Analytical Modeling of Rheological Postbuckling Behavior of Wood-Based Composite Panels Under Cyclic Hygro-Loading

This study was conducted to develop analytical models to predict postbuckling behavior of woodbased composite panels under cyclic humidity conditions. Both the Rayleigh method and von Karman theory of nonlinear plate with imperfection were used to obtain a closed form solution to the hygrobuckling and postbuckling. In addition, mechano-sorptive creep effects were also taken into account for the derivation of analytical models. The closed-form solutions derived for both isotropic and orthotropic materials showed a good agreement with the experimental results in terms of the center deformation of hardboard, especially in the case of the edge movements. The unrecovery deformation was much greater at the first cycle and then decreased as the number of cyclic hygro-loading increased

One-pot Enzymatic Synthesis of Deoxy-thymidine-diphosphate (TDP)-2-deoxy-∝-d-glucose Using Phosphomannomutase

Production of deoxy-thymidine-diphosphate (TDP)-sugars as substrates of glycosyltransferases, has been one of main hurdles for combinatorial antibiotic biosynthesis, which combines sugar moiety with aglycon of various antibiotics. Here, we report the one-pot enzymatic synthesis of TDP-2-deoxy-glucose employing high efficient TMP kinase (TMK; E.C. 2.7.2.12), acetate kinase (ACK; E.C. 2.7.1.21), and TDP-glucose synthase (TGS; E.C. 2.7.7.24) with phosphomannomutase (PMM; E.C. 5.4.2.8). In this study, replacing phosphoglucomutase (PGM; E.C. 5.4.2) by PMM from Escherichia coli gave four times higher specific activity on 2-deoxy-6-phosphate glucose, suggesting that the activity on 2-deoxy-glucose-6-phosphate was mainly affected by PMM activity, not PGM activity. Using an in vitro system starting from TMP and 2-deoxy-glucose-6-phosphate glucose, TDP-2-deoxy-glucose (63% yield) was successfully synthesized. Considering low productivity of NDP-sugars from cheap starting materials, this paper showed how production of NDP-sugars could be enhanced by controlling mutase activity

Silicon germanium photo-blocking layers for a-IGZO based industrial display

Amorphous indium- gallium-zinc oxide (a-IGZO) has been intensively studied for the application to active matrix flat-panel display because of its superior electrical and optical properties. However, the characteristics of a-IGZO were found to be very sensitive to external circumstance such as light illumination, which dramatically degrades the device performance and stability practically required for display applications. Here, we suggest the use for silicon-germanium (Si-Ge) films grown plasmaenhanced chemical vapour deposition (PECVD) as photo-blocking layers in the a-IGZO thin film transistors (TFTs). The charge mobility and threshold voltage (V-th) of the TFTs depend on the thickness of the Si-Ge films and dielectric buffer layers (SiNX), which were carefully optimized to be similar to 200 nm and similar to 300 nm, respectively. As a result, even after 1,000 s illumination time, the V-th and electron mobility of the TFTs remain unchanged, which was enabled by the photo-blocking effect of the Si-Ge layers for a-IGZO films. Considering the simple fabrication process by PECVD with outstanding scalability, we expect that this method can be widely applied to TFT devices that are sensitive to light illumination.

TLR3 signaling is either protective or pathogenic for the development of Theiler's virus-induced demyelinating disease depending on the time of viral infection

Background: We have previously shown that toll-like receptor 3 (TLR3)-mediated signaling plays an important role in the induction of innate cytokine responses to Theiler\u27s murine encephalomyelitis virus (TMEV) infection. In addition, cytokine levels produced after TMEV infection are significantly higher in the glial cells of susceptible SJL mice compared to those of resistant C57BL/6 mice. However, it is not known whether TLR3-mediated signaling plays a protective or pathogenic role in the development of demyelinating disease. Methods: SJL/J and B6; 129S-Tlr3(tm1Flv)/J (TLR3KO-B6) mice, and TLR3KO-SJL mice that TLR3KO-B6 mice were backcrossed to SJL/J mice for 6 generations were infected with Theiler\u27s murine encephalomyelitis virus (2 x 10(5) PFU) with or without treatment with 50 mu g of poly IC. Cytokine production and immune responses in the CNS and periphery of infected mice were analyzed. Results: We investigated the role of TLR3-mediated signaling in the protection and pathogenesis of TMEV-induced demyelinating disease. TLR3KO-B6 mice did not develop demyelinating disease although they displayed elevated viral loads in the CNS. However, TLR3KO-SJL mice displayed increased viral loads and cellular infiltration in the CNS, accompanied by exacerbated development of demyelinating disease, compared to the normal littermate mice. Late, but not early, anti-viral CD4(+) and CD8(+) T cell responses in the CNS were compromised in TLR3KO-SJL mice. However, activation of TLR3 with poly IC prior to viral infection also exacerbated disease development, whereas such activation after viral infection restrained disease development. Activation of TLR3 signaling prior to viral infection hindered the induction of protective IFN-gamma-producing CD4(+) and CD8(+) T cell populations. In contrast, activation of these signals after viral infection improved the induction of IFN-gamma-producing CD4(+) and CD8(+) T cells. In addition, poly IC-pretreated mice displayed elevated PDL-1 and regulatory FoxP3(+) CD4+ T cells in the CNS, while poly IC-post-treated mice expressed reduced levels of PDL-1 and FoxP3(+) CD4(+) T cells. Conclusions: These results suggest that TLR3-mediated signaling during viral infection protects against demyelinating disease by reducing the viral load and modulating immune responses. In contrast, premature activation of TLR3 signal transduction prior to viral infection leads to pathogenesis via over-activation of the pathogenic immune response

N-(2,5-Dimeth­oxy­phen­yl)-N′-(4-hy­droxy­pheneth­yl)urea

In the title compound, C17H20N2O4, the 2,5-dimeth­oxy­phenyl unit is almost planar, with an r.m.s. deviation of 0.015 Å. The dihedral angle between the 2,5-dimeth­oxy­phenyl ring and the urea plane is 20.95 (8)°. The H atoms of the urea NH groups are positioned syn to each other. The mol­ecular structure is stabilized by a short intra­molecular N—H⋯O hydrogen bond. In the crystal, inter­molecular N—H⋯O and O—H⋯O hydrogen bonds link the mol­ecules into a three-dimensional network

1-[3-(Hy­droxy­meth­yl)phen­yl]-3-phenyl­urea

In the title compound, C14H14N2O2, the dihedral angle between the benzene rings is 23.6 (1)°. The H atoms of the urea NH groups are positioned syn to each other. In the crystal, inter­molecular N—H⋯O and O—H⋯O hydrogen bonds link the mol­ecules into a three-dimensional network