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61.
目的研究丙型肝炎病毒(HCV)核心蛋白6号结合蛋白基因(Hcbp6)序列表达的调控机制。方法根据软件对启动子的预测,选取翻译起始密码子ATG上游3256bp及下游180bp的DNA序列,分成5段活性区域,分别以聚合酶链反应技术(PCR),肝母细胞瘤细胞系HePG2基因组DNA为模板,扩增该启动子DNA片段,将其克隆至PCAT3中,构建PCAT3-Hcbp6-P报告基因表达载体,将该质粒分别转染HePG2,NIH3T3细胞,用酶联免疫吸附法检测报告基因编码产物氯霉素乙酰转移酶(CAT)的表达活性。结果发现质粒pCAT3-Hcbp6-1066p和pCAT3-Hcbp6-240p能够指导CAT的表达,其平均吸光度值(4)是PCAT3-basic对照质粒的3.1倍和6.4倍。结论本研究克隆的启动子DNA序列具有转录活性,这一结果为研究HcbP6的调节机制,进一步阐明HCV核心蛋白的作用机制奠定了基础。 相似文献
62.
目的 探讨白细胞介素 10 (IL 10 )在过敏性紫癜血管内皮损伤中的作用及机制。方法 建立人脐静脉内皮细胞 (HUVEC)培养模型 ,ELISA法检测过敏性紫癜患儿外周血单个核细胞 (PB MC)活化后培养上清IL 6、IL 1β、TNF α、IL 10等细胞因子的含量 ;AnnexinV/PI双染色法 ,流式细胞仪检测过敏性紫癜患儿PBMC培养上清所诱导的内皮细胞凋亡率。结果 ①过敏性紫癜组PBMC体外刺激活化后IL 6、IL 1β、TNF α、IL 10等细胞因子的分泌量均明显高于对照组 (P <0 0 1) ,其培养上清诱导的内皮细胞凋亡率 (34 7± 10 3) %明显高于对照组 (3 6± 0 9) %。②抗IL 6、IL 1β、TNF α单克隆抗体联合阻断可明显降低过敏性紫癜患儿PBMC培养上清诱导的内皮细胞凋亡率 (2 2 6±5 9) % ,而抗IL 10单克隆抗体阻断则明显增加过敏性紫癜患儿PBMC培养上清诱导的内皮细胞凋亡率 (5 6 9± 16 5 ) %。③于过敏性紫癜患儿PBMC培养上清加入外源性IL 10 ,可明显降低IL 6、IL 1β、INF α等炎性细胞因子的表达 ,并明显降低内皮细胞凋亡率 (11 8± 3 1) %。结论 IL 10作为机体炎症反应负反馈调节过程中的一个重要枢纽 ,在过敏性紫癜炎症因子所介导的血管内皮损伤中起重要的保护作用。 相似文献
63.
对13例体外循环病人进行了观察,发现体外循环后TXB2/6-keto-PGF1α显著增高,表明体外循环使血小板受损,而血小板受损是体外循环后失血的主要原因之一。 相似文献
64.
腺病毒介导的HSV—tk基因治疗大鼠脑胶质瘤实验研究 总被引:4,自引:0,他引:4
目的:带有HSV-tk基因的重组腺病毒(AdHCMV-tk)结合核苷类似物(NA)治疗大鼠C6脑胶质瘤。方法:用X-gal染色测定AdHCMV-lacZ转染大鼠C6胶质瘤细胞的效率。用AdHCMV-tk/ACV、GCV离体及活体治疗大鼠C6胶质瘤。结果:AdHCMV-lacZ感染C6细胞效率达100%,AdHCMV-tk感染C6细胞,在病毒感染复数为1000时,GCV和ACV半致死剂量分别为3μg/ml和20μg/ml,Ad-HCMV-tk/ACV治疗大鼠C6胶质瘤模型,大鼠生存期超过90天,而对照组分别为17.0±1.6天(生理盐水组)、14.5±1.3天(AdHCMV-lacZ组),P<0.001。结论:重组腺病毒对靶细胞感染效率可达100%,AdHCMV-tk用GCV的杀伤C6胶质瘤细胞比ACV强,而HSV-tk/ACV用腺病毒介导治疗大鼠脑肿瘤疗效显著。 相似文献
65.
本研究选择10μg/ml、20μg/ml、40μg/ml浓度的溴氰菊酯处理白纹伊蚊C6/36细胞,以MMC作为阳性对照物,观察溴氰菊酯处理24h后对C6/36细胞染色体畸变率和姐妹染色单体互换(SCE)频率的影响。结果显示,三个浓度的溴氰菊酯对C6/36细胞染色体畸变率均没有显著影响(P<0.05);溴氰菊酯浓度在40μg/ml时可诱导C6/36细胞SCE频率轻度增高(P>0.05),而溴氰菊酯浓度在10μg/ml、20μg/ml时,对C6/36细胞SCE频率没有诱导作用。表明溴氰菊酯对C6/36细胞的遗传学效应较弱 相似文献
66.
