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排序方式: 共有63条查询结果,搜索用时 31 毫秒
31.
目的:建立注射用右丙亚胺的无菌检查方法。方法:按2005年版《中国药典》无菌检查法中薄膜过滤法进行相关操作,试验菌株为金黄色葡萄球菌、铜绿假单胞菌、枯草芽孢杆菌、生孢梭菌、白色念珠菌、黑曲霉,分别用150、250、350mL氯化钠-蛋白胨缓冲液(pH7.0)冲洗,比较3种冲洗量对检查结果的影响。结果:冲洗量为150mL时,除枯草芽孢杆菌外其它各菌在24~72h内均未见生长,冲洗量为250、350mL时各试验菌株生长良好。结论:所建立的注射用右丙亚胺无菌检查方法准确、可靠。 相似文献
32.
Dalila Belhani Laurent Fanton Fanny Vaillant Jacques Descotes Waheed Manati Alain Tabib Bernard Bui-Xuan Quadiri Timour 《Cardiovascular toxicology》2009,9(2):64-69
Further to our previous observation of post-mortem cardiac lesions after sudden death in several athletes with a history of
anabolic steroid abuse, this study was intended to reproduce these lesions in rabbits administered testosterone oenanthate,
a prototypic anabolic steroid abused by athletes, and to provide evidence for the protective effects of trimetazidine and
dexrazoxane that are used as antianginal and cardioprotective drugs, respectively. Groups of six rabbits each were administered
saline, testosterone, or a combination of testosterone and either trimetazidine or dexrazoxane for 3 months. Histologic cardiac
lesions including necrosis, misshapen cell nuclei, interstitial and endocardial fibrosis, lymphocytic infiltrates, and vascular
dystrophies were observed in testosterone-treated rabbits. In contrast, no significant lesions were observed in the animals
treated with testosterone combined with either trimetazidine or dexrazoxane. This is the first study providing evidence for
testosterone cardiotoxicity following sub-chronic exposure in laboratory animals. In addition, these results suggest the protective
role of trimetazidine and dexrazoxane. 相似文献
33.
Dexrazoxane is highly effective in reducing anthracycline-induced cardiotoxicity and extravasation injury and is used clinically
for these indications. Dexrazoxane has two biological activities: it is a prodrug that is hydrolyzed to an iron chelating
EDTA-type structure and it is also a strong inhibitor of topoisomerase II. Doxorubicin is able to be reductively activated
to produce damaging reactive oxygen species. Iron-dependent cellular damage is thought to be responsible for its cardiotoxicity.
The available experimental evidence supports the conclusion that dexrazoxane reduces doxorubicin cardiotoxicity by binding
free iron and preventing site-specific oxidative stress on cardiac tissue. However, it cannot be ruled out that dexrazoxane
may also be protective through its ability to inhibit topoisomerase II. 相似文献
34.
Robert J 《Cardiovascular toxicology》2007,7(2):135-139
The clinical importance of the cardiotoxicity of anthracyclines requires the availability of preclinical models able to predict
the cardiotoxicity of novel anthracycline analogs in reference to doxorubicin or of cardioprotectors aimed at circumventing
the deleterious effects of these drugs. The reference model has been defined long ago and has proven its validity. Weanling
rabbits given weekly injections of doxorubicin for 4 months developed a cardiomyopathy, which can be assessed from a clinical
and pathological point of view. Models in other animals such as rats or mice were similarly implemented, also with long-term
exposures to the drug, resulting in cardiac failure and severe pathological alterations, which could be graded for comparison.
Starting from the evidence that the damage caused by anthracyclines on cardiomyocytes was immediate after each injection and
that the functional efficiency of the myocardium should be affected long before the morphological alterations become detectable,
we developed a short-term model studying the cardiac performances of isolated perfused hearts of rats that had been treated
within 12 days by repetitive administrations of the molecule(s) to be tested. This model provided the data expected from clinical
experience: epirubicin appeared less cardiotoxic than doxorubicin; liposomal formulations appeared less cardiotoxic than free
drug formulations; dexrazoxane strongly protected against doxorubicin cardiotoxicity. We were then able to show that paclitaxel
could potentialize doxorubicin cardiotoxicity, but that docetaxel did not so; or that a high dose of dexrazoxane brought significantly
higher protection than a conventional dose. Based upon these contributions, we can encourage the use of the short-term model
of isolated perfused rat heart to screen the preclinical cardiotoxicity of anthracycline molecules, formulations and combinations. 相似文献
35.
