Microencapsulation of imidazole curing agent by solvent evaporation method using W/O/W emulsion

The epoxy–imidazole resin system is used to form the anisotropic conducting film. The latent character of the system is very significant. In this study, imidazole (Im) or 2‐methylimidazole (2MI) was encapsulated for the latent curing system to use in the reaction of epoxy resin. Polycaprolactone was used as a wall material, and the solvent evaporation method was used to form the microcapsule using W/O/W emulsion. The shelf life of the microcapsules was studied for the epoxy resin, and the curing behavior of the microcapsules for epoxy resin was examined using a differential scanning calorimeter. The curing times at 150 and 180°C were estimated using an indentation method. The microcapsules of Im or 2MI exhibited a long shelf life for epoxy resin. When comparing the results of the previous methods with the results of this study using the W/O/W emulsion, finer microcapsules were formed and the microcapsule has longer shelf life. © 2012 Wiley Periodicals, Inc. J. Appl. Polym. Sci., 2013Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/98341/1/38767_ftp.pd

Role of G{alpha}12 and G{alpha}13 as Novel Switches for the Activity of Nrf2, a Key Antioxidative Transcription Factor

G{alpha}12 and G{alpha}13 function as molecular regulators responding to extracellular stimuli. NF-E2-related factor 2 (Nrf2) is involved in a protective adaptive response to oxidative stress. This study investigated the regulation of Nrf2 by G{alpha}12 and G{alpha}13. A deficiency of G{alpha}12, but not of G{alpha}13, enhanced Nrf2 activity and target gene transactivation in embryo fibroblasts. In mice, G{alpha}12 knockout activated Nrf2 and thereby facilitated heme catabolism to bilirubin and its glucuronosyl conjugations. An oligonucleotide microarray demonstrated the transactivation of Nrf2 target genes by G{alpha}12 gene knockout. G{alpha}12 deficiency reduced Jun N-terminal protein kinase (JNK)-dependent Nrf2 ubiquitination required for proteasomal degradation, and so did G{alpha}13 deficiency. The absence of G{alpha}12, but not of G{alpha}13, increased protein kinase C {delta} (PKC {delta}) activation and the PKC {delta}-mediated serine phosphorylation of Nrf2. G{alpha}13 gene knockout or knockdown abrogated the Nrf2 phosphorylation induced by G{alpha}12 deficiency, suggesting that relief from G{alpha}12 repression leads to the G{alpha}13-mediated activation of Nrf2. Constitutive activation of G{alpha}13 promoted Nrf2 activity and target gene induction via Rho-mediated PKC {delta} activation, corroborating positive regulation by G{alpha}13. In summary, G{alpha}12 and G{alpha}13 transmit a JNK-dependent signal for Nrf2 ubiquitination, whereas G{alpha}13 regulates Rho-PKC {delta}-mediated Nrf2 phosphorylation, which is negatively balanced by G{alpha}12

In-silico based redesign of CO-dehydrogenase catalyzing the oxidation of toxic waste CO gas for improved O2 resistance and mediator affinity

Carbon monoxide (CO) harmful to most creatures, is largely discharged by industrial processes in steel mill and thermal power plant. Conversion of toxic waste CO gas to safe gas or more valuable chemicals will be a great worth at this point. Interestingly, carbons and high potential electrons from CO-oxidation can be resourced as essential core parts for the chemical products by using CO-dehydrogenase (CODH) and artificial mediator. For industrial application of the enzymatic CO-oxidation, however, key issues remain that most CODHs show oxygen (O2) sensitivity and low-affinity for artificial mediator. Because steel mill waste gas such as blast furnace gas (BFG) commonly contains a little O2 and higher affinity is required to achieve higher reaction rate. In this research, in-silico based approach was used to redesign Carboxydothermus hydrogenoformans CODH (ChCODH) II, capable of increasing O2 resistance and affinity to ethyl viologen (EV) mediator. ChCODHs belong to a group of Ni-Fe containing CODH. Among five known ChCODHs (ChCODH I-V), ChCODH II shows the highest activity toward CO but more O2 sensitive than ChCODH IV. The artificial mediator of EV functions as an electron acceptor for ChCODH II but the affinity of ChCODH II to EV mediator is known poor. As our result, more than 10 folds increase of O2 resistance was achieved for the redesigned ChCODH II enzyme, which will be definitely a working horse in the conversion of waste CO gas into value-added chemicals

Positional Effects of Fluorination in Conjugated Side Chains on Photovoltaic Properties of Donor-Acceptor Copolymers

The position at which conjugated side chains were fluorinated, the meta- or ortho-position in phenyl side chains, was varied to investigate the positional effects of fluorination on the energy levels, crystalline ordering, and photovoltaic properties of the polymers. The fluorine in the ortho-position achieved a lower HOMO energy level than that in the meta-position, but reduced the chain rigidity.1116Ysciescopu

ALTERATIONS IN JOINT KINEMATICS AND KINETICS DURING DOWNHILL RUNNING

The purpose of this investigation was to find how joint kinematics and kinetics during downhill running change compared to level running. Fifteen recreational runners ran on a force plate imbedded treadmill with three different slopes (0 º, -6º, and -9º) at a controlled speed of 3.2 m/s. Ten steps on each slope were selected for analysis. Increased knee flexion with decreased ankle plantar-flexion and hip flexion was found during downhill running compared to level running. Decreased peak propulsive ground reaction force and posterior impulse were found during downhill running compared to level running. Additionally, increased extension moment with increased negative joint power at the knee and decreased plantar-flexion moment with decreased negative joint power at the ankle were found during downhill running compared to level running

Current advances in combining stem cell and gene therapy for neurodegenerative diseases

Neuronal death is the common final pathologic pathway of various neurodegenerative diseases (NDs). Although central nervous system has little regenerative potential, it is expected that damaged neural tissue can be recovered by exogenous supplementation of stem cells; however, stem cell therapy cannot modulate specific causes of NDs, such as accumulation of extracellular amyloid peptides in Alzheimer’s disease. In contrast, gene therapy can deliver therapeutic genes to specific ND targets. Therefore, combining stem cell and gene therapy would have dual treatment mechanisms (regenerating damaged neural tissue and modifying specific causes of NDs) and lead to better clinical outcomes. In this review, we discuss various therapeutic genes that can be used to develop stem cell gene therapy for various NDs and the techniques for how therapeutic genes can be integrated into stem cells