全文获取类型
收费全文 | 1708篇 |
免费 | 128篇 |
国内免费 | 9篇 |
专业分类
耳鼻咽喉 | 14篇 |
儿科学 | 51篇 |
妇产科学 | 122篇 |
基础医学 | 165篇 |
口腔科学 | 48篇 |
临床医学 | 136篇 |
内科学 | 438篇 |
皮肤病学 | 46篇 |
神经病学 | 47篇 |
特种医学 | 172篇 |
外国民族医学 | 1篇 |
外科学 | 171篇 |
综合类 | 59篇 |
一般理论 | 1篇 |
预防医学 | 83篇 |
眼科学 | 11篇 |
药学 | 123篇 |
中国医学 | 1篇 |
肿瘤学 | 156篇 |
出版年
2021年 | 12篇 |
2020年 | 8篇 |
2019年 | 16篇 |
2018年 | 20篇 |
2017年 | 21篇 |
2016年 | 19篇 |
2015年 | 37篇 |
2014年 | 39篇 |
2013年 | 54篇 |
2012年 | 66篇 |
2011年 | 73篇 |
2010年 | 52篇 |
2009年 | 72篇 |
2008年 | 66篇 |
2007年 | 59篇 |
2006年 | 47篇 |
2005年 | 66篇 |
2004年 | 60篇 |
2003年 | 51篇 |
2002年 | 38篇 |
2001年 | 46篇 |
2000年 | 33篇 |
1999年 | 33篇 |
1998年 | 56篇 |
1997年 | 72篇 |
1996年 | 67篇 |
1995年 | 50篇 |
1994年 | 44篇 |
1993年 | 43篇 |
1992年 | 24篇 |
1991年 | 44篇 |
1990年 | 38篇 |
1989年 | 40篇 |
1988年 | 44篇 |
1987年 | 36篇 |
1986年 | 32篇 |
1985年 | 18篇 |
1984年 | 17篇 |
1983年 | 20篇 |
1982年 | 27篇 |
1981年 | 8篇 |
1980年 | 17篇 |
1978年 | 8篇 |
1977年 | 12篇 |
1973年 | 9篇 |
1971年 | 10篇 |
1970年 | 7篇 |
1969年 | 8篇 |
1967年 | 11篇 |
1966年 | 8篇 |
排序方式: 共有1845条查询结果,搜索用时 15 毫秒
71.
72.
Frank E. Kloster MD J. David Bristow MD Arthur J. Seaman MD 《The American journal of cardiology》1971,28(6):675-678
Sixty-three patients receiving anticoagulant therapy with sodium warfarin underwent cardiac catheterization with prothrombin-proconvertin values between 4 and 30 percent. The anticoagulant dose was omitted the day before and resumed the evening of catheterization. Procedures included 43 right heart studies by venous cutdown, 26 transseptal left heart catheterizations, 42 percutaneous retrograde femoral arterial catheterizations, 8 transthoracic cardiac punctures and 55 percutaneous brachial arterial catheterizations.
In 1 patient left hemothorax developed after transthoracic cardiac puncture. In a second minor bleeding from the femoral arterial puncture site occurred after premature ambulation. No extensive bleeding or difficulty in obtaining hemostasis occurred. Cardiac catheterization can be performed with reasonable safety during anticoagulant therapy with the prothrombin-proconvertin time in the therapeutic range. Problems in reestablishing anticoagulant control are avoided, and the patient is not exposed to the increased risk of thromboembolic complications incurred with interrupted therapy. 相似文献
73.
74.
Guscott M Bristow LJ Hadingham K Rosahl TW Beer MS Stanton JA Bromidge F Owens AP Huscroft I Myers J Rupniak NM Patel S Whiting PJ Hutson PH Fone KC Biello SM Kulagowski JJ McAllister G 《Neuropharmacology》2005,48(4):492-502
The affinity of several antidepressant and antipsychotic drugs for the 5-HT7 receptor and its CNS distribution suggest potential in the treatment of psychiatric diseases. However, there is little direct evidence of receptor function in vivo to support this. We therefore evaluated 5-HT7 receptors as a potential drug target by generating and assessing a 5-HT7 receptor knockout mouse. No difference in assays sensitive to potential psychotic or anxiety states was observed between the 5-HT7 receptor knockout mice and wild type controls. However, in the Porsolt swim test, 5-HT7 receptor knockout mice showed a significant decrease in immobility compared to controls, a phenotype similar to antidepressant treated mice. Intriguingly, treatment of wild types with SB-258719, a selective 5-HT7 receptor antagonist, did not produce a significant decrease in immobility unless animals were tested in the dark (or active) cycle, rather than the light, adding to the body of evidence suggesting a circadian influence on receptor function. Extracellular recordings from hypothalamic slices showed that circadian rhythm phase shifts to 8-OH-DPAT are attenuated in the 5-HT7 receptor KO mice also indicating a role for the receptor in the regulation of circadian rhythms. These pharmacological and genetic knockout studies provide the first direct evidence that 5-HT7 receptor antagonists should be investigated for efficacy in the treatment of depression. 相似文献
75.
76.
Asymptomatic small bowel intussusception associated with post-transplant lymphoproliferative disease 总被引:1,自引:0,他引:1
Barshes NR Lee TC Karpen SJ Bristow LJ Quiros-Tejeira RE Goss JA 《Pediatric transplantation》2004,8(2):196-197
Abstract: A 2-yr-old boy who had undergone orthotopic liver transplantation for biliary atresia 6 months prior presented with generalized lymphadenopathy. Physical exam revealed lymphadenopathy only; the patient had no gastrointestinal signs or symptoms. CT was used to evaluate the patient's lymphadenopathy. The findings were consistent with PTLD, and an incidental intussusception causing small bowel obstruction was found. The intussusception was successfully managed expectantly, and the patient's PTLD responded to administration of rituximab. The etiology, diagnosis and management of intussusception is discussed. 相似文献
77.
