Updated on 2023/09/18

写真a

 
TAKEDA Ikuko
 
Organization
Graduate School of Medicine Program in Integrated Medicine Anatomy and Cell Biology Lecturer
Graduate School
Graduate School of Medicine
Undergraduate School
School of Medicine Department of Medicine
Title
Lecturer
External link

Degree 1

  1. 医学(博士) ( 2014.1   広島大学 ) 

Research Interests 3

  1. neuronal circuit

  2. chronic pain

  3. microglia

Research History 3

  1. Nagoya University   Department of Anatomy and Molecular Cell Biology, Graduate School of Medicine   Lecturer

    2022.12

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    Country:Japan

  2. Nagoya University   Department of Anatomy and Molecular Cell Biology Graduate School of Medicine   Assistant Professor

    2021.9 - 2022.11

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  3. Hiroshima University   Assistant Professor

    2015.4 - 2016.4

Education 1

  1. Hiroshima University

    2009.4 - 2014.1

 

Papers 20

  1. Controlled activation of cortical astrocytes modulates neuropathic pain-like behaviour Reviewed International coauthorship International journal

    Ikuko Takeda, Kohei Yoshihara, Dennis L. Cheung, Tomoko Kobayashi, Masakazu Agetsuma, Makoto Tsuda, Kei Eto, Schuichi Koizumi, Hiroaki Wake, Andrew J. Moorhouse, Junichi Nabekura

    Nature Communications   Vol. 13 ( 1 ) page: 4100 - 4100   2022.7

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

    Chronic pain is a major public health problem that currently lacks effective treatment options. Here, a method that can modulate chronic pain-like behaviour induced by nerve injury in mice is described. By combining a transient nerve block to inhibit noxious afferent input from injured peripheral nerves, with concurrent activation of astrocytes in the somatosensory cortex (S1) by either low intensity transcranial direct current stimulation (tDCS) or via the chemogenetic DREADD system, we could reverse allodynia-like behaviour previously established by partial sciatic nerve ligation (PSL). Such activation of astrocytes initiated spine plasticity to reduce those synapses formed shortly after PSL. This reversal from allodynia-like behaviour persisted well beyond the active treatment period. Thus, our study demonstrates a robust and potentially translational approach for modulating pain, that capitalizes on the interplay between noxious afferents, sensitized central neuronal circuits, and astrocyte-activation induced synaptic plasticity.

    DOI: 10.1038/s41467-022-31773-8

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  2. Microglia enable cross-modal plasticity by removing inhibitory synapses. Reviewed International journal

    Akari Hashimoto, Nanami Kawamura, Etsuko Tarusawa, Ikuko Takeda, Yuki Aoyama, Nobuhiko Ohno, Mio Inoue, Mai Kagamiuchi, Daisuke Kato, Mami Matsumoto, Yoshihiro Hasegawa, Junichi Nabekura, Anne Schaefer, Andrew J Moorhouse, Takeshi Yagi, Hiroaki Wake

    Cell reports   Vol. 42 ( 5 ) page: 112383 - 112383   2023.5

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    Language:English   Publishing type:Research paper (scientific journal)  

    Cross-modal plasticity is the repurposing of brain regions associated with deprived sensory inputs to improve the capacity of other sensory modalities. The functional mechanisms of cross-modal plasticity can indicate how the brain recovers from various forms of injury and how different sensory modalities are integrated. Here, we demonstrate that rewiring of the microglia-mediated local circuit synapse is crucial for cross-modal plasticity induced by visual deprivation (monocular deprivation [MD]). MD relieves the usual inhibition of functional connectivity between the somatosensory cortex and secondary lateral visual cortex (V2L). This results in enhanced excitatory responses in V2L neurons during whisker stimulation and a greater capacity for vibrissae sensory discrimination. The enhanced cross-modal response is mediated by selective removal of inhibitory synapse terminals on pyramidal neurons by the microglia in the V2L via matrix metalloproteinase 9 signaling. Our results provide insights into how cortical circuits integrate different inputs to functionally compensate for neuronal damage.

