全文获取类型
收费全文 | 111篇 |
免费 | 9篇 |
国内免费 | 4篇 |
专业分类
儿科学 | 1篇 |
妇产科学 | 1篇 |
基础医学 | 5篇 |
口腔科学 | 1篇 |
临床医学 | 10篇 |
内科学 | 11篇 |
皮肤病学 | 8篇 |
神经病学 | 9篇 |
外科学 | 4篇 |
综合类 | 5篇 |
眼科学 | 1篇 |
药学 | 44篇 |
肿瘤学 | 24篇 |
出版年
2023年 | 3篇 |
2022年 | 3篇 |
2021年 | 6篇 |
2020年 | 4篇 |
2019年 | 3篇 |
2018年 | 1篇 |
2017年 | 2篇 |
2016年 | 3篇 |
2015年 | 5篇 |
2014年 | 2篇 |
2013年 | 13篇 |
2012年 | 4篇 |
2011年 | 1篇 |
2010年 | 3篇 |
2008年 | 2篇 |
2007年 | 1篇 |
2006年 | 8篇 |
2005年 | 1篇 |
2004年 | 1篇 |
2003年 | 9篇 |
2002年 | 3篇 |
2001年 | 4篇 |
2000年 | 2篇 |
1999年 | 1篇 |
1995年 | 1篇 |
1994年 | 1篇 |
1993年 | 2篇 |
1992年 | 3篇 |
1990年 | 2篇 |
1989年 | 2篇 |
1988年 | 1篇 |
1984年 | 3篇 |
1983年 | 3篇 |
1982年 | 3篇 |
1981年 | 3篇 |
1980年 | 3篇 |
1979年 | 2篇 |
1978年 | 5篇 |
1977年 | 1篇 |
1976年 | 2篇 |
1975年 | 1篇 |
1974年 | 1篇 |
排序方式: 共有124条查询结果,搜索用时 15 毫秒
71.
Dusana Majera PhD Zdenek Skrott MSC Jan Bouchal PhD Jirina Bartkova MD PhD Dana Simkova PhD Mariam Gachechiladze MD PhD Jana Steigerova PhD Daniela Kurfurstova MD PhD Jan Gursky PhD Gabriela Korinkova PhD Karel Cwiertka MD PhD Zdenek Hodny MD PhD Martin Mistrik PhD Jiri Bartek MD PhD 《The Prostate》2019,79(4):352-362
72.
H. Faulstich 《Toxicology》1980,18(3):205-211
Two proteins with high affinity for amatoxins have been characterized in calf thymus nucleic, the RNA-polymerase II (or B) and a 100 K protein of unknown function. Most of the toxic effects of amatoxins are based on the inhibited synthesis of mRNA. The 100 K protein may be involved in functions of cytokinesis as suggested by experiments with PtK1 cells and a fluorescent labelled amatoxin. The molecular toxicity of phallotoxins can be understood in terms of their affinity for actin. By interaction with rabbit muscle actin the concentration of action monomers is decreased. In hepatocytes, the phallotoxins change the structure of the microfilamentous web. 相似文献
73.
Bent Krag Mogens Dam Helle Angelo Jytte Molin Christensen 《Acta neurologica Scandinavica》1981,63(6):395-398
Treatment of alcoholics with phenytoin and disulfiram (DI) simultaneously is complicated and inexpedient because of the marked drug interaction. The aim of this study was to investigate whether an interaction exists between DI and carbamazepine (CBZ). The serum levels of CBZ and the metabolite CBZ-10, 11-epoxide were measured by high-pressure liquid chromatography in seven out-patients with epilepsy, on monotherapy with CBZ, before and during two weeks administration of DI. Five patients completed the investigation. None were alcoholics. The changes in the serum levels were insignificant, i.e. without clinical importance. Moreover, uncontrolled clinical experience has not indicated any interaction between DI and CBZ. Thus the influence of DI on the metabolism of CBZ is probably negligible. CBZ is suggested, therefore, when anticonvulsive therapy is needed by alcoholics in treatment with DI. 相似文献
74.
Olof Tottmar Ewa Hellstrm Kerstin Holmberg Kai O. Lindros 《Basic & clinical pharmacology & toxicology》1982,51(3):198-202
Abstract: In rats pretreated with the dopamine-β-hydroxylase (DBH)-inhibitors FLA-57 and FLA-63 (60 mg/kg, intraperitoneally, for 4 and 18 hrs), no effects on the blood acetaldehyde level after ethanol administration or on the activity of the low-Km aldehyde dehydrogenase (ALDH) in the liver were found. FLA-63 but not FLA-57 decreased the rate of ethanol elimination. FLA-63 inhibited the low-Km enzyme in vitro, but much less than the ALDH-inhibitors disulfiram and cyanamide. FLA-57 caused no inhibition in vitro. The results show that the previously observed suppression of ethanol intake in rats by FLA-57 and FLA-63 was not caused by an acetaldehyde-mediated aversion such as during the disulfiram-ethanol reaction. 相似文献
75.
Abstract 1-aminocyclopropanol (ACP) is a potent inhibitor of aldehyde dehydrogenase (ALDH) in vivo and in vitro. Like cyanamide it has a rapid onset of action in vivo with the highest inhibition occurring after 2-24 hrs. and a long duration of action like disulfiram with measurable inhibition after 144 hrs. All the three inhibitors decreased the activity of the mitochondrial low-Km ALDH strongly in vivo, however, in markedly different doses. Cyanamide inhibited the high-Km ALDH only in vivo, whereas in vitro, the high-Km ALDH was unaffected by cyanamide but significantly inhibited by disulfiram and ACP. The inhibition produced by the inhibitors appeared to be irreversible. Acetaldehyde protected the low-Km enzyme at different extents depending on the inhibitor used. The inhibition of ALDH in intoxicated and control rats and its relation to acetaldehyde oxidation and the disulfiram-ethanol reaction are discussed. 相似文献
76.
