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排序方式: 共有196条查询结果,搜索用时 15 毫秒
191.
Saelman EU; Horton LF; Barnes MJ; Gralnick HR; Hese KM; Nieuwenhuis HK; de Groot PG; Sixma JJ 《Blood》1993,82(10):3029-3033
The aim of this investigation was to identify domains of collagen type I that can support platelet adhesion under flow conditions. Four cyanogen bromide (CB) fragments composing 87% of the collagen alpha 1(I)-chain were studied under static and flow conditions. Under static conditions, bovine and human collagen fragment alpha 1(I)CB3 induced aggregate formation, whereas alpha 1(I)CB7 and alpha 1(I)CB8 supported adhesion of dendritic and contact platelets. Bovine alpha 1(I)CB6 weakly supported platelet adhesion. At shear rate 300/s, collagen fragment alpha 1(I)CB3 strongly supported platelet adhesion, whereas lower platelet adhesion was observed to alpha 1(I)CB7 and alpha 1(I)CB8. The fragment alpha 1(I)CB6 did not support platelet adhesion under flow conditions. Adhesion to alpha 1(I)CB3 was completely inhibited by a low concentration (0.6 IgG microgram/mL) of anti-GPIa monoclonal antibody (MoAb), whereas this concentration of antibody partially inhibited adhesion to alpha 1(I)CB7 and alpha 1(I)CB8. At higher concentrations (3 micrograms/mL) the anti-glycoprotein Ia (GPIa) antibody completely inhibited adhesion to alpha 1(I)CB8 and further reduced adhesion to alpha 1(I)CB7. Platelet adhesion to alpha 1(I)CB3, alpha 1(I)CB7, and alpha 1(I)CB8 was strongly inhibited by an anti-GPIb MoAb. A MoAb against the GPIb-binding site of von Willebrand factor (vWF) strongly inhibited platelet adhesion to alpha 1(I)CB7 and alpha 1(I)CB8, whereas platelet adhesion to alpha 1(I)CB3 was not inhibited. We conclude that under flow conditions alpha 1(I)CB3, alpha 1(I)CB7, and alpha 1(I)CB8 support GPIa/IIa-dependent platelet adhesion. The GPIb-vWF interaction is important under flow conditions for adhesion to alpha 1(I)CB7 and alpha 1(I)CB8 and probably also to alpha 1(I)CB3. 相似文献
192.
The electrophoretic mobility distributions of hairy cells, normal monocytes. CLL, and normal lymphocytes isolated from blood were determined by electrophoretic light scattering. Values obtained for hairy cells, 1.52 X 10(-4) cm2/V . sec, were indistinguishable from that of normal monocytes. The mobility of CLL lymphocytes was similar to that of normal B cells. After exposure to neuraminidase, hairy cells revealed a homogeneous distribution with a reduced mobility of 0.55 X 10(-4) cm2/V . sec, while normal monocytes showed a heterogeneous distribution of electrophoretic mobilities suggestive of subpopulations. The electrokinetic behavior of hairy cells thus differs from that or normal and CLL lymphocytes before, and from that of monocytes after, treatment with neuraminidase. The hairy cell therefore possesses a distinct pattern of surface charge properties that clearly distinguish it from the circulating B cells, T cells, or monocytes. 相似文献
193.
Biochemical and functional consequences of dissociation of the platelet membrane glycoprotein IIb-IIIa complex 总被引:10,自引:1,他引:10
The platelet membrane glycoproteins, IIb and IIIa, form a Ca2+- dependent heterodimer complex that functions as the fibrinogen receptor in activated platelets to mediate platelet aggregation. Little is known about factors that affect the IIb-IIIa complex within the platelet membrane. It has been observed that platelets incubated with ethylene glycol tetra-acetic acid (EGTA) at 37 degrees C are unable to aggregate or to bind monoclonal antibodies specific for the IIb-IIIa complex. To determine whether this is due to a dissociation of IIb from IIIa, we developed a method for quantitating the complex on nondenaturing, polyacrylamide gradient gels. Platelets were surface-labeled with 125I and then solubilized and electrophoresed in 0.2% Triton and 10 mmol/L CHAPS. Under these conditions and in the presence of 1 mmol/L Ca2+, glycoproteins IIb and IIIa migrated on the gels as a discrete band at Rf = 0.33. Protein that was eluted from this band bound to an immunoaffinity column specific for the IIb-IIIa complex. In contrast, when the IIb-IIIa complex was solubilized and then dissociated with EGTA, the discrete band at Rf = 0.33 was no longer present, and IIb and IIIa were now found in a broad band at Rf = 0.45 to 0.50. To study IIb and IIIa within the surface membrane, the 125I-labeled platelets were first incubated with 0.5 mmol/L EGTA (1 nmol/L free Ca2+) at 22 degrees C and then solubilized in the absence of EGTA. The IIb and IIIa from these platelets migrated at Rf = 0.33, indicating the presence of the intact IIb-IIIa complex. In contrast, when the platelets were incubated at 37 degrees C for one hour with the EGTA, the discrete band at Rf = 0.33 representing the IIb-IIIa complex gradually disappeared. This phenomenon could not be reversed by adding Ca2+ back to the platelets before solubilization and electrophoresis. This loss of the IIb-IIIa complex from intact platelets was accompanied by (a) a progressive and irreversible decrease in adenosine diphosphate (ADP)-induced platelet aggregation and (b) decreased binding of a complex-dependent monoclonal antibody to the platelets. These studies demonstrate that when platelets are exposed to low Ca2+ at 37 degrees C, the IIb-IIIa heterodimer complexes in their surface membranes are irreversibly disrupted. Because intact IIb-IIIa complexes are required for platelet aggregation, the loss of these complexes may account for the failure of these platelets to aggregate in response to ADP. 相似文献
194.
