Rational Broadcast Protocols against Timid Adversaries

We present a constant-round deterministic broadcast protocol against timid adversaries in the synchronous authenticated setting. A timid adversary is a game-theoretically rational adversary who tries to attack the protocol but prefers the actions to be undetected. Our protocol is secure against such an adversary corrupting t out of n parties for any t < n. The round complexity is 5 for timid adversaries and is at most t + 5 for general malicious adversaries. Our results demonstrate that game-theoretic rationality enables us to circumvent the impossibility of constructing constant-round deterministic broadcast protocols for t = ω(1)

重度大動脈弁狭窄症患者の大動脈弁置換術後における血小板機能および高分子量 von Willebrand 因子多量体の急速な回復

AIM: Patients with severe aortic stenosis (AS) may have bleeding episodes due to the loss of high-molecular-weight (HMW) von Willebrand factor multimers (VWFMs). The absence of HMW-VWFMs and bleeding tendency are usually corrected after aortic valve replacement (AVR). To investigate the process of VWFM recovery and symptoms in patients with severe AS, we analyzed changes in VWF antigen (VWF:Ag), ADAMTS13 activity (ADAMTS13:AC), and platelet thrombus formation under high shear stress conditions. METHODS: Nine patients with severe AS undergoing AVR were analyzed. RESULTS: Evident deficiency of HMW-VWFMs was observed in six patients before surgery, which was rapidly restored within 8 days after AVR. Median levels of VWF:Ag before surgery, on postoperative days (PODs) 1, 8, 15, and 22, and one year after AVR were 78.1%, 130%, 224%, 155%, 134%, and 142%, respectively. In contrast, ADAMTS13:AC was 50.5%, 35.5%, 25.5%, 25.1%, 30.3%, and 84.6%, respectively. Preoperative thrombus formation but not surface coverage was significantly lower than that on POD 22, which was considered as normal level in each patient. Compared with preoperative levels, thrombus volume was significantly lower on POD 1, but rapidly increased by POD 8. CONCLUSION: Bleeding tendency and loss of HMW-VWFMs observed in patients with severe AS before surgery was rapidly corrected after AVR. Instead, patients were in a VWF-predominant state between POD 8 and 22.博士（医学）・乙第1395号・平成29年3月15日Copyright © 2016 Japan Atherosclerosis Society本論文の著作権は日本動脈硬化学会が保持しています。This article is distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License

心臓血管外科領域におけるゼラチンシートの止血効果、癒着防止効果の検討

BACKGROUND:The bi1ayer gelatin sealing sheet was developed as a safe, effective, easy-to-handle and low-cost hemostatic agent. OBJECTIVE:To examine the feasibility of gelatin sealing sheets using a canine aterial hemorrhage mode1. METHODS:In vivo degradation of gelatin sealing sheets was examined by implanting subcutaneously in rats. For the hemostatic and anti-adhesion efficacy investigations, femoral arteries of dogs were pricked with syringe needle to make as mall hole, and a gelatin(i.e. experimental group) or fibrin glue sealing sheet (i.e. control group) was applied on the hole to stop bleeding (n=8). After discontinuation of the bleeding, the skin incisions were closed and re-examined 4 weeks postoperatively. RESULTS:From the degradation study, 4h thermally treated gelatin sheet which degraded within 3 weeks in vivo was chosen for the further hemostatic study. In all cases of gelatin and fibrin glue sealing sheets, bleeding from the needle hole on canine femoral arteries was effectively stopped. Postoperative adhesions and inflammation at the site in the experimental group were significantly less than those in the control group (P<0.01 for adhesion scores). CONCLUSIONS:The gelatin sealing sheet was found to be as effective as the fibrin glue sealing sheet as a surgical hemostatic agent, and more effective in preventing postoperative adhesions.博士（医学）・甲第632号・平成27年3月16日Copyright ©2015 IOS Pres

Effectiveness of Cross‐Linked Gelatin Glue in Canine Lung Surgery Models.

