-Ting Chen, Chien-Yu Chen, Chih-Chieh Chen, Chih-Mei Chen, Chih-Ping Chen, Chih-Ta Chen, Chih-Wei Chen, Chih-Yi Chen, Chin-Chuan Chen, Ching Kit Chen, Ching-Hsuan Chen, Ching-Jung Chen, Ching-Wen Chen, Ching-Yi Chen, Ching-Yu Chen, Chiqi Chen, Chiung Mei Chen, Chiung-Mei Chen, Chixiang Chen, Chong Chen, Chongyang Chen, Christina Y Chen, Christina Yingxian Chen, Christopher S Chen, Chu Chen, Chu-Huang Chen, Chuanbing Chen, Chuannan Chen, Chuanzhi Chen, Chuck T Chen, Chueh-Tan Chen, Chujie Chen, Chun Chen, Chun-An Chen, Chun-Chi Chen, Chun-Fa Chen, Chun-Han Chen, Chun-Houh Chen, Chun-Wei Chen, Chun-Yuan Chen, Chung-Hao Chen, Chung-Hsing Chen, Chung-Hung Chen, Chung-Jen Chen, Chung-Yung Chen, Chunhai Chen, Chunhua Chen, Chunji Chen, Chunjie Chen, Chunlin Chen, Chunnuan Chen, Chunxiu Chen, Chuo Chen, Chuyu Chen, Cindi Chen, Constance Chen, Cuicui Chen, Cuie Chen, Cuilan Chen, Cuimin Chen, Cuncun Chen, D F Chen, D M Chen, D-F Chen, D. Chen, Dafang Chen, Daijie Chen, Daiwen Chen, Daiyu Chen, Dake Chen, Dali Chen, Dan Chen, Dan-Dan Chen, Dandan Chen, Danlei Chen, Danli Chen, Danmei Chen, Danna Chen, Danni Chen, Danxia Chen, Danxiang Chen, Danyang Chen, Danyu Chen, Daoyuan Chen, Dapeng Chen, Dawei Chen, Defang Chen, Dejuan Chen, Delong Chen, Denghui Chen, Dengpeng Chen, Deqian Chen, Dexi Chen, Dexiang Chen, Dexiong Chen, Deying Chen, Deyu Chen, Di Chen, Di-Long Chen, Dian Chen, Dianke Chen, Ding Chen, Diyun Chen, Dong Chen, Dong-Mei Chen, Dong-Yi Chen, Dongli Chen, Donglong Chen, Dongquan Chen, Dongrong Chen, Dongsheng Chen, Dongxue Chen, Dongyan Chen, Dongyin Chen, Du-Qun Chen, Duan-Yu Chen, Duo Chen, Duo-Xue Chen, Duoting Chen, E S Chen, Eleanor Y Chen, Elizabeth H Chen, Elizabeth S Chen, Elizabeth Suchi Chen, Emily Chen, En-Qiang Chen, Erbao Chen, Erfei Chen, Erqu Chen, Erzhen Chen, Everett H Chen, F Chen, F-K Chen, Fa Chen, Fa-Xi Chen, Fahui Chen, Fan Chen, Fang Chen, Fang-Pei Chen, Fang-Yu Chen, Fang-Zhi Chen, Fang-Zhou Chen, Fangfang Chen, Fangli Chen, Fangyan Chen, Fangyuan Chen, Faye H Chen, Fei Chen, Fei Xavier Chen, Feifan Chen, Feifeng Chen, Feilong Chen, Feixue Chen, Feiyang Chen, Feiyu Chen, Feiyue Chen, Feng Chen, Feng-Jung Chen, Feng-Ling Chen, Fenghua Chen, Fengju Chen, Fengling Chen, Fengming Chen, Fengrong Chen, Fengwu Chen, Fengyang Chen, Fred K Chen, Fu Chen, Fu-Shou Chen, Fumei Chen, Fusheng Chen, Fuxiang Chen, Gang Chen, Gao B Chen, Gao Chen, Gao-Feng Chen, Gaoyang Chen, Gaoyu Chen, Gaozhi Chen, Gary Chen, Gary K Chen, Ge Chen, Gen-Der Chen, Geng Chen, Gengsheng Chen, Ginny I Chen, Gong Chen, Gongbo Chen, Gonghai Chen, Gonglie Chen, Guan-Wei Chen, Guang Chen, Guang-Chao Chen, Guang-Yu Chen, Guangchun Chen, Guanghao Chen, Guanghong Chen, Guangjie Chen, Guangju Chen, Guangliang Chen, Guanglong Chen, Guangnan Chen, Guangping Chen, Guangquan Chen, Guangyao Chen, Guangyi Chen, Guangyong Chen, Guanjie Chen, Guanren Chen, Guanyu Chen, Guanzheng Chen, Gui Mei Chen, Gui-Hai Chen, Gui-Lai Chen, Guihao Chen, Guiqian Chen, Guiquan Chen, Guiying Chen, Guo Chen, Guo-Chong Chen, Guo-Jun Chen, Guo-Rong Chen, Guo-qing Chen, Guochao Chen, Guochong Chen, Guofang Chen, Guohong Chen, Guohua Chen, Guojun Chen, Guoliang Chen, Guopu Chen, Guoshun Chen, Guoxun Chen, Guozhong Chen, Guozhou Chen, H Chen, H Q Chen, H T Chen, Hai-Ning Chen, Haibing Chen, Haibo Chen, Haide Chen, Haifeng Chen, Haijiao Chen, Haimin Chen, Haiming Chen, Haining Chen, Haiqin Chen, Haiquan Chen, Haitao Chen, Haiyan Chen, Haiyang Chen, Haiyi Chen, Haiying Chen, Haiyu Chen, Haiyun Chen, Han Chen, Han-Bin Chen, Han-Chun Chen, Han-Hsiang Chen, Han-Min Chen, Hanbei Chen, Hang Chen, Hangang Chen, Hanjing Chen, Hanlin Chen, Hanqing Chen, Hanwen Chen, Hanxi Chen, Hanyong Chen, Hao Chen, Hao Yu Chen, Hao-Zhu Chen, Haobo Chen, Haodong Chen, Haojie Chen, Haoran Chen, Haotai Chen, Haotian Chen, Haoting Chen, Haoyun Chen, Haozhu Chen, Harn-Shen Chen, Haw-Wen Chen, He-Ping Chen, Hebing Chen, Hegang Chen, Hehe Chen, Hekai Chen, Heng Chen, Heng-Sheng Chen, Heng-Yu Chen, Hengsan Chen, Hengsheng Chen, Hengyu Chen, Heni Chen, Herbert Chen, Hetian Chen, Heye Chen, Hong Chen, Hong Yang Chen, Hong-Sheng Chen, Hongbin Chen, Hongbo Chen, Hongen Chen, Honghai Chen, Honghui Chen, Honglei Chen, Hongli Chen, Hongmei Chen, Hongmin Chen, Hongmou Chen, Hongqi Chen, Hongqiao Chen, Hongshan Chen, Hongxiang Chen, Hongxing Chen, Hongxu Chen, Hongyan Chen, Hongyu Chen, Hongyue Chen, Hongzhi Chen, Hou-Tsung Chen, Hou-Zao Chen, Hsi-Hsien Chen, Hsiang-Wen Chen, Hsiao-Jou Cortina Chen, Hsiao-Tan Chen, Hsiao-Wang Chen, Hsiao-Yun Chen, Hsin-Han Chen, Hsin-Hong Chen, Hsin-Hung Chen, Hsin-Yi Chen, Hsiu-Wen Chen, Hsuan-Yu Chen, Hsueh-Fen Chen, Hu Chen, Hua Chen, Hua-Pu Chen, Huachen Chen, Huafei Chen, Huaiyong Chen, Hualan Chen, Huali Chen, Hualin Chen, Huan Chen, Huan-Xin Chen, Huanchun Chen, Huang Chen, Huang-Pin Chen, Huangtao Chen, Huanhua Chen, Huanhuan Chen, Huanxiong Chen, Huaping Chen, Huapu Chen, Huaqiu Chen, Huatao Chen, Huaxin Chen, Huayu Chen, Huei-Rong Chen, Huei-Yan Chen, Huey-Miin Chen, Hui Chen, Hui Mei Chen, Hui-Chun Chen, Hui-Fen Chen, Hui-Jye Chen, Hui-Ru Chen, Hui-Wen Chen, Hui-Xiong Chen, Hui-Zhao Chen, Huijia Chen, Huijiao Chen, Huijie Chen, Huimei Chen, Huimin Chen, Huiqin Chen, Huiqun Chen, Huiru Chen, Huishan Chen, Huixi Chen, Huixian Chen, Huizhi Chen, Hung-Chang Chen, Hung-Chi Chen, Hung-Chun Chen, Hung-Po Chen, Hung-Sheng Chen, I-Chun Chen, I-M Chen, Ida Y-D Chen, Irwin Chen, Ivy Xiaoying Chen, J Chen, Jacinda Chen, Jack Chen, Jake Y Chen, Jason A Chen, Jeanne Chen, Jen-Hau Chen, Jen-Sue Chen, Jennifer F Chen, Jenny Chen, Jeremy J W Chen, Ji-ling Chen, Jia Chen, Jia Min Chen, Jia Wei Chen, Jia-De Chen, Jia-Feng Chen, Jia-Lin Chen, Jia-Mei Chen, Jia-Shun Chen, Jiabing Chen, Jiacai Chen, Jiacheng Chen, Jiade Chen, Jiahao Chen, Jiahua Chen, Jiahui Chen, Jiajia Chen, Jiajing Chen, Jiajun Chen, Jiakang Chen, Jiale Chen, Jiali Chen, Jialing Chen, Jiamiao Chen, Jiamin Chen, Jian Chen, Jian-Guo Chen, Jian-Hua Chen, Jian-Jun Chen, Jian-Kang Chen, Jian-Min Chen, Jian-Qiao Chen, Jian-Qing Chen, Jianan Chen, Jianfei Chen, Jiang Chen, Jiang Ye Chen, Jiang-hua Chen, Jianghua Chen, Jiangxia Chen, Jianhua Chen, Jianhui Chen, Jiani Chen, Jianjun Chen, Jiankui Chen, Jianlin Chen, Jianmin Chen, Jianping Chen, Jianshan Chen, Jiansu Chen, Jianxiong Chen, Jianzhong Chen, Jianzhou Chen, Jiao Chen, Jiao-Jiao Chen, Jiaohua Chen, Jiaping Chen, Jiaqi Chen, Jiaqing Chen, Jiaren Chen, Jiarou Chen, Jiawei Chen, Jiawen Chen, Jiaxin Chen, Jiaxu Chen, Jiaxuan Chen, Jiayao Chen, Jiaye Chen, Jiayi Chen, Jiayuan Chen, Jichong Chen, Jie Chen, Jie-Hua Chen, Jiejian Chen, Jiemei Chen, Jien-Jiun Chen, Jihai Chen, Jijun Chen, Jimei Chen, Jin Chen, Jin-An Chen, Jin-Ran Chen, Jin-Shuen Chen, Jin-Wu Chen, Jin-Xia Chen, Jina Chen, Jinbo Chen, Jindong Chen, Jing Chen, Jing-Hsien Chen, Jing-Wen Chen, Jing-Xian Chen, Jing-Yuan Chen, Jing-Zhou Chen, Jingde Chen, Jinghua Chen, Jingjing Chen, Jingli Chen, Jinglin Chen, Jingming Chen, Jingnan Chen, Jingqing Chen, Jingshen Chen, Jingteng Chen, Jinguo Chen, Jingxuan Chen, Jingyao Chen, Jingyi Chen, Jingyuan Chen, Jingzhao Chen, Jingzhou Chen, Jinhao Chen, Jinhuang Chen, Jinli Chen, Jinlun Chen, Jinquan Chen, Jinsong Chen, Jintian Chen, Jinxuan Chen, Jinyan Chen, Jinyong Chen, Jion Chen, Jiong Chen, Jiongyu Chen, Jishun Chen, Jiu-Chiuan Chen, Jiujiu Chen, Jiwei Chen, Jiyan Chen, Jiyuan Chen, Jonathan Chen, Joy J Chen, Juan Chen, Juan-Juan Chen, Juanjuan Chen, Juei-Suei Chen, Juhai Chen, Jui-Chang Chen, Jui-Yu Chen, Jun Chen, Jun-Long Chen, Junchen Chen, Junfei Chen, Jung-Sheng Chen, Junhong Chen, Junhui Chen, Junjie Chen, Junling Chen, Junmin Chen, Junming Chen, Junpan Chen, Junpeng Chen, Junqi Chen, Junqin Chen, Junsheng Chen, Junshi Chen, Junyang Chen, Junyi Chen, Junyu Chen, K C Chen, Kai Chen, Kai-En Chen, Kai-Ming Chen, Kai-Ting Chen, Kai-Yang Chen, Kaifu