全文获取类型
收费全文 | 10339篇 |
免费 | 1112篇 |
国内免费 | 342篇 |
专业分类
耳鼻咽喉 | 109篇 |
儿科学 | 194篇 |
妇产科学 | 94篇 |
基础医学 | 1170篇 |
口腔科学 | 233篇 |
临床医学 | 1323篇 |
内科学 | 1866篇 |
皮肤病学 | 201篇 |
神经病学 | 548篇 |
特种医学 | 442篇 |
外国民族医学 | 2篇 |
外科学 | 1106篇 |
综合类 | 1102篇 |
现状与发展 | 2篇 |
一般理论 | 4篇 |
预防医学 | 799篇 |
眼科学 | 236篇 |
药学 | 1195篇 |
9篇 | |
中国医学 | 465篇 |
肿瘤学 | 693篇 |
出版年
2024年 | 29篇 |
2023年 | 153篇 |
2022年 | 386篇 |
2021年 | 536篇 |
2020年 | 370篇 |
2019年 | 383篇 |
2018年 | 397篇 |
2017年 | 363篇 |
2016年 | 329篇 |
2015年 | 427篇 |
2014年 | 549篇 |
2013年 | 641篇 |
2012年 | 856篇 |
2011年 | 768篇 |
2010年 | 567篇 |
2009年 | 430篇 |
2008年 | 546篇 |
2007年 | 554篇 |
2006年 | 478篇 |
2005年 | 436篇 |
2004年 | 390篇 |
2003年 | 384篇 |
2002年 | 297篇 |
2001年 | 198篇 |
2000年 | 186篇 |
1999年 | 126篇 |
1998年 | 90篇 |
1997年 | 69篇 |
1996年 | 63篇 |
1995年 | 59篇 |
1994年 | 51篇 |
1993年 | 38篇 |
1992年 | 51篇 |
1991年 | 78篇 |
1990年 | 52篇 |
1989年 | 46篇 |
1988年 | 51篇 |
1987年 | 43篇 |
1986年 | 35篇 |
1985年 | 28篇 |
1984年 | 27篇 |
1983年 | 20篇 |
1982年 | 16篇 |
1980年 | 19篇 |
1979年 | 19篇 |
1978年 | 15篇 |
1975年 | 11篇 |
1974年 | 13篇 |
1973年 | 19篇 |
1969年 | 10篇 |
排序方式: 共有10000条查询结果,搜索用时 0 毫秒
1.
PNPLA3 gene polymorphism and response to lifestyle modification in patients with nonalcoholic fatty liver disease 下载免费PDF全文
2.
Tien‐Yao Tsai Iat‐Lon Leong Ka‐Shun Cheng Lian‐Ru Shiao Tzu‐Hui Su Kar‐Lok Wong Paul Chan Yuk‐Man Leung 《Fundamental & clinical pharmacology》2019,33(1):52-62
A pathological feature in atherosclerosis is the dysfunction and death of vascular endothelial cells (EC). Oxidized low‐density lipoprotein (LDL), known to accumulate in the atherosclerotic arterial walls, impairs endothelium‐dependent relaxation and causes EC apoptosis. A major bioactive ingredient of the oxidized LDL is lysophosphatidylcholine (LPC), which at higher concentrations causes apoptosis and necrosis in various EC. There is hitherto no report on LPC‐induced cytotoxicity in brain EC. In this work, we found that LPC caused cytosolic Ca2+ overload, mitochondrial membrane potential decrease, p38 activation, caspase 3 activation and eventually apoptotic death in mouse cerebral bEND.3 EC. In contrast to reported reactive oxygen species (ROS) generation by LPC in other EC, LPC did not trigger ROS formation in bEND.3 cells. Pharmacological inhibition of p38 alleviated LPC‐inflicted cell death. We examined whether heparin could be cytoprotective: although it could not suppress LPC‐triggered Ca2+ signal, p38 activation and mitochondrial membrane potential drop, it did suppress LPC‐induced caspase 3 activation and alleviate LPC‐inflicted cytotoxicity. Our data suggest LPC apoptotic death mechanisms in bEND.3 might involve mitochondrial membrane potential decrease and p38 activation. Heparin is protective against LPC cytotoxicity and might intervene steps between mitochondrial membrane potential drop/p38 activation and caspase 3 activation. 相似文献
3.
4.
5.
6.
7.
F Boomsma F A van der Hoorn A J Man in 't Veld M A Schalekamp 《Clinica chimica acta; international journal of clinical chemistry》1988,178(1):59-69
We report a reliable method for determining DOPA levels in plasma and cerebrospinal fluid. The method is based on complete conversion of DOPA to dopamine and quantification by HPLC-ECD of the dopamine formed. Lower limit of detection was 0.5 nmol/l. No differences in plasma DOPA levels were found between normal children (0-15 yr, n = 60), normal adults (n = 39) and patients with essential hypertension (n = 40) or Parkinson's disease (no DOPA therapy, n = 30). In normal individuals and in patients with essential hypertension venous plasma levels were higher than arterial levels (10.2 vs 9.3 nmol/l, p less than 0.001, V/A ratio 1.11 (SD 0.08), n = 15). Sympathetic stimuli (standing, tilting, bicycle exercise, tyramine) did not influence DOPA levels. In untreated depressed patients (n = 10) and in non-parkinsonian neurological patients (n = 12) cerebrospinal fluid levels of DOPA were 4.5 (SD 2.4) and 5.2 (SD 1.3) nmol/l respectively. A direct method for the measurement of DOPA by HPLC-ECD after deproteinization of plasma is also described and compared with the conversion method. Good agreement was found when plasma DOPA levels exceeded 0.25 mumol/l (y(conversion method) = 0.943x (direct method) + 0.118; n = 60; r = 0.985). The direct method, because of greater simplicity and the possibility of simultaneous measurement of the DOPA metabolite 3-O-methyldopa, is the method of choice with plasma samples from DOPA-treated patients. In non-DOPA treated individuals the conversion method is superior and has proved to be an accurate and sensitive method for the determination of DOPA levels in plasma and cerebrospinal fluid. 相似文献
8.
9.
10.