Printable polymer actuators from ionic liquid, soluble polyimide, and ubiquitous carbon materials.

We present here printable high-performance polymer actuators comprising ionic liquid (IL), soluble polyimide, and ubiquitous carbon materials. Polymer electrolytes with high ionic conductivity and reliable mechanical strength are required for high-performance polymer actuators. The developed polymer electrolytes comprised a soluble sulfonated polyimide (SPI) and IL, 1-ethyl-3-methylimidazolium bis(trifluoromethanesulfonyl)amide ([C2mim][NTf2]), and they exhibited acceptable ionic conductivity up to 1 × 10(-3) S cm(-1) and favorable mechanical properties (elastic modulus >1 × 10(7) Pa). Polymer actuators based on SPI/[C2mim][NTf2] electrolytes were prepared using inexpensive activated carbon (AC) together with highly electron-conducting carbon such as acetylene black (AB), vapor grown carbon fiber (VGCF), and Ketjen black (KB). The resulting polymer actuators have a trilaminar electric double-layer capacitor structure, consisting of a polymer electrolyte layer sandwiched between carbon electrode layers. Displacement, response speed, and durability of the actuators depended on the combination of carbons. Especially the actuators with mixed AC/KB carbon electrodes exhibited relatively large displacement and high-speed response, and they kept 80% of the initial displacement even after more than 5000 cycles. The generated force of the actuators correlated with the elastic modulus of SPI/[C2mim][NTf2] electrolytes. The displacement of the actuators was proportional to the accumulated electric charge in the electrodes, regardless of carbon materials, and agreed well with the previously proposed displacement model.

Driving mechanisms of ionic polymer actuators having electric double layer capacitor structures.

Two solid polymer electrolytes, composed of a polyether-segmented polyurethaneurea (PEUU) and either a lithium salt (lithium bis(trifluoromethanesulfonyl)amide: Li[NTf2]) or a nonvolatile ionic liquid (1-ethyl-3-methylimidazolium bis(trifluoromethanesulfonyl)amide: [C2mim][NTf2]), were prepared in order to utilize them as ionic polymer actuators. These salts were preferentially dissolved in the polyether phases. The ionic transport mechanism of the polyethers was discussed in terms of the diffusion coefficients and ionic transference numbers of the incorporated ions, which were estimated by means of pulsed-field gradient spin-echo (PGSE) NMR. There was a distinct difference in the ionic transport properties of each polymer electrolyte owing to the difference in the magnitude of interactions between the cations and the polyether. The anionic diffusion coefficient was much faster than that of the cation in the polyether/Li[NTf2] electrolyte, whereas the cation diffused faster than the anion in the polyether/[C2mim][NTf2] electrolyte. Ionic polymer actuators, which have a solid-state electric-double-layer-capacitor (EDLC) structure, were prepared using these polymer electrolyte membranes and ubiquitous carbon materials such as activated carbon and acetylene black. On the basis of the difference in the motional direction of each actuator against applied voltages, a simple model of the actuation mechanisms was proposed by taking the difference in ionic transport properties into consideration. This model discriminated the behavior of the actuators in terms of the products of transference numbers and ionic volumes. The experimentally observed behavior of the actuators was successfully explained by this model.

Colloidal interaction in ionic liquids: effects of ionic structures and surface chemistry on rheology of silica colloidal dispersions.

