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Aluminum phosphate (AlPO4) was found to be an efficient and robust support material to produce optimum metal−support interactions that can reduce significantly Rh loading of automobile catalysts, owing to thermally stable and highly dispersed Rh nanoparticles anchored strongly onto the phosphate surface.

Irradiation with UV light, especially UVB, causes epidermal damage via the induction of apoptosis, inflammatory responses, and DNA damage. Various stressors, including UV light, induce heat shock proteins (HSPs) and the induction, particularly that of HSP70, provides cellular resistance to such stressors. The anti-inflammatory activity of HSP70, such as its inhibition of nuclear factor kappa B (NF-B), was recently revealed. These in vitro results suggest that HSP70 protects against UVB-induced epidermal damage. Here we tested this idea by using transgenic mice expressing HSP70 and cultured keratinocytes. Irradiation of wild-type mice with UVB caused epidermal damage such as induction of apoptosis, which was suppressed in transgenic mice expressing HSP70. UVB-induced apoptosis in cultured keratinocytes was suppressed by overexpression of HSP70. Irradiation of wild-type mice with UVB decreased the cutaneous level of IB-␣ (an inhibitor of NF-B) and increased the infiltration of leukocytes and levels of pro-inflammatory cytokines and chemokines in the epidermis. These inflammatory responses were suppressed in transgenic mice expressing HSP70. In vitro, the overexpression of HSP70 suppressed the expression of pro-inflammatory cytokines and chemokines and increased the level of IB-␣ in keratinocytes irradiated with UVB. UVB induced an increase in cutaneous levels of cyclobutane pyrimidine dimers and 8-hydroxy-2-deoxyguanosine, both of which were suppressed in transgenic mice expressing HSP70. This study provides genetic evidence that HSP70 protects the epidermis from UVB-induced radiation damage. The findings here also suggest that the protective action of HSP70 is mediated by anti-apoptotic, anti-inflammatory, and anti-DNA damage effects.The skin can be structurally classified into several layers, including the most apical layer, the epidermis, containing large numbers of keratinocytes, and a second layer, immediately under this, the dermis, which has a high fibroblast content (1). Skin provides a major interface between the environment and the body and is constantly exposed to an array of physical and chemical stressors. Therefore, in addition to intrinsic causes, harmful exogenous causes are involved in the process of skin damage. Among exogenous harmful agents, UV irradiation is the most relevant to skin damage (photo-damage). UV light can be separated, based on wavelength, into three categories: UVA (320 -400 nm), UVB (290 -320 nm), and UVC (100 -290 nm). Of these, the celldamaging effect of UVA is relatively weak, whereas most UVC is absorbed by the ozone layer (2). Thus, UVB seems to play the central role in photo-damage, such as clinical sunburn, hyperpigmentation, erythema, plaque-like thickening, loss of skin tone, deep furrowing, and fine wrinkle formation, all of which constitute both clinical and cosmetic problems. Furthermore, UVB irradiation induces the development of skin cancer (photo-carcinogenesis) (3). UVB-induced photodamage and photo-carcinogenesis both involve epidermal damage (such as induction...