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Article: [Nursing pharmacology education and active-learning.]

Yanagita, Toshihiko / Kanaoka, Maki / Kinoshita, Yumiko / Takeya, Ryu

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2022 Volume 157, Issue 2, Page(s) 104–109

Abstract: Comprehensive pharmacology education in nursing based on the "Patient-oriented Pharmacology" is effective against the improvement of quality of pharmacotherapy and patient satisfaction. Two active learning programs of practical pharmacotherapy for ... ...

Abstract	Comprehensive pharmacology education in nursing based on the "Patient-oriented Pharmacology" is effective against the improvement of quality of pharmacotherapy and patient satisfaction. Two active learning programs of practical pharmacotherapy for nursing students have been performed in School of Nursing, University of Miyazaki; (1) pharmacotherapy role-play for interprofessional education (IPE) and (2) practical excise for Kampo medicine. Pharmacotherapy role-play for IPE was performed as joint lecture both medical students and nursing students. This pharmacotherapy role-play is named Case & Communication based approach (C&C approach), since it is studied through communication between physicians, nurses and patients based on cases presented beforehand. In the practical excise for Kampo medicine, nursing students studied Kampo medicines and tried to taste 9 frequently used Kampo medicines. These active-learning programs in nursing pharmacology education may be effective for better understanding of pharmacotherapy and patient's feeling, and improvement of students' motivation as a nurse.
MeSH term(s)	Education, Nursing ; Humans ; Interprofessional Relations ; Problem-Based Learning ; Students, Medical
Language	Japanese
Publishing date	2022-02-28
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.21100
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Article ; Online: Altered Fhod3 expression involved in progressive high-frequency hearing loss via dysregulation of actin polymerization stoichiometry in the cuticular plate.

Boussaty, Ely Cheikh / Ninoyu, Yuzuru / Andrade, Leonardo R / Li, Qingzhong / Takeya, Ryu / Sumimoto, Hideki / Ohyama, Takahiro / Wahlin, Karl J / Manor, Uri / Friedman, Rick A

PLoS genetics

2024 Volume 20, Issue 3, Page(s) e1011211

Abstract: Age-related hearing loss (ARHL) is a common sensory impairment with complex underlying mechanisms. In our previous study, we performed a meta-analysis of genome-wide association studies (GWAS) in mice and identified a novel locus on chromosome 18 ... ...

Abstract	Age-related hearing loss (ARHL) is a common sensory impairment with complex underlying mechanisms. In our previous study, we performed a meta-analysis of genome-wide association studies (GWAS) in mice and identified a novel locus on chromosome 18 associated with ARHL specifically linked to a 32 kHz tone burst stimulus. Consequently, we investigated the role of Formin Homology 2 Domain Containing 3 (Fhod3), a newly discovered candidate gene for ARHL based on the GWAS results. We observed Fhod3 expression in auditory hair cells (HCs) primarily localized at the cuticular plate (CP). To understand the functional implications of Fhod3 in the cochlea, we generated Fhod3 overexpression mice (Pax2-Cre+/-; Fhod3Tg/+) (TG) and HC-specific conditional knockout mice (Atoh1-Cre+/-; Fhod3fl/fl) (KO). Audiological assessments in TG mice demonstrated progressive high-frequency hearing loss, characterized by predominant loss of outer hair cells, and a decreased phalloidin intensities of CP. Ultrastructural analysis revealed loss of the shortest row of stereocilia in the basal turn of the cochlea, and alterations in the cuticular plate surrounding stereocilia rootlets. Importantly, the hearing and HC phenotype in TG mice phenocopied that of the KO mice. These findings suggest that balanced expression of Fhod3 is critical for proper CP and stereocilia structure and function. Further investigation of Fhod3 related hearing impairment mechanisms may lend new insight towards the myriad mechanisms underlying ARHL, which in turn could facilitate the development of therapeutic strategies for ARHL.
MeSH term(s)	Animals ; Mice ; Actins/genetics ; Actins/metabolism ; Cochlea/metabolism ; Formins/genetics ; Genome-Wide Association Study ; Hearing ; Hearing Loss, High-Frequency ; Mice, Knockout ; Polymerization
Chemical Substances	Actins ; Fhod3 protein, mouse ; Formins
Language	English
Publishing date	2024-03-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1011211
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Article: 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.

