Vegetation and Socio-economic Structure in Kake-cho, Hiroshima Prefecture

This study analyzed the relationship between rural vegetation and the socioeconomic structure of six villages in Hiroshima Prefecture that consolidated in 1956 to form Kake-cho, a typical mountain town. We measured the area of vegetation in each of the original six villages with a vegetation map (Nakagoshi et al., 1992). A principal component analysis of agricultural and forestry census data from 1970 and 1990 revealed that conifer plantations and deciduous forests were the dominant types of vegetation. The amount of vegetation, 29.7 per square kilometer,[Chris1] was closely related to the agriculture of the region. In 1970, conifer plantations dominated the villages of Kake and Tsubono, but deciduous vegetation and pine forests were more common in the other four villages where farming was the main industry. By 1990, the human population of all six villages had decreased, but the amount of tall vegetation had increased throughout the area. The changes in the amount of vegetation resulted from natural succession, not human activity

自らの意志を表す動詞「やる」 ―日本語母語話者の談話における使われ方と学習者が学ぶべき用法―

「やる」は、日常よく使われる基本語と言える語であるにもかかわらず、初級日本語教科書での扱いは限定的であり、多くの学習者には「やる」の用法を正確に学ぶ機会すら提供されていない。しかし先行研究からは、「やる」には多様な用法があり、特に対象が特定されず使われる場合に自らの意志を表すことがわかる。そこで、日本語母語話者の使用する「やる」を語用論的な角度から分析すると、「発語内の力」が発揮されるという考察に至った。これらを踏まえたうえで、意味論と語用論の側面から「やる」の働きを分類し、日本語教育の学習段階別に「やる」を導入するシラバスを提案する

Electrical storm after cardiac resynchronization therapy in a patient with nonischemic cardiomyopathy: Signal-averaged vector-projected 187-channel electrocardiogram-based risk stratification for lethal arrhythmia

AbstractWe describe treatment of atrial flutter and electrical storm presenting as incessant ventricular tachycardia (VT) after implantation of a cardiac resynchronization therapy defibrillator (CRT-D) in a patient with dilated cardiomyopathy. No prior arrhythmic event had occurred. Our treatment strategy, including amiodarone administration, was guided in part by signal-averaged vector-projected 187-channel electrocardiogram (SAVP-ECG)-based risk stratification for ventricular arrhythmia. Corrected recovery time (RTc) dispersion and Tpeak-end dispersion were used to evaluate transmural dispersion of repolarization. RTc and Tpeak-end dispersion increased during the period of electrical storm. Values were improved 2 years after CRT-D implantation, and the amiodarone was discontinued. The VT has not recurred despite discontinuation of the antiarrhythmic agent. SAVP-ECG-based risk stratification for ventricular arrhythmia proved useful for the management of antiarrhythmic therapy

The Runx1 Transcription Factor Inhibits the Differentiation of Naive CD4+ T Cells into the Th2 Lineage by Repressing GATA3 Expression

Differentiation of naive CD4+ T cells into helper T (Th) cells is controlled by a combination of several transcriptional factors. In this study, we examined the functional role of the Runx1 transcription factor in Th cell differentiation. Naive T cells from transgenic mice expressing a dominant interfering form of Runx1 exhibited enhanced interleukin 4 production and efficient Th2 differentiation. In contrast, transduction of Runx1 into wild-type T cells caused a complete attenuation of Th2 differentiation and was accompanied by the cessation of GATA3 expression. Furthermore, endogenous expression of Runx1 in naive T cells declined after T cell receptor stimulation, at the same time that expression of GATA3 increased. We conclude that Runx1 plays a novel role as a negative regulator of GATA3 expression, thereby inhibiting the Th2 cell differentiation

Alteration of chondroitin sulfate composition on proteoglycan produced by knock-in mouse embryonic fibroblasts whose versican lacks the A subdomain

Versican/proteoglycan-mesenchymal (PG-M) is a large chondroitin sulfate (CS) proteoglycan of the extracellular matrix (ECM) that is constitutively expressed in adult tissues such as dermis and blood vessels. It serves as a structural macromolecule of the ECM, while in embryonic tissue it is transiently expressed at high levels and regulates cell adhesion, migration, proliferation, and differentiation. Knock-in mouse embryonic (Cspg2Δ3/Δ3) fibroblasts whose versican lack the A subdomain of the G1 domain exhibit low proliferation rates and acquire senescence. It was suspected that chondroitin sulfate on versican core protein would be altered when the A subdomain was disrupted, so fibroblasts were made from homozygous Cspg2Δ3/Δ3 mouse embryos to investigate the hypothesis. Analysis of the resulting versican deposition demonstrated that the total versican deposited in the Cspg2Δ3/Δ3 fibroblasts culture was approximately 50% of that of the wild type (WT), while the versican deposited in the ECM of Cspg2Δ3/Δ3 fibroblasts culture was 35% of that of the WT, demonstrating the lower capacity of mutant (Cspg2Δ3/Δ3) versican deposited in the ECM. The analysis of CS expression in the Cspg2Δ3/Δ3 fibroblasts culture compared with wild-type fibroblasts showed that the composition of the non-sulfate chondroitin sulfate isomer on the versican core protein increased in the cell layer but decreased in the culture medium. Interestingly, chondroitin sulfate E isomer was found in the culture medium. The amount of CS in the Cspg2Δ3/Δ3 cell layer of fibroblasts with mutant versican was dramatically decreased, contrasted to the amount in the culture medium, which increased. It was concluded that the disruption of the A subdomain of the versican molecule leads to lowering of the amount of versican deposited in the ECM and the alteration of the composition and content of CS on the versican molecule

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

「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

「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