全文获取类型
收费全文 | 62篇 |
免费 | 5篇 |
国内免费 | 7篇 |
专业分类
儿科学 | 1篇 |
妇产科学 | 1篇 |
基础医学 | 4篇 |
临床医学 | 3篇 |
内科学 | 22篇 |
神经病学 | 1篇 |
特种医学 | 1篇 |
外科学 | 2篇 |
综合类 | 5篇 |
预防医学 | 2篇 |
药学 | 18篇 |
肿瘤学 | 14篇 |
出版年
2018年 | 1篇 |
2017年 | 1篇 |
2015年 | 1篇 |
2014年 | 2篇 |
2013年 | 10篇 |
2011年 | 4篇 |
2010年 | 1篇 |
2008年 | 10篇 |
2007年 | 4篇 |
2006年 | 3篇 |
2005年 | 5篇 |
2004年 | 3篇 |
2003年 | 3篇 |
2002年 | 7篇 |
2001年 | 3篇 |
2000年 | 4篇 |
1998年 | 1篇 |
1997年 | 3篇 |
1995年 | 1篇 |
1991年 | 1篇 |
1988年 | 1篇 |
1987年 | 3篇 |
1983年 | 2篇 |
排序方式: 共有74条查询结果,搜索用时 15 毫秒
1.
2.
M. R. Dobrinska D. E. Furst T. Spiegel W. C. Vincek R. Tompkins D. E. Duggan R. O. Davies H. E. Paulus 《Biopharmaceutics & drug disposition》1983,4(4):347-358
The biliary secretion of sulindac and metabolites after a single 400 mg oral dose of the drug was studied in 3 elective gallbladder surgical patients following placement of an occludable T-tube in the common bile duct. Bile and systemic plasma were sampled at frequent intervals for up to 36 h postdose. The apparent biliary clearance (V?cl,bilc) of the prodrug sulindac is about 25 times greater than that of the pharmacologically active sulfide metabolite. The total biliary flux of drug in normal man with an uninterrupted enterohepatic cycle, calculated from V?cl,bile and historic mean plasma drug AUC values, averages 144 and 12·2 per cent of the dose as sulindac and the sulfide metabolite, respectively. Thus, enterohepatic recycling of the drug in man is principally in the form of the prodrug which not only limits exposure of the intestine to the active moiety but also sustains systemic concentrations of active drug upon reabsorption of the prodrug. 相似文献
3.
Therapeutic potential of sulindac against ischemia-reperfusion-induced myocardial infarction in diabetic and nondiabetic rats
下载免费PDF全文
![点击此处可从《Experimental & Clinical Cardiology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Akula Annapurna Siva Reddy Challa Gomedhikam J Prakash Routhu Kasi Viswanath 《Experimental & Clinical Cardiology》2008,13(2):66-70
BACKGROUND
Diabetes mellitus is an independent risk factor for cardiovascular disease and is also associated with increased susceptibility to cardiovascular complications. It has been suggested that alterations in glucose metabolism and glucose flux via the aldose reductase pathway make the diabetic heart more sensitive to ischemic-reperfusion injury. Previous studies have found sulindac to have inhibitory and anti-inflammatory effects on aldose reductase. The use of aldose reductase inhibitors for the protection of ischemic myocardium is still in an exploratory state.OBJECTIVES
To evaluate the therapeutic potential of sulindac in an in vivo rat model of acute ischemia (30 min) and reperfusion (4 h) in diabetic and nondiabetic rats.METHODS
Diabetes was induced in rats by administering streptozotocin (45 mg/kg, intravenously). Myocardial infarction was induced by occlusion of the left anterior descending coronary artery for 30 min followed by 4 h of reperfusion. Infarct size was measured using the staining agent 2,3,5-triphenyltetrazolium chloride. A lead II electrocardiogram was monitored at various intervals throughout the experiment. Sorbitol dehydrogenase levels in heart tissue, as well as lipid peroxide levels in serum and heart tissue, were estimated spectrophotometrically.RESULTS
Infarct size was increased in diabetic rats in comparison with normal rats. Pretreatment with sulindac significantly reduced infarct size, lipid peroxidation and sorbitol dehydrogenase levels in both diabetic and nondiabetic rats. The degree of cardioprotection was greater in diabetic rats than in nondiabetic rats.CONCLUSIONS
The present study indicates that the observed cardioprotection provided by sulindac in terms of reducing infarct size in normal rats may be due to its combined antioxidant and anti-inflammatory activities. The inhibition of aldose reductase may be responsible for the enhanced cardioprotection observed in diabetic rats treated with sulindac. 相似文献4.
Shigeoka Y Igishi T Matsumoto S Nakanishi H Kodani M Yasuda K Hitsuda Y Shimizu E 《Journal of cancer research and clinical oncology》2004,130(3):146-152
Cell migration is essential for invasive and metastatic phenotypes of cancer cells. Potential chemopreventive agents of cancer—sulindac sulfide, caffeic acid phenethyl ester (CAPE), curcumin, and (+)-catechin—have been reported to interfere with several types of intracellular signaling. In this study, we examined the effects of these agents on transforming growth factor-(TGF-)-induced motility and Akt phosphorylation in A549 cells. Judged by gold particle phagokinesis assay, sulindac sulfide, CAPE, and curcumin suppressed the motility of A549 cells promoted by TGF-. LY294002, a specific inhibitor of phosphatidylinositol 3-kinase(PI3K)/Akt signaling, also suppressed TGF--induced motility and Akt phosphorylation. Sulindac sulfide and CAPE, but not curcumin, suppressed TGF--induced Akt phosphorylation. We conclude that sulindac sulfide and CAPE suppress the motility promoted by TGF- in lung adenocarcinoma cells through the suppression of Akt. Our observations raise the possibility that these agents, except for (+)-catechin, can be applied not only as chemopreventive agents but also as anti-metastatic therapy.Abbreviations CAPE
Caffeic acid phenethyl ester
- TGF-
Transforming growth factor-
- FAK
Focal adhesion kinase
- MMP-2
Matrix metalloproteinase-2 相似文献
5.
