MovieMaker: A Parallel Movie-Making Software for Large Scale Simulations

We have developed a parallel rendering software for scientific visualization of large-scale, three-dimensional, time development simulations. The goal of this software, MovieMaker, is to generate a movie, or a series of visualization images from totally one TB-scale data within one night (or less than 12 hours). The isocontouring, volume rendering, and streamlines are implemented. MovieMaker is a parallel program for the shared memory architecture with dynamic load balancing and overlapped disk I/O.Comment: 3pages, 5figures, submitted to J. Plasma Physcs (special issue for 19th ICNSP

Spreading of Antarctic Bottom Water examined using the CFC-11 distribution simulated by an eddy-resolving OGCM

We have investigated the spreading and pathway of Antarctic Bottom Water(AABW) using the simulated distribution of chlorofluorocarbons(CFCs) in a global eddy-resolving(1/10°) OGCM. Our goal is understanding of the processes and pathways determining the distribution of CFCs in the Southern Ocean, where much of this tracer is entrained by formation of deep and bottom water. The simu- lated high CFC-11 water reveals the newly formed AABW around the Antarctic Continent. The main source regions of AABW in the model are in the Weddell Sea(60°- 30°W ), offshore of Wilkes Land(120°- 160°E ) and in the Ross Sea(170°E -160°W ). In our model, spreading of simulated CFC-11 in the deep Southern Ocean from the newly formed AABW regions is more similar to the observed distribution than in coarse-resolution models. In the Weddell Sea, the high CFC-11 water spreads eastward with the Antarctic Circumpolar Current(ACC) and flows northward to the Argentine Basin. The high CFC-11 water from Wilkes Land joins with the high CFC-11 water from the Ross Sea. Some of the high CFC-11 water from Wilkes Land flows northward toward New Zealand. The high CFC-11 water from the Ross Sea flows eastward with the ACC along the Mid Ocean Ridge and northward to the Southeast Pacific Basin

Multi-Cast Key Distribution: Scalable, Dynamic and Provably Secure Construction

In this paper, we propose a two-round dynamic multi-cast key distribution (DMKD) protocol under the star topology with a central authentication server. Users can share a common session key without revealing any information of the session key to the server, and can join/leave to/from the group at any time even after establishing the session key. Our protocol is scalable because communication and computation costs of each user are independent from the number of users. Also, our protocol is still secure if either private key or session-specific randomness of a user is exposed. Furthermore, time-based backward secrecy is guaranteed by renewing the session key for every time period even if the session key is exposed. We introduce the first formal security definition for DMKD under the star topology in order to capture such strong exposure resilience and time-based backward secrecy. We prove that our protocol is secure in our security model in the standard model

Study on variation of neutral temperature in the polar MLT region using a sodium LIDAR at Tromsø

第2回極域科学シンポジウム/第35回極域宙空圏シンポジウム 11月14日（月） 国立極地研究所 2階大会議

酸化型HMGB-1は間葉系幹細胞/間葉系細胞を介して大腸癌の転移性を促進する

High mobility group box-1 (HMGB1) is known to be a chemotactic factor for mesenchymal stem/stromal cells (MSCs), but the effect of post-translational modification on its function is not clear. In this study, we hypothesized that differences in the oxidation state of HMGB1 would lead to differences in the function of MSCs in cancer. In human colorectal cancer, MSCs infiltrating into the stroma were correlated with liver metastasis and serum HMGB1. In animal models, oxidized HMGB1 mobilized three-fold fewer MSCs to subcutaneous tumors compared with reduced HMGB1. Reduced HMGB1 inhibited the proliferation of mouse bone marrow MSCs (BM-MSCs) and induced differentiation into osteoblasts and vascular pericytes, whereas oxidized HMGB1 promoted proliferation and increased stemness, and no differentiation was observed. When BM-MSCs pretreated with oxidized HMGB1 were co-cultured with syngeneic cancer cells, cell proliferation and stemness of cancer cells were increased, and tumorigenesis and drug resistance were promoted. In contrast, co-culture with reduced HMGB1-pretreated BM-MSCs did not enhance stemness. In an animal orthotopic transplantation colorectal cancer model, oxidized HMGB1, but not reduced HMGB1, promoted liver metastasis with intratumoral MSC chemotaxis. Therefore, oxidized HMGB1 reprograms MSCs and promotes cancer malignancy. The oxidized HMGB1–MSC axis may be an important target for cancer therapy.博士（医学）・甲第874号・令和5年3月15

A statistical study of convective and dynamic instabilities in the polar upper mesosphere above Tromsø

