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991.
R J Santen E Samojlik S A Wells 《The Journal of clinical endocrinology and metabolism》1980,51(3):473-477
Aminoglutethimide (AG) is a potent inhibitor of aromatization in placental microsomes and in peripheral tissues in postmenopausal women. Aromatase inhibitors have been used to block estrogen production and induce breast tumor regression in rodents. To inhibit ovarian estrogen production, we administered various doses of AG and its highly potent D-stereoisomer to premenopausal women with breast carcinoma. However, at no dose level did AG consistently lower estrone and estradiol concentrations in plasma below those observed in normal menstruating women. Uniform increments in LH and FSH were also not observed. Only during the luteal phase were the levels of estradiol (but not estrone) significantly suppressed. These observations are best explained by the possibility that aromatase enzymes in the ovary, as opposed to those in the placenta and in peripheral tissues, are partially resistant to the effects of AG. 相似文献
992.
993.
Beaton DE Bombardier C Katz JN Wright JG Wells G Boers M Strand V Shea B 《The Journal of rheumatology》2001,28(2):400-405
The purpose of this paper is to describe a classification system for studies of responsiveness that was designed to help organize these studies, and identify those with the potential to provide information on minimal clinically important difference (MCID). We developed a 3 dimensional cube into which studies of responsiveness can be categorized based on their evaluation of 3 attributes: 1. individual or group setting; 2. which scores are contrasted; and 3. the type of change or difference being assessed. We present and discuss examples of studies that fit into categories in the classification cube. This classification system helps to focus attention on whether the literature is able to provide information on the specific type of change a person is interested in. It reinforces that the ability of an instrument to detect a certain category of discrimination within the cube does not mean it will necessarily be responsive to another category. The cube has been shown here as a means to separate out studies that address important change. These studies can then be examined as the source of information on MCID. 相似文献
994.
D Grady B Halloran S Cummings S Leveille L Wells D Black N Byl 《The Journal of clinical endocrinology and metabolism》1991,73(5):1111-1117
An unexplained loss of muscle strength occurs with aging. Vitamin D deficiency can cause myopathy and administration of 1,25-dihydroxyvitamin D3 [1,25-(OH2)D3] to persons with low serum concentrations can improve strength. To test the hypothesis that the weakness associated with aging is in part due to inadequate serum concentrations of [1,25-(OH2)D3], we conducted a randomized, controlled, double blinded trial in 98 men and women volunteers over 69 yr old. Treatment consisted of 0.25 micrograms 1,25-(OH)2D3, orally, twice per day or identical placebo for 6 months. Leg muscle strength of the quadriceps was measured with an isokinetic dynamometer. There was no difference between the two groups at 1 week, 1 month, or 6 months of treatment in any of the measures of muscle strength. We conclude that oral administration of 0.5 micrograms 1,25-(OH)2D3/day does not improve muscle strength in older persons. Further research is needed to determine the etiology of the decline in muscle strength associated with aging. 相似文献
995.
Hemoglobin Brisbane is a new hemoglobin variant which produces a mile erythrocytosis. It is not detectable by electrophoresis at pH 8.6 or by isoelectric focusing but it is mildly unstable and gives a positive result with standard stability tests. The new hemoglobin has increased oxygen affinity and reduced co-operativity with a normal Bohr effect and 2,3-DPG binding. Structural analysis shows that a histidine residue has replaced the leucine normally found at position beta 68 (E12). 相似文献
996.
Norihiko Kamioka John Wells Patricia Keegan Stamatios Lerakis Jose Binongo Frank Corrigan Jose Condado Ateet Patel Jessica Forcillo Leslie Ogburn Andy Dong Hope Caughron Amy Simone Bradley Leshnower Chandan Devireddy Kreton Mavromatis Robert Guyton James Stewart Vasilis Babaliaros 《JACC: Cardiovascular Interventions》2018,11(2):107-115
Objectives
This study sought to investigate predictors and safety of next-day discharge (NDD) after transcatheter aortic valve replacement (TAVR).Background
Information about predictors and safety of NDD after TAVR is limited.Methods
The study reviewed 663 consecutive patients who underwent elective balloon-expandable TAVR (from July 2014 to July 2016) at our institution. We first determined predictors of NDD in patients who underwent minimalist transfemoral TAVR. After excluding cases with complications, we compared 30-day and 1-year outcomes between NDD patients and those with longer hospital stay using Cox regression adjusting for the Predicted Risk of Mortality provided by the Society of Thoracic Surgeons. The primary endpoint was the composite of mortality and readmission at 1 year.Results
A total of 150 patients had NDD after TAVR and 210 patients had non-NDD. Mean age and the Society of Thoracic Surgeons Predicted Risk of Mortality were 80.7 ± 8.8 years and 6.6 ± 3.7%, respectively. Predictors of NDD were male sex (odds ratio [OR]: 2.02; 95% confidence interval [CI]: 1.28 to 3.18), absence of atrial fibrillation (OR: 1.62; 95% CI: 1.02 to 2.57), serum creatinine (OR: 0.71; 95% CI: 0.55 to 0.92), and age (OR: 0.95; 95% CI: 0.93 to 0.98). As expected, 84% of patients with complications had non-NDD. After excluding cases with complications, there was no difference in hazard rates of the 30-day composite outcome between NDD and non-NDD (hazard ratio: 0.62; 95% CI: 0.20 to 1.91), but the hazard of the composite outcome at 1 year was significantly lower in the NDD group (hazard ratio: 0.47; 95% CI: 0.27 to 0.81). This difference in the composite outcome can be explained by the lower hazard of noncardiovascular related readmission in the NDD group.Conclusions
Factors predicting NDD include male sex, absence of atrial fibrillation, lower serum creatinine, and younger age. When compared with patients without complications with a longer hospital stay, NDD appears to be safe, achieving similar 30-day and superior 1-year clinical outcomes. 相似文献997.
