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Chiral symmetry and its spontaneous breaking is an essential property of the QCD vacuum and is closely related to the generation of hadron mass. J-PARC E16 experiment measures dielectron spectra in p+A collisions at 30~GeV to study the in-medium spectral change of vector mesons that signals the partial restoration of the broken symmetry. The experiment uses the primary proton beam available at the high-momentum beam line of the J-PARC hadron experimental facility.We performed three proton-beam runs intended for beamline and detector commissioning. We are preparing for the next commissioning run in 2023 and the first physics run. We present the experimental setup, some of the expected results, preparation status, and some findings in the commissioning runs.

J-PARC E16 is an experiment to examine the origin of hadron mass through a systematic measurement of spectral changes of vector mesons in nuclei. The measurement of $e^{+}e^{-}$ pairs from the decay of vector mesons will provide the information of the partial restoration of the chiral symmetry in a normal nuclear density. To resolve a pulse pile-up and achieve good discrimination of $e^{+}$ and $e^{-}$ from the background of a reaction rate of an order of 10 MHz, the data acquisition (DAQ) system uses waveform sampling chips of APV25 and DRS4. The trigger rate and data rate are expected to be 1 kHz and 120–330 MiB/s, respectively. The DAQ system for readout of APV25 and DRS4 were developed, where events were synchronized by common trigger and tag data. The first commissioning in beam, called Run-0a, was performed in June 2020 with about 1/4 of the designed setup. The DAQ worked with a trigger rate of 300 Hz in the Run-0a and the main bottleneck was a large data size of APV25. Further optimization of the DAQ system will improve the performance.

Plasmodium falciparum causes the most severe form of malaria. Acquired immunity against P. falciparum provides insufficient protection even after repeated infections. Therefore, P. falciparum parasites might exploit inhibitory receptors for immune evasion. P. falciparum RIFINs are products of a multigene family consisting of 150–200 genes. Previously, we demonstrated that some RIFINs downregulate the immune response through the leukocyte immunoglobulin-like receptor (LILR) family inhibitory receptor, LILRB1, and leukocyte-associated immunoglobulin-like receptor 1, LAIR1. In this study, we further analyzed the expression of inhibitory receptor ligands on P. falciparum-infected erythrocytes and found that P. falciparum-infected erythrocytes expressed ligands for another LILR family inhibitory receptor, LILRB2, that recognizes HLA class I molecules as a host ligand. Furthermore, we identified that a specific RIFIN was a ligand for LILRB2 by using a newly developed RIFIN expression library. In addition, the domain 3 of LILRB2 was involved in RIFIN binding, whereas the domains 1 and 2 of LILRB2 were involved in the binding to HLA class I molecules. These results suggest that inhibitory receptor LILRB2 is also targeted by RIFIN for immune evasion of P. falciparum similar to LILRB1 and LAIR1.

Many patients with severe COVID-19 suffer from pneumonia, and thus elucidation of the mechanisms underlying the development of such severe pneumonia is important. The ORF8 protein is a secreted protein of SARS-CoV-2, whose in vivo function is not well understood. Here, we analyzed the function of ORF8 protein by generating ORF8-knockout SARS-CoV-2. We found that the lung inflammation observed in wild-type SARS-CoV-2-infected hamsters was decreased in ORF8-knockout SARS-CoV-2-infected hamsters. Administration of recombinant ORF8 protein to hamsters also induced lymphocyte infiltration into the lungs. Similar pro-inflammatory cytokine production was observed in primary human monocytes treated with recombinant ORF8 protein. Furthermore, we demonstrate that the serum ORF8 protein levels are correlated well with clinical markers of inflammation. These results demonstrated that the ORF8 protein is a viral cytokine of SARS-CoV-2 involved in the in the immune dysregulation observed in COVID-19 patients, and that the ORF8 protein could be a novel therapeutic target in severe COVID-19 patients.

