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Optical limiting is a phenomenon widely recognized as the potential application for a protector of human eyes and optical sensors from irradiation with lasers. However, a high optical limiting threshold and low flexibility have restricted such applications. Here, we report that oligothiophene-doped liquid crystals (LCs) function as a low-threshold optical limiter with deformability. Irradiation of dye-doped LCs with a continuous wave (CW) laser beam brings about the formation of diffraction rings, and the number of rings changes depending on the incident light intensity due to their photoinduced molecular reorientation. Utilizing such reorientation enables reversible optical limiting without additional multilayered optical components. In particular, an electric field application to a LC-based optical limiter decreases their optical limiting threshold from 2100 to 25 mW/cm2, and the threshold can be tuned by adjusting the applied voltage. Furthermore, the softness of LCs allows for the fabrication of the deformable optical limiter; optical limiting due to the molecular reorientation occurs even in largely bent states. The low-threshold and deformable optical limiter based on oligothiophene-doped LCs thus will enable one to develop the protector of eyes and optical sensors from glaring light-induced damage.

Irradiation of dye-doped liquid crystals (LCs) with linearly polarized light leads to molecular reorientation, which manifests functional properties for various nonlinear optical (NLO) applications. Material designs with lower light intensity thresholds for molecular reorientation have been explored, and nematic LCs have been one of the most attractive choices because of the high NLO properties. Here we present a different approach to reduce light intensity for reorientation by modifying a substrate surface that controls initial molecular orientation in polymer-stabilized nematic LCs doped with oligothiophene. The surface of the glass substrate was treated with various concentrations of a silane coupler. Water contact angle measurement and analysis of samples using polarized optical microscopy revealed that surface anchoring in the initial state decreased as the silane coupler concentration decreased. The threshold intensity was successfully reduced by 30% simply by optimizing the silane coupler concentration. This finding clearly indicates that weak surface anchoring is key to the reduction of light intensity for molecular reorientation. The molecular orientation of polymer-stabilized nematic liquid crystals (PSLCs) doped with oligothiophene can be easily manipulated using irradiation with linearly polarized light above a threshold intensity. The photoresponsive behavior depended on the initial molecular orientation, as controlled by the surface treatment of PSLC cells. The threshold light intensity for molecular reorientation was successfully reduced by 30% by optimizing the silane coupler concentration because of the decrease in surface anchoring. Thus, weak surface anchoring leads to a reduced threshold light intensity for molecular reorientation.

The calcium hydroxyapatite Ca(10)(PO(4))(6)(OH)(2) (Hap) nanoparticles were prepared by using microreactor and employed these Hap nanoparticles to clarify the adsorption behavior of proteins. The size of Hap particles produced by the microreactor reduced in the order of a hardness of the reaction conditions for mixing Ca(OH)(2) and H(3)PO(4) aqueous solutions, such as flow rates of both solutions and temperature. Finally, the size of the smallest Hap nanoparticle became 2 × 15 nm(2), similar to that of BSA molecule (4 × 14 nm(2)). It is noteworthy that the smallest Hap nanoparticles still possesses rodlike shape, suggesting that particles are grown along c-axis even though the reactants mixed very rapidly in narrow channels of the microreactors. The X-ray diffraction patterns of the Hap nanoparticles revealed that the crystallinity of the materials produced by the microreactor is low. The FTIR measurement indicated that the Hap nanoparticles produced by microreactor were carbonate-substituted type B Hap, where the carbonate ions replace the phosphate ions in the crystal lattice. All the adsorption isotherms of acidic bovine serum albumin (BSA), neutral myoglobin (MGB), and basic lysozyme (LSZ) onto Hap nanoparticles from 1 × 10(-4) mol/dm(3) KCl solution were the Langmuirian type. The saturated amounts of adsorbed BSA (n(S)(BSA)) for the Hap nanoparticles produced by microreactor were decreased with decrease in the mean particle length, and finally it reduced to zero for the smallest Hap nanoparticles. Similar results were observed for the adsorption of LSZ; the saturated amounts of adsorbed LSZ (n(S)(LSZ)) also reduced to zero for the smallest Hap nanoparticles. However, in the case of MGB, the saturated mounts of adsorbed MGB (n(S)(MGB)) are also depressed with decreased in their particle size, but about half of MGB molecules still adsorbed onto the smallest Hap nanoparticles. This difference in the protein adsorption behavior was explained by the difference in the size and flexibility of three kinds of proteins. The reduction of n(S)(BSA) is due to the decrease in the fraction of C sites on the side face of each Hap nanoparticle; i.e., there is not enough area left on the nanoparticle surface to adsorb large BSA molecules even though the BSA molecules are soft and their conformations are alterable. The reduction of n(S)(LSZ) was explained by the reduction of P sites. Further, rigidity of the LSZ molecules was given another possibility of the depression of n(S)(LSZ) for the Hap nanoparticles. However, MGB molecules with small and soft structure were adsorbed on the Hap nanoparticle surface by changing their conformation. We could control the amounts of adsorbed proteins by changing the particle size of Hap in the nanometer range and kinds of proteins. These obtained results may be useful for developing biomimetic materials for bone grafts and successful surgical devices in the biochemical field.

