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María Teruel Jose-Ezequiel Martin Carlos González-Juanatey Raquel López-Mejias Jose A Miranda-Filloy Ricardo Blanco Alejandro Balsa Dora Pascual-Salcedo Luis Rodriguez-Rodriguez Benjamin Fernández-Gutierrez Ana M Ortiz Isidoro González-Alvaro Carmen Gómez-Vaquero Nunzio Bottini Javier Llorca Miguel A González-Gay Javier Martin 《Arthritis research & therapy》2011,13(4):R116-6
Introduction
Acid phosphatase locus 1 (ACP1) encodes a low molecular weight phosphotyrosine phosphatase implicated in a number of different biological functions in the cell. The aim of this study was to determine the contribution of ACP1 polymorphisms to susceptibility to rheumatoid arthritis (RA), as well as the potential contribution of these polymorphisms to the increased risk of cardiovascular disease (CV) observed in RA patients.Methods
A set of 1,603 Spanish RA patients and 1,877 healthy controls were included in the study. Information related to the presence/absence of CV events was obtained from 1,284 of these participants. All individuals were genotyped for four ACP1 single-nucleotide polymorphisms (SNPs), rs10167992, rs11553742, rs7576247, and rs3828329, using a predesigned TaqMan SNP genotyping assay. Classical ACP1 alleles (*A, *B and *C) were imputed with SNP data.Results
No association between ACP1 gene polymorphisms and susceptibility to RA was observed. However, when RA patients were stratified according to the presence or absence of CV events, an association between rs11553742*T and CV events was found (P = 0.012, odds ratio (OR) = 2.62 (1.24 to 5.53)). Likewise, the ACP1*C allele showed evidence of association with CV events in patients with RA (P = 0.024, OR = 2.43).Conclusions
Our data show that the ACP1*C allele influences the risk of CV events in patients with RA. 相似文献104.
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Mercedes García-Bermúdez Raquel López-Mejías Carlos González-Juanatey Alfonso Corrales Gema Robledo Santos Casta?eda José A. Miranda-Filloy Ricardo Blanco Benjamín Fernández-Gutiérrez Alejandro Balsa Isidoro González-Alvaro Carmen Gómez-Vaquero Javier Llorca Javier Martín Miguel A. González-Gay 《PloS one》2012,7(10)
Objective
Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with increased cardiovascular (CV) morbidity and mortality. Since interferon-gamma (IFN-γ) has a direct effect on inflammation, in this study we assessed the potential association of the IFNG functional gene variant rs2430561 with CV disease in patients with RA.Methods
One thousand six hundred and thirty-five patients fulfilling the 1987 American College of Rheumatology classification criteria for RA were genotyped for the IFNG (rs2430561, +874T/A) gene polymorphism using TaqMan genotyping assay. Patients were stratified according to the presence of CV events or not. Logistic regression models to explain the presence of CV disease according to the IFNG rs2430561 allele distribution were performed. The potential influence of this variant in the development of subclinical atherosclerosis was also analyzed in a subgroup of patients with no history of CV events to determine carotid artery intima-media thickness (IMT) (n = 286) and presence of carotid plaques. Levels of the cytokine were determined in a subgroup of patients by ELISA.Results
Adjusted logistic regression model disclosed that presence of the minor allele A was not associated with increased risk of suffering CV events in RA patients. Besides, differences did not achieve statistical significance regarding carotid IMT and presence of carotid plaques in RA patients carrying IFNG rs2430561 variant allele. Levels of IFN-γ were higher in patients who had suffered CV events compared to patients who did not.Conclusion
Our results do not support a role of IFNG rs2430561 (+874T/A) functional gene variant in the development of CV disease in RA patients. 相似文献107.
Francesca Di Nunzio Anne Danckaert Thomas Fricke Patricio Perez Juliette Fernandez Emmanuelle Perret Pascal Roux Spencer Shorte Pierre Charneau Felipe Diaz-Griffero Nathalie J. Arhel 《PloS one》2012,7(9)
The nuclear pore complex (NPC) mediates nucleo-cytoplasmic transport of macromolecules and is an obligatory point of passage and functional bottleneck in the replication of some viruses. The Human Immunodeficiency Virus (HIV) has evolved the required mechanisms for active nuclear import of its genome through the NPC. However the mechanisms by which the NPC allows or even assists HIV translocation are still unknown. We investigated the involvement of four key nucleoporins in HIV-1 docking, translocation, and integration: Nup358/RanBP2, Nup214/CAN, Nup98 and Nup153. Although all induce defects in infectivity when depleted, only Nup153 actually showed any evidence of participating in HIV-1 translocation through the nuclear pore. We show that Nup358/RanBP2 mediates docking of HIV-1 cores on NPC cytoplasmic filaments by interacting with the cores and that the C-terminus of Nup358/RanBP2 comprising a cyclophilin-homology domain contributes to binding. We also show that Nup214/CAN and Nup98 play no role in HIV-1 nuclear import per se: Nup214/CAN plays an indirect role in infectivity read-outs through its effect on mRNA export, while the reduction of expression of Nup98 shows a slight reduction in proviral integration. Our work shows the involvement of nucleoporins in diverse and functionally separable steps of HIV infection and nuclear import. 相似文献
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Customized Treatment in Non-Small-Cell Lung Cancer Based on EGFR Mutations and BRCA1 mRNA Expression
Rafael Rosell Laia Perez-Roca Jose Javier Sanchez Manuel Cobo Teresa Moran Imane Chaib Mariano Provencio Manuel Domine Maria Angeles Sala Ulpiano Jimenez Pilar Diz Isidoro Barneto Jose Antonio Macias Ramon de las Pe?as Silvia Catot Dolores Isla Jose Miguel Sanchez Rafael Ibeas Guillermo Lopez-Vivanco Juana Oramas Pedro Mendez Noemi Reguart Remei Blanco Miquel Taron 《PloS one》2009,4(5)