This paper presents a drowsiness detection model that is capable of sensing the entire range of stages of drowsiness, from weak to strong. The key assumption underlying our approach is that the sitting posture-related index can indicate weak drowsiness that drivers themselves do not notice. We first determined the sensitivity of the posture index and conventional indices for the stages of drowsiness. Then, we designed a drowsiness detection model combining several indices sensitive to weak drowsiness and to strong drowsiness, to cover all drowsiness stages. Subsequently, the model was trained and evaluated on a dataset comprised of data collected from approximately 50 drivers in simulated driving experiments. The results indicated that posture information improved the accuracy of weak drowsiness detection, and our proposed model using the driver’s blink and posture information covered all stages of drowsiness (F1-score 53.6%, root mean square error 0.620). Future applications of this model include not only warning systems for dangerously drowsy drivers but also systems which can take action before their drivers become drowsy. Since measuring the information requires no restrictive equipment such as on-body electrodes, the model presented here based on blink and posture information can be used in several practical applications.

Specific MHC class II alleles are strongly associated with susceptibility to various autoimmune diseases. Although the primary function of MHC class II molecules is to present peptides to helper T cells, MHC class II molecules also function like a chaperone to transport misfolded intracellular proteins to the cell surface. In this study, we found that autoantibodies in patients with Graves’ disease preferentially recognize thyroid-stimulating hormone receptor (TSHR) complexed with MHC class II molecules of Graves’ disease risk alleles, suggesting that the aberrant TSHR transported by MHC class II molecules is the target of autoantibodies produced in Graves’ disease. Mice injected with cells expressing mouse TSHR complexed with MHC class II molecules, but not TSHR alone, produced anti-TSHR autoantibodies. These findings suggested that aberrant self-antigens transported by MHC class II molecules exhibit antigenic properties that differ from normal self-antigens and abrogate self-tolerance, providing a novel mechanism for autoimmunity.

Breakthrough infection is often observed for the SARS-CoV-2 Delta variant, and neutralizing antibody levels are associated with vaccine efficiency1. Recent studies revealed that not only anti-receptor binding domain (RBD) antibodies2 but also antibodies against the N-terminal domain (NTD) play important roles in positively3,4 or negatively4-8 controlling SARS-CoV-2 infectivity. Here, we found that the Delta variant completely escaped from anti-NTD neutralizing antibodies, while increasing responsiveness to anti-NTD infectivity-enhancing antibodies. Cryo-EM analysis of the Delta spike revealed that epitopes for anti-NTD neutralizing antibodies are structurally divergent, whereas epitopes for enhancing antibodies are well conserved with wild-type spike protein. Although Pfizer-BioNTech BNT162b2-immune sera neutralized the original Delta variant, when major anti-RBD neutralizing antibody epitopes remaining in the Delta variant were disrupted, some BNT162b2-immune sera not only lost neutralizing activity but became infection-enhanced. The enhanced infectivity disappeared when the Delta NTD was substituted with the wild-type NTD. Sera of mice immunized by Delta spike, but not wild-type spike, consistently neutralized the Delta variant lacking anti-RBD antibody epitopes without enhancing infectivity. Importantly, SARS-CoV-2 variants with similar mutations in the RBD have already emerged according to the GISAID database and their pseudoviruses were resistant to some BNT162b2-immune sera. These findings demonstrate that mutations in the NTD, as well as the RBD, play an important role in antibody escape by SARS-CoV-2. Development of effective vaccines against emerging variants will be necessary, not only to protect against infection, but also to prevent further mutation of SARS-CoV-2.

Litter decomposition in serpentine ecosystems has been studied solely addressing heavy metals like Ni. We aimed to show how leaf nutrients, cell-wall components and lamina mass per area and microbial communities affect litter decomposition in a cool-temperate serpentine ecosystem. Reciprocal transplant leaf-litter decomposition was observed in three tree species (Clethra barbinervis, Magnolia obovata, and Quercus serrata) common to serpentine and non-serpentine ecosystems. Thirteen litter quality variables of the initial litter and microbial respirations from decomposed litter were assessed. Litter from the serpentine ecosystem decomposed slower than that from the non-serpentine ecosystem. Compared with all species, C. barbinervis showed high heavy metal concentration, cellulose content, and lamina dry mass per area; M. obovata showed low Ca concentration; and Q. serrata exhibited high lignin/N ratio in litter from the serpentine ecosystem. Litter placed in the serpentine site decomposed faster than that placed in the non-serpentine site, but basal microbial respiration rates from litter did not differ between decomposition sites. Litter from serpentine ecosystems adversely influenced decomposition rate owing to its diverse recalcitrant litter quality. Our study suggested the feasibility of litter quality evaluation based on multiple litter traits for better-understanding of litter decomposition in serpentine ecosystems.

