Reelin signaling is essential for correct development of the mammalian brain. Reelin binds to apolipoprotein E receptor 2 and very low-density lipoprotein receptor and induces phosphorylation of Dab1. However, when and where these reactions occur is essentially unknown, and the primary function(s) of Reelin remain unclear.Here

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Efforts have been made to reduce the density of defects in corundum-structured α-Ga2O3 thin films on sapphire substrates by applying quasi-graded α-(Al x Ga1− x )2O3 buffer layers. Transmission electron microscopy images revealed that most strains were located in the α-(Al x Ga1− x )2O3 buffer layers, and that the total density of dislocations in the α-Ga2O3 thin films was successfully decreased by more than one order of magnitude compared with that without buffer layers, that is, the screw and edge dislocation densities were about 3 × 108 and 6 × 108 cm−2, respectively.

Unloading-mediated muscle atrophy is associated with increased reactive oxygen species (ROS) production. We previously demonstrated that elevated ubiquitin ligase casitas B-lineage lymphoma-b (Cbl-b) resulted in the loss of muscle volume (Nakao R, Hirasaka K, Goto J, Ishidoh K, Yamada C, Ohno A, Okumura Y, Nonaka I, Yasutomo K, Baldwin KM, Kominami E, Higashibata A, Nagano K, Tanaka K, Yasui N, Mills EM, Takeda S, Nikawa T. Mol Cell Biol 29: 4798–4811, 2009). However, the pathological role of ROS production associated with unloading-mediated muscle atrophy still remains unknown. Here, we showed that the ROS-mediated signal transduction caused by microgravity or its simulation contributes to Cbl-b expression. In L6 myotubes, the assessment of redox status revealed that oxidized glutathione was increased under microgravity conditions, and simulated microgravity caused a burst of ROS, implicating ROS as a critical upstream mediator linking to downstream atrophic signaling. ROS generation activated the ERK1/2 early-growth response protein (Egr)1/2-Cbl-b signaling pathway, an established contributing pathway to muscle volume loss. Interestingly, antioxidant treatments such as N-acetylcysteine and TEMPOL, but not catalase, blocked the clinorotation-mediated activation of ERK1/2. The increased ROS induced transcriptional activity of Egr1 and/or Egr2 to stimulate Cbl-b expression through the ERK1/2 pathway in L6 myoblasts, since treatment with Egr1/2 siRNA and an ERK1/2 inhibitor significantly suppressed clinorotation-induced Cbl-b and Egr expression, respectively. Promoter and gel mobility shift assays revealed that Cbl-b was upregulated via an Egr consensus oxidative responsive element at −110 to −60 bp of the Cbl-b promoter. Together, this indicates that under microgravity conditions, elevated ROS may be a crucial mechanotransducer in skeletal muscle cells, regulating muscle mass through Cbl-b expression activated by the ERK-Egr signaling pathway.

Issues on tin (Sn) doping in the mist chemical vapor deposition of α-Ga2O3 was attributed to conversion of ionization states of Sn from Sn4+ to Sn2+ and/or out-diffusion of Sn after thermal annealing, resulting in highly resistive films. Silicon (Si) doping, instead, was succeeded by the use of a novel doping source of chloro-(3-cyanopropyl)-dimethylsilane [ClSi(CH3)2((CH2)2CN)]. Si was uniformly incorporated in the α-Ga2O3 films and the electrical properties were stable even after the thermal annealing. The activation ratio as donors was nearly 100%. The carrier (electron) concentration was controlled to the level of 1018 cm-3 by the [Si]/[Ga] ratio in the source solution. The maximum mobility was 31.5 cm2/V⋅s, in contrast to 24 cm2/V⋅s with Sn doping, suggesting advantage of Si doping . However, the reduction in dislocation defects in the α-Ga2O3 films formed owing to heteroepitaxy on sapphire was suggested to be the important subject to be considered in the next stage.