GSTDTAP

浏览/检索结果: 共45条,第1-10条 帮助

限定条件    
已选(0)清除 条数/页:   排序方式:
Characterization of submicron particles by time-of-flight aerosol chemical speciation monitor (ToF-ACSM) during wintertime: aerosol composition, sources, and chemical processes in Guangzhou, China 期刊论文
ATMOSPHERIC CHEMISTRY AND PHYSICS, 2020, 20 (12) : 7595-7615
作者:  Guo, Junchen;  Zhou, Shengzhen;  Cai, Mingfu;  Zhao, Jun;  Song, Wei;  Zhao, Weixiong;  Hu, Weiwei;  Sun, Yele;  He, Yao;  Yang, Chengqiang;  Xu, Xuezhe;  Zhang, Zhisheng;  Cheng, Peng;  Fan, Qi;  Hang, Jian;  Fan, Shaojia;  Wang, Xinming;  Wang, Xuemei
收藏  |  浏览/下载:19/0  |  提交时间:2020/07/06
Impacts of water partitioning and polarity of organic compounds on secondary organic aerosol over eastern China 期刊论文
ATMOSPHERIC CHEMISTRY AND PHYSICS, 2020, 20 (12) : 7291-7306
作者:  Li, Jingyi;  Zhang, Haowen;  Ying, Qi;  Wu, Zhijun;  Zhang, Yanli;  Wang, Xinming;  Li, Xinghua;  Sun, Yele;  Hu, Min;  Zhang, Yuanhang;  Hu, Jianlin
收藏  |  浏览/下载:12/0  |  提交时间:2020/06/29
Sea-ice loss amplifies summertime decadal CO(2)increase in the western Arctic Ocean 期刊论文
NATURE CLIMATE CHANGE, 2020, 10 (7) : 678-+
作者:  Ouyang, Zhangxian;  Qi, Di;  Chen, Liqi;  Takahashi, Taro;  Zhong, Wenli;  DeGrandpre, Michael D.;  Chen, Baoshan;  Gao, Zhongyong;  Nishino, Shigeto;  Murata, Akihiko;  Sun, Heng;  Robbins, Lisa L.;  Jin, Meibing;  Cai, Wei-Jun
收藏  |  浏览/下载:15/0  |  提交时间:2020/06/22
Fast sulfate formation from oxidation of SO2 by NO2 and HONO observed in Beijing haze 期刊论文
NATURE COMMUNICATIONS, 2020, 11 (1)
作者:  Wang, Junfeng;  Li, Jingyi;  Ye, Jianhuai;  Zhao, Jian;  Wu, Yangzhou;  Hu, Jianlin;  Liu, Dantong;  Nie, Dongyang;  Shen, Fuzhen;  Huang, Xiangpeng;  Huang, Dan Dan;  Ji, Dongsheng;  Sun, Xu;  Xu, Weiqi;  Guo, Jianping;  Song, Shaojie;  Qin, Yiming;  Liu, Pengfei;  Turner, Jay R.;  Lee, Hyun Chul;  Hwang, Sungwoo;  Liao, Hong;  Martin, Scot T.;  Zhang, Qi;  Chen, Mindong;  Sun, Yele;  Ge, Xinlei;  Jacob, Daniel J.
收藏  |  浏览/下载:18/0  |  提交时间:2020/06/09
Oncometabolites suppress DNA repair by disrupting local chromatin signalling 期刊论文
NATURE, 2020
作者:  Zhang, Xu;  Lei, Bo;  Yuan, Yuan;  Zhang, Li;  Hu, Lu;  Jin, Sen;  Kang, Bilin;  Liao, Xuebin;  Sun, Wenzhi;  Xu, Fuqiang;  Zhong, Yi;  Hu, Ji;  Qi, Hai
收藏  |  浏览/下载:23/0  |  提交时间:2020/07/03

Metabolites that are elevated in tumours inhibit the lysine demethylase KDM4B, resulting in aberrant hypermethylation of histone 3 lysine 9 and decreased homology-dependent DNA repair.