mRNA-based vaccines provide effective protection against most common SARS-CoV-2 variants. However, identifying likely breakthrough variants is critical for future vaccine development. Here, we found that the Delta variant completely escaped from anti-N-terminal domain (NTD) neutralizing antibodies, while increasing responsiveness to anti-NTD infectivity-enhancing antibodies. Although Pfizer-BioNTech BNT162b2-immune sera neutralized the Delta variant, when four common mutations were introduced into the receptor binding domain (RBD) of the Delta variant (Delta 4+), some BNT162b2-immune sera lost neutralizing activity and enhanced the infectivity. Unique mutations in the Delta NTD were involved in the enhanced infectivity by the BNT162b2-immune sera. Sera of mice immunized by Delta spike, but not wild-type spike, consistently neutralized the Delta 4+ variant without enhancing infectivity. Given the fact that a Delta variant with three similar RBD mutations has already emerged according to the GISAID database, it is necessary to develop vaccines that protect against such complete breakthrough variants.

SARS-CoV-2 infection causes severe symptoms in a subset of patients, suggesting the presence of certain unknown risk factors. Although antibodies against the receptor-binding domain (RBD) of the SARS-CoV-2 spike have been shown prevent SARS-CoV-2 infection, the effects of antibodies against other spike protein domains are largely unknown. Here, we screened a series of anti-spike monoclonal antibodies from COVID-19 patients, and found that some of antibodies against the N-terminal domain (NTD) dramatically enhanced the binding capacity of the spike protein to ACE2, and thus increased SARS-CoV2 infectivity. Surprisingly, mutational analysis revealed that all the infectivity-enhancing antibodies recognized a specific site on the surface of the NTD. The antibodies against this infectivity-enhancing site were detected in all samples of hospitalized COVID-19 patients in the study. However, the ratio of infectivity-enhancing antibodies to neutralizing antibodies differed among patients. Furthermore, the antibodies against the infectivity-enhancing site were detected in 3 out of 48 uninfected donors, albeit at low levels. These findings suggest that the production of antibodies against SARS-CoV-2 infectivity-enhancing site could be considered as a possible exacerbating factors for COVID-19 and that a spike protein lacking such antibody epitopes may be required for safe vaccine development, especially for individuals with pre-existing enhancing antibodies.

Major histocompatibility complex class II (MHC II) molecules are mainly expressed on antigen presentation cells and play an important role in immune response. It has been reported that MHC II molecules are also detected in serum as a soluble form (sMHC II molecules), and they are considered to be involved in the maintenance of self-tolerance. However, the mechanism by which sMHC II molecules are produced remains unclear. Invariant chain (Ii), also called CD74, plays an important role in antigen presentation of MHC II molecules. In the present study, we analyzed the role of Ii on the production of sMHC II molecules. We found that the amount of sMHC II molecules in serum was decreased in Ii-deficient mice compared to wild-type mice. sMHC II molecules were secreted from cells transfected with MHC II molecules and Ii but not from cells transfected with MHC II molecules alone. Moreover, isoform p41 of Ii-transfected cells induced more sMHC II molecules compared to isoform p31-transfected cells. The molecular weight of sMHC II molecules from MHC II and Ii p41-transfected cells was approximately 60 kDa, indicating that sMHC II molecules are a single heterodimer of α and β chains that is not associated with micro-vesicles. From the analysis of Ii-deletion mutants, we found that the luminal domain of Ii p41 is crucial for the production of sMHC II molecules. These results suggested that Ii has an important role in production of sMHC II molecules.

