第 3 回 CIBoGリトリート
第 14 回 NAGOYA グローバルリトリート

名古屋大学医学系研究科
CIBoG 卓越大学院【プログラム・抄録集】

令和 4 年 2 月 19 日（土）cibog@med.nagoyau.ac.jp

目次

第 3 回 CIBoG リトリート（第 14 回 NAGOYA グローバルリトリート）の開催にあたって ……………………………………………………………………………………………… 1
第 3 回 CIBoG リトリート（第 14 回 NAGOYA グローバルリトリート）の開催にあたって 〜実行委員会より〜 ……………………………………………………………… 2
スケジュール …………………………………………………………………………………………………… 3
講演者一覧 ……………………………………………………………………………………………………… 5
口頭発表者一覧 ……………………………………………………………………………………………… 11
発表規定 ……………………………………………………………………………………………………… 15
特別講演抄録 ………………………………………………………………………………………………… 17
医学奨励賞

受賞講演抄録 ……………………………………………………………………………… 19

一般講演抄録 ………………………………………………………………………………………………… 24
口頭発表抄録 ………………………………………………………………………………………………… 28
参加者一覧 …………………………………………………………………………………………………… 44
第 3 回 CIBoG リトリート（第 14 回 NAGOYA グローバルリトリート）実行委員 ………… 51

第 3 回 CIBoG リトリートの開催にあたって
（第 14 回 NAGOYA グローバルリトリート）

名古屋大学大学院医学系研究科長

門松

健治

常に進歩し続ける生命医科学の分野において次代を担う若手研究者の育成は、私たちが属する研究機関の重要な責務であります。この 10 年で生命医科学は劇的な進歩を遂げてきました。
生命医科学ビッグデータを解析して、病気の理解や新たな治療法の開発、さらには病気の発症を未然に防ぐような個別化予防の創成が社会的にも求められ、傑出した研究を行うためには情報科学をはじめとする多様な分野間の連携が必須となっております。

NAGOYA グローバルリトリートは、東海圏の若手研究者が研究分野や所属機関を超えて、幅広く交流し、お互いの研究活動を理解する、またとない機会であり、お互いに探究心を刺激
し合う貴重なイベントです。企画から運営まで全て若手研究者自身が行っている点もその特徴と言えます。
本リトリートは、平成 20 年度にグローバル COE プログラム「機能分子医学への神経疾患・腫瘍の融合拠点」を基盤として初めて開催され、今回が 14 回目です。回数を重ねる中で、神経疾患・腫瘍分野にとどまらず、生物医学領域全体を対象とした会として発展し、現在に至っています。さらに、令和元年度に卓越大学院プログラムとして採用された「情報・生命医科学コンボリューション on グローカルアライアンス卓越大学院（CIBoG 卓越大学院）プログラム」の枠組みの中で開催されました。名古屋大学大学院医学系研究科、国立長寿医療研究センター、
愛知県がんセンター、生理学研究所、愛知県医療療育総合センター 発達障害研究所および名
古屋大学環境医学研究所に、名古屋大学創薬科学研究科、名古屋大学情報学研究科、名古屋大
学生命農学研究科、岐阜大学などを加えた、多くの施設からご参加いただきます。様々なバッ
クグラウンドを持つ若手研究者の参加のもと、活発な議論が行われ、多分野研究の交流の場となることを期待します。
第 14 回を迎えるにあたり、特別講演において大阪大学

茂呂和世先生にご講演頂くことは、

誠に光栄であります。一昨年までであれば「あいち健康プラザ」にて 2 日間の合宿形式の開催でありましたが、今年は新型コロナウイルス感染症（COVID19）の感染状況より、オンライン形
式での 1 日開催となりました。1 日開催ではございますが、今回のリトリートも、特別講演に加え、CIBoG 大学院生を含む大学院生・若手研究者による口頭発表や、一般講演、医学奨励賞受賞講演が設けられ、各施設から推薦された若手研究者による講演も行われます。ご多忙の中、快くご協力頂きました諸先生方に心より御礼を申し上げます。
このリトリートが、若手研究者の皆さんにとって、よい刺激となり、新しい交流がうまれることを願ってやみません。

─1─

第 3 回 CIBoG リトリートの開催にあたって
（第 14 回 NAGOYA グローバルリトリート）〜 実行委員会より 〜
実行委員会代表

名古屋大学大学院医学系研究科

分子生物学

尾崎

智也

I would like to thank all the participants for taking time out of your busy schedules of research,clinical work, and education to join us. Although there may be some shortcomings in the
management of the retreat, I believe that the retreat will provide many opportunities for you toparticipate in cuttingedge research, including special lectures, presentations by colleagues in otherfields, and new encounters through discussions. It will be a great pleasure for us, the planningcommittee, if we can be of any help to you in your research life. Let's enjoy the retreat.
この度、第 3 回 CIBoG リトリート（第 14 回 NAGOYA グローバルリトリート）を開催させて頂くこととなりました。本リトリートは、毎年 2 月に若手研究者育成や東海地区の研究機関の連携などを目的とした学術交流会であり、従来「NAGOYA グローバルリトリート」という名称で 2009 年から開催しておりました。2019 年度より、名古屋大学大学院医学系研究科では卓越
大学院プログラムに採択されたことを受け、本プログラムの通称である CIBoG（Convolutionof Informatics and Biomedical Sciences on Glocal Alliances）が本学術交流会を主催しております。また、名古屋大学大学院医学系研究科が共催となり、周辺の研究機関（国立長寿医療研究センター、愛知県がんセンター、愛知県医療療育総合センター発達障害研究所、生理学研究所）に加え、名古屋大学環境医学研究所、名古屋大学大学院生命農学研究科、創薬科学研究科、情報学研究科、さらに岐阜大学も参画しております。
一昨年までは大府市のあいち健康プラザにて 2 日間の合宿形式で開催されておりましたが、今年は、新型コロナウイルス感染症の拡大に伴い、昨年同様 Web での 1 日開催となりました。

