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51.
Mohamed F. Abdel Rahman Ingy M. Hashad Khaled Abou-Aisha Sahar M. Abdel-Maksoud Mohamed Z. Gad 《Archives of Medical Science》2015,11(3):513-520
Introduction
The enzyme paraoxonase-1 (PON1) represents an endogenous defense mechanism against vascular oxidative stress, thereby contributing to the prevention of atherosclerosis. Several polymorphisms have been reported in the PON1 gene, including Q192R. PON1 phenotype is commonly expressed as the paraoxonase/arylesterase ratio (PON/ARE). The major aim of this study was to investigate the association between PON1 Q192R polymorphism, PON1 phenotypes and the incidence of early-onset acute myocardial infarction (AMI) in Egyptians.Material and methods
The study subjects consisted of 102 AMI patients and 72 age-matched healthy controls. Genotyping and enzyme activities were determined using PCR-RFLP and kinetic spectrophotometric assays, respectively.Results
The genotype distribution for the PON1 gene was significantly different between AMI patients (QQ = 38.24%, QR = 49.02%, RR = 12.75%) and controls (QQ = 66.67%, QR = 25%, RR = 8.33%). Allele frequencies were also significantly different between patients (Q = 62.75%, R = 37.25%) and controls (Q = 79.17%, R = 20.83%). The genotypes QR and RR showed higher risk for AMI compared to the homozygous QQ (odds ratio (OR) = 3.231, p < 0.001). The average PON/ARE ratio in MI patients (1.187 ±0.1) did not differ significantly from controls (1.118 ±0.26). However, it showed a significant difference among different genotypes in both AMI patients (QQ = 0.91 ±0.11, QR = 1.09 ±0.11 and RR = 2.65 ±0.4) (p = 0.0002) and controls (QQ = 0.68 ±0.1, QR = 1.07 ±0.11 and RR = 4.89 ±2.84) (p < 0.0001).Conclusions
PON1 192R allele represents an independent risk factor for early-onset AMI in Egyptians, and PON1 Q192R polymorphism modulates the paraoxonase phenotype. 相似文献52.
John R. Teerlink Beth A. Davison Gad Cotter Aldo P. Maggioni Naoki Sato Ovidiu Chioncel Georg Ertl G. Michael Felker Gerasimos Filippatos Barry H. Greenberg Peter S. Pang Piotr Ponikowski Christopher Edwards Stefanie Senger Sam L. Teichman Olav Wendelboe Nielsen Adriaan A. Voors Marco Metra 《European journal of heart failure》2020,22(2):315-329
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Nonanzit Pérez-Hernández Gilberto Vargas-Alarcón Rocio Arellano-Zapoteco Nancy Martínez-Rodríguez José Manuel Fragoso Gad Aptilon-Duque Rosalinda Posadas-Sánchez Carlos Posadas-Romero Teresa Juárez-Cedillo María Lilia Domínguez-López José Manuel Rodríguez-Pérez 《Experimental and molecular pathology》2014
The purpose of the present study was to establish the role of DDAH gene polymorphisms in the risk of developing myocardial infarction (MI) in a clinical cohort of Mexican patients. One polymorphism (rs1498373) in the DDAH1 and three in the DDAH2 (rs805304, rs3131383, and rs805305) genes were performed by TaqMan genotyping assays in 473 patients with MI and 447 healthy unrelated controls. Similar distribution of DDAH1 and DDAH2 polymorphisms was observed in MI patients and healthy controls. Under a recessive model adjusted for age, gender, and obesity, the rs805304 C allele was associated with decreased risk of MI (OR = 0.70, 95% CI = 0.51–0.96, P = 0.030). The effect of the polymorphisms on various cardiovascular risk factors was analyzed. Under a recessive model adjusted for age and gender, the DDAH2 rs805304 C allele was associated with decreased risk of obesity (OR = 0.35, 95% CI = 0.22–0.57, P = 0.001). The three DDAH2 polymorphisms were in strong linkage disequilibrium. Our results suggest that the rs805304 C allele was associated with decreased risk of MI and decreased risk of obesity. 相似文献
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H Greulich B Kaplan P Mertins TH Chen KE Tanaka CH Yun X Zhang SH Lee J Cho L Ambrogio R Liao M Imielinski S Banerji AH Berger MS Lawrence J Zhang NH Pho SR Walker W Winckler G Getz D Frank WC Hahn MJ Eck DR Mani JD Jaffe SA Carr KK Wong M Meyerson 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(36):14476-14481
We assessed somatic alleles of six receptor tyrosine kinase genes mutated in lung adenocarcinoma for oncogenic activity. Five of these genes failed to score in transformation assays; however, novel recurring extracellular domain mutations of the receptor tyrosine kinase gene ERBB2 were potently oncogenic. These ERBB2 extracellular domain mutants were activated by two distinct mechanisms, characterized by elevated C-terminal tail phosphorylation or by covalent dimerization mediated by intermolecular disulfide bond formation. These distinct mechanisms of receptor activation converged upon tyrosine phosphorylation of cellular proteins, impacting cell motility. Survival of Ba/F3 cells transformed to IL-3 independence by the ERBB2 extracellular domain mutants was abrogated by treatment with small-molecule inhibitors of ERBB2, raising the possibility that patients harboring such mutations could benefit from ERBB2-directed therapy. 相似文献
60.
Roee Admon Dmitry Leykin Gad Lubin Veronika Engert Julie Andrews Jens Pruessner Talma Hendler 《Human brain mapping》2013,34(11):2808-2816
Previous studies have shown that people who develop psychopathology such as posttraumatic stress disorder (PTSD) following stress exposure are characterized by reduced hippocampal (HC) volume and impaired HC functional connectivity with the ventromedial prefrontal cortex (vmPFC). Nevertheless, the exact interrelationship between reduced HC volume and HC‐vmPFC connectivity deficits in the context of stress has yet to be established. Furthermore, it is still not clear whether such neural abnormalities are stress induced or precursors for vulnerability. In this study, we combined measurements of MRI, functional MRI (fMRI), and diffusion tensor imaging (DTI) to prospectively study 33 a priori healthy Israeli soldiers both pre‐ and post‐exposure to stress during their military service. Thus, we were able to assess the contributions of structural and functional features of the HC and its connectivity to the onset and progression of maladaptive response to stress (i.e., increased PTSD symptoms post‐exposure). We found that soldiers with decreased HC volume following military service (i.e., post‐exposure) displayed more PTSD‐related symptoms post‐exposure as well as reduced HC‐vmPFC functional and structural connectivity post‐exposure, compared to soldiers with increased HC volume following military service. In contrast, initial smaller HC volume pre‐exposure did not have an effect on any of these factors. Our results therefore suggest that reduction in HC volume and connectivity with the vmPFC together mark a maladaptive response to stressful military service. As stress‐induced HC volume reductions were previously shown to be reversible, these localized biological markers may carry valuable therapeutic potential. Hum Brain Mapp 34:2808–2816, 2013. © 2012 Wiley Periodicals, Inc. 相似文献