全文获取类型
收费全文 | 2130篇 |
免费 | 146篇 |
国内免费 | 5篇 |
专业分类
耳鼻咽喉 | 42篇 |
儿科学 | 63篇 |
妇产科学 | 53篇 |
基础医学 | 328篇 |
口腔科学 | 32篇 |
临床医学 | 165篇 |
内科学 | 669篇 |
皮肤病学 | 26篇 |
神经病学 | 179篇 |
特种医学 | 94篇 |
外科学 | 291篇 |
综合类 | 13篇 |
预防医学 | 114篇 |
眼科学 | 43篇 |
药学 | 105篇 |
中国医学 | 6篇 |
肿瘤学 | 58篇 |
出版年
2023年 | 9篇 |
2022年 | 23篇 |
2021年 | 36篇 |
2020年 | 27篇 |
2019年 | 44篇 |
2018年 | 47篇 |
2017年 | 35篇 |
2016年 | 48篇 |
2015年 | 61篇 |
2014年 | 64篇 |
2013年 | 77篇 |
2012年 | 172篇 |
2011年 | 159篇 |
2010年 | 71篇 |
2009年 | 63篇 |
2008年 | 117篇 |
2007年 | 138篇 |
2006年 | 120篇 |
2005年 | 105篇 |
2004年 | 107篇 |
2003年 | 110篇 |
2002年 | 87篇 |
2001年 | 36篇 |
2000年 | 49篇 |
1999年 | 52篇 |
1998年 | 29篇 |
1997年 | 15篇 |
1996年 | 15篇 |
1995年 | 11篇 |
1994年 | 11篇 |
1993年 | 11篇 |
1992年 | 25篇 |
1991年 | 27篇 |
1990年 | 15篇 |
1989年 | 15篇 |
1988年 | 19篇 |
1987年 | 28篇 |
1986年 | 13篇 |
1985年 | 18篇 |
1984年 | 9篇 |
1983年 | 10篇 |
1982年 | 6篇 |
1979年 | 16篇 |
1978年 | 7篇 |
1977年 | 6篇 |
1974年 | 7篇 |
1971年 | 7篇 |
1969年 | 9篇 |
1933年 | 13篇 |
1932年 | 10篇 |
排序方式: 共有2281条查询结果,搜索用时 359 毫秒
61.
62.
63.
The haemodynamic effects of intravenous isosorbide dinitrate(Cedocard) in patients with severe acute left ventricular failurehave been assessed using incremental infusion rates from 50to 800µmin1. For most patients most of the fallin pulmonary arterial diastolic pressure occurred by 200µgmin1, with little further fall at higher doses. At 200µgmin1pulmonary arterial diastolic pressure fell from 29 to 23 mgHg(P<0.001), there was no significant change in cardiac index(1.9 to 2.0Lmin1m2) or heart rate (108 to 108beats min1). Despite high doses, no side effects wereobserved. Intravenous isosorbide dinitrate is effective and safe in themanagement of acute severe left ventricular failure. In mostpatients an infusion rate of about 200µg min1 producesoptimal haemodynamic effects. 相似文献
64.
Possible role for mast cell-derived cathepsin G in the adverse remodelling of stenotic aortic valves 总被引:1,自引:1,他引:1
Helske Satu; Syvaranta Suvi; Kupari Markku; Lappalainen Jani; Laine Mika; Lommi Jyri; Turto Heikki; Mayranpaa Mikko; Werkkala Kalervo; Kovanen Petri T.; Lindstedt Ken A. 《European heart journal》2006,27(12):1495-1504
Aims Aortic stenosis (AS) is characterized by extensive remodellingof the valves, including infiltration of inflammatory cells,extracellular matrix degradation, and fibrosis. The molecularmechanisms behind this adverse remodelling have remained obscure.In this article, we study whether cathepsin G, an angiotensinII (Ang II)-forming elastolytic enzyme, contributes to progressionof AS. Methods and results Stenotic aortic valves (n=86) and controlvalves (n=17) were analysed for cathepsin G, transforming growthfactor-ß1 (TGF-ß1), and collagens I andIII with RTPCR and immunohistochemistry. Valvular collagen/elastinratio was quantified by histochemistry. In stenotic valves,cathepsin G was present in mast cells and showed increased expression(P<0.001), which correlated positively (P<0.001) withthe expression levels of TGF-ß1 and collagens I andIII. TGF-ß1 was also present in mast cell-rich areasand cathepsin G induced losartan-sensitive TGF-ß1expression in cultured fibroblasts. Collagen/elastin ratio wasincreased in stenotic valves (P<0.001) and correlated positivelywith smoking (P=0.02). Nicotine in cigarette smoke activatedmast cells and induced TGF-ß1 expression in culturedfibroblasts. Fragmented elastin was observed in stenotic valvescontaining activated cathepsin G-secreting mast cells and innormal valves treated with cathepsin G. Conclusion In stenotic aortic valves, mast cell-derived cathepsinG may cause adverse valve remodelling and AS progression. 相似文献
65.