    DOI: 10.1016/j.celrep.2023.112383

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  3. 特集 慢性疼痛 慢性疼痛とシナプス再編-グリア細胞制御による治療法を目指して

    鍋倉 淳一, 竹田 育子

    BRAIN and NERVE   Vol. 75 ( 3 ) page: 207 - 216   2023.3

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    Publisher:株式会社医学書院  

    DOI: 10.11477/mf.1416202310

    CiNii Research

  4. [Microglial regulation of brain function and pathological changes].

    Wake H, Hashimoto A, Kato D, Takeda I

    Nihon yakurigaku zasshi. Folia pharmacologica Japonica   Vol. 158 ( 5 ) page: 359 - 361   2023

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    Language:Japanese  

    DOI: 10.1254/fpj.23010

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  5. Overexpression of neuronal K+-Cl- co-transporter enhances dendritic spine plasticity and motor learning. Reviewed

    Kayo Nakamura, Andrew John Moorhouse, Dennis Lawrence Cheung, Kei Eto, Ikuko Takeda, Paul Wiers Rozenbroek, Junichi Nabekura

    The journal of physiological sciences : JPS   Vol. 69 ( 3 ) page: 453 - 463   2019.5

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    Language:English   Publishing type:Research paper (scientific journal)  

    The neuronal K+-Cl- cotransporter KCC2 maintains a low intracellular Cl- concentration and facilitates hyperpolarizing GABAA receptor responses. KCC2 also plays a separate role in stabilizing and enhancing dendritic spines in the developing nervous system. Using a conditional transgenic mouse strategy, we examined whether overexpression of KCC2 enhances dendritic spines in the adult nervous system and characterized the effects on spine dynamics in the motor cortex in vivo during rotarod training. Mice overexpressing KCC2 showed significantly increased spine density in the apical dendrites of layer V pyramidal neurons, measured in vivo using two-photon imaging. During modest accelerated rotarod training, mice overexpressing KCC2 displayed enhanced spine formation rates, greater balancing skill at higher rotarod speeds and a faster rate of learning in this ability. Our results demonstrate that KCC2 enhances spine density and dynamics in the adult nervous system and suggest that KCC2 may play a role in experience-dependent synaptic plasticity.

    DOI: 10.1007/s12576-018-00654-5

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  6. Cortical astrocytes prime the induction of spine plasticity and mirror image pain. Reviewed International journal

    Tatsuya Ishikawa, Kei Eto, Sun Kwang Kim, Hiroaki Wake, Ikuko Takeda, Hiroshi Horiuchi, Andrew J Moorhouse, Hitoshi Ishibashi, Junichi Nabekura

    Pain   Vol. 159 ( 8 ) page: 1592 - 1606   2018.8

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    Publishing type:Research paper (scientific journal)  

    Peripheral nerve injury causes maladaptive plasticity in the central nervous system and induces chronic pain. In addition to the injured limb, abnormal pain sensation can appear in the limb contralateral to the injury, called mirror image pain. Because synaptic remodeling in the primary somatosensory cortex (S1) has critical roles in the induction of chronic pain, cortical reorganization in the S1 ipsilateral to the injured limb may also accompany mirror image pain. To elucidate this, we conducted in vivo 2-photon calcium imaging of neuron and astrocyte activity in the ipsilateral S1 after a peripheral nerve injury. We found that cross-callosal inputs enhanced the activity of both S1 astrocytes and inhibitory neurons, whereas activity of excitatory neurons decreased. When local inhibitory circuits were blocked, astrocyte-dependent spine plasticity and allodynia were revealed. Thus, we propose that cortical astrocytes prime the induction of spine plasticity and mirror image pain after peripheral nerve injury. Moreover, this result suggests that cortical synaptic rewiring could be sufficient to cause allodynia on the uninjured periphery.