We have developed a microreactor system for the continuous producting of nanoparticles, and we have clarified the relationship between the mixing performance of reactors and the particle size. First, we evaluated the mixing performance of reactors by carring out the Villermaux–Dushman reaction and determined the experimental conditions for producing AgCl nanoparticles. Next, we developed the microreactor system by including a pressure sensor and an ultrasonic generator in order to prevent the clogging of nanoparticles. Finally, we produced AgCl nanoparticles and evaluated the mixing performance and the particle size. The operating time of the new system was long. Moreover, we found that as the mixing performance improves the size of produced particles decreases and the particle size distribution becomes sharper. We produced AgCl nanoparticles with a size of 86 nm using the microreactor that had the best mixing performance among the three reactors we tested in this study; the coefficient of variation (Cv) of the size distribution of the produced nanoparticles was 26.1%.

Background Cardiac protection by volatile anesthetic-induced preconditioning and ischemic preconditioning have similar signaling pathways. Recently, it was reported that augmentation of protein modified with O-linked β-N-acetylglucosamine (O-GlcNAc) contributes to cardiac protection. This study investigated the role of O-GlcNAc in cardiac protection induced by anesthetic-induced preconditioning. Methods O-GlcNAc-modified proteins were visualized by immunoblotting. Tolerance against ischemia or reperfusion was tested in vivo (n = 8) and in vitro (n = 6). The opening of the mitochondrial permeability transition pore (mPTP) upon oxidative stress was examined in myocytes treated with calcein AM (n = 5). Coimmunoprecipitation and enzymatic labeling were performed to detect the mitochondrial protein responsible for the mPTP opening. Results Isoflurane treatment and the consequent augmentation of O-GlcNAc concentrations reduced the infarct size (26 ± 5% [mean ± SD], P < 0.001) compared with the control. The protective effect of O-GlcNAc was eliminated in the group pretreated with the O-GlcNAc transferase inhibitor alloxan (39 ± 5%, P < 0.001). Myocyte survival also showed the same result in vitro. Formation of the mPTP was abrogated in the isoflurane-treated cells (86 ± 4%, P < 0.001) compared with the control and alloxan-plus-isoflurane-treated cells (57 ± 7%, P < 0.001). Coimmunoprecipitation and enzymatic labeling studies revealed that the O-GlcNAc-modified, voltage-dependent anion channel restained the mPTP opening. Conclusions Isoflurane induced O-GlcNAc modification of mitochondrial voltage-dependent anion channel. This modification inhibited the opening of the mPTP and conferred resistance to ischemia-reperfusion stress.