1 日開催ではございますが、CIBoG 大学院生を含む大学院生・若手研究者による口頭発表や一般講演、医学奨励賞受賞講演、そして特別講演もプログラムに入っており、このリトリートを通じて、この地域で実施されている多くの医学系研究に触れられる内容の濃いプログラムとなっております。
参加者の皆様におかれましては、研究、臨床、教育にお忙しい合間をぬって、ご参加いただ
きありがとうございます。運営に至らない点があるかとは思いますが、特別講演をはじめとする最先端の研究、他分野の同世代研究者の発表、そしてディスカッションを通して皆様の研究が益々発展しますことを実行委員一同お祈り申し上げます。

─2─

スケジュール
2022.2.19
9:00 〜 9:10

開会の辞

9:10 〜10:25

口頭発表 Session A（3 部屋，各 7 演題，各 10 分（7 分発表＋ 3 分質疑応答））

10:25 〜10:30

休憩

10:30 〜11:45

口頭発表 Session B（3 部屋，各 7 演題，各 10 分（7 分発表＋ 3 分質疑応答）)

11:45 〜11:50

休憩

11:50 〜13:15

口頭発表 Session C（3 部屋，各 7 〜 8 演題，各 10 分（7 分発表＋ 3 分質疑応答））

13:15 〜14:00

休憩

14:00 〜15:00

一般講演（3 演題，各 18 分（発表 14 分＋質疑応答 4 分））

15:00 〜15:10

休憩

15:10 〜16:10

特別講演

16:10 〜16:20

休憩

16:20 〜17:35

医学奨励賞受賞講演（4 演題，各 18 分（発表 14 分＋質疑応答 4 分））

17:35 〜17:55

表彰・閉会式茂呂和世先生─3─Schedule
2022.2.19
9:00 〜 9:10

Opening Remarks

9:10 〜10:25（7min presentation & 3min Q&A）

10:25 〜10:30

Break

10:30 〜11:45

Oral Presentations Session B: 3 rooms, 7 titles, 10min each（7min presentation & 3min Q&A）

11:45 〜11:50

Break

11:50 〜13:15（7min presentation & 3min Q&A）

13:15 〜14:00

Break

14:00 〜15:00

General Lectures: 3 titles, 18min each（14min lecture & 4min Q&A）

15:00 〜15:10

Break

15:10 〜16:10

Special Lecture: Dr. Kazuyo Moro（Osaka University）

16:10 〜16:20

Break

16:20 〜17:35

The Medical Research AwardWining Lecture: 4 titles, 18min each
（14min lecture & 4min Q&A）

17:35 〜17:55

Award Ceremony & Closing Remarks

Oral Presentations Session A: 3 rooms, 7 titles, 10min each

Oral Presentations Session C: 3 rooms, 7 or 8 titles, 10min each─4─

講演者一覧
2022.2.19
司会・進行（午前）：羽根

正弥（名古屋大学生命農学研究科

糖鎖生命コア研究所）

9:00 〜 9:10

開会の辞

9:10 〜 10:25

口頭発表 Session A（3 部屋，各 7 演題，各 10 分（7 分発表＋ 3 分質疑応答））

Room 1

座長：日比野絵美（名古屋大学創薬科学研究科 構造分子薬理学）
河谷

Room 2

昌泰（名古屋大学環境医学研究所

神経系分野Ⅱ）

座長：宇野 光平（名古屋大学医学系研究科 総合保健）
藤巻加於梨（名古屋大学医学系研究科

Room 3分子細胞免疫学）

座長：河村奈緒子（岐阜大学 糖鎖生命コア研究所）
植松高史（名古屋大学医学系研究科

神経内科学）

10:25 〜 10:30

休

10:30 〜 11:45

口頭発表 Session B（3 部屋，各 7 演題，各 10 分（7 分発表＋ 3 分質疑応答））

Room 1

座長：羽根 正弥（名古屋大学生命農学研究科 糖鎖生命コア研究所）
髙橋Room 2

憩

秀和（名古屋大学医学系研究科

消化器内科学）

座長：濵口 知成（名古屋大学医学系研究科 神経遺伝情報学）
伊佐次光莉（名古屋大学医学系研究科（保健）リハビリテーション療法学）

Room 3

座長：祖父江 顕（名古屋大学環境医学研究所 病態神経科学）
畑中

11:45 〜 11:50

休理菜（名古屋大学生命農学研究科

憩─5─

糖鎖生命科学）

11:50 〜 13:15
Room 1

口頭発表 Session C（3 部屋，各 7 〜 8 演題，各 10 分（7 分発表＋ 3 分質疑応答））
座長：永田 健一（名古屋大学医学系研究科 機能組織学）
神田

Room 2

Room 3容（名古屋大学環境医学研究所

分子代謝医学）座長：横井聡（名古屋大学医学系研究科

神経内科学）

鈴木

佑治（名古屋大学医学系研究科

分子生物学）

座長：尾崎 智也（名古屋大学医学系研究科 分子生物学）
酒井

13:15 〜 14:00

休

昭平（名古屋大学環境医学研究所

憩

司会・進行（午後）：宇野

14:00 〜 15:00

病態神経科学）光平（名古屋大学医学系研究科

総合保健）

一般講演（3 演題，各 18 分（発表 14 分＋質疑応答 4 分））
座長：小林 憲太（生理学研究所 ウィルスベクター開発室）
岩間信太郎（名古屋大学医学系研究科 糖尿病・内分泌内科学）
篠原充（国立長寿医療研究センター 分子基盤研究部）

