Task Based Learning: Effective Use to Enhance Learner Motivation and Engagement in the EFL Classroom

departmental bulletin pape

1979年プラン・コンタブルに関する一考察-その背景と独自な標準化について-

Articledepartmental bulletin pape

肢体不自由養護学校における機能訓練の位置づけに関する史的考察 ―担当者に視点をあてて―

原著論文Original Papersdepartmental bulletin pape

Differences in clinicopathological characteristics between lipohypertrophy and localized insulin‐derived amyloidosis: A scoping review

Insulin is used as a therapeutic agent in patients with diabetes, and cutaneous lipohypertrophy (LH) and localized insulin-derived amyloidosis (LIDA) are well-known adverse effects associated with insulin injections. The clinical implications, management, assessment methods, and pathological differentiation of LH and LIDA have been recently updated. This review was to update our knowledge of the pathological differentiation, effects of insulin absorption, hypoglycemic events, and recent assessment methods for LH and LIDA. A scoping review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta Analyses extension for Scoping Reviews guidelines. Original studies and case reports in English were also included. PubMed and Scopus databases were searched for keywords to identify papers published up to January 2022. A total of 113 studies were identified through a database search, and 31 were eligible for inclusion in this scoping review. In the 31 studies included in this review, patients with type 2 diabetes had high frequencies of LH and LIDA. LH outcome parameters were assessed using pathological findings and imaging. LIDA is mainly determined by pathological methods, such as hematoxylin and eosin and Congo red staining. Several in vitro and in vivo LIDA models of LIDA have been developed. These results suggest that pathological analysis is required to identify LH and LIDA. It is important to consider LIDA, as it likely influences insulin adsorption and glycemic control. Although several studies have evaluated the LIDA process, little is known about the mechanisms underlying the development of adverse effects associated with insulin injections.Citation: Mukai K, Tanno H, Sugama J, Yanagita T, Kanno E. Differences in clinicopathological characteristics between lipohypertrophy and localized insulin-derived amyloidosis: A scoping review. Chronic Dis Transl Med. 2023 Nov 14;10(1):22-30. doi: 10.1002/cdt3.98. PMID: 38450303; PMCID: PMC10914015

Current Status and Issues of Communication Skills Education in Junior Colleges and Universities

近年，就職時に求められるコミュニケーション能力向上へのニーズや，社会人基礎力の提唱などに伴い，大学や短期大学においてコミュニケーション教育を取り入れる動きが出ている。各大学が独自のプログラムを作成し取り組んでいるが，それらの知見を概観してまとめたものは少ない。本論文では，現在，大学・短期大学において，どのようなコミュニケーション教育が行われているかを概観し,今後の課題を明らかにすることを目的とした。2000年以降の国内の文献を調査した結果，実施したプログラム内容の詳細について記載があった文献が15見出された。その内容について整理した結果，大きく分けて「自己理解・自己成長」「伝えるスキル」「きくスキル」「チームでの問題解決」の４カテゴリーに分類された。また，今後の課題として，綿密な計画に基づいた効果測定（特に一定時間を経ての長期的・持続的効果）が求められることを指摘した。departmental bulletin pape

Formin homology 2 domain–containing 3 (Fhod3) controls neural plate morphogenesis in mouse cranial neurulation by regulating multidirectional apical constriction