Background. Air leakage is a common postoperative complication in pulmonary surgery, and surgical sealants have been developed to prevent or reduce the incidence of air leaks. In this study, we evaluated the efficacy of cross-linked gelatin glue (gelatin plus glutaraldehyde) in canine lung surgery models. Methods. Pulmonary fistulas and injuries were created in dogs and sealed with gelatin glue, fibrin glue, or fibrin glue with a polyglycolic acid (PGA) sheet. Seal-breaking pressures were measured in the fistula model, and pleural adhesions were assessed 28 days postoperatively in the lung injury model. Results. The seal-breaking pressures for canine cadaver and living lung surgeries (; the maximum pressures were 80 and 40 cm H₂O) were respectively: gelatin glue, 77 ± 6 and 32.3 ± 8.9cm H₂O; fibrin glue using spray, 39.2 ± 9.3 and 32 ± 6cm H₂O; fibrin glue using the rub-and-soak method, 35 ± 13.4 and 40 ± 0 cm H₂O; and fibrin glue with a PGA sheet, 55.5 ± 18.2 and 39 ± 2cm H₂O. In the lung injury model, there were no chest wall adhesions in the gelatin and fibrin glue alone groups, while strong adhesions were observed when treated with fibrin glue with a PGA sheet. Conclusions. Gelatin glue's sealing effect was superior to that of fibrin glue while preventing postoperative pleural adhesions. These findings suggest that gelatin glue may be effective as a surgical sealant or anti-adhesion materialin lung surgery

Hot debris dust around HD 106797

Photometry of the A0 V main-sequence star HD 106797 with AKARI and Gemini/T-ReCS is used to detect excess emission over the expected stellar photospheric emission between 10 and 20 micron, which is best attributed to hot circumstellar debris dust surrounding the star. The temperature of the debris dust is derived as Td ~ 190 K by assuming that the excess emission is approximated by a single temperature blackbody. The derived temperature suggests that the inner radius of the debris disk is ~ 14 AU. The fractional luminosity of the debris disk is 1000 times brighter than that of our own zodiacal cloud. The existence of such a large amount of hot dust around HD 106797 cannot be accounted for by a simple model of the steady state evolution of a debris disk due to collisions, and it is likely that transient events play a significant role. Our data also show a narrow spectral feature between 11 and 12 micron attributable to crystalline silicates, suggesting that dust heating has occurred during the formation and evolution of the debris disk of HD 106797.Comment: Accepted to ApJ Letters, 8 pages, 2 figure

Zinc is a novel intracellular second messenger

Zinc is an essential trace element required for enzymatic activity and for maintaining the conformation of many transcription factors; thus, zinc homeostasis is tightly regulated. Although zinc affects several signaling molecules and may act as a neurotransmitter, it remains unknown whether zinc acts as an intracellular second messenger capable of transducing extracellular stimuli into intracellular signaling events. In this study, we report that the cross-linking of the high affinity immunoglobin E receptor (Fcɛ receptor I [FcɛRI]) induced a release of free zinc from the perinuclear area, including the endoplasmic reticulum in mast cells, a phenomenon we call the zinc wave. The zinc wave was dependent on calcium influx and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase activation. The results suggest that the zinc wave is involved in intracellular signaling events, at least in part by modulating the duration and strength of FcɛRI-mediated signaling. Collectively, our findings indicate that zinc is a novel intracellular second messenger

RGMa collapses the neuronal actin barrier against disease-implicated protein and exacerbates ALS

Repulsive guidance molecule A (RGMa) was originally identified as a neuronal growth cone–collapsing factor. Previous reports have demonstrated the multifunctional roles of RGMa mediated by neogenin1. However, the pathogenic involvement of RGMa in amyotrophic lateral sclerosis (ALS) remains unclear. Here, we demonstrated that RGMa concentration was elevated in the cerebrospinal fluid of both patients with ALS and transgenic mice overexpressing the mutant human superoxide dismutase1 (mSOD1 mice). Treatment with humanized anti-RGMa monoclonal antibody ameliorated the clinical symptoms in mSOD1 mice. Histochemical analysis revealed that the anti-RGMa antibody significantly decreased mutant SOD1 protein accumulation in the motor neurons of mSOD1 mice via inhibition of actin depolymerization. In vitro analysis revealed that the anti-RGMa antibody inhibited the cellular uptake of the mutant SOD1 protein, presumably by reinforcing the neuronal actin barrier. Collectively, these data suggest that RGMa leads to the collapse of the neuronal actin barrier and promotes aberrant protein deposition, resulting in exacerbation of the ALS pathology.Shimizu Mikito, Shiraishi Naoyuki, Tada Satoru, et al. RGMa collapses the neuronal actin barrier against disease-implicated protein and exacerbates ALS. Science Advances 9, 686 (2023); https://doi.org/10.1126/sciadv.adg3193