全文获取类型
收费全文 | 518篇 |
免费 | 29篇 |
国内免费 | 22篇 |
专业分类
耳鼻咽喉 | 1篇 |
儿科学 | 54篇 |
基础医学 | 63篇 |
口腔科学 | 13篇 |
临床医学 | 82篇 |
内科学 | 112篇 |
皮肤病学 | 13篇 |
神经病学 | 30篇 |
特种医学 | 108篇 |
外科学 | 27篇 |
综合类 | 7篇 |
预防医学 | 18篇 |
药学 | 29篇 |
肿瘤学 | 12篇 |
出版年
2021年 | 2篇 |
2019年 | 5篇 |
2018年 | 3篇 |
2017年 | 3篇 |
2016年 | 4篇 |
2015年 | 5篇 |
2014年 | 10篇 |
2013年 | 21篇 |
2012年 | 9篇 |
2011年 | 16篇 |
2010年 | 25篇 |
2009年 | 16篇 |
2008年 | 12篇 |
2007年 | 29篇 |
2006年 | 11篇 |
2005年 | 13篇 |
2004年 | 4篇 |
2003年 | 6篇 |
2002年 | 5篇 |
2001年 | 8篇 |
2000年 | 7篇 |
1999年 | 14篇 |
1998年 | 40篇 |
1997年 | 42篇 |
1996年 | 36篇 |
1995年 | 17篇 |
1994年 | 25篇 |
1993年 | 16篇 |
1992年 | 14篇 |
1991年 | 8篇 |
1990年 | 9篇 |
1989年 | 10篇 |
1988年 | 27篇 |
1987年 | 11篇 |
1986年 | 8篇 |
1985年 | 7篇 |
1984年 | 10篇 |
1983年 | 8篇 |
1982年 | 14篇 |
1981年 | 9篇 |
1980年 | 6篇 |
1978年 | 3篇 |
1977年 | 5篇 |
1976年 | 4篇 |
1975年 | 2篇 |
1954年 | 2篇 |
1952年 | 1篇 |
1948年 | 1篇 |
1947年 | 1篇 |
1943年 | 1篇 |
排序方式: 共有569条查询结果,搜索用时 15 毫秒
71.
Many questions about analgesic nephropathy (AN) lack clear-cut answers. We present available evidence for and against proposed answers to many of these questions. These include: (1) Is acetaminophen (AC) nephrotoxic when taken as the sole analgesic? (2) Is the combination of acetylsalicylic acid (ASA) and AC more nephrotoxic than AC taken alone, and if so, why? (3) What are the minimum doses and durations of ingestion required to produce analgesic nephrotoxicity? (4) Is the combination of ASA and AC (a major metabolite of phenacetin) less nephrotoxic than that of phenacetin and ASA combined? (5) Does caffeine in combination with analgesics contribute to nephrotoxicity? (6) What is the incidence of end-stage renal disease (ESRD) due to AN? (7) What uniform diagnostic criteria should be established for AN? (8) What are the earliest anatomic and biochemical abnormalities? (9) What are the mechanisms of renal injury? (10) Does AC cause uroepithelial neoplasia? (11) What research might be most beneficial? Based mainly on associations, some strong, we suggest that AN still exists as a cause of ESRD in the United States, where AC/ASA combinations are available over the counter, and in Canada, where they are not. We also suggest that the evidence needed to recommend that the AC/ASA combination be excluded from over-the-counter analgesic preparations still has limitations. A prospective multicenter study comparing incidence related to AC/ASA in the United States and to AC in Canada and the United States may be needed to answer this question. For such a study to be worthwhile, an adequate incidence in both countries is required. 相似文献
72.
A screening program of 10,040 cigarette-smoking men over 45 years of age was undertaken in an attempt to achieve earlier diagnosis, thereby increasing the cure rate, of oat cell lung cancer. Of the 155 men who were found to have lung cancer, 27 (17%) had confirmed oat cell cancer. Only one case was diagnosed at the first examination. The other 26 cases (called incidence cancer) were diagnosed by subsequent examinations. In 24 of the 26 patients, the tumor was not found until it was advanced (Stage III), and of these patients, only one is alive at 21 months follow-up. Two tumors were diagnosed as oat cell carcinoma at an early stage (Stage I), and both patients are alive with no evidence of disease at seven and 24 months. The screening program used in this study did not succeed in detecting oat cell cancer at an early stage. 相似文献
73.
