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美研究指出颗粒有机碳的温度敏感性比矿质结合态有机碳高53% 快报文章
气候变化快报,2024年第5期
作者:  董利苹
Microsoft Word(15Kb)  |  收藏  |  浏览/下载:525/0  |  提交时间:2024/03/05
Emergent Temperature Sensitivity  Soil Organic Carbon  Mineral Associations  
美研究揭示二氧化碳的温室气体效应将愈发增强 快报文章
气候变化快报,2023年第24期
作者:  秦冰雪
Microsoft Word(15Kb)  |  收藏  |  浏览/下载:389/0  |  提交时间:2023/12/20
CO2  Climate Sensitivity  
德加科研人员提出更精确预测地球温度的新方法 快报文章
气候变化快报,2021年第1期
作者:  廖琴
Microsoft Word(19Kb)  |  收藏  |  浏览/下载:459/0  |  提交时间:2021/01/04
Climate Sensitivity Estimates  Global Temperature Projections  
平衡气候敏感度的温度状态依赖性不可忽视 快报文章
气候变化快报,2020年第18期
作者:  董利苹
Microsoft Word(14Kb)  |  收藏  |  浏览/下载:361/0  |  提交时间:2020/09/20
Eocene  Equilibrium Climate Sensitivity  Proxy Evidence  
国际研究缩小了气候对CO2的敏感性范围 快报文章
气候变化快报,2020年第16期
作者:  裴惠娟
Microsoft Word(14Kb)  |  收藏  |  浏览/下载:379/0  |  提交时间:2020/08/19
Climate Sensitivity  Assessment  
Impact of Higher Spatial Atmospheric Resolution on Precipitation Extremes Over Land in Global Climate Models 期刊论文
JOURNAL OF GEOPHYSICAL RESEARCH-ATMOSPHERES, 2020, 125 (13)
作者:  Bador, Margot;  Boe, Julien;  Terray, Laurent;  Alexander, Lisa, V;  Baker, Alexander;  Bellucci, Alessio;  Haarsma, Rein;  Koenigk, Torben;  Moine, Marie-Pierre;  Lohmann, Katja;  Putrasahan, Dian A.;  Roberts, Chris;  Roberts, Malcolm;  Scoccimarro, Enrico;  Schiemann, Reinhard;  Seddon, Jon;  Senan, Retish;  Valcke, Sophie;  Vanniere, Benoit
收藏  |  浏览/下载:12/0  |  提交时间:2020/08/18
precipitation extremes  multimodel and multiproduct of observations framework  performance of the models  global climate models for CMIP6 and HighResMIP  sensitivity to atmospheric spatial resolution  
热带森林的固碳作用存在温度临界点 快报文章
气候变化快报,2020年第12期
作者:  裴惠娟
Microsoft Word(15Kb)  |  收藏  |  浏览/下载:416/0  |  提交时间:2020/06/19
Tropical Forests  Thermal Sensitivity  
Millennial-scale hydroclimate control of tropical soil carbon storage 期刊论文
NATURE, 2020, 581 (7806) : 63-+
作者:  Lam, Tommy Tsan-Yuk;  Jia, Na;  Zhang, Ya-Wei;  Shum, Marcus Ho-Hin;  Jiang, Jia-Fu;  Zhu, Hua-Chen;  Tong, Yi-Gang;  Shi, Yong-Xia;  Ni, Xue-Bing;  Liao, Yun-Shi;  Li, Wen-Juan;  Jiang, Bao-Gui;  Wei, Wei;  Yuan, Ting-Ting;  Zheng, Kui;  Cui, Xiao-Ming;  Li, Jie;  Pei, Guang-Qian
收藏  |  浏览/下载:25/0  |  提交时间:2020/05/13

Over the past 18,000 years, the residence time and amount of soil carbon stored in the Ganges-Brahmaputra basin have been controlled by the intensity of Indian Summer Monsoon rainfall, with greater carbon destabilization during wetter, warmer conditions.


