<Symposium> Regional Geography and Area Studies Reconsidered Discussion

地誌学とエリアスタディ : 現状と課

Comparison of randomization techniques for low-discrepancy sequences in finance

Low-discrepancy sequence, Quasi-Monte Carlo simulation, Randomization, Error estimation, Derivative pricing, Path dependent option,

HWA1- and HWA2-Mediated Hybrid Weakness in Rice Involves Cell Death, Reactive Oxygen Species Accumulation, and Disease Resistance-Related Gene Upregulation

Hybrid weakness is a type of reproductive isolation in which F1 hybrids of normal parents exhibit weaker growth characteristics than their parents. F1 hybrid of the Oryza sativa Indian cultivars &lsquo;P.T.B.7&prime; and &lsquo;A.D.T.14&prime; exhibits hybrid weakness that is associated with the HWA1 and HWA2 loci. Accordingly, the aim of the present study was to analyze the hybrid weakness phenotype of the &lsquo;P.T.B.7&prime; &times; &lsquo;A.D.T.14&prime; hybrids. The height and tiller number of the F1 hybrid were lower than those of either parent, and F1 hybrid also exhibited leaf yellowing that was not observed in either parent. In addition, the present study demonstrates that SPAD values, an index correlated with chlorophyll content, are effective for evaluating the progression of hybrid weakness that is associated with the HWA1 and HWA2 loci because it accurately reflects degree of leaf yellowing. Both cell death and H2O2, a reactive oxygen species, were detected in the yellowing leaves of the F1 hybrid. Furthermore, disease resistance-related genes were upregulated in the yellowing leaves of the F1 hybrids, whereas photosynthesis-related genes tended to be downregulated. These results suggest that the hybrid weakness associated with the HWA1 and HWA2 loci involves hypersensitive response-like mechanisms

PAPER Special Section on Cryptography and Information Security Digitally Signed Document Sanitizing Scheme with Disclosure Condition Control

SUMMARY A digital signature does not allow any alteration of the document to which it is attached. Appropriate alteration of some signed documents, however, should be allowed because there are security requirements other than that for the integrity of the document. In the disclosure of official information, for example, sensitive information such as personal information or national secrets is masked when an official document is sanitized so that its nonsensitive information can be disclosed when it is demanded by a citizen. If this disclosure is done digitally by using the current digital signature schemes, the citizen cannot verify the disclosed information correctly because the information has been altered to prevent the leakage of sensitive information. That is, with current digital signature schemes, the confidentiality of official information is incompatible with the integrity of that information. This is called the digital document sanitizing problem, and some solutions such as digital document sanitizing schemes and content extraction signatures have been proposed. In this paper, we point out that the conventional digital signature schemes are vulnerable to additional sanitizing attack and show how this vulnerability can be eliminated by using a new digitally signed document sanitizing scheme with disclosure condition control. key words: digital signature, disclosure of official information, privacy issue 1

β-Endorphin Mediates the Development and Instability of Atherosclerotic Plaques

β-Endorphin, an endogenous opioid peptide, and its μ-opioid receptor are expressed in brain, liver, and peripheral tissues. β-Endorphin induces endothelial dysfunction and is related to insulin resistance. We clarified the effects of β-endorphin on atherosclerosis. We assessed the effects of β-endorphin on the inflammatory response and monocyte adhesion in human umbilical vein endothelial cells (HUVECs), foam cell formation, and the inflammatory phenotype in THP-1 monocyte-derived macrophages, and migration and proliferation of human aortic smooth muscle cells (HASMCs) in vitro. We also assessed the effects of β-endorphin on aortic lesions in Apoe−/− mice in vivo. The μ-opioid receptor (OPRM1) was expressed in THP-1 monocytes, macrophages, HASMCs, HUVECs, and human aortic endothelial cells. β-Endorphin significantly increased THP-1 monocyte adhesion to HUVECs and induced upregulation of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin via nuclear factor-κB (NF-κB) and p38 phosphorylation in HUVECs. β-Endorphin significantly increased HUVEC proliferation and enhanced oxidized low-density lipoprotein-induced foam cell formation in macrophages. β-Endorphin also significantly shifted the macrophage phenotype to proinflammatory M1 rather than anti-inflammatory M2 via NF-κB phosphorylation during monocyte-macrophage differentiation and increased migration and apoptosis in association with c-jun-N-terminal kinase, p38, and NF-κB phosphorylation in HASMCs. Chronic β-endorphin infusion into Apoe−/− mice significantly aggravated the development of aortic atherosclerotic lesions, with an increase in vascular inflammation and the intraplaque macrophage/smooth muscle cell ratio, an index of plaque instability. Our study provides the first evidence that β-endorphin contributes to the acceleration of the progression and instability of atheromatous plaques. Thus, μ-opioid receptor antagonists may be useful for the prevention and treatment of atherosclerosis