Neural tube closure requires apical constriction during which contraction of the apical F-actin network forces the cell into a wedged shape, facilitating the folding of the neural plate into a tube. However, how F-actin assembly at the apical surface is regulated in mammalian neurulation remains largely unknown. We report here that formin homology 2 domain–containing 3 (Fhod3), a formin protein that mediates F-actin assembly, is essential for cranial neural tube closure in mouse embryos. We found that Fhod3 is expressed in the lateral neural plate but not in the floor region of the closing neural plate at the hindbrain. Consistently, in Fhod3-null embryos, neural plate bending at the midline occurred normally, but lateral plates seemed floppy and failed to flex dorsomedially. Because the apical accumulation of F-actin and constriction were impaired specifically at the lateral plates in Fhod3-null embryos, we concluded that Fhod3-mediated actin assembly contributes to lateral plate–specific apical constriction to advance closure. Intriguingly, Fhod3 expression at the hindbrain was restricted to neuromeric segments called rhombomeres. The rhombomere-specific accumulation of apical F-actin induced by the rhombomere-restricted expression of Fhod3 was responsible for the outward bulging of rhombomeres involving apical constriction along the anteroposterior axis, as rhombomeric bulging was less prominent in Fhod3-null embryos than in the wild type. Fhod3 thus plays a crucial role in the morphological changes associated with neural tube closure at the hindbrain by mediating apical constriction not only in the mediolateral but also in the anteroposterior direction, thereby contributing to tube closure and rhombomere segmentation, respectively.Citeation: Sulistomo HW, Nemoto T, Yanagita T, Takeya R. Formin homology 2 domain-containing 3 (Fhod3) controls neural plate morphogenesis in mouse cranial neurulation by regulating multidirectional apical constriction. J Biol Chem. 2019 Feb 22;294(8):2924-2934. doi: 10.1074/jbc.RA118.005471. Epub 2018 Dec 20. PMID: 30573686; PMCID: PMC6393623

非妊時BMIおよび妊娠中の体重増加量と出生体重に関する検討

第3回日本DOHaD研究会学術集会 抄録集 【ポスター発表】journal articl

Changes in TRPV1 Receptor, CGRP, and BDNF Expression in Rat Dorsal Root Ganglion with Resiniferatoxin-Induced Neuropathic Pain: Modulation by Pulsed Radiofrequency Applied to the Sciatic Nerve

Pulsed radiofrequency (PRF) is a safe method of treating neuropathic pain by generating intermittent electric fields at the needle tip. Resiniferatoxin (RTX) is an ultrapotent agonist of transient receptor potential vanilloid subtype-1 (TRPV1) receptors. We investigated the mechanism of PRF using a rat model of RTX-induced neuropathic pain. After administering RTX intraperitoneally, PRF was applied to the right sciatic nerve. We observed the changes in TRPV1, calcitonin gene-related peptide (CGRP), and brain-derived neurotrophic factor (BDNF) in the dorsal root ganglia by western blotting. Expressions of TRPV1 and CGRP were significantly lower in the contralateral (RTX-treated, PRF-untreated) tissue than in control rats (p<0.0001 and p<0.0001, respectively) and the ipsilateral tissues (p<0.0001 and p<0.0001, respectively). BDNF levels were significantly higher in the contralateral tissues than in the control rats (p<0.0001) and the ipsilateral tissues (p<0.0001). These results suggest that, while TRPV1 and CGRP are decreased by RTX-induced neuronal damage, increased BDNF levels result in pain development. PRF may promote recovery from neuronal damage with concomitant restoration of TRPV1 and CGRP, and exert its analgesic effect by reversing BDNF increase. Further research is required to understand the role of TRPV1 and CGRP restoration in improving mechanical allodynia.Citation: Koshida T, Maruta T, Tanaka N, Hidaka K, Kurogi M, Nemoto T, Yanagita T, Takeya R, Tsuneyoshi I. Changes in TRPV1 Receptor, CGRP, and BDNF Expression in Rat Dorsal Root Ganglion with Resiniferatoxin-Induced Neuropathic Pain: Modulation by Pulsed Radiofrequency Applied to the Sciatic Nerve. Acta Med Okayama. 2023 Aug;77(4):359-364. doi: 10.18926/AMO/65741. PMID: 37635135

How was cognitive behavioural therapy for mood disorder implemented in Japan? A retrospective observational study using the nationwide claims database from FY2010 to FY2015

