The neural cell recognition molecule NB-3, also referred to as contactin-6, is expressed prominently in the developing nervous system after birth and its deficiency has been shown to cause impairment in motor coordination. Here, we investigated the contribution of NB-3 to cerebellar development, focusing on lobule 3 where NB-3 was expressed in granule cells but not in Purkinje cells. In the developing molecular layer, the neural cell recognition molecules TAG-1, L1, and NB-3 formed distinct expression zones from the external granule cell layer to the internal granule cell layer (IGL), respectively. The NB-3-immunoreactive zone did not overlap with TAG-1-immunoreactive zone. By contrast, the L1-immunoreactive zone overlapped with both the TAG-1- and NB-3-immunoreactive zones. NB-3-positive puncta overlapped with vesicular glutamate transporter 1, a presynaptic marker and were apposed close to metabotropic glutamate receptor 1A, a postsynaptic marker, indicating that NB-3 is localized presynaptically at glutamatergic synapses between parallel fibers and Purkinje cells. In NB-3 knockout mice, L1 immunoreactive signals were increased in the IGL at postnatal day (P) 5, suggesting the increase in the number of immature granule cells of the IGL. In addition, the density of parallel fiber synaptic terminals was reduced in NB-3 knockout mice relative to wild-type mice at P5 to P10. In parallel with these findings, caspase-dependent cell death was significantly increased in the NB- 3-deficient cerebellum at P15. Collectively, our results indicate that NB-3 deficiency affects synapse formation during postnatal cerebellar development.

Diffusion of self-atoms and co-implanted carbon (C) and boron (B) in silicon (Si) has been simultaneously observed using natSi/28Si isotope heterostructures. The supersaturation of Si self-interstitials (I’s) is investigated through the 30Si diffusion. The experimental results showed that Si self-diffusion was enhanced, that is, the I is more severely supersaturated, while B diffusion near the kink region was reduced with higher C dose. We also found slower dissolution of immobile BI clusters. C diffusion was not significant, indicating the formation of immobile CI clusters. These results indicate that the reduction of B diffusion is not due to the trapping of I by C, if any, but due to the retardation of BI cluster dissolution by the presence of C to decrease the amount of mobile B. The Si self-diffusion is enhanced by the dissolution of CI clusters to emit I.

The effect of surface modification on the tensile strength of the bonded interface of Al alloy and SUS304 stainless steel was investigated by SEM observations of interfacial microstructures and fractured surfaces. Aluminum surfaces were modified by boiling in 5% aqueous solution of NaOH for 20 s and 99.7% Acetic acid for 60 s. Bonding was performed at bonding temperature of 753 ~ 813 K under a pressure of 6 MPa (bonding time of 1.8 ks). As a result of surface modification, bonded joints were obtained at a bonding temperature 20 K lower than that required for non-modified surfaces, and the bonded strength was comparable to that of the maximum load.