Koshida, Tomohiro / Maruta, Toyoaki / Tanaka, Nobuhiko / Hidaka, Kotaro / Kurogi, Mio / Nemoto, Takayuki / Yanagita, Toshihiko / Takeya, Ryu / Tsuneyoshi, Isao

Acta medica Okayama

2023 Volume 77, Issue 4, Page(s) 359–364

Abstract: 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. ...

Abstract	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.
MeSH term(s)	Animals ; Rats ; Antineoplastic Agents ; Brain-Derived Neurotrophic Factor ; Calcitonin Gene-Related Peptide ; Ganglia, Spinal ; Neuralgia/chemically induced ; Neuralgia/therapy ; Pulsed Radiofrequency Treatment ; Sciatic Nerve ; TRPV Cation Channels
Chemical Substances	Antineoplastic Agents ; Brain-Derived Neurotrophic Factor ; Calcitonin Gene-Related Peptide (JHB2QIZ69Z) ; resiniferatoxin (A5O6P1UL4I) ; TRPV1 receptor ; Bdnf protein, rat ; TRPV Cation Channels
Language	English
Publishing date	2023-08-28
Publishing country	Japan
Document type	Journal Article
ZDB-ID	188415-3
ISSN	0386-300X ; 0001-6152
ISSN	0386-300X ; 0001-6152
DOI	10.18926/AMO/65741
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Article ; Online: Extracellular signal-regulated kinase phosphorylation enhancement and Na

Hidaka, Kotaro / Maruta, Toyoaki / Koshida, Tomohiro / Kurogi, Mio / Kage, Yohko / Kouroki, Satoshi / Shirasaka, Tetsuro / Takeya, Ryu / Tsuneyoshi, Isao

Molecular pain

2022 Volume 18, Page(s) 17448069221089784

Abstract: Pulsed radiofrequency (PRF) therapy is one of the most common treatment options for neuropathic pain, albeit the underlying mechanism has not been hitherto elucidated. In this study, we investigated the efficacy and mechanism of PRF therapy on ... ...

Abstract	Pulsed radiofrequency (PRF) therapy is one of the most common treatment options for neuropathic pain, albeit the underlying mechanism has not been hitherto elucidated. In this study, we investigated the efficacy and mechanism of PRF therapy on resiniferatoxin (RTX)-induced mechanical allodynia, which has been used as a model of postherpetic neuralgia (PHN). Adult male rats were intraperitoneally injected with a vehicle or RTX. Furthermore, PRF current was applied on a unilateral sciatic nerve in all RTX-treated rats. On both ipsilateral and contralateral sides, the paw mechanical withdrawal thresholds were examined and L4-6 dorsal root ganglia (DRG) were harvested. In the DRG of rats with RTX-induced mechanical allodynia, Na
MeSH term(s)	Animals ; Diterpenes ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Ganglia, Spinal ; Humans ; Hyperalgesia/therapy ; Male ; NAV1.7 Voltage-Gated Sodium Channel/metabolism ; Neuralgia/chemically induced ; Neuralgia/therapy ; Neuralgia, Postherpetic ; Neurons ; Phosphorylation ; Radiofrequency Therapy ; Rats ; Rats, Sprague-Dawley ; Sodium Channels ; Tramadol/pharmacology ; Up-Regulation
Chemical Substances	Diterpenes ; NAV1.7 Voltage-Gated Sodium Channel ; Scn9a protein, rat ; Sodium Channels ; Tramadol (39J1LGJ30J) ; resiniferatoxin (A5O6P1UL4I) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
Language	English
Publishing date	2022-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2174252-2
ISSN	1744-8069 ; 1744-8069
ISSN (online)	1744-8069
ISSN	1744-8069
DOI	10.1177/17448069221089784
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Article: Altered Fhod3 Expression Involved in Progressive High-Frequency Hearing Loss via Dysregulation of Actin Polymerization Stoichiometry in The Cuticular Plate.