    DOI: 10.1097/j.pain.0000000000001248

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  7. The roles of cortical astrocytes in chronic pain and other brain pathologies. Reviewed International journal

    Kei Eto, Sun Kwang Kim, Ikuko Takeda, Junichi Nabekura

    Neuroscience research   Vol. 126   page: 3 - 8   2018.1

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    Publishing type:Research paper (scientific journal)  

    Astrocytes are the most abundant cell type in the brain. Several decades ago, they were considered to be only support cells in the central nervous system. Recent studies using advanced technologies have clarified that astrocytes play more active roles in regulating neuronal function and remodeling synaptic structures by releasing molecules called gliotransmitters. In addition to various physiological functions, astrocytes are activated under disease conditions, such as chronic pain, releasing molecules that in turn cause reorganization of the central nervous system microstructure and disrupt behavior in pathological conditions. In the present review, we summarize cortical astrocyte function in chronic pain and other neurological disorders and discuss the role of astrocytes in brain pathologies.

    DOI: 10.1016/j.neures.2017.08.009

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  8. Neurological Complications in Eosinophilic Granulomatosis with Polyangiitis (EGPA): The Roles of History and Physical Examinations in the Diagnosis of EGPA. Reviewed

    Hiroshi Oiwa, Sho Mokuda, Tomoyasu Matsubara, Masamoto Funaki, Ikuko Takeda, Takemori Yamawaki, Kazuhiko Kumagai, Eiji Sugiyama

    Internal medicine (Tokyo, Japan)   Vol. 56 ( 22 ) page: 3003 - 3008   2017.11

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    Publishing type:Research paper (scientific journal)  

    Objective To investigate the clinical symptoms, the physical and neurological findings, and the clinical course of neurological complications in eosinophilic granulomatosis with polyangiitis (EGPA). Methods A retrospective chart review of EGPA cases managed by two referral hospitals was performed, with a focus on the neurological findings. The study analyzed the symptoms at the onset of EGPA and investigated their chronological relationship. The patient delay (the delay between the onset of symptoms and the initial consultation), and the physician delay (the delay from consultation to the initiation of therapy) were determined and compared. The involved nerves were identified thorough a neurological examination. The cases with central nervous system (CNS) involvement were described. Results The average duration of symptoms prior to the initiating of therapy for sensory disturbances, motor deficits, rash, edema, and fever was 23, 5, 21, 18, and 24 days, respectively. Among the EGPA-specific symptoms, sensory disturbance was often the first symptom (63%), and was usually followed by the appearance of rash within four days (63%). The average physician delay (32.9±38.3 days) was significantly longer than the average patient delay (7.9±7.8 days; p=0.010). Reduced touch sensation in the superficial peroneal area, and weakness of dorsal flexion of the first toe secondary to deep peroneal nerve involvement, were highly sensitive for identifying the presence of peripheral nerve involvement in our series of patients with EGPA. Two cases, with CNS involvement, had multiple skin lesions over their hands and feet (Janeway lesions). Conclusion Japanese physicians are not always familiar with EGPA. It is important for us to consider this disease, when an asthmatic patient complains about the new onset of an abnormal sensation in the distal lower extremities, which is followed several days later by rash.

    DOI: 10.2169/internalmedicine.8457-16

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  9. A case of chronic inflammatory demyelinating polyradiculoneuropathy after treatment with pegylated interferon ?-2a in a patient with chronic hepatitis B virus infection Reviewed

    Hiroyuki Naito, Ikuko Takeda, Akiko Segawa, Masataka Tsuge, Hirofumi Maruyama, Masayasu Matsumoto

    Clinical neurology   Vol. 56 ( 10 )   2016.9

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    Language:Japanese   Publishing type:Research paper (scientific journal)  

  10. CD34+/CD144+ Circulating Endothelial Cells as an Indicator of Carotid Atherosclerosis Reviewed

    Journal of stroke and cerebrovascular diseases: the official journal of National Stroke Association   Vol. 24 ( 3 ) page: 583 - 590   2014.12

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jstrokecerebrovasdis.2014.10.001