66.
Andrej Petri? Scott A. Johnson Hung V. Pham Ying Li Simon ?eh Amalija Golobi? Eric D. Agdeppa Gerald Timbol Jie Liu Gyochang Keum Nagichettiar Satyamurthy Vladimir Kepe Kendall N. Houk Jorge R. Barrio 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(41):16492-16497
The positron-emission tomography (PET) probe 2-(1-[6-[(2-fluoroethyl)(methyl)amino]-2-naphthyl]ethylidene) (FDDNP) is used for the noninvasive brain imaging of amyloid-β (Aβ) and other amyloid aggregates present in Alzheimer’s disease and other neurodegenerative diseases. A series of FDDNP analogs has been synthesized and characterized using spectroscopic and computational methods. The binding affinities of these molecules have been measured experimentally and explained through the use of a computational model. The analogs were created by systematically modifying the donor and the acceptor sides of FDDNP to learn the structural requirements for optimal binding to Aβ aggregates. FDDNP and its analogs are neutral, environmentally sensitive, fluorescent molecules with high dipole moments, as evidenced by their spectroscopic properties and dipole moment calculations. The preferred solution-state conformation of these compounds is directly related to the binding affinities. The extreme cases were a nonplanar analog t-butyl-FDDNP, which shows low binding affinity for Aβ aggregates (520 nM Ki) in vitro and a nearly planar tricyclic analog cDDNP, which displayed the highest binding affinity (10 pM Ki). Using a previously published X-ray crystallographic model of 1,1-dicyano-2-[6-(dimethylamino)naphthalen-2-yl]propene (DDNP) bound to an amyloidogenic Aβ peptide model, we show that the binding affinity is inversely related to the distortion energy necessary to avoid steric clashes along the internal surface of the binding channel. 相似文献
67.
68.
69.
Meriläinen S Mäkelä J Koivukangas V Jensen HA Rimpiläinen E Yannopoulos F Mäkelä T Alestalo K Vakkala M Koskenkari J Ohtonen P Koskela M Lehenkari P Karttunen T Juvonen T 《Hepato-gastroenterology》2012,59(114):599-606
Background/Aims: To examine whether intestinal bacterial translocation occurs early in acute mild and severe pancreatitis and whether the intestinal expression of tight junction proteins (claudins-2, -3, -4, -5, -7), apoptosis or proliferation would explain the possible translocation. Methodology: Fifteen pigs were randomized to controls (n=5) or to develop mild edematous pancreatitis (n=5, saline infusion to pancreatic duct) or severe necrotic pancreatitis (n=5, taurocholic acid infusion). Translocation was studied by measuring bacterial cultures from portal vein blood and mesenteric lymph nodes. Immunohistochemical expression of the tight junction proteins, apoptosis rate (TUNEL) and Ki-67 were analyzed quantitatively from the epithelium of the jejunum and colon. Results: There was no bacterial translocation during the 6 hours followup, nor changes in the expression of tight junction proteins claudins-2 and -5 in jejunum or colon. Saturation and proportional area of claudin-3 staining decreased in the colon, as did claudins-4 and -7 staining in the jejunum of the necrotic pancreatitis group. Increased apoptosis was found in all samples from controls and the edematous pancreatitis group but not in jejunum in the necrotic pancreatitis group. Ki-67 activity tended to increase in the upper half of the villus in edematous and necrotic pancreatitis. There were no changes in the basic histology. Conclusions: The major finding of this study was that bacterial translocation from the gut is not present at the beginning of acute pancreatitis. Tight junction proteins claudin-2 and -5 do not become altered in the early stages of pancreatitis. Claudin-3 decreases in the colon and claudins-4 and -7 in the jejunum in necrotic pancreatitis. Laparotomy itself causes increased apoptosis in the colon and the jejunum. 相似文献
70.