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991.
992.
Antonio Rivero-Juarez Francisco Tellez Maria Isabel Mayorga Dolores Merino Nuria Espinosa Juan Macias Rosario Palacios María Paniagua Antonio Collado Omar Mohamed Javier Perez-Stachowski Jose Hernandez-Quero Elisa Fernandez-Fuertes Antonio Rivero 《Clinical microbiology and infection》2021,27(5):800-801
993.
Isabel Gmez-Monterrey Rosario Gonzlez Muiz Concepcin Prez-Martín María Lpez de Ceballos Joaquín Del Río M. Teresa García-Lpez 《Archiv der Pharmazie》1992,325(5):261-265
Non-rhamnose-containing phosphoramidon analogues, in which the amide bond was replaced by the isosteric ketomethylene group, have been synthesized in order to stabilize these compounds to peptidase degradation. The key step in this synthesis was suitable alkylation of a 4-ketodiester, prepared from Z-Leu chloromethyl ketone and dimethyl malonate. The ketomethylene dipeptide derivatives P-Leu psi (COCH2)(RS)Xaa-OMe (Xaa = Trp, Phe) are good inhibitors of thermolysin, ACE and specially enkephalinase. 相似文献
994.
Rosario Gil-Benso Concha Lpez-Gins Pilar Soriano Sergio Almenar Carlos Vazquez Antonio Llombart-Bosch 《Genes, chromosomes & cancer》1994,10(3):210-212
Angiosarcoma of the breast is quite rare, and the development of cutaneous angiosarcoma after segmental mastectomy and radiation therapy is even less common. A cytogenetic analysis of a mammary angiosarcoma arising in a breast after previous irradiation and segmental mastectomy for infiltrating ductal carcinoma revealed multiple clonal rearrangements involving chromosomes X, 1, 2, 3, 4, 5, 6, 7, 8, 9, 15, 17, 20, and 22. No cytogenetically analyzed angiosarcomas of the breast have been reported before. Genes Chromosom Cancer 10:210–212 (1994). © 1994 Wiley-Liss, Inc. 相似文献
995.
Christoph Schwarzer Günther Sperk Rosario Samanin Massimo Rizzi Marco Gariboldi Annamaria Vezzani 《Brain Research Reviews》1996,22(1):27-50
Recent studies have demonstrated that neuropeptide expression in forebrain neurons is responsive to changes in physiological activity. This is particularly true in the hippocampus where the expression of various neuropeptides has been reported to change in distinct neuronal populations in response to seizure activity. The aim of this work is to review and integrate the information on the pathological changes and functional modifications in neuropeptide systems of the hippocampal formation in kindling and other models of limbic epilepsy. This will be done by presenting a study in which we investigated the changes in the expression of somatostatin, neuropeptide Y (NPY), neurokinin B (NKB) and cholecystokinin-octapeptide (CCK) in the rat hippocampal principal neurons during and after kindling of the hippocampus using immunocytochernistry and in situ hybridization analysis of mRNA. NPY-IR was transiently expressed in the granule cells/mossy fibres after the preconvulsive stage 2 and 2 days but not 1 week after three consecutive tonic-clonic seizures (stage 5). A more pronounced increase was observed in NKB-IR lasting for 1 week after kindling acquisition. Only the NKB mRNA expression was enhanced in granule cells at these intervals. At stages 2 and 5, somatostatin- and NPY-IR and their mRNA levels were markedly increased in intemeurons in the deep hilus and in the polymorphic cell layer and their presumed projections to the outer molecular layer of the dentate gyrus. NKB- and CCK-IR and their mRNAs were highly expressed in basket cells at both stages of kindling. Their IR was increased in the inner molecular layer of the dentate gyrus in the ventral hippocampus. Peptide-containing neurons in the hilus appeared well preserved in spite of a reduction of Nissl stained cells by 24% in the stimulated and contralateral hippocampus at stage 5. In the hippocampus proper, somatostatin and NPY-IR were enhanced in the stratum lacunosum moleculare while CCK-IR fibres and its mRNA were particularly expressed in the pyramidal cell layer. The number of somatostatin-, NKB- and CCK-IR cells was increased in the subiculum. The intensity of these changes was similar 2 days after stages 2 or 5 of kindling. Less pronounced effects were observed 1 week after kindling completion. These results, in the frame of the literature data, suggest that lasting functional changes occur in distinct neuropeptide-containing neurons during limbic epileptogenesis. This may have profound effects on synaptic transmission and contribute to modulate hippocampal excitability. 相似文献
996.
