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可变误差多面体法用于多种维生素的同时测定 总被引:11,自引:0,他引:11
本文基于对多元校正分析模型的简要讨论,探索了应用可变误差多面体法同时测定维生索B1,B2,B6和烟酰胺的可行性。其结果准确度和精密度均较满意。维生素B1,B2,B6及烟酰胺的回收率分别是99.8±0.9%(CV),100.1±0.8%(CV),100.2±2.1%,100.1±0.7%(CV)。结果表明,通过公式KS=ASCST(CSCST)-1计算校正系数矩阵KS,并结合可变误差多面体法这一直接求解方法,能有效地提高分析结果的准确度,克服组分间的交互作用及病态,是多元校正分析的较佳策略之一。 相似文献
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Kaukola T Herva R Perhomaa M Pääkkö E Kingsmore S Vainionpää L Hallman M 《Pediatric research》2006,59(3):478-483
Intrauterine inflammation may relate to neurologic disability among preterm children. We investigated the relationship between chorioamnionitis, cord serum cytokines, and neurologic outcome. Sixty-one consecutively born very preterm extremely low birth weight (ELBW) infants were prospectively enrolled. Histologic inflammation in placenta and umbilical cord and vascular pathology were evaluated. Cord sera were analyzed for five proinflammatory cytokines. Serial brain ultrasound and magnetic resonance imaging were performed for evaluation of intraventricular hemorrhage (IVH grade I-III) and white matter damage (WMD: cystic periventricular leukomalacia or IVH grade IV). Neurologic and neurocognitive outcomes were assessed at the corrected age of 2 y. The incidences of HCA, WMD, and abnormal neurologic outcome were 48%, 13% and 19%, respectively. HCA or high IL-6 in cord serum predicted spontaneous preterm labor with high accuracy. HCA increased the risk of IVH grade II-III. In HCA, without either clinical chorioamnionitis or histologic placental perfusion defect, the children had a low risk of WMD (0%) and a low risk of abnormal neurologic outcome (6%). In HCA, the concentration of IL-6 in cord serum was lower in children with abnormal neurologic outcome than in children with normal neurologic outcome. In HCA and placental perfusion defect (compound defect) the risk of abnormal neurologic outcome was high. Compound placental defect and WMD additively predicted abnormal neurologic outcome. We propose that HCA together with other insults (placental perfusion defect or maternal systemic infection) increases the risk of poor neurologic outcome in very preterm ELBW infants. 相似文献
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A novel protein tyrosine phosphatase gene is mutated in progressive myoclonus epilepsy of the Lafora type (EPM2) 总被引:13,自引:5,他引:8
Serratosa JM; Gomez-Garre P; Gallardo ME; Anta B; de Bernabe DB; Lindhout D; Augustijn PB; Tassinari CA; Malafosse RM; Topcu M; Grid D; Dravet C; Berkovic SF; de Cordoba SR 《Human molecular genetics》1999,8(2):345-352
Progressive myoclonus epilepsy of the Lafora type or Lafora disease (EPM2;
McKusick no. 254780) is an autosomal recessive disorder characterized by
epilepsy, myoclonus, progressive neurological deterioration and
glycogen-like intracellular inclusion bodies (Lafora bodies). A gene for
EPM2 previously has been mapped to chromosome 6q23- q25 using linkage
analysis and homozygosity mapping. Here we report the positional cloning of
the 6q EPM2 gene. A microdeletion within the EPM2 critical region, present
inhomozygosis in an affected individual, was found to disrupt a novel gene
encoding a putative protein tyrosine phosphatase (PTPase). The gene,
denoted EPM2, presents alternative splicing in the 5' and 3' end regions.
Mutational analysis revealed that EPM2 patients are homozygous for
loss-of-function mutations in EPM2. These findings suggest that Lafora
disease results from the mutational inactivation of a PTPase activity that
may be important in the control of glycogen metabolism.
相似文献
107.
Wei Li John C. Detter Harvey J. Weiss Elisabeth M. Cramer Qing Zhang Edward K. Novak Rmi Favier Stephen F. Kingsmore Richard T. Swank 《Molecular genetics and metabolism》2000,71(4):599
Hermansky-Pudlak syndrome (HPS) is a recessively inherited disease with dysfunction of several related subcellular organelles including platelet-dense granules, melanosomes, and lysosomes. Our recent identification of the mutation in murine Rab geranylgeranyl transferase α-subunit gene (Rabggta) in one mouse model of HPS, the gunmetal mouse, suggested that human patients with similar phenotypes might have mutations in the human orthologous RABGGTA gene. This prompted reanalysis of the 5′-untranslated structure of the human RABGGTA gene in normal individuals and in patients with deficiencies of platelet-dense granules (αδ-SPD), alpha granules (α-SPD or gray platelet syndrome, GPS) or alpha plus dense granules (αδ-SPD). We report the complete sequence of intron α of RABGGTA and demonstrate that exon α is immediately upstream of intron α. The exon/intron structural organization of the 5′-untranslated region (UTR) of human RABGGTA was found to be similar to that of the mouse Rabggta gene. However, exons α and introns α are not homologous between mouse and human. Features of the 5′-UTR of RABGGTA suggest it is a housekeeping gene. While obvious disease-causing mutations of human RABGGTA were not found in our existing SPD patients by sequencing its entire coding region, several polymorphisms of RABGGTA including a putative cryptic splicing mutation in intron 4 were identified. Knowledge of the 5′-UTR structure of RABGGTA and its common polymorphisms will be useful for mutation screening or linkage analysis in patients with albinism, thrombocytopenia, or platelet SPD. 相似文献
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