A polymerized complex (PC) technique was applied to the preparation of a highly active photocatalyst, K 2 La 2 Ti 3 O 10 , with a layered perovskite type structure to decompose H 2 O into H 2 and O 2 . The catalyst prepared by the PC technique had a higher photocatalytic activity than that prepared by conventional solid-state reaction method.

Production of type I collagen declines during aging, leading to skin thinning and impaired function. Prostaglandin E2 (PGE2) is a pleiotropic lipid mediator that is synthesized from arachidonic acid by the sequential actions of cyclooxygenases (COX) and PGE synthases (PTGES). PGE2 inhibits collagen production by fibroblasts in vitro. We report that PTGES1 and COX2 progressively increase with aging in sun-protected human skin. PTGES1 and COX2 mRNA was increased 3.4-fold and 2.7-fold, respectively, in the dermis of elderly (>80 years) versus young (21-30 years) individuals. Fibroblasts were the major cell source of both enzymes. PGE2 levels were increased 70% in elderly skin. Fibroblasts in aged skin display reduced spreading due to collagen fibril fragmentation. To investigate the relationship between spreading and PGE2 synthesis, fibroblasts were cultured on micropost arrays or hydrogels of varying mechanical compliance. Reduced spreading/mechanical force resulted in increased expression of both PTGES1 and COX2 and elevated levels of PGE2. Inhibition of PGE2 synthesis by diclofenac enhanced collagen production in skin organ cultures. These data suggest that reduced spreading/mechanical force of fibroblasts in aged skin elevates PGE2 production, contributing to reduced collagen production. Inhibition of PGE2 production may be therapeutically beneficial for combating age-associated collagen deficit in human skin.

Perovskite PbTiO 3 powders were prepared by a polymerized complex technique at relatively low temperatures, viz. 400-600 °C. Heating of a mixed solution of citric acid (CA), ethylene glycol (EG), and Pb and Ti ions with a molar ratio of Pb/Ti/CA/EG ) 1/1/10/40 at 130 °C produced a yellowish transparent polymeric gel without any precipitation, which after pyrolysis at 300 °C was converted to a powder precursor for PbTiO 3 . We suggest, based on the results of Raman and 13 C NMR spectroscopies, that a heterometallic (Pb,Ti)-CA 3 chelate complex formed in a starting Pb/Ti/CA/EG solution and it was thermally stable upon polymerization at 130 °C. Chemical analyses showed no PbO loss during calcination of powder precursors at 400-700 °C, which led to the conclusion that a solid-state reaction between isolated PbO and TiO 2 particles was not responsible for PbTiO 3 formation, but PbTiO 3 formed directly by thermal decomposition of the powder precursor above 400 °C.

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Chronic exposure of human skin to solar ultraviolet (UV) irradiation causes premature skin aging, which is characterized by reduced type I collagen production and increased fragmentation of the dermal collagenous extracellular matrix. This imbalance of collagen homeostasis is mediated, in part, by elevated expression of the matricellular protein cysteine-rich protein 61 (CCN1), in dermal fibroblasts, the primary collagen producing cell type in human skin. Here, we report that the actions of CCN1 are mediated by induction of interleukin 1β (IL-1β). CCN1 and IL-1β are strikingly induced by acute UV irradiation, and constitutively elevated in sun-exposed prematurely aged human skin. Elevated CCN1 rapidly induces IL-1β, inhibits type I collagen production, and upregulates matrix metalloproteinase-1, which degrades collagen fibrils. Blockade of IL-1β actions by IL-1 receptor antagonist largely prevents the deleterious effects of CCN1 on collagen homeostasis. Furthermore, knockdown of CCN1 significantly reduces induction of IL-1β by UV irradiation, and thereby partially prevents collagen loss. These data demonstrate that elevated CCN1promotes inflammaging and collagen loss via induction of IL-1β and thereby contributes to the pathophysiology of premature aging in chronically sun-exposed human skin.