The transfer of sweat to the skin surface without leakage is important for the homeostatic regulation of skin and is impaired in atopic dermatitis. Although the precise composition of the leakage barrier remains obscure, there is a large contribution from claudins, the major components of tight junctions. In humans, claudin-1, -3, and -15 are expressed on sweat ducts, and claudin-3 and -10 are expressed on secretory coils. Although only two claudins are expressed in murine sweat glands, we found that the expression of claudin-3 is conserved. Atopic dermatitis lesional skin had decreased claudin-3 expression in sweat glands, which was accompanied by sweat leakage. This critical role in water barrier function was confirmed in Cldn3 and Cldn3 mice and those with experimentally decreased claudin-3. Our results show the crucial role of claudin-3 in preventing sweat gland leakage and suggest that the pathogenesis of dermatoses accompanied by hypohidrosis involves abnormally decreased claudin-3.
The reactivities of toluene, rn-xylene, phenol and benzene on mono-and multi-layer V/Ti and V/Zr oxides prepared by the gas-phase method have been studied by FTIR spectroscopy. It is found that Lewis-acidic sites (vanadium ion) play an important role in the formation of n-complexes of toluene, rn-xylene and benzene. The methyl group of the n-complex is dehydrogenated by the V -0 species to form benzyl species and benzaldehyde. On the other hand, phenol is adsorbed via its oxygen with its benzene ring oriented perpendicular to the surface. From spectral similarities, it is concluded that benzene is adsorbed to form mono-and/or disubstituted species. The activity of V=O species on the monolayer catalyst is higher than that on the multilayer catalyst.
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