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Summary Symbiontic zooxanthellae found in the stomach of the giant clamTridacna gigas are of exogenous origin. They become available to the clam following their mass expulsion from heat-stressed hermatypic corals. The frequent appearance of these mini-plankton blooms also permits the primary production of zooxanthellae to become an available food source for other filter-feeding reef organisms rather than remaining imprisoned within the tissues of corals.We are grateful to personnel of the Mid-Pacific Marine Laboratory, Enewetak Atoll, Marshall Islands, and Friday Harbor Laboratories Washington, for providing services and facilities where portions of this study were performed. Financial support was provided by the US Department of Energy and by operating grants from the National Research Council of Canada. We thank Drs Eugene N. Kozloff and Richard R. Strathmann for comments. 相似文献
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Quantitative studies with antilymphocytic antibody 总被引:7,自引:0,他引:7
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Mitral valve action and the mode of ventricular filling 总被引:2,自引:0,他引:2
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Growth processes in teeth distinguish modern humans from Homo erectus and earlier hominins. 总被引:3,自引:0,他引:3
A modern human-like sequence of dental development, as a proxy for the pace of life history, is regarded as one of the diagnostic hallmarks of our own genus Homo. Brain size, age at first reproduction, lifespan and other life-history traits correlate tightly with dental development. Here we report differences in enamel growth that show the earliest fossils attributed to Homo do not resemble modern humans in their development. We used daily incremental markings in enamel to calculate rates of enamel formation in 13 fossil hominins and identified differences in this key determinant of tooth formation time. Neither australopiths nor fossils currently attributed to early Homo shared the slow trajectory of enamel growth typical of modern humans; rather, both resembled modern and fossil African apes. We then reconstructed tooth formation times in australopiths, in the approximately 1.5-Myr-old Homo erectus skeleton from Nariokotome, Kenya, and in another Homo erectus specimen, Sangiran S7-37 from Java. These times were shorter than those in modern humans. It therefore seems likely that truly modern dental development emerged relatively late in human evolution. 相似文献
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Neale BM Kou Y Liu L Ma'ayan A Samocha KE Sabo A Lin CF Stevens C Wang LS Makarov V Polak P Yoon S Maguire J Crawford EL Campbell NG Geller ET Valladares O Schafer C Liu H Zhao T Cai G Lihm J Dannenfelser R Jabado O Peralta Z Nagaswamy U Muzny D Reid JG Newsham I Wu Y Lewis L Han Y Voight BF Lim E Rossin E Kirby A Flannick J Fromer M Shakir K Fennell T Garimella K Banks E Poplin R Gabriel S DePristo M Wimbish JR Boone BE Levy SE Betancur C Sunyaev S Boerwinkle E Buxbaum JD Cook EH Devlin B 《Nature》2012,485(7397):242-245
Autism spectrum disorders (ASD) are believed to have genetic and environmental origins, yet in only a modest fraction of individuals can specific causes be identified. To identify further genetic risk factors, here we assess the role of de novo mutations in ASD by sequencing the exomes of ASD cases and their parents (n = 175 trios). Fewer than half of the cases (46.3%) carry a missense or nonsense de novo variant, and the overall rate of mutation is only modestly higher than the expected rate. In contrast, the proteins encoded by genes that harboured de novo missense or nonsense mutations showed a higher degree of connectivity among themselves and to previous ASD genes as indexed by protein-protein interaction screens. The small increase in the rate of de novo events, when taken together with the protein interaction results, are consistent with an important but limited role for de novo point mutations in ASD, similar to that documented for de novo copy number variants. Genetic models incorporating these data indicate that most of the observed de novo events are unconnected to ASD; those that do confer risk are distributed across many genes and are incompletely penetrant (that is, not necessarily sufficient for disease). Our results support polygenic models in which spontaneous coding mutations in any of a large number of genes increases risk by 5- to 20-fold. Despite the challenge posed by such models, results from de novo events and a large parallel case-control study provide strong evidence in favour of CHD8 and KATNAL2 as genuine autism risk factors. 相似文献