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991.
Roger Suau Marta Vidal Ruth Aguilar Gemma Ruiz-Olalla Miquel Vázquez-Santiago Chenjerai Jairoce Augusto J. Nhabomba Ben Gyan David Dosoo Kwaku Poku Asante Seth Owusu-Agyei Joseph J. Campo Luis Izquierdo David Cavanagh Ross L. Coppel Virander Chauhan Evelina Angov Sheetij Dutta Carlota Dobaño 《Vaccine》2021,39(4):687-698
BackgroundThe evaluation of immune responses to RTS,S/AS01 has traditionally focused on immunoglobulin (Ig) G antibodies that are only moderately associated with protection. The role of other antibody isotypes that could also contribute to vaccine efficacy remains unclear. Here we investigated whether RTS,S/AS01E elicits antigen-specific serum IgA antibodies to the vaccine and other malaria antigens, and we explored their association with protection.MethodsNinety-five children (age 5–17 months old at first vaccination) from the RTS,S/AS01E phase 3 clinical trial who received 3 doses of RTS,S/AS01E or a comparator vaccine were selected for IgA quantification 1 month post primary immunization. Two sites with different malaria transmission intensities (MTI) and clinical malaria cases and controls, were included. Measurements of IgA against different constructs of the circumsporozoite protein (CSP) vaccine antigen and 16 vaccine-unrelated Plasmodium falciparum antigens were performed using a quantitative suspension array assay.ResultsRTS,S vaccination induced a 1.2 to 2-fold increase in levels of serum/plasma IgA antibodies to all CSP constructs, which was not observed upon immunization with a comparator vaccine. The IgA response against 13 out of 16 vaccine-unrelated P. falciparum antigens also increased after vaccination, and levels were higher in recipients of RTS,S than in comparators. IgA levels to malaria antigens before vaccination were more elevated in the high MTI than the low MTI site. No statistically significant association of IgA with protection was found in exploratory analyses.ConclusionsRTS,S/AS01E induces IgA responses in peripheral blood against CSP vaccine antigens and other P. falciparum vaccine-unrelated antigens, similar to what we previously showed for IgG responses. Collectively, data warrant further investigation of the potential contribution of vaccine-induced IgA responses to efficacy and any possible interplay, either synergistic or antagonistic, with protective IgG, as identifying mediators of protection by RTS,S/AS01E immunization is necessary for the design of improved second-generation vaccines.Clinical trial registration: ClinicalTrials.gov: NCT008666191. 相似文献
992.
993.
Animal models have been used extensively to investigate the biology of fracture healing and spinal fusion. The goal of each spinal fusion model is to try and reproduce the correct sequence of events during osseous healing in humans. Animal models allow us the capability of dialing in fusion rates and fusion parameters depending upon the study conditions. These models have become invaluable in assessing the clinical potential of emerging technologies such as recombinant growth factors and gene therapy. 相似文献
994.
Role for macrophage migration inhibitory factor in acute respiratory distress syndrome 总被引:18,自引:0,他引:18
The critical role of macrophage migration inhibitory factor (MIF) in mediating inflammatory lung injury in acute respiratory distress syndrome (ARDS) has been raised recently. The present study has identified enhanced MIF protein expression in alveolar capillary endothelium and infiltrating macrophages in lung tissues from ARDS patients. The possibility that MIF up-regulates its synthesis in an autocrine fashion in ARDS was tested using cultured endothelial cells stimulated with MIF and a murine model of lipopolysaccharide (LPS)-induced acute lung injury. MIF induced significant MIF and tumour necrosis factor (TNF)-alpha synthesis in cultured endothelial cells and the effect was blocked by neutralizing anti-MIF antibody. A similar blocking effect was observed when MIF-stimulated endothelial cells were pretreated with neutralizing anti-TNF-alpha antibody or glucocorticoid, supporting the notion that MIF induced TNF-alpha production via an amplifying pro-inflammatory loop. Treatment with anti-MIF or glucocorticoid effectively attenuated pulmonary pathology and the synthesis of MIF or TNF-alpha in mice with LPS-induced acute lung injury. Mildly augmented expression of aquaporin 1 (AQP1) was also detected in alveolar capillary endothelium in ARDS. In vitro studies revealed that both MIF and TNF-alpha induced a small increase of AQP1 synthesis in cultured endothelial cells. These findings suggest that MIF plays a crucial pathological role leading to alveolar inflammation in ARDS. Anti-MIF and early glucocorticoid therapy may represent a novel therapeutic approach for reducing alveolar inflammation in ARDS. 相似文献
995.
