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IJ Simpson MP Sulbaek Andersen S Meinardi L Bruhwiler NJ Blake D Helmig FS Rowland DR Blake 《Nature》2012,488(7412):490-494
After methane, ethane is the most abundant hydrocarbon in the remote atmosphere. It is a precursor to tropospheric ozone and it influences the atmosphere's oxidative capacity through its reaction with the hydroxyl radical, ethane's primary atmospheric sink. Here we present the longest continuous record of global atmospheric ethane levels. We show that global ethane emission rates decreased from 14.3 to 11.3 teragrams per year, or by 21 per cent, from 1984 to 2010. We attribute this to decreasing fugitive emissions from ethane's fossil fuel source--most probably decreased venting and flaring of natural gas in oil fields--rather than a decline in its other major sources, biofuel use and biomass burning. Ethane's major emission sources are shared with methane, and recent studies have disagreed on whether reduced fossil fuel or microbial emissions have caused methane's atmospheric growth rate to slow. Our findings suggest that reduced fugitive fossil fuel emissions account for at least 10-21 teragrams per year (30-70 per cent) of the decrease in methane's global emissions, significantly contributing to methane's slowing atmospheric growth rate since the mid-1980s. 相似文献
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Fish (cartilaginous: elasmobranch and bony: osteichthyan actinopterygian) and reptile (crocodile) microfossils comprising scales and teeth have been examined from a series of limestone samples in the Upper Jurassic of France and Germany to gauge the possibilities of using them for correlation between fully marine and hypo-or hyper-saline (non-marine) deposits. 相似文献
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Fish (cartilaginous: elasmobranch and bony: osteichthyan actinopterygian) and reptile (crocodile) microfossils comprising scales and teeth have been examined from a series of limestone samples in the Upper Jurassic of France and Germany to gauge the possibilities of using them for correlation between fully marine and hypo-or hyper-saline (non-marine) deposits. 相似文献
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Stoepker C Hain K Schuster B Hilhorst-Hofstee Y Rooimans MA Steltenpool J Oostra AB Eirich K Korthof ET Nieuwint AW Jaspers NG Bettecken T Joenje H Schindler D Rouse J de Winter JP 《Nature genetics》2011,43(2):138-141
DNA interstrand crosslink repair requires several classes of proteins, including structure-specific endonucleases and Fanconi anemia proteins. SLX4, which coordinates three separate endonucleases, was recently recognized as an important regulator of DNA repair. Here we report the first human individuals found to have biallelic mutations in SLX4. These individuals, who were previously diagnosed as having Fanconi anemia, add SLX4 as an essential component to the FA-BRCA genome maintenance pathway. 相似文献
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An opioid benzodiazepine 总被引:5,自引:0,他引:5
D R?mer H H Büscher R C Hill R Maurer T J Petcher H Zeugner W Benson E Finner W Milkowski P W Thies 《Nature》1982,298(5876):759-760
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Biallelic mutations in PALB2 cause Fanconi anemia subtype FA-N and predispose to childhood cancer 总被引:1,自引:0,他引:1
Reid S Schindler D Hanenberg H Barker K Hanks S Kalb R Neveling K Kelly P Seal S Freund M Wurm M Batish SD Lach FP Yetgin S Neitzel H Ariffin H Tischkowitz M Mathew CG Auerbach AD Rahman N 《Nature genetics》2007,39(2):162-164
PALB2 was recently identified as a nuclear binding partner of BRCA2. Biallelic BRCA2 mutations cause Fanconi anemia subtype FA-D1 and predispose to childhood malignancies. We identified pathogenic mutations in PALB2 (also known as FANCN) in seven families affected with Fanconi anemia and cancer in early childhood, demonstrating that biallelic PALB2 mutations cause a new subtype of Fanconi anemia, FA-N, and, similar to biallelic BRCA2 mutations, confer a high risk of childhood cancer. 相似文献
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The BRCA1-interacting helicase BRIP1 is deficient in Fanconi anemia 总被引:19,自引:0,他引:19
Levran O Attwooll C Henry RT Milton KL Neveling K Rio P Batish SD Kalb R Velleuer E Barral S Ott J Petrini J Schindler D Hanenberg H Auerbach AD 《Nature genetics》2005,37(9):931-933
Seven Fanconi anemia-associated proteins (FANCA, FANCB, FANCC, FANCE, FANCF, FANCG and FANCL) form a nuclear Fanconi anemia core complex that activates the monoubiquitination of FANCD2, targeting FANCD2 to BRCA1-containing nuclear foci. Cells from individuals with Fanconi anemia of complementation groups D1 and J (FA-D1 and FA-J) have normal FANCD2 ubiquitination. Using genetic mapping, mutation identification and western-blot data, we identify the defective protein in FA-J cells as BRIP1 (also called BACH1), a DNA helicase that is a binding partner of the breast cancer tumor suppressor BRCA1. 相似文献
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