Via-switch FPGA with transistor-free programmability enabling energy-efficient near-memory parallel computation

We are developing field-programmable gate arrays (FPGAs) with a new non-volatile switch called via-switch. In via-switch FPGAs (VS-FPGAs), the via-switches required for reconfiguration are placed in the routing layer so that the entire transistor layer can be utilized for computing, and higher implementation density can be achieved compared to conventional SRAM FPGAs. Furthermore, since arithmetic units and memories for computing can be placed under the via-switch crossbar for routing, large-scale parallel operations can be realized where the memory and the arithmetic unit are adjacent to each other. These features enable operation with high energy efficiency. This article reports 65 nm prototype fabrication results and predicted the performance of the VS-FPGA designed for AI applications. We also present the developed application mapping flow and crossbar programming method. The VS-FPGA closes the gap between FPGA and application-specific integrated circuits (ASIC) with the performance advantage of the via-switch and via-switch copy scheme for FPGA-to-ASIC migration, contributing to the expansion of the FPGA usage

Star formation in self-gravitating disks in active galactic nuclei. I. Metallicity gradients in broad line regions

It has been suggested that the high metallicity generally observed in active galactic nuclei (AGNs) and quasars originates from ongoing star formation in the self-gravitating part of accretion disks around the supermassive black holes. We designate this region as the star forming (SF) disk, in which metals are produced from supernova explosions (SNexp) while at the same time inflows are driven by SNexp-excited turbulent viscosity to accrete onto the SMBHs. In this paper, an equation of metallicity governed by SNexp and radial advection is established to describe the metal distribution and evolution in the SF disk. We find that the metal abundance is enriched at different rates at different positions in the disk, and that a metallicity gradient is set up that evolves for steady-state AGNs. Metallicity as an integrated physical parameter can be used as a probe of the SF disk age during one episode of SMBH activity. In the SF disk, evaporation of molecular clouds heated by SNexp blast waves unavoidably forms hot gas. This heating is eventually balanced by the cooling of the hot gas, but we show that the hot gas will escape from the SF disk before being cooled, and diffuse into the BLRs forming with a typical rate of \sim 1\sunmyr. The diffusion of hot gas from a SF disk depends on ongoing star formation, leading to the metallicity gradients in BLR observed in AGNs. We discuss this and other observable consequences of this scenario.Comment: 11 pages, 5 Figures, ApJ, Vol. 737, in pres

siRNAs compete with miRNAs for methylation by HEN1 in Arabidopsis

Plant microRNAs (miRNAs) and small interfering RNAs (siRNAs) bear a 2′-O-methyl group on the 3′-terminal nucleotide. This methyl group is post-synthetically added by the methyltransferase protein HEN1 and protects small RNAs from enzymatic activities that target the 3′-OH. A mutagenesis screen for suppressors of the partial loss-of-function hen1-2 allele in Arabidopsis identified second-site mutations that restore miRNA methylation. These mutations affect two subunits of the DNA-dependent RNA polymerase IV (Pol IV), which is essential for the biogenesis of 24 nt endogenous siRNAs. A mutation in RNA-dependent RNA polymerase 2, another essential gene for the biogenesis of endogenous 24-nt siRNAs, also rescued the defects in miRNA methylation of hen1-2, revealing a previously unsuspected, negative influence of siRNAs on HEN1-mediated miRNA methylation. In addition, our findings imply the existence of a negative modifier of HEN1 activity in the Columbia genetic background

TRANSPORT AND TRANSFORMATION OF CHEMICAL COMPONENTS IN THE GROUNDWATER FLOW SYSTEM OF JAKARTA METROPOLITAN AREA

ABSTRACT The aim of this study is to examine the transport and transformation of chemical components within the groundwater flow in Jakarta area, and to evaluate the effects of accelerated urbanization on it. The collected data showed that the current hydraulic potential in the Jakarta metropolitan area is below sea level because of prior excess abstraction of groundwater. The distribution of Cl- and Mn2- concentration in groundwater suggests that the decline in hydraulic potential has caused the intrusion of seawater to shallow groundwater and the movement of shallow groundwater into deep groundwater. It implies an accumulation of contaminants in deep aquifers. On the other hands, the presentation of NO3--N in groundwater is suggested to be attenuated by the processes of denitrification and dilution in the coastal area