Chen, Kaijian Chen, Kailang Chen, Kaili Chen, Kaina Chen, Kaiquan Chen, Kan Chen, Kang Chen, Kang-Hua Chen, Kangyong Chen, Kangzhen Chen, Katharine Y Chen, Katherine C Chen, Ke Chen, Kecai Chen, Kehua Chen, Kehui Chen, Kelin Chen, Ken Chen, Kenneth L Chen, Keping Chen, Kequan Chen, Kevin Chen, Kewei Chen, Kexin Chen, Keyan Chen, Keyang Chen, Keying Chen, Keyu Chen, Keyuan Chen, Kuan-Jen Chen, Kuan-Ling Chen, Kuan-Ting Chen, Kuan-Yu Chen, Kuangyang Chen, Kuey Chu Chen, Kui Chen, Kun Chen, Kun-Chieh Chen, Kunmei Chen, Kunpeng Chen, L B Chen, L F Chen, Lan Chen, Lang Chen, Lankai Chen, Lanlan Chen, Lanmei Chen, Le Chen, Le Qi Chen, Lei Chen, Lei-Chin Chen, Lei-Lei Chen, Leijie Chen, Lena W Chen, Leqi Chen, Letian Chen, Lexia Chen, Li Chen, Li Jia Chen, Li-Chieh Chen, Li-Hsien Chen, Li-Hsin Chen, Li-Hua Chen, Li-Jhen Chen, Li-Juan Chen, Li-Mien Chen, Li-Nan Chen, Li-Tzong Chen, Li-Zhen Chen, Li-hong Chen, Lian Chen, Lianfeng Chen, Liang Chen, Liang-Kung Chen, Liangkai Chen, Liangsheng Chen, Liangwan Chen, Lianmin Chen, Liaobin Chen, Lichang Chen, Lichun Chen, Lidian Chen, Lie Chen, Liechun Chen, Lifang Chen, Lifen Chen, Lifeng Chen, Ligang Chen, Lihong Chen, Lihua Chen, Lijin Chen, Lijuan Chen, Lili Chen, Limei Chen, Limin Chen, Liming Chen, Lin Chen, Lina Chen, Linbo Chen, Ling Chen, Ling-Yan Chen, Lingfeng Chen, Lingjun Chen, Lingli Chen, Lingxia Chen, Lingxue Chen, Lingyi Chen, Linjie Chen, Linlin Chen, Linna Chen, Linxi Chen, Linyi Chen, Liping Chen, Liqiang Chen, Liugui Chen, Liujun Chen, Liutao Chen, Lixia Chen, Lixian Chen, Liyun Chen, Lizhen Chen, Lizhu Chen, Lo-Yun Chen, Long Chen, Long-Jiang Chen, Longqing Chen, Longyun Chen, Lu Chen, Lu Hua Chen, Lu-Biao Chen, Lu-Zhu Chen, Lulu Chen, Luming Chen, Luyi Chen, Luzhu Chen, M Chen, M L Chen, Man Chen, Man-Hua Chen, Mao Chen, Mao-Yuan Chen, Maochong Chen, Maorong Chen, Marcus Y Chen, Mark I-Cheng Chen, Max Jl Chen, Mechi Chen, Mei Chen, Mei-Chi Chen, Mei-Chih Chen, Mei-Hsiu Chen, Mei-Hua Chen, Mei-Jie Chen, Mei-Ling Chen, Mei-Ru Chen, Meilan Chen, Meilin Chen, Meiling Chen, Meimei Chen, Meiting Chen, Meiyang Chen, Meiyu Chen, Meizhen Chen, Meng Chen, Meng Xuan Chen, Meng-Lin Chen, Meng-Ping Chen, Mengdi Chen, Menglan Chen, Mengling Chen, Mengping Chen, Mengqing Chen, Mengting Chen, Mengxia Chen, Mengyan Chen, Mengying Chen, Mian-Mian Chen, Miao Chen, Miao-Der Chen, Miao-Hsueh Chen, Miao-Yu Chen, Miaomiao Chen, Miaoran Chen, Michael C Chen, Michelle Chen, Mien-Cheng Chen, Min Chen, Min-Hsuan Chen, Min-Hu Chen, Min-Jie Chen, Ming Chen, Ming-Fong Chen, Ming-Han Chen, Ming-Hong Chen, Ming-Huang Chen, Ming-Huei Chen, Ming-Yu Chen, Mingcong Chen, Mingfeng Chen, Minghong Chen, Minghua Chen, Minglang Chen, Mingling Chen, Mingmei Chen, Mingxia Chen, Mingxing Chen, Mingyang Chen, Mingyi Chen, Mingyue Chen, Minjian Chen, Minjiang Chen, Minjie Chen, Minyan Chen, Mo Chen, Mu-Hong Chen, Muh-Shy Chen, Mulan Chen, Mystie X Chen, Na Chen, Naifei Chen, Naisong Chen, Nan Chen, Ni Chen, Nian-Ping Chen, Ning Chen, Ning-Bo Chen, Ning-Hung Chen, Ning-Yuan Chen, Ningbo Chen, Ningning Chen, Nuan Chen, On Chen, Ou Chen, Ouyang Chen, P P Chen, Pan Chen, Paul Chih-Hsueh Chen, Pei Chen, Pei-Chen Chen, Pei-Chun Chen, Pei-Lung Chen, Pei-Yi Chen, Pei-Yin Chen, Pei-zhan Chen, Peihong Chen, Peipei Chen, Peiqin Chen, Peixian Chen, Peiyou Chen, Peiyu Chen, Peize Chen, Peizhan Chen, Peng Chen, Peng-Cheng Chen, Pengxiang Chen, Ping Chen, Ping-Chung Chen, Ping-Kun Chen, Pingguo Chen, Po-Han Chen, Po-Ju Chen, Po-Min Chen, Po-See Chen, Po-Sheng Chen, Po-Yu Chen, Qi Chen, Qi-An Chen, Qian Chen, Qianbo Chen, Qianfen Chen, Qiang Chen, Qiangpu Chen, Qiankun Chen, Qianling Chen, Qianming Chen, Qianping Chen, Qianqian Chen, Qianxue Chen, Qianyi Chen, Qianyu Chen, Qianyun Chen, Qianzhi Chen, Qiao Chen, Qiao-Yi Chen, Qiaoli Chen, Qiaoling Chen, Qichen Chen, Qifang Chen, Qihui Chen, Qili Chen, Qinfen Chen, Qing Chen, Qing-Hui Chen, Qing-Juan Chen, Qing-Wei Chen, Qingao Chen, Qingchao Chen, Qingchuan Chen, Qingguang Chen, Qinghao Chen, Qinghua Chen, Qingjiang Chen, Qingjie Chen, Qingliang Chen, Qingmei Chen, Qingqing Chen, Qingqiu Chen, Qingshi Chen, Qingxing Chen, Qingyang Chen, Qingyi Chen, Qinian Chen, Qinsheng Chen, Qinying Chen, Qiong Chen, Qiongyun Chen, Qiqi Chen, Qitong Chen, Qiu Jing Chen, Qiu-Jing Chen, Qiu-Sheng Chen, Qiuchi Chen, Qiuhong Chen, Qiujing Chen, Qiuli Chen, Qiuwen Chen, Qiuxia Chen, Qiuxiang Chen, Qiuxuan Chen, Qiuyun Chen, Qiwei Chen, Qixian Chen, Qu Chen, Quan Chen, Quanjiao Chen, Quanwei Chen, Qunxiang Chen, R Chen, Ran Chen, Ranyun Chen, Ray-Jade Chen, Ren-Hui Chen, Renjin Chen, Renwei Chen, Renyu Chen, Robert Chen, Roger Chen, Rong Chen, Rong-Hua Chen, Rongfang Chen, Rongfeng Chen, Rongrong Chen, Rongsheng Chen, Rongyuan Chen, Roufen Chen, Rouxi Chen, Ru Chen, Rucheng Chen, Ruey-Hwa Chen, Rui Chen, Rui-Fang Chen, Rui-Min Chen, Rui-Pei Chen, Rui-Zhen Chen, Ruiai Chen, Ruibing Chen, Ruijing Chen, Ruijuan Chen, Ruilin Chen, Ruimin Chen, Ruiming Chen, Ruiqi Chen, Ruisen Chen, Ruixiang Chen, Ruixue Chen, Ruiying Chen, Rujun Chen, Runfeng Chen, Runsen Chen, Runsheng Chen, Ruofan Chen, Ruohong Chen, Ruonan Chen, Ruoyan Chen, Ruoying Chen, S Chen, S N Chen, S Pl Chen, S-D Chen, Sai Chen, San-Yuan Chen, Sean Chen, Sen Chen, Shali Chen, Shan Chen, Shanchun Chen, Shang-Chih Chen, Shang-Hung Chen, Shangduo Chen, Shangsi Chen, Shangwu Chen, Shangzhong Chen, Shanshan Chen, Shanyuan Chen, Shao-Ke Chen, Shao-Peng Chen, Shao-Wei Chen, Shao-Yu Chen, Shao-long Chen, Shaofei Chen, Shaohong Chen, Shaohua Chen, Shaokang Chen, Shaokun Chen, Shaoliang Chen, Shaotao Chen, Shaoxing Chen, Shaoze Chen, Shasha Chen, She Chen, Shen Chen, Shen-Ming Chen, Sheng Chen, Sheng-Xi Chen, Sheng-Yi Chen, Shengdi Chen, Shenghui Chen, Shenglan Chen, Shengnan Chen, Shengpan Chen, Shengyu Chen, Shengzhi Chen, Shi Chen, Shi-Qing Chen, Shi-Sheng Chen, Shi-Yi Chen, Shi-You Chen, Shibo Chen, Shih-Jen Chen, Shih-Pin Chen, Shih-Yin Chen, Shih-Yu Chen, Shilan Chen, Shiming Chen, Shin-Wen Chen, Shin-Yu Chen, Shipeng Chen, Shiqian Chen, Shiqun Chen, Shirui Chen, Shiuhwei Chen, Shiwei Chen, Shixuan Chen, Shiyan Chen, Shiyao Chen, Shiyi Chen, Shiyu Chen, Shou-Tung Chen, Shoudeng Chen, Shoujun Chen, Shouzhen Chen, Shu Chen, Shu-Fen Chen, Shu-Gang Chen, Shu-Hua Chen, Shu-Jen Chen, Shuai Chen, Shuai-Bing Chen, Shuai-Ming Chen, Shuaijie Chen, Shuaijun Chen, Shuaiyin Chen, Shuaiyu Chen, Shuang Chen, Shuangfeng Chen, Shuanghui Chen, Shuchun Chen, Shuen-Ei Chen, Shufang Chen, Shufeng Chen, Shuhai Chen, Shuhong Chen, Shuhuang Chen, Shuhui Chen, Shujuan Chen, Shuliang Chen, Shuming Chen, Shunde Chen, Shuntai Chen, Shunyou Chen, Shuo Chen, Shuo-Bin Chen, Shuoni Chen, Shuqin Chen, Shuqiu Chen, Shuting Chen, Shuwen Chen, Shuyi Chen, Shuying Chen, Si Chen, Si-Ru Chen, Si-Yuan Chen, Si-Yue Chen, Si-guo Chen, Sien-Tsong Chen, Sifeng Chen, Sihui Chen, Sijia Chen, Sijuan Chen, Sili Chen, Silian Chen, Siping Chen, Siqi Chen, Siqin Chen, Sisi Chen, Siteng Chen, Siting Chen, Siyi Chen, Siyu Chen, Siyu S Chen, Siyuan Chen, Siyue Chen, Size Chen, Song Chen, Song-Mei Chen, Songfeng Chen, Suet N Chen, Suet Nee Chen, Sufang Chen, Suipeng Chen, Sulian Chen, Suming Chen, Sun Chen, Sung-Fang Chen, Suning Chen, Sunny Chen, Sy-Jou Chen, Syue-Ting Chen, Szu-Chi Chen, Szu-Chia Chen, Szu-Chieh Chen, Szu-Han Chen, Szu-Yun Chen, T Chen, Tai-Heng Chen, Tai-Tzung Chen, Tailai Chen, Tan-Huan Chen, Tan-Zhou Chen, Tania Chen, Tao Chen, Tian Chen, Tianfeng Chen, Tianhang Chen, Tianhong Chen, Tianhua Chen, Tianpeng Chen, Tianran Chen, Tianrui Chen, Tiantian Chen, Tianzhen Chen, Tielin Chen, Tien-Hsing Chen, Ting Chen, Ting-Huan Chen, Ting-Tao Chen, Ting-Ting Chen, Tingen Chen, Tingtao Chen, Tingting Chen, Tom Wei-Wu Chen, Tong Chen, Tongsheng Chen, Tse-Ching Chen, Tse-Wei Chen, TsungYen Chen, Tuantuan Chen, Tzu-An Chen, Tzu-Chieh Chen, Tzu-Ju Chen, Tzu-Ting Chen, Tzu-Yu