全文获取类型
收费全文 | 418篇 |
免费 | 22篇 |
国内免费 | 19篇 |
专业分类
儿科学 | 33篇 |
妇产科学 | 11篇 |
基础医学 | 45篇 |
口腔科学 | 8篇 |
临床医学 | 48篇 |
内科学 | 71篇 |
皮肤病学 | 13篇 |
神经病学 | 11篇 |
特种医学 | 111篇 |
外科学 | 35篇 |
综合类 | 10篇 |
预防医学 | 18篇 |
眼科学 | 9篇 |
药学 | 14篇 |
中国医学 | 2篇 |
肿瘤学 | 20篇 |
出版年
2024年 | 1篇 |
2021年 | 1篇 |
2020年 | 5篇 |
2019年 | 4篇 |
2018年 | 10篇 |
2017年 | 4篇 |
2016年 | 6篇 |
2015年 | 7篇 |
2014年 | 10篇 |
2013年 | 12篇 |
2012年 | 6篇 |
2011年 | 11篇 |
2010年 | 15篇 |
2009年 | 21篇 |
2008年 | 11篇 |
2007年 | 17篇 |
2006年 | 6篇 |
2005年 | 5篇 |
2004年 | 3篇 |
2003年 | 2篇 |
2002年 | 4篇 |
2001年 | 7篇 |
2000年 | 2篇 |
1999年 | 10篇 |
1998年 | 31篇 |
1997年 | 38篇 |
1996年 | 28篇 |
1995年 | 18篇 |
1994年 | 17篇 |
1993年 | 17篇 |
1992年 | 1篇 |
1991年 | 6篇 |
1990年 | 11篇 |
1989年 | 20篇 |
1988年 | 12篇 |
1987年 | 9篇 |
1986年 | 8篇 |
1985年 | 10篇 |
1984年 | 4篇 |
1983年 | 8篇 |
1982年 | 6篇 |
1981年 | 2篇 |
1980年 | 11篇 |
1979年 | 1篇 |
1978年 | 1篇 |
1977年 | 6篇 |
1976年 | 7篇 |
1975年 | 5篇 |
1970年 | 1篇 |
1968年 | 1篇 |
排序方式: 共有459条查询结果,搜索用时 15 毫秒
51.
优秀女子赛艇运动员比赛前后血乳酸、血尿素及血清肌酸激酶跟踪测试 总被引:1,自引:1,他引:1
目的:跟踪测试优秀女子赛艇运动员比赛前后血乳酸、血尿素及血清肌酸激酶的变化,探讨女子赛艇运动员机体能量物质代谢和赛后疲劳恢复的特点。方法:选取2005-07/09湖北省水上运动中心优秀女子运动员14名,其中国家健将级运动员7名,国家一级运动员7名;平均年龄(22±4)岁,训练年限(4.1±1.4)年,身高(174.2±3.1)cm,体质量(68.6±4.7)kg。14名运动员分别于2000m划艇比赛当日晨空腹、赛前15min、赛后5min,1h及24h抽取指尖血60μL,进行血乳酸、血尿素、血清肌酸激酶检测。结果:14名运动员全部进入结果分析。①比赛前后运动员血乳酸水平的变化:运动员空腹血乳酸水平为(1.22±0.45)mmol/L,赛前15min为(2.89±0.49)mmol/L。赛后5min血乳酸浓度高达(11.51±1.72)mmol/L,与空腹水平比较差异有显著性意义(t=3.077,P<0.01)。赛后24h血乳酸浓度显著下降至(1.76±0.24)mmol/L,与空腹水平基本接近(t=0.027,P>0.05)。②比赛前后运动员血尿素水平的变化:与空腹血尿素水平比较,运动员赛后5min血尿素浓度明显升高[(5.45±0.47),(6.13±1.00)mmol/L;t=2.416,P<0.05]。赛后24h血尿素浓度下降至(5.94±0.85)mmol/L,仍高于空腹水平(t=2.682,P<0.05)。③比赛前后运动员血清肌酸激酶活性的变化:与赛前比较,运动员赛后5min血清肌酸激酶活性明显升高[(3.38±1.58),(6.13±3.25)nkat/L;t=4.968,P<0.01]。赛后1h血清肌酸激酶活性开始下降,至赛后24h与赛前基本相似(t=1.537,P>0.05)。结论:①赛后5min血乳酸、血尿素、血清肌酸激酶活性显著高于赛前,赛后1h血乳酸消除迅速,但仍未恢复到正常水平。提示赛艇是一种以糖酵解系统为主、无氧 有氧代谢混合型供能的运动项目。②赛艇比赛使酸性产物生成增多,血乳酸、血尿素、血清肌酸激酶可作为运动强度和机能恢复的指标。③赛艇比赛后至少24h内,机体处于蛋白质降解增强状态,建议恢复期增加饮食糖和蛋白质摄入量,以促进合成代谢,加快功能恢复过程。 相似文献
52.