Boussaty, Ely Cheikh / Ninoyu, Yuzuru / Andrade, Leo / Li, Qingzhong / Takeya, Ryu / Sumimoto, Hideki / Ohyama, Takahiro / Wahlin, Karl J / Manor, Uri / Friedman, Rick A

bioRxiv : the preprint server for biology

2023

Abstract: Age-related hearing loss (ARHL) is a common sensory impairment with comlex underlying mechanisms. In our previous study, we performed a meta-analysis of genome-wide association studies (GWAS) in mice and identified a novel locus on chromosome 18 ... ...

Abstract	Age-related hearing loss (ARHL) is a common sensory impairment with comlex underlying mechanisms. In our previous study, we performed a meta-analysis of genome-wide association studies (GWAS) in mice and identified a novel locus on chromosome 18 associated with ARHL specifically linked to a 32 kHz tone burst stimulus. Consequently, we investigated the role of Formin Homology 2 Domain Containing 3 (Fhod3), a newly discovered candidate gene for ARHL based on the GWAS results. We observed Fhod3 expression in auditory hair cells (HCs) and primarily localized at the cuticular plate (CP). To understand the functional implications of Fhod3 in the cochlea, we generated Fhod3 overexpression mice (Pax2-Cre+/-; Fhod3Tg/+) (TG) and HC-specific conditional knockout mice (Atoh1-Cre+/-; Fhod3fl/fl) (KO). Audiological assessments in TG mice demonstrated progressive high-frequency hearing loss, characterized by predominant loss of outer HCs and decrease phalloidin intensities of CP. Ultrastructural analysis revealed shortened stereocilia in the basal turn cochlea. Importantly, the hearing and HC phenotype in TG mice were replicated in KO mice. These findings indicate that Fhod3 plays a critical role in regulating actin dynamics in CP and stereocilia. Further investigation of Fhod3-related hearing impairment mechanisms may facilitate the development of therapeutic strategies for ARHL in humans.
Language	English
Publishing date	2023-08-27
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.07.20.549974
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Article ; Online: Differential effects of the formin inhibitor SMIFH2 on contractility and Ca

Sakata, Koji / Matsuyama, Sho / Kurebayashi, Nagomi / Hayamizu, Kengo / Murayama, Takashi / Nakamura, Kunihide / Kitamura, Kazuo / Morimoto, Sachio / Takeya, Ryu

Genes to cells : devoted to molecular & cellular mechanisms

2021 Volume 26, Issue 8, Page(s) 583–595

Abstract: Genetic mutations in actin regulators have been emerging as a cause of cardiomyopathy, although the functional link between actin dynamics and cardiac contraction remains largely unknown. To obtain insight into this issue, we examined the effects of ... ...

Abstract	Genetic mutations in actin regulators have been emerging as a cause of cardiomyopathy, although the functional link between actin dynamics and cardiac contraction remains largely unknown. To obtain insight into this issue, we examined the effects of pharmacological inhibition of formins, a major class of actin-assembling proteins. The formin inhibitor SMIFH2 significantly enhanced the cardiac contractility of isolated frog hearts, thereby augmenting cardiac performance. SMIFH2 treatment had no significant effects on the Ca
MeSH term(s)	Animals ; Calcium Signaling ; Cells, Cultured ; Heart/drug effects ; Heart/physiology ; Mice ; Mice, Inbred C57BL ; Myocardial Contraction ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/physiology ; Rana catesbeiana ; Ryanodine Receptor Calcium Release Channel/metabolism ; Species Specificity ; Thiones/pharmacology ; Uracil/analogs & derivatives ; Uracil/pharmacology
Chemical Substances	Ryanodine Receptor Calcium Release Channel ; SMIFH2 compound ; Thiones ; Uracil (56HH86ZVCT)
Language	English
Publishing date	2021-06-17
Publishing country	England
Document type	Journal Article
ZDB-ID	1330000-3
ISSN	1365-2443 ; 1356-9597
ISSN (online)	1365-2443
ISSN	1356-9597
DOI	10.1111/gtc.12873
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Article ; Online: Formin homology 2 domain-containing 3 (Fhod3) controls neural plate morphogenesis in mouse cranial neurulation by regulating multidirectional apical constriction.

