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A Pannella G Ragaglia F Laboranti M Fossa G L Picchio M Zambianchi P Zanotto 《Minerva chirurgica》1992,47(18):1441-1447
Acute pathologies of the biliary tract in geriatric patients were examined in this study taking into account the major causes, treatment used and results obtained. All patients aged over 65 who had been hospitalised during the past 17 years for acute pathologies of the biliary tract (564 cases, equivalent to 34.2% of all in-patients suffering from acute biliary pathologies) were included in the study. These patients were then subdivided into 3rd and 4th age groups (65-74 and < 75 years respectively). The results obtained in the 3rd age group (267 patients, 60%) showed the greatest number of cases of inflammatory lithiasic disease of the cholecystus (61.2%) and VBP (17.7%), whereas 45 patients, equivalent to 49.5%, presented tumours with jaundice. Out of a total of 179 cases in patients in the 4th age group, equivalent to 39.3%, 119 (66.5%) were suffering from lithiasic cholecystitis and 16 (8.9%) from calcolosis of the VBP with jaundice. Cancer of the pancreas head was diagnosed in 27 patients (58.7%), whereas 9 (19.6%) had obstruent cancer of the biliary tract. The Authors conclude that both the preoperative preparation, the choice of operation and postoperative treatment give satisfactory results with a very low early mortality (0.8% in non-tumour cases and 6.9% in tumour cases). 相似文献
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Studies of proteins that inhibit tissue factor activity have generally been conducted using either an extracted tissue homogenate ("thromboplastin") or tissue factor protein reconstituted into phospholipid vesicles rather than with tissue factor expressed in cell membranes (its physiological environment). In the present study, a human fibroblast cell strain was used to evaluate the effects of lipoprotein associated coagulation inhibitor (LACI), placental anticoagulant protein (PAP), and apolipoprotein A-II (apo A-II) on human tissue factor in cell membranes. LACI was tested from 7.8 to 500 pmol/L on fibroblasts cultured at cell densities ranging from 3,500 to 9,925 cells/well, and caused a progressive inhibition of tissue factor activity. PAP was tested from 3.9 nmol/L to 1 mumol/L at cell densities ranging from 4,500 to 15,400 cells/well and caused up to 83% inhibition of tissue factor activity. Inhibition by these proteins appeared to be influenced by cell density as well as whether the cells were intact or disrupted. Apo A-II, up to 1 mumol/L, did not inhibit the tissue factor activity of intact or disrupted fibroblasts at any cell density examined even though it did inhibit the activity of tissue factor in phospholipid vesicles. Of these inhibitors of tissue factor-dependent activation of factor X, LACI was the most effective in suppressing the generation of factor Xa activity. The effects obtained with apo A-II are clearly dependent on the nature of the tissue factor preparation with which it is tested. The disparity between the inhibitory effect of apo A-II on the activity of tissue factor reconstituted into lipid vesicles and the absence of effect on the activity of tissue factor remaining in cell membranes serves to reemphasize the necessity of reexamining results obtained with model systems using as nearly physiological reagents as possible. 相似文献
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Myosin VIIA gene: heterogeneity of the mutations responsible for Usher syndrome type IB 总被引:8,自引:1,他引:8
Levy G; Levi-Acobas F; Blanchard S; Gerber S; Larget-Piet D; Chenal V; Liu XZ; Newton V; Steel KP; Brown SD; Munnich A; Kaplan J; Petit C; Weil D 《Human molecular genetics》1997,6(1):111-116
Usher syndrome is recognized as the most frequent cause of hereditary
deaf-blindness. Usher syndrome type I (USH1), the most severe form of the
disease, is characterized by profound congenital sensorineural deafness,
constant vestibular dysfunction, and retinitis pigmentosa of prepubertal
onset. This form is genetically heterogeneous and five loci (USH1A-E) have
been mapped thusfar. However, only the gene responsible for USH1 B (which
accounts for approximately 75% of USH1 cases) has been characterized. It
encodes a long-tailed unconventional myosin, myosin VIIA, with a predicted
2215 amino acid sequence. Primers covering the complete myosin VIIA coding
sequence as well as the 3' non coding sequence were designed, allowing
direct sequence analysis of each of the 48 coding exons and flanking splice
sites in seven patients affected by USH1. Four novel mutations were thereby
identified. The possibility should now be considered of a sequence-based
prenatal diagnosis in some of the families affected by this very severe
form of Usher syndrome.
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Evolutionary silencing of the human elastase I gene (ELA1) 总被引:6,自引:0,他引:6