Lead-free (Na 0:5 K 0:5 )NbO 3 (NKN) powders and thin films were fabricated from stoichiometric (Na/K ¼ 50=50), 4 mol % excess (52/52, 53/51, and 55/49), and 10 mol % excess (55/55, 56/54, 58/52, and 60/50) precursor solutions by the sol-gel process. The NKN55/55 powder heat-treated at 800 C showed an orthorhombic phase and rectangular grains whose size was estimated to be about 300 nm. With increasing Na/K ratio, grain size increased to about 1 mm and the cubic-tetragonal (T c ) phase transition peak emerged at 392 C in a differential thermal analysis (DTA) curve. On the other hand, single-phase NKN thin films were fabricated at 600 C from the (Na,K)-excess precursor solutions (58/52 and 60/50). In particular, the NKN58/ 52 thin film showed a low leakage current density (10 À7 A/cm 2 at 40 kV/cm), and the maximum polarization P max and dielectric constant " r at 1 kHz were 9.1 mC/cm 2 and 725, respectively.

Mast cells are widely distributed in the connective tissue of the body, but are particularly prominent in tissues such as skin. An increased number of mast cells can be found in the dermis under inflammatory conditions and ultraviolet (UV) exposed skin. Previous investigations have identified matrix metalloproteinases (MMPs) as key enzymes in the degradation of extra cellular matrix (ECM). This study reports about the potential contribution of human mast cell tryptase as a new triggering enzyme in matrix degradation process. Recent studies suggest that mast cell-derived proteases can activate MMPs. We investigated both the degradation of cellular matrix components and activation of MMPs by human tryptase. Mast cells are increased in photoaged skin and the increase of mast cell tryptase in UV irradiated skin was confirmed. Human mast cell tryptase was purified from human tonsils by a series of standard chromatographic procedures. Degradation of collagen type I was achieved by incubation of human type I collagen with tryptase and the fragments were quantified by SDS-PAGE and staining with Coomassie Brilliant Blue 250-R (CBB). Treatment with tryptase resulted in the activation of proMMP-9 as revealed by gelatinolytic activity in type IV collagen zymography. When tryptase was incubated with human type IV collagen, gradual degradation of intact collagen was detected by Western blotting. Furthermore, type IV collagen degradation was observed in the basement membrane (BM) of a three-dimensional (3D) skin model. Degranulation of mast cells, which release tryptase, can activate MMPs and causes direct damage to ECM proteins. These findings strongly implicate that tryptase either alone or in conjunction with activation of MMPs, can participate in ECM damage and the possible destruction of BM leading to photoaging.

The skin photoaging is characterized by keratinocyte hyperproliferation and degradation of collagen fibers, causing skin wrinkling and laxity and melanocyte proliferation that leads to pigmentation. UV is considered to be a major cause of such skin changes. It is well established that nuclear factor B (NF-B) is activated upon UV irradiation and induces various genes including interleukin-1 (IL-1), tumor necrosis factor ␣ (TNF␣), and matrix metalloprotease-1 (MMP-1). It is also known that basic fibroblast growth factor (bFGF) production is induced by UV and promotes the proliferation of skin keratinocytes and melanocytes. We found that UVB, IL-1, and TNF␣ induced NF-B activation and then produced MMP-1 and bFGF in HaCaT keratinocytes and skin fibroblasts. In this experiment, we examined if parthenolide, an NF-B inhibitor, could block the UVB-mediated skin changes. We found that parthenolide could effectively inhibit the gene expression mediated by NF-B and the production of bFGF and MMP-1 from cells overexpressing p65, a major subunit of NF-B. We also found that parthenolide could inhibit the UVB-induced proliferation of keratinocytes and melanocytes in the mouse skin. These findings suggest that NF-B inhibitors should be useful for the prevention of skin photoaging.

Skin aging is the aging process of skin tissue due to elastin and collagen breakdown. Collagen and elastin are protein of connective tissue in skin dermis that serves to regenerate the skin for firmness and flexibility maintained. Sunlight is composed by three main parts according to their wavelengths, namely UVA, UVB, and UVC where the intensity of UVB sunlight is most active. UVB generates the production superoxide anion (O 2-) which is main free radical in the skin surface. It attacked the cell membrane and subsequently form a new ROS and decrease antioxidants enzymatic excesively. Excessive ROS production resulting overexpression of AP-1 which activated Matrix metalloproteinases lead to collagen breakdown and photoaging. This paper discusses the affinity and interaction of isorhamnetin to CYP1A1 causing inactivation of AP-1 using molecular docking program. CYP1A1 is protein member of cytochrome P450 superfamily of enzymes encoded by the CYP1A1 gene. Cytochrome P450 used as oxidazing catalist in metabolic pathways steroids, fatty acids, xenobiotics, including drugs, toxins and carcinogens. This study consist of two stages: (1) isorhamnetin-CYP1A1 docking and α-naphthoflavone-CYP1A1 redocking (2) ∆G scores, inhibitory constant, and bonding interaction between ligan-reseptor analysis. Gibbs energy and inhibitory (∆G) constant (Ki) showed stability interaction between isorhamnetin and CYP1A1. Based on the ∆G score isorhamnetin has higher potential as CYP1A1 inhibitor than-naphthoflavoneα. Isorhamnetin-CYP1A1 get-10,3 kcal/mol and 11,34 µM and-naphthoflavoneα get-9,1 kcal/mol and 228,4 µM. Isorhamnetin-CYP1A1 binded by 4 π bondingand2hydrogen bonding. The result presented the potential of isorhamnetin to decreased AP-1 expressioan through CYP1A1 inhibition.

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Lead- and bismuth-free Ba(Ti1-x Zr x )O3 (BTZ) thin films were fabricated on Pt(111)/Ti/SiO2/Si(100) substrates by the chemical solution deposition (CSD) process. The BaTiO3 and BTZ005 thin films fabricated by the conventional process were observed to have a remarkable difference in grain size along the depth of the thin film. The microstructure of the BaTiO3 and BTZ005 thin films was improved by additional sintering process, and their grain sizes were increased to about 60 and 40 nm, respectively, by additional sintering at 800°C for 1 h. The dielectric constant ε r and piezoelectric constant d 33 of the BaTiO3 thin film consisting of large grains by the additional sintering at 800°C for 1 h were found to be about 375 and 14.5 pm/V. But, ε r and d 33 of the BTZ005 thin film changed negligibly with increasing of the grain size.

The critical behaviour of fully directed Levy flight on a square lattice is studied using the Monte Carlo method. The obtained critical exponents U, ull and U _ are independent of the parameter U. This seems to be interesting compared with the Levy flight previously discussed by Halley and Nakanishi, for which U depends on U in addition to d. It also indicates that the introduction of the direction plays a dominant role in directed Levy flight just as in directed SAW, with U, ull and U _ independent of d.

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