自然由来重金属等を含む地盤材料の適正利用に関する研究

京都大学新制・論文博士博士(地球環境学)乙第13628号論地環博第18号京都大学大学院地球環境学舎地球環境学専攻(主査)教授 勝見 武, 准教授 高井 敦史, 教授 安原 英明, 教授 越後 信哉学位規則第4条第2項該当Doctor of Global Environmental StudiesKyoto UniversityDFA

What is a proper definition of spin current? -- Lessons from the Kane-Mele Model

Spin current, a key concept in spintronics that carries spin angular momentum, has a non-unique definition due to the non-conservation of spins in solids. While two primary definitions exist -- conventional spin current and conserved spin current -- their validity has not been quantitatively examined. Here, we examine the validity of these definitions of spin current by comparing their spin Hall conductivities to the spin accumulation on edges of materials calculated in a real-time evolution simulation. Employing the Kane-Mele model with the Rashba term, which explicitly violates spin conservation, we reveal that the spin Hall conductivities calculated under both definitions fail to reproduce the simulated results of spin accumulation when the Rashba term is large. Our results suggest that the standard definitions of spin current and the associated spin Hall conductivity do not give an accurate quantitative estimate of spin accumulation. This conclusion indicates that real-time simulations are necessary to accurately estimate spin accumulation on edges/surfaces of materials.Comment: 5 pages, 3 figure

Autoantibodies to low-density-lipoprotein-receptor-related protein 2 (LRP2) in systemic autoimmune diseases

We previously reported that autoantibodies (autoAbs) to the main epitope on CD69 reacted to its homologous amino acid sequence in low-density-lipoprotein-receptor-related protein 2 (LPR2), a multiligand receptor for protein reabsorption. In this study, we have investigated the prevalence, autoepitope distribution, and clinical significance of the autoAbs to LRP2 in patients with systemic autoimmune diseases. Using six recombinant proteins (F2–F7) for LRP2 and one for CD69, we detected autoAbs to LRP2 in sera of patients with rheumatoid arthritis (RA), systemic lupus erythematosus, Behçet's disease, systemic sclerosis, and osteoarthritis and then mapped autoepitopes by Western blotting. The autoAbs to LRP2 were detected in 87% of the patients with rheumatoid arthritis, 40% of those with systemic lupus erythematosus, 35% of those with systemic sclerosis, 15% of those with osteoarthritis, and 3% of those with Behçet's disease. Multiple epitopes on LRP2 were recognized by most of the anti-LRP2(+ )serum samples. All of the tested anti-CD69 autoAb(+ )samples reacted to LRP2-F3 containing the homologous sequence to the main epitope of CD69; however, only 38% of the anti-LRP2-F3(+ )samples reacted to CD69. Clinically, the existence of the autoAbs to LRP2-F4, -F5, and -F6 correlated with the presence of proteinuria in RA. This study revealed that LRP2 is a major autoantigen in RA. The autoAbs to LRP2 are probably produced by the antigen-driven mechanism and the autoimmunity to LRP2 may spread to include CD69. The anti-LRP2 autoAbs may play pathological roles by inhibiting the reabsorbing function of LRP2

The epigenetic function of androgen receptor in prostate cancer progression

Androgen and androgen deprivation (castration) therapies, including androgen receptor antagonists, are clinically used to treat patients with prostate cancer. However, most hormone-dependent prostate cancer patients progress into a malignant state with loss of hormone-dependency, known as castration (drug)-resistant prostate cancer (CRPC), after prolong androgen-based treatments. Even in the CRPC state with irreversible malignancy, androgen receptor (AR) expression is detectable. An epigenetic transition to CRPC induced by the action of AR-mediated androgen could be speculated in the patients with prostate cancer. Androgen receptors belongs to the nuclear receptor superfamily with 48 members in humans, and acts as a ligand-dependent transcriptional factor, leading to local chromatin reorganization for ligand-dependent gene regulation. In this review, we discussed the transcriptional/epigenetic regulatory functions of AR, with emphasis on the clinical applications of AR ligands, AR protein co-regulators, and AR RNA coregulator (enhancer RNA), especially in chromatin reorganization, in patients with prostate cancer