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排序方式: 共有2169条查询结果,搜索用时 125 毫秒
31.
32.
L1 knockout mice show dilated ventricles, vermis hypoplasia and impaired exploration patterns 总被引:8,自引:3,他引:8
Fransen E; D'Hooge R; Van Camp G; Verhoye M; Sijbers J; Reyniers E; Soriano P; Kamiguchi H; Willemsen R; Koekkoek SK; De Zeeuw CI; De Deyn PP; Van der Linden A; Lemmon V; Kooy RF; Willems PJ 《Human molecular genetics》1998,7(6):999-1009
L1 is a neural cell adhesion molecule mainly involved in axon guidance and
neuronal migration during brain development. Mutations in the human L1 gene
give rise to a complex clinical picture, with mental retardation,
neurologic abnormalities and a variable degree of hydrocephalus. Recently,
a transgenic mouse model with a targeted null mutation in the L1 gene was
generated. These knockout (KO) mice show hypoplasia of the corticospinal
tract. Here we have performed further studies of these KO mice including
magnetic resonance imaging of the brain, neuropathological analysis and
behavioral testing. The ventricular system was shown to be abnormal with
dilatation of the lateral ventricles and the 4th ventricle, and an altered
shape of the Sylvius aqueduct. Additionally, the cerebellar vermis of the
KO mice is hypoplastic. Their exploratory behavior is characterized by
stereotype peripheral circling reminiscent of that of rodents with induced
cerebellar lesions.
相似文献
33.
PJ Hallam P. Mannucci A. Tripodi D. Bevan B. Lawsen L. Tengborn A. Wacey DN Coopel 《Clinical genetics》1998,54(3):231-233
Hallam PJ, Mannucci P, Tripodi A, Bevan D, Laursen B, Tengborn L, Wacey A, Cooper DN. Three novel PROC gene lesions causing protein C deficiency. Clin Genet 1998: 54: 231–233. 0 Munksgaard, 1998
Missense mutations. three of them novel (Am210→Val, Asn248→ Ile, Ah355→Val), were found in the protein c ( PROC ) genes of 7 patients with inherited protein C deficiency associated with venous thrombosis. Comparison with the phenotypic effects of mutations in the analogous residues of factor IX causing hdernophilia B and the use of molecular modelling has provided explanations as to how these lesions might alter either the structure, function or secretion of the protein C molecules encoded. 相似文献
Missense mutations. three of them novel (Am210→Val, Asn248→ Ile, Ah355→Val), were found in the protein c ( PROC ) genes of 7 patients with inherited protein C deficiency associated with venous thrombosis. Comparison with the phenotypic effects of mutations in the analogous residues of factor IX causing hdernophilia B and the use of molecular modelling has provided explanations as to how these lesions might alter either the structure, function or secretion of the protein C molecules encoded. 相似文献
34.
35.
In the peripheral blood (PBL) of juvenile chickens three populations of B cells have previously been distinguished based on life-span and origin of cells within each population. In this report we show that the largest PBL B cell subset, population 1 B cells, which are short-lived cells corresponding to about 60% of PBL B cells and the vast majority of bursal emigrants, exit from the bursa directly from the follicular cortex. This conclusion is based on the specific labeling of rapidly dividing cortical lymphocytes with bromodeoxyuridine, followed by their detection in the periphery prior to the appearance of bromodeoxyuridine labeled cells in the bursa medulla. Furthermore, the rate of emigration of cortical lymphocytes, 1.00 ± 0.1% of PBL B cells per hour, is indistinguishable from the emigration rate of B cells from the bursa as a whole. The anatomical organization of the bursa has evolved to focus gut-derived antigens from the bursal lumen into the lymphoid follicles. The emigration of cortical bursal cells is discussed in relation to the exposure of bursal lymphocytes to extrinsic antigen. 相似文献
36.