Preparation of factor IX deficient human plasma by immunoaffinity chromatography using a monoclonal antibody 总被引:1,自引:0,他引:1
Goodall AH; Kemble G; O'Brien DP; Rawlings E; Rotblat F; Russell GC; Janossy G; Tuddenham EG 《Blood》1982,59(3):664-670
A murine hybridoma clone is described that grows continuously in culture and produces a monoclonal antibody we have called Royal Free Monoclonal Antibody to factor IX No. 1 (RFF-IX/1). This has high affinity for a coagulation site on factor IX. RFF-IX/1 immobilised on sepharose can be used to deplete factor IX from normal human plasma. This immunoaffinity depleted plasma is indistinguishable from severe Christmas disease plasma and can be used as the substrate in a one stage coagulation assay for factor IX. The affinity column has high capacity and can be regenerated so that large scale production from normal plasma of factor IX deficient plasma as a diagnostic reagent is now feasible. 相似文献
53.
High-molecular-weight kininogen is exclusively membrane bound on endothelial cells to influence activation of vascular endothelium 总被引:3,自引:1,他引:3
An important biologic function of high-molecular-weight kininogen (HK) is to deliver bradykinin (BK) to its cellular receptors. Internalization and degradation of HK may provide a mechanism by which endothelial cells modulate the production of BK and control its activities. Therefore, we investigated the binding and subsequent distribution of biotinylated-HK (biotin-HK) associated with human umbilical vein endothelial cells (HUVEC). HUVEC bound 3 to 4 times more HK and with greater avidity at 1 to 3 hours at 37 degrees C than at 4 degrees C (Bmax = 1.0 +/- 0.02 x 10(7) molecules/cell, kd = 7 +/- 3 nmol/L v Bmax = 2.6 +/- 0.2 x 10(6) molecules/cell, kd = 46 +/- 8 nmol/L). However, there was no evidence that the difference was caused by internalization of HK at the higher temperature. First, the same amount of biotin-HK was associated with nonpermeabilized and permeabilized HUVEC using buffers containing 20 to 50 mumol/L zinc ion in the absence or presence of 2 mmol/L calcium ion. Second, binding of biotin-HK to HUVEC was approximately 92% reversible at 1 hour when the cells were maintained at both 37 degrees C and 4 degrees C. Third, neither chloroquine nor primaquine altered the amount of biotin-HK bound to HUVEC. Fourth, biotin-HK bound to HUVEC was almost completely removed by pronase. Fifth, the nonpermeable dye, crystal violet, almost completely quenched the fluorescence signal emitted by HUVEC-associated fluorescein isothiocyanate (FITC) HK. Finally, the localization of HUVEC-bound FITC-HK was restricted to the membrane as shown by laser scanning confocal microscopy. The expression of HK binding sites had an absolute requirement for metabolic energy, but was not dependent on new protein synthesis. Membrane-bound HK contributed to the anticoagulant nature of endothelial cells by blocking human alpha-thrombin binding and its resultant induction of prostacyclin formation. These studies indicate that HK is not internalized by HUVEC, but remains primarily on cell surfaces to be accessible for BK liberation and to modulate the binding and actions of alpha-thrombin. 相似文献
54.
