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    表紙(和文目次)、裏表紙(英文目次)、編集後記、奥付 Vol.20 (2024.04)

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    The Psychological Impact of COVID-19 Infection on Pregnant and Postpartum Women : A Scoping Review

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    目的:スコーピングレビューを行いCOVID-19陽性となった妊産婦の体験を明らかにすることにより、精神状態は悪化するのか、どのような囚子が影響するのかを網羅的に明らかにすることである。以上からCOVID-19陽性妊産婦への精神的支援を示唆することである。方法: Arksey & 0'malley(2005)の方法論的フレームワークと友利ら(2020)のスコーピングレビューのための報告ガイドライン日本語版: PRISMA-ScR.に基づき行った。結果:9件の英語の文献を対象とした。1) 量的研究結果の概要は、抑うつ、不安の発症率、ストレスレベル、EPSDスコアはCOVID-19陽性者の方が陰性または末検査より高かった。2) COVID-19 陽性者の精神的影響への関連因子は、妊娠回数、睡眠不足、NICU入院、低出生体重児、ミルク哺乳、母児異室、早期母子接触なし、高学歴、勤労女性、より悪い産科歴、年齢が高いこと、妊娠初期、妊娠週数が進んでいることが抽出された。3) 質的記述研究の概要で抽出されたテーマは、[心理社会的・精神的問題] [対処のメカニズム] [リスク] [保護] [変化] [スタッフや支援者からの無視や孤立感] [出産後の新生児分離]であった。考察:妊娠経過が正常から逸脱しやすいハイリスク妊産婦は元々精神状況が悪化しやすく、COVID-19陽性となることでさらに身体的リスクを高め精神状態の悪化に繋がっている。COVID-19陽性によって変化したケアが母児分離の状況を作り、妊産婦のストレス、不安、罪悪感が増している。結論: COVID-19 陽性妊産婦への精神的支援として、妊娠早期から心身の健康管理を行うこと、出産時の経験が肯定的なものとなるようなケアを行うことが必要である。PURPOSE: To examine the psychological impact of COVID-19 infection on pregnant and postpartum women.METHOD: This is a scoping review based on Arksey and O'Malley's methodological framework and the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews Guidelines.RESULTS: Nine English-language references were included in this study. 1)Depression, anxiety, stress, and Edinburgh Postnatal Depression Scale scores were higher in women who tested positive for COVID-19 than in those who tested negative for COVID-19 or were not tested. 2) Related factors of psychological impact in COVID-19-positive women were: gravidity, delicery pain, pleep deprivation, neonatal intensive care unit admission, low birth weight, milk feeding, rooming out for mother and infact, no skin to skin contact, higher education, working women, first pregnancy trimester, obstetric history, country, COVID-19 epidemic month, and age. 3) Themes identified in the qualitative descriptive research summary were [psychosocial issues], [coping mechanisms], [risk], [protection], [change], [neglect,isolation], and [difficulty with neonatal separation]. CONCLUSION; Psychological support for COVID-19-positive pregnant women should include mental and ohysical health care from the early stages of pregnancy, and care to ensure that the birth experience is a positive one

    表在性皮膚脂肪腫性母斑の超音波所見:この腫瘍と他の軟部腫瘍との鑑別点は?

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    Nevus lipomatosus cutaneous superficialis is a rare, benign hamartoma characterized by mature adipocyte proliferation in the dermis. It is frequently difficult to distinguish clinically from soft tissue tumors, including lipoma, neurofibroma, venous malformation, and angiolipoma. Notably, the classical form, which shows multiple and sometimes enlarged nodules, is difficult to differentiate from liposarcoma based on clinical examination, computed tomography, and magnetic resonance imaging findings. Therefore, to ascertain the utility of ultrasonography in diagnosing nevus lipomatosus cutaneous superficialis, sonographic examinations were performed on eight patients with nevus lipomatosus cutaneous superficialis. All patients had ill-defined hyperechoic masses in the dermis or from the dermis to the subcutis, and the posterior echoes were attenuated in seven patients. Color Doppler sonography revealed no blood flow to the lesions. Ultrasound images were created using the reflections of ultrasound waves at interfaces with different acoustic impedances. Therefore, it is assumed that, in nevus lipomatosus cutaneous superficialis, the ultrasound beam is scattered by ectopic mature adipocytes intermingled with collagen bundles, which are shown as hyperechoic masses. Furthermore, the scattering of the ultrasound beam is thought to reduce tissue penetration, which may attenuate the posterior echo.権利情報:© 2023 Japanese Dermatological Association. This is the peer reviewed version of the following article: [https://onlinelibrary.wiley.com/doi/10.1111/1346-8138.16998], which has been published in final form at [https://doi.org/10.1111/1346-8138.16998]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions

    低用量持続的腎代替療法と急性腎障害を有する重症患者の死亡率との関連の検討

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    Rationale & objective: Continuous kidney replacement therapy (CKRT) is preferred when available for hemodynamically unstable acute kidney injury (AKI) patients in the intensive care unit (ICU). The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommend a delivered CKRT dose of 20-25mL/kg/h; however, in Japan the doses are typically below this recommendation due to government health insurance system restrictions. This study investigated the association between mortality and dose of CKRT. Study design: Single-center retrospective cohort study. Setting & participants: Critically ill patients with AKI treated with CKRT at a tertiary Japanese university hospital between January 1, 2012, and December 31, 2021. Exposure: Delivered CKRT doses below or above the median. Outcome: 90-day mortality after CKRT initiation. Analytical approach: Multivariable Cox regression analysis and Kaplan-Meier analysis. Results: The study population consisted of 494 patients. The median age was 72 years, and 309 patients (62.6%) were men. Acute tubular injury was the leading cause of AKI, accounting for 81.8%. The median delivered CKRT dose was 13.2mL/kg/h. Among the study participants, 456 (92.3%) received delivered CKRT doses below 20mL/kg/h, and 204 (41.3%) died within 90 days after CKRT initiation. Multivariable Cox regression analysis revealed increased mortality in the below-median group (HR, 1.73 [95% CI, 1.19-2.51], P=0.004). Additionally, a significant, inverse, nonlinear association between 90-day mortality and delivered CKRT dose was observed using delivered CKRT dose as a continuous variable. Limitations: Single-center, retrospective, observational study. Conclusions: A lower delivered CKRT dose was independently associated with higher 90-day mortality among critically ill patients who mostly received dosing below the current KDIGO recommendations.権利情報:© 2024 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved

    日本人2型糖尿病患者におけるエネルギー摂取量と体重に対するカナグリフロジンとテネリグリプチンの比較:CANTABILE試験のサブ解析

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    Background: While the Sodium-glucose co-transporter 2 (SGLT2) inhibitors and dipeptidyl peptidase-4 (DPP4) are widely used for the glycemic control in type 2 diabetes mellitus, the differences in the effects of SGLT2 inhibitors and DPP4 inhibitors on energy intake and diabetes-related indicators are unclear. Methods: This was a subanalysis of the CANTABILE study which compared the effects of canagliflozin and teneligliptin on metabolic factors in Japanese patients with Type 2 diabetes. The changes at 24 weeks from the baseline of the diabetes-related indicators including Hemoglobin A1c (HbA1c), energy intake and body weight were compared between the canagliflozin and teneligliptin groups. Results: Seventy-five patients in the canagliflozin group and 70 patients in the teneligliptin group were analyzed. A significant decrease in HbA1c was observed in both groups. In the teneligliptin group, although energy intake was significantly reduced, there was no significant change in body weight. Conversely, in the canagliflozin group, although energy intake tended to increase, body weight significantly decreased. Conclusion: Canagliflozin and teneligliptin have different effects on the dietary status of patients with Type 2 diabetes. Our result suggests that canagliflozin can manage blood glucose without weight gain, even with increased energy intake.権利情報:© The Author(s) 2024. This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

    肺由来脱細胞化マトリックスシートを用いた ES 細胞から肺細胞への分化誘導

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    Various extracellular matrix (ECM) in the lungs regulate tissue development and homeostasis, as well as provide support for cell structures. However, few studies regarding the effects of lung cell differentiation using lung-derived ECM (LM) alone have been reported. The present study investigated the capability of lung-derived matrix sheets (LMSs) to induce lung cell differentiation using mouse embryonic stem (ES) cells. Expressions of lung-related cell markers were significantly upregulated in ES-derived embryoid bodies (EBs) cultured on an LMS for two weeks. Moreover, immunohistochemical analysis of EBs grown on LMSs revealed differentiation of various lung-related cells. These results suggest that an LMS can be used to promote differentiation of stem cells into lung cells.権利情報:© 2023 Elsevier Inc. All rights reserved

