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排序方式: 共有277条查询结果,搜索用时 15 毫秒
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Computed tomography of hepatic cavernous hemangioma 总被引:4,自引:0,他引:4
C Ashida E K Fishman E A Zerhouni F H Herlong S S Siegelman 《Journal of computer assisted tomography》1987,11(3):455-460
Fifty hepatic hemangiomas in 38 patients were evaluated by CT using sequential scanning following bolus injection. Lesions were assessed for the following CT features: (a) low density lesion on unenhanced scan; (b) early peripheral contrast enhancement; (c) progressive opacification from the periphery to the center; (d) a delay of at least 3 min before total opacification; and (e) eventual isodense appearance with or without unopacified cleft. The criteria for diagnosis of hepatic hemangioma were (d) and (e) plus at least two of the remaining three features. Forty-eight lesions were identified by CT; 38 displayed all five features, five lesions were missing one feature, and five lesions did not meet the criteria for diagnosis. Larger lesions required a significantly longer period to opacify (p less than 0.05). The positive predictive value of CT in the diagnosis of hemangioma was 100%. 相似文献
4.
一些保肝药物对原代培养大鼠肝细胞糖原合成功能的影响 总被引:1,自引:0,他引:1
本文参照PO Seglen的方法并加以修改,建立了原代培养大鼠肝细胞糖原合成功能的测定体系。观察到联苯双酯既能使正常肝细胞合成糖原增加88%,又能保护肝细胞完全拮抗四氯化碳对其功能的损伤;银耳多糖能使四氯化碳对肝细胞糖原合成功能的损伤减轻57%;去甲斑蝥素10μg/ml能增加肝细胞糖原合成,浓度增加到100μg/ml时,此作用减弱,1000μg/ml则明显抑制糖原的合成,而且在10~100μg/ml浓度时,即能加强四氯化碳的损伤作用;100μg/ml CL1500和熊果酸二钠单独应用可增加肝细胞糖原合成,但与四氯化碳同时应用,反而加重对糖原合成的抑制作用。 相似文献
5.
Neulen J; Raczek S; Pogorzelski M; Grunwald K; Yeo TK; Dvorak HF; Weich HA; Breckwoldt M 《Molecular human reproduction》1998,4(3):203-206
Vascularization is a prominent event during corpus luteum formation,
providing low density lipoproteins for steroid biosynthesis and enabling
transport of secreted steroids. The process of vascularization is
controlled by specific regulators. Vascular endothelial growth factor
(VEGF), otherwise named vascular permeability factor (VPF), induces
endothelial cell proliferation as well as angiogenesis in vivo and
increases capillary permeability. Here we report the expression of VEGF/VPF
mRNA by cultured human luteinized granulosa cells (GC) for at least 10
days. Without HCG VEGF/VPF expression declined after day 4 and by day 10
was reduced to approximately 30% of the value at day 4. However, after
culture in the presence of 1 U/ml human chorionic gonadotrophin (HCG),
expression of VEGF/VPF mRNA by GC was four times greater than control
experiments by day 10, and increased 100% from day 4 to day 10.
Simultaneously, HCG supplementation increased VEGF/VPF secretion by GC.
Medium VEGF/VPF on day 3 was 13 pM without and 11 pM with HCG. Medium
VEGF/VPF on day 10 was 6 pM without HCG and 29 pM with HCG. These results
suggest that vascularization of the corpus luteum is induced by
HCG-mediated effects of VEGF/VPF.
相似文献
6.
The UTX gene escapes X inactivation in mice and humans 总被引:7,自引:3,他引:7
Greenfield A; Carrel L; Pennisi D; Philippe C; Quaderi N; Siggers P; Steiner K; Tam PP; Monaco AP; Willard HF; Koopman P 《Human molecular genetics》1998,7(4):737-742
We recently have identified a ubiquitously transcribed mouse Y chromosome
gene, Uty , which encodes a tetratricopeptide repeat (TPR) protein. A
peptide derived from the UTY protein confers H-Y antigenicity on male
cells. Here we report the characterization of a widely transcribed X-linked
homologue of Uty , called Utx , which maps to the proximal region of the
mouse X chromosome and which detects a human X-linked homologue at Xp11.2.
Given that Uty is ubiquitously transcribed, we assayed for Utx expression
from the inactive X chromosome (Xi) in mice and found that Utx escapes X
chromosome inactivation. Only Smcx and the pseudoautosomal Sts gene on the
mouse X chromosome have been reported previously to escape inactivation.
The human UTX gene was also found to be expressed from Xi. We discuss the
significance of these data for our understanding of dosage compensation of
X-Y homologous genes in humans and mice.
相似文献
7.
8.
Dal Zotto L; Quaderi NA; Elliott R; Lingerfelter PA; Carrel L; Valsecchi V; Montini E; Yen CH; Chapman V; Kalcheva I; Arrigo G; Zuffardi O; Thomas S; Willard HF; Ballabio A; Disteche CM; Rugarli EI 《Human molecular genetics》1998,7(3):489-499
We have recently reported isolation of the gene responsible for X- linked
Opitz G/BBB syndrome, a defect of midline development. MID1 is located on
the distal short arm of the human X chromosome (Xp22. 3) and encodes a
novel member of the B box family of zinc finger proteins. We have now
cloned the murine homolog of MID1 and performed preliminary expression
studies during development. Mid1 expression in undifferentiated cells in
the central nervous, gastrointestinal and urogenital systems suggests that
abnormal cell proliferation may underlie the defect in midline development
characteristic of Opitz syndrome. We have also found that Mid1 is located
within the mouse pseudoautosomal region (PAR) in Mus musculus , while it
seems to be X- specific in Mus spretus. Therefore, Mid1 is likely to be a
recent acquisition of the M. musculus PAR. Genetic and FISH analyses also
demonstrated a high frequency of unequal crossovers in the murine PAR,
creating spontaneous deletion/duplication events involving Mid1. These data
provide evidence for the first time that genetic instability of the PAR may
affect functionally important genes. In addition, we show that MID1 is the
first example of a gene subject to X-inactivation in man while escaping it
in mouse. These data contribute to a better understanding of the molecular
content and evolution of the rodent PAR.
相似文献
9.
10.
A Mocroft B Neesgard R Zangerle A Rieger A Castagna V Spagnuolo A Antinori FC Lampe M Youle JJ Vehreschild C Mussini V Borghi J Begovac C Duvivier HF Gunthard A Rauch J Tiraboschi N Chkhartishvili N Bolokadze F Wit JC Wasmuth S De Wit C Necsoi C Pradier V Svedhem C Stephan K Petoumenos H Garges F Rogatto L Peters L Ryom 《HIV medicine》2020,21(9):599-606