Airway resistance, lung compliance and enhanced pause (PenH) were

Airway resistance, lung compliance and enhanced pause (PenH) were

measured in naive, sensitized and saline or allergen-challenged Selleck NVP-BSK805 wild-type (WT) and ANXA1(-/-) mice. Total and allergen-specific antibodies were measured in the serum.\n\nResults We show that allergen-specific and total IgE, IgG2a and IgG2b levels were significantly higher in ANXA1(-/-) mice. Furthermore, naive ANXA1(-/-) mice displayed higher airway hypersensitivity to inhaled Mch, and significant differences were also observed in allergen-sensitized and allergen-challenged ANXA1(-/-) mice compared with WT mice.\n\nConclusions In conclusion, ANXA1(-/-) mice possess multiple features characteristic to allergic asthma, such as airway hyperresponsiveness and enhanced antibody responses, suggesting that ANXA1 plays a critical regulatory role in the development of asthma.”
“We investigated the potential Selleck INCB024360 role of pentraxin 3 (PTX3) in Henoch-Schonlein purpura (HSP), a common multisystemic vasculitis affecting children, as a predictor of Henoch-Schonlein purpura nephritis (HSPN). A total of 108 cases consisting of 34 children with HSP, 37 children with HSPN, and 37 healthy control

children were enrolled in this prospective study from March 2010 to February 2013. Blood and urine samples were collected to measure plasma PTX3, C-reactive protein (CRP), serum creatinine, blood urea nitrogen (BUN), urine microalbumin (MALB), and beta 2-microglobulin (beta 2-MG). Median plasma PTX3 concentrations were significantly higher in children with HSPN and HSP than in control subjects before treatment (6.99, 4.18-9.78 ng/ml; 3.19, 1.13-4.27 ng/ml; 1.24, 0.87-2.08 ng/ml, respectively; all p < 0.05). Median plasma PTX3 concentrations were also significantly higher in children with

HSPN than in children with HSP before treatment (6.99, 4.18-9.78 vs. 3.19, 1.13-4.27 ng/ml; p < 0.05). After treatment, Sapanisertib median plasma PTX3 concentrations significantly decreased in children with HSP (from 3.19, 1.13-4.27 to 1.08, 0.65-2.19 ng/ml; p < 0.05) and HSPN (from 6.99, 4.18-9.78 to 1.29, 1.01-2.26 ng/ml; p < 0.05). Plasma PTX3 concentration was positively correlated with CRP (rho = 0.532, p = 0.001), MALB (rho = 0.606, p < 0.001), beta 2-MG (rho = 0.490, p = 0.002), and 24-h urinary protein quantity (rho = 0.650, p < 0.001) in children with HSPN. Considering vasculitis, we found that PTX3 could be used as a more efficient potential predictor of HSPN than CRP as indicated by the area under the receiver operating characteristic (ROC) curve (AUC(ROC)) of PTX3 (AUC(ROC) = 0.837; p < 0.001) and CRP (AUC(ROC) = 0.514; p = 0.845). The threshold PTX3 concentration with optimal sensitivity and specificity was 4.30 ng/ml (sensitivity73.0 %, specificity79.6 %). Conclusion: PTX3 seems to have an important role in multisystemic vasculitis of HSP, may be involved in the development of HSPN, and used as an early biomarker to predict HSPN.

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