58 research outputs found

    Double-Free-Layer Stochastic Magnetic Tunnel Junctions with Synthetic Antiferromagnets

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    Stochastic magnetic tunnel junctions (sMTJ) using low-barrier nanomagnets have shown promise as fast, energy-efficient, and scalable building blocks for probabilistic computing. Despite recent experimental and theoretical progress, sMTJs exhibiting the ideal characteristics necessary for probabilistic bits (p-bit) are still lacking. Ideally, the sMTJs should have (a) voltage bias independence preventing read disturbance (b) uniform randomness in the magnetization angle between the free layers, and (c) fast fluctuations without requiring external magnetic fields while being robust to magnetic field perturbations. Here, we propose a new design satisfying all of these requirements, using double-free-layer sMTJs with synthetic antiferromagnets (SAF). We evaluate the proposed sMTJ design with experimentally benchmarked spin-circuit models accounting for transport physics, coupled with the stochastic Landau-Lifshitz-Gilbert equation for magnetization dynamics. We find that the use of low-barrier SAF layers reduces dipolar coupling, achieving uncorrelated fluctuations at zero-magnetic field surviving up to diameters exceeding (D100D\approx 100 nm) if the nanomagnets can be made thin enough (1\approx 1-22 nm). The double-free-layer structure retains bias-independence and the circular nature of the nanomagnets provides near-uniform randomness with fast fluctuations. Combining our full sMTJ model with advanced transistor models, we estimate the energy to generate a random bit as \approx 3.6 fJ, with fluctuation rates of \approx 3.3 GHz per p-bit. Our results will guide the experimental development of superior stochastic magnetic tunnel junctions for large-scale and energy-efficient probabilistic computation for problems relevant to machine learning and artificial intelligence

    Magnetization dynamics and its scattering mechanism in thin CoFeB films with interfacial anisotropy

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    Studies of magnetization dynamics have incessantly facilitated the discovery of fundamentally novel physical phenomena, making steady headway in the development of magnetic and spintronics devices. The dynamics can be induced and detected electrically, offering new functionalities in advanced electronics at the nanoscale. However, its scattering mechanism is still disputed. Understanding the mechanism in thin films is especially important, because most spintronics devices are made from stacks of multilayers with nanometer thickness. The stacks are known to possess interfacial magnetic anisotropy, a central property for applications, whose influence on the dynamics remains unknown. Here, we investigate the impact of interfacial anisotropy by adopting CoFeB/MgO as a model system. Through systematic and complementary measurements of ferromagnetic resonance (FMR), on a series of thin films, we identify narrower FMR linewidths at higher temperatures. We explicitly rule out the temperature dependence of intrinsic damping as a possible cause, and it is also not expected from existing extrinsic scattering mechanisms for ferromagnets. We ascribe this observation to motional narrowing, an old concept so far neglected in the analyses of FMR spectra. The effect is confirmed to originate from interfacial anisotropy, impacting the practical technology of spin-based nanodevices up to room temperature.Comment: 23 pages,3 figure

    Giant voltage control of spin Hall nano-oscillator damping

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    Spin Hall nano-oscillators (SHNOs) are emerging spintronic devices for microwave signal generation and oscillator based neuromorphic computing combining nano-scale footprint, fast and ultra-wide microwave frequency tunability, CMOS compatibility, and strong non-linear properties providing robust large-scale mutual synchronization in chains and two-dimensional arrays. While SHNOs can be tuned via magnetic fields and the drive current, neither approach is conducive for individual SHNO control in large arrays. Here, we demonstrate electrically gated W/CoFeB/MgO nano-constrictions in which the voltage-dependent perpendicular magnetic anisotropy, tunes the frequency and, thanks to nano-constriction geometry, drastically modifies the spin-wave localization in the constriction region resulting in a giant 42 % variation of the effective damping over four volts. As a consequence, the SHNO threshold current can be strongly tuned. Our demonstration adds key functionality to nano-constriction SHNOs and paves the way for energy-efficient control of individual oscillators in SHNO chains and arrays for neuromorphic computing

    CMOS + stochastic nanomagnets: heterogeneous computers for probabilistic inference and learning

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    Extending Moore's law by augmenting complementary-metal-oxide semiconductor (CMOS) transistors with emerging nanotechnologies (X) has become increasingly important. Accelerating Monte Carlo algorithms that rely on random sampling with such CMOS+X technologies could have significant impact on a large number of fields from probabilistic machine learning, optimization to quantum simulation. In this paper, we show the combination of stochastic magnetic tunnel junction (sMTJ)-based probabilistic bits (p-bits) with versatile Field Programmable Gate Arrays (FPGA) to design a CMOS + X (X = sMTJ) prototype. Our approach enables high-quality true randomness that is essential for Monte Carlo based probabilistic sampling and learning. Our heterogeneous computer successfully performs probabilistic inference and asynchronous Boltzmann learning, despite device-to-device variations in sMTJs. A comprehensive comparison using a CMOS predictive process design kit (PDK) reveals that compact sMTJ-based p-bits replace 10,000 transistors while dissipating two orders of magnitude of less energy (2 fJ per random bit), compared to digital CMOS p-bits. Scaled and integrated versions of our CMOS + stochastic nanomagnet approach can significantly advance probabilistic computing and its applications in various domains by providing massively parallel and truly random numbers with extremely high throughput and energy-efficiency

