Starting from an historical perspective, ethical issues in publishing are discussed and technical suggestions on how to get the final draft accepted for publication are outlined. Contributing towards medical science is a great pleasure to be experienced and shared. (C) 2008 Elsevier Ltd. All rights reserved.”
“Objective: Hsa-miR-148a expression is decreased in Osteoarthritis (OA) cartilage, but its functional role in cartilage has never been studied. Therefore, our aim was to investigate the effects of overexpressing
hsa-miR-148a on cartilage metabolism of OA chondrocytes.
Design: OA chondrocytes were transfected with a miRNA precursor for hsa-miR-148a or a miRNA Evofosfamide cell line precursor negative control. After 3, 7, 14 and 21 days, real-time PCR was performed to examine gene expression levels of aggrecan (ACAN), type I, II, selleck chemicals llc and X collagen (COL1A1, COL2A1, COl10A1), matrix metallopeptidase 13 (MMP13), a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) and the serpin peptidase
inhibitor, clade H (heat shock protein 47), member 1 (SERPINH1). After 3 weeks, DNA content and proteoglycan and collagen content and release were determined. Type II collagen was analyzed at the protein level by Western blot.
Results: Overexpression of hsa-miR-148a had no effect on ACAN, COL1A1 and SERPINH1 gene expression, but increased COL2A1 and decreased COL10A1, MMP13 and ADAMTS5 gene expression. Luciferase reporter assay confirmed
direct interaction of miR-148a and COL10A1, MMP13 and ADAMTS5. The matrix deposited by the miR-148a overexpressing cells contained more proteoglycans and collagen, in particular type II collagen. Proteoglycan and collagen release into the culture medium was inhibited, but total collagen production was increased.
Conclusion: Overexpression of hsa-miR-148a inhibits hypertrophic differentiation and increases the production Apoptosis Compound Library manufacturer and deposition of type II collagen by OA chondrocytes, which is accompanied by an increased retention of proteoglycans. Hsa-miR-148a might be a potential disease-modifying compound in OA, as it promotes hyaline cartilage production. (C) 2013 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.”
“We aimed to investigate the possible spasmolytic activity of ent-7 alpha-acetoxytrachyloban-18-oic acid (1) and ent-7 alpha-hydroxytrachyloban-18-oic acid (2) on smooth muscle models. In male rat aorta and rat uterus, both diterpenes were unable to trigger spasmolytic action. However, 2 relaxed guinea-pig trachea: Compounds 1 and 2 antagonised, significantly and concentration-dependently, carbachol- and histamine-induced phasic contractions in guinea-pig ileum.