目的 :研究注射用右雷佐生细菌内毒素检查的试验方法。方法 :按中国药典 2 0 0 0年版 (二部 )附录方法和指导原则。结果 :注射用右雷佐生对鲎试剂灵敏度在 0 0 6EU/ml以下时有干扰。结论 :选用高灵敏度的鲎试剂可对注射用右雷佐生进行细菌内毒素检查。 相似文献
36.
Fabio Galetta Ferdinando Franzoni Giulia Cervetti Nadia Cecconi Angelo Carpi Mario Petrini Gino Santoro 《Biomedicine & Pharmacotherapy》2005,59(10):94-544
BACKGROUND AND OBJECTIVE: Aim of the present study was to assess the effect of epirubicin-based chemotherapy on QT interval dispersion in patients with aggressive non-Hodgkin lymphoma (NHL), and the effect of dexrazoxane supplementation. Prolongation of QT dispersion may not only represent a sensitive tool in identifying the first sign of anthracycline-induced cardiotoxicity, but it may serve also in identifying patients who are at risk of arrhythmic events. METHODS: Twenty untreated patients, 相似文献
37.
Lubomir Elbl Hana Hrstkova Iva Tomaskova Jaroslav Michalek 《Supportive care in cancer》2006,14(2):128-136
Background The authors conducted a retrospective study to determine whether dexrazoxane (ICRF-187) would reduce late anthracycline-induced cardiotoxicity in patients treated in childhood for hematological malignancy.Patients and methods The authors examined 108 patients (63 male, 45 female) 5–29 years old, (median 15 years). All patients were in long-term remission of their malignancy. The cardioprotection was given to 68 patients (39 male, 29 female), and standard treatment was used in 40 patients (24 male, 16 female). Dexrazoxane (cardioxane, Chiron Company, The Netherlands) was given in 20:1 ratio to anthracycline. The follow-up time was 2–20 years (mean 7 years). The control group consisted of 41 volunteers (22 males, 19 females) 4–31 years old (median 18 years). The cardiotoxicity has been defined as the presence of heart failure or the decline of shortening fraction below 30% or ejection fraction (EF) below 55%. The end-systolic wall stress (ESS), myocardial performance index (MPI; Tei index), and parameters of left ventricular diastolic filling were also assessed.Results The anthracycline cardiomyopathy with the presence of heart failure was diagnosed in only one patient treated with a standard regimen. The pathological decline of fractional shortening was present in three (5%) and six (15%) patients with and without cardioprotection given, respectively. Similarly, none of the patients with cardioprotection revealed a pathological value of EF, while four (10%) patients without cardioprotection showed an EF decrease. Finally, ESS and isovolumic relaxation time were pathologically increased in the group without cardioprotection in comparison to the controls and to the group with cardioprotection. However, the MPI was significantly increased in both groups of patients.Conclusions Dexrazoxane reduces the risk of late clinical and subclinical cardiotoxicity and does not affect the response rates to chemotherapy and overall survival during the median follow-up period of 7 years (follow-up period 2–20 years). 相似文献
38.
