Atmospheric‐pressure nonthermal plasma was used to synthesize ammonia from nitrogen and hydrogen over ruthenium catalysts. Formation of NH3 in a N2‐H2 mixture altered the plasma characteristics due to the low ionization potential of NH3 (10.15 eV). The optimum gas ratio was found at N2:H2 = 4:1 by volume (i.e., N2‐rich conditions). When plasma was operated at a temperature below 250 °C, the NH3 concentration increased linearly with increasing specific input energy (SIE). For the Ru(2)‐Mg(5)/γ‐Al2O3 catalyst at 250 °C, pulse energization was four times more efficient than the AC energization case. The presence of RuO2 was found to be beneficial for the NH3 synthesis via plasma‐catalysis. The addition of a small amount of O2 was found to be effective for the in situ regeneration of the deactivated catalyst. The effect of metal promoters was in the order of Mg > K > Cs > no promoter.

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Protein L-isoaspartyl methyltransferase (PIMT) is suggested to play a role in the repair of aged protein spontaneously incorporated with isoaspartyl residues. We generated PIMT-deficient mice by targeted disruption of the PIMT gene to elucidate the biological role of the gene in vivo. PIMT-deficient mice died from progressive epileptic seizures with grand mal and myoclonus between 4 and 12 weeks of age. An anticonvulsive drug, dipropylacetic acid (DPA), improved their survival but failed to cure the fatal outcome. L-Isoaspartatate, the putative substrate for PIMT, was increased ninefold in the brains of PIMT-deficient mice. The brains of PIMT-deficient mice started to enlarge after 4 weeks of age when the apical dendrites of pyramidal neurons in cerebral cortices showed aberrant arborizations with disorganized microtubules. We conclude that methylation of modified proteins with isoaspartyl residues is essential for the maintenance of a mature CNS and that a deficiency in PIMT results in fatal progressive epilepsy in mice.

Direct conversion of dilute CO2 contained in power plant or industrial exhaust gas and the atmosphere into high-concentration hydrocarbons without a need of separate CO2 capture and purification processes is one of the awaited technologies in envisioned low-carbon societies. In this study, we investigated the performance of integrated CO2 capture and reduction to CH4 over Nibased dual functional catalysts promoted with Na, K and Ca. Ni/Na-γ-Al2O3 exhibited the highest activity for integrated CO2 (5% CO2) capture and reduction, achieving high CO2 conversion (>96%) and CH4 selectivity (>93%). In addition, very low concentration CO2 (100 ppm CO2) was successfully converted to 11.5% CH4 at the peak point (>1000 times higher concentration than that of the supplied CO2) over Ni/Na-γ-Al2O3. The Ni-based dual functional catalyst exhibited a high CO2 conversion exceeding 90%, even when 20%O2 was present during CO2 capture. Furthermore, an increased operation pressure had positive impacts on both CO2 capture and CH4 formation, and these advantageous effects were also observed when CO2 concentration was at the level of atmospheric CO2 (100-400 ppm). As pressure increased from 0.1 to 0.9 MPa, CH4 production capacity with 400 ppm CO2 was enhanced from 111 to 160 µmol gcat -1 . The approach in combination with the efficient catalyst shows encouraging promises for CO2 utilization, enabling direct air capture-conversion to value-added chemicals.CH4 productivity increased from 188 to 266 μmol gcat −1 . In addition, the effect of pressure on catalyst performance was also investigated at very low CO2 levels of 100 and 400 ppm, and high pressure was found to positively affect both CO2 capture and CH4 formation. These results suggest that high pressure enhances the CO2 absorption and CH4 formation capacities of dual-functional catalysts and allows for efficient integrated CO2 capture and reduction into CH4 even at atmospheric levels of CO2. The approach, in combination with the efficient catalyst, is promising for CO2 utilization, thus enabling direct air capture-conversion to value-added chemicals.

Transforming growth factor-beta (TGF-beta) is a multifunctional polypeptide which plays a crucial role in the regulation of cell proliferation, differentiation, and organogenesis. In the present study, we investigated the expression of signaling receptors for TGF-beta in developing mice by in situ hybridization, revealing a significant difference in the expression of TGF-beta type I and type II receptors. Unexpectedly, the TGF-beta type I receptors were exclusively expressed without any detectable expression of the TGF-beta type II receptors in developing cerebral cortices. In primary cortical neurons, a neutralizing antibody for TGF-beta significantly reduced the expression of bcl-2 and subsequently induced neuronal cell death, indicating that TGF-beta functions as a survival factor for cortical neurons in vitro. Consistent with the result of in situ hybridization, the TGF-beta, type I but not type II receptors were detected in primary cortical neurons by affinity crosslink and RT-PCR analyses. The concomitant expression of TGF-beta2 and the TGF-beta type I receptors in developing cerebral cortices suggests that the TGF-beta signaling system plays a pivotal role in neuronal differentiation and that unidentified components may be involved in TGF-beta signaling in the development of the central nervous system.