A subgroup of SGS3-like proteins act redundantly in RNA-directed DNA methylation

Plant specific SGS3-like proteins are composed of various combinations of an RNA-binding XS domain, a zinc-finger zf-XS domain, a coil–coil domain and a domain of unknown function called XH. In addition to being involved in de novo 2 (IDN2) and SGS3, the Arabidopsis genome encodes 12 uncharacterized SGS3-like proteins. Here, we show that a group of SGS3-like proteins act redundantly in RNA-directed DNA methylation (RdDM) pathway in Arabidopsis. Transcriptome co-expression analyses reveal significantly correlated expression of two SGS3-like proteins, factor of DNA methylation 1 (FDM1) and FDM2 with known genes required for RdDM. The fdm1 and fdm2 double mutations but not the fdm1 or fdm2 single mutations significantly impair DNA methylation at RdDM loci, release transcriptional gene silencing and dramatically reduce the abundance of siRNAs originated from high copy number repeats or transposons. Like IDN2 and SGS3, FDM1 binds dsRNAs with 5′ overhangs. Double mutant analyses also reveal that IDN2 and three uncharacterized SGS3-like proteins FDM3, FDM4 and FDM5 have overlapping function with FDM1 in RdDM. Five FDM proteins and IDN2 define a group of SGS3-like proteins that possess all four-signature motifs in Arabidopsis. Thus, our results demonstrate that this group of SGS3-like proteins is an important component of RdDM. This study further enhances our understanding of the SGS3 gene family and the RdDM pathway

Trapping of CDC42 C-terminal variants in the Golgi drives pyrin inflammasome hyperactivation

CDC42-C末端異常症に於ける炎症病態を解明 --ゴルジ体への異常蓄積がパイリンインフラマソーム形成を過剰促進--. 京都大学プレスリリース. 2022-05-02.Mutations in the C-terminal region of the CDC42 gene cause severe neonatal-onset autoinflammation. Effectiveness of IL-1β–blocking therapy indicates that the pathology involves abnormal inflammasome activation; however, the mechanism underlying autoinflammation remains to be elucidated. Using induced-pluripotent stem cells established from patients carrying CDC42[R186C], we found that patient-derived cells secreted larger amounts of IL-1β in response to pyrin-activating stimuli. Aberrant palmitoylation and localization of CDC42[R186C] protein to the Golgi apparatus promoted pyrin inflammasome assembly downstream of pyrin dephosphorylation. Aberrant subcellular localization was the common pathological feature shared by CDC42 C-terminal variants with inflammatory phenotypes, including CDC42[*192C*24] that also localizes to the Golgi apparatus. Furthermore, the level of pyrin inflammasome overactivation paralleled that of mutant protein accumulation in the Golgi apparatus, but not that of the mutant GTPase activity. These results reveal an unexpected association between CDC42 subcellular localization and pyrin inflammasome activation that could pave the way for elucidating the mechanism of pyrin inflammasome formation

