全文获取类型
收费全文 | 252120篇 |
免费 | 17820篇 |
国内免费 | 1130篇 |
专业分类
耳鼻咽喉 | 2787篇 |
儿科学 | 6498篇 |
妇产科学 | 4595篇 |
基础医学 | 32945篇 |
口腔科学 | 4557篇 |
临床医学 | 25331篇 |
内科学 | 53611篇 |
皮肤病学 | 3383篇 |
神经病学 | 24283篇 |
特种医学 | 8399篇 |
外国民族医学 | 11篇 |
外科学 | 38475篇 |
综合类 | 3456篇 |
一般理论 | 318篇 |
预防医学 | 21433篇 |
眼科学 | 6561篇 |
药学 | 16972篇 |
6篇 | |
中国医学 | 361篇 |
肿瘤学 | 17088篇 |
出版年
2023年 | 1339篇 |
2022年 | 2413篇 |
2021年 | 5439篇 |
2020年 | 3263篇 |
2019年 | 5301篇 |
2018年 | 5953篇 |
2017年 | 4472篇 |
2016年 | 4961篇 |
2015年 | 5828篇 |
2014年 | 8605篇 |
2013年 | 11799篇 |
2012年 | 18015篇 |
2011年 | 18899篇 |
2010年 | 10576篇 |
2009年 | 9427篇 |
2008年 | 16595篇 |
2007年 | 17451篇 |
2006年 | 17305篇 |
2005年 | 17282篇 |
2004年 | 16193篇 |
2003年 | 15042篇 |
2002年 | 14061篇 |
2001年 | 2104篇 |
2000年 | 1602篇 |
1999年 | 2322篇 |
1998年 | 3068篇 |
1997年 | 2563篇 |
1996年 | 2184篇 |
1995年 | 2095篇 |
1994年 | 1746篇 |
1993年 | 1572篇 |
1992年 | 1259篇 |
1991年 | 1152篇 |
1990年 | 1000篇 |
1989年 | 974篇 |
1988年 | 967篇 |
1987年 | 945篇 |
1986年 | 951篇 |
1985年 | 964篇 |
1984年 | 1217篇 |
1983年 | 1123篇 |
1982年 | 1365篇 |
1981年 | 1313篇 |
1980年 | 1145篇 |
1979年 | 703篇 |
1978年 | 747篇 |
1977年 | 635篇 |
1976年 | 584篇 |
1975年 | 469篇 |
1974年 | 472篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
101.
Ming Zhao Cheng Simon C F Rawlinson Andrew A Pitsillides Gul Zaman Subburaman Mohan David J Baylink Lance E Lanyon 《Journal of bone and mineral research》2002,17(4):593-602
The mechanism by which mechanical strain and estrogen stimulate bone cell proliferation was investigated using monolayer cultures of human osteoblastic TE85 cells and female human primary (first-passage) osteoblasts (fHOBs). Both cell types showed small but statistically significant dose-dependent increases in [3H]thymidine incorporation in response to 17beta-estradiol and to a single 10-minute period of uniaxial cyclic strain (1 Hz). In both cell types, the peak response to 17beta-estradiol occurred at 10(-8) - 10(-7) M and the peak response to strain occurred at 3500 microstrain ((mu)epsilon). Both strain-related and 17beta-estradiol-related increases in [3H]thymidine incorporation were abolished by the estrogen receptor (ER) modulator ICI 182,780 (10-8 M). Tamoxifen (10(-9) - 10(-8) M) increased [3H]thymidine incorporation in both cell types but had no effect on their response to strain. In TE85 cells, tamoxifen reduced the increase in [3H]thymidine incorporation associated with 17beta-estradiol to that of tamoxifen alone but had no such effect in fHOBs. In TE85 cells, strain increased medium concentrations of insulin-like growth factor (IGF) II but not IGF-I, whereas 17beta-estradiol increased medium concentrations of IGF-I but not IGF-II. Neutralizing monoclonal antibody (MNAb) to IGF-I (3 microg/ml) blocked the effects of 17beta-estradiol and exogenous truncated IGF-I (tIGF-I; 50 ng/ml) but not those of strain or tIGF-II (50 ng/ml). Neutralizing antibody to IGF-II (3 microg/ml) blocked the effects of strain and tIGF-II but not those of 17beta-estradiol or tIGF-I. MAb aIR-3 (100 ng/ml) to the IGF-I receptor blocked the effects on [3H]thymidine incorporation of strain, tIGF-II, 17beta-estradiol, and tIGF-I. HOBs and TE85 cells, act similarly to rat primary osteoblasts and ROS 17/2.8 cells in their dose-related proliferative responses to strain and 17beta-estradiol, both of which can be blocked by the ER modulator ICI 182,780. In TE85 cells (as in rat primaries and ROS 17/2.8 cells), the response to 17beta-estradiol is mediated by IGF-I, and the response to strain is mediated by IGF-II. Human cells differ from rat cells in that tamoxifen does not block their response to strain and reduces the response to 17beta-estradiol in TE85s but not primaries. In both human cell types (unlike rat cells) the effects of strain and IGF-II as well as estradiol and IGF-I can be blocked at the IGF-I receptor. 相似文献
102.