We have studied the convective (or static) and dynamic instabilities between 80 and 100 km above Tromsø (69.6° N, 19.2° E) using temperature and wind data of 6 min and 1 km resolutions primarily almost over a solar cycle obtained with the sodium lidar at Tromsø. First, we have calculated Brunt–Väisälä frequency (N) for 339 nights obtained from October 2010 to December 2019, and the Richardson number (Ri) for 210 nights obtained between October 2012 to December 2019. Second, using those values (N and Ri), we have calculated probabilities of the convective instability (N2<0) and the dynamic instability (0≤Ri<0.25) that can be used for proxies for evaluating the atmospheric stability. The probability of the convective instability varies from about 1% to 24% with a mean value of 9%, and that of the dynamic instability varies from 4 to 20% with a mean value of 10%. Third, we have compared these probabilities with the F10.7 index and local K-index. The probability of the convective instability shows a dependence (its correlation coefcient of 0.45) of the geomagnetic activity (local K-index) between 94 and 100 km, suggesting an auroral infuence on the atmospheric stability. The probability of the dynamic instability shows a solar cycle dependence (its correlation coefcient being 0.54). The probability of the dynamic instability shows the dependence of the 12 h wave amplitude (meridional and zonal wind components) (C.C.=0.52). The averaged potential energy of gravity waves shows decrease with height between 81 and 89 km, suggesting that dissipation of gravity waves plays an important role (at least partly) in causing the convective instability below 89 km. The probability of the convective instability at Tromsø appears to be higher than that at middle/low latitudes, while the probability of the dynamic instability is similar to that at middle/low latitudes

中鎖脂肪酸と糖質の併用摂取は癌関連骨格筋萎縮から保護する

Skeletal muscle volume is associated with prognosis of cancer patients. Maintenance of skeletal muscle is an essential concern in cancer treatment. In nutritional intervention, it is important to focus on differences in metabolism between tumor and skeletal muscle. We examined the influence of oral intake of glucose (0%, 10%, 50%) and 2% medium-chain fatty acid (lauric acid, LAA, C12:0) on tumor growth and skeletal muscle atrophy in mouse peritoneal metastasis models using CT26 mouse colon cancer cells and HT29 human colon cancer cells. After 2 weeks of experimental breeding, skeletal muscle and tumor were removed and analyzed. Glucose intake contributed to prevention of skeletal muscle atrophy in a sugar concentration-dependent way and also promoted tumor growth. LAA ingestion elevated the level of skeletal muscle protein and suppressed tumor growth by inducing tumor-selective oxidative stress production. When a combination of glucose and LAA was ingested, skeletal muscle mass increased and tumor growth was suppressed. Our results confirmed that although glucose is an important nutrient for the prevention of skeletal muscle atrophy, it may also foster tumor growth. However, the ingestion of LAA inhibited tumor growth, and its combination with glucose promoted skeletal muscle integrity and function, without stimulating tumor growth. These findings suggest novel strategies for the prevention of skeletal muscle atrophy.博士（医学）・甲第733号・令和2年3月16日© 2019 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License(https://creativecommons.org/licenses/by-nc/4.0/), which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes

The Novel Monoclonal Antibody 9F5 Reveals Expression of a Fragment of GPNMB/Osteoactivin Processed by Furin-like Protease(s) in a Subpopulation of Microglia in Neonatal Rat Brain

To differentiate subtypes of microglia (MG), we developed a novel monoclonal antibody, 9F5, against one subtype (type 1) of rat primary MG. The 9F5 showed high selectivity for this cell type in Western blot and immunocytochemical analyses and no cross‐reaction with rat peritoneal macrophages (Mφ). We identified the antigen molecule for 9F5: the 50‐ to 70‐kDa fragments of rat glycoprotein nonmetastatic melanoma protein B (GPNMB)/osteoactivin, which started at Lys170. In addition, 9F5 immunoreactivity with GPNMB depended on the activity of furin‐like protease(s). More important, rat type 1 MG expressed the GPNMB fragments, but type 2 MG and Mφ did not, although all these cells expressed mRNA and the full‐length protein for GPNMB. These results suggest that 9F5 reactivity with MG depends greatly on cleavage of GPNMB and that type 1 MG, in contrast to type 2 MG and Mφ, may have furin‐like protease(s) for GPNMB cleavage. In neonatal rat brain, amoeboid 9F5+ MG were observed in specific brain areas including forebrain subventricular zone, corpus callosum, and retina. Double‐immunοstaining with 9F5 antibody and anti‐Iba1 antibody, which reacts with MG throughout the CNS, revealed that 9F5+ MG were a portion of Iba1+ MG, suggesting that MG subtype(s) exist in vivo. We propose that 9F5 is a useful tool to discriminate between rat type 1 MG and other subtypes of MG/Mφ and to reveal the role of the GPNMB fragments during developing brain