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81.
目的观察丙丁酚对载脂蛋白E-/-小鼠主动脉粥样硬化斑块形成及主动脉凝集素样氧化型低密度脂蛋白受体1表达的影响,以探讨丙丁酚调节血脂以外的可能的抗动脉粥样硬化作用机制。方法将21只4周龄的雄性载脂蛋白E-/-小鼠随机分成基础饮食对照组、高脂饮食对照组和高脂饮食加丙丁酚组 相似文献
82.
目的本文检测血管内皮生长因子(VEGF)和基质金属蛋白酶(MMP-9)在大肠癌患者血清中的水平,探讨其与大肠癌恶性程度、浸润、转移的关系。方法用ELISA法对48例大肠癌患者及40例正常对照者血清VEGF和MMP-9进行检测。结果大肠癌患者血清VEGF、MMP-9的水平分别为(665.8±232.8)ng/L;(532.7±208.9)ug/L。显著高于对照组(391.6±135.2)ng/L;(317.8±132.2)ug/L(P<0.01)。并与组织分化程度、Duke’s分期有关。低分化者及C、D期患者较中、高度分化及A、B期高(P<0.01)。结论大肠癌患者血清VEGF和MMP-9水平增高,与肿瘤的组织分化程度、转移、分期有关,提示VEGF、MMP-9对大肠癌恶性程度的判断有一定的价值。 相似文献
83.
目的:探讨细胞活素肿瘤坏死因子-α(TNF-α)、SNAP(S-Nitroso-Nacetyl-penicillamine)对胰腺癌细胞产生血管内皮生长因子A、C(VEGF-A、C)的调节.方法:用Northern杂交和Western杂交法分析6种人胰腺癌细胞株中VEGF-A、C基因和蛋白的表达;以TNF-α或SNAP刺激其中两个细胞株后用逆转录-聚合酶链式反应技术(RT-PCR)分析其VEGF-A、C基因的表达.结果:Northern杂交法显示这6种胰腺癌细胞株均有4.1kb VEGF-A基因和2.4kb VEGF-C基因的表达;Western杂交法显示它们均有分子量为43kD的VEGF-A蛋白质和分子量为55kD的VEGF-C蛋白质的表达.RT-PCR分析法显示:TNF-α使细胞株COLO-357产生VEGF-A、VEGF-C mRNA分别减少约1~2.5倍、1~2倍,使细胞株CAPAN-1产生VEGF-A、VEGF-C mRNA分别减少约1倍、1.6~2.5倍;而SNAP刺激细胞株COLO-357产生VEGF-A mRNA增加约5倍,刺激细胞株CAPAN-1产生VEGF-A mRNA增加约4倍,但对这两种细胞株产生VEGF-C mRNA均无明显刺激作用.结论:细胞活素TNF-α和低氧通过调节血管内皮生长因子A、C的表达而影响胰腺癌细胞的生物学特性,抑制癌细胞的增殖,促进其凋亡、死亡或进展、恶化. 相似文献
84.
本文对52例肝硬化门脉高压性胃粘膜损害患者临床分析表明,肝功能损害与胃粘膜病变有显著相关性,而与胃底食道静脉曲张没有显著相关性。同一组病人中PHG与GEV的发生率虽有差异,但认为这种差异的临床意义不大。结合文献对PHG的发生机理和诊断治疗进行了讨论 相似文献
85.
J. G. Boonstra Johan W. van der Pijl Yves F. C. Smets Herman H. P. J. Lemkes Jan Ringers Leendert A. van Es F. J. van der Woude Jan A. Bruijn 《Transplant international》1997,10(6):451-456
To examine the incidence of interstitial and vascular
rejection in pancreas allografts and its impact on graft survival, we studied 36 percutaneous pancreas biopsies and 10 pancreas
transplantectomy specimens from 32 patients who had undergone simultaneous pancreas-kidney transplantation. Interstitial rejection
(IR) was predominantly found in the biopsies, while vascular rejection (VR) was most prominent in the transplantectomies.
Pancreas graft survival was significantly decreased for pancreas grafts that had suffered from vascular rejection when compared
to those with only interstitial rejection. Potential rejection markers, i. e., serum amylase, glucose, creatinine, and urinary
amylase, did not correlate with histological signs of rejection, although increased levels of serum amylase were, in all but
one case, associated with rejection.We conclude that a percutaneous pancreas biopsy remains the most reliable method to determine
pancreas rejection, and that by distinguishing between IR andVR, a pancreas biopsy may provide important diagnostic as well
as prognostic information.
Received: 6 March 1997 Received after revision: 5 June 1997 Accepted: 30 June 1997 相似文献
86.