  11. Safety Evaluation of Substituting Clopidogrel for Ticlopidine in Japanese Patients with Ischemic Stroke—Hiroshima Ticlopidine, Clopidogrel Safe Exchange Trial Reviewed

    Journal of stroke and cerebrovascular diseases: the official journal of National Stroke Association   Vol. 23 ( 6 )   2014.7

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    Language:English  

  12. Isolated Unilateral Hypoglossal Nerve Paralysis Caused by Internal Carotid Artery Dissection Reviewed

    Journal of stroke and cerebrovascular diseases: the official journal of National Stroke Association   Vol. 23 ( 8 )   2014.7

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    Language:English  

  13. Fiber Type-Specific Expression of Low-Density Lipoprotein Receptor-Related Protein 6 in Human Skeletal Muscles Reviewed

    Pathobiology   Vol. 81 ( 2 ) page: 94 - 99   2014.1

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

  14. Autosomal recessive Andersen–Tawil syndrome with a novel mutation L94P in Kir2.1 Invited Reviewed

    Neurology and Clinical Neuroscience     2013.7

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

  15. Cancer-associated ischemic stroke is associated with elevated D-dimer and fibrin degradation product levels in acute ischemic stroke with advanced cancer Invited Reviewed

    Geriatrics & Gerontology International     2012.1

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    Language:English  

  16. Clinical characteristics of ischemic stroke in elderly patients with cancer Invited Reviewed

    Japanese Journal of Geriatrics     2011.1

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    Language:Japanese  

  17. Two Cases of Cerebral Embolism Caused by Apical Thrombi in Midventricular Obstructive Cardiomyopathy Invited Reviewed

    Internal Medicine     2011.1

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    Authorship:Lead author   Language:English  

  18. Efficacy of the Free Radical Scavenger, Edaravone, for Motor Palsy of Acute Lacunar Infarction Invited Reviewed

    Internal Medicine     2009.1

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    Language:English  

  19. Two Populations of microglial cells isolated from rat primary mixed glial cultures Reviewed

    Journal of Neuroscience Research     2003.7

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    Language:English  

  20. Effects of norepinephrine on rat cultured microglial cells that express alpha1, alpha2, beta1 and beta2 adrenergic receptors Reviewed

    Neuropharmacology     2002.11

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    Language:English  

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Books 1

  1. 糖尿病診療ガイドライン

    竹田育子,大槻俊輔,松本昌泰( Role: Joint author ,  糖尿病における脳血管障害のリスク)

    南山堂  2011.2  ( ISBN:978-4-525-23821-6

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    Total pages:422  

MISC 11

  1. 一次体性感覚野アストロサイトの活動制御による痛み関連行動の治療 Invited

    竹田育子

      Vol. 2   2023.4

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    Authorship:Lead author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (other)  

  2. 体の「痛い」を脳から治す ―痛みに関わる神経回路を標的とした疼痛の新たな治療戦略― Invited

    竹田育子

    神経科学トピックス     2023.2

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    Authorship:Lead author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (other)  

  3. ミクログリアによる脳機能制御と病態時の変化 Invited

    和氣弘明、橋本明香里、加藤大輔、竹田育子

    日本薬理学雑誌   Vol. 158 ( 5 )   2023

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    Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

    DOI: https://doi.org/10.1254/fpj.23010

  4. ミクログリアとシナプス機能

    和氣弘明、橋本明香里、竹田育子、加藤大輔

        2022.11

  5. ミクログリアの生理機能と病態 Invited

    渋下碧、竹田育子、和氣弘明

    炎症と免疫   Vol. 30 ( 3 )   2022.4

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    Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

  6. 大脳皮質体性感覚野における神経回路の再構築 Invited

    竹田育子,江藤圭,鍋倉淳一

    ペインクリニック   Vol. 39   page: 35 - 41   2018

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    Authorship:Lead author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

  7. The roles of cortical astrocytes in chronic pain and other brain pathologies. Invited

    Eto K, Kim SK, Takeda I, Nabekura J

    Neuroscience Research   Vol. 126   page: 3 - 8   2018

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    Authorship:Last author   Language:English  