Rejuvenation of aged T cells for effective adoptive cancer immunotherapy
籠谷勇紀 （愛知県がんセンター

腫瘍免疫応答研究分野）

Development of sialic acid chemistry and its application to glycan syntheses
河村奈緒子 （岐阜大学

糖鎖生命コア研究所）

Properties of 2'5'linked oligonucleotides with a conformationally locked sugar conformation in anNform.
定池雅司 （名古屋大学創薬科学研究科

15:00 〜 15:10

休

15:10 〜 16:10

特別講演（1 演題）
座長：坪田
足立

基盤創薬学専攻）憩

庄真（名古屋大学医学系研究科
雄太（愛知県がんセンター

分子生物学）

がん標的治療 TR 分野）

The identification of ILC2 has changed the concept of type 2 immune diseases
茂呂

和世 （大阪大学大学院 医学系研究科 生体防御学教室／大阪大学 免疫学フロン
ティア研究センター 免疫・アレルギー／理化学研究所 生命医科学研究センター 自然免疫システム研究チーム）

─6─

16:10 〜 16:20

休

16:20 〜 17:35

医学奨励賞受賞講演（4 演題，各 18 分（発表 14 分＋質疑応答 4 分）
）
座長：吉崎

憩

嘉一（発達障害研究所

障害モデル研究部門）

小西

博之（名古屋大学医学系研究科

機能組織学）阪本

考司（名古屋大学医学系研究科

呼吸器内科学）

Splicing regulation of large exons secures phaseseparation of transcription factors in vertebrates
河地

利彦 （名古屋大学医学系研究科

神経遺伝情報学）

CD4+ T cells are essential for the development of destructive thyroiditis induced by anti–PD1 antibody inthyroglobulinimmunized mice安田康紀 （名古屋大学医学部附属病院

糖尿病・内分泌内科）

Neutrophil/lymphocyte ratio as a predictor of lymph node metastasis in extramammary Paget s disease
江畑

葵 （名古屋大学医学系研究科

皮膚科学）

Embryonal erythropoiesis and aging exploit ferroptosis/Lysosomal nitric oxide determines transition from
autophagy to ferroptosis after exposure to plasmaactivated Ringer's lactate
Hao Zheng （名古屋大学医学系研究科 生体反応病理学）

17:35 〜 17:55

表彰、閉会式─7─

List of speakers
2022.2.19
Moderators：Masaya Hane（GlycoLife Science, Nagoya University Institute for Glycocore
Research（iGCORE））

9:00 〜 9:10

9:10 〜 10:25
Room 1

Opening Remarks

Oral Presentations Session A: 3 rooms, 7 titles, 10min each（7min presentation & 3min Q&A）

Chairs：Emi Hibino（Structural Molecular Pharmacology, Nagoya University Graduate Schoolof Pharmaceutical Sciences）
Masahiro Kawatani（Neuroscience II, Nagoya University Research Institute ofEnvironmental Medicine（RIEM））

Room 2Chairs：Kohei Uno（Nagoya University Graduate School of Medicine（Health Sciences））
Kaori Fujimaki（Immunology, Nagoya University Graduate School of Medicine）

Room 3Chairs：Naoko Komura（Gifu University Institute for Glycocore Research（iGCORE））
Takashi Uematsu（Neurology, Nagoya University Graduate School of Medicine）

10:25 〜 10:30

Break

10:30 〜 11:45

Oral Presentations Session B: 3 rooms, 7 titles, 10min each（7min presentation & 3min Q&A）

Room 1Chairs：Masaya Hane（GlycoLife Science, Nagoya University Institute for Glycocore
Research（iGCORE））
Hidekazu Takahashi（Gastroenterology, Nagoya University Graduate School of
Medicine）

Room 2Chairs：Tomonari Hamaguchi（Neurogenetics, Nagoya University Graduate School of
Medicine）
Hikari Isaji（Occupational Therapy, Nagoya University Graduate School of Medicine（Health Sciences））

Room 3Chairs：Akira Sobue（Neuroscience and Pathobiology, Nagoya University Research Instituteof Environmental Medicine（RIEM））
Rina Hatanaka（GlycoLife Science, Nagoya University Graduate School of
Bioagricultural Sciences）

11:45 〜 11:50

Break

─8─

11:50 〜 13:15
Room 1

Oral Presentations Session C: 3 rooms, 7 or 8 titles, 10min each（7min presentation & 3min Q&A）

Chairs：Kenichi Nagata（Functional Anatomy and Neuroscience, Nagoya University Graduate
School of Medicine）
Hiro Kohda（Molecular Medicine and Metabolism, Nagoya University ResearchInstitute of Environmental Medicine（RIEM））

Room 2Chairs：Satoshi Yokoi（Neurology, Nagoya University Graduate School of Medicine）
Yuji Suzuki（Molecular Biology, Nagoya University Research Institute ofEnvironmental Medicine（RIEM））

Room 3Chairs：Tomoya Ozaki（Molecular Biology, Nagoya University Graduate School of Medicine）
Shohei Sakai（Neuroscience and Pathobiology, Nagoya University Research Instituteof Environmental Medicine（RIEM））

13:15 〜 14:00

BreakModerators：Kohei Uno（Nagoya University Graduate School of Medicine（Health Sciences））