    ADAMTS13によるvon Willebrand因子の制御はマウスにおけるLPS誘発肺炎病態を改善する

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    The relationship between von Willebrand factor (VWF) and inflammation has attracted considerable attention in recent years. VWF, which is stored in the Weibel-Palade bodies (WPBs) of endothelial cells (ECs), is released from WPBs in response to inflammatory stimuli and is thought to contribute to inflammation by promoting leukocyte extravasation. In this study, lung injury model mice were produced by intratracheal injection with lipopolysaccharides. The severity of lung inflammation was evaluated in mice with different genotypes (wild-type, Vwf-/-, Adamts13-/-) and mice treated with drugs that inhibit VWF function. Lung inflammation was significantly ameliorated in Vwf-/- mice compared with wild-type mice. Furthermore, inflammation was significantly suppressed in wild-type mice treated with anti-VWF A1 antibody or recombinant human ADAMTS13 compared with the untreated control group. The underlying mechanism appears to be an increased VWF/ADAMTS13 ratio at the site of inflammation and the interaction between blood cell components, such as leukocytes and platelets, and the VWF A1 domain, which promotes leukocyte infiltration into the lung. This study suggested that ADAMTS13 protein and other VWF-targeting agents may be a novel therapeutic option for treatment of pulmonary inflammatory diseases.権利情報:© Japanese Society of Hematology 2023. This version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use, but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: https://doi.org/10.1007/s12185-023-03668-

    アンジオテンシンⅡ受容体拮抗剤とネプリライシン阻害剤の併用が肝星状細胞の活性化を抑制し,肝線維化を抑制する

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    The renin-angiotensin-aldosterone system has gained attention due to its role as a mediator of liver fibrosis and hepatic stellate cell (HSC) activation. Meanwhile, the natriuretic peptide (NP) system, including atrial NP (ANP) and C-type NP (CNP), is a counter-regulatory hormone regulated by neprilysin. Although the combination of an angiotensin receptor and a neprilysin inhibitor (sacubitril/valsartan: SAC/VAL) has shown clinical efficacy in patients with heart failure, its potential effects on hepatic fibrosis have not been clarified. This study assessed the effects of SAC/VAL in carbon tetrachloride (CCl4)-induced murine liver fibrosis as well as the in vitro phenotypes of HSCs. Treatment with SAC and VAL markedly attenuated CCl4-induced liver fibrosis while reducing α-SMA+-HSC expansion and decreasing hepatic hydroxyproline and mRNA levels of pro-fibrogenic markers. Treatment with SAC increased plasma ANP and CNP levels in CCl4-treated mice, and ANP effectively suppressed cell proliferation and TGF-β-stimulated MMP2 and TIMP2 expression in LX-2 cells by activating guanylate cyclase-A/cGMP/protein kinase G signaling. Meanwhile, CNP did not affect the pro-fibrogenic activity of LX-2 cells. Moreover, VAL directly inhibited angiotensin II (AT-II)-stimulated cell proliferation and the expression of TIMP1 and CTGF through the blockade of the AT-II type 1 receptor/protein kinase C pathway. Collectively, SAC/VAL may be a novel therapeutic treatment for liver fibrosis.権利情報:© 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)

    治療用抗KIR抗体1-7F9は活性化ヒトNK細胞の膠芽腫細胞株、およびそれに由来する膠芽腫マウスモデルに対する抗腫瘍効果を抑制する

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    Glioblastoma (GBM) is the leading malignant intracranial tumor, where prognosis for which has remained extremely poor for two decades. Immunotherapy has recently drawn attention as a cancer treatment, including for GBM. Natural killer (NK) cells are immune cells that attack cancer cells directly and produce antitumor immunity-related cytokines. The adoptive transfer of expanded and activated NK cells is expected to be a promising GBM immunotherapy. We previously established an efficient expansion method that produced highly purified, activated primary human NK cells, which we designated genuine induced NK cells (GiNKs). The GiNKs demonstrated antitumor effects in vitro and in vivo, which were less affected by blockade of the inhibitory checkpoint receptor programmed death 1 (PD-1). In the present study, we assessed the antitumor effects of GiNKs, both alone and combined with an antibody targeting killer Ig-like receptor 2DLs (KIR2DL1 and DL2/3, both inhibitory checkpoint receptors of NK cells) in vitro and in vivo with U87MG GBM-like cells and the T98G GBM cell line. Impedance-based real-time cell growth assays and apoptosis detection assays revealed that the GiNKs exhibited growth inhibitory effects on U87MG and T98G cells by inducing apoptosis. KIR2DL1 blockade attenuated the growth inhibition of the cell lines in vitro. The intracranial administration of GiNKs prolonged the overall survival of the U87MG-derived orthotopic xenograft brain tumor model. The KIR2DL1 blockade did not enhance the antitumor effects; rather, it attenuated it in the same manner as in the in vitro experiment. GiNK immunotherapy directly administered to the brain could be a promising immunotherapeutic alternative for patients with GBM. Furthermore, KIR2DL1 blockade appeared to require caution when used concomitantly with GiNKs.権利情報:© 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)

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