An experiment at J-PARC, E16 experiment, which aims to measure the spectral modification of vector meson in nuclear matter is planned. The experiment will measure light vector mesons (ρ/ω/ϕ mesons) generated in nuclear target through the 30 GeV p+A reactions. The mass spectra can be reconstructed with e^+e^− pairs originating from their decays. The spectral modification in finite baryon density is studied systematically. The detail of the experimental plan and expected results are presented with a particular focus on first physics run.

Antibodies against the receptor-binding-domain of the SARS-CoV-2 spike protein prevent SARS-CoV-2 infection. However, the effects of antibodies against other spike protein domains are largely unknown. Here, we screened a series of anti-spike monoclonal antibodies from COVID-19 patients, and found that some of antibodies against the N-terminal-domain (NTD) induced the open conformation of receptor binding domain (RBD) and thus enhanced the binding capacity of the spike protein to ACE2 and infectivity of SARS-CoV-2. Mutational analysis revealed that all the infectivity-enhancing antibodies recognized a specific site on the NTD. Structural analysis demonstrated that all the infectivity-enhancing antibodies bound to NTD in a similar manner. The antibodies against this infectivity-enhancing site were detected at high levels in severe patients. Moreover, we identified antibodies against the infectivity-enhancing site in uninfected donors, albeit at a lower frequency. These findings demonstrate that not only neutralizing antibodies but also enhancing antibodies are produced during SARS-CoV-2 infection., A subset antibodies that are detected in patients with severe COVID-19 target a specific region of the N terminal domain of the spike protein and enhance binding of the virus to the ACE2 receptor.

We constructed a hadron blind detector (HBD) using a finely segmented pad readout. The finely segmented pad readout enabled us to adopt an advanced particle identification method which applies a threshold to the number of pad hits in addition to the total amount of collected charge. The responses of the detector to electrons and pions were evaluated using a negatively charged secondary beam at 1.0 GeV/c containing 20% electrons at the J-PARC K1.1BR beam line. We observed 7.3 photoelectrons per incident electron. Using the advanced particle identification method, an electron detection efficiency of 83% was achieved with a pion rejection factor of 120. The method improved the pion rejection by approximately a factor of five, compared to the one which just applies a threshold to the amount of collected charge. The newly introduced finely segmented pad readout was found to be effective in rejecting pions.

The radial and vertical distributions of radiocesium in tree stems were investigated to understand radiocesium transfer to trees at an early stage of massive contamination from the Fukushima nuclear disaster. A conifer species (Japanese red pine) and a broad-leaved species (Japanese konara oak) were selected to determine whether the radiocesium contamination pattern differs between species. Stem disks were collected at several heights and separated into outer bark, inner bark, and wood. The radiocesium concentration was the highest in the outer bark, followed by that in the inner bark and wood. The vertical distribution of the radiocesium concentration at each stem part differed between the species. The difference between species in radiocesium concentration of the outer bark could be explained by presence or absence of leaves at the time of the disaster. However, the reasons for the differences between species in the radiocesium concentration of the inner bark and wood are unclear. The radial distribution in the wood of the studied species showed a common pattern across stem disk heights and species. However, the radiocesium concentration ratio between sapwood and inner bark was significantly different between species. Although the radial contamination pattern in the wood was similar in the studied species during the early stage of contamination, the radiocesium transport pathway and allocation would be different between the species, and the contamination pattern will likely be different between the species at later stages. Continued investigations are important for understanding the radiocesium cycle and the accumulation of radiocesium in the tree stems of each species.