Chen, Tzy-Yen Chen, Valerie Chen, W Chen, Wai Chen, Wan Jun Chen, Wan-Tzu Chen, Wan-Yan Chen, Wan-Yi Chen, Wanbiao Chen, Wanjia Chen, Wanjun Chen, Wanling Chen, Wantao Chen, Wanting Chen, Wanyin Chen, Wei Chen, Wei J Chen, Wei Ning Chen, Wei-Cheng Chen, Wei-Cong Chen, Wei-Fei Chen, Wei-Hao Chen, Wei-Hui Chen, Wei-Kai Chen, Wei-Kung Chen, Wei-Lun Chen, Wei-Min Chen, Wei-Peng Chen, Wei-Ting Chen, Wei-Wei Chen, Wei-Yu Chen, Wei-xian Chen, Weibo Chen, Weican Chen, Weichan Chen, Weicong Chen, Weihao Chen, Weihong Chen, Weihua Chen, Weijia Chen, Weijie Chen, Weili Chen, Weilun Chen, Weina Chen, Weineng Chen, Weiping Chen, Weiqin Chen, Weiqing Chen, Weirui Chen, Weisan Chen, Weitao Chen, Weitian Chen, Weiwei Chen, Weixian Chen, Weixin Chen, Weiyi Chen, Weiyong Chen, Wen Chen, Wen-Chau Chen, Wen-Jie Chen, Wen-Pin Chen, Wen-Qi Chen, Wen-Tsung Chen, Wen-Yi Chen, Wenbiao Chen, Wenbing Chen, Wenfan Chen, Wenfang Chen, Wenhao Chen, Wenhua Chen, Wenjie Chen, Wenjun Chen, Wenlong Chen, Wenqin Chen, Wensheng Chen, Wenshuo Chen, Wentao Chen, Wenting Chen, Wentong Chen, Wenwen Chen, Wenwu Chen, Wenxi Chen, Wenxing Chen, Wenxu Chen, Willian Tzu-Liang Chen, Wu-Jun Chen, Wu-Xian Chen, Wuyan Chen, X Chen, X R Chen, X Steven Chen, Xi Chen, Xia Chen, Xia-Fei Chen, Xiaguang Chen, Xiameng Chen, Xian Chen, Xian-Kai Chen, Xianbo Chen, Xiancheng Chen, Xianfeng Chen, Xiang Chen, Xiang-Bin Chen, Xiang-Mei Chen, XiangFan Chen, Xiangding Chen, Xiangjun Chen, Xiangli Chen, Xiangliu Chen, Xiangmei Chen, Xiangna Chen, Xiangning Chen, Xiangqiu Chen, Xiangyu Chen, Xiankai Chen, Xianmei Chen, Xianqiang Chen, Xianxiong Chen, Xianyue Chen, Xianze Chen, Xianzhen Chen, Xiao Chen, Xiao-Chen Chen, Xiao-Hui Chen, Xiao-Jun Chen, Xiao-Lin Chen, Xiao-Qing Chen, Xiao-Quan Chen, Xiao-Wei Chen, Xiao-Yang Chen, Xiao-Ying Chen, Xiao-chun Chen, Xiao-he Chen, Xiao-ping Chen, Xiaobin Chen, Xiaobo Chen, Xiaochang Chen, Xiaochun Chen, Xiaodong Chen, Xiaofang Chen, Xiaofen Chen, Xiaofeng Chen, Xiaohan Chen, Xiaohong Chen, Xiaohua Chen, Xiaohui Chen, Xiaojiang S Chen, Xiaojie Chen, Xiaojing Chen, Xiaojuan Chen, Xiaojun Chen, Xiaokai Chen, Xiaolan Chen, Xiaole L Chen, Xiaolei Chen, Xiaoli Chen, Xiaolin Chen, Xiaoling Chen, Xiaolong Chen, Xiaolu Chen, Xiaomeng Chen, Xiaomin Chen, Xiaona Chen, Xiaonan Chen, Xiaopeng Chen, Xiaoping Chen, Xiaoqian Chen, Xiaoqing Chen, Xiaorong Chen, Xiaoshan Chen, Xiaotao Chen, Xiaoting Chen, Xiaowan Chen, Xiaowei Chen, Xiaowen Chen, Xiaoxiang Chen, Xiaoxiao Chen, Xiaoyan Chen, Xiaoyang Chen, Xiaoyin Chen, Xiaoyong Chen, Xiaoyu Chen, Xiaoyuan Chen, Xiaoyun Chen, Xiatian Chen, Xihui Chen, Xijun Chen, Xikun Chen, Ximei Chen, Xin Chen, Xin-Jie Chen, Xin-Ming Chen, Xin-Qi Chen, Xinan Chen, Xing Chen, Xing-Lin Chen, Xing-Long Chen, Xing-Zhen Chen, Xingdong Chen, Xinghai Chen, Xingxing Chen, Xingyi Chen, Xingyong Chen, Xingyu Chen, Xinji Chen, Xinlin Chen, Xinpu Chen, Xinqiao Chen, Xinwei Chen, Xinyan Chen, Xinyang Chen, Xinyi Chen, Xinyu Chen, Xinyuan Chen, Xinyue Chen, Xinzhuo Chen, Xiong Chen, Xiqun Chen, Xiu Chen, Xiu-Juan Chen, Xiuhui Chen, Xiujuan Chen, Xiuli Chen, Xiuping Chen, Xiuxiu Chen, Xiuyan Chen, Xixi Chen, Xiyao Chen, Xiyu Chen, Xu Chen, Xuan Chen, Xuancai Chen, Xuanjing Chen, Xuanli Chen, Xuanmao Chen, Xuanwei Chen, Xuanxu Chen, Xuanyi Chen, Xue Chen, Xue-Mei Chen, Xue-Qing Chen, Xue-Xin Chen, Xue-Yan Chen, Xue-Ying Chen, XueShu Chen, Xuechun Chen, Xuefei Chen, Xuehua Chen, Xuejiao Chen, Xuejun Chen, Xueli Chen, Xueling Chen, Xuemei Chen, Xuemin Chen, Xueqin Chen, Xueqing Chen, Xuerong Chen, Xuesong Chen, Xueting Chen, Xueyan Chen, Xueying Chen, Xufeng Chen, Xuhui Chen, Xujia Chen, Xun Chen, Xuxiang Chen, Xuxin Chen, Xuzhuo Chen, Y Chen, Y D I Chen, Y Eugene Chen, Y M Chen, Y P Chen, Y S Chen, Y U Chen, Y-D I Chen, Y-D Ida Chen, Ya Chen, Ya-Chun Chen, Ya-Nan Chen, Ya-Peng Chen, Ya-Ting Chen, Ya-xi Chen, Yafang Chen, Yafei Chen, Yahong Chen, Yajie Chen, Yajing Chen, Yajun Chen, Yalan Chen, Yali Chen, Yan Chen, Yan Jie Chen, Yan Q Chen, Yan-Gui Chen, Yan-Jun Chen, Yan-Ming Chen, Yan-Qiong Chen, Yan-yan Chen, Yanan Chen, Yananlan Chen, Yanbin Chen, Yanfei Chen, Yanfen Chen, Yang Chen, Yang-Ching Chen, Yang-Yang Chen, Yangchao Chen, Yanghui Chen, Yangxin Chen, Yanhan Chen, Yanhua Chen, Yanjie Chen, Yanjing Chen, Yanli Chen, Yanlin Chen, Yanling Chen, Yanming Chen, Yann-Jang Chen, Yanping Chen, Yanqiu Chen, Yanrong Chen, Yanru Chen, Yanting Chen, Yanyan Chen, Yanyun Chen, Yanzhu Chen, Yanzi Chen, Yao Chen, Yao-Shen Chen, Yaodong Chen, Yaosheng Chen, Yaowu Chen, Yau-Hung Chen, Yaxi Chen, Yayun Chen, Yazhuo Chen, Ye Chen, Ye-Guang Chen, Yeh Chen, Yelin Chen, Yen-Chang Chen, Yen-Chen Chen, Yen-Cheng Chen, Yen-Ching Chen, Yen-Fu Chen, Yen-Hao Chen, Yen-Hsieh Chen, Yen-Jen Chen, Yen-Ju Chen, Yen-Lin Chen, Yen-Ling Chen, Yen-Ni Chen, Yen-Rong Chen, Yen-Teen Chen, Yewei Chen, Yi Chen, Yi Feng Chen, Yi-Bing Chen, Yi-Chun Chen, Yi-Chung Chen, Yi-Fei Chen, Yi-Guang Chen, Yi-Han Chen, Yi-Hau Chen, Yi-Heng Chen, Yi-Hong Chen, Yi-Hsuan Chen, Yi-Hui Chen, Yi-Jen Chen, Yi-Lin Chen, Yi-Ru Chen, Yi-Ting Chen, Yi-Wen Chen, Yi-Yung Chen, YiChung Chen, YiPing Chen, Yian Chen, Yibing Chen, Yibo Chen, Yidan Chen, Yiding Chen, Yidong Chen, Yiduo Chen, Yifa Chen, Yifan Chen, Yifang Chen, Yifei Chen, Yih-Chieh Chen, Yihao Chen, Yihong Chen, Yii-Der Chen, Yii-Der I Chen, Yii-Derr Chen, Yii-der Ida Chen, Yijiang Chen, Yijun Chen, Yike Chen, Yilan Chen, Yilei Chen, Yili Chen, Yilin Chen, Yiming Chen, Yin-Huai Chen, Ying Chen, Ying-Cheng Chen, Ying-Hsiang Chen, Ying-Jie Chen, Ying-Jung Chen, Ying-Lan Chen, Ying-Ying Chen, Yingchun Chen, Yingcong Chen, Yinghui Chen, Yingji Chen, Yingjie Chen, Yinglian Chen, Yingting Chen, Yingxi Chen, Yingying Chen, Yingyu Chen, Yinjuan Chen, Yintong Chen, Yinwei Chen, Yinzhu Chen, Yiru Chen, Yishan Chen, Yisheng Chen, Yitong Chen, Yixin Chen, Yiyin Chen, Yiyun Chen, Yizhi Chen, Yong Chen, Yong-Jun Chen, Yong-Ping Chen, Yong-Syuan Chen, Yong-Zhong Chen, YongPing Chen, Yongbin Chen, Yongfa Chen, Yongfang Chen, Yongheng Chen, Yonghui Chen, Yongke Chen, Yonglu Chen, Yongmei Chen, Yongming Chen, Yongning Chen, Yongqi Chen, Yongshen Chen, Yongshuo Chen, Yongxing Chen, Yongxun Chen, You-Ming Chen, You-Xin Chen, You-Yue Chen, Youhu Chen, Youjia Chen, Youmeng Chen, Youran Chen, Youwei Chen, Yu Chen, Yu-Bing Chen, Yu-Cheng Chen, Yu-Chi Chen, Yu-Chia Chen, Yu-Chuan Chen, Yu-Fan Chen, Yu-Fen Chen, Yu-Fu Chen, Yu-Gen Chen, Yu-Han Chen, Yu-Hui Chen, Yu-Ling Chen, Yu-Ming Chen, Yu-Pei Chen, Yu-San Chen, Yu-Si Chen, Yu-Ting Chen, Yu-Tung Chen, Yu-Xia Chen, Yu-Xin Chen, Yu-Yang Chen, Yu-Ying Chen, Yuan Chen, Yuan-Hua Chen, Yuan-Shen Chen, Yuan-Tsong Chen, Yuan-Yuan Chen, Yuan-Zhen Chen, Yuanbin Chen, Yuanhao Chen, Yuanjia Chen, Yuanjian Chen, Yuanli Chen, Yuanqi Chen, Yuanwei Chen, Yuanwen Chen, Yuanyu Chen, Yuanyuan Chen, Yubin Chen, Yucheng Chen, Yue Chen, Yue-Lai Chen, Yuebing Chen, Yueh-Peng Chen, Yuelei Chen, Yuewen Chen, Yuewu Chen, Yuexin Chen, Yuexuan Chen, Yufei Chen, Yufeng Chen, Yuh-Lien Chen, Yuh-Ling Chen, Yuh-Min Chen, Yuhan Chen, Yuhang Chen, Yuhao Chen, Yuhong Chen, Yuhui Chen, Yujie Chen, Yule Chen, Yuli Chen, Yulian Chen, Yulin Chen, Yuling Chen, Yulong Chen, Yulu Chen, Yumei Chen, Yun Chen, Yun-Ju Chen, Yun-Tzu Chen, Yun-Yu Chen, Yundai Chen, Yunfei Chen, Yunfeng Chen, Yung-Hsiang Chen, Yung-Wu Chen, Yunjia Chen, Yunlin Chen, Yunn-Yi Chen, Yunqin Chen, Yunshun Chen, Yunwei Chen, Yunyun Chen, Yunzhong Chen, Yunzhu Chen, Yupei Chen, Yupeng Chen, Yuping Chen, Yuqi Chen, Yuqin Chen, Yuqing Chen, Yuquan Chen, Yurong Chen, Yushan Chen, Yusheng Chen, Yusi Chen, Yuting Chen, Yutong Chen, Yuxi Chen, Yuxian Chen, Yuxiang Chen, Yuxin Chen, Yuxing Chen, Yuyan Chen, Yuyang Chen, Yuyao Chen, Z Chen, Zan Chen, Zaozao Chen, Ze-Hui Chen, Ze-Xu Chen, Zechuan Chen, Zemin Chen, Zetian Chen, Zexiao Chen, Zeyu Chen, Zhanfei Chen, Zhang-Liang