ジョセイ ショクイキ ト シテノ ヒセイキ ロウドウ カンコク ノ ヒセイキ ロウドウ オ メグッテ

本研究は韓国の女性非正規雇用労働者に焦点をあて，女性職域がどのように選択されるかにつ いて論じるものである。韓国では，通貨危機と世界同時不況を経て非正規化が深化しており，女性の 側の選択は構造的に大幅に制約されている。2007年には非正規雇用の濫用防止と格差の是正を目的と した非正規雇用労働者保護関連法が施行されたものの現実とのギャップは開いたままである。そのよ うな中でも，非正規雇用労働者の就業意識には正規雇用労働者と明確な違いがあり，非正規雇用の選 択に「自発的」と見られるものを多く含んでいる。それは時に「戦略的」と呼ぶべきであろう。非正 規雇用の選択要因は複合的なものであるが，非正規雇用を含む女性職域の選択はジェンダー・ステレ オタイプを再生産するという点を含めて更なる検討を要する。This study argues about the choices of ‘female-dominated work area\u27 focusing on fe­male non-regular workers in Korea. The 1997 monetary crisis and the global recession in 2008 brought a further deterioration of non-regularization in labor market. Thus women\u27s choices of work areas are structurally restricted. Although the Acts on the Protection of Non-regular Employees were enacted in 2007，the gap between the Acts and the reality is not filled. Under this situation work values of non-regular workers differ from the ones of regular workers and lots of their choices seem to be made voluntarily. Factors of the choices of non-regular employment are multi-layered， however，further investigation isneeded including an aspect of reproduction of gender-stereotype

チュウショウ キギョウ ニオケル ジョセイ ヤクイン トリシマリヤク ト ジョセイ トウヨウ : ロンテン ノ サクテイ ニ ムケテ

日本の雇用において中小企業は重大な役割を果たしている。本稿は、その中小企業における女性役員・取締役のあり方が大企業と異なっているのか、異なっているとすればどのように異なっているのか、又その要因は何かを明らかにする前段階として、この課題を見るべき論点を明らかにするためのものである。そのため、ヒアリング調査は経営者であると同時に周辺企業を俯瞰する立場にあり、自らもまた働く女性として経験を積んで来た女性を対象とした。ヒアリングを通して得た知見により、今後検証を進めるにあたっての論点は以下のとおりとした。第1は、「役員・取締役に至る経緯」、第2は「システム整備」である。第1点は、女性管理職・役員にまで至った要因は何であったのかである。第2点は具体的な就業環境のシステム整備に力点をおくものである。そこには、育児休業などの制度整備が重要であることは言うまでもないが、ここではそのような制度を補完するものとして、もっとも具体的な人事管理システムとしての「業務の配分」や「働き方」のシステム整備を取り上げることとした

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

Relationship between Exhaled Nitric Oxide Measured by Two Offline Methods and Bronchial Hyperresponsiveness in Japanese Adults with Asthma

Background: Exhaled nitric oxide (eNO) is a useful marker of eosinophilic airway inflammation in asthmatics. There have been no studies to show the relationship between eNO measured by offline methods and the degree of bronchial hyperresponsiveness in asthmatic patients treated with inhaled corticosteroids. Methods: The study population comprised asthmatics at our outpatient clinic. We measured eNO levels by two methods (“eNOs” was measured with a Sievers kit; and “eNOc” was measured with a kit from the Center for Environmental Information Science, Japan). We also used spirometry to test bronchial hyperresponsiveness to acetylcholine (PC20Ach). Results: We recruited 192 stable asthmatics. There was a significant relationship between eNOs and eNOc (r = 0.919, p < 0.001). LogPC20Ach levels were negatively correlated with eNOs or eNOc levels (eNOs, r = −0.31, p < 0.001; eNOc, r = −0.23, p = 0.0013). We classified the subjects into two groups based on eNOs levels ((A) the subjects with high eNOs levels (n = 92) and (B) the subjects with normal eNOs levels (n = 100) ); logPC20Ach was significantly correlated with eNOs (r = −0.34, p = 0.001) or eNOc (r = −0.28, p = 0.0075) but not correlated with %FEV1 in (A), whereas logPC20Ach was not significantly correlated with eNO but significantly correlated with %FEV1 (r = 0.33, p = 0.002) in (B). Conclusions: Levels of eNOs and eNOc were correlated with the degree of bronchial hyperresponsiveness to acetylcholine in adult asthmatics treated with inhaled corticosteroids. Our findings suggest that offline monitoring of eNO will facilitate the management of bronchial asthma in patients treated with these drugs

Inhibition of transforming growth factor-β signaling in myeloid cells ameliorates aortic aneurysmal formation in Marfan syndrome.

Increased transforming growth factor-β (TGF-β) signaling contributes to the pathophysiology of aortic aneurysm in Marfan syndrome (MFS). Recent reports indicate that a small but significant number of inflammatory cells are infiltrated into the aortic media and adventitia in MFS. However, little is known about the contribution of myeloid cells to aortic aneurysmal formation. In this study, we ablated the TGF-β type II receptor gene Tgfbr2 in myeloid cells of Fbn1C1039G/+ MFS mice (Fbn1C1039G/+;LysM-Cre/+;Tgfbr2fl/fl mice, hereinafter called Fbn1C1039G/+;Tgfbr2MyeKO) and evaluated macrophage infiltration and TGF-β signaling in the aorta. Aneurysmal formation with fragmentation and disarray of medial elastic fibers observed in MFS mice was significantly ameliorated in Fbn1C1039G/+;Tgfbr2MyeKO mice. In the aorta of Fbn1C1039G/+;Tgfbr2MyeKO mice, both canonical and noncanonical TGF-β signals were attenuated and the number of infiltrated F4/80-positive macrophages was significantly reduced. In vitro, TGF-β enhanced the migration capacity of RAW264.7 macrophages. These findings suggest that TGF-β signaling in myeloid cells promotes aortic aneurysmal formation and its inhibition might be a novel therapeutic target in MFS