全文获取类型
收费全文 | 4796篇 |
免费 | 375篇 |
国内免费 | 34篇 |
专业分类
耳鼻咽喉 | 115篇 |
儿科学 | 72篇 |
妇产科学 | 46篇 |
基础医学 | 645篇 |
口腔科学 | 192篇 |
临床医学 | 494篇 |
内科学 | 1444篇 |
皮肤病学 | 83篇 |
神经病学 | 312篇 |
特种医学 | 231篇 |
外科学 | 704篇 |
综合类 | 81篇 |
一般理论 | 2篇 |
预防医学 | 194篇 |
眼科学 | 95篇 |
药学 | 198篇 |
1篇 | |
中国医学 | 5篇 |
肿瘤学 | 291篇 |
出版年
2021年 | 58篇 |
2020年 | 39篇 |
2019年 | 70篇 |
2018年 | 78篇 |
2017年 | 64篇 |
2016年 | 73篇 |
2015年 | 99篇 |
2014年 | 133篇 |
2013年 | 153篇 |
2012年 | 198篇 |
2011年 | 241篇 |
2010年 | 141篇 |
2009年 | 146篇 |
2008年 | 200篇 |
2007年 | 207篇 |
2006年 | 236篇 |
2005年 | 222篇 |
2004年 | 242篇 |
2003年 | 171篇 |
2002年 | 179篇 |
2001年 | 189篇 |
2000年 | 182篇 |
1999年 | 127篇 |
1998年 | 101篇 |
1997年 | 75篇 |
1996年 | 48篇 |
1995年 | 54篇 |
1994年 | 57篇 |
1993年 | 50篇 |
1992年 | 99篇 |
1991年 | 86篇 |
1990年 | 99篇 |
1989年 | 89篇 |
1988年 | 77篇 |
1987年 | 77篇 |
1986年 | 81篇 |
1985年 | 77篇 |
1984年 | 52篇 |
1983年 | 44篇 |
1982年 | 33篇 |
1981年 | 33篇 |
1980年 | 25篇 |
1979年 | 48篇 |
1978年 | 34篇 |
1977年 | 35篇 |
1976年 | 33篇 |
1975年 | 24篇 |
1974年 | 35篇 |
1973年 | 30篇 |
1968年 | 24篇 |
排序方式: 共有5205条查询结果,搜索用时 15 毫秒
101.
Hiddemann W Spiekermann K Buske C Feuring-Buske M Braess J Haferlach T Schoch C Kern W Schnittger S Berdel W Wörmann B Heinecke A Sauerland C Büchner T;German AML Cooperative Group 《Critical reviews in oncology/hematology》2005,56(2):235-245
Genetic and molecular techniques have provided increasing insights into the biology of acute myeloid leukemia (AML). These investigations showed that AML is not a homogeneous disease but a heterogeneous group of biologically different subentities. These subentities are currently primarily defined by cytogenetics by which three main subgroups can be discriminated: AML with balanced translocations, AML with unbalanced aberrations and AML without cytogenetically detectable aberrations. Within the latter group molecular alterations are identified in more than half of cases such as NPM mutations, FLT3 mutations, MLL duplications and mutations of CEBP-alpha. The clinical meaning of these findings is illustrated by substantial differences in response to therapy and long-term outcome. As demonstrated by the recent multicenter trial of the German AML Cooperative Group (AMLCG) and other studies intensification of induction therapy may improve the results in distinct subtypes but fails to do so in others. Therefore, new strategies need to be explored which incorporate the knowledge about the biology of AML to develop biology adapted treatment strategies. This process has just begun and is predominantly determined by the availability of new agents and their evaluation in clinical phase I and II studies. A variety of targets are currently explored and some trials have yielded promising results already. The step towards a biology adapted treatment of AML is long and requires the combined efforts of researchers, clinicians and the pharmaceutical industry. The first steps towards this goal have been taken and give rise to the hope for more effective and more specific therapies of AML. 相似文献
102.
103.
104.
105.
106.
