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41.
硫酸镁对普鲁帕酮致心律失常的干预作用 总被引:1,自引:0,他引:1
目的探讨静脉滴注硫酸镁对普鲁帕酮致心律失常作用的干预效果。方法将92例心律失常患者随机分为对照组和干预组,每组46例。两组均口服普鲁帕酮,干预组同时静脉滴注硫酸镁,于治疗1周后常规心电图观察心律失常变化及致心律失常作用。结果心律失常消失率对照组为43.4%(20/46)、干预组为82.6%(39/46),致心律失常率对照组为19.6%、干预组为4.4%,两组比较有统计学意义(P<0.01)。结论普鲁帕酮抗心律失常同时有致心律失常作用,使用硫酸镁干预可降低致心律失常发生率。 相似文献
42.
目的:建立从小鼠骨髓中分离、纯化、培养、扩增树突状细胞(DC)前体的方法,研究细胞因子IL-4对小鼠DC体外增殖、分化成熟的影响.方法:将健康小鼠股骨骨髓细胞分离,去除悬浮细胞,将贴壁细胞分为2组,第1组加入重组细胞/巨噬细胞集落刺激因子(GM-CSF)培养;第2组加入GM-CSF和白细胞介素-4(IL-4)联合培养.诱导的DC经相差显微镜观察.结果:分离的DC前体经8~9d的培养,镜下随机取8个视野进行细胞计数,第1组细胞数量是85.38±3.42;第2组细胞数量是119.25±3.96,两组间DC数量有显著差异(t=3.19,P<0.05).且细胞纯度达90%以上,具有典型的树枝状或裙褶状突起.结论:用GM-CSF和IL- 4联合作用更能促进DC的体外扩增及分化. 相似文献
43.
目的观察抑酸药(法莫替丁、鼠李铋镁)对马来酸多潘立酮(健胃药)在健康人体药代动力学的影响。方法10名健康受试者未服和服用抑酸药后,单剂量口服马来酸多潘立酮10mg,用LC/MS/MS测定血药浓度,用Win-NonLin5.0软件计算药代动力学参数,并用Spss12.0软件比较主要药代动力学参数。结果未服和服用抑酸药后,单剂量口服马来酸多潘立酮,其药代动力学参数如下:tmax分别为(0.85±0.24)、(2.20±1.78)h,Cmax分别为(9.68±5.37)、(7.18±4.12)μg.L-1,AUC0~tn分别为(38.18±19.76)、(49.96±10.35)μg.h.L-1。显示服用抑酸药后,马来酸多潘立酮的tmax延长,有显著性差异(P=0.04);AUC0-tn增加,峰浓度降低,但无显著性差异(分别为P=0.1、0.06)。结论在健康人体内,法莫替丁、鼠李铋镁不影响马来酸多潘立酮的吸收程度;但使其吸收速度减慢。 相似文献
44.
戴晓慧 《中国卫生标准管理》2021,(5):72-74
目的 观察阴式子宫瘢痕妊娠病灶清除术治疗剖宫产术后瘢痕妊娠的意义.方法 选取我院2018年10月—2019年10月收治的64例剖宫产术后瘢痕妊娠患者的临床资料,根据手术方案的不同,将实施阴式子宫瘢痕妊娠病灶清除术的病例作为观察组(n=33),将选择腹腔镜子宫瘢痕妊娠病灶消除术的病例作为对照组(n=31).比较两组手术疗... 相似文献
45.
目的:股骨颈脆性骨折是后果最严重、医疗花费最高和病死率最高的骨质疏松性骨折类型。股骨颈几何参数(femoral neck geometric parameters,FNGPs)是反映股骨颈几何学特征的重要参数,与股骨颈强度和脆性骨折风险密切相关。股骨颈脆性骨折的发病率存在明显的种族差异,但FNGPs是否有种族差异尚未明确。本研究旨在比较中国女性与日本女性FNGPs的差异。方法:本研究为横断面研究,从湖南省长沙市及周边地区招募女性健康志愿者3 859名,年龄为10.0~86.0(45.7±17.1)岁。测量并记录研究对象的体重、身高,并计算其体重指数(body mass index,BMI),采用双能X线骨密度测量仪测量研究对象的股骨颈投射骨面积(bone area, BA)和股骨颈骨密度(bone mineral density,BMD)。采用BA和/或BMD计算各种FNGPs,包括股骨颈轴长中点的外周直径(outer diameter,OD)、横截面积(cross-sectional area,CSA)、平均皮质厚度(cortical thickness,CT)、内皮质直径(endo... 相似文献
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48.
针刺镇痛在临床上被广泛应用。针刺的神经传导通路与机体痛觉传导通路基本相似,对周围神经和中枢神经均有一定的影响,因此推断这可能是针刺缓解疼痛的一种调节机制。本文总结了近五年针刺治疗各种疼痛疾病的机制研究,从传导通路上分析得知针刺能激发神经元活性,改善周围神经的病理变化,增加神经元之间突触传递,修复受损的周围神经以缓解疼痛。此外,应用针刺或加用电针治疗痛症,能改善大脑内与疼痛相关各功能区之间的联系,对镇痛起到一定的中枢调控作用。在研究中还发现针刺能减少病变区炎性反应和细胞凋亡,增加细胞自噬和血管调节因子的表达。这些反应之间常存在一定的相互作用,共同缓解机体疼痛症状。然而,临床中针刺手法及辅助方法众多,治疗选取的相关穴位各异,根据疾病定位定性后选择最优组合方式是今后总结经验的重要目标。 相似文献
49.