A preterm neonate exposed antenatally to sulindac and dexamethasone was found to have a localised ileal perforation soon after birth. Unlike necrotising enterocolitis, drug-mediated ischaemic focal small-bowel perforation is associated with a benign clinical course and good prognosis when promptly treated. As antenatal sulindac and dexamethasone are being used with increasing frequency in obstetrics, all rare and life-threatening complications should be reported so that the benefits and risks can be critically assessed. 相似文献
6.
舒林酸在防治小鼠大肠癌中对p53和 p21WAF1影响的初步研究 总被引:2,自引:1,他引:2
目的:细胞凋亡受到抑制与大肠癌的发生有密切联系。近年来发现长期应用舒林酸等非甾体抗炎药(NSAID)对人的结肠癌、直肠癌和癌前病变的发生发展有预防作用。本实验试图通过对凋亡调控基因的观察,初步探讨舒林酸抗肿瘤作用可能存在的分子机制。方法:利用二甲肼诱发的小鼠实验性大肠癌动物模型,采用TUNEL原位杂交和免疫组化染色的方法,分别标记细胞凋亡、p53、p21阳性细胞,多阶段地动态观察诱癌过程中蛋白表达的变化和舒林酸对它们的影响。结果:p53蛋白表达阳性细胞密度随着病变加重而增加,p21阳性细胞密度升高趋势不明显,预防组、治疗组的p53和p21阳性率都与模型组无显著性差异(P>0.05)。预防组和治疗组中p53低于模型组(P<0.05),p21表达则高于模型组(P<0.05)。结论:舒林酸可以通过上调p21的表达,抑制突变型p53的表达,诱导细胞凋亡,抑制肿瘤形成和进展。 相似文献
7.
Summary A 37-year-old woman died after 18 days from her starting to take sulindac for low back pain. Based on her clinical course and the autopsy findings, the cause of her death was Lyell syndrome (toxic epidermal necrolysis) induced by sulindac. This case is described together with the legal aspects of medical malpractice to which it gave rise. 相似文献
8.
Krier F Brion M Debrus B Lebrun P Driesen A Ziemons E Evrard B Hubert P 《Journal of pharmaceutical and biomedical analysis》2011,54(4):694-700
The European Pharmacopoeia describes a liquid chromatography (LC) method for the quantification of sulindac, using a quaternary mobile phase including chloroform and with a rather long run time. In the present study, a new method using a short sub-2 μm column, which can be used on a classical HPLC system, was developed. The new LC conditions (without chloroform) were optimised by means of a new methodology based on design of experiments in order to obtain an optimal separation. Four factors were studied: the duration of the initial isocratic step, the percentage of organic modifier at the beginning of the gradient, the percentage of organic modifier at the end of the gradient and the gradient time. The optimal condition allows the separation of sulindac and of its 3 related impurities in 6 min instead of 18 min. Finally, the method was successfully validated using an accuracy profile approach in order to demonstrate its ability to accurately quantify these compounds. 相似文献
9.
《Toxicology in vitro》2011,25(5):1075-1084
The effects of arsenic trioxide (ATO) in combination with sulindac (SUL), sulindac sulfide (SS) or sulindac sulfone (SF) on human (Jurkat, HL-60, K562 and HPB-ALL) and mouse (EL-4) leukemic cell lines were investigated. The cells showed different sensitivity to sulindacs (2.5-200 μM) with SS being the most cytotoxic (72 h WST-1 reduction test). The cytotoxicity of ATO was enhanced by combination with sulindacs. The combination of ATO (1 μM) with SS or SF at concentrations over 50 μM induced considerable cytotoxicity in all cell lines. Normal human lymphocytes exposed for 48 h to the combinations showed smaller decrease in viability. Measurements of Jurkat, HL-60 and K562 cells exposed to ATO (1 μM) and sulindacs (100 μM or 200 μM for K562 cells) indicated apoptosis as the main cell death mechanism. The mitochondrial membrane potential measurements (JC-1 probe) indicated an active involvement of mitochondria in the process. The results did not indicate involvement of an inhibitory effect of the combinations on NF-κB activity in Jurkat, HL-60 and K562 cells. 相似文献
10.
To study the disposition of the anti-inflammatory drug sulindac, its active sulphide metabolite, and the inactive sulphone metabolite, sulindac (200 mg twice daily) was given to eight elderly subjects for at least 14 consecutive days. The drug was then ceased for 72 hours, and suitable samples were collected to study its elimination. The mean steady-state concentration for sulindac was 5.0 μg/ml, for sulindac sulphide was 6.5 μg/ml, and for sulindac sulphone was 13.2 μg/ml. These are approximately twice the reported steady-state levels for the respective redox forms in healthy young adults. The mean half-lives of sulindac, sulindac sulphide, and sulindac sulphone were 18.3 hours, 22.3 hours, and 54.6 hours, respectively. One patient who had mildly abnormal liver function tests developed more severe abnormalities whilst receiving sulindac. These returned towards normal after cessation of treatment. This patient had the highest steadystate plasma concentration of sulindac sulphone. It is concluded that care should be taken with the use of sulindac in the elderly, and control of patients' symptoms should be attempted with lower doses of the drug before the standard dose of 200 mg twice daily is administered. 相似文献