To understand the important factors that dominate colloidal stability in ionic liquids (ILs), rheology of the dispersions of hydrophilic and hydrophobic silica nanoparticles were investigated in ILs with different ionic structures. The dispersion of hydrophilic silica nanoparticles in [BF(4)] anion-based ILs and in an IL containing a hydroxyl group, 1-(2-hydroxyethyl)-3-methylimidazolium bis(trifluoromethane sulfonyl)amide ([C(2)OHmim][NTf(2)]), showed an intriguing shear thickening response. Nonflocculation of the hydrophilic silica nanoparticles in the [BF(4)] anion-based ILs and in [C(2)OHmim][NTf(2)], where the interparticle electrostatic repulsion appears to be depressed, suggests that an IL-based steric hindrance or solvation force provides an effective repulsive barrier for the colloidal aggregation. On the other hand, the other dispersions presented shear thinning behavior with an increase in shear rates and gelled at relatively low particle concentrations. The elastic modulus (G') of the gels formed by the hydrophilic silica was correlated with the polarity scale, lambda(Cu), of the ILs, indicating that the silica-IL interactions, especially the silica-anion interactions, appear to affect the rheological behavior, even in flocculated systems. All the ILs used in this study can be solidified by the addition of hydrophobic silica particles. The rheological behavior of the silica colloidal dispersions was strongly affected by the ionic structure of the ILs and the surface structure of the silica particles.

Arsenite-induced thymus atrophy is mediated by cell cycle arrest: a characteristic downregulation of E2F-related genes revealed by a microarray approach.

Thymus atrophy is induced by a variety of chemicals, including environmental contaminants and is used as a sensitive index to detect their adverse effects on lymphocytes. In the present study we adopted a toxicogenomics approach to identify the pathways that mediate the atrophy induced by arsenite. We also analyzed gene expression changes observed in the course of thymus atrophy by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), dexamethasone (DEX), and estradiol (E2), to determine whether arsenite induces atrophy by activating an arsenite-specific pathway or the same pathways as other chemicals. These compounds were intraperitoneally administered to C57BL/6 mice at doses that reduce thymus weight by approximately 30% within 3 days, and gene expression changes in the thymus 24 h after the administration were analyzed by using microarrays and real-time PCR. The microarray analysis showed that arsenite specifically downregulates a variety of E2F target genes that are involved in cell cycle progression. The same genes were also downregulated when mouse B-cell lymphoma A20 cells were exposed to arsenite. Arsenite exposure of the A20 cells was confirmed to induce cell cycle arrest, mainly in the G(1) phase, and reduce cell number. Cell cycle arrest in the G(1) phase was also confirmed to occur in the thymocytes of the arsenite-exposed mice. These results indicate that arsenite induces thymus atrophy through E2F-dependent cell cycle arrest. The results of this study also show that analysis of gene expression in thymuses is a useful method of obtaining clues to the pathways that mediate the effects of atrophy-inducing chemicals.

Exercise-induced liver beta2-microglobulin expression is related to lower IgG clearance in the blood.

Voluntary wheel running exercise induced higher antigen-specific IgG in circulating blood is well recognized in mice. This antibody response may be regulated by an exercise-induced mechanism that protects against IgG catabolism. The recent hypothesis that the beta2-microglobulin gene is implicated in IgG protection is investigated further on mice voluntary wheel running. Male C57BL/6N mice were intraperitoneally immunized with 0.375microg/kg (body weight) of tetanus toxoid to induce primary and secondary antibody responses. At the peak concentration of blood tetanus toxoid specific IgG in this experiment, we administered (125)I-labeled mouse IgG. To determine how (125)I-IgG half-life is prolonged in voluntary wheel running exercised mice, we observed the tissue radioactivity (125)I-IgG. Significantly higher blood IgG concentrations were demonstrated in the exercised group compared to non-exercised group (P<.05). The mean value of radioactivity in the liver was higher in the exercised group (P<.05). Furthermore, extracted IgG concentration of exercised mouse liver was higher than that of non-exercised group (P<.05). Immunohistochemical analysis showed dramatically increased tissue IgG in the liver of the exercised group (P<.05). The gene expression of beta2-microglobulin was up-regulated in the exercised mouse liver (P<.05). There is a significant correlation between liver accumulation of (125)I-IgG and (125)I-IgG concentration in the blood (P<.05). In addition, there is a significant correlation between extracted total hepatic IgG and beta2-microglobulin in the liver (P<.05). These findings indicate that voluntary wheel running exercise-induced liver beta2-microglobulin expression is related to lower IgG clearance in the blood.