(C) 2013 Elsevier Inc. All rights reserved.”
“The aim of the present study was to compare the bioavailability of escitalopram (CAS 128196-01-0) from two escitalopram oxalate (CAS 219861-08-2) tablets (escitalopram 10 mg tablet as test preparation and 10 mg tablet commercially available original tablet of the drug as reference preparation) in 20 Chinese healthy male volunteers, aged between 19 and 27. The study was conducted according to an open, randomized, single blind, 2-way crossover study design with a wash-out phase of 14 d. Blood samples for pharmacokinetic profiling were taken up to 156 It
post-dose, and escitalopram plasma concentrations were determined with a validated liquid chromatography-electrospray ionization-mass
spectrometry (LC-ESI-MS) method. Maximum plasma concentrations (C(max)) of AZD2014 clinical trial 9.85 +/- 1.79 ng/ml (test) and 9.92 +/- 2.14 ng/ml (reference) were achieved. Areas under the plasma concentration-time curve (AUC(0 – infinity)) of 428.40 +/- 140.25 ng . h/ml (test) and 413.73 +/- 144.81 ng . h/ml (reference), AUC(0 – t) of 401.33 +/- 120.61 ng . h/ml (test), 385.42 +/- see more 117.73 ng . h/ml (reference) were calculated. The median T(max) was 4.3 +/- 1.8 h, 4.1 +/- 1.5 h for test and reference formulation, respectively. Plasma elimination half-lives (t(1/2)) of 36.30 +/- 8.93 h (test), 36.70 +/- 9.99 h (reference) were determined. Both primary target parameters, AUC(0 – infinity) and AUC(0 – t) were tested parametrically by analysis of variance (ANOVA) and relative bioavailabilities were 105.1 +/- 10.8% for AUC(0 – infinity) 104.9 +/- 11.1% for AUC(0 – t). Bioequivalence between test and reference preparation was demonstrated for both parameters, AUC(0 – infinity) and AUC(0 – t). The 90% confidence MLN2238 cell line intervals of the T/R-ratios of logarithmically transformed data were in the generally accepted range of 80%-125%. That means that the test formulation is bioequivalent to the reference formulation for escitalopram.”
“2-Chloro-3-(4-oxocyclohexa-2,5-dienylideneamino)-1,4-dihydronaphthalene-1,4-diones
maintained in the conc. sulfuric acid undergo cyclization affording in a high yield 6-chloro-10,12a-dihydroqD-7H,12aH-benzo[c]phenoxazin-5-ones whose structure is proved by XRD analysis.”
“Objective: To investigate the molecular etiologic causes of sporadic nonsyndromic hearing loss in Chinese children.
Methods: 179 sporadic nonsyndromic hearing loss children were subjected to microarray-based mutation detection for nine hot spot mutations in four of the most common deafness-related genes, including GJB2, SLC26A4, GJB3, and 12s rRNA.
Results: The incidence of positive genetic errors was 43.58% with the current set of target genes in sporadic nonsyndromic hearing loss children. Among them, 25.14% of cases had genetic defects in GJB2, 16.76% of cases had pathogenic mutations in SLC26A4, 1.12% of cases were caused by 12s rRNA mutations, and GJB3 mutation was detected in 0.