Sulistomo, Hikmawan Wahyu / Nemoto, Takayuki / Yanagita, Toshihiko / Takeya, Ryu

The Journal of biological chemistry

2018 Volume 294, Issue 8, Page(s) 2924–2934

Abstract: 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 ... ...

Abstract	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.
MeSH term(s)	Actin Cytoskeleton/metabolism ; Animals ; Cells, Cultured ; Female ; Formins ; Mice ; Mice, Knockout ; Microfilament Proteins/physiology ; Morphogenesis ; Neural Plate/cytology ; Neural Plate/physiology ; Neural Tube/cytology ; Neural Tube/physiology ; Neurulation
Chemical Substances	Fhod3 protein, mouse ; Formins ; Microfilament Proteins
Language	English
Publishing date	2018-12-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA118.005471
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Article: [Role-play for pharmacology education: active learning through the Case & Communication based approach].

Yanagita, Toshihiko / Nemoto, Takayuki / Takeya, Ryu

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2015 Volume 146, Issue 2, Page(s) 115–118

MeSH term(s)	Communication ; Problem-Based Learning ; Role Playing ; Students, Medical
Language	Japanese
Publishing date	2015-08
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.146.115
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Article ; Online: Selective optogenetic activation of NaV1.7-expressing afferents in NaV1.7-ChR2 mice induces nocifensive behavior without affecting responses to mechanical and thermal stimuli.

Maruta, Toyoaki / Hidaka, Kotaro / Kouroki, Satoshi / Koshida, Tomohiro / Kurogi, Mio / Kage, Yohko / Mizuno, Seiya / Shirasaka, Tetsuro / Yanagita, Toshihiko / Takahashi, Satoru / Takeya, Ryu / Tsuneyoshi, Isao

PloS one

2022 Volume 17, Issue 10, Page(s) e0275751

Abstract: In small and large spinal dorsal root ganglion neurons, subtypes of voltage-gated sodium channels, such as NaV1.7, NaV1.8, and NaV1.9 are expressed with characteristically localized and may play different roles in pain transmission and intractable pain ... ...

Abstract	In small and large spinal dorsal root ganglion neurons, subtypes of voltage-gated sodium channels, such as NaV1.7, NaV1.8, and NaV1.9 are expressed with characteristically localized and may play different roles in pain transmission and intractable pain development. Selective stimulation of each specific subtype in vivo may elucidate its role of each subtype in pain. So far, this has been difficult with current technology. However, Optogenetics, a recently developed technique, has enabled selective activation or inhibition of specific neural circulation in vivo. Moreover, optogenetics had even been used to selectively excite NaV1.8-expressing dorsal root ganglion neurons to induce nocifensive behavior. In recent years, genetic modification technologies such as CRISPR/Cas9 have advanced, and various knock-in mice can be easily generated using such technology. We aimed to investigate the effects of selective optogenetic activation of NaV1.7-expressing afferents on mouse behavior. We used CRISPR/Cas9-mediated homologous recombination to generate bicistronic NaV1.7-iCre knock-in mice, which express iCre recombinase under the endogenous NaV1.7 gene promoter without disrupting NaV1.7. The Cre-driver mice were crossed with channelrhodopsin-2 (ChR2) Cre-reporter Ai32 mice to obtain NaV1.7iCre/+;Ai32/+, NaV1.7iCre/iCre;Ai32/+, NaV1.7iCre/+;Ai32/Ai32, and NaV1.7iCre/iCre;Ai32/Ai32 mice. Compared with wild-type mice behavior, no differences were observed in the behaviors associated with mechanical and thermal stimuli exhibited by mice of the aforementioned genotypes, indicating that the endogenous NaV1.7 gene was not affected by the targeted insertion of iCre. Blue light irradiation to the hind paw induced paw withdrawal by mice of all genotypes in a light power-dependent manner. The threshold and incidence of paw withdrawal and aversive behavior in a blue-lit room were dependent on ChR2 expression level; the strongest response was observed in NaV1.7iCre/iCre;Ai32/Ai32 mice. Thus, we developed a non-invasive pain model in which peripheral nociceptors were optically activated in free-moving transgenic NaV1.7-ChR2 mice.
MeSH term(s)	Animals ; Channelrhodopsins/metabolism ; Ganglia, Spinal/metabolism ; Mice ; Mice, Transgenic ; NAV1.7 Voltage-Gated Sodium Channel/metabolism ; Optogenetics ; Pain/genetics ; Recombinases/metabolism
Chemical Substances	Channelrhodopsins ; NAV1.7 Voltage-Gated Sodium Channel ; Recombinases ; Scn9a protein, mouse
Language	English
Publishing date	2022-10-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0275751
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Article ; Online: Fhod1, an actin-organizing formin family protein, is dispensable for cardiac development and function in mice.

