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81.
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83.
Sysmex RAM-1与FCM定量分析网织红细胞的比较研究 总被引:1,自引:0,他引:1
目的评价Sysmex RAM-1(下称RAM-1)及流式细胞术(FCM)定量分析网织红细胞(RET)的性能.方法以 RAM-1及FCM定量分析RET,并将其113例测定结果与手工法的测定结果相比较.结果 RAM-1测定RET正常(65.5×109/L)、轻度增高(104.7×109/L)和明显增高(324.8×109/L)标本批内重复性的变异系数(CV)分别为5.89%、5.92%和3.51%,批间重复性CV为5.22%,总重复性CV<5%;RET在5×109/L~480×109/L范围内线性良好(r RAM-1=0.9998, r FCM=0.9974,P<0.001).RAM-1 分析RET在标本采集后48小时内结果稳定; RAM-1、FCM携带污染率分别为0和1.245%; RAM-1、FCM与手工法测定RET结果之间有良好的相关性,r分别为0.9760、0.9632(P<0.001).受试者工作曲线分析显示, RAM-1与FCM的灵敏度分别为0.95和0.83, 特异性分别为0.81和0.78;受试者工作曲线下面积RAM-1为0.999和0.972,而FCM为0.990、0.900.结论 RAM-1测定RET具有简便、准确、精密度高、线性好、可提供多参数并优于FCM等特点. 相似文献
84.
Electrophoretic analysis of glycoprotein enzymes in the sialidoses and mucolipidoses 总被引:2,自引:2,他引:0
D. M. SWALLOW J. S. O'BRIEN† A. T. HOOGEVEEN† D. W. BUCK§ 《Annals of human genetics》1981,45(1):29-37
Ten enzymes, all known to be glycoproteins, were examined by electrophoresis or gel isoelectric focusing in 12 different patients with primary or secondary sialidase deficiency. Aberrant electrophoretic mobilities of many of the enzymes attributable to abnormal sialylation were found in all the patients. In ten of the patients seven of the enzymes were affected. The unaffected enzymes were β -galactosidase, alkaline phosphatase and β -glucuronidase. In the cells from the two patients with I cell disease (mucolipidosis II) in which sialidase is one of many deficient enzymes, β -galactosidase, α -galactosidase, α -fucosidase and α -mannosidase were undetectable, alkaline phosphatase showed a normal electrophoretic mobility and acid phosphatase, adenosine deaminase, α -glucosidase and β -D- N -acetylhexosaminidase showed aberrant mobilities. 相似文献
85.
Functional activity of granulocytes from healthy individuals and from patients with acute leukemia in remission was studied. The increase of heat production rate (metabolic activity) after stimulation of the blood cells with in vitro formed immune complexes was measured by microcalorimeters of heat conduction type. It was demonstrated that increased heat production rate after exposure to immune complexes was significantly lower (p<0.0005) in 9 patients with acute leukemia with a remission duration of less than 6 months than in 25 healthy volunteers. 相似文献
86.
A. LAMOUR C. SOUBRANE M. ICHEN Y. L. PENNEC D. KHAYAT P. YOUINOU 《European journal of clinical investigation》1993,23(2):97-101
Abstract. A sandwich enzyme-linked immunosorbent assay was developed to assess Fc-gamma receptor III (Fc γ RIII), based on a combination of two non-competing monoclonal antibodies. This receptor was detectable in the serum of eight out of 23 patients with primary Sjögren's syndrome and two out of 23 normal controls. The proportion of FcγRIII-carrying polymorphonuclear (PMN) cells was lower (P < 0.05) in the patients with cell-free Fc γ RIII (90·4 ± 7.5%) than in the remainder (84.8 ± 8.3%). The PMN cell functions were evaluated and the diminished adherence (71.7, geometric mean) and chemotaxis (1.23) paralleled the Fc γ RIII release. The relative inefficiency of PMN cells in SS might be due to phagocytosis of immune complexes. 相似文献
87.
