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231.
Effect of decapacitation factor on the oxygen uptake of rabbit spermatozoa recovered from the uterus 总被引:2,自引:0,他引:2
I. G. White J. C. Rodger Dr. R. N. Murdoch W. L. Williams T. O. Abney 《Cellular and molecular life sciences : CMLS》1975,31(1):80-81
Résumé L'addition d'un facteur de décapacitation préparé à partir du plasma séminal de lapin et de taureau a généralement produit une augmentation supplémentaire de l'absorption d'oxygène, quand il a été ajouté à la suspension de spermatozoïdes enlevée de l'utérus. Le facteur de décapacitation n'a exercé aucun effet stimulant similaire sur les spermatozoïdes de lapin avant l'incubation dans l'utérus et n'a montré lui-même aucune absorption d'oxygène appréciable.
Dr.I. G. White is indebted to the Population Council for a fellowship and to the Australian Research Grants Committee for financial support. The authors are indebted to ProfessorC. W. Emmens for his interest and advice. 相似文献
Dr.I. G. White is indebted to the Population Council for a fellowship and to the Australian Research Grants Committee for financial support. The authors are indebted to ProfessorC. W. Emmens for his interest and advice. 相似文献
232.
233.
Zhang B Cunningham MA Nichols WC Bernat JA Seligsohn U Pipe SW McVey JH Schulte-Overberg U de Bosch NB Ruiz-Saez A White GC Tuddenham EG Kaufman RJ Ginsburg D 《Nature genetics》2003,34(2):220-225
Mutations in LMAN1 (also called ERGIC-53) result in combined deficiency of factor V and factor VIII (F5F8D), an autosomal recessive bleeding disorder characterized by coordinate reduction of both clotting proteins. LMAN1 is a mannose-binding type 1 transmembrane protein localized to the endoplasmic reticulum-Golgi intermediate compartment (ERGIC; refs. 2,3), suggesting that F5F8D could result from a defect in secretion of factor V and factor VIII (ref. 4). Correctly folded proteins destined for secretion are packaged in the ER into COPII-coated vesicles, which subsequently fuse to form the ERGIC. Secretion of certain abundant proteins suggests a default pathway requiring no export signals (bulk flow; refs. 6,7). An alternative mechanism involves selective packaging of secreted proteins with the help of specific cargo receptors. The latter model would be consistent with mutations in LMAN1 causing a selective block to export of factor V and factor VIII. But approximately 30% of individuals with F5F8D have normal levels of LMAN1, suggesting that mutations in another gene may also be associated with F5F8D. Here we show that inactivating mutations in MCFD2 cause F5F8D with a phenotype indistinguishable from that caused by mutations in LMAN1. MCFD2 is localized to the ERGIC through a direct, calcium-dependent interaction with LMAN1. These findings suggest that the MCFD2-LMAN1 complex forms a specific cargo receptor for the ER-to-Golgi transport of selected proteins. 相似文献
234.
Positional cloning of a quantitative trait locus on chromosome 13q14 that influences immunoglobulin E levels and asthma 总被引:20,自引:0,他引:20
235.
Mutations in the genes encoding 11beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase interact to cause cortisone reductase deficiency 总被引:12,自引:0,他引:12
236.
Monoclonal antibodies inhibit prion replication and delay the development of prion disease 总被引:19,自引:0,他引:19
White AR Enever P Tayebi M Mushens R Linehan J Brandner S Anstee D Collinge J Hawke S 《Nature》2003,422(6927):80-83
Prion diseases such as Creutzfeldt-Jakob disease (CJD) are fatal, neuro-degenerative disorders with no known therapy. A proportion of the UK population has been exposed to a bovine spongiform encephalopathy-like prion strain and are at risk of developing variant CJD. A hallmark of prion disease is the transformation of normal cellular prion protein (PrP(C)) into an infectious disease-associated isoform, PrP(Sc). Recent in vitro studies indicate that anti-PrP monoclonal antibodies with little or no affinity for PrP(Sc) can prevent the incorporation of PrP(C) into propagating prions. We therefore investigated in a murine scrapie model whether anti-PrP monoclonal antibodies show similar inhibitory effects on prion replication in vivo. We found that peripheral PrP(Sc) levels and prion infectivity were markedly reduced, even when the antibodies were first administered at the point of near maximal accumulation of PrP(Sc) in the spleen. Furthermore, animals in which the treatment was continued remained healthy for over 300 days after equivalent untreated animals had succumbed to the disease. These findings indicate that immunotherapeutic strategies for human prion diseases are worth pursuing. 相似文献
237.
238.
Remains of Homo erectus from Bouri, Middle Awash, Ethiopia 总被引:5,自引:0,他引:5
Asfaw B Gilbert WH Beyene Y Hart WK Renne PR WoldeGabriel G Vrba ES White TD 《Nature》2002,416(6878):317-320
The genesis, evolution and fate of Homo erectus have been explored palaeontologically since the taxon's recognition in the late nineteenth century. Current debate is focused on whether early representatives from Kenya and Georgia should be classified as a separate ancestral species ('H. ergaster'), and whether H. erectus was an exclusively Asian species lineage that went extinct. Lack of resolution of these issues has obscured the place of H. erectus in human evolution. A hominid calvaria and postcranial remains recently recovered from the Dakanihylo Member of the Bouri Formation, Middle Awash, Ethiopia, bear directly on these issues. These approximately 1.0-million-year (Myr)-old Pleistocene sediments contain abundant early Acheulean stone tools and a diverse vertebrate fauna that indicates a predominantly savannah environment. Here we report that the 'Daka' calvaria's metric and morphological attributes centre it firmly within H. erectus. Daka's resemblance to Asian counterparts indicates that the early African and Eurasian fossil hominids represent demes of a widespread palaeospecies. Daka's anatomical intermediacy between earlier and later African fossils provides evidence of evolutionary change. Its temporal and geographic position indicates that African H. erectus was the ancestor of Homo sapiens. 相似文献
239.
Gardner MJ Hall N Fung E White O Berriman M Hyman RW Carlton JM Pain A Nelson KE Bowman S Paulsen IT James K Eisen JA Rutherford K Salzberg SL Craig A Kyes S Chan MS Nene V Shallom SJ Suh B Peterson J Angiuoli S Pertea M Allen J Selengut J Haft D Mather MW Vaidya AB Martin DM Fairlamb AH Fraunholz MJ Roos DS Ralph SA McFadden GI Cummings LM Subramanian GM Mungall C Venter JC Carucci DJ Hoffman SL Newbold C Davis RW Fraser CM Barrell B 《Nature》2002,419(6906):498-511
The parasite Plasmodium falciparum is responsible for hundreds of millions of cases of malaria, and kills more than one million African children annually. Here we report an analysis of the genome sequence of P. falciparum clone 3D7. The 23-megabase nuclear genome consists of 14 chromosomes, encodes about 5,300 genes, and is the most (A + T)-rich genome sequenced to date. Genes involved in antigenic variation are concentrated in the subtelomeric regions of the chromosomes. Compared to the genomes of free-living eukaryotic microbes, the genome of this intracellular parasite encodes fewer enzymes and transporters, but a large proportion of genes are devoted to immune evasion and host-parasite interactions. Many nuclear-encoded proteins are targeted to the apicoplast, an organelle involved in fatty-acid and isoprenoid metabolism. The genome sequence provides the foundation for future studies of this organism, and is being exploited in the search for new drugs and vaccines to fight malaria. 相似文献