Whereas high-dose ultraviolet B (UVB) is detrimental to the epidermal permeability barrier, suberythemal doses of UVB are used to treat atopic dermatitis (AD), which is characterized by defective permeability barrier and antimicrobial function. As epidermal permeability barrier and antimicrobial peptide (AMP) expression are coregulated and interdependent functions, we hypothesized that suberythemal doses of UVB exposure could regulate AMP expression in parallel with permeability barrier function. Hairless mice were exposed to 40 mJ cm(-2) UVB (about 1/2 minimal erythema dose) daily for 1 or 3 days. Twenty-four hours after the last exposure, epidermal barrier function was assessed and skin specimens were taken for western blotting, immunohistochemistry, and quantitative reverse transcription-PCR for mouse beta-defensin (mBD)-2, mBD3 and cathelin-related antimicrobial peptide (CRAMP). mRNA levels of the vitamin D receptor (VDR), 1alpha-hydroxylase and key epidermal lipid synthetic enzymes were also quantified. After 3 days of UVB exposure, acceleration of barrier recovery and augmentation in expression of epidermal differentiation markers (for example, involucrin and filaggrin) occurred in parallel with increased mBD2, mBD3, and CRAMP expression at both the mRNA and protein level. VDR, 1alpha-hydroxylase, and the major epidermal lipid synthetic enzymes were also upregulated. When an inhibitor of 1alpha, 25 dihydroxyvitamin D(3) formation, ketoconazole, was applied immediately after UVB exposure, the cutaneous vitamin D system was inhibited, which in turn blocked epidermal lipid synthesis, AMP expression, and permeability barrier homeostasis, suggesting that the beneficial effect of low-dose UVB depends, at least in part, on activation of the cutaneous vitamin D system. Our results provide new insights into the mechanisms whereby low-dose UVB comprises effective therapy for AD.

Cellular behavior can be influenced by the chemical and physical surface characteristics of biomedical substrates. To understand the relationships between various topographical surface patterns and cellular activities, various types of pattern models have been developed and examined in a range of sizes (microscale, nanoscale, and hierarchical structures consisting of both) and shapes (pillar, hole, groove, grate, grid, and island). Here, we review fabrication methods for obtaining physically patterned microscale and nanoscale surfaces, and discuss the relationships between cellular responses and physically patterned surfaces, which could be applied to various biomedical scaffolds used in tissue engineering applications.

Recently, various functional devices based on printing technologies have been of paramount interest, owing to their characteristic processing advantages along with excellent device performance. In particular, printable metallic electrodes have drawn attention in a variety of optoelectronic applications; however, research into printable metallic nanoparticles has been limited mainly to the case of an environmentally stable Ag phase. Despite its earth-abundance and highly conductive nature, the Cu phase, to date, has not been exploited as an ambient atmosphere-processable, printable material due to its critical oxidation problem in air. In this study, we demonstrate a facile route for generating highly conductive, flexible Cu electrodes in air by introducing the well-optimized photonic sintering at a time frame of 10(-3) s, at which the photon energy, rather than conventional thermal energy, is instantly provided. It is elucidated here how the surface oxide-free, printed Cu particulate films undergo chemical structural/microstructural evolution depending on the instantly irradiated photon energy, and a successful demonstration is provided of large-area, flexible, printed Cu conductors on various substrates, including polyimide (PI), polyethersulfone (PES), polyethylene terephthalate (PET), and paper. The applicability of the resulting printed Cu electrodes is evaluated via implementation into both flexible capacitor devices and indium-gallium-zinc oxide (IGZO) flexible thin-film transistors.

This study was undertaken to evaluate the effect of 3D printed polycaprolactone (PCL)/β-tricalcium phosphate (β-TCP) scaffold containing bone demineralized and decellularized extracellular matrix (bdECM) and human recombinant bone morphogenetic protein-2 (rhBMP-2) on bone regeneration. Scaffolds were divided into PCL/β-TCP, PCL/β-TCP/bdECM, and PCL/β-TCP/bdECM/BMP groups. In vitro release kinetics of rhBMP-2 were determined with respect to cell proliferation and osteogenic differentiation. These three reconstructive materials were implanted into 8 mm diameter calvarial bone defect in male Sprague-Dawley rats. Animals were sacrificed four weeks after implantation for micro-CT, histologic, and histomorphometric analyses. The findings obtained were used to calculate new bone volumes (mm3) and new bone areas (%). Excellent cell bioactivity was observed in the PCL/β-TCP/bdECM and PCL/β-TCP/bdECM/BMP groups, and new bone volume and area were significantly higher in the PCL/β-TCP/bdECM/BMP group than in the other groups (p < .05). Within the limitations of this study, bdECM printed PCL/β-TCP scaffolds can reproduce microenvironment for cells and promote adhering and proliferating the cells onto scaffolds. Furthermore, in the rat calvarial defect model, the scaffold which printed rhBMP-2 loaded bdECM stably carries rhBMP-2 and enhances bone regeneration confirming the possibility of bdECM as rhBMP-2 carrier.

Melt-plotted poly (ɛ-caprolactone) (PCL) has been widely applied in various tissue regenerations. However, its hydrophobic nature has hindered its usage in wider tissue engineering applications. In this study, we present the development of a porous and multilayered PCL scaffold, which shows outstanding hydrophilic properties and has a roughened surface consisting of homogeneously distributed nanosized pits. The scaffold was obtained using an innovative oxygen plasma treatment. This technology can induce variable nanoscale surface roughness, which is difficult from traditional plasma treatment. Osteoblast-like cells were cultured on the scaffolds and several cellular responses (cell viability, fluorescence images [live/dead cells, nucleus, and actin cytoskeleton], ALP activity, and calcium mineralization) were assessed for untreated PCL and conventionally plasma-treated PCL scaffolds. The data indicated that an appropriate roughness (654 ± 91 nm) of the PCL scaffold processed with the new plasma treatment induced more advantageous responses for the cells, compared with untreated scaffolds and traditional plasma-treated scaffolds.

To understand the relationship between surface patterns and cellular activities, various types of pattern models have been investigated. In this study, we suggest a new surface pattern model, which replicates proliferated cells. We used osteoblast-like cells (MG63) as a target cell pattern and constructed various cell-imprinted surfaces using an electric field assisted casting method for different culturing times (4 h and 7 and 14 days). On the basis of scanning electron microscopy images and three-dimensional topographical optical images, we acquired the cells' unique patterns and used them for replicating patterned substrates. We then cultured MG63 cells in the patterned surfaces for 7 and 14 days to observe various cellular activities, cell viability, alkaline phosphatase (ALP) activity, and mineralization. Higher cellular activities were observed on the roughened surface as compared with the smooth surface. In particular, we obtained the most appropriate roughness value (R(a) = 702 ± 87 nm) from proliferated cells cultured over 14 days. On the basis of these findings, we demonstrate a new biomimical surface model that enhances cellular activities at the cell-substrate interface.

Background: Topical calcineurin inhibitors (TCIs) such as pimecrolimus and tacrolimus have recently been used for dermatologic diseases including atopic dermatitis instead of topical glucocorticoids, because they display comparable efficacy, but less-frequent side effects. Although even short-term topical glucocorticoid compromise epidermal permeability barrier homeostasis, the effects of TCI on barrier function have not yet been reported. However, viral infections such as eczema herpeticum and molluscum contagiosum, which could indicate an impaired skin barrier, continue to occur with TCI use in atopic dermatitis.

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