The last few years have seen increasing concerns among anaesthetistsabout the risks of pharmacological prophylaxis for thromboembolicdisease. Increased bleeding during or after surgery is one concern,but of greater significance is the possibility of an increasedpredisposition to haematoma formation when regional block isused. Most of the recent consideration of this problem has beenin relation to vertebral canal haematoma formation after centralnerve block. Some thought must be given also to the possibilityof haematoma formation after peripheral techniques when thetarget nerve is deeply placed so that pressure cannot be usedto control bleeding after needle insertion. However, this reviewwill be focused on vertebral canal haematoma. 相似文献
78.
Bayol A Bristow A Charton E Girard M Jongen P 《Pharmeuropa bio / the Biological Standardisation Programme, EDQM》2004,2004(1):35-45
Human Growth hormone (hGH, somatotrophin) is a 22 kDa, 191 amino-acid single chain protein produced by somatroph cells of the anterior pituitary gland. It is the major physiological regulator of growth, and deficiencies in growth hormone levels have long been recognized as the underlying cause of growth disorders (dwarfism). The ability of exogenous hGH to restore normal rates of growth in both human and animal models of growth retardation has long been recognized and the use of hGH in therapy goes back several decades. Initial preparations were prepared by extraction and purification from cadaveric pituitary tissue, and since 1984, hGH has been prepared by recombinant Deoxyribosenucleic acid (rDNA) technology. As is usually the case with "biologicals", characterization of the drug substance depended on a combination of physico-chemical and biological methods, and the hGH molecule became well characterized fairly early in its life as a drug. Indeed, by 1980 the major degradation forms and structural variants of the hGH molecule had been described and reviewed. Little satisfactory progress had been made in refining biological assays for hGH, and, although in vitro assays were described, potency-defining assays remained dependant on the whole body growth response in rats, and were both invasive and imprecise. In the early 1990's a series of collaborative studies on analysis of recombinant hGH (somatropin) established that available bioassays were much less selective that physico-chemical methods in detecting and quantifying structural degradation, and 1994 saw an international consensus to replace the bioassays with physico-chemical analytical methods for the routine batch release of somatropin. During the last decade in most markets somatropin has, unusually for a protein, been subject to batch release and control dependent entirely on physico-chemical analysis, without the routine use of any form of bioassay. During that time there has been a continuous development and refinement of methods, and the identification of a range of structural variants and degradation products of the molecule. The present review sets out to summarise the current knowledge on physico-chemical analytical methods for somatropin, and the structural variants that have been identified and characterized. A survey of available biological analytical methods is beyond the scope of this review, as is consideration of the earlier pituitary preparations and the recombinant 192 amino-acid methionyl form of the molecule (somatrem), although it is likely that many of the methods and variants described would be equally applicable to somatrem. 相似文献
79.
The p53 protein family and radiation sensitivity: Yes or no? 总被引:9,自引:0,他引:9
The p53 tumor suppressor protein is a key mediator of an ATM-dependent DNA damage response cascade following cellular exposure to ionizing radiation. The p53-family members, p63 and p73, are highly similar to p53, yet are differentially activated by IR, UV and cis-platinum via ATM and c-abl/ATR signaling pathways. Loss of function of p53 can occur by mutation or degradation; giving rise to alterations in G(1) and G(2) cell cycle checkpoint control, cell death, DNA repair and genetic stability. The end result of these alterations can be the generation of radioresistant mutant tumor cells. Indeed, in isogenic systems, loss of p53 or p73 function has been associated with decreased chemosensitivity and radiosensitivity, in vitro. However, clinical data supporting a role for p53 genotype as an independent predictive factor for radiotherapy outcome continues to be controversial due to variable endpoints in clinical trial design and in methodology in detecting p53 function. Nonetheless, in carefully controlled radiotherapy studies where mutations in p53 have been detected using DNA sequencing or functional assays, the presence of mutant p53 can be associated with decreased local control following radiotherapy. This suggests that novel molecular treatment strategies specifically designed to re-institute normal p53 function within resistant tumors can be used as combined modality protocols to improve local control and maintain a therapeutic ratio. A future challenge lies in the pre-therapy determination of a 'molecular therapeutic ratio' for individual patients which could allow for specific prognostication based on p53 functional status and subsequent individualized therapy. 相似文献
80.
Beta-adrenergic signaling mechanisms are of central importance to cardiovascular health and disease. Modulation of these pathways represents an important pharmacologic approach to the treatment of heart failure and hypertension. Advances in molecular genetics have identified genetic polymorphisms in the human beta-adrenergic receptor genes; some of this variation predicts changes in protein sequence/structure, and potentially changes in function, of the b-adrenergic receptors. This article reviews the current state of knowledge and understanding of the genetic variation present in the three human beta-adrenergic receptor genes. Already, variation in these genes has been associated with observed differences in several cardiovascular phenotypes. This work has led to the demonstration of functional differences in activity between receptors with certain known polymorphisms and "wild-type" receptors. An understanding of these polymorphisms is key to the development of studies of how differences in drug response/effects may be mediated by these polymorphisms. Such studies are anticipated to provide a foundation for the development of novel pharmacologic approaches where selection of and dosing of cardiovascular therapy is tailored to individuals on the basis of each patient's specific genetic makeup. 相似文献