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设计了一个非专业人士能够使用、最简化的气候敏感模型,用来研究人类活动所导致的全球变暖的幅度问题.在1990年的第一次IPCC评估报告中,IPCC对其报告中预测的未来全球变暖幅度很有信心,但是随后的观测结果显示全球的变暖幅度只有预测的一半.而自2001年起,全球变暖出现停滞,但是仅仅考虑到二氧化碳浓度的增加,很少有模型能够模拟出这一变化.在已出版的IPCC第五次评估报告的草稿中,IPCC大幅度削减了近期变暖的幅度,并以专家评估代替了模型预测.但是报告中关于未来气候长期变化的预测仍被保留.如果把IPCC模型的总反馈从1.9 W m–2 K–1调整到1.5 W m–2 K–1,气候敏感模型中模拟的温度将从3.2 K降至2.2 K.同时由于反馈很可能是净负反馈,更合适的估计应该是1.0 K.1.0 K是一个能够实现的增幅,21世纪的实际变暖将会小于1 K.即使燃烧所有可开采的化石燃料也不会使全球变暖的幅度超过2.2 K,这一增加幅度也将趋于平稳.本文认为解决IPCC第四、五次报告中评估方法的差异非常关键.一旦这些差异得到解决,人类活动导致的全球变暖在22世纪以及几个世纪以后的平稳态将有可能不会超过IPCC当前模型预测的1/3~1/2.  相似文献   
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对烟碱类农药在水体中残留情况及对水生生物产生的直接和间接影响的研究进行了综述。重点对水生脊椎类动物(鱼类、两栖类)及非脊椎类动物(蜉蝣、大型蚤)的急性和慢性毒性,及通过生物群落、食物链因素对鱼类种群层面的间接影响研究进行了总结,认为烟碱类农药对于水生脊椎类生物的急性毒性远小于非脊椎类生物,同时在低浓度下其对水生生物具有长期的慢性毒性和影响。通过对已有研究数据的分析,讨论了烟碱类农药在风险评价过程中的间接影响效应,指出通过食物链富集及传递作用,烟碱类农药对于非靶标生物的群落和种群数量具有重要的影响。  相似文献   
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Adult height is a model polygenic trait, but there has been limited success in identifying the genes underlying its normal variation. To identify genetic variants influencing adult human height, we used genome-wide association data from 13,665 individuals and genotyped 39 variants in an additional 16,482 samples. We identified 20 variants associated with adult height (P < 5 x 10(-7), with 10 reaching P < 1 x 10(-10)). Combined, the 20 SNPs explain approximately 3% of height variation, with a approximately 5 cm difference between the 6.2% of people with 17 or fewer 'tall' alleles compared to the 5.5% with 27 or more 'tall' alleles. The loci we identified implicate genes in Hedgehog signaling (IHH, HHIP, PTCH1), extracellular matrix (EFEMP1, ADAMTSL3, ACAN) and cancer (CDK6, HMGA2, DLEU7) pathways, and provide new insights into human growth and developmental processes. Finally, our results provide insights into the genetic architecture of a classic quantitative trait.  相似文献   
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Multiple ovulations are uncommon in humans, cattle and many breeds of sheep. Pituitary gonadotrophins and as yet unidentified ovarian factors precisely regulate follicular development so that, normally, only one follicle is selected to ovulate. The Inverdale (FecXI) sheep, however, carries a naturally occurring X-linked mutation that causes increased ovulation rate and twin and triplet births in heterozygotes (FecXI/FecX+; ref. 1), but primary ovarian failure in homozygotes (FecXI/FecXI; ref. 2). Germ-cell development, formation of the follicle and the earliest stages of follicular growth are normal in FecXI/FecXI sheep, but follicular development beyond the primary stage is impaired. A second family unrelated to the Inverdale sheep also has the same X-linked phenotype (Hanna, FecXH). Crossing FecXI with FecXH animals produces FecXI/FecXH infertile females phenotypically indistinguishable from FecXI/FecXI females. We report here that the FecXI locus maps to an orthologous chromosomal region syntenic to human Xp11.2-11.4, which contains BMP15, encoding bone morphogenetic protein 15 (also known as growth differentiation factor 9B (GDF9B)). Whereas BMP15 is a member of the transforming growth factor beta (TGFbeta) superfamily and is specifically expressed in oocytes, its function is unknown. We show that independent germline point mutations exist in FecXI and FecXH carriers. These findings establish that BMP15 is essential for female fertility and that natural mutations in an ovary-derived factor can cause both increased ovulation rate and infertility phenotypes in a dosage-sensitive manner.  相似文献   
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