全文获取类型
收费全文 | 67343篇 |
免费 | 6847篇 |
国内免费 | 2043篇 |
专业分类
耳鼻咽喉 | 661篇 |
儿科学 | 1723篇 |
妇产科学 | 620篇 |
基础医学 | 4235篇 |
口腔科学 | 536篇 |
临床医学 | 10641篇 |
内科学 | 12184篇 |
皮肤病学 | 508篇 |
神经病学 | 4420篇 |
特种医学 | 2601篇 |
外国民族医学 | 2篇 |
外科学 | 6781篇 |
综合类 | 12854篇 |
现状与发展 | 3篇 |
预防医学 | 4907篇 |
眼科学 | 963篇 |
药学 | 6627篇 |
103篇 | |
中国医学 | 4445篇 |
肿瘤学 | 1419篇 |
出版年
2024年 | 258篇 |
2023年 | 1152篇 |
2022年 | 2334篇 |
2021年 | 3450篇 |
2020年 | 3380篇 |
2019年 | 2665篇 |
2018年 | 2432篇 |
2017年 | 2859篇 |
2016年 | 2851篇 |
2015年 | 2484篇 |
2014年 | 4641篇 |
2013年 | 4632篇 |
2012年 | 3832篇 |
2011年 | 4004篇 |
2010年 | 3312篇 |
2009年 | 3060篇 |
2008年 | 3121篇 |
2007年 | 3344篇 |
2006年 | 2963篇 |
2005年 | 2516篇 |
2004年 | 2045篇 |
2003年 | 1797篇 |
2002年 | 1540篇 |
2001年 | 1449篇 |
2000年 | 1167篇 |
1999年 | 1019篇 |
1998年 | 844篇 |
1997年 | 791篇 |
1996年 | 689篇 |
1995年 | 706篇 |
1994年 | 625篇 |
1993年 | 481篇 |
1992年 | 534篇 |
1991年 | 419篇 |
1990年 | 356篇 |
1989年 | 308篇 |
1988年 | 299篇 |
1987年 | 280篇 |
1986年 | 221篇 |
1985年 | 233篇 |
1984年 | 226篇 |
1983年 | 141篇 |
1982年 | 166篇 |
1981年 | 109篇 |
1980年 | 86篇 |
1979年 | 96篇 |
1978年 | 98篇 |
1977年 | 48篇 |
1976年 | 57篇 |
1975年 | 39篇 |
排序方式: 共有10000条查询结果,搜索用时 156 毫秒
31.
目的探讨不同手术方法治疗复杂胫骨平台骨折临床疗效。方法选择2016年1月—2018年12月84例复杂胫骨平台骨折患者,随机分组。单侧锁定钢板内固定组选择单侧锁定钢板内固定手术,双侧切口双侧解剖钢板内固定组选择双侧切口双侧解剖钢板内固定。分析手术操作时间、手术失血、平均住院天数以及复杂胫骨平台骨折愈合时间;治疗前后患者视觉模拟评分和Rasmussen膝关节功能评分;膝关节僵硬发生率。结果双侧切口双侧解剖钢板内固定组视觉模拟评分和Rasmussen膝关节功能评分、手术操作时间、手术失血、平均住院天数以及复杂胫骨平台骨折愈合时间、膝关节僵硬发生率和单侧锁定钢板内固定组比较有优势,P<0.05。结论复杂胫骨平台骨折患者实施双侧切口双侧解剖钢板内固定可获得较好效果。 相似文献
32.
目的 通过阿霉素(Dox)复制大鼠慢性心力衰竭(CHF)模型,观察Liguzinediol对CHF大鼠心功能的影响。方法 通过血流动力学观察Liguzinediol对Dox(腹腔注射,2 mg/kg)诱导的CHF大鼠左心室内压最大上升/下降速率(±dp/dtmax)、左心室内压(LVSP)、动脉收缩压(ASP)、动脉舒张压(ADP)和心率(HR)的变化;观察Liguzinediol对血清一氧化氮(NO)、一氧化氮合成酶(NOS)、超氧化物歧化酶(SOD)、肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)以及血浆中丙二醛(MDA)的影响。结果 Liguzinediol能增加LVSP、+dp/dtmax、ASP、ADP、AP、HR,降低-dp/dtmax(P<0.05~0.01);降低NO、iNOS以及MDA的浓度,同时增强了SOD的活性(P<0.05~0.01);抑制IL-6和TNF-α的生成(P<0.05~0.01)。结论 Liguzinediol可明显改善Dox诱导的CHF大鼠血流动力学指标,减少模型大鼠炎症因子的释放以及抑制氧自由基的生成。 相似文献
33.