14:00 〜 15:00

General Lectures: 3 titles, 18min each（14min lecture & 4min Q&A）

Chairs：Kenta Kobayashi（Viral Vector Development, National Institute for Physiological
Sciences（NIPS））
Shintaro Iwama（Endocrinology and Diabetes, Nagoya University Graduate School of
Medicine）
Mitsuru Shinohara（Aging Neurobiology, National Center for Geriatrics andGerontology）
Rejuvenation of aged T cells for effective adoptive cancer immunotherapy
Yuki Kagoya（Division of Immune Response, Aichi Cancer Center Research Institute
Division of Cellular Oncology, Department of Cancer Diagnostics andTherapeutics, Nagoya University Graduate School of Medicine）

Development of sialic acid chemistry and its application to glycan syntheses
Naoko Komura（Gifu University Institute for Glycocore Research（iGCORE））
Properties of 2'5'linked oligonucleotides with a conformationally locked sugar conformation in an Nform.
Masashi Sadaike（Division of Structural Molecular Pharmacology, Nagoya University Graduate
School of Pharmaceutical Sciences）

15:00 〜 15:10

Break

─9─

15:10 〜 16:10

Special Lecture: 1 title

Chairs：Shoma Tsubota（Molecular Biology, Nagoya University Graduate School of Medicine）
Yuta Adachi（Molecular Therapeutics, Aichi Cancer Center）
The identification of ILC2 has changed the concept of type 2 immune diseases
Kazuyo Moro （Professor, Laboratory for Innate Immune Systems, Department of Microbiology
and Immunology, Graduate School of Medicine, Osaka University
Laboratory for Innate Immune Systems, RIKEN Center for Integrative Medical
Sciences（IMS））

16:10 〜 16:20

Break

16:20 〜 17:35

The Medical Research AwardWining Lecture: 4 titles, 18min each
（14min lecture & 4min Q&A）

Chairs：Kaichi Yoshizaki（Disease Model, Institute for Developmental Research）
Hiroyuki Konishi（Functional Anatomy and Neuroscience, Nagoya University
Graduate School of Medicine）
Koji Sakamoto（Respiratory Medicine, Nagoya University Graduate School of
Medicine）
Splicing regulation of large exons secures phaseseparation of transcription factors in vertebrates
Toshihiko Kawachi （Neurogenetics, Nagoya University Graduate School of Medicine）
CD4+ T cells are essential for the development of destructive thyroiditis induced by anti–PD1 antibody inthyroglobulinimmunized mice
Yoshinori Yasuda （Endocrinology and Diabetes, Nagoya University Hospital）
Neutrophil/lymphocyte ratio as a predictor of lymph node metastasis in extramammary Paget s disease
Aoi Ebata （Dermatology, Nagoya University Graduate School of Medicine）
Embryonal erythropoiesis and aging exploit ferroptosis/Lysosomal nitric oxide determines transition from
autophagy to ferroptosis after exposure to plasmaactivated Ringer's lactate
Hao Zheng （Pathology and Biological Responses, Nagoya University Graduate School of
Medicine）

17:35 〜 17:55

Award Ceremony & Closing Remarks

─ 10 ─

List of Oral Presenters＊ Please note that the time may change slightly due to the extension and replacement of presentations.
Session No/Time Room No

Presentation Time/No

Name

Department or Division

1

Yumiko Kasugai

Cancer Epidemiology Aichi Cancer Centerand Prevention

9:20 〜 9:30

2

Hinano Komura

GlycoLife Science

Nagoya University Graduate Carbohydratebinding properties of
School of Bioagricultural
a novel sialic acid binding site on
Sciences, iGCORE
Siglec99:30 〜 9:40

3

Yoko Tanaka

Psychiatry

Nagoya University Graduate Relationship between driving andSchool of Medicine
gaze indices using a driving simulator

9:40 〜 9:50

4

Katsunori Yogo

Medical Quantum
Science

Nagoya University Graduate         School of Medicine (Health nanoparticles on plasmid DNA
Sciences)damage induced by therapeutic MV
Xrays9:50 〜 10:00

5

Hiroto Ito

Neuroscience II

Nagoya University Research         
Institute of Environmental sleep is involved in abnormal REM
Medicine (RIEM)
sleep architecture in narcolepsy

10:00 〜 10:10

6

Dong Yutao

Neuropsychopharmacology Nagoya University Graduate Dynamic changes and functionsand Hospital Pharmacy
School of Medicine
       
motivative behavior

10:10 〜 10:20

7

Paniz
Farshadyeganeh

Neurogenetics

Nagoya University Graduate Elucidation of the functional
School of Medicine
      
    
glucosaminefructose6phosphate
aminotransferase isomerizing 1(GFPT1)

9:10 〜 9:20

1

Ting Wang

Neuroscience andPathobiology

Nagoya University Research        
Institute of Environmental       
Medicine (RIEM)
in Alzheimer's disease mice

9:20 〜 9:30

2

Kaichi Yoshizaki

Disease Model

Aichi Developmental!    "#$%*+- Disability Center Institutemice was enhanced in the presence
for Developmental Research  /    "#$%*+-    ;%*"< mice.