The storage of organic carbon in the terrestrial biosphere directly affects atmospheric concentrations of carbon dioxide over a wide range of timescales. Within the terrestrial biosphere, the magnitude of carbon storage can vary in response to environmental perturbations such as changing temperature or hydroclimate(1), potentially generating feedback on the atmospheric inventory of carbon dioxide. Although temperature controls the storage of soil organic carbon at mid and high latitudes(2,3), hydroclimate may be the dominant driver of soil carbon persistence in the tropics(4,5)  however, the sensitivity of tropical soil carbon turnover to large-scale hydroclimate variability remains poorly understood. Here we show that changes in Indian Summer Monsoon rainfall have controlled the residence time of soil carbon in the Ganges-Brahmaputra basin over the past 18,000 years. Comparison of radiocarbon ages of bulk organic carbon and terrestrial higher-plant biomarkers with co-located palaeohydrological records(6) reveals a negative relationship between monsoon rainfall and soil organic carbon stocks on a millennial timescale. Across the deglaciation period, a depletion of basin-wide soil carbon stocks was triggered by increasing rainfall and associated enhanced soil respiration rates. Our results suggest that future hydroclimate changes in tropical regions are likely to accelerate soil carbon destabilization, further increasing atmospheric carbon dioxide concentrations.


  
What users of global risk indicators should know 期刊论文
GLOBAL ENVIRONMENTAL CHANGE-HUMAN AND POLICY DIMENSIONS, 2020, 62
作者:  Visser, H.;  de Bruin, S.;  Martens, A.;  Knoop, J.;  Ligtvoet, W.
收藏  |  浏览/下载:10/0  |  提交时间:2020/07/02
Campbell'  s law  Composite indicators  Global data sets  Metadata  Uncertainty and sensitivity analysis  
A dominant autoinflammatory disease caused by non-cleavable variants of RIPK1 期刊论文
NATURE, 2020, 577 (7788) : 109-+
作者:  Tao, Panfeng;  Sun, Jinqiao;  Wu, Zheming;  Wang, Shihao;  Wang, Jun;  Li, Wanjin;  Pan, Heling;  Bai, Renkui;  Zhang, Jiahui;  Wang, Ying;  Lee, Pui Y.;  Ying, Wenjing;  Zhou, Qinhua;  Hou, Jia;  Wang, Wenjie;  Sun, Bijun;  Yang, Mi;  Liu, Danru;  Fang, Ran;  Han, Huan;  Yang, Zhaohui;  Huang, Xin;  Li, Haibo;  Deuitch, Natalie;  Zhang, Yuan;  Dissanayake, Dilan;  Haude, Katrina;  McWalter, Kirsty;  Roadhouse, Chelsea;  MacKenzie, Jennifer J.;  Laxer, Ronald M.;  Aksentijevich, Ivona;  Yu, Xiaomin;  Wang, Xiaochuan;  Yuan, Junying;  Zhou, Qing
收藏  |  浏览/下载:23/0  |  提交时间:2020/07/03

Activation of RIPK1 controls TNF-mediated apoptosis, necroptosis and inflammatory pathways(1). Cleavage of human and mouse RIPK1 after residues D324 and D325, respectively, by caspase-8 separates the RIPK1 kinase domain from the intermediate and death domains. The D325A mutation in mouse RIPK1 leads to embryonic lethality during mouse development(2,3). However, the functional importance of blocking caspase-8-mediated cleavage of RIPK1 on RIPK1 activation in humans is unknown. Here we identify two families with variants in RIPK1 (D324V and D324H) that lead to distinct symptoms of recurrent fevers and lymphadenopathy in an autosomaldominant manner. Impaired cleavage of RIPK1 D324 variants by caspase-8 sensitized patients'  peripheral blood mononuclear cells to RIPK1 activation, apoptosis and necroptosis induced by TNF. The patients showed strong RIPK1-dependent activation of inflammatory signalling pathways and overproduction of inflammatory cytokines and chemokines compared with unaffected controls. Furthermore, we show that expression of the RIPK1 mutants D325V or D325H in mouse embryonic fibroblasts confers not only increased sensitivity to RIPK1 activation-mediated apoptosis and necroptosis, but also induction of pro-inflammatory cytokines such as IL-6 and TNF. By contrast, patient-derived fibroblasts showed reduced expression of RIPK1 and downregulated production of reactive oxygen species, resulting in resistance to necroptosis and ferroptosis. Together, these data suggest that human non-cleavable RIPK1 variants promote activation of RIPK1, and lead to an autoinflammatory disease characterized by hypersensitivity to apoptosis and necroptosis and increased inflammatory response in peripheral blood mononuclear cells, as well as a compensatory mechanism to protect against several pro-death stimuli in fibroblasts.