Building Secure and Anonymous Communication Channel: Formal Model and its Prototype Implementation

Various techniques need to be combined to realize anonymously authenticated communication. Cryptographic tools enable anonymous user authentication while anonymous communication protocols hide users' IP addresses from service providers. One simple approach for realizing anonymously authenticated communication is their simple combination, but this gives rise to another issue; how to build a secure channel. The current public key infrastructure cannot be used since the user's public key identifies the user. To cope with this issue, we propose a protocol that uses identity-based encryption for packet encryption without sacrificing anonymity, and group signature for anonymous user authentication. Communications in the protocol take place through proxy entities that conceal users' IP addresses from service providers. The underlying group signature is customized to meet our objective and improve its efficiency. We also introduce a proof-of-concept implementation to demonstrate the protocol's feasibility. We compare its performance to SSL communication and demonstrate its practicality, and conclude that the protocol realizes secure, anonymous, and authenticated communication between users and service providers with practical performance.Comment: This is a preprint version of our paper presented in SAC'14, March 24-28, 2014, Gyeongju, Korea. ACMSAC 201

The Effect of Dietary Zinc on Vascular Function with Aging

Aging is associated with the development of vascular dysfunction, which is attributed to cardiovascular diseases (CVD) [14]. Researching possible intervention methods that promote healthy vascular aging is therefore a great biomedical priority. Essential nutrient zinc (Zn) is involved with many important biological processes including those believed to be associated with vascular function such as antiinflammatory and antioxidant activities [1]. However, specific mechanisms are still unknown, and investigation of the effect of zinc on vascular function is limited. Using the data collected through the Integrative Physiology of Aging Laboratory (IPA), we tested the hypothesis that zinc deficiency is linked with vascular dysfunction in healthy middle age/older adults (MA/O) (n=289, Ages 50-79). Correlational analysis as well as between-group analysis (low-zinc status versus high-zinc status; low zinc-body mass ratio versus high zinc-body mass ratio) showed no significant relationship between zinc intake and direct vascular health measures such as Pulse Wave Velocity (PWV) and vasodilation measures (endothelium dependent dilation/endothelium independent dilation). However, improvements in humoral factors such as TNF-α, oxidized LDL, and NADPH oxidase were observed with higher dietary zinc intake. Although the result was inconsistent, this study supports other literature’s argument on zinc’s anti-inflammatory and anti-oxidant properties. Discrepancy in the result suggests the necessity for further research identifying zinc’s promising capability in preventing CVD

Cysteinyl Leukotrienes and Their Receptors; Emerging Concepts

Cysteinyl leukotrienes (cys-LTs) are potent mediators of inflammation derived from arachidonic acid through the 5-lipoxygenase/leukotriene C4 synthase pathway. The derivation of their chemical structures and identification of their pharmacologic properties predated the cloning of their classical receptors and the development of drugs that modify their synthesis and actions. Recent studies have revealed unanticipated insights into the regulation of cys-LT synthesis, the function of the cys-LTs in innate and adaptive immunity and human disease, and the identification of a new receptor for the cys-LTs. This review highlights these studies and summarizes their potential pathobiologic and therapeutic implications

Diazipine, a novel photoaffinity probe for dihydropyridine receptors of calcium channels

AbstractA new 1,4-dihydropyridine photoaffinity ligand, [3H]diazipine, has been assessed by binding and photolabeling, and compared with a currently used [3H]Diazipine reversibly binds to skeletal muscle Ca2+ channels with a similar affinity of [3H]azidopine, but [3H]diazipine labels the channels two times more efficiently and no release of the incorporated amount is observed after dithiothreitol treatment

N-Nitroso-β-lactams as β-lactamase inhibitor

AbstractN-Nitroso-β-phenyl-β-lactam has been found to be a specific inhibitor of β-lactamase. N-Nitroso-α-phenyl-β-lactam, by contrast, was virtually ineffective although a transient inhibition of short duration was observed. The acyl enzyme derived from the β-phenyl isomer is presumably involved in a cross-linking reaction, whereas that from the α-phenyl isomer was quenched by spontaneous hydrolysis without formation of a covalent bond. No inhibitory effect of the β-phenyl isomer on chymotrypsin has been observed

Leukotrienes provide an NFAT-dependent signal that synergizes with IL-33 to activate ILC2s.

Group 2 innate lymphoid cells (ILC2s) and type 2 helper T cells (Th2 cells) are the primary source of interleukin 5 (IL-5) and IL-13 during type 2 (allergic) inflammation in the lung. In Th2 cells, T cell receptor (TCR) signaling activates the transcription factors nuclear factor of activated T cells (NFAT), nuclear factor κB (NF-κB), and activator protein 1 (AP-1) to induce type 2 cytokines. ILC2s lack a TCR and respond instead to locally produced cytokines such as IL-33. Although IL-33 induces AP-1 and NF-κB, NFAT signaling has not been described in ILC2s. In this study, we report a nonredundant NFAT-dependent role for lipid-derived leukotrienes (LTs) in the activation of lung ILC2s. Using cytokine reporter and LT-deficient mice, we find that complete disruption of LT signaling markedly diminishes ILC2 activation and downstream responses during type 2 inflammation. Type 2 responses are equivalently attenuated in IL-33- and LT-deficient mice, and optimal ILC2 activation reflects potent synergy between these pathways. These findings expand our understanding of ILC2 regulation and may have important implications for the treatment of airways disease

Atmospheric Environment, Radioactivity and Organic Pollutants in Pan- Japan Sea Area (AERO-PJS)

金沢大学大学院自然科学研究科Scedule:17-18 March 2003, Vemue: Kanazawa, Japan, Kanazawa Citymonde Hotel, Project Leader : Hayakawa, Kazuichi, Symposium Secretariat: XO kamata, Naoto, Edited by:Kamata, Naoto

Analysis of Reactive Oxygen Metabolites (ROMs) after Cardiovascular Surgery as a Marker of Oxidative Stress

The transient systemic low perfusion that occurs during cardiovascular surgery leads to oxidative stress and the production of free radicals. A systemic increase of various markers of oxidative stress has been shown to occur during cardiopulmonary bypass (CPB). However, these markers have not been adequately evaluated because they seem to be reactive and short-lived. Here, oxidative stress was measured using the free radical analytical system (FRAS 4) assessing the derivatives of reactive oxygen metabolites (d-ROMs) and biological antioxidant potential (BAP). Blood samples were taken from 21 patients undergoing elective cardiovascular surgery. CPB was used in 15 patients, and abdominal aortic aneurysm (AAA) surgery without CPB was performed in 6. Measurements of d-ROMs and BAP were taken before surgery, 1 day, 1 week, and 2 weeks after surgery, and oxidative stress was evaluated. The d-ROM level increased gradually after cardiovascular surgery up to 2 weeks. Over time, the d-ROM level after surgery involving CPB became higher than that after AAA surgery. This difference reached statistical significance at 1 week and lasted to 2 weeks. The prolongation of CPB was prone to elevate the d-ROM level whereas the duration of the aortic clamp in AAA surgery had no relation to the d-ROM level. The BAP was also elevated after surgery, and was positively correlated with the level of d-ROMs. In this study, patients who underwent cardiovascular surgery involving CPB had significant oxidative damage. The production of ROMs was shown to depend on the duration of CPB. Damage can be reduced if CPB is avoided. When CPB must be used, shortening the CPB time may be effective in reducing oxidative stress