Propionibacterium acnes, an anaerobic pathogen, plays an important role in the pathogenesis of acne and seems to initiate the inflammatory process by producing proinflammatory cytokines. In order to demonstrate the anti-inflammatory effects and action mechanisms of magnolol and honokiol, several methods were employed. Through DPPH and SOD activity assays, we found that although both magnolol and honokiol have antioxidant activities, honokiol has relatively stronger antioxidant activities than magnolol {[for DPPH assay, % of DPPH bleaching of magnolol and honokiol (500 microM magnolol: 19.8%; 500 microM honokiol: 67.3%)]; [for SOD assay, SOD activity (200 microM magnolol: 53.4%; 200 microM honokiol: 64.3%)]}. Moreover, the production of interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-alpha) induced by P. acnes in THP-1 cells, a human monocytic cell line, was reduced by magnolol and honokiol {[for IL-8 (10 microM magnolol: 42.7% inhibition; 10 microM honokiol: 51.4% inhibition)]; [for TNF-alpha (10 microM magnolol: 20.3% inhibition; 10 microM honokiol: 39.0% inhibition)]}. Cyclooxygenase-2 (Cox-2) activity was also suppressed by them [(15 microM magnolol: 45.8% inhibition), (15 microM honokiol: 66.3% inhibition)]. Using a nuclear factor-kappaB (NF-kappaB) luciferase reporter assay system and Western analysis, we identified that magnolol and honokiol exert their anti-inflammatory effects by inhibiting the NF-kappaB element, which exists in Cox-2, IL-8, and TNF-alpha promoters [(15 microM magnolol: 44.8% inhibition), (15 microM honokiol: 42.3% inhibition)]. Of particular note is that magnolol and honokiol operate downstream of the MEKK-1 molecule. Together with their previously known antibacterial activity against P. acnes and based on these results, we suggest that magnolol and honokiol may be introduced as possible acne-mitigating agents.

Skin aging appears to be principally related to a decrease in the levels of type I collagen, the primary component of the skin dermis. Asiaticoside, a saponin component isolated from Centella asiatica, has been shown to induce type I collagen synthesis in human dermal fibroblast cells. However, the mechanism underlying asiaticoside-induced type I collagen synthesis, especially at a molecular level, remains only partially understood. In this study, we have attempted to characterize the action mechanism of asiaticoside in type I collagen synthesis. Asiaticoside was determined to induce the phosphorylation of both Smad 2 and Smad 3. In addition, we detected the asiaticoside-induced binding of Smad 3 and Smad 4. In a consistent result, the nuclear translocation of the Smad 3 and Smad 4 complex was induced via treatment with asiaticoside, pointing to the involvement of asiaticoside in Smad signaling. In addition, SB431542, an inhibitor of the TGFbeta receptor I (TbetaRI) kinase, which is known to be an activator of the Smad pathway, was not found to inhibit both Smad 2 phosphorylation and Type 1 collagen synthesis induced by asiaticoside. Therefore, our results show that asiaticoside can induce type I collagen synthesis via the activation of the TbetaRI kinase-independent Smad pathway.

In mammalian melanocytes, melanin synthesis is controlled by tyrosinase, the critical enzyme in the melanogenic pathway. A recent report showed that the stimulation of melanogenesis by glycyrrhizin (GR) is because of an increased tyrosinase expression at mRNA and protein levels. But, the molecular events of melanogenesis induced by GR remain to be elucidated. In this study, using B16 melanoma cells, we showed that GR activated activator protein-1 (AP-1) and cyclic response filament "CRE" promoters, but not the nuclear factor-kappaB promoter. In addition, although GR stimulated mitogen-activated protein (MAP) kinase, p42/44(mapk), consistent with GR-induced AP-1 promoter activation, GR-induced melanogenesis was not blocked by PD98059, an MEK1 inhibitor, suggesting that MAPkinase induced by GR does not have a direct effect on the level of melanin content. But, GR-induced melanogenesis was inhibited by an inhibitor of protein kinase A (H-89). This result was further confirmed by the fact that GR induced the phosphorylation of CRE binding protein (CREB) and inhibition of glycogen synthase kinase 3beta phosphorylation as well as the production of cAMP, indicating that GR induces melanogenesis through cAMP signaling. In addition, the fact that GR-induced CRE activation was blocked by H-89 but GR-induced increase of cAMP production was not suggests that GR operates upstream of protein kinase A.

Escherichia coli (E. coli) and other bacteria are propelled through water by several helical flagella, which are rotated by motors embedded at random points on the cell wall. Depending on the handedness and rotation sense, the motion of the flagella induces a flow field that causes them to wrap around each other and form a bundle. Our objective is to understand and model the mechanics of this process. Full-scale flagella are 10 lm in length, 20 nm in diameter, and turn at a rate of 100 Hz. To accurately simulate bundling at a more easily observable scale, we built a scale model in which 20-cm-long helices are rotated in 100,000 cp silicone oil (Poly-di-methyl-siloxane). The highly viscous oil ensures an appropriately low Reynolds number. We developed a macro-scale particle image velocimetry (PIV) system to measure the full-field velocity distribution for rotating rigid helices and rotating flexible helices. In the latter case, the helices were made from epoxy-filled plastic tubing to give approximately the same ratio of elastic to viscous stresses as in the full-scale flagella. Comparison between PIV measurements and slender-body calculations shows good agreement for the case of rigid helices. For the flexible helices, we find that the flow field generated by a bundle in the steady state is well approximated by the flow generated by a single rigid helix with twice the filament radius.

Results concerning the design and fabrication of electromagnetic actuators, and their application to affect the wall shear stress in a fully turbulent channel flow are discussed. The actuators utilize a Lorentz force to induce fluid motion due to the interaction between a magnetic field and a current density. The actuators are comprised of spanwise-aligned rows of permanent magnets interlaced with surface-mounted electrodes, segmented to allow the Lorentz force to be propagated in the spanwise direction. Problems commonly associated with electromagnetic flow control-electrolysis, bubble formation, and electrode corrosion are substantially reduced, and in most cases eliminated by the use of a conductive polymer coating. The actuators generate velocity profiles with a penetration depth into the flow of approximately 1 mm ͑set by the electrode/magnet pitch͒ and maximum velocities of approximately 4 cm/s. The actuation velocities are found to scale linearly with forcing voltage and frequency. The electrical to mechanical efficiency is found to be very low (Ϸ10 Ϫ4 ), primarily due to the limitations on the magnetic field strength and the low conductivity of the working fluid ͑saltwater͒. The actuators are used in a fully turbulent low Reynolds number channel flow and their effect on the turbulent skin friction is measured using a direct measurement of drag. Maximum drag reductions of approximately 10% are measured when the flow is forced using a spanwise oscillating Lorentz force. A scaling argument for the optimal amplitude of the current density is developed. The efficiency of this method for drag reduction, and its application at higher Reynolds numbers is also discussed.