首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   19249篇
  免费   1244篇
  国内免费   80篇
耳鼻咽喉   216篇
儿科学   392篇
妇产科学   307篇
基础医学   2634篇
口腔科学   1595篇
临床医学   1539篇
内科学   4049篇
皮肤病学   449篇
神经病学   1742篇
特种医学   421篇
外国民族医学   1篇
外科学   3051篇
综合类   59篇
一般理论   3篇
预防医学   1588篇
眼科学   331篇
药学   1291篇
中国医学   128篇
肿瘤学   777篇
  2023年   177篇
  2022年   164篇
  2021年   727篇
  2020年   478篇
  2019年   631篇
  2018年   815篇
  2017年   561篇
  2016年   589篇
  2015年   685篇
  2014年   915篇
  2013年   1106篇
  2012年   1631篇
  2011年   1820篇
  2010年   929篇
  2009年   789篇
  2008年   1204篇
  2007年   1244篇
  2006年   1048篇
  2005年   937篇
  2004年   783篇
  2003年   648篇
  2002年   554篇
  2001年   293篇
  2000年   218篇
  1999年   218篇
  1998年   92篇
  1997年   70篇
  1996年   50篇
  1995年   54篇
  1994年   35篇
  1993年   39篇
  1992年   85篇
  1991年   84篇
  1990年   81篇
  1989年   73篇
  1988年   79篇
  1987年   66篇
  1986年   59篇
  1985年   60篇
  1984年   41篇
  1983年   31篇
  1982年   21篇
  1979年   38篇
  1978年   30篇
  1975年   26篇
  1974年   31篇
  1973年   36篇
  1969年   19篇
  1967年   21篇
  1966年   23篇
排序方式: 共有10000条查询结果,搜索用时 796 毫秒
1.
2.
3.
4.
5.
6.
Acute lung injury (ALI) caused by systemic inflammatory response remains a leading cause of morbidity and mortality in critically ill patients. Management of patients with sepsis is largely limited to supportive therapies, reflecting an incomplete understanding of the underlying pathophysiology. Furthermore, there have been limited advances in the treatments for ALI. In this study, lung function and a histological analysis were performed to evaluate the impact of transient receptor potential vanilloid‐1 receptor (TRPV1) antagonist (capsazepine; CPZ) on the lipopolysaccharide (LPS)‐induced lung injury in mice. For this, adult mice pre‐treated with CPZ or vehicle received intraperitoneal injections of LPS or saline and 24 hr after, the mice were anaesthetized, and lung mechanics was evaluated. The LPS‐challenged mice exhibited substantial mechanical impairment, characterized by increases in respiratory system resistance, respiratory system elastance, tissue damping and tissue elastance. The pre‐treatment with CPZ prevented the increase in respiratory system resistance and decreased the increase in tissue damping during endotoxemia. In addition, mice pre‐treated with CPZ had an attenuated lung injury evidenced by reduction on collapsed area of the lung parenchyma induced by LPS. This suggests that the TRPV1 antagonist capsazepine has a protective effect on lung mechanics in ALI during endotoxemia and that it may be a target for enhanced therapeutic efficacy in ALI.  相似文献   
7.
8.
Delayed contrast enhancement after injection of a gadolinium-chelate (Gd-chelate) is a reference imaging method to detect myocardial tissue changes. Its localization within the thickness of the myocardial wall allows differentiating various pathological processes such as myocardial infarction (MI), inflammatory myocarditis, and cardiomyopathies. The aim of the study was first to characterize benign myocarditis using quantitative delayed-enhancement imaging and then to investigate whether the measure of the extracellular volume fraction (ECV) can be used to discriminate between MI and myocarditis.In 6 patients with acute benign myocarditis (32.2 ± 13.8 year-old, subepicardial late gadolinium enhancement [LGE]) and 18 patients with MI (52.3 ± 10.9 year-old, subendocardial/transmural LGE), myocardial T1 was determined using the Modified Look-Locker Imaging (MOLLI) sequence at 3 Tesla before and after Gd-chelate injection. T1 values were compared in LGE and normal regions of the myocardium. The myocardial T1 values were normalized to the T1 of blood, and the ECV was calculated from T1 values of myocardium and blood pre- and post-Gd injection.In both myocarditis and MI, the T1 was lower in LGE regions than in normal regions of the left ventricle. T1 of LGE areas was significantly higher in myocarditis than in MI (446.8 ± 45.8 vs 360.5 ± 66.9 ms, P = 0.003) and ECV was lower in myocarditis than in MI (34.5 ± 3.3 vs 53.8 ± 13.0 %, P = 0.004).Both inflammatory process and chronic fibrosis induce LGE (subepicardial in myocarditis and subendocardial in MI). The present study demonstrates that the determination of T1 and ECV is able to differentiate the 2 histological patterns.Further investigation will indicate whether the severity of ECV changes might help refine the predictive risk of LGE in myocarditis.  相似文献   
9.
10.
Objective:The present study evaluates a training program for fitting different hearing protection devices (HPDs) based on personal attenuation rating (PAR) before, immediately after, and six months after training.Methods:A total of 67 workers from a public university in the city of São Paulo, Brazil, were invited to participate in the measurement of PARs for foam and silicone protectors through the 3M™ E-A-Rfit Validation System. Two evaluations were performed for each protector at each sampling date: one after reading printed material (the package instructions) and another after being trained by an audiologist. The same procedures were repeated after six months. The final sample consisted of 30 individuals. ANOVA was used for statistical analysis.Results:Larger PAR values were observed after training by the audiologist, and smaller values were observed after six months. Then, after re-training, the values increased again. There were no statistically significant differences in PAR among the HPDs tested. Even after the two training sessions, 23 to 27% of the subjects did not obtain adequate PAR values.Conclusion:These findings emphasize the need for continual worker training in the correct fit of earplug HPDs and the importance of longitudinal PAR monitoring. In addition, some workers, despite the training provided, did not adapt to the HPDs used. Therefore, it is essential that other protection methods and/or other HPD types are made available to these individuals.Key words: Hearing, noise-induced hearing loss, occupational health, personal protective equipment, hearing protection devices  相似文献   
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号