Thick GaN layers were grown by hydride vapor phase epitaxy (HVPE) with the aim of using these layers as a homoepitaxial substrate to improve device quality of laser diodes or light emitting diodes. HVPE is very useful for thick layer growth since the growth rate can reach from several ten up to one hundred micron per hour. In this experiment, the growth began as selective growth through openings formed in a SiO2 mask. Facets consisting of {1101} planes were formed in the early stage and a continuous film developed from the coalescence of these facets on the SiO2 mask. As a result, GaN layers with a dislocation density as low as 6×107 cm-2 were grown on 2-inch-diameter sapphire wafers. These GaN layers were crack-free and had mirror-like surface.

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Forty patients with squamous cell carcinoma of the oral cavity were treated with bleomycin prior to undergoing surgery. The degree of the clinical effect of bleomycin and the postoperative clinical course of each case were estimated from the viewpoint of correlation with the mode of invasion. A strong correlation was found among the mode of invasion, bleomycin sensitivity, and clinical course. A slight effect of bleomycin and poor prognosis existed in the group with a diffuse invasion of mode of invasion, while the greatest effect of bleomycin and good clinical course were achieved in the group with a welldefined tumor‐host borderline.

We have characterized by transmission electron microscopy (TEM) defect structures in GaN films grown selectively in hydride vapor-phase epitaxy (HVPE). In this experiment, growth was achieved on SiO2-stripe-patterned GaN layers that had been grown by metalorganic vapor-phase epitaxy (MOVPE) on sapphire substrates. Cross-sectional TEM revealed unambiguously that most of the dislocations, which originated from threading dislocations vertically aligned in the MOVPE-grown layer, propagated laterally around the SiO2 mask in the HVPE-grown film before the film thickness amounted to about 5 μm. This change of the propagation direction prevented the dislocations from crossing the film to the surface region and thus principally led to a drastic reduction in the threading dislocation density in thicker films.

It is well-established that heat shock proteins (HSPs)-peptides complexes elicit antitumor responses in prophylactic and therapeutic immunization protocols. HSPs such as gp96 and Hsp70 have been demonstrated to undergo receptor-mediated uptake by APCs with subsequent representation of the HSP-associated peptides to MHC class I molecules on APCs, facilitating efficient cross-presentation. On the contrary, despite its abundant expression among HSPs in the cytosol, the role of Hsp90 for the cross-presentation remains unknown. We show here that exogenous Hsp90-peptide complexes can gain access to the MHC class I presentation pathway and cause cross-presentation by bone marrow-derived dendritic cells. Interestingly, this presentation is TAP independent, and followed chloroquine, leupeptin-sensitive, as well as cathepsin S-dependent endosomal pathways. In addition, we show that Hsp90-chaperoned precursor peptides are processed and transferred onto MHC class I molecules in the endosomal compartment. Furthermore, we demonstrate that immunization with Hsp90-peptide complexes induce Ag-specific CD8+ T cell responses and strong antitumor immunity in vivo. These findings have significant implications for the design of T cell-based cancer immunotherapy.