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141.
142.
Hellmer HH  Kauker F  Timmermann R  Determann J  Rae J 《Nature》2012,485(7397):225-228
The Antarctic ice sheet loses mass at its fringes bordering the Southern Ocean. At this boundary, warm circumpolar water can override the continental slope front, reaching the grounding line through submarine glacial troughs and causing high rates of melting at the deep ice-shelf bases. The interplay between ocean currents and continental bathymetry is therefore likely to influence future rates of ice-mass loss. Here we show that a redirection of the coastal current into the Filchner Trough and underneath the Filchner-Ronne Ice Shelf during the second half of the twenty-first century would lead to increased movement of warm waters into the deep southern ice-shelf cavity. Water temperatures in the cavity would increase by more than 2 degrees Celsius and boost average basal melting from 0.2 metres, or 82 billion tonnes, per year to almost 4 metres, or 1,600 billion tonnes, per year. Our results, which are based on the output of a coupled ice-ocean model forced by a range of atmospheric outputs from the HadCM3 climate model, suggest that the changes would be caused primarily by an increase in ocean surface stress in the southeastern Weddell Sea due to thinning of the formerly consolidated sea-ice cover. The projected ice loss at the base of the Filchner-Ronne Ice Shelf represents 80 per cent of the present Antarctic surface mass balance. Thus, the quantification of basal mass loss under changing climate conditions is important for projections regarding the dynamics of Antarctic ice streams and ice shelves, and global sea level rise.  相似文献   
143.
通过对蚁群算法和粒子群算法分别进行改进,利用两种算法自身优势相结合的方式建立一种蚁群粒子群算法,以提高云计算资源调度效率,解决云计算中资源调度方案优化问题.实验结果表明,该算法所消耗的时间更少,效果更好.  相似文献   
144.
目的:研究高河菜提取物对小鼠消化道动力的影响.方法:采用炭末推进实验观察高河菜提取物对阿托品所致小鼠小肠推进抑制的影响;采用甲基橙胃残留率的方法观察高河菜提取物对阿托品所致小鼠胃排空抑制的影响.结果:高河菜提取物2g/kg能明显拮抗阿托品对小鼠小肠推进抑制的作用;高河菜提取物2g/kg、1g/kg和0.5g/kg均能拮抗阿托品对小鼠胃排空抑制的作用.结论:高河菜提取物对阿托品所致小鼠胃肠功能障碍有明显的改善作用.  相似文献   
145.
目的研究三次图的完全扩容图的连通度。方法利用反证法。结果与结论3-连通三次图的完全扩容图也是3-连通三次图。  相似文献   
146.
Both serotonin (5-HT) and neuropeptide Y have been shown to affect a variety of mammalian behaviors, including aggression. Here we show in Drosophila melanogaster that both 5-HT and neuropeptide F, the invertebrate homolog of neuropeptide Y, modulate aggression. We show that drug-induced increases of 5-HT in the fly brain increase aggression. Elevating 5-HT genetically in the serotonergic circuits recapitulates these pharmacological effects, whereas genetic silencing of these circuits makes the flies behaviorally unresponsive to the drug-induced increase of 5-HT but leaves them capable of aggression. Genetic silencing of the neuropeptide F (npf) circuit also increases fly aggression, demonstrating an opposite modulation to 5-HT. Moreover, this neuropeptide F effect seems to be independent of 5-HT. The implication of these two modulatory systems in fly and mouse aggression suggest a marked degree of conservation and a deep molecular root for this behavior.  相似文献   
147.
Systematic efforts are underway to decipher the genetic changes associated with tumor initiation and progression. However, widespread clinical application of this information is hampered by an inability to identify critical genetic events across the spectrum of human tumors with adequate sensitivity and scalability. Here, we have adapted high-throughput genotyping to query 238 known oncogene mutations across 1,000 human tumor samples. This approach established robust mutation distributions spanning 17 cancer types. Of 17 oncogenes analyzed, we found 14 to be mutated at least once, and 298 (30%) samples carried at least one mutation. Moreover, we identified previously unrecognized oncogene mutations in several tumor types and observed an unexpectedly high number of co-occurring mutations. These results offer a new dimension in tumor genetics, where mutations involving multiple cancer genes may be interrogated simultaneously and in 'real time' to guide cancer classification and rational therapeutic intervention.  相似文献   
148.
Mammalian podocytes, the key determinants of the kidney’s filtration barrier, differentiate from columnar epithelial cells and several key determinants of apical–basal polarity in the conventional epithelia have been shown to regulate podocyte morphogenesis and function. However, little is known about the role of Crumbs, a conserved polarity regulator in many epithelia, for slit-diaphragm formation and podocyte function. In this study, we used Drosophila nephrocytes as model system for mammalian podocytes and identified a conserved function of Crumbs proteins for cellular morphogenesis, nephrocyte diaphragm assembly/maintenance, and endocytosis. Nephrocyte-specific knock-down of Crumbs results in disturbed nephrocyte diaphragm assembly/maintenance and decreased endocytosis, which can be rescued by Drosophila Crumbs as well as human Crumbs2 and Crumbs3, which were both expressed in human podocytes. In contrast to the extracellular domain, which facilitates nephrocyte diaphragm assembly/maintenance, the intracellular FERM-interaction motif of Crumbs is essential for regulating endocytosis. Moreover, Moesin, which binds to the FERM-binding domain of Crumbs, is essential for efficient endocytosis. Thus, we describe here a new mechanism of nephrocyte development and function, which is likely to be conserved in mammalian podocytes.  相似文献   
149.
Through exomic sequencing of ten hepatitis C virus (HCV)-associated hepatocellular carcinomas (HCC) and subsequent evaluation of additional affected individuals, we discovered novel inactivating mutations of ARID2 in four major subtypes of HCC (HCV-associated HCC, hepatitis B virus (HBV)-associated HCC, alcohol-associated HCC and HCC with no known etiology). Notably, 18.2% of individuals with HCV-associated HCC in the United States and Europe harbored ARID2 inactivation mutations, suggesting that ARID2 is a tumor suppressor gene that is relatively commonly mutated in this tumor subtype.  相似文献   
150.
Although thoracic aortic aneurysms and dissections (TAAD) can be inherited as a single-gene disorder, the genetic predisposition in the majority of affected people is poorly understood. In a multistage genome-wide association study (GWAS), we compared 765 individuals who had sporadic TAAD (STAAD) with 874 controls and identified common SNPs at a 15q21.1 locus that were associated with STAAD, with odds ratios of 1.6-1.8 that achieved genome-wide significance. We followed up 107 SNPs associated with STAAD with P < 1 × 10(-5) in the region, in two separate STAAD cohorts. The associated SNPs fall into a large region of linkage disequilibrium encompassing FBN1, which encodes fibrillin-1. FBN1 mutations cause Marfan syndrome, whose major cardiovascular complication is TAAD. This study shows that common genetic variants at 15q21.1 that probably act via FBN1 are associated with STAAD, suggesting a common pathogenesis of aortic disease in Marfan syndrome and STAAD.  相似文献   
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