Sato H Lagan AL Alexopoulou C Vassilakis DA Ahmad T Pantelidis P Veeraraghavan S Renzoni E Denton C Black C Wells AU du Bois RM Welsh KI 《Arthritis and rheumatism》2004,50(2):558-564
OBJECTIVE: Scleroderma is characterized by the presence of 3 predominant, yet almost mutually exclusive, antibodies: anticentromere antibody (ACA), antitopoisomerase antibody, and anti-RNA polymerase antibody. The purpose of this study was to investigate tumor necrosis factor (TNF) polymorphisms in scleroderma, with the specific aim of determining whether TNF polymorphisms would prove to be stronger markers for ACA than class II major histocompatibility complex (MHC). METHODS: We studied 214 UK white scleroderma patients and 354 healthy controls. All subjects were investigated for 5 TNF promoter region polymorphisms by sequence-specific polymerase chain reaction. RESULTS: We showed that an NF-kappaB binding site polymorphism (known to be functionally relevant) in the TNF promoter region was present in 51.8% of patients with ACA and 16.3% of patients without ACA (chi(2) = 25.1, P = 0.000004 [corrected P = 0.00002]). Using haplotype mapping, we showed that this was a primary TNF association that could explain the previous weak links between ACA production and class II MHC alleles. In marked contrast to our ACA results, HLA class II (especially DRB1*11) appeared to be primary in that it could explain the weaker TNF association with antitopoisomerase production. Further, we observed a separate TNF haplotype to be associated with scleroderma per se, although the level of significance was much lower (chi(2) = 8.7, P = 0.003 [corrected P = 0.02]). CONCLUSION: We believe these findings may have importance both for the directional pathogenesis of scleroderma progression and for the treatment of scleroderma with anti-TNF agents. 相似文献
998.
Activation of MAP kinase-activated protein kinase 2 in human neutrophils after phorbol ester or fMLP peptide stimulation 总被引:3,自引:0,他引:3
In response to extracellular stimulation, one of the earliest events in human neutrophils is protein phosphorylation, which mediates signal transduction and leads to the regulation of cellular functions. Mitogen- activated protein (MAP) kinases are rapidly activated by a variety of mitogens, cytokines, and stresses. The activated MAP kinases in turn regulate their substrate molecules by phosphorylation. MAP kinase- activated protein (MAPKAP) kinase 2, a Ser/Thr kinase, has been shown to be phosphorylated by p38 MAP kinase both in vivo and in vitro. Phosphorylation of the Thr-334 site of MAPKAP kinase 2 results in a conformational change with subsequent activation of the enzyme. To better define the role of MAPKAP kinase 2 in the activation of human neutrophils, its enzymatic activity was measured after stimulation by either a phorbol ester (phorbol myristate acetate [PMA]), a potent protein kinase C activator, or the tripeptide fMLP, which is a chemotactic factor. The in vitro kinase assays indicate that both PMA and fMLP stimulated a transient increase in the enzymatic activity of cellular MAPKAP kinase 2. The induced kinase activation was concentration-dependent and reached a maximum at 5 minutes for PMA and 1 minute for fMLP. To identify potential substrate molecules for MAPKAP kinase 2, a highly active kinase mutant was generated by mutating the MAP kinase phosphorylation site in the C-terminal region. The replacement of threonine 334 with alanine resulted in a marked augmentation of catalytic activity. Analysis of in vitro protein phosphorylation in the presence of the active kinase indicates that a 60-kD cytosolic protein (p60) was markedly phosphorylated and served as the major substrate for MAPKAP kinase 2 in human neutrophils. Based on the MAPKAP kinase 2 phosphorylation site of Hsp27, a competitive inhibitory peptide was synthesized. This competitive inhibitory peptide specifically inhibited MAPKAP kinase 2 enzymatic activity, as well as the in vitro and in vivo kinase-induced p60 phosphorylation. To assess the contribution of MAPKAP kinase 2 in neutrophil function, the oxidative burst response after manipulation of endogenous kinase activity was measured. Intracellular delivery of the competitive inhibitory peptide into human neutrophils reduced both PMA- and fMLP- stimulated superoxide anion production. Thus, the results strongly suggest that MAPKAP kinase 2 is involved in the activation of human neutrophils. 相似文献
999.
1000.