Chen, Zhang-Yuan Chen, Zhangcheng Chen, Zhanghua Chen, Zhangliang Chen, Zhanglin Chen, Zhangxin Chen, Zhanjuan Chen, Zhao Chen, Zhao-Xia Chen, ZhaoHui Chen, Zhaojun Chen, Zhaoli Chen, Zhaolin Chen, Zhaoran Chen, Zhaowei Chen, Zhaoyao Chen, Zhe Chen, Zhe-Ling Chen, Zhe-Sheng Chen, Zhe-Yu Chen, Zhebin Chen, Zhehui Chen, Zhelin Chen, Zhen Bouman Chen, Zhen Chen, Zhen-Hua Chen, Zhen-Yu Chen, Zhencong Chen, Zhenfeng Chen, Zheng Chen, Zheng-Zhen Chen, Zhenghong Chen, Zhengjun Chen, Zhengling Chen, Zhengming Chen, Zhenguo Chen, Zhengwei Chen, Zhengzhi Chen, Zhenlei Chen, Zhenyi Chen, Zhenyue Chen, Zheping Chen, Zheren Chen, Zhesheng Chen, Zheyi Chen, Zhezhe Chen, Zhi Bin Chen, Zhi Chen, Zhi-Hao Chen, Zhi-bin Chen, Zhi-zhe Chen, Zhiang Chen, Zhichuan Chen, Zhifeng Chen, Zhigang Chen, Zhigeng Chen, Zhiguo Chen, Zhihai Chen, Zhihang Chen, Zhihao Chen, Zhiheng Chen, Zhihong Chen, Zhijian Chen, Zhijian J Chen, Zhijing Chen, Zhijun Chen, Zhimin Chen, Zhinan Chen, Zhiping Chen, Zhiqiang Chen, Zhiquan Chen, Zhishi Chen, Zhitao Chen, Zhiting Chen, Zhiwei Chen, Zhixin Chen, Zhixuan Chen, Zhixue Chen, Zhiyong Chen, Zhiyu Chen, Zhiyuan Chen, Zhiyun Chen, Zhizhong Chen, Zhong Chen, Zhongbo Chen, Zhonghua Chen, Zhongjian Chen, Zhongliang Chen, Zhongxiu Chen, Zhongzhu Chen, Zhou Chen, Zhouji Chen, Zhouliang Chen, Zhoulong Chen, Zhouqing Chen, Zhuchu Chen, Zhujun Chen, Zhuo Chen, Zhuo-Yuan Chen, ZhuoYu Chen, Zhuohui Chen, Zhuojia Chen, Zi-Jiang Chen, Zi-Qing Chen, Zi-Yang Chen, Zi-Yue Chen, Zi-Yun Chen, Zian Chen, Zifan Chen, Zihan Chen, Zihang Chen, Zihao Chen, Zihe Chen, Zihua Chen, Zijie Chen, Zike Chen, Zilin Chen, Zilong Chen, Ziming Chen, Zinan Chen, Ziqi Chen, Ziqing Chen, Zitao Chen, Zixi Chen, Zixin Chen, Zixuan Chen, Ziying Chen, Ziyuan Chen, Zoe Chen, Zongming E Chen, Zongnan Chen, Zongyou Chen, Zongzheng Chen, Zugen Chen, Zuolong Chen
articles
Huimei Chen, Aida Moreno-Moral, Francesco Pesce +24 more · 2019 · Nature communications · Nature · added 2026-04-24
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
no PDF DOI: 10.1038/s41467-019-12060-5
WWP2
Wen-Ting Hsiao, Hui-Min Su, Kuan-Pin Su +5 more · 2019 · Nutrition research and practice · added 2026-04-24
Docosahexaenoic acid (DHA), an n-3 long chain polyunsaturated fatty acid (LCPUFA), is acquired by dietary intake or the The tissue DHA concentrations and mRNA levels of genes participating in DHA bios Show more
Docosahexaenoic acid (DHA), an n-3 long chain polyunsaturated fatty acid (LCPUFA), is acquired by dietary intake or the The tissue DHA concentrations and mRNA levels of genes participating in DHA biosynthesis were compared among PPARα homozygous (KO), heterozygous (HZ), and wild type (WT) mice (Exp I), and between WT mice treated with clofibrate (PPARα agonist) or those not treated (Exp II). In ExpII, the expression levels of the proteins associated with DHA function in the brain cortex and retina were also measured. An n3-PUFA depleted/replenished regimen was applied to mitigate the confounding effects of maternal DHA. PPARα ablation reduced the hepatic LCPUFA enzyme expression was altered by PPARα. Either PPARα deficiency or activation-decreased tissue DHA concentration is a stimulus for further studies to determine the functional significance. Show less
📄 PDF DOI: 10.4162/nrp.2019.13.4.286
FADS1
Siteng Chen, Ning Zhang, Jialiang Shao +2 more · 2019 · Journal of Cancer · added 2026-04-24
📄 PDF DOI: 10.7150/jca.30307
MACF1
Fang-Zhou Chen, Ying Zhao, Hui-Zhao Chen · 2019 · International journal of molecular medicine · added 2026-04-24
Alzheimer's disease (AD) is a chronic neurodegenerative disease that often occurs at a slow pace yet deteriorates with time. MicroRNAs (miRs) have been demonstrated to offer novel therapeutic hope for Show more
Alzheimer's disease (AD) is a chronic neurodegenerative disease that often occurs at a slow pace yet deteriorates with time. MicroRNAs (miRs) have been demonstrated to offer novel therapeutic hope for disease treatment. The aim of the present study was to investigate the effect of miR‑98 on amyloid β (Aβ)‑protein production, oxidative stress and mitochondrial dysfunction through the Notch signaling pathway by targeting hairy and enhancer of split (Hes)‑related with YRPW motif protein 2 (HEY2) in mice with AD. A total of 70 Kunming mice were obtained and subjected to behavioral assessment. The levels of oxidative stress‑related proteins glutathione peroxidase, reduced glutathione, superoxide dismutase, malondialdehyde, acetylcholinesterase and Na+‑K+‑ATP were measured. Morphological changes in brain tissue, HEY2‑positivity levels, neuronal apoptotic index (AI) and neuron mitochondrial DNA (mtDNA) levels were also determined. Subsequently, the levels of miR‑98 and the mRNA and protein levels of HEY2, Jagged1, Notch1, Hes1, Hes5, β‑amyloid precursor protein, B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein in tissues and hippocampal neurons were determined by reverse transcription‑quantitative polymerase chain reaction and western blot analyses, respectively. Finally, hippocampal neuron viability and apoptosis were determined using an MTT assay and flow cytometry, respectively. The levels of miR‑98‑targeted HEY2 and miR‑98 were low and the levels of HEY2 were high in the AD mice. The AD mice exhibited poorer learning and memory abilities, oxidative stress function, and morphological changes of pyramidal cells in the hippocampal CA1 region. Furthermore, the AD mice exhibited increased protein levels of HEY2 and AI in the CA1 region of brain tissues with reduced mtDNA levels and dysfunctional neuronal mitochondria. miR‑98 suppressed hippocampal neuron apoptosis and promoted hippocampal neuron viability by inactivating the Notch signaling pathway via the inhibition of HEY2. In conclusion, the results demonstrated that miR‑98 reduced the production of Aβ and improved oxidative stress and mitochondrial dysfunction through activation of the Notch signaling pathway by binding to HEY2 in AD mice. Show less
📄 PDF DOI: 10.3892/ijmm.2018.3957
HEY2
Zhao Chen, Dongmei Sun, Xiaoli Bi +7 more · 2019 · Phytomedicine : international journal of phytotherapy and phytopharmacology · Elsevier · added 2026-04-24
The selection of active compounds for the quality evaluation of traditional Chinese medicine (TCM), specifically complex formulas, remains a challenge for researchers, as components selected as indexe Show more
The selection of active compounds for the quality evaluation of traditional Chinese medicine (TCM), specifically complex formulas, remains a challenge for researchers, as components selected as indexes usually have no clear relation with the therapeutic effects of interest. As a suggested resolution, quality control markers (Q-markers) showed good perspective for discriminating numerous compounds found for specific efficacies. In the presented study, the components of the Yinlan (YL) capsule, a TCM patent formula comprising four ingredients, were evaluated and selected for their lipid regulatory effects using principles for Q-marker selection. The mechanism of TCM therapeutic effects involves several pathways and targets that combine to become an integrated action in the body. Therefore, it is assumed that specific compounds in YL should have good affinity for related targets and obvious effects (both up- and downregulating). Thus, a series of experiments, including cytobiology, animal-based pharmacodynamics, computer-assisted drug design, conventional content determination and pharmacokinetics, would be helpful for the selection and final confirmation of Q-markers. The capsule was first administered to Wistar mice fed a high-fat diet and tested for their triglycerides (TG) and total cholesterol (TC) values to evaluate the effectiveness of YL. Then, liver tissue was extracted for gene expression. According to the results, the