Rabbit model for in vivo study of anthracycline-induced heart failure and for the evaluation of protective agents 总被引:4,自引:0,他引:4
Simůnek T Klimtová I Kaplanová J Mazurová Y Adamcová M Sterba M Hrdina R Gersl V 《European journal of heart failure》2004,6(4):377-387
BACKGROUND: Cardiac toxicity associated with chronic administration of anthracycline (ANT) antibiotics represents a serious complication of their use in anticancer chemotherapy, but can also serve as a useful experimental model of cardiomyopathy and congestive heart failure. AIMS: In this study, a model of chronic ANT cardiotoxicity induced by repeated i.v. daunorubicin (DAU) administration to rabbits was tested. METHODS: Three groups of animals were used: (1) control group-10 animals received i.v. saline; (2) 11 animals received DAU (3 mg/kg, i.v.); (3) 5 animals received the model cardioprotective agent dexrazoxane (DEX, 60 mg/kg, i.p.), 30 min prior to DAU. All substances were administered once weekly, for 10 weeks. The DAU-induced heart damage and protective action of DEX were determined and quantitated with the use of histopathology, invasive haemodynamic measurements (e.g. left ventricular pressure changes-dP/dt(max), dP/dt(min)), non-invasive systolic function examinations (left ventricular ejection fraction, PEP/LVET index) and biochemical analysis of cardiac troponin T plasma concentrations. RESULTS: All the employed methods showed unambiguously pronounced heart impairment in the DAU group, with the development of both systolic and diastolic heart failure, as well as significant reduction of DAU-cardiotoxicity in DEX-pretreated animals. Other toxicities were acceptable. CONCLUSION: The presented model has been approved to be consistent and reliable and it can serve as a basis for future determinations and comparisons of chronic cardiotoxic effects of various drugs, as well as for the evaluation of potential cardioprotectants. 相似文献
39.
目的 观察右丙亚胺对老年女性乳腺癌患者接受表阿霉素化疗时的心脏保护作用.万法 选取2008年5月至2011年11月84例年龄>65岁乳腺癌术后接受CEF方案及TE方案化疗的患者,随机分为两组:试验组42例,接受含表阿霉素方案化疗加右丙亚胺;对照组42例,接受含表阿霉素方案化疗不加右丙亚胺.所有患者连续随访2年,监测患者心肌钙蛋白T(cTnT)、左心室射血分数(LVEF)的变化情况,以及化疗毒性反应情况.结果 试验组患者心肌钙蛋白T(cTnT)的升高、左心室射血分数(LVEF)的下降均低于对照组,两组患者化疗毒性反应无差别,心脏毒性事件发生率差异无统计学意义.结论 对于老年乳腺癌患者,应用表阿霉素化疗从第一周期开始就已产生了心脏毒性.联合应用右丙亚胺能降低表阿霉素对老年乳腺癌患者引起的心脏毒性,而并不加重患者非心脏毒性反应,可增加老年乳腺j癌患者的治疗机会. 相似文献
40.
Dexrazoxane (ICRF-187) protects cardiac myocytes against doxorubicin by preventing damage to mitochondria 总被引:4,自引:0,他引:4
The clinically approved antioxidant cardioprotective agent dexrazoxane (ICRF-187) was examined for its ability to protect
neonatal rat cardiac myocytes from doxorubicin-induced damage. Doxorubicin is thought to induce oxidative stress on the heart
muscle, both through reductive activation to its semiquinone form, and by the production of hydroxyl radicals mediated by
its complex with iron. Hydrolyzed dexrazoxane metabolites prevent site-specific iron-based oxygen radical damage by displacing
iron from doxorubicin and chelating free and loosely bound iron. The mitochondrial stain Mito Tracker Green GM and doxorubicin
were shown by epifluorescence microscopy to accumulate in the myocyte mitochondria. An epifluorescence microscopic image analysis
method to measure mitochondrial damage was developed using the mitochondrial membrane potential sensing ratiometric dye JC-1.
This method was used to show that dexrazoxane protected against doxorubicin-induced depolarization of the myocyte mitochondrial
membrane. Dexrazoxane also attenuated doxorubichin-induced oxidation of intracellular dichlorofluorescin. Annexin V-FITC/propidium
iodide staining of myocytes was used to demonstrate that, depending on the concentration, doxorubicin caused both apoptotic
and necrotic damage. These results suggest that doxorubicin may be cardiotoxic by damaging the mitochondria and dexrazoxane
may be protective by preventing iron-based oxidative damage. 相似文献