Deregulation of metabolism and disruption of genome integrity are hallmarks of cancer(1). Increased levels of the metabolites 2-hydroxyglutarate, succinate and fumarate occur in human malignancies owing to somatic mutations in the isocitrate dehydrogenase-1 or -2 (IDH1 or IDH2) genes, or germline mutations in the fumarate hydratase (FH) and succinate dehydrogenase genes (SDHA, SDHB, SDHC and SDHD), respectively(2-4). Recent work has made an unexpected connection between these metabolites and DNA repair by showing that they suppress the pathway of homology-dependent repair (HDR)(5,6) and confer an exquisite sensitivity to inhibitors of poly (ADP-ribose) polymerase (PARP) that are being tested in clinical trials. However, the mechanism by which these oncometabolites inhibit HDR remains poorly understood. Here we determine the pathway by which these metabolites disrupt DNA repair. We show that oncometabolite-induced inhibition of the lysine demethylase KDM4B results in aberrant hypermethylation of histone 3 lysine 9 (H3K9) at loci surrounding DNA breaks, masking a local H3K9 trimethylation signal that is essential for the proper execution of HDR. Consequently, recruitment of TIP60 and ATM, two key proximal HDR factors, is substantially impaired at DNA breaks, with reduced end resection and diminished recruitment of downstream repair factors. These findings provide a mechanistic basis for oncometabolite-induced HDR suppression and may guide effective strategies to exploit these defects for therapeutic gain.


  
Changing rapid weather variability increases influenza epidemic risk in a warming climate 期刊论文
ENVIRONMENTAL RESEARCH LETTERS, 2020, 15 (4)
作者:  Liu, Qi;  Tan, Zhe-Min;  Sun, Jie;  Hou, Yayi;  Fu, Congbin;  Wu, Zhaohua
收藏  |  浏览/下载:10/0  |  提交时间:2020/07/02
influenza epidemic  rapid weather variability  North mid-latitude  climate change  predictable model  
Notch signalling drives synovial fibroblast identity and arthritis pathology 期刊论文
NATURE, 2020, 582 (7811) : 259-+
作者:  Han, Xiaoping;  Zhou, Ziming;  Fei, Lijiang;  Sun, Huiyu;  Wang, Renying;  Chen, Yao;  Chen, Haide;  Wang, Jingjing;  Tang, Huanna;  Ge, Wenhao;  Zhou, Yincong;  Ye, Fang;  Jiang, Mengmeng;  Wu, Junqing;  Xiao, Yanyu;  Jia, Xiaoning;  Zhang, Tingyue;  Ma, Xiaojie;  Zhang, Qi;  Bai, Xueli;  Lai, Shujing;  Yu, Chengxuan;  Zhu, Lijun;  Lin, Rui;  Gao, Yuchi;  Wang, Min;  Wu, Yiqing;  Zhang, Jianming;  Zhan, Renya;  Zhu, Saiyong;  Hu, Hailan;  Wang, Changchun;  Chen, Ming;  Huang, He;  Liang, Tingbo;  Chen, Jianghua;  Wang, Weilin;  Zhang, Dan;  Guo, Guoji
收藏  |  浏览/下载:43/0  |  提交时间:2020/07/03

NOTCH3 signalling is shown to be the underlying driver of the differentiation and expansion of a subset of synovial fibroblasts implicated in the pathogenesis of rheumatoid arthritis.


