Inhibitory Action of Quercetin on Eosinophil Activation in Vitro.
Inhibitory action of quercetin on eosinophil activation in vitro.
Evid Based Complement Alternat Med. 2013; 2013: 127105
Sakai-Kashiwabara M, Asano K
The influence of quercetin on eosinophil functions was examined in vitro and in vivo. The first set of experiments was undertaken to examine whether quercetin could suppress eosinophilia and IgE hyperproduction induced by Mesocestoides corti infection in BALB/c mice. The number of peripheral blood eosinophils and IgE levels were examined 21 days after infection. Oral administration of quercetin for 21 days could not suppress both peripheral blood eosinophilia and IgE hyperproduction, even when 20.0?mg/kg quercetin was used for treatment. The second part of the experiment was designed to examine the influence of quercetin on eosinophil activation induced by SCF stimulation in vitro. Eosinophils were obtained from M. corti-infected mice and stimulated with SCF in the presence of various concentrations of quercetin for 24?h. The addition of quercetin into cell cultures could suppress eosinophil activation induced by SCF stimulation as assessed by measuring the contents of RANTES, MIP-1 ? , ECP, and MBP in culture supernatants. The minimum concentration of quercetin which caused significant suppression of factor secretion was 5.0? ? M. These results may suggest that quercetin will be a good candidate for the supplement on the management of eosinophil-mediated diseases, such as allergic rhinitis and asthma. HubMed – rehab
Community-based rehabilitation: Working in partnership with eye care.
Community Eye Health. 2013; 26(81): 14
Weber J
A compound heterozygote SLC26A2 mutation resulting in robin sequence, mild limbs shortness, accelerated carpal ossification, and multiple epiphysial dysplasia in two Brazilian sisters. A new intermediate phenotype between diastrophic dysplasia and recessive multiple epiphyseal dysplasia.
Am J Med Genet A. 2013 Jul 9;
Zechi-Ceide RM, Moura PP, Raskin S, Richieri-Costa A, Guion-Almeida ML
Mutations in solute carrier family 26 (sulfate transporter), member 2 (SLC26A2) gene result in a spectrum of autosomal recessive chondrodysplasias that range from the mildest recessive form of multiple epiphysial dysplasia (rMED) through the most common diastrophic dysplasia (DTD) to lethal atelosteogenesis type II and achondrogenesis IB. The clinical variability has been ascribed to quantitative effect of mutations of the sulfate transporter activity. Here we describe two Brazilian sisters, born to healthy and non consanguineous parents, with Robin sequence, mild shortening of upper and lower limbs, brachymetacarpalia/tarsalia, additional and accelerated carpal ossification, marked genu valgum, and multiple epiphysial dysplasia. This phenotype was intermediate between DTD and rMED, and both girls have a compound heterozygous mutations for the SLC26A2, a Finnish founder mutation (c.-26?+?2T>C), and R279W. This combination of mutations has been observed in individuals with different phenotypes, including DTD, DTD variant, and rMED. The distinct phenotype of our cases reinforces the hypothesis that other factors may be influencing the phenotype as previously suggested. © 2013 Wiley Periodicals, Inc. HubMed – rehab
RBPj?-dependent Notch signaling is required for articular cartilage and joint maintenance.
Arthritis Rheum. 2013 Jul 9;
Mirando AJ, Liu Z, Moore T, Lang A, Kohn A, Osinski AM, O’Keefe RJ, Mooney RA, Zuscik MJ, Hilton MJ
Objective: Osteoarthritis (OA) is a degenerative disease resulting in severe joint cartilage destruction and disability. While the mechanisms underlying the development and progression of OA are poorly understood, gene mutations have been identified within cartilage-related signaling molecules implicating impaired cell signaling in OA and joint disease. The Notch pathway has recently been identified as a crucial regulator of growth plate cartilage development and components are expressed in joint tissues. Therefore, we set out to investigate a novel role for Notch signaling in joint cartilage development, maintenance, and the pathogenesis of joint disease. Methods: We performed the first mouse genetic studies in which the core Notch signaling component, RBPj?, was tissue-specifically deleted within joints. The Prx1Cre transgene removed Rbpj? floxed alleles in mesenchymal joint precursor cells, while the Col2Cre(ERT2) transgene specifically deleted Rbpj? in postnatal chondrocytes. Articular chondrocyte cultures were also utilized to examine Notch regulation of gene expression. Results: Loss of Notch signaling in mesenchymal joint precursor cells does not affect embryonic joint development, but rather results in an early, progressive OA-like pathology. Additionally, partial loss of Notch signaling in postnatal cartilage results in progressive joint cartilage degeneration and an age-related OA-like pathology. Inhibition of Notch signaling alters expression of the ECM-related factors: COL2A1, PRG4, COL10A1, MMP13, and ADAMTSs. Conclusions: These data have identified the RBPj?-dependent Notch pathway as: 1) a novel pathway involved in joint maintenance and articular cartilage homeostasis, 2) a critical regulator of articular cartilage ECM-related molecules, and 3) a potentially important therapeutic target for OA-like joint disease. © 2013 American College of Rheumatology. HubMed – rehab