compounds in YL with good affiliation were selected and determined using UHPLC-MS-MS, and those with adequate results in the capsule were chosen as Q-marker candidates. Finally, pharmacokinetics research was performed; the candidates with desirable metabolite and bioavailability parameters were confirmed as Q-markers of YL. YL capsule was capable of lowering TG and TC levels. For target selection, the expression of LXR mRNA increased significantly at all three tested dosages. Downstream genes, such as LCAT, CYP7A1, and ABCA1, and intestinal FXR mRNA also showed significant increases in expression. For screening of the Q-marker candidates, 5 compounds were selected according to abovementioned results. The pharmacokinetics research demonstrated that the rats exploited lupeol and ginsenoside Rb3 in a desirable pattern with adequate bioavailability, which confirmed their roles as lipid regulatory Q-markers. The YL capsule was demonstrated to have obvious lipid regulatory effects, which are mainly exerted by targeting LXR and its related pathway. Lupeol and ginsenoside Rb3 were validated as Q-markers that represent the anti-hyperlipidemia activity of the capsule. Show less
no PDF DOI: 10.1016/j.phymed.2019.152896
NR1H3
Ying-Zhu Rao, Rong Chen, Yong Zhang +1 more · 2019 · General and comparative endocrinology · Elsevier · added 2026-04-24
Melanocortin-4 receptor (MC4R) and melanocortin receptor accessory protein 2 (MRAP2) play important roles in the melanocortin system, and interaction of MC4R and MRAP2 is suggested to play pivotal rol Show more
Melanocortin-4 receptor (MC4R) and melanocortin receptor accessory protein 2 (MRAP2) play important roles in the melanocortin system, and interaction of MC4R and MRAP2 is suggested to play pivotal role in energy balance of vertebrates. Orange-spotted grouper (Epinephelus coioides) is a widely cultured marine fish with high economic value in Asia. To explore potential interaction between grouper MC4R and MRAP2, herein we cloned grouper mc4r and mrap2. Grouper mc4r consisted of a 981 bp ORF encoding a putative protein of 327 amino acids, while the grouper mrap2 consisted of a 696 bp ORF encoding a putative protein of 232 amino acids. Sequence and phylogenetic analysis revealed that the grouper MC4R and MRAP2 were highly homologous at amino acid levels to several teleost MC4Rs and MRAP2s, respectively. qRT-PCR results showed that both mc4r and mrap2 were expressed primarily in the central nervous system. In the periphery, these genes were expressed more widely in male fish. The cloned grouper MC4R was functional, exhibiting high constitutive activity in cAMP pathway, capable of binding to three peptide agonists and increasing intracellular cAMP production dose-dependently. MRAP2 significantly decreased basal and agonist-stimulated cAMP signaling. MRAP2 also increased basal ERK1/2 activation but decreased ligand-induced stimulation when expressed at high levels. These data will facilitate future investigation of these molecules in regulating diverse physiological processes in orange-spotted grouper. Show less
no PDF DOI: 10.1016/j.ygcen.2019.113234
MC4R
Jie Zhao, Jian-Wei Liang, Hui-Liang Xue +8 more · 2019 · Leukemia · Nature · added 2026-04-24
Acute promyelocytic leukemia (APL) is characterized by t(15;17)(q22;q21), resulting in a PML-RARA fusion that is the master driver of APL. A few cases that cannot be identified with PML-RARA by using Show more
Acute promyelocytic leukemia (APL) is characterized by t(15;17)(q22;q21), resulting in a PML-RARA fusion that is the master driver of APL. A few cases that cannot be identified with PML-RARA by using conventional methods (karyotype analysis, FISH, and RT-PCR) involve abnormal promyelocytes that are fully in accordance with APL in morphology, cytochemistry, and immunophenotype. To explore the mechanisms involved in pathogenesis and recurrence of morphologically diagnosed APL, we performed comprehensive variant analysis by next-generation sequencing in 111 pediatric patients morphologically diagnosed as APL. Structural variant (SV) analysis in 120 DNA samples from both diagnosis and relapse stage identified 95 samples with RARA rearrangement (including 94 with PML-RARA and one with NPM-RARA) and two samples with KMT2A rearrangement. In the eligible 13 RNA samples without any RARA rearrangement at diagnosis, one case each with CPSF6-RARG, NPM1-CCDC28A, and TBC1D15-RAB21 and two cases with a TBL1XR1-RARB fusion were discovered. These uncovered fusion genes strongly suggested their contributions to leukemogenesis as driver alternations and APL phenotype may arise by abnormalities of other members of the nuclear receptor superfamily involved in retinoid signaling (RARB or RARG) or even by mechanisms distinct from the formation of aberrant retinoid receptors. Single-nucleotide variant (SNV) analysis in 77 children (80 samples) with RARA rearrangement showed recurrent alternations of primary APL in FLT3, WT1, USP9X, NRAS, and ARID1A, with a strong potential for involvement in pathogenesis, and WT1 as the only recurrently mutated gene in relapsed APL. WT1, NPM1, NRAS, FLT3, and NSD1 were identified as recurrently mutated in 17 primary samples without RARA rearrangement and WT1, NPM1, TP53, and RARA as recurrently mutated in 9 relapsed samples. The survival of APL with RARA rearrangement is much better than without RARA rearrangement. Thus, patients morphologically diagnosed as APL that cannot be identified as having a RARA rearrangement are more reasonably classified as a subclass of AML other than APL, and individualized treatment should be considered according to the genetic abnormalities. Show less
no PDF DOI: 10.1038/s41375-018-0338-z
RAB21
Liping Hou, Shangduo Chen, Hongxing Chen +8 more · 2019 · Chemosphere · Elsevier · added 2026-04-24
Natural and synthetic progestins in receiving streams can disrupt the normal endocrine systems of fish. Norethindrone (NET) is a widely used synthetic progestin that often appears in wastewater efflue Show more
Natural and synthetic progestins in receiving streams can disrupt the normal endocrine systems of fish. Norethindrone (NET) is a widely used synthetic progestin that often appears in wastewater effluents. For this research, adult female western mosquitofish (Gambusia affinis) were exposed to NET at three concentrations. The effects of NET on the following biological factors were evaluated: the histology of the ovaries and livers, the anal fin morphology, and transcription of genes related to steroidogenesis signaling pathways in the livers. After 42 d exposure to NET at 33.0 ng L Show less
no PDF DOI: 10.1016/j.chemosphere.2018.10.130
HSD17B12
Meiyi Zhou, Jing Shao, Cheng-Yang Wu +17 more · 2019 · Diabetes · added 2026-04-24
Recent studies implicate a strong association between elevated plasma branched-chain amino acids (BCAAs) and insulin resistance (IR). However, a causal relationship and whether interrupted BCAA homeos Show more
Recent studies implicate a strong association between elevated plasma branched-chain amino acids (BCAAs) and insulin resistance (IR). However, a causal relationship and whether interrupted BCAA homeostasis can serve as a therapeutic target for diabetes remain to be established experimentally. In this study, unbiased integrative pathway analyses identified a unique genetic link between obesity-associated IR and BCAA catabolic gene expression at the pathway level in human and mouse populations. In genetically obese ( Show less
📄 PDF DOI: 10.2337/db18-0927
BCKDK
Yu Xu, Huawei Wang, Yujian Zeng +11 more · 2019 · Surgical oncology · Elsevier · added 2026-04-24
The aberrant expression of ceroid-lipofuscinosis 3 (CLN3) has been reported in a variety of human malignancies. However, the role of CLN3 in the progression and prognosis of hepatocellular carcinoma ( Show more
