Performance Evaluation of SCTP wth Adaptive Multistreamiing over LEO Satellite Networks

科研費報告書収録論文(課題番号:17500030/研究代表者:加藤寧/インターネットと高親和性を有する次世代低軌道衛星ネットワークに関する基盤研究

Supporting IP/LEO satellite networks by handover-independent IP mobility management

科研費報告書収録論文(課題番号:14380172・基盤研究(B)(2) ・H14～H15/研究代表者:根元, 義章/トラヒックパターンの時系列解析に基づく次世代広域不正アクセス自動追跡システム

Clinical course of focal choroidal excavation in Vogt-Koyanagi-Harada disease

We describe focal choroidal excavation (FCE) in a case of Vogt–Koyanagi–Harada (VKH) disease and compare the findings with different chorioretinal conditions. A 55-year-old man was diagnosed with VKH based on panuveitis and exudative retinal detachments. Spectral-domain optical coherence tomography demonstrated a dome-shaped protrusion with a nonconforming pattern at the fovea, which had been detected as a conforming pattern 1 year before the onset. The FCE pattern returned into a conforming pattern following corticosteroid therapy. These findings suggest that the natively existent FCE could be affected by pathophysiological changes of VKH as well as other chorioretinal conditions

Cu-NMR study on the disordered quantum spin magnet with the Bose-glass ground state

Cu-NMR study has been performed on the disordered spin-gap system Tl1-xKxCuCl3 In the high-field H > HC=\Delta/\mu_B, where \Delta is the spin-gap, the hyperfine field becomes extremely inhomogeneous at low temperatures due to the field-induced magnetic order, indicating that the ordered spin state must be different from the pure TlCuCl3. In the low field H < HC, a saturating behavior in the longitudinal nuclear spin relaxation rate 1/T1 was observed at low temperatures, indicating existence of the magnetic ground state proposed to be Bose-glass phase by Fisher.Comment: RHMF200

Generation of cytotoxic T cell responses to an HLA-A24 restricted epitope peptide derived from wild-type p53

Mutations in the p53 gene are the most common genetic alterations found in human tumours, and these mutations result in high levels of p53 protein in the tumour cells. Since the expression levels of wild-type p53 in nonmalignant tissue are usually much lower in contrast, the p53 protein is an attractive target for cancer immunotherapy. We tested p53 encoded HLA-A24 binding peptides for their capacity to elicit anti-tumour cytotoxic T lymphocytes (CTL) in vitro. These peptides were in murine p53-derived cytotoxic peptides, which were being presented to CTL by H-2K d and H-2K b molecules, because the HLA-A24 peptide binding motifs were similar to the H-2K d and H-2K b. For CTL induction, we used CD8+T lymphocytes from the peripheral blood mononuclear cells (PBMC) of healthy donors and the peptides from pulsed dendritic cells as antigen-presenting cells. We identified the peptide, p53-161 (AIYKQSQHM), which was capable of eliciting CTL lines that lysed tumour cells expressing HLA-A24 and p53. The effectors lysed C1RA24 cells (p53+, HLA-A*2402 transfectant), but not their parental cell lines C1R (p53+, HLA-A,B null cell). These results strongly indicate that the CTL exerts cytotoxic activity in HLA-A24's restricted manner. The identification of this novel p53 epitope for CTL offers the possibility to design and develop specific immunotherapeutic approaches for treating tumours with p53 mutation in HLA-A24-positive patients. © 2001 Cancer Research Campaign http://www.bjcancer.co