Objectives To clarify the dissemination status of cognitive behavioural therapy (CBT) in Japan under the national health insurance scheme. Design Retrospective observational study. Setting National Database of Health Insurance Claims and Specific Health Checkups of Japan. Participants Patients who received CBT under the national health insurance scheme from fiscal years (FY) 2010 to 2015. Primary and secondary outcome measures We estimated the change rate and the standardised claim ratio (SCR) for the number of patients receiving CBT and analysed the association between the CBT status and several regional factors. Results We found that (a) a total of 60 304 patients received CBT during the study period; (b) the number of patients receiving CBT was highest in the first year (−1.8% from FY2010 to FY2015); (c) the number of patients who received CBT per 100 000 population decreased (or remained at zero) in most prefectures (32 out of 47); (d) there was a maximum 424.7-fold difference between prefectures in the standardised claim ratio for CBT and (e) the number of registered CBT institutions was significantly associated with the number of patients who received CBT. Conclusions The provision of CBT did not increase in the first 6 years (FY2010–2015) after its coverage in Japan’s national health insurance scheme. Further studies including a questionnaire survey of registered CBT institutions are required to get more detailed information on the dissemination of CBT in Japan.Citation: Hayashi Y, Yoshinaga N, Sasaki Y, Tanoue H, Yoshimura K, Kadowaki Y, Arimura Y, Yanagita T, Ishida Y. How was cognitive behavioural therapy for mood disorder implemented in Japan? A retrospective observational study using the nationwide claims database from FY2010 to FY2015. BMJ Open. 2020 May 5;10(5):e033365. doi: 10.1136/bmjopen-2019-033365. PMID: 32376747; PMCID: PMC7223011

Comparison of Nocifensive Behavior in NaV1.7–, NaV1.8–, and NaV1.9–Channelrhodopsin‐2 Mice by Selective Optogenetic Activation of Targeted Sodium Channel Subtype‐Expressing Afferents

Voltage-gated sodium channels, including NaV1.7, NaV1.8, and NaV1.9, play important roles in pain transmission and chronic pain development. However, the specific mechanisms of their action remain unclear, highlighting the need for in vivo stimulation studies of these channels. Optogenetics, a novel technique for targeting the activation or inhibition of specific neural circuits using light, offers a promising solution. In our previous study, we used optogenetics to selectively excite NaV1.7-expressing neurons in the dorsal root ganglion of mice to induce nocifensive behavior. Here, we further characterize the impact of nocifensive behavior by activation of NaV1.7, NaV1.8, or NaV1.9-expressing neurons. Using CRISPR/Cas9-mediated homologous recombination, NaV1.7-iCre, NaV1.8-iCre, or NaV1.9-iCre mice expressing iCre recombinase under the control of the endogenous NaV1.7, NaV1.8, or NaV1.9 gene promoter were produced. These mice were then bred with channelrhodopsin-2 (ChR2) Cre-reporter Ai32 mice to obtain NaV1.7-ChR2, NaV1.8-ChR2, or NaV1.9-ChR2 mice. Blue light exposure triggered paw withdrawal in all mice, with the strongest response in NaV1.8-ChR2 mice. These light sensitivity differences observed across NaV1.x-ChR2 mice may be dependent on ChR2 expression or reflect the inherent disparities in their pain transmission roles. In conclusion, we have generated noninvasive pain models, with optically activated peripheral nociceptors. We believe that studies using optogenetics will further elucidate the role of sodium channel subtypes in pain transmission.Citation: Maruta T, Kouroki S, Kurogi M, Hidaka K, Koshida T, Miura A, Nakagawa H, Yanagita T, Takeya R, Tsuneyoshi I. Comparison of Nocifensive Behavior in NaV1.7-, NaV1.8-, and NaV1.9-Channelrhodopsin-2 Mice by Selective Optogenetic Activation of Targeted Sodium Channel Subtype-Expressing Afferents. J Neurosci Res. 2024 Oct;102(10):e25386. doi: 10.1002/jnr.25386. PMID: 39364619