The aberrant expression of ceroid-lipofuscinosis 3 (CLN3) has been reported in a variety of human malignancies. However, the role of CLN3 in the progression and prognosis of hepatocellular carcinoma (HCC) remains unknown. In this study, we found that CLN3 was frequently upregulated in HCC clinical samples and HCC-derived cell lines and was significantly correlated with an APF serum level ≥20 μg/L, a tumour size ≥5 cm, multiple tumours, and the absence of encapsulation. Kaplan-Meier showed that CLN3 upregulation predicted shorter recurrence-free survival (RFS) and overall survival (OS) time in HCC patients. Cox regression analysis revealed that CLN3 upregulation was an independent risk factor for RFS and OS. A functional study demonstrated that the knockdown of CLN3 expression profoundly suppressed the growth and metastasis of HCC cells both in vitro and in vivo. Mechanistic investigation revealed that the EGFR/PI3K/AKT pathway was essential for mediating CLN3 function. In conclusion, our results provide the first evidence that CLN3 contributes to tumour progression and metastasis and offer a potential prognostic predictor and therapeutic target for HCC. Show less
no PDF DOI: 10.1016/j.suronc.2018.12.003
CLN3
Jenna Holland, Joyce Sorrell, Emily Yates +12 more · 2019 · Cell reports · Elsevier · added 2026-04-24
The melanocortin system is a brain circuit that influences energy balance by regulating energy intake and expenditure. In addition, the brain-melanocortin system controls adipose tissue metabolism to Show more
The melanocortin system is a brain circuit that influences energy balance by regulating energy intake and expenditure. In addition, the brain-melanocortin system controls adipose tissue metabolism to optimize fuel mobilization and storage. Specifically, increased brain-melanocortin signaling or negative energy balance promotes lipid mobilization by increasing sympathetic nervous system input to adipose tissue. In contrast, calorie-independent mechanisms favoring energy storage are less understood. Here, we demonstrate that reduction of brain-melanocortin signaling actively promotes fat mass gain by activating the lipogenic program and adipocyte and endothelial cell proliferation in white fat depots independently of caloric intake via efferent nerve fibers conveyed by the common hepatic branch of the vagus nerve. Those vagally regulated obesogenic signals also contribute to the fat mass gain following chronic high-fat diet feeding. These data reveal a physiological mechanism whereby the brain controls energy stores that may contribute to increased susceptibility to obesity. Show less
📄 PDF DOI: 10.1016/j.celrep.2019.04.089
MC4R
Ching-Feng Cheng, Hui-Chen Ku, Jing-Jy Cheng +7 more · 2019 · Communications biology · Nature · added 2026-04-24
Billions of people have obesity-related metabolic syndromes such as diabetes and hyperlipidemia. Promoting the browning of white adipose tissue has been suggested as a potential strategy, but a drug s Show more
Billions of people have obesity-related metabolic syndromes such as diabetes and hyperlipidemia. Promoting the browning of white adipose tissue has been suggested as a potential strategy, but a drug still needs to be identified. Here, genetic deletion of activating transcription factor 3 ( Show less
📄 PDF DOI: 10.1038/s42003-019-0624-y
MLXIPL
Huiling Tang, Wenbing Nie, Jinna Xiao +3 more · 2019 · RSC advances · Royal Society of Chemistry · added 2026-04-24
The galactoglucan ACP2 was isolated from cultured
📄 PDF DOI: 10.1039/c8ra10347j
ACP2
Brandon Eilertson, Liang Chen, Audrey Li +3 more · 2019 · The Journal of antimicrobial chemotherapy · Oxford University Press · added 2026-04-24
To examine the epidemiology of β-lactam resistance in 'clonal group 258' (CG258), a successful KPC clonal group, over 14 years. Isolates were collected from 1999 to 2013 for a study of antibiotic resi Show more
To examine the epidemiology of β-lactam resistance in 'clonal group 258' (CG258), a successful KPC clonal group, over 14 years. Isolates were collected from 1999 to 2013 for a study of antibiotic resistance in Enterobacteriaceae in New York City; 515 bloodstream isolates had antibiotic susceptibility data available and 436 were available for a CG258 PCR assay. The 56 resulting CG258 isolates were characterized by MLST, capsular type and ESBL and KPC carriage. KPC-positive isolates were assessed for common KPC plasmid types, KPC subtype and Tn4401 isoform. RT-PCR revealed 56 isolates were CG258. Seventeen of the 56 CG258 isolates were phenotypically susceptible to all carbapenems (all KPC negative). Five out of 17 susceptible isolates were of the cps-2 (wzi154) capsule type; none was cps-1 (wzi29). Nineteen out of 28 KPC-2 isolates were cps-1 (wzi29) and 8/10 KPC-3 isolates carried cps-2 (wzi154); however, cps-2 (wzi154) predominated among KPC-2-positive isolates in 2003 and 2004. KPC-2 was first detected in 2003 and KPC-3 was first detected in 2006. KPC-harbouring plasmids pKpQIL (all Tn4401a) and pBK30683 (all Tn4401d) were detected in 16/38 and 6/38 carbapenem-resistant isolates, respectively. CG258-lineage Klebsiella pneumoniae isolates were completely absent in 1999, but common in 2003. Twenty-one percent of CG258 isolates were susceptible to carbapenems in addition to lacking both common ESBL and blaKPC-mediated resistance. The cps-2 (wzi154) capsule type was common in both these susceptible isolates and in early KPC-2-harbouring isolates, suggesting it was the initial capsule type in CG258. Carbapenem-resistant isolates carried common KPC-harbouring plasmids with the same KPC and Tn4401 isoforms, suggesting frequent clonal spread. Show less
no PDF DOI: 10.1093/jac/dky394
CPS1
D L Tian, R J Guo, Y M Li +8 more · 2019 · Poultry science · added 2026-04-24
This experiment was conducted to evaluate the effects of lysine deficiency or excess on growth and the expression of lipid metabolism genes in slow-growing birds. A total of 360 one-day-old chicks wer Show more
This experiment was conducted to evaluate the effects of lysine deficiency or excess on growth and the expression of lipid metabolism genes in slow-growing birds. A total of 360 one-day-old chicks were randomly divided into 3 groups, with 6 replicates of 20 birds each. The birds fed the basal diet with a total lysine 0.60% (LL), 1.00% (ML), or 1.40% (HL). The amount of lysine (ML) as the control group, LL and HL as the experimental group, the trial period last 3 wk. The results showed that compared with ML, LL significantly decreased average daily gain and average daily feed intake and remarkably increased feed conversion ratio of birds at 21 day old (P < 0.01), while the above indices in HL had no significant effects (P > 0.05). Besides, LL reduced the pectoral muscle rate (P < 0.01) and decreased the percentage of abdominal fat significantly (P < 0.05). In addition, compared with ML, the expression of fatty acid binding protein 1 (FABP1), acetyl-CoA carboxylase (ACC), malic enzyme (ME), and sterol regulatory element binding protein 1 (SREBP1c) mRNA of liver in LL was significantly decreased (P < 0.05), and the expression of cholesteryl ester transfer protein (CETP) mRNA was significantly increased (P < 0.01), whereas LL had no significant effects on the expression of peroxisome proliferator activated receptor alpha (PPARα) mRNA (P > 0.05). Moreover, compared with ML, HL significantly reduced the expression of FABP1, ACC, ME, SREBP-1c, and PPARα mRNA in the liver (P < 0.05), and had no significant effects on the expression of CETP mRNA (P > 0.05). The results of current research suggest that dietary lysine deficiency could reduce the growth and fat deposition of slow-growing broilers mainly by downregulating the expression of lipid synthesis genes. Show less
no PDF DOI: 10.3382/ps/pez041
CETP

SarcTrack.