High molecular weight kininogen: localization in the unstimulated and activated platelet and activation by a platelet calpain(s) 总被引:5,自引:0,他引:5
High mol wt kininogen (HMWK), the major cofactor-substrate of the contact phase of coagulation, is contained within and secreted by platelets. Studies have been performed to localize platelet HMWK in both the unstimulated and activated platelet and to ascertain the effect of platelet enzymes on HMWK itself. On platelet subcellular fractionation, platelet HMWK was localized to alpha-granules, and platelets from a patient with a deficiency of these granules (gray platelet syndrome) had 28% normal platelet HMWK. Platelet HMWK, in addition to being secreted from the platelet, was also localized to the surface of the platelet when activated. Using a competitive enzyme- linked immunosorbent assay for HMWK as an indirect antibody consumption assay, the external membrane of thrombin-activated platelets as well as the releasate from these stimulated platelets had 17 ng HMWK antigen/10(8) platelets available, whereas unstimulated platelets and their supernatant had only 4.9 and 4.2 ng HMWK/10(8) platelets present, respectively. The anti-HMWK antibody consumption by activated normal platelets was specific for membrane-expressed platelet HMWK, since activated platelets from a patient with total kininogen deficiency did not adsorb the anti-HMWK antibody. Enzymes in the cytosolic fraction of platelets cleaved 125I-HMWK (mol wt 120,000) into a mol wt 100,000 polypeptide as well as smaller products at mol wt 74,000, mol wt 62,000, mol wt 47,000, and a few components below mol wt 45,000. No cleavage products were observed when DFP and leupeptin were present. The cleavage of HMWK was specifically prevented by inhibitors of calcium-activated cysteine proteases (leupeptin, N-ethylmaleimide, iodoacetamide, and EDTA) but not by inhibitors of serine proteases (DFP, benzamidine, soybean trypsin inhibitor, or aprotinin). Platelet cytosol increased the coagulant activity of exogenous purified HMWK with maximum HMWK coagulant activity (35-fold) occurring within ten minutes of exposure to platelet cytosol. Treatment of platelet cytosol with leupeptin prevented the increase in the coagulant activity of exogenous HMWK. These studies indicate that activated platelets express platelet HMWK on their external membrane and platelet enzymes can cleave and increase the coagulant activity of exogenous HMWK. 相似文献
55.
56.
Hartdorff Caroline M Frank Kneepkens CM van Dijk Alice EM Stok Anita Engels Michelle AH Gemke Reinoud JBJ Kindermann Angelika 《Tijdschrift voor kindergeneeskunde》2013,81(1):11-11
Tijdschrift voor Kindergeneeskunde - 相似文献
57.
Zollikofer CL; Cragg AH; Einzig S; Castaneda-Zuniga WR; Castaneda F; Rysavy JA; Bruhlmann WF; Shebuski RJ; Amplatz K 《Radiology》1983,149(3):681-685
To prevent platelet aggregation following percutaneous transluminal angioplasty (PTA), cyclooxygenase inhibitors such as acetylsalicylic acid (ASA) and indomethacin are recommended. However, ASA blocks both the proaggregating effects of thromboxane (TXA2) and the antiaggregating and vasodilating effects of prostacyclin (PGI2). The authors measured the contractile response of dilated canine carotid arteries in situ and in vitro using an isometric force transducer. Following PTA, contraction of the arterial wall was significantly reduced (p less than 0.01). By blocking cyclooxygenase with indomethacin (3 micrograms/ml), contraction was greatly improved (p less than 0.001). These results suggest that PTA may result in marked release of prostacyclin by the damaged arterial wall, which could account for the decreased responsiveness of the artery to exogenous norepinephrine. 相似文献
58.
