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91.
92.
Anja Becher 《Scandinavian journal of gastroenterology》2013,48(6):645-653
Objective. The mortality associated with malignant complications of gastroesophageal reflux disease (GERD) is well recognized. The aim of this systematic review was to assess the less well-examined mortality associated with GERD and its non-malignant complications, including esophageal erosions, ulcers, bleeding, perforation and strictures. Material and methods. Studies reporting mortality in GERD and its non-malignant complications were identified via systematic PubMed searches, and previously unpublished population mortality statistics from public access databases. Results. Three countries were examined (USA, UK, Finland). Cohort studies (n=3) in the UK showed a 1.16- to 1.6-fold increase in risk of death in individuals with GERD compared with the general population, the majority of deaths being due to cardiac disease. Population data indicate that GERD and its likely esophageal complications were the cause of death in 685 and 521 cases, respectively, in the USA (year: 2003) (age-adjusted mortality: 2.3/million and 1.8/million, respectively), and in 36 and 349 cases, respectively, in England and Wales (2004) (0.6/million and 5.4/million, respectively). In Finland (2000), GERD-related mortality was 4.6/million. Mortality from GERD and its likely esophageal complications increased with age, and was between 1.2-fold and 1.8-fold higher in men than in women. Cohort studies in the USA are inconsistent on mortality risk associated with surgical therapy. Time-trend data suggest that mortality from GERD and its non-malignant complications has been increasing. Conclusions. Data from Europe and the USA show that GERD and its non-malignant complications can on rare occasions cause death. 相似文献
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96.
Xanthelasmas of the upper gastrointestinal tract 总被引:1,自引:0,他引:1
Gencosmanoglu R Sen-Oran E Kurtkaya-Yapicier O Tozun N 《Journal of gastroenterology》2004,39(3):215-219
Background Gastric xanthelasma is a benign and uncommon lesion with a variably reported frequency, while esophageal and duodenal xanthelasmas are quite rare.Methods Seventeen patients who had the diagnosis of xanthelasma in the upper gastrointestinal tract were analyzed retrospectively with respect to their demographic, clinical, endoscopic, and histopathologic features. All lesions suspected as xanthelasma were totally removed by either hot biopsy forceps or a snare with the technique of endoscopic mucosal resection.Results The incidence of upper gastrointestinal xanthelasmas in 7320 patients who had upper gastro-intestinal endoscopy was 0.23%. There were 9 (53%) men and 8 (47%) women, with a median age of 50 years (range, 24–80 years). The most common location of xanthelasmas was the stomach (76%), followed by the esophagus (12%) and duodenum (12%). All lesions were observed as yellow-white colored plaques at endoscopy. Multiple xanthelasmas were detected in 4 patients (24%); in the duodenum in 2, esophagus in 1, and stomach in 1. One patient had xanthelasma within a gastric hyperplastic polyp. The size of the lesion was less than 5mm in diameter in 14 (82%) patients and between 5 and 10mm in diameter in 3 (18%). Thirteen (76%) patients had moderate to severe atrophic gastritis, while the remainder had normal gastric mucosa.Conclusions Xanthelasmas of the upper gastrointestinal tract were mostly located in the stomach in the present series, which includes the second and third reported cases of duodenal xanthelasma, the second case of xanthelasma developed within a hyperplastic gastric polyp, and the fourth and the fifth cases of esophageal xanthelasma. 相似文献
97.
Gerold J. Wetscher MD Debasis Bagchi PhD Galen Perdikis MD Manashi Bagchi PhD Elizabeth J. Redmond FRCS Paul R. Hinder Dr. Karl Glaser MD Dr. Ronald A. Hinder MD PhD 《Digestive diseases and sciences》1995,40(4):853-858
Oxidative stress induced by nicotine was investigated in the esophageal mucosa of rats. The homogenized mucosa was incubated for 30 min with 50, 100, 200, 400, and 800 ng/mg protein/ml nicotine or with 200 ng/mg protein/ml nicotine for 15, 30, 45, and 60 min. Esophageal mucosa was also incubated for 30 min with 200 ng/mg protein/ml nicotine with or without the scavengers superoxide dismutase (SOD), catalase, SOD + catalase, inactivated SOD, inactivated catalase, or albumin. Incubation with 0.9% NaCl served as control. There was a strong correlation between chemiluminescence and the nicotine dose (r=0.75) or the nicotine incubation time (r=0.77). Thirty-minute incubation of the esophageal mucosa with 200 ng/mg protein/ml nicotine increased chemiluminescence 5.5-fold and lipid peroxidation 3.3-fold. This response was dampened by SOD or catalase and abolished by SOD + catalase. Inactivated enzymes or albumin had no scavenging effect. These results demonstrate that nicotine causes oxidative stress to the esophageal mucosa. 相似文献
98.