9:30 〜 9:40

3

Norihiko Yokoi

MembranePhysiology

National Institute forPhysiological Sciences(NIPS)

9:40 〜 9:50

4

Hiro Kohda

Molecular Medicine
and Metabolism

Nagoya University Research Molecular mechanism underlying
Institute of Environmental cell deathtriggered adipose tissue
/     
Medicine (RIEM)
obesity

9:50 〜 10:00

5Miki Umeda

Virology

Nagoya University Graduate Molecular mechanisms of HCoV
229E coronavirus entry
School of Medicine

10:00 〜 10:10

6

Wenda Li

Mori Lab

Nagoya University Graduate Spatially Variant Biases Considered
School of Informatics
Selfsupervised Depth Estimation
Based on Laparoscopic Videos

10:10 〜 10:20

7

Koyo Tsujikawa

Neurology

Nagoya University Graduate Actin/      A
School of Medicine
drives tau aggregation and contributes
to progressive supranuclear palsy
pathology

Session A

Room 2Title

9:10 〜 9:20

Room 1

9:1010:25

Institute─ 11 ─

Association between germline
pathogenic variants and breast
cancer risk in Japanese women: the
HERPACC study.

LGI1ADAM22 levels to regulate
seizure thresholds in miceSession No/Time Room No

Session A
9:1010:25

Presentation Time/No

Name

Session B

Institute

Title

9:10 〜 9:20

1

Mika Takai

Hematology andOncology

Nagoya University Graduate Screening with invitro spheroids
School of Medicine
     = 
ibrutinib for IVLBCL

9:20 〜 9:30

2

Yuya Hara

Virology

Nagoya University Graduate >    %? 
School of Medicine
a tegument network hub via
comprehensive analyses of intraviral
EpsteinBarr virus proteinprotein
interactions

9:30 〜 9:40

3

Shohei Sakai

Neuroscience andPathobiology

Nagoya University Research TBK selectively eliminates
Institute of Environmental pathogenic monomeric TDP43 via
humoral factors
Medicine (RIEM)

9:40 〜 9:50

4

Rinako Tanaka

Neuropsychopharmacology Nagoya University Graduate @    kinase inhibitor,and Hospital Pharmacy
School of Medicine
fasudil, on cognitive impairments
induced by methamphetamine
administration in mice carrying
mutations of the Arhgap10 gene

9:50 〜 10:00

5

Yuji Suzuki

Molecular Biology

Nagoya University Graduate Regulation of phosphorylation
School of Medicine
on a neuronal adaptor protein
by enzymelinked receptors forglycosaminoglycans

10:00 〜 10:10

6

Yujun Zhou

Bioorganic
Chemistry

Gifu University Graduate
School of Natural Scienceand Technology, iGCORE

10:10 〜 10:20

7

Yoshiyuki Kishimoto Neurology

Nagoya University Graduate A novel device to evaluate upper
School of Medicine
/   [   

10:30 〜 10:40

1

Mai Horiuchi

Neuroscience andPathobiology

Nagoya University Research Sigma 1 receptor prevents ATAD3A
Institute of Environmental dimerization to maintain normal
Medicine (RIEM)
mitochondrial function

10:40 〜 10:50

2

Takumi Kagawa

Occupational andNagoya University Graduate Intranasal levels of lead as an
Environmental Health School of Medicine/     
rhinitis in humans and mice

10:50 〜 11:00

3

Yusuke Yamaga

Hematology andOncology

Nagoya University Graduate \     " associated
School of Medicine
//     of the malignant lymphoma
microenvironment to AntiCD20
antibody therapy

11:00 〜 11:10

4

Yoshinori Oda

Structural Biology

Nagoya University Graduate Structural basis of local anesthetics
School of Pharmaceuticalbinding to voltagegated sodium
channels
Sciences

11:10 〜 11:20

5

Mona Alhussein
Aboalela

Cancer Immune
Therapy ResearchCenterNagoya University Graduate @  "; \   <
School of Medicine
Tumors by Armed Oncolytic virus       "; \ therapy

11:20 〜 11:30

6

Yohei Tsukamoto

Molecular andCellular Biology

Nagoya University Graduate 3ʼ Sialyllactose on Notch: Notch1
School of Medicine
         ]linked, 3ʼsialyllactosylated glycans

11:30 〜 11:40

7

Ayuka Murakami

Neurology

Nagoya University Graduate Metabolome and transcriptome
School of Medicine
analysis on muscle of sporadic
inclusion body myositis

10:30 〜 10:40

1Kazuhiro Kumagai

Immunology

Nagoya University Graduate Tumor   
School of Medicine
metabolism inhibition may promote
CD8+ TILs activation and enhance =    

10:40 〜 10:50

2

Kasumi Maekawa

Neuroscience andPathobiology

Nagoya University Research Testosterone regulates theInstitute of Environmental    
Medicine (RIEM)
androgen receptor in Alzheimerʼ s
disease mice

Room 3

Room 1

Department or Division

10:3011:45

Synthesis and Evaluation of (S)5'CAminopropyl and (S)5'CAminopropyl2'/ 
      Room 2

─ 12 ─

Session No/Time Room No

Room 2Presentation Time/No

Name

Department or Division

Institute

10:50 〜 11:00

3

Seita Tomida

Glycobiochemistry

Gifu University Graduate
School of Natural Scienceand Technology, iGCORE

11:00 〜 11:10

4

Monami Kihara

Molecular
Biotechnology

Nagoya University Graduate ;[   ; SARSCoV2
School of Bioagricultural
Spike Human Monoclonal Antibody
Sciencesfrom Single B Cells of COVID19
Infected Patients Using Cellfree
Protein Synthesis System

11:10 〜 11:20

5Masataka Kusano

Molecular
Microbiology

Nagoya University Graduate Analysis of bst1+ that regulates
School of Pharmaceutical   Sciences

11:20 〜 11:30

6

NawaratRattanajearakul

Endocrinology andMetabolism

National Institute forPhysiological Sciences(NIPS)

11:30 〜 11:40

7

Hiromi Tamada

Functional Anatomy
and Neuroscience

Nagoya University Graduate >*<@`      
School of Medicine        q;><x
and microglial activation around AIS
after nerve injury