Conclusion Pancreatic adenocarcinoma, the human tumor with the highest incidence of K-ras mutations, is one of the leading causes of cancer death and has a very poor prognosis. Over the past few years, a molecular
genetic profile of pancreatic cancer has started to emerge: K-ras mutations in at least 90% of cases, MTS1 alterations (somatic mutations and homozygous deletions) in 80%, p53 mutations in
about 70%, as well as multiple sites of allelic loss in cancer cells. The detection of K-ras mutations is done by using one of several PCR-based methods. A modified allele-specific ligation assay recently described
appears particularly simple and reproducible. The possibility of pancreatic ductal lesions being the early precursors of pancreatic
cancer has gained support from the finding of frequent K-ras mutations in these lesions. Although K-ras mutations are a defining event in pancreatic ductal carcinogenesis, it is unclear in which genetic context they occur. K-ras mutations as markers of cancer cells have been detected in clinical specimens from patients, including stool and blood, raising
the possibility of early diagnosis. In addition K-ras can be a molecular target for therapeutic intervention, as illustrated with the use of farnesylation inhibitors. 相似文献
107.
M J Kern U Deligonul S Tatineni H Serota F Aguirre T C Hilton 《Journal of the American College of Cardiology》1991,18(3):718-729
To assess the use of adenosine as an alternative agent for determination of coronary vasodilator reserve, hemodynamics and coronary blood flow velocity were measured at rest and during peak hyperemic responses to continuous intravenous adenosine infusion (50, 100 and 150 micrograms/kg per min for 3 min) and intracoronary papaverine (10 mg) in 34 patients (17 without [group 1] and 17 with [group 2] significant left coronary artery disease), and in 17 patients (11 without and 6 with left coronary artery disease) after low dose (2.5 mg) intravenous bolus injection of adenosine. The maximal adenosine dose did not change mean arterial pressure (-10 +/- 14% and -6 +/- 12% for groups 1 and 2, respectively) but increased the heart rate (15 +/- 18% and 13 +/- 16, respectively). For continuous adenosine infusions, mean coronary flow velocity increased 64 +/- 104%, 122 +/- 94% and 198 +/- 59% and 15 +/- 51%, 110 +/- 95% and 109 +/- 86% in groups 1 and 2, respectively for each of the three doses. Mean coronary flow velocity increased significantly after 100 and 150 micrograms/kg of adenosine and 10 mg of intracoronary papaverine (48 +/- 25, 52 +/- 19 and 54 +/- 21 cm/s, respectively; all p less than 0.05 vs. baseline) and was significantly higher than in group 2 (37 +/- 24, 32 +/- 16, 41 +/- 23 cm/s; all p less than 0.05 vs. group 1). The coronary vasodilator reserve ratio (calculated as the ratio of hyperemic to basal mean flow velocity) for adenosine and papaverine was 2.94 +/- 1.50 and 2.94 +/- 1.00, respectively, in group 1 and was significantly and similarly reduced in group 2 (2.16 +/- 0.81 and 2.38 +/- 0.78, respectively; both p less than 0.05 vs. group 1). Low dose bolus injection of adenosine increased mean velocity equivalently to that after continuous infusion of 100 micrograms/kg, but less than after papaverine. There was a strong correlation between adenosine infusion and papaverine for both mean coronary flow velocity and coronary vasodilator reserve ratio (r2 = 0.871 and 0.325; SEE = 0.068 and 0.189, respectively; both p less than 0.0005). No patient had significant arrhythmias or prolongation of the corrected QT (QTc) interval with adenosine, but papaverine increased the QT (QTc) interval from 445 +/- 44 to 501 +/- 43 ms (p less than 0.001 vs. both maximal adenosine and baseline) and produced nonsustained ventricular tachycardia in one patient.(ABSTRACT TRUNCATED AT 400 WORDS) 相似文献
108.
Daria Capece Daniel DAndrea Federica Begalli Laura Goracci Laura Tornatore James L. Alexander Alessandra Di Veroli Shi-Chi Leow Thamil S. Vaiyapuri James K. Ellis Daniela Verzella Jason Bennett Luca Savino Yue Ma James S. McKenzie Maria Luisa Doria Sam E. Mason Kern Rei Chng Hector C. Keun Gary Frost Vinay Tergaonkar Katarzyna Broniowska Walter Stunkel Zoltan Takats James M. Kinross Gabriele Cruciani Guido Franzoso 《The Journal of clinical investigation》2021,131(11)
109.
110.