The Bitcoin Network as Platform for Trans-Organizational Attribute Authentication

WEB2015 : The Third International Conference on Building and Exploring Web Based Environments , May 24-29, 2015 , Rome, ItalyThe role-based access control (RBAC) is a natural and versatile model of the access control principle. In the real world, it is common that an organization provides a service to a user who owns a certain role that was issued by a different organization. However, such a trans-organizational RBAC is not common in a computer network because it is difficult to establish both the security that prohibits malicious impersonation of roles and the flexibility that allows small organizations/individual users to fully control their own roles. This study proposes a system that makes use of Bitcoin technology to realize a trans-organizational RBAC mechanism. Bitcoin, the first decentralized digital currency, is a payment network that has become a platform for innovative ideas. Bitcoin’s technology, including its protocol, cryptography, and open-source nature, has built a good reputation and has been applied in other applications, such as trusted timestamping. The proposed system uses Bitcoin technology as a versatile infrastructure to represent the trust and endorsement relationship that are essential in RBAC and to realize a challenge-response authentication protocol that verifies a user's ownership of roles

Benzalkonium Chloride Accelerates the Formation of the Amyloid Fibrils of Corneal Dystrophy-associated Peptides

This research was originally published in the Journal of Biological Chemistry. Yusuke Kato, Hisashi Yagi, Yuichi Kaji, Tetsuro Oshika and Yuji Goto. Benzalkonium Chloride Accelerates the Formation of the Amyloid Fibrils of Corneal Dystrophy-associated Peptides. J. Biol. Chem. 2013; 288, 25109-25118. © the American Society for Biochemistry and Molecular Biolog

Photodynamic therapy on corneal dystrophy on the basis of molecular mechanism.

科学研究費助成事業 研究成果報告書：基盤研究(C)2012-2014課題番号:2459261

Hybrid-BFT: Optimistically Responsive Synchronous Consensus with Optimal Latency or Resilience

Optimistic responsiveness was introduced to shorten the latency of a synchronous Byzantine consensus protocol that is inherently lower bounded by the pessimistic bound on the network delay $\Delta$. It states that a protocol makes a decision with latency on the order of actual network delay $\delta$ if the number of actual faults is significantly smaller than $f$, which is the worst-case allowed. In this paper, we investigate if a Byzantine consensus can simultaneously achieve (i) optimistic responsiveness, and (ii) optimal latency of $\Delta + O(\delta)$ in the presence of $f$ faults. To do this, we provide a tight upper bound on the number of actual faults by showing matching feasibility and infeasibility results. Furthermore, we present a simple leader-based Byzantine fault-tolerant (BFT) replication protocol as a practical application. Even while being able to rotate leaders after every decision, our protocol simultaneously achieves average latency of (i) $3\delta$ under optimistic condition and (ii) $1.5\Delta + O(\delta)$ (or $3\Delta + O(\delta)$) in the presence of $f$ faults, which is more than a factor of two better than current state-of-the-art rotating-leader BFT protocols

VEGF\u3csub\u3e164\u3c/sub\u3e-Mediated Inflammation is Required for Pathological, but Not Physiological, Ischemia-Induced Retinal Neovascularization

Hypoxia-induced VEGF governs both physiological retinal vascular development and pathological retinal neovascularization. In the current paper, the mechanisms of physiological and pathological neovascularization are compared and contrasted. During pathological neovascularization, both the absolute and relative expression levels for VEGF164 increased to a greater degree than during physiological neovascularization. Furthermore, extensive leukocyte adhesion was observed at the leading edge of pathological, but not physiological, neovascularization. When a VEGF164-specific neutralizing aptamer was administered, it potently suppressed the leukocyte adhesion and pathological neovascularization, whereas it had little or no effect on physiological neovascularization. In parallel experiments, genetically altered VEGF164-deficient (VEGF120/188) mice exhibited no difference in physiological neovascularization when compared with wild-type (VEGF+/+) controls. In contrast, administration of a VEGFR-1/Fc fusion protein, which blocks all VEGF isoforms, led to significant suppression of both pathological and physiological neovascularization. In addition, the targeted inactivation of monocyte lineage cells with clodronate-liposomes led to the suppression of pathological neovascularization. Conversely, the blockade of T lymphocyte–mediated immune responses with an anti-CD2 antibody exacerbated pathological neovascularization. These data highlight important molecular and cellular differences between physiological and pathological retinal neovascularization. During pathological neovascularization, VEGF164 selectively induces inflammation and cellular immunity. These processes provide positive and negative angiogenic regulation, respectively. Together, new therapeutic approaches for selectively targeting pathological, but not physiological, retinal neovascularization are outlined

