全文获取类型
收费全文 | 1978篇 |
免费 | 75篇 |
国内免费 | 20篇 |
专业分类
耳鼻咽喉 | 57篇 |
儿科学 | 50篇 |
妇产科学 | 58篇 |
基础医学 | 127篇 |
口腔科学 | 104篇 |
临床医学 | 104篇 |
内科学 | 493篇 |
皮肤病学 | 9篇 |
神经病学 | 100篇 |
特种医学 | 106篇 |
外科学 | 549篇 |
综合类 | 15篇 |
预防医学 | 93篇 |
眼科学 | 37篇 |
药学 | 100篇 |
肿瘤学 | 71篇 |
出版年
2023年 | 21篇 |
2022年 | 26篇 |
2021年 | 65篇 |
2020年 | 28篇 |
2019年 | 38篇 |
2018年 | 64篇 |
2017年 | 40篇 |
2016年 | 41篇 |
2015年 | 46篇 |
2014年 | 84篇 |
2013年 | 140篇 |
2012年 | 189篇 |
2011年 | 191篇 |
2010年 | 121篇 |
2009年 | 103篇 |
2008年 | 136篇 |
2007年 | 169篇 |
2006年 | 129篇 |
2005年 | 102篇 |
2004年 | 84篇 |
2003年 | 81篇 |
2002年 | 83篇 |
2001年 | 9篇 |
2000年 | 10篇 |
1999年 | 8篇 |
1998年 | 8篇 |
1997年 | 3篇 |
1996年 | 5篇 |
1995年 | 6篇 |
1994年 | 4篇 |
1993年 | 5篇 |
1992年 | 4篇 |
1991年 | 3篇 |
1990年 | 3篇 |
1989年 | 2篇 |
1988年 | 2篇 |
1987年 | 2篇 |
1985年 | 1篇 |
1984年 | 2篇 |
1983年 | 2篇 |
1982年 | 3篇 |
1981年 | 3篇 |
1977年 | 1篇 |
1973年 | 1篇 |
1972年 | 1篇 |
1971年 | 1篇 |
1939年 | 3篇 |
排序方式: 共有2073条查询结果,搜索用时 15 毫秒
51.
Engvall M Sjögreen L Kjellberg H Robertson A Sundell S Kiliaridis S 《European journal of oral sciences》2007,115(3):192-197
Myotonic dystrophy or dystrophia myotonica (DM) is a hereditary neuromuscular multisystem disease with a varying clinical expressivity and severity. The objective of this study was to assess the oral health in children with myotonic dystrophy and to compare it with a control group. Fifty-six DM patients, aged 2.7-18.0 yr, were compared with age- and gender-matched control patients with respect to caries, plaque, and gingivitis. Oral function and signs of temporomandibular dysfunction (TMD) were assessed, and the ability to co-operate in dental treatment was estimated. Questionnaires concerning eating habits, dental care, traumatic injuries to teeth, and orofacial function were also used. The DM patients had significantly more caries, plaque, and gingivitis than did control patients. They had more TMD problems and lower co-operation ability than the healthy control persons. General sedation was frequently needed to carry through dental treatment. DM patients are at risk of caries, gingivitis and TMD problems, and need intensified prophylactic care. Behavior management problems are common. 相似文献
52.
Strong association of interleukin-4 (-590 C/T) polymorphism with increased risk for oral squamous cell carcinoma in Europeans 总被引:1,自引:0,他引:1
53.
