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Specificity of a rodent alpha(α)6 nicotinic acetylcholine receptor subunit antibody
Alpha(α)6-containing nicotinic acetylcholine receptors (nAChRs) have been implicated in nicotine reward and reinforcement. To date, a commercially available, validated α6 nAChR subunit antibody has not been reported. To evaluate a commercially available neuronal α6 nAChR subunit antibody we performed quantitative western blots on protein from the ventral tegmental area of wild type Sprague Dawley rats. As a first approach to determine the specificity of the antibody, we used a control antigen to block the α6 antibody from binding. Next, we tested the antibody in brain tissue of wild type and α6 knockout (KO) C57BL/6J mice. The α6 antibody was present at a higher than expected molecular weight (63 versus 57 kDa) and the control antigen blocked the α6 antibody, suggesting specificity. However, when we genetically validated the antibody, bands were present in both α6 KO mice and C57BL/6J samples. Taken together, our study highlights the necessity to genetically validate antibodies when possible and we report that a commercially available α6 nAChR subunit antibody is non-specific
Incidence and Seroprevalence of Avian Influenza in a Cohort of Backyard Poultry Growers, Egypt, August 2015–March 2019
Does endotoxaemia contribute to osteoarthritis in obese patients?
OA (osteoarthritis) is a degenerative condition associated with obesity. A number of metabolic explanations have been proposed to explain the association between obesity and OA in non-weight-bearing joints; however, none of these hypotheses have been demonstrated empirically. In the present Hypothesis article, we recognize that obesity is associated with compromised gut mucosa, translocation of microbiota and raised serum LPS (lipopolysaccharide). The consequent activation of the innate immune response leads to increased serum titres of inflammatory mediators in obese patients, with both local and systemic markers of inflammation associated with onset and progression of OA. Furthermore, a number of workers have shown that articular cartilage repair is impaired by a range of inflammatory mediators, both in vitro and in vivo. We propose that metabolic endotoxaemia, caused by impaired gastric mucosa and low-grade chronic inflammation, may contribute to the onset and progression of OA in obese patients. This may account for the association between obesity and OA at non-weight-bearing joints which cannot be explained by biomechanical factors