996.
单片微机化微弱发光测量仪及其在肿瘤研究中的初步应用 总被引:2,自引:0,他引:2
单片微机化微弱发光测量仪由中科院生物物理所和北京科龙生物医学技术开发公司研制成功。该仪器适用于肿瘤研究中生物医学样品的微弱发光的测量。测量样品的重复性优于0.8%,稳定性优于0.5%,线性相关系数达0.9997,不仅可以进行样品的发光强度测量,还可以进行动力学曲线的测量以及样品发射光谱的测量。光谱在400nm-750nm范围内。测量方式可选择手动、半自动和自动计时三种。测量结果表明,荷瘤裸鼠血液微 相似文献
997.
牛磺酸对大鼠心脏模拟缺血再灌注损伤的保护作用 总被引:2,自引:0,他引:2
在离体大鼠心脏模拟缺血再灌注(I/R)损伤的模型上观察了牛磺酸的心肌保护作用。实验结果发现预先给大鼠牛磺酸灌胃(300mg/kg)三日或再灌注同时给药(20mmol/L),对心肌均有保护作用,明显减少心肌细胞内的Mb、LDH的漏出,降低心肌MDA的生成,减轻细胞内钙的聚集,促进心肌ATP含量的恢复。在本实验条件下预防应用牛磺酸较再灌注的同时应用更为有效,表现为更大程度地减少LDH漏出,抑制心肌MDA生成和钙聚集。结果证明牛磺酸具有心肌保护作用,对于防治心肌I/R损伤可能具有临床应用价值。 相似文献
998.
999.
Angiotensin-II stimulates nitric oxide release in isolated perfused renal resistance arteries 总被引:3,自引:0,他引:3
C. Thorup Mark Kornfeld Joseph M. Winaver Michael S. Goligorsky Leon C. Moore 《Pflügers Archiv : European journal of physiology》1998,435(3):432-434
Nitric oxide (NO) has been implicated as a modulator of the vascular effects of angiotensin II (ANG II) in the kidney. We
used a NO-sensitive microelectrode to study the effect of ANG II on NO release, and to determine the effect of selective inhibition
of the ANG II subtype I receptor (AT1) with losartan (LOS) and candesartan (CAN). NO release from isolated and perfused renal
resistance arteries was measured with a porphyrin-electroplated, carbon fiber. The vessels were microdissected from isolated
perfused rat kidneys and perfused at constant flow and pressure in vitro. The NO-electrode was placed inside the glass collection
cannula to measure vessel effluent NO concentration. ANG II stimulated NO release in a dose-dependent fashion: 0.1 nM, 10 nM
and 1000 nM ANG II increased NO-oxidation current by 85±18 pA (n = 11), 148±22 pA (n = 11), and 193±29 pA (n = 11), respectively. These currents correspond to changes in effluent NO concentration of 3.4±0.5 nM, 6.1±1.1 nM, and 8.2±1.3 nM,
respectively. Neither LOS (1 μM) nor CAN (1 nM) significantly affected basal NO production, but both AT1-receptor blockers
markedly blunted NO release in response to ANG II (10 nM): 77±6% inhibition with LOS (n = 8) and 63±9% with CAN (n = 8). These results are the first to demonstrate that ANG II stimulates NO release in isolated renal resistance arteries,
and that ANG II-induced NO release is blunted by simultaneous AT1-receptor blockade. Our findings suggest that endothelium-dependent
modulation of ANG II-induced vasoconstriction in renal resistance arteries is mediated, at least in part, by AT1-receptor-dependent
NO release.
Received: 24 September 1997 / Accepted: 20 October 1997 相似文献
1000.