Filipa Ponte Ha-Neui Kim Srividhya Iyer Li Han Maria Almeida Stavros C Manolagas 《Journal of bone and mineral research》2020,35(8):1441-1451
CXCL12 is abundantly expressed in reticular cells associated with the perivascular niches of the bone marrow (BM) and is indispensable for B lymphopoiesis. Cxcl12 promotes osteoclastogenesis and has been implicated in pathologic bone resorption. We had shown earlier that estrogen receptor α deletion in osteoprogenitors and estrogen deficiency in mice increase Cxcl12 mRNA and protein levels in the BM plasma, respectively. We have now generated female and male mice with conditional deletion of a Cxcl12 allele in Prrx1 targeted cells (Cxcl12∆Prrx1) and show herein that they have a 90% decrease in B lymphocytes but increased erythrocytes and adipocytes in the marrow. Ovariectomy increased the expression of Cxcl12 and B-cell number in the Cxcl12f/f control mice, but these effects were abrogated in the Cxcl12∆Prrx1 mice. Cortical bone mass was not affected in Cxcl12∆Prrx1 mice. Albeit, the cortical bone loss caused by ovariectomy was greatly attenuated. Most unexpectedly, the rate of bone turnover in sex steroid–sufficient female or male Cxcl12∆Prrx1 mice was dramatically increased, as evidenced by a more than twofold increase in several osteoblast- and osteoclast-specific mRNAs, as well as increased mineral apposition and bone formation rate and increased osteoclast number in the endosteal surface. The magnitude of the Cxcl12∆Prrx1-induced changes were much greater than those caused by ovariectomy or orchidectomy in the Cxcl12f/f mice. These results strengthen the evidence that CXCL12 contributes to the loss of cortical bone mass caused by estrogen deficiency. Moreover, they reveal for the first time that in addition to its effects on hematopoiesis, CXCL12 restrains bone turnover—without changing the balance between resorption and formation—by suppressing osteoblastogenesis and the osteoclastogenesis support provided by cells of the osteoblast lineage. © 2020 American Society for Bone and Mineral Research. 相似文献
54.
Hua Shen Andrea G Schwartz Roberto Civitelli Stavros Thomopoulos 《Journal of bone and mineral research》2020,35(8):1494-1503
The enthesis is a mineralized fibrocartilage transition that attaches tendon to bone and is vital for musculoskeletal function. Despite recent studies demonstrating the necessity of muscle loading for enthesis formation, the mechanisms that regulate enthesis formation and mechanoresponsiveness remain unclear. Therefore, the current study investigated the role of the gap junction protein connexin 43 in these processes by deleting Gja1 (the Cx43 gene) in the tendon and enthesis. Compared with their wild-type (WT) counterparts, mice lacking Cx43 showed disrupted entheseal cell alignment, reduced mineralized fibrocartilage, and impaired biomechanical properties of the supraspinatus tendon entheses during postnatal development. Cx43-deficient mice also exhibited reduced ability to complete a treadmill running protocol but no apparent deficits in daily activity, metabolic indexes, shoulder muscle size, grip strength, and major trabecular bone properties of the adjacent humeral head. To examine enthesis mechanoresponsiveness, young adult mice were subjected to modest treadmill exercise. Gja1 deficiency in the tendon and enthesis reduced entheseal anabolic responses to treadmill exercise: WT mice had increased expression of Sox9, Ihh, and Gli1 and increased Brdu incorporation, whereas Cx43-deficient mice showed no changes or decreased levels with exercise. Collectively, the results demonstrated an essential role for Cx43 in postnatal tendon enthesis formation, function, and response to loading; results further provided evidence implicating a link between Cx43 function and the hedgehog signaling pathway. © 2020 American Society for Bone and Mineral Research. 相似文献
55.
Athanasiou Stavros Pitsouni Eleni Douskos Athanasios Salvatore Stefano Loutradis Dimitrios Grigoriadis Themos 《Lasers in medical science》2020,35(1):1-11
Lasers in Medical Science - A systematic review and meta-analysis was undertaken to assess the efficacy and safety of intravaginal energy-based therapies (laser and radiofrequency) on sexual health... 相似文献
56.
57.