The present study examined the influences of dopamine (DA) receptor stimulation on enkephalin (Met5-enkephalin; ME) and tachykinin (substance P; SP) systems of basal ganglia of Sprague-Dawley rats, lesioned as neonates with 6-hydroxydopamine (6-OHDA). It has been proposed that the neonatal 6-OHDA-lesioned rat could serve as a model for the DA deficiency and self-injurious behavior (SIB) observed in the childhood neurological disorder. Lesch-Nyhan syndrome. In agreement with earlier work, the present study found that the neonatal 6-OHDA treatment at 3 days of age, reduced DA and caused an increase in ME and a decrease in SP content in the striatum and substantia nigra, when tested as adults. Administration of the DA precursor, L-dihydroxyphenylalanine (L-DOPA), to lesioned animals, induced SIB; increased DA and DOPAC levels; produced a greater decrease (-64%) in SP levels in the striatum and substantia nigra than was observed with lesion alone (-28%). The L-DOPA-induced decrease in SP levels and the SIB observed in the lesioned animals were blocked by pretreatment with the D1 receptor antagonist, SCH-23390. Moreover, administration of the D1 receptor agonist, SKF-38393, but not the D2 agonist, LY-171555, to lesioned animals mimicked the L-DOPA responses in all respects, except that the agonists did not alter DA or DOPAC levels. None of the DA agonists or antagonists treatments affected lesion-induced increase in ME levels in the striatum. These results indicate for the first time, that SIB precipitated by DA agonists in neonatal dopaminergic denervated animals, is associated with a marked and selective decrease in SP in the striatonigral SP neurons. This process has two components: (a) a retarded development of the SP system due to neonatal dopaminergic denervation: and (b) a depletion of the remaining SP, presumably by enhanced release due to D1 DA receptor-mediated activation of striatonigral SP neurons. 相似文献
67.
Unfractionated cytokines have been shown to induce in vitro proliferation of neonatal rat Schwann cells but the nature of the mitogen(s) is not known. A mixture of rabbit antibodies specific for recombinant interleukin-1α (IL-1α) and interleukin-1β (IL-1β) inhibited Schwann cell proliferation induced by unfractionated human cytokines whereas antibodies to interleukin-2 (IL-2) and control IgG did not. However, purified human IL-1 and recombinant human IL-1α or β did not induce Schwann cell proliferation on their own. 相似文献
68.
Robert J. Carey 《Psychopharmacology》1991,104(4):463-469
Sprague-Dawley rats with unilateral 6-OHDA substantia nigra lesions were given combined scopolamine (0.5 mg/kg IP) and apomorphine (0.05 mg/kg SC) treatments. In this animal model, scopolamine, when administered separately, induces ipsilateral rotation and apomorphine, contralateral rotation. When these drugs are co-administered at 0.5 mg/kg and 0.05 mg/kg dose levels, respectively, animals rotate in the contralateral direction, creating the opportunity for the stimulus effect of scopolamine to become associated with the response effect of apomorphine. In tests with scopolamine (0.5 mg/kg), animals that previously had scopolamine and apomorphine co-administered rotated contralaterally in the test chamber, thereby behaving as if they had received apomorphine. Thus, scopolamine exhibited a functionally acquired conditioned stimulus (CS) property by eliciting the apomorphine response of contralateral rotation as a conditioned response. This acquired CS property was extinguished with separate scopolamine trials and reacquired following one scopolamine-apomorphine co-administration trial. 相似文献
69.
70.
Effects of antimicrobial agents on spontaneous and endotoxin-induced cytokine release of human peripheral blood mononuclear cells 总被引:2,自引:0,他引:2
U. Krehmeier M. Bardenheuer G. Voggenreiter U. Obertacke F. U. Schade M. Majetschak 《Journal of infection and chemotherapy》2002,8(2):194-197
Because the immunomodulatory effects of antibiotics could possibly influence the degree of the systemic and local response
to infection, knowledge of their intrinsic influence on the host's inflammatory response appears to be essential. Therefore,
this study investigated the effects of frequently used antimicrobial agents (β-lactams, quinolones gentamicin, vancomycin
and metronidazole) on the in-vitro tumor necrosis factor (TNF)-α and interleukin (IL)-6 production of isolated human peripheral
blood mononuclear cells (PBMNC), cultured with or without endotoxin, in comparison with those effects obtained in a whole-blood
assay system. In the presence of ciprofloxacin, ofloxacin, gentamicin, vancomycin, and metronidazole, a significant inhibition
of the endotoxin-stimulated TNF-α production of human peripheral blood mononuclear cells (PBMNC) was found at therapeutic
levels. Only ofloxacin showed a significant inhibitory influence on the endotoxin-induced IL-6 production of PBMNC. In the
whole-blood assay, significant effects were not detectable. None of the antibiotics showed cytotoxicity. It is concluded that,
at present, the direct immunological effects of antibiotics should be interpreted carefully with regard to the experimental
conditions, and regardless of the therapeutic implications. To assess the potential direct immunomodulatory effect of antimicrobial
agents, different cell culture procedures should be used.
Received: October 19, 2001 / Accepted: February 15, 2002 相似文献