10:30 〜 10:40

1

Hirotake Misu

Endocrinology andMetabolism

National Institute forPhysiological Sciences(NIPS)

10:40 〜 10:50

2

Shurui Chen

Immunology

Nagoya University Graduate Comprehensive Analysis of Pathways
School of Medicine
Involved in Liposomal Gene Transfer

10:50 〜 11:00

3

Fumie Mitani

Cancer Cell
Regulation

Aichi Cancer Center

11:00 〜 11:10

4

Takeru Shiina

Mori Lab

Nagoya University Graduate } @    > acinar
School of Informatics
Airways from MicroCT Volumes of
Resected Human Lungs

11:10 〜 11:20

5

Yudai Tamada

Preventive Medicine

Nagoya University Graduate <     School of Medicine
heated tobacco products and its   [   - ~The JASTIS study 20172020

11:20 〜 11:30

6

Kei Hashimoto

Neuroscience andPathobiology

Nagoya University Research A hydrophobic residue is critical
Institute of Environmental for species   
canine SOD1 with E40K mutation in
Medicine (RIEM)
canine degenerative myelopathy

11:30 〜 11:40

7

He Zhang

Immunology

Nagoya University Graduate A Novel Antibody Drug Conjugate
School of Medicine
Targeting CCR8+ Tumor    Regulatory T Cells Induces a Strong
Antitumor Immunity

11:50 〜 12:00

1

Yoshitaka Adachi

Hematology andOncology

Nagoya University Graduate Genomewide CRISPR screen in
School of Medicine
human CAR\    "%#as negative regulator of CART cells     

12:00 〜 12:10

2

Yohei Sugimoto

Genome Dynamics

Nagoya University Research Biochemical analysis of molecular
Institute of Environmental mechanisms dealing with AP site
HMCES crosslink
Medicine (RIEM)

12:10 〜 12:20

3

Yuki Aoyama

Molecular Cell
Biology

Nagoya University Graduate Elucidation of the pathogenesis of
School of Medicine
Alzheimer's disease focusing on thewhite matter function

12:20 〜 12:30

4Emi Hibino

Structural Molecular
Pharmacology

Nagoya University Graduate Structure of glycyrrhizin binding to
School of Pharmaceutical      ]PDZ1
Sciencesdomain of tight junctions and its
function

Session B
10:3011:45

Room 3Session C
11:5013:15

Title
Functions of FUT8 stem region

Role of NPY"_   
the PVH in carbohydrate selection inmice@induced changes in
the hypothalamic neural circuits
controlling energy metabolism;     
    ;`{|*
mTORmediated activation oflysosome function

Room 1

─ 13 ─

Session No/Time Room No

Presentation Time/No

Name

Department or Division

Institute

Title

12:30 〜 12:40

5

Shaochuan Zhang

Neurogenetics

Nagoya University Graduate Characterization of compound
School of Medicine
heterozygous mutation derived from
DOK7relatedCMS patient

12:40 〜 12:50

6Kenji Sakakibara

Neurology

Nagoya University Graduate AIbased livecellimage analysis
School of Medicine
for spinal and bulbar muscularatrophy pathology

12:50 〜 13:00

7

Atefeh Joudaki

Neurogenetics

Nagoya University Graduate {    <  @   
School of Medicine
SingleNucleotide Variants (SNVs)      

11:50 〜 12:00

1

Ritsuko Shimogawa

Neuroscience andPathobiology

Nagoya University Research     \Institute of Environmental like receptor 7 agonistinduced
mouse model for systemic lupus
Medicine (RIEM)
erythematosus

12:00 〜 12:10

2

Md. Kamal Uddin

Virology

Nagoya University Graduate EpsteinBarr Virus BBLF1 isSchool of Medicine>   @= ! @

12:10 〜 12:20

3

Masahiro Nishimura Creative Physical
Therapy

Nagoya University Graduate Analysis of Dynamic Postural
School of of Medicine
Control Related to TrunkLower(Health Sciences)@   "    }
Initiation

12:20 〜 12:30

4Masahiro Kawatani

Neuroscience II

Nagoya University Research <          
Institute of Environmental do not have a role in motorrelated
Medicine (RIEM)
membrane potential dynamics in     

12:30 〜 12:40

5

Ryosuke Ichihara

Tumor Pathology

Nagoya University Graduate `   associated
School of Medicine
protein 8 is a marker of a subset
of cancer  //  pancreatic cancer

12:40 〜 12:50

6

Bushra Samira

Neurogenetics

Nagoya University Graduate The downregulation of PTBP1
School of Medicine
promotes alternative splicing of
AGRN mRNA essential for AChR
clustering

12:50 〜 13:00

7

Akihiro Fukushima

Integrative
Physiology

Nagoya University Graduate ;       School of Medicine
that regulates metabolism

13:00 〜 13:10

8

Tomoki Hirunagi

Neurology

Nagoya University Graduate @induced Ampk activation
School of Medicine
ameliorates polyglutaminemediatedneuromuscular degeneration in
SBMA mice

11:50 〜 12:00

1

Yuko Tashima

Molecular andCellular Biology

Nagoya University Graduate Analysis of mechanism to control the
School of Medicine  ]\"_   /
detecting abnormal Oglycosylation

12:00 〜 12:10

2

Midori Shibushita

Molecular Cell
Biology

Nagoya University Graduate Visualizing neuronal circuit activity
School of Medicine
underling sensory abnormalities ofASD

12:10 〜 12:20

3

Yutaro Nagasawa

Center for Brain
Research

National Institute forPhysiological Sciences(NIPS)