Yu-si CHENG De-zai DAI Yin DAI 《中国药理学报》2009,(8):1099-1106
Aim: Spatial dispersion of bioactive substances in the myocardium could serve as pathological basis for arrhythmogenesis and cardiac impairment by β-adrenoceptor stimulation. We hypothesized that dispersed NADPH oxidase, protein kinase Cε (PKCε), early response gene (ERG), and matrix metalloproteinase 9 (MMP-9) across the heart by isoproterenol (ISO) medication might be mediated by the endothelin (ET) - ROS pathway. We aimed to verify if ISO induced spatially heterogeneous distribution of pPKCε, NAPDH oxidase, MMP-9 and ERG could be mitigated by either an ET receptor antagonist CPU0213 or iNOS inhibitor aminoguanidine. Methods:Rats were treated with ISO (1 mg/kg sc) for 10 days, and drug interventions (mg/kg) either CPU0213 (30 sc) or aminoguanidine (100 ip) were administered on days 8-10. Expression of NADPH oxidase, MMP-9, ERG, and PKCε in the left and right ventricle (LV, RV) and septum (S) were measured separately. Results: Ventricular hypertrophy was found in the LV, S, and RV, in association with dispersed QTc and oxidative stress in ISO-treated rats. mRNA and protein expression of MMP-9, PKCε, NADPH oxidase and ERG in the LV, S, and RV were obviously dispersed, with augmented expression mainly in the LV and S. Dispersed parameters were re-harmonized by either CPU0213, or aminoguanidine. Conclusion: We found at the first time that ISO-induced dispersed distribution of pPKCε, NADPH oxidase, MMP-9, and ERG in the LV, S, and RV of the heart, which were suppressed by either CPU0213 or aminoguanidine. It indicates that the ET-ROS pathway plays a role in the dispersed distribution of bioactive substances following sustained β-receptor stimulation. 相似文献
50.
Aim: Paeonol (2'-hydroxy-4'-methoxyacetophenone) from Cortex moutan root is a potential therapeutic agent for atherosclerosis. This study sought to investigate the mechanisms underlying anti-inflammatory effects of paeonol in rat vascular endothelial cells (VECs) in vitro.
Methods: VECs were isolated from rat thoracic aortas. The cells were pretreated with paeonol for 24 h, and then stimulated with ox-LDL for another 24 h. The expression of microRNA-21 (miR-21) and PTEN in VECs was analyzed using qRT-PCR. The expression of PTEN protein was detected by Western blotting. TNF-α release by VECs was measured by ELISA.
Results: Ox-LDL treatment inhibited VEC growth in dose- and time-dependent manners (the value of IC50 was about 20 mg/L at 24 h). Furthermore, ox-LDL (20 mg/L) significantly increased miR-21 expression and inhibited the expression of PTEN, one of downstream target genes of miR-21 in VECs. In addition, ox-LDL (20 mg/L) significantly increased the release of TNF-α from VECs. Pretreatment with paeonol increased the survival rate of ox-LDL-treated VECs in dose- and time-dependent manners. Moreover, paeonol (120 μmol/L) prevented ox-LDL-induced increases in miR-21 expression and TNF-α release, and ox-LDL-induced inhibition in PTEN expression. A dual-luciferase reporter assay showed that miR-21 bound directly to PTEN's 3'-UTR, thus inhibiting PTEN expression. In ox-LDL treated VECs, transfection with a miR-21 mimic significantly increased miR-21 expression and inhibited PTEN expression, and attenuated the protective effects of paeonol pretreatment, whereas transfection with an miR-21 inhibitor significantly decreased miR-21 expression and increased PTEN expression, thus enhanced the protective effects of paeonol pretreatment.
Conclusion: miR-21 is an important target of paeonol for its protective effects against ox-LDL-induced VEC injury, which may play critical roles in development of atherosclerosis. 相似文献
Methods: VECs were isolated from rat thoracic aortas. The cells were pretreated with paeonol for 24 h, and then stimulated with ox-LDL for another 24 h. The expression of microRNA-21 (miR-21) and PTEN in VECs was analyzed using qRT-PCR. The expression of PTEN protein was detected by Western blotting. TNF-α release by VECs was measured by ELISA.
Results: Ox-LDL treatment inhibited VEC growth in dose- and time-dependent manners (the value of IC50 was about 20 mg/L at 24 h). Furthermore, ox-LDL (20 mg/L) significantly increased miR-21 expression and inhibited the expression of PTEN, one of downstream target genes of miR-21 in VECs. In addition, ox-LDL (20 mg/L) significantly increased the release of TNF-α from VECs. Pretreatment with paeonol increased the survival rate of ox-LDL-treated VECs in dose- and time-dependent manners. Moreover, paeonol (120 μmol/L) prevented ox-LDL-induced increases in miR-21 expression and TNF-α release, and ox-LDL-induced inhibition in PTEN expression. A dual-luciferase reporter assay showed that miR-21 bound directly to PTEN's 3'-UTR, thus inhibiting PTEN expression. In ox-LDL treated VECs, transfection with a miR-21 mimic significantly increased miR-21 expression and inhibited PTEN expression, and attenuated the protective effects of paeonol pretreatment, whereas transfection with an miR-21 inhibitor significantly decreased miR-21 expression and increased PTEN expression, thus enhanced the protective effects of paeonol pretreatment.
Conclusion: miR-21 is an important target of paeonol for its protective effects against ox-LDL-induced VEC injury, which may play critical roles in development of atherosclerosis. 相似文献