74.
75.
76.
77.
Oyen RH; Gielen JL; Van Poppel HP; Verbeken EK; Van Damme BJ; Baert LV; Baert AL 《Radiology》1988,169(3):705-707
Abdominal radiography, excretory urography, retrograde pyelography, and computed tomography were performed in two patients who had undergone retrograde pyelography with thorium dioxide (Thorotrast) approximately 40 years ago. Both patients developed a transitional cell carcinoma due to suburothelial thorium deposition. Typical thorium densities were demonstrated at CT in the peripelvicalyceal area as well as in retroperitoneal lymph nodes. Elderly patients in whom radiographic examination reveals retained Thorotrast in the kidney should be followed up because of the high risk of renal carcinoma. 相似文献
78.
79.
TN Kakuda M Schöller-Gyüre G De Smedt G Beets F Aharchi MP Peeters K Vandermeulen BJ Woodfall RMW Hoetelmans 《HIV medicine》2009,10(3):173-181
Objective
Two open‐label, randomized, cross‐over trials in healthy volunteers were conducted to investigate the pharmacokinetic interaction between etravirine and tenofovir disoproxil fumarate.Methods
Etravirine was administered as either 800 mg twice a day (bid) (phase II formulation in Study 1) or 200 mg bid (phase III formulation in Study 2) for 8 days followed by a 12 h pharmacokinetic evaluation. After a minimum of 14 days washout, tenofovir disoproxil fumarate 300 mg once a day was administered for 16 days. Volunteers were randomized to receive co‐administration of etravirine with tenofovir disoproxil fumarate on either days 1–8 or days 9–16 followed by a 12 h pharmacokinetic evaluation for etravirine on day 8 or 16, respectively. Plasma and urine tenofovir concentrations were determined on days 8 and 16 over 24 h.Results
The least square mean (LSM) ratio [90% confidence interval (CI)] for the area under the plasma concentration–time curve from 0 to 12 h (AUC12 h) for etravirine co‐administered with tenofovir disoproxil fumarate vs. etravirine alone was 0.69 (0.61–0.79) and 0.81 (0.75–0.88) in Studies 1 and 2, respectively. The LSM ratio (90% CI) for the effect of etravirine on tenofovir AUC24 h was 1.16 (1.09–1.23) in Study 1 and 1.15 (1.09–1.21) in Study 2.Conclusions
These alterations are not considered clinically relevant for either drug and no dose adjustment is necessary when etravirine and tenofovir disoproxil fumarate are co‐administered. 相似文献80.
D Hofer K Paul K Fantur M Beck A Roubergue A Vellodi BJ Poorthuis H Michelakakis B Plecko E Paschke 《Clinical genetics》2010,78(3):236-246
Hofer D, Paul K, Fantur K, Beck M, Roubergue A, Vellodi A, Poorthuis BJ, Michelakakis H, Plecko B, Paschke E. Phenotype determining alleles in GM1 gangliosidosis patients bearing novel GLB1 mutations. GM1 gangliosidosis manifests with progressive psychomotor deterioration and dysostosis of infantile, juvenile, or adult onset, caused by alterations in the structural gene coding for lysosomal acid ß‐galactosidase (GLB1). In addition, allelic variants of this gene can result in Morquio B disease (MBD), a phenotype with dysostosis multiplex and entire lack of neurologic involvement. More than 100 sequence alterations in the GLB1 gene have been identified so far, but only few could be proven to be predictive for one of the GM1 gangliosidosis subtypes or MBD. We performed genotype analyses in 16 GM1 gangliosidosis patients of all phenotypes and detected 28 different genetic lesions. Among these, p.I55FfsX16, p.W65X, p.F107L, p.H112P, p.C127Y, p.W161X, p.I181K, p.C230R, p.W273X, p.R299VfsX5, p.A301V, p.F357L, p.K359KfsX23, p.L389P, p.D448V, p.D448GfsX8, and the intronic mutation IVS6‐8A>G have not been published so far. Due to their occurrence in homozygous patients, four mutations could be correlated to a distinct GM1 gangliosidosis phenotype. Furthermore, the missense mutations from heteroallelic patients and three artificial nonsense mutations were characterized by overexpression in COS‐1 cells, and the subcellular localization of the mutant proteins in fibroblasts was assessed. The phenotype specificity of 10 alleles can be proposed on the basis of our results and previous data. 相似文献