Conducting Super-Hydrophobic Thin Film for Electric Heating Applications.

Frost presents a serious problem for the human environment, resulting in such phenomena as downed power lines, damaged crops and stalled aircraft. In addition, frost and ice accumulation significantly decrease the performance of ships, wind turbines, and HVAC systems with high failure risk. Super-hydrophobic (SH) surface can be an appropriate solution for frost problems, due to its anti-icing properties that can prevent ice nucleation on the surface. In addition, in the case of conducting SH surface using carbon nanotubes (CNTs) as a filler, it can form an excellent heating unit, owing to the resistive heating effect. The purpose of this study is to produce a large-area conducting SH film that can prevent ice nucleus and remove ice formation rapidly. High aspect ratio carbon nanotubes (CNTs) as a conducting filler and adhesive polymer resin as a binder were used to form coating layer. In addition, silica particles (~7 nm) were used to stabilize nano-size roughness of the SH surface. Wet and dry etching processes were used on the substrate to improve wettability and to produce organic functional groups. To evaluate the de-icing effect, the fabricated SH surface was rapidly heated to 150 °C by applying voltage.

PPARdelta promotes wound healing by up-regulating TGF-beta1-dependent or -independent expression of extracellular matrix proteins.

Although the peroxisome proliferator-activated receptor (PPAR) delta has been implicated in the wound healing process, its exact role and mechanism of action have not been fully elucidated. Our previous findings showed that PPARdelta induces the expression of the transforming growth factor (TGF)-beta1, which has been implicated in the deposit of extracellular matrix proteins. Here, we demonstrate that administration of GW501516, a specific PPARdelta ligand, significantly promoted wound closure in the experimental mouse and had a profound effect on the expression of collagen types I and III, alpha-smooth muscle actin, pSmad3 and TGF-beta1, which play a pivotal role in wound healing processes. Activation of PPARdelta increased migration of human epidermal keratinocytes and dermal fibroblasts in in vitro scrape-wounding assays. Addition of a specific ALK5 receptor inhibitor SB431542 significantly suppressed GW501516-induced migration of human keratinocytes and fibroblasts. In these cells, activated PPARdelta also induced the expression of collagen types I and III and fibronectin in a TGF-beta1-dependent or -independent manner. The effect of PPARdelta on the expression of type III collagen was dually regulated by the direct binding of PPARdelta and Smad3 to a direct repeat-1 site and a Smad-binding element, respectively, of the type III gene promoter. Taken together, these results demonstrated that PPARdelta plays an important role in skin wound healing in vivo and that it functions by accelerating extracellular matrix-mediated cellular interactions in a process mediated by the TGF-beta1/Smad3 signaling-dependent or - independent pathway.

Down-regulation of aldose reductase renders J774A.1 cells more susceptible to acrolein- or hydrogen peroxide-induced cell death.

Aldose reductase (AR) is abundantly expressed in a variety of cell lineages and has been implicated in the cellular response against oxidative stress. However, the exact functional role of AR against oxidative stress remains relatively unclear. This study investigated the role of AR in acrolein- or hydrogen peroxide-induced apoptosis using the J774.A.1 macrophage cell line. Ablation of AR with a small interference RNA or inhibition of AR activity significantly enhanced the acrolein- or hydrogen peroxide-induced generation of reactive oxygen species and aldehydes, leading to increased apoptotic cell death. Blockade of AR activity in J774A.1 cells markedly augmented the acrolein- or hydrogen peroxide-induced translocation of Bax to mitochondria along with reduced Bcl-2 and increased release of cytochrome c from the mitochodria. Taken together, these findings indicate that AR plays an important role in the cellular response against oxidative stress, by sequestering the reactive molecules generated in cells exposed to toxic substances.