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1.
Roberto V.P. Ribeiro Mitesh V. Badiwala Danny Ramzy Laura C. Tumiati Vivek Rao 《The Journal of thoracic and cardiovascular surgery》2019,157(2):615-625.e1
Objective
Hypertonic saline (HTS) has potent immune and vascular effects. We assessed recipient pretreatment with HTS on allograft function in a porcine model of heart transplantation and hypothesized that HTS infusion would limit endothelial and left ventricular (LV) dysfunction following transplantation.Methods
Heart transplants were performed after 6 hours of cold ischemic storage. Recipient pigs were randomized to treatment with or without HTS (7.5% NaCl) before cardiopulmonary bypass (CPB). Using a myograft apparatus, coronary artery endothelial-dependent (Edep) and -independent (Eind) relaxation was assessed. LV performance was determined using pressure-volume loop analysis. Pulmonary interleukin (IL)-2, IL-6, and tumor necrosis factor (TNF)-α expression was measured.Results
Weaning from CPB and LV performance after transplantation were improved in HTS-treated animals. Successful weaning from CPB was greater in the HTS-treated hearts (8 of 8 vs 2 of 8; P < .05). Mean LV functional recovery was improved in the HTS-treated animals, as assessed by preload recruitable stroke work (65 ± 10% vs 27 ± 10%; P < .001) and end-systolic elastance (55 ± 7% vs 37 ± 4%; P < .001). Treatment with HTS resulted in improved Edep (mean maximum elastance [Emax], 56 ± 5% vs 37 ± 7%; P < .001) and Eind (mean Emax%, 77 ± 6% vs 52 ± 4%; P < .001) vasorelaxation compared with control. Pulmonary expression of IL-2, IL-6, and TNF-α increased following transplantation, whereas HTS therapy attenuated IL production (P < .001). Transplantation increased plasma TNF-α levels and LV TNF-α expression, whereas HTS prevented this up-regulation (P < .001).Conclusions
Recipient HTS pretreatment preserves allograft vasomotor and LV function, and HTS therapy limits CPB-induced injury. HTS may be a novel recipient intervention to prevent graft dysfunction. 相似文献2.
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Bryan E.K. Guevara Suhail Saleem Wan‐Ting Chen Pa‐Fan Hsiao Yu‐Hung Wu 《Journal of cutaneous pathology》2019,46(5):347-352
Lucio phenomenon is an atypical reaction of leprosy, characterized by vasculitic lesions that can mimic antiphospholipid syndrome (APS) clinically. Distinguishing the two can be difficult as antiphospholipid autoantibodies may be present in patients with leprosy. We report on a 32‐year‐old female patient presenting with a sudden onset of fever, hemorrhagic bullae, and skin necrosis on her lower legs. She was treated for APS due to the presence of antiphospholipid antibodies but had an inadequate response. A skin biopsy revealed thrombotic vasculopathy and necrotizing vasculitis associated with aggregation of foam cells in the perivascular area and subcutis, with acid‐fast bacilli in the histiocytes and blood vessel walls. Direct immunofluorescence showed IgM, C3, and fibrinogen deposition in the superficial and deep dermal blood vessels. The pathology confirmed the diagnosis of Lucio phenomenon, and appropriate therapy was given. It is essential to evaluate the patient comprehensively, including clinical, serological, and pathological aspects, to obtain the correct diagnosis. 相似文献
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Nobumichi Takeuchi Hiroshi Shimada Koichiro Misuta Akira Nakano 《Journal of hepato-biliary-pancreatic sciences》1997,4(1):119-122
We surgically treated a patient with biliary stricture and portal vein occlusion, after operation for gastric cancer with lymphadenectomy along the hepatoduodenal ligament, that had led to choledochal stone formation and a dilatated parabiliary venous system. A 57-year-old man without hepatic dysfunction exhibited hepatic duct dilatation with choledochal stone on ultrasonography and percutaneous transhepatic cholangiography, respectively. Pharmacoportography revealed occlusion of the portal vein and dilatation of the parabiliary venous system. Of various preoperative imaging studies used, enhanced computed tomography was most useful for delineating the surgical anatomy of the hepatoduodenal ligament. Complete preservation of the dilatated vessels, which functioned as the main portal collateral pathway, resulted in a successful choledocho-jejunostomy, with an uneventful postoperative course. 相似文献
7.