  8. 発達・病態における神経回路再編成 Invited

    江藤圭,竹田育子,鍋倉淳一

    実験医学   Vol. 36   page: 125 - 132   2018

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    Authorship:Last author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)  

  9. 突発性ミオグロビン尿で発症した脂質代謝異常症の一例 Reviewed

    増田 沙季, 倉重 毅志, 同道 頼子, 竹田 育子, 上野 弘貴, 西野 一三, 丸山 博文

    臨床神経学   Vol. 57 ( 5 ) page: 251 - 251   2017.5

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    Language:Japanese   Publisher:(一社)日本神経学会  

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  10. 平衡機能障害・運動失調 Invited

    竹田育子,山脇健盛

    medicina   Vol. 49 ( 4 ) page: 614 - 616   2012

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    Authorship:Lead author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)  

  11. 麻痺/しびれ Invited

    竹田育子,山脇健盛

    診断と治療   Vol. 99 ( 1 ) page: 31 - 35   2011

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    Authorship:Lead author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)  

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Presentations 16

  1. The role of astrocytes in V2L neuronal remodeling following vision loss International conference

    Ikuko Takeda

    ISN-ESN meeting  2023.8.12 

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    Event date: 2023.8

    Language:English   Presentation type:Poster presentation  

    Venue:Porto   Country:Portugal  

  2. アストロサイトが関与する高次視覚野感覚統合機序

    竹田育子

    第6回グリアデコーディング領域会議  2023.7.17  グリアデコード

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    Event date: 2023.7

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  3. The role of glial cells in cross-modal plasticity

    2023.7.7 

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    Event date: 2023.7

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  4. Astrocyte-mediated neuronal circuit remodeling in higher visual cortex induced by sensory deprivation International conference

    2023.4.27  CSH Asia

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    Event date: 2023.4

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  5. Astrocyte-mediated neuronal circuit remodeling in higher visual cortex induced by sensory deprivation

    2023.3.15 

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    Event date: 2023.3

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  6. アストロサイトが誘導する神経回路再編成 Invited

    竹田育子

    次世代脳  2022.12.16  次世代脳プロジェクト

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    Event date: 2022.12

    Language:Japanese   Presentation type:Public lecture, seminar, tutorial, course, or other speech  

    Venue:オンライン   Country:Japan  

  7. ミクログリアによる異種感覚の可塑性

    竹田育子

    学術変革A iPlasticity 夏の領域会議  2022.8.3  学術変革A iPlasticity

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    Event date: 2022.8

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京   Country:Japan  

  8. The alteration of astrocytes in cross-modal plasticity

    Ikuko Takeda

    Neuro2022  2022.7.1 

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    Event date: 2022.6 - 2022.7

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  9. 一次体性感覚野のアストロサイトによる慢性疼痛への治療的アプローチ

    竹田 育子、Dennis L. Chung、和氣 弘明、鍋倉 淳一

    第127回日本解剖学会総会・全国学術集会  2022.3.28 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Poster presentation  

  10. Modulating astrocytes activation reorganizes noxious circuits in chronic pain

    Ikuko Takeda, Dennis L. Cheung, Hiroaki Wake, Junichi Nabekura

    2022.3.17 

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    Event date: 2022.3

    Language:English   Presentation type:Poster presentation  

  11. Modulating astrocyte activity reverse allodynia in chronic pain

    Ikuko Takeda

    2022.1.18 

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    Event date: 2022.1

    Language:English   Presentation type:Oral presentation (general)  

  12. ミクログリアによる異種感覚の可塑性構築機序

    竹田 育子

    学術変革A臨界期生物学2021年領域班会議  2022.1.14 

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    Event date: 2022.1

    Language:Japanese   Presentation type:Oral presentation (general)  