34.
35.
36.
Shunsuke Iriyama Haruyo Yamanishi Naomi Kunizawa Tetsuji Hirao Satoshi Amano 《Experimental dermatology》2019,28(3):247-253
Daily exposure to sunlight is known to affect the structure and function of the epidermal basement membrane (BM), as well as epidermal differentiation and epidermal barrier function. The aim of this study is to clarify whether the inhibition of BM‐degrading enzymes such as heparanase and matrix metalloproteinase 9 (MMP‐9) can improve the epidermal barrier function of facial skin, which is exposed to the sun on a daily basis. 1‐(2‐hydroxyethyl)‐2‐imidazolidinone (HEI) was synthesized as an inhibitor of both heparanase and MMP‐9. HEI inhibited not only the BM damage at the DEJ but also epidermal proliferation, differentiation, water contents and transepidermal water loss abnormalities resulting from ultraviolet B (UVB). This was determined in this study by the use of UVB‐induced human cultured skins as compared with the control without HEI. Moreover, topical application of HEI improved epidermal barrier function by increasing water content and decreasing transepidermal water loss in daily sun‐exposed facial skin as compared with non‐treated skins. These results suggest that the inhibition of both heparanase and MMP‐9 is an effective way to care for regularly sun‐exposed facial skin by protecting the BM from damage. 相似文献
37.
Marginal rate-based analyses are widely used for the analysis of recurrent events in clinical trials. In many areas of application, the events are not instantaneous but rather signal the onset of a symptomatic episode representing a recurrent infection, respiratory exacerbation, or bout of acute depression. In rate-based analyses, it is unclear how to best handle the time during which individuals are experiencing symptoms and hence are not at risk. We derive the limiting value of the Nelson-Aalen estimator and estimators of the regression coefficients under a semiparametric rate-based model in terms of an underlying two-state process. We investigate the impact of the distribution of the episode durations, heterogeneity, and dependence on the asymptotic and finite sample properties of standard estimators. We also consider the impact of these features on power in trials designed to test intervention effects on rate functions. An application to a trial of individuals with herpes simplex virus is given for illustration. 相似文献
38.
《Journal of thoracic oncology》2019,14(8):1360-1369
IntroductionInherited susceptibility to lung cancer risk in never-smokers is poorly understood. The major reason for this gap in knowledge is that this disease is relatively uncommon (except in Asians), making it difficult to assemble an adequate study sample. In this study we conducted a genome-wide association study on the largest, to date, set of European-descent never-smokers with lung cancer.MethodsWe conducted a two-phase (discovery and replication) genome-wide association study in never-smokers of European descent. We further augmented the sample by performing a meta-analysis with never-smokers from the recent OncoArray study, which resulted in a total of 3636 cases and 6295 controls. We also compare our findings with those in smokers with lung cancer.ResultsWe detected three genome-wide statistically significant single nucleotide polymorphisms rs31490 (odds ratio [OR]: 0.769, 95% confidence interval [CI]: 0.722–0.820; p value 5.31 × 10-16), rs380286 (OR: 0.770, 95% CI: 0.723–0.820; p value 4.32 × 10-16), and rs4975616 (OR: 0.778, 95% CI: 0.730–0.829; p value 1.04 × 10-14). All three mapped to Chromosome 5 CLPTM1L-TERT region, previously shown to be associated with lung cancer risk in smokers and in never-smoker Asian women, and risk of other cancers including breast, ovarian, colorectal, and prostate.ConclusionsWe found that genetic susceptibility to lung cancer in never-smokers is associated to genetic variants with pan-cancer risk effects. The comparison with smokers shows that top variants previously shown to be associated with lung cancer risk only confer risk in the presence of tobacco exposure, underscoring the importance of gene-environment interactions in the etiology of this disease. 相似文献
39.
40.