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排序方式: 共有402条查询结果,搜索用时 15 毫秒
1.
高效液相色谱法检测血中表阿霉素的研究 总被引:2,自引:0,他引:2
用ZorbaxC-8柱成功地分离了阿霉素、表阿霉素及其代谢产物。在此基础上建立了用阿霉素作内标物定量测定表阿霉素的分析方法,其最低检测限为2ng/ml,线性范围10-300ng/ml。 相似文献
2.
环孢素A体外抗曼氏血吸虫作用的观察 总被引:1,自引:0,他引:1
MF1小鼠实验感染曼氏血吸虫尾蚴1周、3周和6周后,分别经肺静脉和门静脉灌注取虫。实验显示,药物体外抗曼氏血吸虫的作用呈时间、剂量和虫龄依赖方式,童虫和雄虫对药物更敏感。 相似文献
3.
A single oral administration of orthophenylphenol (OPP, 1400 mg/kg; about half the LD50) to male Fischer 344 rats produced an elevation of serum transaminase activity 24 h later. Pretreatment with l-buthionine-S,R-sulfoximine (BSO, 900 mg/kg) in the OPP-treated rats potentiated the hepatic and renal damage which was accompanied by necrosis. Six hours after the administration of OPP (700 or 1400 mg/kg), hepatic and renal glutathione (GSH) levels decreased with increasing dosage. Hepatic GSH depletion with OPP was enhanced with BSO pretreatment and the recovery of GSH in both organs was slow in the high-dose OPP group. These results suggest that hepatic and renal damage is associated with a serious and prolonged GSH depletion. When either phenyl-p-benzoquinone (PBQ) or phenylhydroquinone (PHQ), which are intermediates of OPP, was administered orally to rats at 700 or 1400 mg/kg, the mortality with the high dose of PBQ was 75% at 24 h. The serum transaminase activity and UN level increased with the low dose of PBQ, accompanied by necrotic hepatocytes. The toxic effects of PHQ on kidney or liver were less than those on PBQ. These observations suggest that the liver and kidney may be target organs for toxic actions of a large dose of OPP and its intermediate, PBQ.Part of this work was presented at IInd International ISSX Meeting Xenobiotic Metabolism and Disposition, May 16–20, 1988, Kobe, Japan 相似文献
4.
本实验采用单标记和双标记法,分别检测4种苯并(a)芘代谢产物(anti-BPDE,syn-BPDE,3-OH-BP和9-OH-BP)对BALB/3T3细胞DNA合成和程序外DNA合成(UDS)的影响,结果表明,anti-BPDE、syn-BPDE、3-OH-BP和9-OH-BP均在不同程度上使BALB/3T3细胞DNA合成增加,但只有anti-BPDE、3-OH-BP和9-OH-BP可诱发BALB/3T3细胞的UDS,说明这些苯并(a)芘代谢产物可损伤BALB/3T3细胞的DNA,同时,这种效应与苯并(a)芘代谢产物的立体结构有关。 相似文献
5.
The disposition of the plasticizer di-(2-ethylhexyl) phthalate (DEHP) and four of its major metabolites was studied in male rats given single infusions of a DEHP emulsion in doses of 5, 50 or 500 mg DEHP/kg body weight. Plasma concentrations of DEHP and metabolites were followed for 24 h after the start of the infusion. The kinetics of the primary metabolite mono-(2-ethylhexyl) phthalate (MEHP) was studied separately.The concentrations of DEHP in plasma were at all times considerably higher than those of MEHP, and the concentrations of MEHP were much higher than those of the other investigated metabolites. In animals given 500 mg DEHP/kg, the areas under the plasma concentration-time curves (AUCs) of the other investigated metabolites were at most 15% of that of MEHP. Parallel decreases in the plasma concentrations of DEHP, MEHP and the and (-1) oxidized metabolites indicated that the elimination of DEHP was the rate-limiting step in the disposition of the metabolites. This was partly supported by the observation that the clearance of MEHP was higher than that of DEHP. Nonlinear increases in the AUCs of DEHP and MEHP indicated saturation in the formation as well as the elimination of the potentially toxic metabolite MEHP. 相似文献
6.