Sanematsu, Fumiyuki / Kanai, Ami / Ushijima, Tomoki / Shiraishi, Aki / Abe, Takaya / Kage, Yohko / Sumimoto, Hideki / Takeya, Ryu

Cytoskeleton (Hoboken, N.J.)

2019 Volume 76, Issue 2, Page(s) 219–229

Abstract: The formin family proteins have the ability to regulate actin filament assembly, thereby functioning in diverse cytoskeletal processes. Fhod3, a cardiac member of the family, plays a crucial role in development and functional maintenance of the heart. ... ...

Abstract	The formin family proteins have the ability to regulate actin filament assembly, thereby functioning in diverse cytoskeletal processes. Fhod3, a cardiac member of the family, plays a crucial role in development and functional maintenance of the heart. Although Fhod1, a protein closely-related to Fhod3, has been reported to be expressed in cardiomyocytes, the role of Fhod1 in the heart has still remained elusive. To know the physiological role of Fhod1 in the heart, we disrupted the Fhod1 gene in mice by replacement of exon 1 with a lacZ reporter gene. Histological lacZ staining unexpectedly revealed no detectable expression of Fhod1 in the heart, in contrast to intensive staining in the lung, a Fhod1-containing organ. Consistent with this, expression level of the Fhod1 protein in the heart was below the lower limit of detection of the present immunoblot analysis with three independent anti-Fhod1 antibodies. Homozygous Fhod1-null mice did not show any defects in gross and histological appearance of the heart or upregulate fetal cardiac genes that are induced under stress conditions. Furthermore, Fhod1 ablation did not elicit compensatory increase in expression of other formins. Thus, Fhod1 appears to be dispensable for normal development and function of the mouse heart, even if a marginal amount of Fhod1 is expressed in the heart.
MeSH term(s)	Actins/metabolism ; Animals ; Cardiomyopathies/embryology ; Cardiomyopathies/genetics ; Cardiomyopathies/pathology ; Fetal Proteins/deficiency ; Fetal Proteins/genetics ; Fetal Proteins/metabolism ; Formins/deficiency ; Formins/genetics ; Formins/metabolism ; Gene Deletion ; Gene Expression Regulation, Developmental ; Gene Targeting ; Heart/diagnostic imaging ; Heart/embryology ; Mice, Knockout ; Sarcomeres/metabolism
Chemical Substances	Actins ; FHOD1 protein, mouse ; Fetal Proteins ; Fhod3 protein, mouse ; Formins
Language	English
Publishing date	2019-04-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2534372-5
ISSN	1949-3592 ; 1949-3584
ISSN (online)	1949-3592
ISSN	1949-3584
DOI	10.1002/cm.21523
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