Conclusions: Our study suggests that exogenous bFGF promotes articular cartilage repair by up-regulating the levels of multiple GFs, but administration at an early stage is required. (C) 2013 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.”
“A sensitive and selective liquid chromatography-mass spectrometry (LC-MS) method for determination of sulpiride in rabbit plasma was developed YM155 and validated. The analyte and internal standard (IS) were extracted from plasma by liquid liquid extraction using ethyl acetate, and chromatography im volved Agilent Extend-C18 column (2.1 mm x 50 mm, 35 mu m) using 0.2 % formic

acid in water and acetonitrile (60: 40, v/v) as a mobile phase. Detection involved positive ion mode electrospray ionization (ESI), and selective ion monitoring (SIM) mode was used for quantification of target fragment ions m/z 342.0 for sulpiride and m/z 294.8 for estazolam (internal standard, IS). The assay

was linear over the range of 10-2000 ng/mL for sulpiride, with a lower limit of quantitation (LLOQ) of 10 ng/mL for sulpiride. Intra- and inter-day precisions were less than 12 % and the accuracies were in the range of 94.1-108.7 % for sulpiride. This developed method was successfully applied for the determination of sulpiride in rabbit plasma for pharmacokinetic study.”
“Objective: Wnt/beta-catenin signaling plays C59 Wnt manufacturer an integral and complex role in cartilage development and maintenance. beta-catenin signaling has been linked to osteoarthritis (OA), but the role of Lrp6-mediated Wnt/beta-catenin signaling during OA remains unexplored. Mutations in the Wnt/beta-catenin co-receptors LRP5 and LRP6 (low-density lipoprotein-related receptors 5 and 6) result in skeletal abnormalities, which tend to be more severe in Lrp6 mutant mice. We examined OA development, chondrocyte and osteoblast behavior, and beta-catenin A-1155463 signaling after ligament and meniscus damage in mice with global heterozygous deletion of Lip6.

Design: Ligament and meniscus damage was surgically induced in Lrp6(+/-) and wild-type (WT) mice, and evidence of joint disease was assessed by Microcomputed tomography (micro-CT)

and histology. Wnt/beta-catenin signaling, proliferation, apoptosis, chondrogenesis, osteogenesis, and catabolic enzyme activity were measured.

Results: Relative to WT mice, Lip6(+/-) mice had lower nuclear beta-catenin signaling within articular cartilage. After surgery, osteophytes and reduced articular cartilage were apparent in WT mice, but more severe in Lip6(+/-) animals. Impairments to trabecular bone geometry occurred for WT and Lip6(+/-) mice after surgery. Relative to WT mice, Lip6(+/-) mice had reduced trabecular BMD and thickness, and Cyclin D1 and Lip6 gene expression after surgery. There was an increase in apoptotic cells and serum matrix metalloproteinase-9 (MMP9) for Lip6(+/-) mice after surgery, but no differences in cell proliferation occurred.