Barrett's食管的研究现状 总被引:1,自引:0,他引:1
黄颖秋 《世界华人消化杂志》2007,15(24):2567-2571
Barrett's食管是以食管下段逐步肠化及不典型增生为主要特征的食管腺癌癌前状态.本文系统阐述了Barrett's食管定义、发病机制、诊断方法、环氧化酶2(COX-2)等癌基因治疗及内镜下激光、黏膜下切除、光动力治疗等最新进展,为Barrett's食管发病机制的揭示、早期诊断、根治性治疗以及食管腺癌的预防提供了新的思路. 相似文献
99.
Loss of heterozygosity on chromosome 17p predicts neoplastic progression in Barrett's esophagus 总被引:2,自引:0,他引:2
Dolan K Morris AI Gosney JR Field JK Sutton R 《Journal of gastroenterology and hepatology》2003,18(6):683-689
BACKGROUND AND AIM: Endoscopic surveillance for adenocarcinoma in patients with Barrett's esophagus is costly, with one cancer detected every 48-441 patient years of follow up. Genetic abnormalities, including loss of heterozygosity at sites of tumor suppressor genes, have been detected in malignant and premalignant Barrett's esophagus. The aim of this prospective study was to determine if loss of heterozygosity analysis could identify patients with Barrett's esophagus at greatest risk of adenocarcinoma, for whom endoscopic surveillance is most appropriate. METHODS: Loss of heterozygosity analysis was performed on endoscopic biopsies from 48 patients as part of a Barrett's surveillance program using 14 microsatellite markers shown previously to detect loss of heterozygosity in more than 30% of esophageal adenocarcinomas. Patients were followed up endoscopically for a median of 5 years. RESULTS: Loss of heterozygosity was detected in nine patients. Three patients with loss of heterozygosity on chromosome 5q or 9p did not progress beyond metaplasia. Loss of heterozygosity at 17p11.1-p13 was detected in six patients, all of whom demonstrated dysplasia and/or carcinoma during follow up (four low-grade dysplasia, one high-grade dysplasia and one adenocarcinoma). CONCLUSION: Loss of heterozygosity at 17p11.1-p13 on chromosome 17p identifies patients with Barrett's esophagus at risk of neoplastic progression and can supplement histology in determining the frequency of endoscopy during surveillance. 相似文献
100.
Malignant degeneration of Barrett''s esophagus: the role of the Ki-67 proliferation fraction, expression of E-cadherin and p53 总被引:5,自引:0,他引:5
Barrett's columnar epithelium with dysplasia is the most important risk factor for adenocarcinoma of the distal esophagus. The molecular mechanisms responsible for progression of columnar metaplasia to dysplasia and invasive carcinoma are mostly unknown. We investigated expression of the tumor suppressor gene p53, E-cadherin expression and cell proliferation in the metaplasia-dysplasia-carcinoma sequence of esophageal adenocarcinoma. In 24 patients with R0-resected adenocarcinomas of the distal esophagus we evaluated the expression of E-cadherin (antibody HECD-1), mutated p53 (antibody DO1) and cell proliferation (antibody MiB1) by immunohistochemistry in sections of adenocarcinoma, columnar metaplasia, with and without dysplasia, and in squamous epithelium of the esophagus. No p53 immunoreactivity was seen in sections of normal squamous epithelium or columnar metaplasia. Fifty per cent of invasive adenocarcinomas stained positive for mutated p53. The p53 expression correlated with the T-category (P = 0.048) and the N-category (P = 0.024). There was a significant decrease in the expression of E-cadherin from columnar metaplasia to dysplasia and to esophageal adenocarcinoma (P < 0.0001). Expression of E-cadherin in columnar metaplasia without dysplasia was similar to that seen in normal squamous epithelium of the esophagus. The Ki-67 proliferation fraction increased significantly from normal squamous epithelium to columnar metaplasia to dysplasia and to invasive carcinoma (P < 0.001), with a marked expansion of the proliferative component. There was no correlation between cell proliferation, E-cadherin expression and the tumor stage. In contrast to the alterations in the p53 expression, a decreased E-cadherin expression and the expansion of the proliferative component represent an early phenomenon in the malignant degeneration of Barrett's esophagus. This might aid in the early detection of esophageal adenocarcinoma. 相似文献