Rosario Maroto María-Teresa de la Fuente Pedro Zapater Francisco Abad Enrique Esquerro Antonio G. García 《Brain research》1996,714(1-2)
External Ca2+ entry through various Ca t+-channel subtypes is responsible for the large oscillations of the cytosolic Ca2+ concentrations, [Ca2+]i, and cell death induced by veratridine in primary cultures of bovine chromaffin cells. Blockade by ω-conotoxin GVIA (GVIA) of N-type Ca2+ channels, by ω-agatoxin GIVA (IVA) of P-type Ca2+ channels, or by furnidipine of L-type Ca2+ channels did not afford cytoprotection. However, ω-conotoxin MVIIC (MVIIC), a wide-spectrum blocker of N-, P- and Q-type Ca2+ channels greatly protected the cells against the cytotoxic effects of veratridine. Furnidipine further enhanced the cytoprotecting effects of MVIIC. MVIIC but not fumidipine, markedly reduced the oscillations of [Ca2+]i induced by veratridine in single fura-2-loaded chromaffin cells. The results suggest that Ca2+ entry through any of the different Ca2+ channel subtypes present in bovine chromaffin cells might be cytotoxic. They also support two ideas: (i) that wide-spectrum neuronal Ca2+ channel blockers (i.e. MVIIC) might be better cytoprotecting agents than more specific neuronal Ca2+ channel blockers (i.e., GVIA, IVA, furnidipine); and (ii) that combined Ca2+ channel blockers may provide greater cytoprotection than single compounds. 相似文献
997.
2nd Congress of the International Society for Quality of Life Research Author Index 相似文献
998.
999.
The major metabolites of the carcinogen dibenz[a,j]acridine formed in rodent liver microsomal preparations were trans-3,4-dihydroxy-3,4-dihydrodibenz[a,j]acridine (DBAJAC-3,4-DHD) and dibenz[a,j]acridine 5,6-oxide (DBAJAC 5,6-oxide) [Gill et al. (1987) Carcinogenesis 8, 425-431]. The enantiomers of DBAJAC-3,4-DHD were prepared from the separable diastereoisomeric esters with (+)-endo-1,4,5,6,7,7-hexachlorobicyclo[2.2.1]hept-5-ene-2-carboxyl ic acid (HCA). The absolute configuration of trans-3(R),4(R)-dihydroxy-1,2,3,4-tetrahydrodibenz[a,j]acridine was assigned by conversion to the bis[p-(dimethylamino)benzoate] and examination of the exciton coupling in its circular dichroic (CD) spectrum. The 3(R),4(R)-tetrahydrodiol was converted to DBAJAC-3(R),4(R)-DHD. The enantiomers of DBAJAC 5,6-oxide were partially resolved by chiral stationary-phase chromatography, and subsequent methoxide attack afforded two enantiomerically enriched isomeric ethers from each fraction. The structures of the two ethers from each enantiomer were determined, and from their 1H NMR spin-spin coupling between the H5 and H6 signals and the CD spectra of the ethers, the absolute configuration of the ethers, and hence the 5,6-oxides, was determined. The enantiomeric composition of the 3,4-dihydrodiol and 5,6-oxide formed as microsomal metabolites of rat liver preparations was 69% 3R,4R and 81% 5R,6S, respectively. When rats were pretreated with 3-methylcholanthrene (MC), these percentages were 70% and 5%, indicating a reversed stereochemical preference for oxide formation in the MC-induced preparation. Results are also presented for phenobarbitone-induced rat liver and mouse liver preparations. 相似文献
1000.