The J-PARC E16 experiment has been proposed to measure the mass spectrum of ϕ mesons in nuclear matter to study the origin of QCD mass. The ϕ mesons are identified in the e + e − decay channel and the mass of these ϕ mesons is reconstructed using the momenta of the e + and e − pairs. A tracking detector for this experiment is composed of a position sensitive device that employs Gas Electron Multipliers (GEMs) with a two-dimensional readout board. The ionization electrons are amplified with a triple-GEM stack. The required position resolution is 100 μ m up to an incidence angle of 30°. Position resolutions and efficiencies of the tracking device are evaluated using a π − beam with a momentum of 1.0 GeV/ c at the J-PARC K1.1BR beam line. A position resolution of better than 100 μ m is obtained by calculating the center of gravity of the charges on the readout strips when tracks arrive perpendicularly at the detector plane. Timing information of charge clusters is essential to improve the position resolutions for the inclined tracks. The arrival times of the charge clusters are derived from the wave forms collected by flash ADC modules. Using the arrival times of the clusters, the obtained position resolution is better than 100 μ m for the track inclinations of 15° and 30°. The detection efficiency is also investigated as a function of the GEM gains, and the operational voltage is optimized.

A beam profile monitor for 1-GeV region gamma-ray beams has been developed using an X-ray flat panel sensor. In order to increase its sensitivity to gamma-rays, a converter plate was placed on the input window. We tested its sensitivity to input gamma-ray photons with various types of converter plates. The output brightness of the pixels was found to be correlated to the number of electrons and positrons converted from the gamma-ray photons. A measured profile of the 1-GeV region gamma-ray beams obtained with a 1-mm thick lead plate was consistent with the beam profile measured with plastic scintillator hodoscopes. It suggested that the X-ray flat panel sensor was sufficiently applicable to the beam profile monitor for 1-GeV region gamma-ray beams.

Extracellular vesicles (EVs) such as exosomes and microvesicles serve as messengers of intercellular network, allowing exchange of cellular components between cells. EVs carry lipids, proteins and RNAs derived from their producing cells and have potential as biomarkers specific to cell types and even cellular states. However, conventional methods (such as ultracentrifugation or polymeric precipitation) for isolating EVs have disadvantages regarding purity and feasibility. Here, we have developed a novel method for EV purification by using Tim4 protein, which specifically binds the phosphatidylserine displayed on the surface of EVs. Because the binding is Ca2+-dependent, intact EVs can be easily released from Tim4 by adding Ca2+ chelators. Tim4 purification, which we have applied to cell conditioned media and biofluids, is capable of yielding EVs of a higher purity than those obtained using conventional methods. The lower contamination found in Tim4-purified EV preparations allows more EV-specific proteins to be detected by mass spectrometry, enabling better characterization and quantification of different EV populations’ proteomes. Tim4 protein can also be used as a powerful tool for quantification of EVs in both ELISA and flow cytometry formats. Thus, the affinity of Tim4 for EVs will find abundant applications in EV studies.

1 RIKEN Nishina Center, RIKEN, Saitama 351-0198, Japan 2KEK, High Energy Accelerator Research Organization, Ibaraki 305-0801, Japan 3Center for Nuclear Study, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan 4Department of Physics, University of Tokyo, Tokyo 113-0033, Japan 5Japan Synchrotron Radiation Research Institute, Hyogo 679-5198, Japan 6Department of Physics, Kyoto University, Kyoto 113-0033, Japan 7Hiroshima University, Hiroshima 739-8526, Japan 8Research Center for Nuclear Physics, Osaka University, Ibaraki, Osaka 567-0047, Japan

DNA polymerases delta and epsilon (pol delta and epsilon) are the major replicative polymerases and possess 3'-5' proofreading exonuclease activities that correct errors arising during DNA replication in the yeast Saccharomyces cerevisiae. This study measures the fidelity of the holoenzyme of wild-type pol epsilon, the 3'-5' exonuclease-deficient pol2-4, a +1 frameshift mutator for homonucleotide runs, pol2C1089Y, and pol2C1089Y pol2-4 enzymes using a synthetic 30-mer primer/100-mer template. The nucleotide substitution rate for wild-type pol epsilon was 0.47 x 10(-5) for G:G mismatches, 0.15 x 10(-5) for T:G mismatches, and less than 0.01 x 10(-5) for A:G mismatches. The accuracy for A opposite G was not altered in the exonuclease-deficient pol2-4 pol epsilon; however, G:G and T:G misincorporation rates increased 40- and 73-fold, respectively. The pol2C1089Y pol epsilon mutant also exhibited increased G:G and T:G misincorporation rates, 22- and 10-fold, respectively, whereas A:G misincorporation did not differ from that of wild type. Since the fidelity of the double mutant pol2-4 pol2C1089Y was not greatly decreased, these results suggest that the proofreading 3'-5' exonuclease activity of pol2C1089Y pol epsilon is impaired even though it retains nuclease activity and the mutation is not in the known exonuclease domain.