103.
104.
Guerard W. Byrne Johannes M. Schirmer David N. Fass Sumeet S. Teotia Walter K. Kremers Hui Xu Bashoo Naziruddin Henry D. Tazelaar John S. Logan Christopher G. A. McGregor 《American journal of transplantation》2005,5(5):1011-1020
Microvascular thrombosis is a prominent feature in cardiac delayed xenograft rejection (DXR). We investigated the impact of warfarin or low-molecular-weight heparin (LMWH) anti-coagulation on xenograft function using a heterotopic pig-to-primate model. Donor hearts were from CD46 transgenic pigs and baboon immunosuppression included tacrolimus, sirolimus, anti-CD20 and TPC, an alpha-galactosyl-polyethylene glycol conjugate. Three groups of animals were studied. Group 1 (n = 9) was treated with warfarin, Group 2 (n = 13) with LMWH and Group 3, received no anti-coagulant drugs. The median duration of xenograft function was 20 days (range 3-62 days), 18 days (range 5-109 days) and 15 days (range 4-53 days) in Groups 1 to 3 respectively. Anti-coagulation achieved the targeted international normalized prothrombin ratio (INR) and anti-factor Xa levels consistent with effective in vivo therapy yet, no significant impact on median xenograft function was observed. At rejection, a similar histology of thrombosis and ischemia was apparent in each group and the levels of fibrin deposition and platelet thrombi in rejected tissue was the same. Anti-coagulation with warfarin or LMWH did not have a significant impact on the onset of DXR and microvascular thrombosis. However, a role for specific anti-coagulant strategies to achieve long-term xenograft function cannot be excluded. 相似文献
105.
106.
Joseph F Malouf Manfredi Ballo Heidi M Connolly David O Hodge Regina M Herges Charles J Mullany Fletcher A Miller 《Journal of the American Society of Echocardiography》2005,18(3):252-256
The purpose of this study was to provide, in a large number of patients, comprehensive Doppler echocardiographic assessment of normal St Jude Medical mitral valve prosthesis function using Doppler-derived hemodynamic variables, including the mitral valve prosthesis-to-left ventricular outflow tract time-velocity integral ratio and prosthesis performance index. The pressure half-time was less than 130 milliseconds in all patients, and all but one patient had either a peak early mitral diastolic velocity of 2 m/s or less or a mitral valve prosthesis-to-left ventricular outflow tract time-velocity integral ratio of less than 2.2. There was a significant (P < .001) negative correlation between the prosthesis performance index and prosthesis size. This negative correlation suggests that there is more efficient use of the in vitro geometric orifice area with smaller prostheses. 相似文献
107.
OBJECTIVE: This study was designed to investigate potential areas of practice for the clinical laboratory scientist (CLS) and to propose a graduate curriculum to prepare the practitioner for an advanced level of practice. DESIGN: Meta-analysis of PharmD, physician assistant, physical therapy, and nurse practitioner curricula focusing on academic and clinical advanced practice was used to develop an educational model and curriculum for a professional doctorate in clinical laboratory science (CLS). MAIN OUTCOME MEASURE: (1) New educational model for CLS advanced practice; (2) A proposed curriculum for a Doctorate of Clinical Laboratory Science degree. RESULTS: A new curriculum model was adapted from established healthcare educational models. CONCLUSION: Although there is a need for a baccalaureate degree in CLS there is also a role for expanded education and responsibilities for CLS practitioners. The CLS Advanced Practitioner design focuses on moving students from the baccalaureate level to the doctoral level and prepares the individual to become an integral part of the healthcare team. 相似文献
108.
