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91.
Cross-modal interactions between visual understanding and linguistic processing substantially contribute to the remarkable robustness of human language processing.We argue that the formation of cross-modal referential links is a prerequisite for the occurrence of cross-modal interactions between vision and language.In this paper we examine a computational model for a cross-modal reference formation with respect to its robustness against conceptual underspecification in the visual modality.This investigation is motivated by the fact that natural systems are well capable of establishing a cross-modal reference between modalities with different degrees of conceptual specification.In the investigated model,conceptually underspecified context information continues to drive the syntactic disambiguation of verb-centered syntactic ambiguities as long as the visual context contains the situation arity information of the visual scene. 相似文献
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Proteome survey reveals modularity of the yeast cell machinery 总被引:4,自引:0,他引:4
Gavin AC Aloy P Grandi P Krause R Boesche M Marzioch M Rau C Jensen LJ Bastuck S Dümpelfeld B Edelmann A Heurtier MA Hoffman V Hoefert C Klein K Hudak M Michon AM Schelder M Schirle M Remor M Rudi T Hooper S Bauer A Bouwmeester T Casari G Drewes G Neubauer G Rick JM Kuster B Bork P Russell RB Superti-Furga G 《Nature》2006,440(7084):631-636
Protein complexes are key molecular entities that integrate multiple gene products to perform cellular functions. Here we report the first genome-wide screen for complexes in an organism, budding yeast, using affinity purification and mass spectrometry. Through systematic tagging of open reading frames (ORFs), the majority of complexes were purified several times, suggesting screen saturation. The richness of the data set enabled a de novo characterization of the composition and organization of the cellular machinery. The ensemble of cellular proteins partitions into 491 complexes, of which 257 are novel, that differentially combine with additional attachment proteins or protein modules to enable a diversification of potential functions. Support for this modular organization of the proteome comes from integration with available data on expression, localization, function, evolutionary conservation, protein structure and binary interactions. This study provides the largest collection of physically determined eukaryotic cellular machines so far and a platform for biological data integration and modelling. 相似文献
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Kugathasan S Baldassano RN Bradfield JP Sleiman PM Imielinski M Guthery SL Cucchiara S Kim CE Frackelton EC Annaiah K Glessner JT Santa E Willson T Eckert AW Bonkowski E Shaner JL Smith RM Otieno FG Peterson N Abrams DJ Chiavacci RM Grundmeier R Mamula P Tomer G Piccoli DA Monos DS Annese V Denson LA Grant SF Hakonarson H 《Nature genetics》2008,40(10):1211-1215
Inflammatory bowel disease (IBD) is a common inflammatory disorder with complex etiology that involves both genetic and environmental triggers, including but not limited to defects in bacterial clearance, defective mucosal barrier and persistent dysregulation of the immune response to commensal intestinal bacteria. IBD is characterized by two distinct phenotypes: Crohn's disease (CD) and ulcerative colitis (UC). Previously reported GWA studies have identified genetic variation accounting for a small portion of the overall genetic susceptibility to CD and an even smaller contribution to UC pathogenesis. We hypothesized that stratification of IBD by age of onset might identify additional genes associated with IBD. To that end, we carried out a GWA analysis in a cohort of 1,011 individuals with pediatric-onset IBD and 4,250 matched controls. We identified and replicated significantly associated, previously unreported loci on chromosomes 20q13 (rs2315008[T] and rs4809330[A]; P = 6.30 x 10(-8) and 6.95 x 10(-8), respectively; odds ratio (OR) = 0.74 for both) and 21q22 (rs2836878[A]; P = 6.01 x 10(-8); OR = 0.73), located close to the TNFRSF6B and PSMG1 genes, respectively. 相似文献
97.
Sun J Zheng SL Wiklund F Isaacs SD Purcell LD Gao Z Hsu FC Kim ST Liu W Zhu Y Stattin P Adami HO Wiley KE Dimitrov L Sun J Li T Turner AR Adams TS Adolfsson J Johansson JE Lowey J Trock BJ Partin AW Walsh PC Trent JM Duggan D Carpten J Chang BL Grönberg H Isaacs WB Xu J 《Nature genetics》2008,40(10):1153-1155
We carried out a fine-mapping study in the HNF1B gene at 17q12 in two study populations and identified a second locus associated with prostate cancer risk, approximately 26 kb centromeric to the first known locus (rs4430796); these loci are separated by a recombination hot spot. We confirmed the association with a SNP in the second locus (rs11649743) in five additional populations, with P = 1.7 x 10(-9) for an allelic test of the seven studies combined. The association at each SNP remained significant after adjustment for the other SNP. 相似文献
98.