酮洛芬的伏安行为研究 总被引:4,自引:0,他引:4
在0.1mol·L-1H2SO4溶液中,酮洛芬有一灵敏的还原伏安峰。当搅拌富集40s、扫速100mV·s-1时,其峰电位Ep=-0.80V(vs.Ag/AgCl)。用线性扫描和循环伏安法、脉冲极谱等手段研究该体系的伏安行为,特别是吸附性和电极反应机理,测得体系αn=1.05,α=0.53,参与电极反应的H+数为2。实验表明,该体系属一有吸附性的不可逆过程,可用于痕量酮洛芬的测定。其检测限,对吸附伏安法可达1.0×10-9mol·L-1,对示波极谱法则为5.0×10-8mol·L-1。 相似文献
195.
196.
异丙酚激活蛋白激酶C对心肌缺血再灌注损伤的保护作用 总被引:4,自引:0,他引:4
目的:观察异丙酚对大鼠离体心肌缺血再灌注的影响及蛋白激酶C激活的作用。方法:实验于2004-04/2005-03在河北省医学科学院药研室完成。48只大鼠离体心脏随机分为6组,每组8只。分别为:正常对照组,持续灌注Lock液65min;缺血再灌注模型组,用含脂肪乳对照的灌流液灌注15min后,以钳夹主动脉灌注管造成全心常温缺血25min后,恢复再灌注30min,灌流液与预灌时相同;异丙酚15,30,60μmol/L组,缺血前和再灌期的灌流液中分别含相应浓度的异丙酚,余同缺血再灌注模型组;异丙酚60μmol/L 蛋白激酶抑制剂5μmol/L组,灌流液中含5μmol/L的chelerythrine的灌流液,其余同异丙酚60μmol/L组。实验评估:①Powerlab/8s仪记录各组平衡末、缺血前及再灌30min时心率、左室发展压、左室舒张末压、左室压力变化速率、冠状动脉流量等心功能指标。②测定冠状动脉流出液中乳酸脱氢酶、磷酸肌酸激酶活性。③透射电镜观察心肌细胞超微结构变化。④差速离心提取心肌线粒体,测定线粒体超氧化物岐化酶、谷胱甘肽过氧化物酶、ATP酶活性和丙二醛含量。结果:48只大鼠均进入结果分析。①平衡灌注末、缺血前各组间心功能指标差异无显著性(P>0.05),再灌注30min末,异丙酚30,60μmol/L组左室发展压、左室压力变化速率、冠状动脉流量明显高于缺血再灌注模型组(P<0.05),左室舒张末压明显低于缺血再灌注模型组(P<0.05)。异丙酚60μmol/L 蛋白激酶C抑制剂5μmol/L组左室发展压、左室压力变化速率、冠状动脉流量明显低于单纯异丙酚60μmol/L组(P<0.05),但仍高于与缺血再灌注模型组(P<0.05)。②心肌缺血再灌后,冠状动脉流出液中乳酸脱氢酶和肌酸激酶活性明显高于正常对照组(P<0.05)。异丙酚30,60μmol/L组、异丙酚60μmol/L 蛋白激酶C抑制剂5μmol/L组乳酸脱氢酶、肌酸激酶活性明显低于缺血再灌注模型组(P<0.05),异丙酚60μmol/L 蛋白激酶C抑制剂5μmol/L组乳酸脱氢酶和肌酸激酶活性与异丙酚60μmol/L组无明显差异。③与缺血再灌注模型组相比,异丙酚组心肌损伤明显减轻,尤其是60μmol/L组,心肌纤维排列均匀,线粒体膜结构完整,仅轻度水肿,嵴清晰,糖原可见。异丙酚60μmol/L 蛋白激酶C抑制剂5μmol/L组心肌超微结构显示损伤程度重于异丙酚60μmol/L组。④异丙酚30,60μmol/L、异丙酚60μmol/L 蛋白激酶C抑制剂5μmol/L组丙二醛含量低于缺血再灌注模型组(P<0.05),ATP酶、超氧化物歧化酶、谷胱甘肽过氧化物酶活性明显高于缺血再灌注模型组(P<0.05)。异丙酚60μmol/L组与异丙酚60μmol/L 蛋白激酶C抑制剂5μmol/L组相比,上述指标无明显差异。结论:异丙酚对离体大鼠心肌缺血再灌注损伤有保护作用,可能与其抗脂质过氧化和激活蛋白激酶C有关。 相似文献