Cesium-137 (137Cs) accumulation by mushrooms and trees was evaluated based on the aggregated transfer factor (T ag) value at one and a half years after the Fukushima Daiichi Nuclear Power Plant accident. Our results suggest that (1) some genera of fungi tend to accumulate more 137Cs than others, (2) not only 137Cs concentration of the substrates but also its availability for fungi is an important factor determining the 137Cs concentration in mushrooms and (3) ectomycorrhizal fungi do not necessarily enhance 137Cs uptake by host plants when compared to arbuscular mycorrhizal fungi.

The yeast Saccharomyces cerevisiaeCdc7p/Dbf4p protein kinase complex was purified to near homogeneity from insect cells. The complex efficiently phosphorylated yeast Mcm2p and less efficiently the remaining Mcm proteins or other replication proteins. Significantly, when pretreated with alkaline phosphatase, Mcm2p became completely inactive as a substrate, suggesting that it must be phosphorylated by other protein kinase(s) to be a substrate for the Cdc7p/Dbf4p complex. Mutant Cdc7p/Dbf4p complexes containing either Cdc7-1p or Dbf4-1∼5p were also partially purified from insect cells and characterized in vitro. Furthermore, the autonomously replicating sequence binding activity of variousdbf4 mutants was also analyzed. These studies suggest that the autonomously replicating sequence-binding and Cdc7p protein kinase activation domains of Dbf4p collaborate to form an active Cdc7p/Dbf4p complex and function during S phase in S. cerevisiae. It is shown that Rad53p phosphorylates the Cdc7p/Dbf4p complex in vitro and that this phosphorylation greatly inhibits the kinase activity of Cdc7p/Dbf4p. This result suggests that Rad53p controls the initiation of chromosomal DNA replication by regulating the protein kinase activity associated with the Cdc7p/Dbf4p complex.

Resection of DNA double-strand break (DSB) ends, which results in 3(') single-stranded tails, is an early event of DSB repair and can be a critical determinant in choice of repair pathways and eventual genome stability. Current techniques for examining resection are restricted to model in vivo systems with defined substrates (i.e., HO-endonuclease targets). We present here a robust assay that can analyze not only the resection of site-specific DSBs which typically have "clean" double-strand ends but also random "dirty-ended" DSBs such as those generated by ionizing radiation and chemotherapeutic agents. The assay is based on our finding that yeast chromosomes with single-stranded DNA tails caused by resection are less mobile during pulsed-field gel electrophoresis (PFGE) than those without a tail. In combination with the use of a circular chromosome and enzymatic trimming of single-stranded DNA, resection of random DSBs can be easily detected and analyzed. This mobility-shift assay provides a unique opportunity to examine the mechanisms of resection, early events in DSB repair, as well as factors involved in pathway regulation.

The continuity of duplex DNA is generally considered a prerequisite for chromosome continuity. However, as previously shown in yeast as well as human cells, the introduction of a double-strand break (DSB) does not generate a chromosome break (CRB) in yeast or human cells. The transition from DSB to CRB was found to be under limited control by the tethering function of the RAD50/MRE11/XRS2 (MRX) complex. Using a system for differential fluorescent marking of both sides of an endonuclease-induced DSB in single cells, we found that nearly all DSBs are converted to CRBs in cells lacking both exonuclease 1 (EXO1) activity and MRX complex. Thus, it appears that some feature of exonuclease processing or resection at a DSB is critical for maintaining broken chromosome ends in close proximity. In addition, we discovered a thermal sensitive (cold) component to CRB formation in an MRX mutant that has implications for chromosome end mobility and/or end-processing.