The CTLA-4 gene region of chromosome 2q33 is linked to, and associated with, type 1 diabetes. Belgian Diabetes Registry 总被引:8,自引:1,他引:8
Nistico L; Buzzetti R; Pritchard LE; Van der Auwera B; Giovannini C; Bosi E; Larrad MT; Rios MS; Chow CC; Cockram CS; Jacobs K; Mijovic C; Bain SC; Barnett AH; Vandewalle CL; Schuit F; Gorus FK; Tosi R; Pozzilli P; Todd JA 《Human molecular genetics》1996,5(7):1075-1080
Susceptibility to autoimmune insulin-dependent (type 1) diabetes mellitus
is determined by a combination of environmental and genetic factors, which
include variation in MHC genes on chromosome 6p21 (IDDM1) and the insulin
gene on chromosome 11p15 (IDDM2). However, linkage to IDDM1 and IDDM2
cannot explain the clustering of type 1 diabetes in families, and a role
for other genes is inferred. In the present report we describe linkage and
association of type 1 diabetes to the CTLA-4 gene (cytotoxic T lymphocyte
associated-4) on chromosome 2q33 (designated IDDM12). CTLA-4 is a strong
candidate gene for T cell- mediated autoimmune disease because it encodes a
T cell receptor that mediates T cell apoptosis and is a vital negative
regulator of T cell activation. In addition, we provide supporting evidence
that CTLA-4 is associated with susceptibility to Graves' disease, another
organ- specific autoimmune disease.
相似文献
59.
al-Wakeel JS; Mitwalli AH; Huraib S; al-Mohaya S; Abu-Aisha H; Chaudhary AR; al-Majed SA; Memon N 《Nephrology, dialysis, transplantation》1997,12(7):1420-1424
High serum fluoride (F-) in patients with chronic renal failure (CRF) and
end-stage renal disease (ESRD) is associated with risk of renal
osteodystrophy and other bone changes. This study was done to determine F-
in normal healthy controls and patients with ESRD on haemodialysis (HD) or
peritoneal dialysis (PD). Seventeen healthy controls (12 males, 5 females)
and 39 ESRD patients on dialysis (17 males, 22 females) were recruited in
the study in a community with 47.4 +/- 3.28 microM/l (range 44-51 microM/l)
of F- content in drinking water. Control subjects showed a mean serum F-
concentration of 1.08 +/- 0.350 microM/l. Males in control group showed
slightly higher F- levels (1.15 +/- 0.334, range 0.55-1.9 microM/l) than
females (0.92 +/- 0.370, range 0.6-1.5 microM/l). Mean serum F-
concentration did not correlate significantly with age and sex among
control subjects, whereas such correlation was observed in patients with
ESRD on dialysis. Mean serum F- concentration was significantly higher in
patients on dialysis (2.67 +/- 1.09, range 0.8-5.2 microM/l) than normal
controls. When grouped according to sex, the mean serum F- concentration in
males (3.05 +/- 1.04, range 1.8-5.2 microM/l) was significantly higher than
females (2.38 +/- 1.08, range 0.8-5.2 microM/l). When patients were grouped
according to age, it was observed that F- concentration was significantly
higher in patients with age groups 21-70 (2.86 +/- 1.05) than those with
age group 13-20 years (1.42 +/- 0.531). Thus F- concentration correlated
with age and sex, being higher in males and above 20 years. Despite
appreciable clearance of F- (39-90%) across the peritoneum, patients on
CAPD showed higher serum F- concentration than those on HD (3.1 +/- 1.97 vs
2.5 +/- 1.137 microM/l). Of the total 39 patients on dialysis 39% had their
serum F- concentration above 3.0 microM/l, posing the risk of renal
osteodystrophy.
相似文献
60.