Eugene J. Sato Megan L. Killian Anthony J. Choi Evie Lin Mary C. Esparza Leesa M. Galatz Stavros Thomopoulos Samuel R. Ward 《Journal of orthopaedic research》2014,32(9):1111-1116
Rotator cuff tears can cause irreversible changes (e.g., fibrosis) to the structure and function of the injured muscle(s). Fibrosis leads to increased muscle stiffness resulting in increased tension at the rotator cuff repair site. This tension influences repairability and healing potential in the clinical setting. However, the micro‐ and meso‐scale structural and molecular sources of these whole‐muscle mechanical changes are poorly understood. Here, single muscle fiber and fiber bundle passive mechanical testing was performed on rat supraspinatus and infraspinatus muscles with experimentally induced massive rotator cuff tears (Tenotomy) as well as massive tears with chemical denervation (Tenotomy + BTX) at 8 and 16 weeks post‐injury. Titin molecular weight, collagen content, and myosin heavy chain profiles were measured and correlated with mechanical variables. Single fiber stiffness was not different between controls and experimental groups. However, fiber bundle stiffness was significantly increased at 8 weeks in the Tenotomy + BTX group compared to Tenotomy or control groups. Many of the changes were resolved by 16 weeks. Only fiber bundle passive mechanics was weakly correlated with collagen content. These data suggest that tendon injury with concomitant neuromuscular compromise results in extra‐cellular matrix production and increases in stiffness of the muscle, potentially complicating subsequent attempts for surgical repair. © 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:1111–1116, 2014. 相似文献
58.
59.
Stavros Ioannidis Spyridon Kampantais Anastasios Ioannidis Konstantinos Gkagkalidis Ioannis Vakalopoulos Chrysovalantis Toutziaris Christos Patsialas Leonidas Laskaridis Panagiotis Dimopoulos Georgios Dimitriadis 《Urological research》2014,42(6):527-532
The aim of the study is to determine whether dermal scarification is equally effective for treating acute renal colic compared to diclofenac sodium intramuscular therapy. A prospective, randomized controlled study was conducted with methodologic rigor based on CONSORT criteria. A total of 291 patients, aged ≥18 years, suffering from acute renal colic were included in this trial and randomly assigned in two groups. Patients in the first group (A) received endodermal injection (dermal scarification) of 1 ml normal saline at the area of intensity of pain. The second group (B) received 75 mg diclofenac sodium by intramuscular injection. The success of each method defined the primary end point. Pain intensity before and after treatment was assessed using a visual analog scale. The time onset and the duration of analgesia were also recorded. There was no significant difference between the two groups regarding hematuria (p = 0.158), stone identification at KUB (p = 0.751) and mean pain intensity (p = 0.609) before treatment initiation. The method was successful in 75.5 % of patients in group A and 74.3 % of patients in group B (p = 0.812). Mean pain reduction was comparable, 5.65 ± 3.05 in group A and 5.34 ± 2.99 in group B (p = 0.379), with dermal scarification eliciting its effect considerably faster, whereas the duration of analgesia was longer in the diclofenac group (p < 0.05). In conclusion, dermal scarification could constitute an alternative method for treating renal colic as it is equally effective compared to the standard treatment of diclofenac sodium. 相似文献
60.
Ian P Harrison Stavros Selemidis 《Clinical and experimental pharmacology & physiology》2014,41(8):533-542
Reactive oxygen species (ROS), the cellular products of myriad physiological processes, have long been understood to lead to cellular damage if produced in excess and to be a causative factor in cancer through the oxidation and nitration of various macromolecules. Reactive oxygen species influence various hallmarks of cancer, such as cellular proliferation and angiogenesis, through the promotion of cell signalling pathways intrinsic to these processes and can also regulate the function of key immune cells, such as macrophages and regulatory T cells, which promote angiogenesis in the tumour environment. Herein we emphasize the family of NADPH oxidase enzymes as the most likely source of ROS, which promote angiogenesis and tumourigenesis through signalling pathways within endothelial, immune and tumour cells. In this review we focus on the pharmacological inhibitors of NADPH oxidases and suggest that, compared with traditional anti‐oxidants, they are likely to offer better alternatives for suppression of tumour angiogenesis. Despite the emerging enthusiasm towards the use of NADPH oxidase inhibitors for cancer therapy, this field is still in its infancy; in particular, there is a glaring lack of knowledge of the roles of NADPH oxidases in in vivo animal models and in human cancers. Certainly a clearer understanding of the relevant signalling pathways influenced by NADPH oxidases during angiogenesis in cancer is likely to yield novel therapeutic approaches. 相似文献