[en] The efficacy of hyperthermia for malignancies depend on various vasophsiological factors in the tumor, Such as pH, blood flow and oxygen tension. The present animal experiment was performed to ascertain how the effect of hyperthermia can be enhanced by administration of hydralazine (HYD), a vasodilator, which is known to decrease the local blood flow selectively and accordingly, decelerate thermal diffusion in the tumor. HYD (2-5mg/kg) was injected intraperitoneally 20 min before hyperthermia, which was done for 20-30 min at. 43 .deg. C by the use of a thermo-static water bath. The tumor quadrupling time was 4.5 days in the untreated FM3A group, 5.4 days in the HYD treated FM3A group, 8.5 days in the heat alone FM3A group and 11.2 days in the HYD plus heat treated FM3A group. Those in the respective SCC- VII group were 7.7 days, 9.0 days , 11.1 days and 14.0 days respectively. The enhancement ratio was 2.48 in the treatment for FM3A tumor and 1.81 in the treatment for SCC- VII tumor. Thus, these results indicate that HYD can increase the therapeutic efficiency of local hyperthermia treatment by inducing the change of microenvironment i.e. low pH, tumor hypoxia, deficient nutrition secondary to blood flow diminution which increase the sensitivity of tumor to heat

[en] This paper reviews recent experience with drugs that have been found to increase blood flow in tumours and to sensitize them to radiation. (UK)

No abstract available

[en] Short note

[en] Syntheses of |24-¹⁴C|3β,20xi-dihydroxy-23-norchol-5-enoic acid, |24-¹⁴C|3β20xi-dihydroxy-23-norcholanoic acid and |24-¹⁴C|20xi-hydroxy-3-oxo-23-norchol-4-enoic acid were accomplished by the reaction of ethyl |1-¹⁴C|bromoacetate in Reformatsky conditions, with suitable 20-keto-pregnane derivatives. Dehydration of these products afforded |24-¹⁴C|3β-hydroxy-23-norchola-5,20(22)E-dienoic acid, |24-¹⁴C|3β-hydroxy-23-norchol-20(22)E-enoic acid and |24-¹⁴C|3-oxo-23-norchola-4,20(22)E-dienoic acid respectively. The products were characterized by spectroscopic (IR, ¹H NMR, MS) methods. (author)

No abstract available

No abstract available

[en] To compare antihypertensive effect of fixed dose combination Hydrochlorothiazide-Amiloride and Amlodipine in patients of mild essential hypertension. After fulfilling the inclusion criteria of mild essential hypertension, defined as per recommendations of Seventh Joint National Committee (JNC 7) for treatment of Hypertension as stage 1 hypertension, systolic blood pressure (SBP) amlodipine and hydrochlorthiazide-amiloride 140-159-mmHg and Diastolic blood pressure(DBP) greater or equal to 90-99-mmHg, 100 patients were randomized into two study groups using a table of random numbers. Group 1 received tab amlodipine (5 mg) and Group 2 received tab hydrocholrthiazide-amiloride (25 mg-2.5mg). Informed written consent was taken. The patients were followed on subsequent visits (6 in total) for five months and systolic and diastolic blood pressure was recorded carefully. All the data thus obtained were processed and analyzed using SPSS version 10.0. Mean and standard deviation (SD) were calculated for age, diastolic and systolic blood pressure. In group 1 the drop in mean SBP between first and last visit was 15.42 mm Hg. In group 2 the drop in mean SBP between first and last visit was 18.34 mm Hg. In group 1, the drop in mean DBP between first and last visit was 10.08 mm Hg. In group 2 the drop in mean DBP between first and last visit was 14.65 mmHg. Mean drop in SBP of both the groups were compared with each other and found to be significantly different (P=0.003). Similarly mean drop in DBP of both the groups were compared with each other and found to be significant statistically (P=0.001). Hydrochlorothiazide-Amiloride had significantly better antihypertensive effect than Amlodipine in patients of mild essential hypertension at the end of five months therapy. (author)

[en] The stability of captopril in powder papers under three different storage conditions was determined. Captopril 12.5-mg tablets were triturated with lactose to a final concentration of 2 mg of captopril in 100 mg of powder. A total of 240 powder papers were prepared and stored in class A prescription vials (80 papers), 002G plastic zip-lock bags (80 papers), and Moisture Proof Barrier Bags (80 papers). Immediately after preparation and at 1, 2, 3, 4, 8, 12, and 24 weeks of storage at room temperature, powder papers under each storage condition were reweighed and the contents were assayed for captopril concentration by a stability-indicating high-performance liquid chromatographic method. More than 90% of the initial captopril concentration was retained under all storage conditions during the first 12 weeks of the study. Captopril disulfide, a degradation product, was detected in one sample stored in a plastic zip-lock bag at 24 weeks. Captopril was stable for the entire 24-week period in powder papers stored in either the class A prescription vial or the Moisture Proof Barrier Bag. Captopril in powder papers is stable for at least 12 weeks when stored at room temperature under all three storage conditions

[en] Mammalian target of rapamycin complex (mTORC) regulates various cellular processes including proliferation, growth, migration and differentiation. In this study, we showed that mTORC1 regulates platelet-derived growth factor (PDGF)-induced phenotypic conversion of vascular smooth muscle cells (VSMCs). Stimulation of contractile VSMCs with PDGF significantly reduced the expression of contractile marker proteins in a time- and dose-dependent manner. In addition, angiotensin II (AngII)-induced contraction of VSMCs was completely blocked by the stimulation of VSMCs with PDGF. PDGF-dependent suppression of VSMC marker gene expression was significantly blocked by inhibition of phosphatidylinositol 3-kinase (PI3K), extracellular signal-regulated kinase (ERK), and mTOR whereas inhibition of p38 MAPK had no effect. In particular, inhibition of mTORC1 by rapamycin or by silencing of Raptor significantly blocked the PDGF-dependent phenotypic change of VSMCs whereas silencing of Rictor had no effect. In addition, loss of AngII-dependent contraction by PDGF was significantly retained by silencing of Raptor. Inhibition of mTORC1 by rapamycin or by silencing of Raptor significantly blocked PDGF-induced proliferation of VSMCs. Taken together, we suggest that mTORC1 plays an essential role in PDGF-dependent phenotypic changes of VSMCs. - Graphical abstract: Regulation of VSMC phenotype by PDGF-dependent activation of mTORC1. - Highlights: • The expression of contractile marker proteins was reduced by PDGF stimulation. • PDGF-dependent phenotypic conversion of VSMCs was blocked by inhibition of mTOR. • PDGF-induced proliferation of VSMCs was attenuated by inhibition of mTORC1. • mTORC1 plays a critical role in PDGF-dependent phenotypic conversion of VSMCs