12:20 〜 12:30

4

Takahiro Nakagawa

Animal Cell Function Nagoya University Graduate @         
School of Bioagricultural     
Sciences, iGCORE
development

12:30 〜 12:40

5

Zhiwen Wu

Immune Response

Aichi Cancer Center

12:40 〜 12:50

6Shinichiro
Horigane

Neuroscience I

Nagoya University Research Calcium transients control aInstitute of Environmental morphogenetic cycle underlying
Medicine (RIEM)
neuronal migratory movement

12:50 〜 13:00

7

Kaori Fujimaki

Immunology

Nagoya University Graduate Elucidation of the mechanism of
School of Medicine >"   = 
advancedstage cancer

Room 1Room 2

Session C
11:5013:15

Room 3

─ 14 ─

@  }@   "?       
synapses"        \cell population

発表規定
口頭発表
① スライドは英語で表記して下さい。
② 1 ページ目には必ず氏名、講座名等を英語で記載してください。
③ スライドのサイズ、枚数の指定はありません。
④ 持ち時間約 7 分とし ､ 英語でご発表下さい（質疑応答は 3 分）。
⑤ 当日までに接続テストを行って下さい。
⑥ 発表者は 10 分程度の余裕を持って待機して下さい。
⑦ 時間厳守でご協力お願いいたします。

注意事項
Web 開催ですので、ポスターや発表内容のダウンロードや写真撮影は厳禁とご理解ください。

─ 15 ─

特別講演抄録

Special Lecture

The identification of ILC2 has changed the conceptof type 2 immune diseases
Speaker

Kazuyo Moro

Affiliation

Professor, Laboratory for Innate Immune Systems, Department ofMicrobiology and Immunology, Graduate School of Medicine,
Osaka University
Laboratory for Innate Immune Systems, RIKEN Center for
Integrative Medical Sciences (IMS)

Contact

kazuyo.moro@riken.jp} ?      q>%"?x      ?       ?                / >%"? 
tissue-resident cells, and derived from common lymphoid progenitor, similar to other lymphocytes such as T cells andB cells. While T cells are activated by antigen, ILC2s are activated by cytokines, lipids, and hormones, and produce    ?    >%#   @     >%"?          >%
induces secretion of mucin as well as airway hyperreactivity. GM-CSF from ILC2s involves in bone homeostasis, and>%    [ >@               ]      
research groups have joined this research field and identified new immune responses that are regulated by ILC2s.
In particular, the importance of ILC2s in allergic diseases has received a fair amount of attention and new evidence               /     /        >%"?     <    /   >%"?    ?   
research to suppress ILC2s and development of drugs targeting ILC2s have been actively conducted. In this talk, I          >%"?     /     >%"?
References _  `   \ ]  ` | {        >%"?            - @Med. 218 (2021).
2. Moro K, Kabata H, Tanabe M, Koga S, Takeno N, Mochizuki M, Fukunaga K, Asano K, Betsuyaku T & Koyasu S. Interferon and IL27 antagonize the function of group 2 innate lymphoid cells and type 2 innate immune responses. Nat Immunol. 17, 76-86 (2016).
3. Moro K, Yamada T, Tanabe M, Takeuchi T, Ikawa T, Kawamoto H, Furusawa J, Ohtani M, Fujii H & Koyasu S. Innate production of T
(H) 2 cytokines by adipose tissue-associated c-Kit (+) Sca-1 (+) lymphoid cells. Nature. 463, 540-544 (2010).

─ 17 ─

医学奨励賞 受賞講演抄録

Medical Research Award Lectures 1

Splicing regulation of large exons secures phase-separation oftranscription factors in vertebrates
Speaker

Toshihiko Kawachi

Affiliation

Neurogenetics, Nagoya University Graduate School of Medicine

Contact

t0asdvb@hotmail.com%     /     /                                     >          
<<          q<%"@x \   "    <
LCEs recruit two splicing factors, hnRNP K and SRSF3. hnRNP K induces the splicing
suppression of S3-LCEs, which is mitigated by SRSF3 to achieve constitutive splicingof S3-LCEs. SRSF3 depletion deletes intrinsically disordered regions (IDRs) of transcription factors by skipping S3%"@        / @   "                                [   /  %
splicing regulation by hnRNP K and SRSF3 secures their proper phase separation of transcription factors in vertebrates.
References\ | ; `                    /      The EMBO Journal, 40:e107485 (2021).
\    /  [

─ 19 ─

Medical Research Award Lectures 2

CD4+ T cells are essential for the development of destructive thyroiditis
induced by anti–PD-1 antibody in thyroglobulin-immunized mice
Speaker

Yoshinori Yasuda

Affiliation

Endocrinology and Diabetes, Nagoya University Hospital

Contacty-yasuda@med.nagoya-u.ac.jp

Immune-related adverse events induced by anti–programmed cell death–1 antibodies(PD-1-Ab), including destructive thyroiditis (thyroid-irAE), are thought to be caused by
activated T cells. However, the T cell subsets that are directly responsible for damaging
self-organs remain unclear. To clarify which T cell subsets are involved in the developmentof thyroid-irAE, a mouse model of thyroid-irAE was analyzed. PD-1-Ab administration 2.5
months after immunization with thyroglobulin caused destructive thyroiditis. Thyroiditis
was completely prevented by previous depletion of CD4+ T cells and partially prevented by depleting CD8+ T cells.
\ [           "+ \  /               with thyroglobulin were increased in the cervical lymph nodes of mice with thyroid-irAE compared with controls.
_           "+ \               /    >>         ;@ ;     "+ T
cells from cervical lymph nodes in mice with thyroid-irAE caused destruction of thyroid follicular architecture in the             [           "+ T        "?$     /            ;@   / {;/      \            
CD4+ T cells activated by PD-1-Ab in the pathogenesis of thyroid-irAE.