目的:观察卡托普利(CaP)对自发性高血压大鼠(SHR)血管平滑肌细胞(VSMC)增殖的作用及对原癌基因及抑癌基因的影响。方法:氚-胸腺嘧啶核苷(3H-TdR)参入,电镜,原位来交及Northernblot杂交。结果:CaP在降低SHR血压同时,能减少VSMC的线粒体,粗面内质网及3H-TdR参入量(P<0.01),并能逆转c-fos,c-myc,c-sis原癌基因mRNA表达增强(P<0.05或0.01),p53抑癌基因mRNA表达减弱(P<0.01)。结论:Cap能抑制SHR的VSMC增殖,与癌基因调控的分子生物学机制有关。 相似文献
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Marta Méndez-López Magdalena Méndez Fernando Sánchez-Patán Isabel Casado Maria-Angeles Aller Laudino López Maria-Teresa Corcuera Maria-Jose Alonso Maria-Paz Nava Jaime Arias Jorge-Luis Arias 《Journal of gastrointestinal surgery》2007,11(2):187-194
To obtain a new model of chronic portal hypertension in the rat, two classical methods to produce portal hypertension, partial portal vein ligation and the oral administration of thioacetamide (TAA), have been combined. Male Wistar rats were divided into four groups: 1 (control; n?=?10), 2 [triple partial portal vein ligation (TPVL); n?=?9], 3 (TAA; n?=?11), and 4 (TPVL plus TAA; n?=?9). After 3 months, portal pressure, types of portosystemic collateral circulation, laboratory hepatic function tests (aspartate aminotransferase, alanine aminotransferase, bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase) and liver histology were studied. The animals belonging to group 2 (TPVL) developed extrahepatic portosystemic collateral circulation, associated with mesenteric venous vasculopathy without hepatic destructurization or portal hypertension. Animals from group 3 (TAA) developed cirrhosis and portal hypertension but not extrahepatic portosystemic collateral circulation, or mesenteric venous vasculopathy. Finally, the animals from group 4 (TPVL?+?TAA) developed cirrhosis, portal hypertension, portosystemic collateral circulation, and mesenteric venous vasculopathy. The association of TPVL and TAA can be used to obtain a model of chronic portal hypertension in the rat that includes all the alterations that patients with hepatic cirrhosis usually have. This could, therefore, prove to be a useful tool to study the pathophysiological mechanisms involved in these alterations. 相似文献
10.
门静脉主干缩窄法制备SD大鼠门静脉高压症模型时最佳口径的探讨 总被引:1,自引:0,他引:1
目的 探讨缩窄门静脉主干法制备SD大鼠门静脉高压症模型时的最佳缩窄口径.方法 SD大鼠70只,随机分为正常组和6个实验组,每组各10只.正常组行假手术.各实验组分别按照5、6、7、8、9、12号针头的缩窄口径行门静脉主干缩窄术.观察各组大鼠术后累积死亡率,术后状态,术前、术后即刻及术后2周时的门静脉压力,术后2周时的食管组织学变化和脾指数.结果 5、6、7、8、9、12号针头缩窄组术后3 d时大鼠的累积死亡率分别为100%、80%、70%、20%、10%、0%,与缩窄程度正相关.8、9、12号组的大鼠存活状态明显好于5、6、7号组.5、6、7、8、9、12号组术后即刻门静脉压力分别为:(5.836±0.275)、(4.557±0.419)、(3.856±0.576)、(3.343±0.433)、(2.708±0.309)、(1.957±0.358)kPa,7、8、9、12号组术后2周时门静脉压力分别为:(2.163±0.424)、(1.956±0.172)、(1.841±0.202)、(1.232±0.154)kPa,均较正常(0.881±0.165)kPa显著升高(P<0.05).术后2周,7、8、9、12号组大鼠食管下段黏膜下层平均血管数目分别为:(3.94±0.83)、(3.58±0.63)、(3.14±0.64)、(2.02±0.62)个,与正常组(1.65±0.62)个比较,除12号组外均有增多(P<0.01);固有层平均血管数目分别为:(2.24±0.64)、(2.05±0.29)、(1.52±0.28)、(0.93±0.19)个,与正常组(0.82±0.18)比较,除第12组外均增多(P<0.01);黏膜下层血管口径分别为:(4.52±1.51)、(4.05±1.23)、(3.75±1.11)、(2.03±0.86)μm,除第12组外均增大(P<0.01);脾指数分别为:(4.21±0.93)、(4.06±0.68)、(3.84 4±0.71)、(3.31±0.69)除12号组外也较正常增加(P<0.01).结论 缩窄门静脉主干可成功制成大鼠门静脉高压症模型;其最佳缩窄口径应该是:大鼠体重200 g左右时用8号针头(直径0.8mm),大鼠体重300 g左右时用9号针头(直径0.9 mm). 相似文献