SHG-specificity of cellular Rootletin filaments enables naïve imaging with universal conservation

Despite growing demand for truly naïve imaging, label-free observation of cilium-related structure remains challenging, and validation of the pertinent molecules is correspondingly difficult. In this study, in retinas and cultured cells, we distinctively visualized Rootletin filaments in rootlets in the second harmonic generation (SHG) channel, integrated in custom coherent nonlinear optical microscopy (CNOM) with a simple, compact, and ultra-broadband supercontinuum light source. This SHG signal was primarily detected on rootlets of connecting cilia in the retinal photoreceptor and was validated by colocalization with anti-Rootletin staining. Transfection of cells with Rootletin fragments revealed that the SHG signal can be ascribed to filaments assembled from the R234 domain, but not to cross-striations assembled from the R123 domain. Consistent with this, Rootletin-depleted cells lacked SHG signal expected as centrosome linker. As a proof of concept, we confirmed that similar fibrous SHG was observed even in unicellular ciliates. These findings have potential for broad applications in clinical diagnosis and biophysical experiments with various organisms

VEGF164-mediated Inflammation Is Required for Pathological, but Not Physiological, Ischemia-induced Retinal Neovascularization

Hypoxia-induced VEGF governs both physiological retinal vascular development and pathological retinal neovascularization. In the current paper, the mechanisms of physiological and pathological neovascularization are compared and contrasted. During pathological neovascularization, both the absolute and relative expression levels for VEGF(164) increased to a greater degree than during physiological neovascularization. Furthermore, extensive leukocyte adhesion was observed at the leading edge of pathological, but not physiological, neovascularization. When a VEGF(164)-specific neutralizing aptamer was administered, it potently suppressed the leukocyte adhesion and pathological neovascularization, whereas it had little or no effect on physiological neovascularization. In parallel experiments, genetically altered VEGF(164)-deficient (VEGF(120/188)) mice exhibited no difference in physiological neovascularization when compared with wild-type (VEGF(+/+)) controls. In contrast, administration of a VEGFk-1/Fc fusion protein, which blocks all VEGF isoforms, led to significant suppression of both pathological and physiological neovascularization. In addition, the targeted inactivation of monocyte lineage cells with clodronate-liposomes led to the suppression of pathological neovascularization. Conversely, the blockade of T lymphocyte-mediated immune responses with an anti-CD2 antibody exacerbated pathological neovascularization. These data highlight important molecular and cellular differences between physiological and pathological retinal neovascularization. During pathological neovascularization, VEGF(164) selectively induces inflammation and cellular immunity. These processes provide positive and negative angiogenic regulation, respectively. Together, new therapeutic approaches for selectively targeting pathological, but not physiological, retinal neovascularization are outlined

VEGF164-mediated Inflammation Is Required for Pathological, but Not Physiological, Ischemia-induced Retinal Neovascularization

Hypoxia-induced VEGF governs both physiological retinal vascular development and pathological retinal neovascularization. In the current paper, the mechanisms of physiological and pathological neovascularization are compared and contrasted. During pathological neovascularization, both the absolute and relative expression levels for VEGF164 increased to a greater degree than during physiological neovascularization. Furthermore, extensive leukocyte adhesion was observed at the leading edge of pathological, but not physiological, neovascularization. When a VEGF164-specific neutralizing aptamer was administered, it potently suppressed the leukocyte adhesion and pathological neovascularization, whereas it had little or no effect on physiological neovascularization. In parallel experiments, genetically altered VEGF164-deficient (VEGF120/188) mice exhibited no difference in physiological neovascularization when compared with wild-type (VEGF+/+) controls. In contrast, administration of a VEGFR-1/Fc fusion protein, which blocks all VEGF isoforms, led to significant suppression of both pathological and physiological neovascularization. In addition, the targeted inactivation of monocyte lineage cells with clodronate-liposomes led to the suppression of pathological neovascularization. Conversely, the blockade of T lymphocyte–mediated immune responses with an anti-CD2 antibody exacerbated pathological neovascularization. These data highlight important molecular and cellular differences between physiological and pathological retinal neovascularization. During pathological neovascularization, VEGF164 selectively induces inflammation and cellular immunity. These processes provide positive and negative angiogenic regulation, respectively. Together, new therapeutic approaches for selectively targeting pathological, but not physiological, retinal neovascularization are outlined