Spracklin DK Emery ME Thummel KE Kharasch ED 《Acta anaesthesiologica Scandinavica》2003,47(6):765-770
BACKGROUND: Cytochrome P4502E1(CYP2E1)-mediated oxidation of halothane to a reactive intermediate (trifluoroacyl chloride) that covalently binds to hepatic proteins forming trifluoroacetylated neoantigens is believed to be the initiating event in a complex immunologic cascade culminating in antibody formation and severe hepatic necrosis ('halothane hepatitis') in susceptible patients. Trifluoroacyl chloride may also hydrolyze to the stable metabolite trifluoroacetic acid (TFA). CYP2E1 inactivation by disulfiram or its primary metabolite, diethyldithiocarbamate, inhibits human halothane oxidation to TFA in vitro and in vivo. Nevertheless, disulfiram effects on hepatic protein trifluoroacetylation by halothane in vivo are unknown. This investigation tested the hypotheses that disulfiram prevents halothane-dependent protein trifluoroacetylation in vivo, and that TFA represents a biomarker for hepatic protein trifluoroacetylation. METHODS: Rats were pretreated with isoniazid (CYP2E1 induction), isoniazid followed by disulfiram (CYP2E1 inhibition), or nothing (controls), then anesthetized with halothane or nothing (controls). Plasma and urine TFA were quantified by ion HPLC; hepatic microsomal TFA-proteins were analyzed by Western blot. RESULTS: CYP2E1 induction increased both TFA and TFA-protein formation compared with uninduced halothane-treated rats. Disulfiram, even after CYP2E1 induction, nearly abolished both TFA and TFA-protein formation. Pretreatments similarly affected both TFA and TFA-protein formation across all groups. CONCLUSIONS: Disulfiram inhibition of CYP2E1-mediated halothane oxidation prevents hepatic protein trifluoroacetylation. Based on the concordance between TFA and TFA-protein formation, TFA appears to be a valid biomarker for TFA-protein formation. Disulfiram inhibition of human halothane oxidation in vivo, previously assessed by diminished TFA formation, probably also confers inhibition of hepatic TFA-protein formation. 相似文献
77.
About 50% of alcoholic patients relapse within 3 months of treatment. Previous studies have suggested that disulfiram may help to prevent such relapse. The aim of our study was to assess the efficacy and safety of long-term disulfiram treatment in alcohol dependence of adolescents. In this double-blind, placebo-controlled study we recruited 26 adolescents, aged 16 - 19 years, with chronic or episodic alcohol dependence. Patients were allocated treatment randomly with disulfiram (200 mg daily) or placebo for 90 days. Patients were assessed on the day treatment started and on days 30 and 90 by interview, self-report, questionnaire and laboratory screening. Patients were classified as abstinent, relapsing or non-attending. Time to first treatment failure (relapse or non-attendance) was the primary outcome measure. The disulfiram (n =13) and placebo (n = 13) groups were well matched in terms of baseline demographic and alcohol-related variables. Thirteen disulfiram-treated and 13 placebo-treated patients completed the treatment phase; seven (1 vs. 6) relapsed, five (3 vs. 2) refused to continue treatment, three (1 vs. 2) had concurrent illness and two (1 vs. 1) had adverse side effects. At the end of treatment, seven disulfiram-treated and two placebotreated patients had been abstinent continuously (p= 0.0063). Mean cumulative abstinence duration was significantly greater in the disulfiram group than in the placebo group [68.5 (SD 37.5) vs. 29.7 (19.0) days; p =0.012]. Apart from occasional diarrhoea, there was no difference in side effects between groups. In some cases, disulfiram may be an effective and well-tolerated pharmacological adjunct to psychosocial and behavioural treatment programmes for treatment of adolescent alcohol-dependent patients. [Niederhofer H, Staffen W. Comparison of disulfiram and placebo in treatment of alcohol dependence of adolescents. Drug Alcohol Rev 2003;22:295 - 297] 相似文献
78.
79.
T. Lysbo Svendsen M. Brandt Kristensen J. Mølholm Hansen L. Skovsted 《European journal of clinical pharmacology》1976,9(5-6):439-441
Summary Diphenylhydantoin (DPH) and tolbutamide serum levels were studied in ten volunteers before and after 4 days of disulfiram treatment. The mean DPH half life incresed significantly from 11.0±1.2 h to 19.0±3.3 h, and the mean DPH metabolic clearance rate decreased significantly from 51.2±17.2 ml/min to 33.9±12.0 ml/min during medication. No significant changes in the half life or metabolic clearance rate of tolbutamide was observed. 相似文献
80.
Inclusions, structurally similar to Lafora's bodies, are described in the liver cells of three chronic alcoholic patients who stopped drinking after disulfiram treatment. The inclusions were strongly positive with PAS and methenamine silver stains. Shikata stain for HBsAg was negative. On electron microscopy the inclusions are not membrane-bound and contain glycogen beta-granules, secondary lysosomes containing lamellar structures, lipid droplets and filaments; the SER was almost completely lost. In the patient least affected, the cells bearing inclusions were predominantly periportal in location, as is usual in Lafora's disease. In the two other patients the change involved the whole lobule. The possibility of an induced carbohydrate metabolic disorder, which could be due to the disulfiram, a drug that interferes with the activity of several hepatic enzymes is discussed. The presence of appearances suggestive of SER breakdown could also be interpreted as a manifestation of 'disuse atrophy' due to alcohol withdrawal. 相似文献