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841.
V Jackson J Breiden S Gibbons L Dickinson DJ Back M Brennan EO Connor N Boyle C Fleming S Coulter‐Smith SH Khoo 《HIV medicine》2011,12(3):166-173
Objectives
The aim of the study was to determine total and unbound lopinavir (LPV) plasma concentrations in HIV‐infected pregnant women receiving lopinavir/ritonavir (LPV/r tablet) undergoing therapeutic drug monitoring (TDM) during pregnancy and postpartum.Methods
Women were enrolled in the study who were receiving the LPV/r tablet as part of their routine prenatal care. Demographic and clinical data were collected and LPV plasma (total) and ultrafiltrate (unbound) concentrations were determined in the first, second and third trimesters using high‐performance liquid chromatography–tandem mass spectrometry (HPLC‐MS/MS). Postpartum sampling was performed where applicable. Antepartum and postpartum trough concentrations (Ctrough) were compared independently [using analysis of variance (anova )] and on a longitudinal basis (using a paired t‐test).Results
Forty‐six women were enrolled in the study (38 Black African). Forty women initiated LPV/r treatment in pregnancy. Median (range) gestation at initiation was 25 (15–36) weeks and median (range) baseline CD4 count and viral load were 346 (14–836) cells/μL and 8724 (<50–267408) HIV‐1 RNA copies/mL, respectively. Forty women (87%) had LPV concentrations above the accepted minimum effective concentration for wild‐type virus (MEC; 1000 ng/mL). Geometric mean (95% confidence interval [CI]) total LPV concentrations in the first/second [3525 (2823–4227) ng/mL; n=16] and third [3346 (2813–3880) ng/mL; n=43] trimesters were significantly lower relative to postpartum [5136 (3693–6579) ng/mL; n=12] (P=0.006). In a paired analysis (n=12), LPV concentrations were reduced in the third trimester [3657 (2851–4463) ng/mL] vs. postpartum (P=0.021). No significant differences were observed in the LPV fraction unbound (fu%). Conclusions The above target concentrations achieved in the majority of women and similarities in the fu% suggest standard dosing of the LPV/r tablet is appropriate during pregnancy. However, reduced LPV concentrations in the second/third trimesters and potentially compromised adherence highlight the need for TDM‐guided dose adjustment in certain cases. 相似文献842.
Mahendra Jain Rakhee Kapadia Ravirajsinh N Jadeja Menaka C Thounaojam Ranjitsinh V Devkar SH Mishra 《Asian Pacific Journal of Tropical Biomedicine》2011,1(6):443-447
Objective
To evaluate the cytotoxicity and hepatoprotective potentials of extracts, fractions or isolated compound from the leaves of Feronia limonia (F. limonia).Methods
Qualitative phytochemical analysis of extracts, fractions or compound was performed by means of thin layer chromatography and spectroscopic assays. The % purity of compound was measured by analytical HPLC. Extracts, fractions or compound have been individually evaluated for their cytotoxicity effects (10, 20, 100, 250, 500, 750 and 1 000 µg/mL). Based on the inhibitory concentration (IC50) obtained from the cell viability assay, graded concentrations of extracts, fractions or isolated compound were assessed (10, 20, 50, 100, 200 µg/mL) for its hepatoprotective potential against CCl4-induced hepatotoxicity by monitoring activity levels of serum glutamatic pyruvatic transaminase (SGPT) and serum glutamic oxaloacetic transaminase (SGOT).Results
Results indicated that the methanol extract of F. limonia was non-toxic and hepatoprotective in nature as compared with the petroleum ether extract. The acetone fraction of methanolic extract also showed similar properties but the subsequent two fractions were cytotoxic. However, the pure compound isolated from the penultimate fraction of methanolic extract was non-toxic and hepatoprotective in nature. Biochemical investigations (SGOT, SGPT) further corroborated these cytological observations.Conclusions
It can be concluded from this study that F. limonia methanol extract, some fractions and pure isolated compound herein exhibit hepatoprotective activity. However, cytotoxicity recorded in the penultimate fraction and investigation of structural details of pure compound warrants further study. 相似文献843.
Corson K Doak MN Denneson L Crutchfield M Soleck G Dickinson KC Gerrity MS Dobscha SK 《Pain medicine (Malden, Mass.)》2011,12(10):1490-1501
844.
D Sachs CF Villarreal FQ Cunha CA Parada SH Ferreira 《British journal of pharmacology》2009,156(5):826-834
Background and purpose:
Protein kinase (PK) A and the ε isoform of PKC (PKCε) are involved in the development of hypernociception (increased sensitivity to noxious or innocuous stimuli) in several animal models of acute and persistent inflammatory pain. The present study evaluated the contribution of PKA and PKCε to the development of prostaglandin E2 (PGE2)-induced mechanical hypernociception.Experimental approach:
Prostaglandin E2-induced mechanical hypernociception was assessed by constant pressure rat paw test. The activation of PKA or PKCε was evaluated by radioactive enzymic assay in the dorsal root ganglia (DRG) of sensory neurons from the hind paws.Key results:
Hypernociception induced by PGE2 (100 ng) by intraplantar (i.pl.) injection, was reduced by i.pl. treatment with inhibitors of PKA [A-kinase-anchoring protein St-Ht31 inhibitor peptide (AKAPI)], PKCε (PKCεI) or adenylyl cyclase. PKA activity was essential in the early phase of the induction of hypernociception, whereas PKC activity was involved in the maintenance of the later phase of hypernociception. In the DRG (L4-L5), activity of PKA increased at 30 min after injection of PGE2 but PKC activity increased only after 180 min. Moreover, i.pl. injection of the catalytic subunit of PKA induced hypernociception which was markedly reduced by pretreatment with an inhibitor of PKCε, while the hypernociception induced by paw injection of PKCε agonist was not affected by an inhibitor of PKA (AKAPI).Conclusions and implications:
Taken together, these findings are consistent with the suggestion that PKA activates PKCε, which is a novel mechanism of interaction between these kinases during the development of PGE2-induced mechanical hypernociception. 相似文献845.
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