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Aim
To compare the evaluation of retinographies by a teleophthalmology nurse and primary care physicians (PCP) with an ophthalmologist referral hospital (gold standard).Methods
Cross-sectional study on a random sample of 337 patients on the teleophthalmology programme from January 2010 to January 2015. We analyzed the diagnostic evaluation (whether or not it presented findings of RD) and the therapeutic assessment (whether or not referral to the opthalmology department was needed) which were conducted independently on the sample retinographies by the PCP, a nurse and an ophthalmologist (gold standard). Reliability and concordance between the gold standard and the PCP and the nurse were checked and the statistical analyses were supported using SPSSv.23.00 software and diagnostic test reliability calculators (EPIDAT 4.1).Results
In the diagnosis of RD, the nurse presented: sensitivity (S): 0.96; specificity (Sp): 0.89; PPV: 0.58; NPV: 0.99; Kappa index: 0.67 and PCP: S: 0.98; Sp: 0.99; PPV: 0.96; NPV: 0.99; Kappa index: 0.96.In the referral to ophthalmology assessed by the nurse: S: 0.83; Sp: 0.83; PPV: 0.51; NPV: 0.96; Kappa Index: 0.53 and PCP: S: 0.62; Sp: 0.76; PPV: 0.36; NPV: 0.90; Kappa index: 0.29.Conclusions
A nursing teleophthalmology programme could perform population screening for RD with the same quality as PCP. This would increase coverage, in addition to providing better use of resources by avoiding intermediate patient appointments through PCP and increased health savings. 相似文献![点击此处可从《Journal of thrombosis and haemostasis》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Essentials
- Eisenmenger syndrome is characterised by thrombotic and hemorrhagic risks of unclear aetiology.
- Calibrated automated thrombography was used to assess these coagulation derangements.
- Platelet activity supported abnormalities in procoagulant and anticoagulant pathway function.
- Endothelin‐1 antagonism appeared to ameliorate these derangements.
Summary
Aims
The mechanisms underlying the competing thrombotic and hemorrhagic risks in Eisenmenger syndrome are poorly understood. We aimed to characterize derangements of blood coagulation and to assess the effect of dual endothelin‐1 receptor antagonism in modulating hemostasis in this rare disorder.Methods
In a 10‐month recruitment period at a tertiary cardiology referral center, during which time there were over 14 000 outpatient consultations, consecutive subjects with Eisenmenger syndrome being considered for macitentan therapy (n = 9) and healthy volunteers (n = 9) were recruited. Plasma thrombin generation in platelet‐rich and platelet‐poor plasma was assessed by calibrated automated thrombography prior to and following therapy.Results
Median peak plasma thrombin generation was higher in platelet‐rich plasma obtained from Eisenmenger syndrome subjects relative to controls (median peak thrombin [25th–75th percentile]: 228.3 [206.5–258.6] nm vs. 169.9 [164.3–215.8] nm ), suggesting a critical mechanistic role for platelets in supporting abnormal hypercoagulability in Eisenmenger syndrome. Abnormal enhanced sensitivity to the anticoagulant activity of activated protein C was also observed in platelet‐rich plasma in Eisenmenger syndrome, suggesting that derangements of platelet activity may influence the activity of anticoagulant pathways in a manner that might promote bleeding in this disease state. Following 6 months of macitentan therapy, attenuations in the derangements in both procoagulant and anticoagulant pathways were observed.Conclusions
Abnormal platelet activity contributes to derangements in procoagulant and anticoagulant pathways in Eisenmenger syndrome. Therapies targeting the underlying vascular pathology appear to ameliorate these derangements and may represent a novel strategy for the management of the competing prothrombotic and hemorrhagic tendencies in this disorder.![点击此处可从《International journal of clinical practice》网站下载免费的PDF全文](/ch/ext_images/free.gif)
![点击此处可从《Family relations》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Introduction
The prevalence of Barrett's esophagus has been calculated at between 1.3 and 1.6%. There is little information with respect to this in Mexico.Aim
To determine the frequency and characteristics of Barrett's esophagus in patients that underwent endoscopy at a national referral center, within a 10-year time frame.Material and methods
The databases of the pathology and gastrointestinal endoscopy departments of the Instituto Nacional de Ciencias Médicas y Nutrición “Salvador Zubirán” were analyzed, covering the period of January 2002 to December 2012. Patients with a histologic diagnosis of Barrett's esophagus were included. The variables of age, sex, the presence of dysplasia/esophageal adenocarcinoma, Barrett's esophagus length, and follow-up were analyzed.Results
Of 43,639 upper gastrointestinal endoscopies performed, 420 revealed Barrett's esophagus, corresponding to a frequency of 9.6 patients for every 1,000 endoscopies. Of those patients, 66.9% (n = 281) were men, mean patient age ± SD was 57.2 ± 15.3 years, 223 patients (53%) presented with long-segment Barrett's esophagus, and 197 (47%) with short-segment Barrett's esophagus. Dysplasia was not present in 339 patients (80.7%). Eighty-one (19.3%) patients had some grade of dysplasia or cancer: 48/420 (11.42%) presented with low-grade dysplasia, 20/420 (4.76%) with high-grade dysplasia, and 13/420 (3.1%) were diagnosed with esophageal cancer arising from Barrett's esophagus. Mean follow-up time was 5.6 years.Conclusions
The frequency of Barrett's esophagus was 9.6 cases for every 1,000 upper gastrointestinal endoscopies performed. Dysplasia was not documented in the majority of the patients with Barrett's esophagus and they had no histopathologic changes during follow-up. A total of 19.3% of the patients presented with dysplasia or cancer. 相似文献Areas covered: Multiple cells, molecules, and genes interplay with early life environmental factors in the pathophysiology of EoE to converge in the esophageal epithelium at the center of disease pathogenesis. Epithelial cells constitute a mayor cytokine source for TSLP and Calpain-14; an impaired epithelial barrier function allowing penetration of food and microbiota-derived antigens is involved in triggering and maintaining inflammation. Eosinophil and mast cell-derived products, including TGFβ, together with IL-1β and TNFα, promote epithelial mesenchymal transition in EoE, contributing to tissue remodeling by synthetizing and depositing extracellular matrix in subepithelial layers. This article aims to provide a state-of-the-art update on the pathophysiology of EoE applied to clinical practice, and latest research and developments with potential interest to improve the diagnosis and treatment of patients with EoE are revised.
Expert commentary: Preliminary approaches have provided promising results toward incorporating minimally invasive methods for patient diagnosis and monitoring in clinical practice. Early diagnosis and optimized therapies will allow for personalized medicine in EoE. 相似文献