    発症早期ALS患者に対する超高用量メチルコバラミンの有効性・安全性について : ランダム化比較試験

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    Importance: Post hoc analysis in a phase 2/3 trial indicated ultra-high dose methylcobalamin slowed decline of the Revised Amyotrophic Lateral Sclerosis Functional Rating Scale (ALSFRS-R) total score at week 16 as well as at week 182, without increase of adverse events, in patients with amyotrophic lateral sclerosis (ALS) who were enrolled within 1 year from onset. Objective: To validate the efficacy and safety of ultra-high dose methylcobalamin for patients with ALS enrolled within 1 year of onset. Design: A multicenter, placebo-controlled, double-blind, randomized phase 3 trial with 12-week observation and 16-week randomized period, conducted from October 2017 to September 2019. Setting: Twenty-five neurology centers in Japan. Participants: Patients with ALS diagnosed within 1 year of onset by the updated Awaji criteria were initially enrolled. Of those, patients fulfilling the following criteria after 12-week observation were eligible for randomization: 1- or 2-point decrease in ALSFRS-R total score, a percent forced vital capacity over 60%, no history of noninvasive respiratory support and tracheostomy, and being ambulant. The target number was 64 in both methylcobalamin and placebo groups. Of 203 patients enrolled in the observation, 130 patients (age, 61.0 ± 11.7 years; female, 56) met the criteria and were randomly assigned through an electronic web-response system to methylcobalamin or placebo (65 for each). Of these, 129 patients were eligible for the full analysis set, and 126 completed the double-blind stage. Interventions: Intramuscular injection of methylcobalamin 50 mg or placebo twice weekly for 16 weeks. Main outcomes and measures: The primary endpoint was change in ALSFRS-R total score from baseline to week 16 in the full analysis set. Results: The least-squares mean difference in ALSFRS-R total score at week 16 of the randomized period was 1.97 points greater with methylcobalamin than placebo (−2.66 versus −4.63; 95% CI, 0.44–3.50; P = 0.012). The incidence of adverse events was similar between the two groups. Conclusions and relevance: Ultra-high dose methylcobalamin was efficacious in slowing functional decline and safe in the 16-week treatment period in ALS patients in the early stage and with moderate progression rate. Trial registration: UMIN-CTR Identifier: UMIN000029588 (umin.ac.jp/ctr); ClinicalTrials.gov Identifier: NCT03548311 (clinicaltrials.gov

    The whole blood transcriptional regulation landscape in 465 COVID-19 infected samples from Japan COVID-19 Task Force

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    「コロナ制圧タスクフォース」COVID-19患者由来の血液細胞における遺伝子発現の網羅的解析 --重症度に応じた遺伝子発現の変化には、ヒトゲノム配列の個人差が影響する--. 京都大学プレスリリース. 2022-08-23.Coronavirus disease 2019 (COVID-19) is a recently-emerged infectious disease that has caused millions of deaths, where comprehensive understanding of disease mechanisms is still unestablished. In particular, studies of gene expression dynamics and regulation landscape in COVID-19 infected individuals are limited. Here, we report on a thorough analysis of whole blood RNA-seq data from 465 genotyped samples from the Japan COVID-19 Task Force, including 359 severe and 106 non-severe COVID-19 cases. We discover 1169 putative causal expression quantitative trait loci (eQTLs) including 34 possible colocalizations with biobank fine-mapping results of hematopoietic traits in a Japanese population, 1549 putative causal splice QTLs (sQTLs; e.g. two independent sQTLs at TOR1AIP1), as well as biologically interpretable trans-eQTL examples (e.g., REST and STING1), all fine-mapped at single variant resolution. We perform differential gene expression analysis to elucidate 198 genes with increased expression in severe COVID-19 cases and enriched for innate immune-related functions. Finally, we evaluate the limited but non-zero effect of COVID-19 phenotype on eQTL discovery, and highlight the presence of COVID-19 severity-interaction eQTLs (ieQTLs; e.g., CLEC4C and MYBL2). Our study provides a comprehensive catalog of whole blood regulatory variants in Japanese, as well as a reference for transcriptional landscapes in response to COVID-19 infection

    DOCK2 is involved in the host genetics and biology of severe COVID-19

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    「コロナ制圧タスクフォース」COVID-19疾患感受性遺伝子DOCK2の重症化機序を解明 --アジア最大のバイオレポジトリーでCOVID-19の治療標的を発見--. 京都大学プレスリリース. 2022-08-10.Identifying the host genetic factors underlying severe COVID-19 is an emerging challenge. Here we conducted a genome-wide association study (GWAS) involving 2, 393 cases of COVID-19 in a cohort of Japanese individuals collected during the initial waves of the pandemic, with 3, 289 unaffected controls. We identified a variant on chromosome 5 at 5q35 (rs60200309-A), close to the dedicator of cytokinesis 2 gene (DOCK2), which was associated with severe COVID-19 in patients less than 65 years of age. This risk allele was prevalent in East Asian individuals but rare in Europeans, highlighting the value of genome-wide association studies in non-European populations. RNA-sequencing analysis of 473 bulk peripheral blood samples identified decreased expression of DOCK2 associated with the risk allele in these younger patients. DOCK2 expression was suppressed in patients with severe cases of COVID-19. Single-cell RNA-sequencing analysis (n = 61 individuals) identified cell-type-specific downregulation of DOCK2 and a COVID-19-specific decreasing effect of the risk allele on DOCK2 expression in non-classical monocytes. Immunohistochemistry of lung specimens from patients with severe COVID-19 pneumonia showed suppressed DOCK2 expression. Moreover, inhibition of DOCK2 function with CPYPP increased the severity of pneumonia in a Syrian hamster model of SARS-CoV-2 infection, characterized by weight loss, lung oedema, enhanced viral loads, impaired macrophage recruitment and dysregulated type I interferon responses. We conclude that DOCK2 has an important role in the host immune response to SARS-CoV-2 infection and the development of severe COVID-19, and could be further explored as a potential biomarker and/or therapeutic target
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