This change is explained by considering the filtering effect of the beam patterns of the BLD by the SF. Further, we show that the signal and then the signal-to-noise ratio of the transmission spectra of a sample are enhanced by using the SF compared with our previous work. (C) 2011 American Institute of Physics. [doi:10.1063/1.3639296]“
“Background: Trichophyton-induced superficial skin mycosis is a common infectious human disease, but the immunological mechanism against Trichophyton infection is unclear with regard to many points. Since Trichophyton cannot colonize mice, guinea
pigs were used in previous experiments on Trichophyton infection. However, it is difficult to perform immunological and genetic selleck chemicals analyses in guinea pigs.
Objective: The objective of this study was to establish a mouse Trichophytin-associated inflammation model of superficial skin mycosis in which immunological check details and genetic analyses can be performed.
Methods: We established a mouse Trichophyton-induced contact hypersensitivity model by applying Trichophytin, the Trichophyton antigen, extracted from Trichophyton mentagrophytes, to mice. Using a Th1-dominant strain, C57BL/6, and a Th2-dominant strain, BALB/c, we investigated
the expression of inflammatory cytokines and receptors of the innate immune system for fungi, TLR4, TLR2, and dectin-1, and their influences on responses of the acquired immune system.
Results: In C57BL/6 mice, expressions of IFN-gamma and IL-17 A in regional lymph nodes and IL-1 beta, IFN-gamma, IL-6, and IL-23 in the inflammatory auricular skin were enhanced by Trichophytin challenge, suggesting that not only Th1 cells but also Th17 cells were induced. In BALB/c mice, expressions of IL-4 in regional lymph nodes, and TSLP and IL-4 in the auricular
skin were enhanced by Trichophytin challenge. Interestingly, dectin-1-neutralizing LCL161 nmr antibody inhibited the promotion of IFN-gamma production in C57BL/6 mice, and dectin-1-expressing immune cells had crucial actions in Trichophyton-induced IFN-gamma production.
Conclusion: These results suggest that inflammatory mediators differently regulate Trichophytin-induced contact hypersensitivity on the basis of the status of host immunity. (C) 2012 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.”
“Background: Metabolic consequences of vitamin D deficiency have become a recent research focus. Maternal vitamin D status is thought to influence musculoskeletal health in children, but its relation with offspring metabolic risk is not known.
Objective: We aimed to examine the association between maternal vitamin D status and anthropometric variables, body composition, and cardiovascular risk markers in Indian children.