Hemoglobin Setif produces pseudosickling of red cells in vitro; the nature of the process and the conditions that "trigger" it are unknown. Studies of red cells, hemolysates, purified hemoglobin solutions, and artificial mixtures of Hb A and Setif suggest that pseudosickling is produced by intracellular crystallization of insoluble hemoglobin. Increased tonicity of the suspending medium accentuates the process, probably by causing a rise in intracellular hemoglobin concentration. If precipitates from A/Setif mixtures are analyzed, they always contain Hb A, suggesting an unusual mechanism for the process. Despite the fact that osmolality in the renal medulla is similar to that which produces pseudosickling in vitro, carriers do not have renal dysfunction of the type found in patients with sickle cell disease. 相似文献
37.
Khadka J. Ratcliffe J. Hutchinson C. Cleland J. Mulhern B. Lancsar E. Milte R. 《Quality of life research》2022,31(9):2849-2865
Quality of Life Research - To evaluate the construct (convergent and known group) validity of the Quality-of-Life-Aged Care Consumer (QOL-ACC), an older-person-specific quality-of-life measure... 相似文献
38.
Wolf Rasmus Trap Ratcliffe Julie Chen Gang Jeppesen Pia 《Quality of life research》2021,30(6):1747-1756
Quality of Life Research - The Child Health Utility 9D (CHU9D) currently represents the only preference-based health-related quality-of-life instrument designed exclusively from its inception for... 相似文献
39.
Ratcliffe J 《Health policy (Amsterdam, Netherlands)》1993,25(1-2):169-183
This paper focuses upon a number of features of the NHS reforms which are external to the new market created by the purchaser-provider split. Initially, the market and the problems associated with its operation are examined. Particular consideration is given to the extent to which these problems are likely to hinder the achievement of the Government's objective of improved efficiency in the NHS. Each of the provider, purchaser and consumer sectors of the market is then examined more closely in relation to the extra-market incentives present. It is argued that these incentives do have the potential to complement the purchaser-provider split in encouraging improvements in efficiency. However, in several instances, the incentives are either the wrong incentives or are too weak to have any real impact in changing behaviour. In conclusion, it is argued that there is a need for more direct incentive structures to be introduced if improvements in efficiency are to be realised. 相似文献
40.
Dr. B. D. Keavney C. R. K. Dudley I. M. Stratton R. R. Holman D. R. Matthews P. J. Ratcliffe R. C. Turner 《Diabetologia》1995,38(8):948-952
Summary The deletion allele of the insertion/deletion polymorphism of the angiotensin-converting enzyme gene has been suggested to be an independent risk factor for myocardial infarction, particularly in subjects judged to be low-risk by the criteria of lipid status and body mass index. In a prospective, matched case-control study, we have investigated the role of this polymorphism as a risk factor for myocardial infarction in 173 newly-diagnosed British Caucasian non-insulin-dependent diabetic subjects taken from the United Kingdom Prospective Diabetes Study who subsequently developed myocardial infarction and 297 control subjects from the same study population matched for known cardiovascular risk factors including age at diagnosis of diabetes, gender, blood pressure, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride and smoking habit. A trend towards increased risk conferred by homozygosity for the deletion allele was observed in cases (odds ratio 1.63, p=0.09). When the population was stratified according to the matched risk factors, the deletion allele was associated with myocardial infarction in those with low plasma low-density lipoprotein cholesterol (odds ratio 3.67, p=0.002), or low triglyceride (odds ratio 3.14, p=0.005). The strongest association of the deletion allele with myocardial infarction was observed in subjects with both low low-density lipoprotein cholesterol and low triglyceride levels (odds ratio 9.0, p<0.001). These results show that the deletion allele is a risk factor for myocardial infarction in non-insulin-dependent diabetic patients who have a favourable lipid profile.Abbreviations ACE
angiotensin-converting enzyme
- MI
myocardial infarction
- I/D polymorphism
insertion/deletion polymorphism
- I allele
insertion allele
- D allele
deletion allele
- DD genotype
homozygosity for the deletion allele
- UKPDS
United Kingdom Prospective Diabetes Study 相似文献