  13. Modulating astrocyte activation reorganizes noxious circuits in chronic pain

    Ikuko Takeda, Hiroaki Wake, Junichi Nabekura

    2021.12.17 

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    Event date: 2021.12

  14. Activated astrocytes as a therapeutic approach adjust noxious circuits in chronic pain International coauthorship

    Ikuko Takeda, Dennis L. Cheung, Junichi Nabekura

    2021.7.28 

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    Event date: 2021.7

    Language:English   Presentation type:Poster presentation  

  15. Astrocyte rehabilitate noxious circuits

    Ikuko Takeda

    the 98th Annual Meeting of The Physiological Society of Japan, the 126th Annual Meeting of The Japanese Association of Anatomists  2021.3.29 

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    Event date: 2021.3

    Language:English   Presentation type:Symposium, workshop panel (public)  

  16. Reactivation of astrocytes can reverse chronic pain

    Ikuko Takeda

    The 10th NIPS-PRI-BRINU Joint Symposium  2021.3.12 

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    Event date: 2021.3

    Language:English   Presentation type:Poster presentation  

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Research Project for Joint Research, Competitive Funding, etc. 1

  1. 色から迫る慢性疼痛治療と神経回路基盤編成

    Grant number:2600007301  2022.4 - 2023.3

    堀科学芸術振興財団 研究費助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\1000000

KAKENHI (Grants-in-Aid for Scientific Research) 6

  1. ミクログリアによる異種感覚の可塑性構築機序

    Grant number:21H05688  2021.9 - 2023.3

    科学研究費助成事業  学術変革領域研究(A)

    竹田 育子

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    Authorship:Principal investigator 

    Grant amount:\7800000 ( Direct Cost: \6000000 、 Indirect Cost:\1800000 )

  2. Cheromotherapy relieves pain by neural circuit organisation

    Grant number:23K06825  2023.4 - 2026.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship:Principal investigator 

    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

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  3. Development of pain treatment using color

    2023.4 - 2024.3

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  4. 感覚モダリティ理解のためのミクログリア・シナプス接触の多角的解析

    Grant number:20KK0170  2020.10 - 2024.3

    国際共同研究加速基金(国際共同研究強化(B))

    和氣 弘明

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    Authorship:Coinvestigator(s) 

    本国際研究では中枢神経系唯一の免疫細胞であるミクログリアに着目し、ミクログリアがシナプスの構造的・機能的可塑性を修飾する背景を踏まえ、多角的階層的な技術を相互補完することによって、ミクログリアのシナプスに対する時間的(発達・成熟)および空間(脳領域)特異的な生理機能を明らかにする。さらにこれを異種感覚の可塑的変化のメカニズムに繋げ、そこから精神病態を考察する。

  5. S1 astrocytes are therapeutic target for chronic pain

    Grant number:20K16510  2020.4 - 2022.3

    Grant-in-Aid for Early-Career Scientists

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    Authorship:Principal investigator 

    Grant amount:\3900000 ( Direct Cost: \3000000 、 Indirect Cost:\900000 )

  6. Astrocytic modulation of tauopathy

    Grant number:17K16133  2017.4 - 2019.3

    Takeda Ikuko

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    Authorship:Principal investigator 

    Grant amount:\3640000 ( Direct Cost: \2800000 、 Indirect Cost:\840000 )

    This study is to find a new tool to specifically activate astrocytes for a novel therapeutic target of tauopathy. To induce astrocyte activation, I used hM3Dq(Gq)-DREADD under GFAP promter. Astrocytes exprssed hM3Dq(Gq)-DREADD showed the increase of long-term Ca2+ transients via G protein signaling following CNO intraperitoneal injection. Activated astrocytes increased spine turnover rates in long-term spine imaging during CNO injection, possibly rewiring neural circuits.

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Teaching Experience (On-campus) 10

  1. 基礎医学体験実習

    2023

  2. 解剖学実習

    2023

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    頭頸部解剖

  3. 基礎セミナーA

    2023

  4. 骨解剖実習

    2023

  5. 神経解剖実習

    2022

  6. 解剖学実習

    2022

  7. 骨解剖実習

    2022

  8. 基礎セミナーA

    2022

  9. Neuroanatomy

    2022

  10. 基礎生物学II

    2021

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