Christopher N Toepfer, Arun Sharma, Marcelo Cicconet +13 more · 2019 · Circulation research · added 2026-04-24
Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) in combination with CRISPR/Cas9 genome editing provide unparalleled opportunities to study cardiac biology and disease. However, Show more
Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) in combination with CRISPR/Cas9 genome editing provide unparalleled opportunities to study cardiac biology and disease. However, sarcomeres, the fundamental units of myocyte contraction, are immature and nonlinear in hiPSC-CMs, which technically challenge accurate functional interrogation of contractile parameters in beating cells. Furthermore, existing analysis methods are relatively low-throughput, indirectly assess contractility, or only assess well-aligned sarcomeres found in mature cardiac tissues. We aimed to develop an analysis platform that directly, rapidly, and automatically tracks sarcomeres in beating cardiomyocytes. The platform should assess sarcomere content, contraction and relaxation parameters, and beat rate. We developed SarcTrack, a MatLab software that monitors fluorescently tagged sarcomeres in hiPSC-CMs. The algorithm determines sarcomere content, sarcomere length, and returns rates of sarcomere contraction and relaxation. By rapid measurement of hundreds of sarcomeres in each hiPSC-CM, SarcTrack provides large data sets for robust statistical analyses of multiple contractile parameters. We validated SarcTrack by analyzing drug-treated hiPSC-CMs, confirming the contractility effects of compounds that directly activate (CK-1827452) or inhibit (MYK-461) myosin molecules or indirectly alter contractility (verapamil and propranolol). SarcTrack analysis of hiPSC-CMs carrying a heterozygous truncation variant in the myosin-binding protein C ( MYBPC3) gene, which causes hypertrophic cardiomyopathy, recapitulated seminal disease phenotypes including cardiac hypercontractility and diminished relaxation, abnormalities that normalized with MYK-461 treatment. SarcTrack provides a direct and efficient method to quantitatively assess sarcomere function. By improving existing contractility analysis methods and overcoming technical challenges associated with functional evaluation of hiPSC-CMs, SarcTrack enhances translational prospects for sarcomere-regulating therapeutics and accelerates interrogation of human cardiac genetic variants. Show less
no PDF DOI: 10.1161/CIRCRESAHA.118.314505
MYBPC3
Joel Gelernter, Ning Sun, Renato Polimanti +25 more · 2019 · Nature neuroscience · Nature · added 2026-04-24
Post-traumatic stress disorder (PTSD) is a major problem among military veterans and civilians alike, yet its pathophysiology remains poorly understood. We performed a genome-wide association study an Show more
Post-traumatic stress disorder (PTSD) is a major problem among military veterans and civilians alike, yet its pathophysiology remains poorly understood. We performed a genome-wide association study and bioinformatic analyses, which included 146,660 European Americans and 19,983 African Americans in the US Million Veteran Program, to identify genetic risk factors relevant to intrusive reexperiencing of trauma, which is the most characteristic symptom cluster of PTSD. In European Americans, eight distinct significant regions were identified. Three regions had values of P < 5 × 10 Show less
no PDF DOI: 10.1038/s41593-019-0447-7
KANSL1
Heather J Finlay, Ji Jiang, Richard Rampulla +18 more · 2019 · ACS medicinal chemistry letters · ACS Publications · added 2026-04-24
Lead optimization of the diphenylpyridylethanamine (DPPE) and triphenylethanamine (TPE) series of CETP inhibitors to improve their pharmaceutical profile is described. Polar groups at the
no PDF DOI: 10.1021/acsmedchemlett.9b00086
CETP
Hong-Li Guo, Xia Jing, Jie-Yu Sun +7 more · 2019 · Current pharmaceutical design · Bentham Science · added 2026-04-24
Valproic acid (VPA) as a widely used primary medication in the treatment of epilepsy is associated with reversible or irreversible hepatotoxicity. Long-term VPA therapy is also related to increased ri Show more
Valproic acid (VPA) as a widely used primary medication in the treatment of epilepsy is associated with reversible or irreversible hepatotoxicity. Long-term VPA therapy is also related to increased risk for the development of non-alcoholic fatty liver disease (NAFLD). In this review, metabolic elimination pathways of VPA in the liver and underlying mechanisms of VPA-induced hepatotoxicity are discussed. We searched in PubMed for manuscripts published in English, combining terms such as "Valproic acid", "hepatotoxicity", "liver injury", and "mechanisms". The data of screened papers were analyzed and summarized. The formation of VPA reactive metabolites, inhibition of fatty acid β-oxidation, excessive oxidative stress and genetic variants of some enzymes, such as CPS1, POLG, GSTs, SOD2, UGTs and CYPs genes, have been reported to be associated with VPA hepatotoxicity. Furthermore, carnitine supplementation and antioxidants administration proved to be positive treatment strategies for VPA-induced hepatotoxicity. Therapeutic drug monitoring (TDM) and routine liver biochemistry monitoring during VPA-therapy, as well as genotype screening for certain patients before VPA administration, could improve the safety profile of this antiepileptic drug. Show less
no PDF DOI: 10.2174/1381612825666190329145428
CPS1
Mengxue Pan, Wei Hong, Ye Yao +12 more · 2019 · Stem cells international · added 2026-04-24
Estrogen is very important to the differentiation of B lymphocytes; B lymphopoiesis induced by OVX was supposedly involved in osteoporosis. But the effects of B lymphocytes on the osteogenic different Show more
Estrogen is very important to the differentiation of B lymphocytes; B lymphopoiesis induced by OVX was supposedly involved in osteoporosis. But the effects of B lymphocytes on the osteogenic differentiation of bone mesenchymal stem cells (BMSCs) are not clear. In this study, we detected bone quality and bone loss in a trabecular bone by electronic universal material testing machine and microcomputed tomography (micro-CT) in OVX and splenectomized-ovariectomy (SPX-OVX) rats. Additionally, changes in lymphocytes (B lymphocyte, CD4 Show less
📄 PDF DOI: 10.1155/2019/8150123
HEY2
Ke Liu, Li Ma, Timothy Y Y Lai +5 more · 2019 · Eye and vision (London, England) · BioMed Central · added 2026-04-24
Neovascular age-related macular degeneration (AMD) and polypoidal choroidal vasculopathy (PCV) are sight-threatening maculopathies with both environmental and genetic risk factors. We have previously Show more
Neovascular age-related macular degeneration (AMD) and polypoidal choroidal vasculopathy (PCV) are sight-threatening maculopathies with both environmental and genetic risk factors. We have previously shown relative risks posed by genes of the complement pathways to neovascular AMD and PCV. In this study, we investigated the haplotype-tagging single nucleotide polymorphisms (SNPs) in the The results revealed none of the six tagging SNPs of the This study showed no statistical significance in the genetic association of Show less
📄 PDF DOI: 10.1186/s40662-019-0161-2
CETP
Feng Ye, Hongwei Gao, Lin Xiao +19 more · 2019 · International journal of cancer · Wiley · added 2026-04-24
Although the genotype-phenotype for familial medullary thyroid carcinoma (FMTC) is well studied, only few low susceptibility risk loci were identified for familial non-medullary thyroid carcinoma (FNM Show more
Although the genotype-phenotype for familial medullary thyroid carcinoma (FMTC) is well studied, only few low susceptibility risk loci were identified for familial non-medullary thyroid carcinoma (FNMTC). The aim of this study is to screen and identify high-penetrate genes for FNMTC. A total of 34 families with more than two first-degree relatives diagnosed as papillary thyroid cancer without other familial syndrome were recruited. Whole exome and target gene sequencing were performed for candidate variants. These variants were screened and analyzed with ESP6500, ExAC, 1000 genomes project, and the Cancer Genome Atlas (TCGA) with SIFT score and Polyphen2 prediction. Finally, we identified recurrent genetic mutation of MAP2K5 variants c.G961A and c.T1100C (p. A321T and p.M367 T) as susceptibility loci for FNMTC. The frequencies of MAP2K5 c.G961A and c.T1100C were found, 0.0385 and 0.0259 in FNMTC and 0 and 0.00022523 in healthy Chinese controls (n = 2200, P < 0.001), respectively. Both variants were located in the protein kinase domain. The functional study showed that MAP2K5 A321T or M367 T could consistently phosphorylate downstream protein ERK5 on site Ser731 + Thr733 or Ser496, promoting nuclear translocation and subsequently altering target gene expressions. Our data revealed that MAP2K5 variants A321T or M367 T can activate MAP2K5-ERK5 pathway, alter downstream gene expression, and subsequently induce thyroid epithelial cell malignant transformation. While classic MAP2K1/2(MEK1/2)-ERK1/2 signaling is well known for driving sporadic NMTC, our research indicated that MAP2K5 (MEK5) is a susceptibility gene for FNMTC. These findings highlight the potential application of MAP2K5 for molecular diagnosis as well as early prevention. Show less
no PDF DOI: 10.1002/ijc.31825
MAP2K5
Qiang Yang, Pingxian Wu, Kai Wang +11 more · 2019 · Genomics · Elsevier · added 2026-04-24
Growth and fat deposition are important economic traits due to the influence on production in pigs. In this study, a dataset of 1200 pigs with 345,570 SNPs genotyped by sequencing (GBS) was used to co Show more
Growth and fat deposition are important economic traits due to the influence on production in pigs. In this study, a dataset of 1200 pigs with 345,570 SNPs genotyped by sequencing (GBS) was used to conduct a GWAS with single-marker regression method to identify SNPs associated with body weight and backfat thickness (BFT) and to search for candidate genes in Landrace and Yorkshire pigs. A total of 27 and 13 significant SNPs were associated with body weight and BFT, respectively. In the region of 149.85-149.89 Mb on SSC6, the SNP (SSC6: 149876737) for body weight and the SNP (SSC6: 149876507) for BFT were in the same locus region (a gap of 230 bp). Two SNPs were located in the DOCK7 gene, which is a protein-coding gene that plays an important role in pigmentation. Two SNPs located on SSC8: 54567459 and SSC11: 33043081 were found to overlap weight and BFT; however, no candidate gene was found in these regions. In addition, based on other significant SNPs, two positional candidate genes, NSRP1 and CADPS, were proposed to influence weight. In conclusion, this is the first study report using GBS data to identify the significant SNPs for weight and BFT. A total of four particularly interesting SNPs and one potential candidate genes (DOCK7) were found for these traits in domestic pigs. This study improves our knowledge to better understand the complex genetic architecture of weight and BFT, but further validation studies of these candidate loci and genes are recommended in pigs. Show less