TAKEJI UMEMURA NOBUYOSHI YAMAMURA ATSUO NAGATA ATSUSHI SHIBATA KUNIHIKO YAMASHITA TAKEO OHATA TAKEO YAMADA TSUTOMU KATSUYAMA KENDO KIYOSAWA 《Journal of gastroenterology and hepatology》1998,13(5):471-474
A 66-year-old female with liver cirrhosis was treated by transcatheter arterial embolization (TAE) for a small hepatocellular carcinoma. She developed steatonecrosis with tenderness which occurred in the upper abdomen after TAE. The hepatic falciform artery from the middle hepatic artery was detected by arteriography. Necrosis in the upper abdomen was considered to be due to ischaemic changes caused by micromaterials for embolization of this artery, injuries of hepatic arterial endothelia slowly caused by carcinostatics, and chemotoxicity. It was considered that such complication as observed in this patient should be taken into consideration when performing TAE. 相似文献
88.
L. U. LAMM INGE-LIS THORSEN G. BRUUN PETERSEN† J. JØRGENSEN K. HENNINGSEN‡ BENTE BECH§ F. KISSMEYER-NIELSEN 《Annals of human genetics》1975,38(4):383-390
Lod scores from a study in 229 families of the linkage relations of HL-A-PGM3 to 19 marker loci and cystic fibrosis are reported. The data exclude that ADA belongs to this linkage group while they give weak support for the inclusion of P. There is weak evidence for linkage of cystic fibrosis to PGM3, but none for linkage to HL-A. No new suggestive linkages appeared. 相似文献
89.
The postmortem changes (0.5, 1, 2, 3, 5, 7 and 10 hours) in pyramidal neurons of the area CAI of the hippocampus of rats have been studied with the light and electron microscope. 1. (light microscopy) In the pyramidal neurons that have undergone 0.5- and 1-hour postmortem autolysis (postmortem autolysis for 0.5 and 1 hours), no remarkable changes were found. In the neurons which had undergone 2- or 3-hour postmortem autolysis, nuclei were slightly edematous and the perineuronal spaces were slightly disintegrated. In the neurons which had undergone more than 5-hour postmortem autolysis, these changes were more prominent. 2. (electron microscopy) The aggregation of the nuclear chromatin was already observed in the neurons which had undergone 0.5- or 1-hour postmortem autolysis. In the cytoplasm, the swelling of mitochondria, Golgi vesicles and the disintegration tion of myelin sheath were partly observed in the neurons which had undergone 0.5-hour postmortem autolysis. Within 1-hour postmortem period, the dilatation of the endoplasmic reticulum in the neurons and the swelling of the processes of astrocytes were distinguishable. These alterations proceeded gradually in the course of time. With regard to the postmortem changes, the autolysis and the other artefacts such as pH, osmolality and concentration of the fixative and hypoxic or ischaemic factor were discussed. 相似文献
90.
When the antidepressant amoxapine is taken in overdose, it can cause metabolic acidosis, brain damage and sometimes death. In previous studies, biochemical evidence has been presented that amoxapine disrupts reactions of membrane-associated multi-enzyme complexes, and mitochondrial energy conservation may be one of the first systems affected. Three in vitro systems were investigated to determine whether general membrane disruption or more specific mitochondrial effects of amoxapine could be responsible for toxicity and for lactic acid accumulation. In Saccharomyces cerevisiae, increased amoxapine concentrations led to decreased oxygen uptake associated with decreased survival of cells. In Chinese hamster ovary cells in culture, an initial increase in oxygen uptake was observed up to 10 μg amoxapine/ml and a decrease thereafter. At drug levels that caused an increased oxygen uptake, there was increased lactic acid output by cells, but no observable toxicity. At higher drug levels, the decreased oxygen uptake was accompanied by cell death, reduced lactic acid output and a change in the mitochondrial cristae configuration. Cell death in both of the above systems was attributed to interference with energy conservation. Isolated, beating guinea-pig hearts perfused with 5 μg amoxapine/ml stopped after 13 min, but no lactic acid accumulated. This may be explained by the membrane-stabilizing activity of the drug. In an arrested perfused heart, increased concentrations of amoxapine stimulated oxygen consumption and lactic acid production. Hence, membrane-stabilizing activity alone is not adequate to explain the action of amoxapine on isolated cells, and on the perfused arrested heart, or the clinical pattern of overdose, and disruption of energy conservation in cells is likely to be involved also. 相似文献