http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Utilization of Sunitinib for Renal Cell Cancer: an Egyptian University hospital experience
Ezz El Din, M Asian Pacific Journal of Cancer Prevention 2016 Asian Pacific journal of cancer prevention Vol.17 No.7
Background: Metastatic renal cell carcinoma (mRCC) status as poor prognosis improved with the introduction of tyrosine-kinase inhibitors, especially sunitinib. There is sparse data reporting from our region on use of sunitinib in metastatic RCC. Thus the present study explores sunitinib usage at our institute. Materials and Methods: An unselected population of patients with metastatic RCC receiving sunitinib was analyzed with respect to patient characteristics, response, toxicity, and outcomes. Results: Fourty-nine patients with a median age of 50.5 years (range 21-71 years) were included. Most were male (61.2%). Twenty‑one (42.9%) had metastatic disease at presentation. Sunitinib was first line therapy in 45. Conventional clear cell carcinoma was the most common pathology present (39 patients; 79.59 %). The most common site of metastasis was the lung (75.5%). Most patients (30) were started at a dose of 50 mg once a day for 4 weeks and then 2 weeks rest. Clinical benefit rate was 73.5% (n= 36), and 22.5% (n= 11) demonstrated progressive disease at first imaging evaluation within the first 3-6 months. The following objective response performed for patients was 48.9% (n=24) and progression at 24.5 % (n=12). The median follow‑up was 16 months (range, 4-34 months), the overall estimated median PFS was 9 months and the estimated median OS was 15 months. Conclusions: This study demonstrated sunitinib is tolerable and effective in advanced/metastatic RCC Egyptian patients and indicates we should further seek second and third lines to increase survival equivalence as reported in the worldwide literature.
Synthesis and Biological Investigations of New Thiazolidinone and Oxadiazoline Coumarin Derivatives
Abd Elhafez, Omaima Mohamed,El Khrisy, Ezz El Din Ahmed Mohamed,Badria, Farid,Fathy, Alaa El Din Mohamed The Pharmaceutical Society of Korea 2003 Archives of Pharmacal Research Vol.26 No.9
Ethyl (coumarin-4-oxy)acetate 1 was prepared through the reaction of 4-hydroxycoumarin with ethyl bromoacetate. Compound 1 was allowed to react with hydrazine hydrate to produce coumarin-4-oxyacetic hydrazide 2. The synthesis of N-(arylidene and alkylidene)-coumarin-4-oxyacetic hydrazones 3-20 was performed. The preparation of 2-substituted-3-[(coumarin-4-oxy) acetamido]thiazolidinones 21-26 and 2-[(coumarin-4-oxy )methyl]-4-acetyl-5-substituted-$\Delta^2$-1,3,4-oxadiazolines 27-33 was performed by the reaction of the hydrazones 3, 4, 7, 9, 12, 14 with mercaptoacetic acid and the hydrazones 3, 4, 5, 7, 12, 15, 16 with acetic anhydride, respectively. The antiviral activities, cytotoxicities and structure-activity relationship (SAR) towards different microorganisms of the prepared compounds were studied.
Ahmed H. Eid,Noha F. Abdelkader,Ola M. Abd El-Raouf,Hala M. Fawzy,Ezz-El-Din S. El-Denshary 대한약학회 2016 Archives of Pharmacal Research Vol.39 No.12
The clinical application of the anticancer drugcisplatin is limited by its deleterious side effects, includingmale reproductive toxicity. In this context, the potentialprotective effect of carvedilol on testicular and spermatologicaldamage induced by cisplatin in male Sprague–Dawley rats was investigated. Carvedilol was orallyadministered at a dose of 10 mg/kg for 2 weeks, and cisplatinwas given as a single intraperitoneal injection of10 mg/kg on the 12th day to induce toxicity. Cisplatinsignificantly reduced reproductive organ weight, spermcount and sperm motility, and increased sperm abnormalitiesand histopathological damage of testicular tissue. Inaddition, it resulted in a significant decline in serumtestosterone as well as levels of testicular enzymatic andnon-enzymatic antioxidants (superoxide dismutase, catalase,glutathione peroxides, and reduced glutathione). Moreover, cisplatin remarkably augmented malondialdehyde,nitric oxide, tumor necrosis factor-a, and nuclearfactor-kappa B contents in testicular tissue. Conversely,carvedilol administration markedly mitigated cisplatin-inducedtesticular and spermatological injury as demonstratedby suppression of oxidative/nitrosative andinflammatory burden, amendment of antioxidant defenses,enhancement of steroidogenesis and spermatogenesis, andmitigation of testicular histopathological damage. Thecurrent study reveals a promising protective action ofcarvedilol against cisplatin-induced reproductive toxicityby virtue of its anti-inflammatory and antioxidantproperties.