no PDF DOI: 10.1016/j.ygeno.2018.11.002
DOCK7
Yanjun Li, Yingyu Chen · 2019 · Advances in experimental medicine and biology · Springer · added 2026-04-24
AMPK is an evolutionarily conserved serine/threonine-protein kinase that acts as an energy sensor in cells and plays a key role in the upregulation of catabolism and inactivation of anabolism. Under v Show more
AMPK is an evolutionarily conserved serine/threonine-protein kinase that acts as an energy sensor in cells and plays a key role in the upregulation of catabolism and inactivation of anabolism. Under various physiological and pathological conditions, AMPK can be phosphorylated by an upstream kinase and bind to AMP or ADP rather than ATP, leading to its activation. Activated AMPK regulates a variety of metabolic processes, including autophagy. AMPK promotes autophagy directly by phosphorylating autophagy-related proteins in the mTORC1, ULK1, and PIK3C3/VPS34 complexes or indirectly by regulating the expression of autophagy-related genes downstream of transcription factors such as FOXO3, TFEB, and BRD4. AMPK can also upregulate the autophagic degradation of mitochondria (mitophagy), as it can induce fragmentation of damaged mitochondria in the network and promote the translocation of the autophagy machinery to damaged mitochondria. In this section, we will detail the molecular structure of AMPK, how its activity is regulated, and its pivotal role in regulating autophagy and mitophagy. Show less
no PDF DOI: 10.1007/978-981-15-0602-4_4
PIK3C3
Xiaojie Chen, Lin Wei, Zhijun Zhu +3 more · 2019 · Pediatric transplantation · Blackwell Publishing · added 2026-04-24
We introduce the indications, technique, results of our experience using donor's RGEA as interposition vessel to solve hepatic artery reconstruction problems in P-LDLT. A retrospective analysis of P-L Show more
We introduce the indications, technique, results of our experience using donor's RGEA as interposition vessel to solve hepatic artery reconstruction problems in P-LDLT. A retrospective analysis of P-LDLT for children with metabolic diseases from June 2013 to November 2018 in our center was carried out. The arterial conditions, reconstruction methods, and prognosis were analyzed. A total of 73 children with metabolic diseases underwent P-LDLT during the period. The LLF was the main graft, accounting for 71.2%. The donor's RGEA was utilized in five cases. There were three children with OTCD and two children with deficiency of CPS1 and MSUD, respectively. In three cases, the grafts' left hepatic arteries were anastomosed with the recipients' PHA using donors' RGEA as interposition vessel. In other two cases, the donors' RGEA was interposed between graft's MHA and the recipient's bifurcation of PHA and GDA. The average follow-up time was 19.7 ± 15.9 month. There were two cases of artery thrombosis or occlusion, and the incidence was 2.7%. No arterial complications occurred in children using RGEA (follow-up time 5.0 ± 3.4 months). In P-LDLT for patients with metabolic diseases, the application of RGEA as an interposition vessel can solve caliber mismatch and short arteries problem and achieve good results. Compared with traditional arterial anastomosis, it may reduce the incidence of arterial complications. Show less
no PDF DOI: 10.1111/petr.13418
CPS1
Syed Aun Muhammad, Nighat Fatima, Rehan Zafar Paracha +2 more · 2019 · Journal of biological research (Thessalonike, Greece) · BioMed Central · added 2026-04-24
Alopecia or hair loss is a complex polygenetic and psychologically devastating disease affecting millions of men and women globally. Since the gene annotation and environmental knowledge is limited fo Show more
Alopecia or hair loss is a complex polygenetic and psychologically devastating disease affecting millions of men and women globally. Since the gene annotation and environmental knowledge is limited for alopecia, a systematic analysis for the identification of candidate biomarkers is required that could provide potential therapeutic targets for hair loss therapy. We designed an interactive framework to perform a meta-analytical study based on differential expression analysis, systems biology, and functional proteomic investigations. We analyzed eight publicly available microarray datasets and found 12 potential candidate biomarkers including three extracellular proteins from the list of differentially expressed genes with a Our integrative approach helps to prioritize the biomarkers that ultimately lessen the economic burden of experimental studies. It will also be valuable to discover mutants in genomic data in order to increase the identification of new biomarkers for similar problems. Show less
📄 PDF DOI: 10.1186/s40709-019-0094-x
GPRC5B
Guanglin Xing, Hongyang Jing, Lei Zhang +9 more · 2019 · eLife · added 2026-04-24
Neuromuscular junction is a synapse between motoneurons and skeletal muscles, where acetylcholine receptors (AChRs) are concentrated to control muscle contraction. Studies of this synapse have contrib Show more
Neuromuscular junction is a synapse between motoneurons and skeletal muscles, where acetylcholine receptors (AChRs) are concentrated to control muscle contraction. Studies of this synapse have contributed to our understanding of synapse assembly and pathological mechanisms of neuromuscular disorders. Nevertheless, underlying mechanisms of NMJ formation was not well understood. To this end, we took a novel approach - studying mutant genes implicated in congenital myasthenic syndrome (CMS). We showed that knock-in mice carrying N88K, a prevalent CMS mutation of Rapsyn (Rapsn), died soon after birth with profound NMJ deficits. Rapsn is an adapter protein that bridges AChRs to the cytoskeleton and possesses E3 ligase activity. In investigating how N88K impairs the NMJ, we uncovered a novel signaling pathway by which Agrin-LRP4-MuSK induces tyrosine phosphorylation of Rapsn, which is required for its self-association and E3 ligase activity. Our results also provide insight into pathological mechanisms of CMS. Show less
no PDF DOI: 10.7554/eLife.49180
RAPSN

G

Min Chen, Eric A Wilson, Zhenzhong Cui +8 more · 2019 · Molecular metabolism · Elsevier · added 2026-04-24
G We created mice (DMHGsKO) with G DMHGsKO mice developed severe, early-onset obesity associated with hyperphagia and reduced energy expenditure and locomotor activity, along with impaired brown adipo Show more
G We created mice (DMHGsKO) with G DMHGsKO mice developed severe, early-onset obesity associated with hyperphagia and reduced energy expenditure and locomotor activity, along with impaired brown adipose tissue thermogenesis. Studies in mice with loss of MC4R in the DMH suggest that defective DMH MC4R/G DMH G Show less
📄 PDF DOI: 10.1016/j.molmet.2019.04.005
MC4R
Raj Karthik, Bhuvanenthiran Mutharani, Shen-Ming Chen +5 more · 2019 · Journal of materials chemistry. B · Royal Society of Chemistry · added 2026-04-24
The current study reports a new, simple and fast method using a flake-like dysprosium molybdate (Dy2MoO6; FL-DyM) nanostructured material to detect the antibiotic drug metronidazole (METZ). This nanoc Show more
The current study reports a new, simple and fast method using a flake-like dysprosium molybdate (Dy2MoO6; FL-DyM) nanostructured material to detect the antibiotic drug metronidazole (METZ). This nanocomposite material was employed on the surface of a glassy carbon electrode (GCE) to develop the electrode (FL-DyM/GCE). Further, the synthesized FL-DyM was systematically characterized by powder X-ray diffraction (XRD), Raman spectroscopy, scanning electron microscopy (SEM), transmission electron microscopy (TEM), energy-dispersive X-ray diffraction (EDS), elemental mapping, X-ray photoelectron spectroscopy (XPS), and Brunauer-Emmett-Teller (BET) analyses. Cyclic (CV) and differential pulse voltammetry (DPV) techniques were used to study the electrochemical properties. The FL-DyM/GCE-based sensor demonstrated excellent selectivity and sensitivity for the detection of the drug METZ, which could be attributed to the strong affinity of FL-DyM towards the -NO2 group in METZ, and the good electrocatalytic activity and conductivity of FL-DyM. The fabrication and optimization of the working electrode were accomplished with CV and DPV obtained by scan rate and pH studies. Compared to the bare GCE and other rare-earth metal molybdates, the FL-DyM/GCE sensor displayed a superior electrocatalytic activity response for METZ detection. The sensor demonstrated a good linear relationship over the concentration range of 0.01-2363 μM. The quantification and detection limits were found to be 0.010 μM and 0.0030 μM, respectively. The FL-DyM/GCE sensor displayed excellent selectivity, repeatability, reproducibility, and stability for the detection of METZ in human urine and commercial METZ tablet samples, which validates the new technique for efficient drug sensing in practical applications. Show less
no PDF DOI: 10.1039/c9tb01020c
DYM
Sixuan Qu, Zhaoli Yang, Hongdi Tao +4 more · 2019 · Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology · added 2026-04-24
Objective To investigate the expression of semaphorin 6D (SEMA6D) and Snail and their clinicopathological implications in gastric cancer. Methods 54 cases of gastric cancer tissues and 26 paracancerou Show more
Objective To investigate the expression of semaphorin 6D (SEMA6D) and Snail and their clinicopathological implications in gastric cancer. Methods 54 cases of gastric cancer tissues and 26 paracancerous gastric mucosa were collected for detecting the expression of SEMA6D and Snail by immunohistochemistry and Western blot analysis. The co-localization of SEMA6D and Snail was observed by immunofluorescence double staining and laser scanning confocal microscopy. The correlation between SEMA6D and Snail and their relationships with the clinicopathological features of the patients were analyzed. Results Compared with the paracancerous gastric mucosa, the protein expression of SEMA6D and Snail in the gastric cancer significantly increased, and there was a significant co-localization of SEMA6D and Snail in gastric cancer. Further statistical analysis showed that the expression of SEMA6D and Snail in gastric cancer was positively correlated with the degree of differentiation, invasion, lymph node metastasis and TNM stage. Conclusion The high expression of SEMA6D and Snail in gastric cancer are related to the malignant clinicopathological indexes of gastric cancer. Show less
no PDF
SNAI1