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The oxygen evolution reaction (OER) at anode requires high overpotential and is still challenging. The metallic core-oxyhydroxide layer structure is an efficient method to lower an overpotential. We synthesized Fe rich FeCo core-Co rich FeCo oxyhydroxide layer with a different particle size of 173 nm, 225 nm, and 387 nm (FeCo 173, 225, 387) through a difference in the reduction rate of Fe/Co precursors using facile modified polyol synthesis. To investigate the effect of conductivity, CoFe2O4 nanoparticles of 80–130 nm were synthesized. Among samples, FeCo 173 showed remarkable catalytic performance of 316 mV at a current density of 10 mA/cm2 in 0.1 M KOH compared to RuO2 (408 mV), FeCo 225 (323 mV), FeCo 387 (334 mV), CoFe2O4 (382 mV). Moreover, FeCo 173 showed good stability for 60,000 s while RuO2 showed a gradual increase in overpotential to maintain 10 mA/cm2 after 15,000 s in chronopotentiometry. The excellent performance was attributed to Fe-rich metallic core, a small amount of Fe doping into CoOOH, and the synergic effect between the active site of Co rich FeCoOOH and conductive Fe rich metallic core. Following this result, it shows that the use of such FeCo electrodes has advantages in the production of hydrogen via electrochemical water oxidation.

Although stroke elicits progressive cognitive decline and is a leading cause of dementia, molecular interplay between stroke and Alzheimer's disease (AD) pathology has not been fully elucidated. Furthermore, studies on the effects of post-stroke rehabilitation on AD pathology are limited. We evaluated the acute effect of stroke on tau modification, and the molecular effects of task-specific training (TST) on tau modification using a model of photochemically-induced thrombosis (PIT)-induced cortical infarction. Following PIT in the dominant side of sensorimotor cortex, the rehabilitation group received 4-weeks of TST rehabilitation once daily by single pellet reaching training, whereas the sedentary control group did not received any type of training. Cortical expression levels of proteins related to tau modification were evaluated on post-stroke day 1 (PSD1) and 28; functional tests were also evaluated performed every week. The expression levels of acetyl-tau, phosphorylated-tau (p-tau), cyclooxygenase-2 and Akt-mTORC1-p70S6K pathway in infarcted cortices on PSD1 were significantly greater, whereas the expression levels of p-AMPK were significantly lower than in the paired contralateral sides. TST rehabilitation for 4 weeks greatly improved functional motor performance but not memory, which concurred with the down-regulations of ipsilateral p-AMPK, cyclooxygenase-2, Akt-mTORC1-p70S6K pathway, and p-tau in rehabilitation group. PIT-induced cortical infarction was found to induce cortical tau modification through the Akt-mTORC1-p70S6K activation, and to suppress the expression of AMPK-related proteins. TST rehabilitation greatly improved motor function, but not memory, and suppressed p-tau expression and neuroinflammation. Nevertheless, the role of TST-mediated regulation of tau hyperphosphorylation required further clarification.

Objective : To investigate cortical regions related to voluntary blinking. Methods : Transcranial magnetic stimulation (TMS) was applied to the facial motor cortex (M1) and the midline frontal region (Fz) in 10 healthy subjects with eyes opened and closed. Motor-evoked potentials were recorded from the orbicularis oculi (OOC), orbicularis oris (OOR), abductor digiti minimi and tibialis anterior using surface and needle electromyography electrodes. Facial M waves and blink reflex were measured using supramaximal electrical stimulation of the facial and supraorbital nerves. Results : TMS at Fz elicited 3 waves in OOC with no response in other tested muscles except for the early wave in OOR. Facial M1 stimulation produced only early and late waves. Because of their latencies, shapes, and relationship to coil position and stimulation intensity, early and late waves appeared to be analogous to the facial M wave and R1 component of the blink reflex. The intermediate wave at 6–8 ms latency was elicited in OOC by Fz stimulation with eyes closed. Conclusions : Since its latency matches the central conduction time of other cranial muscles and it has characteristic of muscle activation-related facilitation, the intermediate wave is presumably related to cortical stimulation. This result provides evidence that the cortical center for the upper facial movements, including blinking, is not principally located in the facial M1, but rather in the mesial frontal region.

alpha-Synuclein, an acidic neuronal protein of 140 amino acids, is extremely heat-resistant and is natively unfolded. Recent studies have demonstrated that alpha-synuclein has chaperone activity both in vitro and in vivo, and that this activity is lost upon removing its C-terminal acidic tail. However, the detailed mechanism of the chaperone action of alpha-synuclein remains unknown. In this study, we investigated the molecular mechanism of the chaperone action of alpha-synuclein by analyzing the roles of its N-terminal and C-terminal domains. The N-terminal domain (residues 1-95) was found to bind to substrate proteins to form high molecular weight complexes, whereas the C-terminal acidic tail (residues 96-140) appears to be primarily involved in solubilizing the high molecular weight complexes. Because the substrate-binding domain and the solubilizing domain for chaperone function are well separated in alpha-synuclein, the N-terminal-binding domain can be substituted by other proteins or peptides. Interestingly, the resultant engineered chaperone proteins appeared to display differential efficiency and specificity in terms of the chaperone function, which depended upon the nature of the binding domain. This finding implies that the C-terminal acidic tail of alpha-synuclein can be fused with other proteins or peptides to engineer synthetic chaperones for specific purposes.

≥177mg/dl. In addition, we identified 473 individuals (64.3%men) with the metabolic syndrome (MetS) according to the updated ATP III criteria. The mean±SD of hs-CRP was 1.3±2.9 mg/l for the 5,879 individuals who had neither the HTGW phenotype nor the MetS, 2.0±2.5 mg/l for those who had the HTGW phenotype and no MetS, 2.7±2.6 for 473 individuals with the MetS and no HTGW phenotype, while those who had both atherogenic disorders had a hsCRP concentration of 2.8±2.3 mg/l. Conclusion: In this cohort of apparently healthy non-diabetic employed individuals, the HTGW phenotype had a similar prevalence as the MetS and was associated with the presence of low grade inflammation. The inflammatory machinery could be a pathophysiologic link between this dysmetabolism and atherothrombosis. In addition, it looks as if the HTGW phenotype is relatively prevalent and could be a simple and inexpensive way to single out individuals at risk for future CAD.