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“This work is concerned with development and AZD5153 mw validation of chromatographic and spectophotometric methods for analysis of Mebeverine HCl (MEH), Diloxanide furoate (DF) and Metronidazole (MET) in Dimetrol (R) tablets – spectrophotometric and RP-HPLC methods using UV detection. The developed spectrophotometric methods depend on determination of MEH and DF in the combined dosage form using the successive derivative ratio spectra method which depends on derivatization of the obtained ratio spectra in two steps using methanol as a solvent and measuring MEH at 226.4-232.2 mu (peak to peak) and DF at 260.6-264.8
nm (peak to peak). While MET concentrations were determined using first derivative (D-1) at lambda = 327 nm using the same solvent. The chromatographic method depends on HPLC separation on ODS column and elution with a mobile
phase consisting water: methanol: triethylamine (25: 75: 0.5, by volume, orthophosphoric acid to pH = 4). Pumping the mobile phase at 0.7 ml min(-1) with UV at 230 nm. Factors affecting the developed methods were studied and optimized, moreover, they have been validated as per ICH guideline and the results demonstrated that the suggested methods are reproducible, reliable and can be applied for routine use with short time of analysis. Statistical analysis of the two developed methods with each other using F and student’s-t tests showed no significant difference.”
“OBJECTIVE: Endostatin is a potent endogenous inhibitor of angiogenesis. It is derived from the proteolytic check details cleavage of collagen XVIII, which is encoded by the COL18A1 gene.
A polymorphic COL18A1 allele encoding the functional polymorphism p.D104N impairs the activity of endostatin, resulting in a decreased ability to inhibit angiogenesis. This polymorphism has been previously analyzed in many types of cancer and has been considered a phenotype modulator in some benign and malignant tumors. However, these data are controversial, and different results have been reported for the same tumor types, such as prostate and breast cancer. The purpose of this study was to genotype the p.D104N variant in a cohort of pediatric and adult patients with adrenocortical tumors and to determine its possible association with the biological behavior of adrenocortical tumors.
METHODS: DNA Selleck Elafibranor samples were obtained from 38 pediatric and 56 adult patients (0.6-75 yrs) with adrenocortical tumors. The DNA samples were obtained from peripheral blood, frozen tissue or paraffin-embedded tumor blocks when blood samples or fresh frozen tissue samples were unavailable. Restriction fragment length polymorphism analysis was used to genotype the patients and 150 controls. The potential associations of the p.D104N polymorphism with clinical and histopathological features and oncologic outcome (age of onset, tumor size, malignant tumor behavior, and clinical syndrome) were analyzed.