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71.
M.V. Lind L. Lauritzen H. Vestergaard T. Hansen O. Pedersen M. Kristensen A.B. Ross 《Nutrition, metabolism, and cardiovascular diseases : NMCD》2018,28(4):402-410
Background and aims
Alterations to one-carbon metabolism, especially elevated plasma homocysteine (Hcy), have been suggested to be both a cause and a consequence of the metabolic syndrome (MS). A deeper understanding of the role of other one-carbon metabolites in MS, including s-adenosylmethionine (SAM), s-adenosylhomocysteine (SAH), and the methylation capacity index (SAM:SAH ratio) is required.Methods and results
118 men and women with MS-risk factors were included in this cross-sectional study and cardiometabolic outcomes along with markers of one-carbon metabolism, including fasting plasma SAM, SAH, Hcy and vitamin B12 concentrations, were analysed. Multiple linear regression models were also used to examine the association between plasma one-carbon metabolites and cardiometabolic health features.We found that fasting plasma concentrations of Hcy, SAM and SAH were all positively correlated with markers of adiposity, including BMI (increase in BMI per 1-SD increase in one-carbon metabolite: 0.92 kg/m2 95% CI (0.28; 1.56), p = 0.005; 0.81 (0.15; 1.47), p = 0.02; 0.67 (?0.01; 1.36), p = 0.05, respectively). Hcy, but not SAM, SAH or SAM:SAH ratio was associated with BMI and body fat percentage after mutual adjustments. SAM concentrations were associated with higher fasting insulin (9.5% 95% CI (0.3; 19.5) per SD increase in SAM, p = 0.04), HOMA-IR (10.8% (0.8; 21.9), p = 0.03) and TNF-α (11.8% (5.0; 19.0), p < 0.001).Conclusion
We found little evidence for associations between SAM:SAH ratio and cardiometabolic variables, but higher plasma concentrations of SAM, SAH and Hcy are related to an overall higher risk of metabolic dysfunctions.The studies were registered at www.clinicaltrials.gov (NCT01719913 & NCT01731366). 相似文献72.
Dr. Doris H. B. Palvio M.D. Erik Steen Kristensen M.D. Erling Falk M.D. 《Diseases of the colon and rectum》1985,28(10):746-748
A case of a carcinoid tumor arising in a Meckel's diverticulum is reported. By the time of detection, the tumor had spread
to the mesentery causing ischemia of the small intestine due to the associated vascular elastosis. 相似文献
73.
I. H. Lambert D. M. Kristensen J. B. Holm O. H. Mortensen 《Acta physiologica (Oxford, England)》2015,213(1):191-212
Taurine is often referred to as a semi‐essential amino acid as newborn mammals have a limited ability to synthesize taurine and have to rely on dietary supply. Taurine is not thought to be incorporated into proteins as no aminoacyl tRNA synthetase has yet been identified and is not oxidized in mammalian cells. However, taurine contributes significantly to the cellular pool of organic osmolytes and has accordingly been acknowledged for its role in cell volume restoration following osmotic perturbation. This review describes taurine homeostasis in cells and organelles with emphasis on taurine biophysics/membrane dynamics, regulation of transport proteins involved in active taurine uptake and passive taurine release as well as physiological processes, for example, development, lung function, mitochondrial function, antioxidative defence and apoptosis which seem to be affected by a shift in the expression of the taurine transporters and/or the cellular taurine content. 相似文献
74.
75.
Bach A Clausen BH Møller M Vestergaard B Chi CN Round A Sørensen PL Nissen KB Kastrup JS Gajhede M Jemth P Kristensen AS Lundström P Lambertsen KL Strømgaard K 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(9):3317-3322
Inhibition of the ternary protein complex of the synaptic scaffolding protein postsynaptic density protein-95 (PSD-95), neuronal nitric oxide synthase (nNOS), and the N-methyl-D-aspartate (NMDA) receptor is a potential strategy for treating ischemic brain damage, but high-affinity inhibitors are lacking. Here we report the design and synthesis of a novel dimeric inhibitor, Tat-NPEG4(IETDV)(2) (Tat-N-dimer), which binds the tandem PDZ1-2 domain of PSD-95 with an unprecedented high affinity of 4.6 nM, and displays extensive protease-resistance as evaluated in vitro by stability-measurements in human blood plasma. X-ray crystallography, NMR, and small-angle X-ray scattering (SAXS) deduced a true bivalent interaction between dimeric inhibitor and PDZ1-2, and also provided a dynamic model of the conformational changes of PDZ1-2 induced by the dimeric inhibitor. A single intravenous injection of Tat-N-dimer (3 nmol/g) to mice subjected to focal cerebral ischemia reduces infarct volume with 40% and restores motor functions. Thus, Tat-N-dimer is a highly efficacious neuroprotective agent with therapeutic potential in stroke. 相似文献
76.
Kristensen T Broesby-Olsen S Vestergaard H Bindslev-Jensen C Møller MB;Mastocytosis Centre Odense University Hospital 《European journal of haematology》2012,89(1):42-46
It is presently accepted that the KIT D816V mutation is detectable in tissues with neoplastic mast cells in most patients with indolent systemic mastocytosis. In this study, neoplastic mast cells were detected in bone marrow, but not in peripheral blood, by flow cytometry in all 25 included cases of indolent systemic mastocytosis. However, the KIT D816V mutation was detected using mutation-specific qPCR in both bone marrow and peripheral blood in all 25 cases, demonstrating for the first time that the KIT D816V mutation is consistently present in non-mast cells in indolent systemic mastocytosis and that these cells are circulating in peripheral blood. 相似文献
77.
78.
79.
80.
Jens Kristensen Michael Maeng Ulrik Markus Mortensen Jette Berg Michael Rehling Torsten Toftegaard Nielsen 《Scandinavian cardiovascular journal : SCJ》2013,47(1-2):115-120
Objective Previous experimental studies indicate that glutamine or glutamate may provide cardioprotection by improving the oxidative metabolism in myocardial ischemia. We investigated the effect of glutamine or glutamate, given during reperfusion, on resulting infarct size and hemodynamic recovery. Design A porcine coronary occlusion model was applied. Infusions were initiated 15 min before reperfusion and supplemented with intracoronary bolus doses at reperfusion. The primary outcome measure was infarct size in relation to area at risk determined by a standard tissue staining procedure. Secondary outcome measures were the hemodynamic variables. Results The infarct sizes as a proportion of the area at risk (mean±SD) were: control group, 0.64±0.19 (n=9); glutamine group, 0.87±0.07 (p<0.05 vs control group) (n=8); glutamate group, 0.72±0.11 (n=9). Glutamine increased systemic vascular resistance, while glutamate preserved cardiac output during infusion. Conclusion Substrate supplementation with the anaplerotic precursors glutamine and glutamate is ineffective as adjunctive therapy for severe myocardial ischemia. Beneficial effects documented in less complex experimental systems could not be transferred to a more pathophysiological relevant model. 相似文献