The Cdc7–Dbf4 complex is a conserved serine/threonine protein kinase essential for the initiation of eukaryotic DNA replication. Although an mcm5–bob1 mutation bypasses lethality conferred by mutations in CDC7 or DBF4, the Δcdc7 mcm5–bob1 mutant is sensitive to hydroxyurea (HU), which induces replication stress. To elucidate the reasons for HU sensitivity conferred by deletion of CDC7, we examined the role of Cdc7–Dbf4 in the replication checkpoint. We found that in Cdc7–Dbf4-deficient cells exposed to replication stress, Rad53 remains in a hypophosphorylated form, anaphase spindle is elongated, and checkpoint-specific transcription is not induced. The hypophosphorylated Rad53 exhibits a low autophosphorylation activity, and recombinant Cdc7–Dbf4 phosphorylates Rad53 in vitro. These results suggest that Cdc7–Dbf4 is required for full activation of Rad53 in response to replication stress.

The J-PARC E16 experiment was proposed to investigate the restoration of chiral symmetry at the normal nuclear density. E16 will systematically measure in-medium mass of vector mesons at J-PARC Hadron Experimental Facility using a 30-GeV proton beam with an intensity of 2 x 1010 protons per pulse. The E16 spectrometer was designed to detect e+e- from slowly moving vector meson, particularly the meson. The detector system consists of GEM tracker, Gas Cerenkov detector based on GEM and electromagnetic calorimeter made of lead-glass, whose number of channels reaches about 100,000 in total. The readout electronics, trigger system and data acquisition system for the detectors have been developed, for which level-1 trigger rate of 1-2 kHz is required under several 10 MHz interaction rate. The preparation is underway for the first beam time in 2017.

At the J-PARC E16 experiment[1], we measure mass spectra of vector mesons in nuclei from the e+e- decay channel with high precision and high statistics. We have developed the trigger system consisting of newly developed ASD ASICs which can extract signals from the GEM foil used as a cathode plane of the induction gap in a GEM chamber and digital electronics using FPGAs which processes binary signals from the ASIC.

DAQ-Middleware is a software framework for network-distributed data acquisition (DAQ) systems. We adopted the framework for the J-PARC E16 experiment, which requires a DAQ bandwidth of more than 660 MB/spill (two-second spill per six-second cycle). We developed a prototype for the DAQ software and confirmed that the prototype's total throughput satisfies the requirements of the experiment.

This manuscript was withdrawn at the request of the authors.

This paper proposes a method of extracting skeleton interactively for 3D character animation. A skeleton is automatically and interactively generated from the object data of 3D models in a process that consists of five steps: 1) transformation into a low polygon model from the original model composed of a large number of polygons; 2) calculation of the sum of the geodesic distance from specific points to all vertices on the 3D model; 3) subdivision of the 3D model using the sum of geodesic distances; 4) generation of skeleton joints (skeleton nodes) on each boundary surface between those subdivision areas; and 5) connection of all skeleton nodes. We also propose a method for flexible skeleton generation using boundary shapes and the sum of geodesic distances. After generating the skeleton, various animations can be created by interpolating key poses created from user manipulation of skeleton joints. Since skeletons can be generated with this method where specified by users, users are expected to create interactively flexible animations of 3D models.

In enterohemorrhagic Escherichia coli, Shiga toxin is produced by lysogenic prophages. We have isolated the prophage VT2-Sa that is responsible for production of Shiga toxin type 2 protein, and determined the complete nucleotide sequence of this phage DNA. The entire DNA sequence consisted of 60,942 bp, exhibiting marked similarity to the 933W phage genome. However, several differences were observed in the immunity and replication regions, where cI, cII, cIII, N, cro, O, and P genes were present: Predicted amino acid sequences of N, cI, cro, O and P in the VT2-Sa genome did not show significant similarity to the counterparts of the 933W genome; however its cI showed higher similarity to lambda. Furthermore, O and P closely resembled those of phage HK022. These observations suggest that the various degrees of homology observed in the immunity and replication regions of VT2-Sa could have resulted from frequent recombination events among the lambdoid phages, and that these regions play a key role as a functional unit for phage propagation in competition with other lambdoid phages.