R. Kirsten E. Kirsten J. Wolff 《Pflügers Archiv : European journal of physiology》1969,307(3):154-166
Summary Since ether anesthesia lowered ATP by 25% in red, but not in white muscle, and only when the spinal neurones were intact, we suggested that small or intermediate muscle units were activated under ether anesthesia [8].In order to prove this postulate, some glycolytic metabolites, known to rise under muscular activation, are studied in the white musculus adductor magnus and in the red musculus pyramidalis of the rat: glucose-1-phosphate, glucose-6-phosphate, fructose-6-phosphate, fructose-1-6-diphosphate, -glycerophosphate, lactate, pyruvate, and dihydroxyacetone phosphate.The conditions compared are: Inactin (5-ethyl-5(methyl-propyl)-2-thiobarbituric acid)-anesthesia, diethyl ether anesthesia, and tetanic contraction under Inactin anesthesia.The histological assay with Sudan-black B staining shows 34.2±7.3% dark fibers in m. pyramidalis and 0.2±4.8% dark fibers in m. adductor magnus.Glucose-1-phosphate, fructose-1-6-diphosphate, and -glycerophosphate are elevated under ether anesthesia in both muscles versus Inactin anesthesia by 100–200%.Lactate in both muscles and pyruvate in the red muscle are slightly elevated under ether (by 40%) versus Inactin anesthesia.Under tetanic contraction the metabolites studied rise considerably in both muscles.As glycogen is lowered in rat muscle under ether [9], the present results suggest an activation of glycogen phosphorylase and of phosphofructokinase in both the red and the white muscle under ether anesthesia, which results in augmented glycolysis.The comparatively small increment of pyruvate and lactate in the presence of a high increment of -glycerophosphate under ether anesthesia is considered to indicate an asynchronous activation of fibers with unimpaired circulation and oxidative metabolism. 相似文献
7.
苯及其代谢产物在小鼠骨髓中形成DNA加合物的实验研究 总被引:3,自引:0,他引:3
目的 观察苯及其主要代谢产物苯酚、氢醌、苯醌及苯酚和氢醌联合染毒在小鼠骨髓中形成的 D N A 加合物及其髓性毒性。方法 改进的32 P 后标记方法。结果 苯及其主要代谢产物均能在小鼠骨髓细胞中形成至少1 种 D N A 加合物,相对加合物水平从0 .85 ×10 - 8 ~6 .78 ×10 - 8 不等。骨髓细胞计数结果表明:单独染苯酚或氢醌,对小鼠骨髓细胞均没有抑制作用,但二者联合染毒对小鼠却表现出增强的髓性毒作用。结论 苯及其主要代谢产物均能在小鼠骨髓细胞中形成 D N A 加合物,苯的代谢产物形成的 D N A 加合物与髓性毒性有关。 相似文献
8.
Aetiologically different models of experimental acute renal failure were induced in rats by the administration of glycerol, mercuric chloride and gentamicin, respectively, to different groups. Quinine levels in plasma and urine of the rats with induced renal failure were determined and pharmacokinetic parameters (eliminationt
1/2, CL
p
,V, CLR AUC0–) of the drug were derived and compared with values obtained from control rats following intraperitoneal administration of a 10 mg/kg body-weight dose of quinine. Results showed that each of the three compounds caused an up to 25-fold increase in the plasma levels of the drug and a marked decrease in the levels of the metabolite 3-hydroxyquinine. All the pharmacokinetic parameters determined for the rats with renal impairment were markedly different when compared to control. The high plasma quinine levels observed in the rats with renal failure could be largely due to the marked decrease inV and reduced metabolism. Also, in the rats with renal impairment, no correlation was observed between the increased plasma urea levels and plasma quinine levels or disposition of the drug. The results of the study suggest that quinine should be used with caution in patients with renal impairment. The plasma urea levels, as a measure of renal function, might not provide a suitable index for determining quinine dosage. 相似文献
9.
10.