The synovium is a mesenchymal tissue composed mainly of fibroblasts, with a lining and sublining that surround the joints. In rheumatoid arthritis the synovial tissue undergoes marked hyperplasia, becomes inflamed and invasive, and destroys the joint(1,2). It has recently been shown that a subset of fibroblasts in the sublining undergoes a major expansion in rheumatoid arthritis that is linked to disease activity(3-5)  however, the molecular mechanism by which these fibroblasts differentiate and expand is unknown. Here we identify a critical role for NOTCH3 signalling in the differentiation of perivascular and sublining fibroblasts that express CD90 (encoded by THY1). Using single-cell RNA sequencing and synovial tissue organoids, we found that NOTCH3 signalling drives both transcriptional and spatial gradients-emanating from vascular endothelial cells outwards-in fibroblasts. In active rheumatoid arthritis, NOTCH3 and Notch target genes are markedly upregulated in synovial fibroblasts. In mice, the genetic deletion of Notch3 or the blockade of NOTCH3 signalling attenuates inflammation and prevents joint damage in inflammatory arthritis. Our results indicate that synovial fibroblasts exhibit a positional identity that is regulated by endothelium-derived Notch signalling, and that this stromal crosstalk pathway underlies inflammation and pathology in inflammatory arthritis.


  
Production of Ancient Dissolved Organic Carbon in Arctic Ocean Sediment: A Pathway of Carbon Cycling in the Extreme Environment 期刊论文
GEOPHYSICAL RESEARCH LETTERS, 2020, 47 (5)
作者:  Fu, Wenjing;  Qi, Yuanzhi;  Liu, Yanguang;  Wang, Xuchen;  Druffel, Ellen R. M.;  Xu, Xiaomei;  Ren, Peng;  Sun, Shuwen;  Fan, Di
收藏  |  浏览/下载:13/0  |  提交时间:2020/07/02
Biodiversity constraint indicator establishment and its optimization for urban growth: framework and application (vol 14, 125006, 2019) 期刊论文
ENVIRONMENTAL RESEARCH LETTERS, 2020, 15 (3)
作者:  Sun, Chuanzhun;  Xu, Shan;  Qi, Wei;  Chen, Cheng;  Deng, Yu;  Pei, Nancai;  Koenig, Hannes J.
收藏  |  浏览/下载:4/0  |  提交时间:2020/07/02
Hyperactivation of sympathetic nerves drives depletion of melanocyte stem cells 期刊论文
NATURE, 2020, 577 (7792) : 676-+
作者:  Zhao, Ruozhu;  Chen, Xin;  Ma, Weiwei;  Zhang, Jinyu;  Guo, Jie;  Zhong, Xiu;  Yao, Jiacheng;  Sun, Jiahui;  Rubinfien, Julian;  Zhou, Xuyu;  Wang, Jianbin;  Qi, Hai
收藏  |  浏览/下载:12/0  |  提交时间:2020/07/03

Empirical and anecdotal evidence has associated stress with accelerated hair greying (formation of unpigmented hairs)(1,2), but so far there has been little scientific validation of this link. Here we report that, in mice, acute stress leads to hair greying through the fast depletion of melanocyte stem cells. Using a combination of adrenalectomy, denervation, chemogenetics(3,4), cell ablation and knockout of the adrenergic receptor specifically in melanocyte stem cells, we find that the stress-induced loss of melanocyte stem cells is independent of immune attack or adrenal stress hormones. Instead, hair greying results from activation of the sympathetic nerves that innervate the melanocyte stem-cell niche. Under conditions of stress, the activation of these sympathetic nerves leads to burst release of the neurotransmitter noradrenaline (also known as norepinephrine). This causes quiescent melanocyte stem cells to proliferate rapidly, and is followed by their differentiation, migration and permanent depletion from the niche. Transient suppression of the proliferation of melanocyte stem cells prevents stress-induced hair greying. Our study demonstrates that neuronal activity that is induced by acute stress can drive a rapid and permanent loss of somatic stem cells, and illustrates an example in which the maintenance of somatic stem cells is directly influenced by the overall physiological state of the organism.


Stress induces hair greying in mice through depletion of melanocyte stem cells, which is mediated by the activation of sympathetic nerves rather than through immune attack or adrenal stress hormones.