Quantitatively distinct requirements for signaling-competent cell spreading on engineered versus natural adhesion ligands. 总被引:1,自引:0,他引:1
Gabriel P Richman David A Tirrell Anand R Asthagiri 《Journal of controlled release》2005,101(1-3):3-12
To design synthetic microenvironments that elicit desired cell behaviors, we must better understand the molecular mechanisms by which cells interact with candidate biomaterials. Using cell lines with distinct alpha5beta1 integrin expression profiles, we demonstrate that this integrin mediates cell spreading on substrata coated with genetically engineered artificial extracellular matrix (aECM) proteins containing the RGD sequence (RGD-containing aECM protein [aRGD]) but lacking the PHSRN synergy site. Furthermore, aRGD-mediated adhesion stimulates an intracellular focal adhesion kinase (FAK) signal that is indicative of integrin tethering. Although both aRGD and the natural ECM protein fibronectin (FN) support alpha5beta1 integrin-mediated cell spreading, quantitative single-cell analysis revealed that aRGD-mediated spreading requires ten-fold greater threshold amount of integrin expression than FN-mediated spreading. Our analysis demonstrates that aRGD-based substrata mediate both biophysical (cell spreading) and biochemical (FAK signaling) events via the alpha5beta1 integrin, albeit with efficacy quantitatively distinct from that of natural ECM proteins that possess the full spectrum of adhesion and synergy domains. 相似文献
109.
Leslee J. Shaw Romalisa Miranda-Peats Piotr Slomka John Friedman Sean W. Hayes Daniel S. Berman Gary V. Heller Marcin Dada William E. Boden Paul Casperson Robert A. O’Rourke Ronald Schwartz William S. Weintraub David J. Maron Spencer King Koon Teo Pamela Hartigan 《Journal of nuclear cardiology》2006,13(5):685-698
Background Stress gated myocardial perfusion single photon emission computed tomography (gSPECT) is increasingly used before and after
intercurrent therapeutic intervention and is the basis for ongoing evaluation in the Department of Veterans Affairs clinical
outcomes utilizing revascularization and aggressive drug evaluation (COURAGE) trial.
Methods and Results The COURAGE trial is a North American multicenter randomized clinical trial that enrolled 2287 patients to aggressive medical
therapy vs percutaneous coronary intervention plus aggressive medical therapy. Three COURAGE nuclear substudies have been
designed. The goals of substudy 0 are to examine the diagnostic accuracy of the extent and severity of inducible ischemia
at baseline in COURAGE patients compared with patient symptoms and quantitative coronary angiography and to explore the relationship
between inducible ischemia and the benefit from revascularization when added to medical therapy. Substudy 1 will correlate
the extent and severity of provocative ischemia with the frequency, quality, and instability of recurrent symptoms in postcatheterization
patients. Substudy 2 (n _ 300) will examine the usefulness of sequential gSPECT monitoring 6 to 18 months after therapeutic
intervention. Together, these nuclear substudies will evaluate the role of gSPECT to determine the effectiveness of aggressive
risk-factor modifications, lifestyle interventions, and anti-ischemic medical therapies with or without revascularization
in reducing patients’ ischemic burdens.
Conclusions The unfolding of evidence on the application of gSPECT in trials such as COURAGE defines a new era for nuclear cardiology.
We hope the evidence that emerges from the COURAGE trial will further establish the role of nuclear imaging in the evidence-based
management of patients with stable coronary disease.
The COURAGE trial was supported by the Cooperative Studies Program of the Department of Veterans Affairs Office of Research
and Development in collaboration with the Canadian Institutes of Health Research. Unrestricted research grants were obtained
from Merck & Co; Pfizer Pharmaceuticals; Bristol-Myers Squibb Medical Imaging; Astellas Pharma; Kos Pharmaceuticals; Data
Scope; Astra Zeneca Pharmaceuticals; Astra-Zeneca-Canada; Schering-Plough Coorporation, Ltd; Sanofi-Aventis, Inc; First Horizon;
and GE Healthcare. All industrial funding for this trial was directed through the Department of Veterans Affairs. Additional
funding for this substudy was provided by grants to the Department of Veterans Affairs and Canadian Institutes of Health Research
from Astellas Pharma and Bristol-Myers-Squibb Medical Imaging. 相似文献
110.
Williamson Kathleen A.; Hever Ann M.; Rainger Joe; Rogers R. Curtis; Magee Alex; Fiedler Zdenek; Keng Wee Teik; Sharkey Freddie H.; McGill Niolette; Hill Clare J.; Schneider Adele; Messina Mario; Turnpenny Peter D.; Fantes Judy A.; van Heyningen Veronica; FitzPatrick David R. 《Human molecular genetics》2006,15(12):2030
Table 1 相似文献