54只大白鼠随机分三组,用不同方法修复坐骨神经缺损,术后60天和90天取材,作电生理、组织学和电镜观察的比较,结果表明:游离神经移植+血管植入方法和带血管蒂神经移植效果同样好,二者均显著优于单纯游离神经移植。 相似文献
87.
de Caro R. Parenti A. Capitanio G. Ori C. Bracco F. Ricchieri G. L. 《Acta neurochirurgica》1990,104(1-2):73-76
Summary A vascular malformation, consisting of a venous vessel bridgeing the right inferior petrosal sinus and the anterior spinal veins, was found in the posterior fossa. The vessel presented a ring-like course around the right trigeminal root, and it was parallel and dorsal to the basilar artery. The malformation was associated with cutaneous and hepatic angiomas and peri-osteal lipomas. It had been clinically silent for 52 years, when it thrombosed causing death. The authors think that, within a general mesenchymopatic state, this is a result of the persistence of an embryonal cerebral venous pattern. 相似文献
88.
门脉高压性胃病患者的胃壁血气变化 总被引:1,自引:0,他引:1
作者观测了43例门脉高压症患者股动脉血PO2、胃网膜有动静脉胃壁支血PO2、胃壁支静脉及肘静脉血pH、HCO3-和胃网膜右静脉压力,其中23例并有非出血期门脉高压性胃病。结果表明:①门脉高压症患者的股动脉血PO2低于对照组;②门脉高压症患者胃网膜右动静脉胃壁支血氧分压差低于对照组,胃网膜右静脉压力高于对照组,胃壁支静脉血pH和HCO3-低于对照组和同组肘静脉血。并有门脉高压性胃病者这些变化更为显著。提示门脉高压性胃病的发病机制在于门脉系压力增高、胃粘膜下动静脉短路开放、胃粘膜缺血缺氧和胃壁局部酸中毒。 相似文献
89.
Claudia Linde Cornelia Löffler Christina Kessler U. Quast 《Naunyn-Schmiedeberg's archives of pharmacology》1997,356(4):467-474
In vascular smooth muscle, openers of ATP-dependent potassium channels (K
ATP channels), such as P1075 (N-cyano-N’-(1,1-dimethylpropyl)-N’’-3-pyridylguanidine), produce relaxation. In this study we have investigated the effects of thiol-modifying agents on the
binding of P1075 and on the 86Rb+ efflux stimulating and vasorelaxant effects of the opener in rat aortic rings. The increase in 86Rb+ efflux induced by P1075 was taken as a qualitative measure of K+ channel opening. The hydrophilic SH-group-oxidizing substance, thimerosal (1 to 100μM), abolished specific binding of [3H]-P1075 with an IC50 value of 7.6±1.2μM; at 30μM, the half time for inhibition was 38min. Two other thiol-oxidizing agents, PMB (4-hydroxy-mercuribenzoic
acid) and DTBNP (2,2’-dithio-bis(5-nitropyridine)), inhibited binding up to 86% and 44%, respectively. The disulphide bond
reducing substance, DTT (1,4-dithiothreitol, 0.1 to 1mM), reduced [3H]-P1075 binding by up to 20% and partially reversed the inhibitory effect of thimerosal. In 86Rb+ efflux experiments, thimerosal (3 to 100μM) concentration-dependently increased basal efflux but inhibited P1075-stimulated
tracer efflux with an IC50 value of 7±1μM. The inhibitory effect occurred with a half-time of approximately 8min and was essentially reversed by DTT.
In rings precontracted with noradrenaline, thimerosal inhibited the vasorelaxant effect in a noncompetitive manner, shifting
the concentration-relaxation curves to the right and reducing maximum relaxation.The data show that oxidation of thiol groups
interferes with the binding of the K
ATP channel opener, P1075; concomitantly, the 86Rb+ efflux stimulating and the vasorelaxant effects are inhibited. Reduction of disulphide bonds by DTT has only minor effects
on the action of P1075. Collectively, the results suggest that intact thiol groups are essential for the functioning of the
KATP channel in rat aorta. The different kinetics governing the inhibition of opener binding and of opener-stimulated 86Rb+ efflux suggest that the SH-groups involved in the two processes differ in their accessibility to thimerosal and/or in their
reactivity.
Received: 7 April / Accepted: 9 July 1997 相似文献
90.
应用原位杂交技术,观察了二乙基亚硝胺(DEN)诱发大鼠肝癌前病变组织中胎盘型谷胱甘肽S转移酶(GST-P)mRNA的表达。结果显示,GST-PmRNA主要在癌前病变肝组织中的变异灶及灶外卵圆形细胞内表达,且在变异灶间或和同一灶内阳性细胞间表达程度不尽一致,而正常肝、再生肝组织中未见其表达。提示在分子水平上变异灶细胞及卵圆型细胞可能成为实验性肝癌的癌前期细胞 相似文献