First Data Release of the Hyper Suprime-Cam Subaru Strategic Program

The Hyper Suprime-Cam Subaru Strategic Program (HSC-SSP) is a three-layered imaging survey aimed at addressing some of the most outstanding questions in astronomy today, including the nature of dark matter and dark energy. The survey has been awarded 300 nights of observing time at the Subaru Telescope and it started in March 2014. This paper presents the first public data release of HSC-SSP. This release includes data taken in the first 1.7 years of observations (61.5 nights) and each of the Wide, Deep, and UltraDeep layers covers about 108, 26, and 4 square degrees down to depths of i~26.4, ~26.5, and ~27.0 mag, respectively (5sigma for point sources). All the layers are observed in five broad bands (grizy), and the Deep and UltraDeep layers are observed in narrow bands as well. We achieve an impressive image quality of 0.6 arcsec in the i-band in the Wide layer. We show that we achieve 1-2 per cent PSF photometry (rms) both internally and externally (against Pan-STARRS1), and ~10 mas and 40 mas internal and external astrometric accuracy, respectively. Both the calibrated images and catalogs are made available to the community through dedicated user interfaces and database servers. In addition to the pipeline products, we also provide value-added products such as photometric redshifts and a collection of public spectroscopic redshifts. Detailed descriptions of all the data can be found online. The data release website is https://hsc-release.mtk.nao.ac.jp/.Comment: 34 pages, 20 figures, 7 tables, moderate revision, accepted for publication in PAS

Extracellular Release of HMGB1 as an Early Potential Biomarker for the Therapeutic Response in a Xenograft Model of Boron Neutron Capture Therapy

Boron neutron capture therapy (BNCT) is a non-invasive therapeutic technique for treating malignant tumors, however, methods to evaluate its therapeutic efficacy and adverse reactions are lacking. High mobility group box 1 (HMGB1) is an inflammatory molecule released during cell death. Therefore, we aimed to investigate HMGB1 as a biomarker for BNCT response, by examining the early responses of tumor cells to 10B-boronophenylalanine (BPA)-based BNCT in the Kyoto University Nuclear Reactor. Extracellular HMGB1 release was significantly increased in human squamous carcinoma SAS and melanoma A375 cells 24 h after neutron irradiation but not after γ-irradiation. At 3 days post-BPA-based BNCT irradiation in a SAS xenograft mouse model, plasma HMGB1 levels were higher than those in the non-irradiation control, and HMGB1 was detected in both nuclei and cytoplasm in tumor cells. Additionally, increased plasma HMGB1 levels post-BNCT irradiation were detected even when tumors decreased in size. Collectively, these results indicate that the extracellular HMGB1 release occurs at an early stage and is persistent when tumors are reduced in size; therefore, it is a potential biomarker for evaluating the therapeutic response during BNCT

The Non-Catalytic Carboxyl-Terminal Domain of ARFGAP1 Regulates Actin Cytoskeleton Reorganization by Antagonizing the Activation of Rac1

The regulation of the actin cytoskeleton and membrane trafficking is coordinated in mammalian cells. One of the regulators of membrane traffic, the small GTP-binding protein ARF1, also activates phosphatidylinositol kinases that in turn affect actin polymerization. ARFGAP1 is a GTPase activating protein (GAP) for ARF1 that is found on Golgi membranes. We present evidence that ARFGAP1 not only serves as a GAP for ARF1, but also can affect the actin cytoskeleton.As cells attach to a culture dish foci of actin appear prior to the cells flattening and spreading. We have observed that overexpression of a truncated ARFGAP1 that lacks catalytic activity for ARF, called GAP273, caused these foci to persist for much longer periods than non-transfected cells. This phenomenon was dependent on the level of GAP273 expression. Furthermore, cell spreading after re-plating or cell migration into a previously scraped area was inhibited in cells transfected with GAP273. Live cell imaging of such cells revealed that actin-rich membrane blebs formed that seldom made protrusions of actin spikes or membrane ruffles, suggesting that GAP273 interfered with the regulation of actin dynamics during cell spreading. The over-expression of constitutively active alleles of ARF6 and Rac1 suppressed the effect of GAP273 on actin. In addition, the activation of Rac1 by serum, but not that of RhoA or ARF6, was inhibited in cells over-expressing GAP273, suggesting that Rac1 is a likely downstream effector of ARFGAP1. The carboxyl terminal 65 residues of ARFGAP1 were sufficient to produce the effects on actin and cell spreading in transfected cells and co-localized with cortical actin foci.ARFGAP1 functions as an inhibitor upstream of Rac1 in regulating actin cytoskeleton. In addition to its GAP catalytic domain and Golgi binding domain, it also has an actin regulation domain in the carboxyl-terminal portion of the protein