DE Neafsey K Galinsky RH Jiang L Young SM Sykes S Saif S Gujja JM Goldberg S Young Q Zeng SB Chapman AP Dash AR Anvikar PL Sutton BW Birren AA Escalante JW Barnwell JM Carlton 《Nature genetics》2012,44(9):1046-1050
We sequenced and annotated the genomes of four P. vivax strains collected from disparate geographic locations, tripling the number of genome sequences available for this understudied parasite and providing the first genome-wide perspective of global variability in this species. We observe approximately twice as much SNP diversity among these isolates as we do among a comparable collection of isolates of P. falciparum, a malaria-causing parasite that results in higher mortality. This indicates a distinct history of global colonization and/or a more stable demographic history for P. vivax relative to P. falciparum, which is thought to have undergone a recent population bottleneck. The SNP diversity, as well as additional microsatellite and gene family variability, suggests a capacity for greater functional variation in the global population of P. vivax. These findings warrant a deeper survey of variation in P. vivax to equip disease interventions targeting the distinctive biology of this neglected but major pathogen. 相似文献
99.
Höglinger GU Melhem NM Dickson DW Sleiman PM Wang LS Klei L Rademakers R de Silva R Litvan I Riley DE van Swieten JC Heutink P Wszolek ZK Uitti RJ Vandrovcova J Hurtig HI Gross RG Maetzler W Goldwurm S Tolosa E Borroni B Pastor P;PSP Genetics Study Group Cantwell LB Han MR Dillman A van der Brug MP Gibbs JR Cookson MR Hernandez DG Singleton AB Farrer MJ Yu CE Golbe LI Revesz T Hardy J Lees AJ Devlin B Hakonarson H Müller U Schellenberg GD 《Nature genetics》2011,43(7):699-705
Progressive supranuclear palsy (PSP) is a movement disorder with prominent tau neuropathology. Brain diseases with abnormal tau deposits are called tauopathies, the most common of which is Alzheimer's disease. Environmental causes of tauopathies include repetitive head trauma associated with some sports. To identify common genetic variation contributing to risk for tauopathies, we carried out a genome-wide association study of 1,114 individuals with PSP (cases) and 3,247 controls (stage 1) followed by a second stage in which we genotyped 1,051 cases and 3,560 controls for the stage 1 SNPs that yielded P ≤ 10(-3). We found significant previously unidentified signals (P < 5 × 10(-8)) associated with PSP risk at STX6, EIF2AK3 and MOBP. We confirmed two independent variants in MAPT affecting risk for PSP, one of which influences MAPT brain expression. The genes implicated encode proteins for vesicle-membrane fusion at the Golgi-endosomal interface, for the endoplasmic reticulum unfolded protein response and for a myelin structural component. 相似文献
100.
McCarroll SA Kuruvilla FG Korn JM Cawley S Nemesh J Wysoker A Shapero MH de Bakker PI Maller JB Kirby A Elliott AL Parkin M Hubbell E Webster T Mei R Veitch J Collins PJ Handsaker R Lincoln S Nizzari M Blume J Jones KW Rava R Daly MJ Gabriel SB Altshuler D 《Nature genetics》2008,40(10):1166-1174
Dissecting the genetic basis of disease risk requires measuring all forms of genetic variation, including SNPs and copy number variants (CNVs), and is enabled by accurate maps of their locations, frequencies and population-genetic properties. We designed a hybrid genotyping array (Affymetrix SNP 6.0) to simultaneously measure 906,600 SNPs and copy number at 1.8 million genomic locations. By characterizing 270 HapMap samples, we developed a map of human CNV (at 2-kb breakpoint resolution) informed by integer genotypes for 1,320 copy number polymorphisms (CNPs) that segregate at an allele frequency >1%. More than 80% of the sequence in previously reported CNV regions fell outside our estimated CNV boundaries, indicating that large (>100 kb) CNVs affect much less of the genome than initially reported. Approximately 80% of observed copy number differences between pairs of individuals were due to common CNPs with an allele frequency >5%, and more than 99% derived from inheritance rather than new mutation. Most common, diallelic CNPs were in strong linkage disequilibrium with SNPs, and most low-frequency CNVs segregated on specific SNP haplotypes. 相似文献