─ 20 ─

Medical Research Award Lectures 3

Neutrophil/lymphocyte ratio as a predictor of lymph node metastasis
in extramammary Paget’s disease
Speaker

Aoi EbataAffiliation

Dermatology, Nagoya University Graduate School of Medicine

Contact

aoi.ebata@gmail.com\        {   q@`{x     
detect lymph node metastasis at an early stage. Therefore, biomarkers that predict the risk       [ >          
the potential of neutrophil-to-lymphocyte ratio (NLR) in peripheral blood samples asa biomarker for the risk of lymph node metastasis in EMPD. This study involved 137
EMPD patients who underwent sentinel lymph node biopsy (SLNB) at our hospital from` ?  ` ??         /  %  <%         */                %      %        \  %        %       %   $   
whose NLRs were no more than 3, and 23% and 8% each of them showed sentinel lymph node metastasis (SLNM).
\    <%`         %  \     <%`       %      \          ?  / <%   <     q$x <%` >        # /  $    q\/ x    /    /     ##     <%      %     /       <%    _    %  /       %`  @`{   
References ; /  <  / - \ {  ! !  <   {   *         * 
ratio as a predictor of long-term mortality in breast cancer patients. Med Oncol, 30:432 (2013).
2. Huang W, Huang J, Liu Q, Lin F, He Z, Zeng Z et al. Neutrophil-lymphocyte ratio is a reliable predictive marker for early-stage
/    " @   q]x ?~?? q?#x
3. Ma J, Kuzman J, Ray A, Lawson BO, Khong B, Xuan S et al. Neutrophil-to-lymphocyte Ratio (NLR) as a predictor for recurrence inpatients with stage III melanoma. Sci Rep, 8:4044 (2018).
&ŝŐƵƌĞ͘ǆƚƌĂŵĂŵŵĂƌǇWĂŐĞƚ͛ƐŝƐĞĂƐĞŽĐĐƵƌƌĞĚŝŶƚŚĞŝŶŐƵŝŶĂůƌĞŐŝŽŶ─ 21 ─

Medical Research Award Lectures 4

Embryonal erythropoiesis and aging exploit ferroptosis/Lysosomal
nitric oxide determines transition from autophagy to ferroptosis after
exposure to plasma-activated Ringer's lactate
Speaker

Hao Zheng

Affiliation

Pathology and Biological Responses, Nagoya University Graduate
School of Medicine

Contactzhenghao@med.nagoya-u.ac.jp             [   q>>x  
   _    ?    q_@x      
by a HNEJ-1 mouse monoclonal antibody is a robust immunohistochemical technology tolocate ferroptosis in tissues in combination with morphological nuclear information, basedon various models of ferroptosis. We observed a significant age-dependent increase inferroptosis in various organs, which was accompanied by iron accumulation. Epidermal ferroptosis in ageing SAMP8
mice was significantly promoted by high-fat or carbohydrate-restricted diets. During embryogenesis of Fischer-344
rats, we found ferroptosis in nucleated erythrocytes at E13.5, which disappeared in enucleated erythrocytes at E18.5.
Administration of a ferroptosis inhibitor significantly delayed erythrocyte enucleation. Our results demonstrate theinvolvement of ferroptosis in physiological processes.
Non-thermal plasma (NTP), an engineered technology            *apoptosis specifically in various-type cancer cells. NTPactivated Ringer's lactate (PAL) is another modality forcancer therapy at preclinical stage. Here we found that PAL
induces selective ferroptosis of malignant mesothelioma
cells, where metabolome screening identified upregulated      q]x    {;%   ]/    /      {;% 
with time-dependent increase, which was responsible  / ]   q]<x   ]         
compartment. Not only ferrostatin-1 but inhibitors for .NO * ]<      {;% 
ferroptosis accompanied autophagic process in the earlyphase transforming into the later phase with boosted lipid   \ ]   
is central in PAL-induced ferroptosis.
References
1. Hao Zheng, Li Jiang, Tsuyoshi Tsuduki, Marcus Conrad, Shinya\  @/          
    ?$# q??x
2. Shinya Toyokuni, Izumi Yanatori, Yashiro Motooka, Li Jiang.
Ferroptosis at the crossroads of infection, aging and cancer. Cancer
Science, 111, 2665–2671 (2020).
3. Li Jiang, Hao Zheng, Qinying Lyu, Shotaro Hayashi, Kotaro
Sato, Yoshitaka Sekido, Kae Nakamura, Hiromasa Tanaka, Kenji
Ishikawa, Hiroaki Kajiyama, Masaaki Mizuno, Masaru Hori, Shinya\       q??x

─ 22 ─

一般講演抄録

General Lectures 1

Rejuvenation of aged T cells for effective adoptive cancer
immunotherapy
Speaker

Yuki Kagoya

Affiliation

Division of Immune Response, Aichi Cancer Center ResearchInstitute
Division of Cellular Oncology, Department of Cancer Diagnostics
and Therapeutics, Nagoya University Graduate School of Medicine

Contacty.kagoya@aichi-cc.jp

Adoptive cancer immunotherapy, in which antitumor T cells are prepared in vitro
and infused back into the patient, is a promising therapeutic option for patients withadvanced cancer. Especially, CD19-directed chimeric antigen receptor (CAR)-engineered
T cells have shown unprecedented efficacy against relapsed or refractory B cell malignancies. However, adoptive
immunotherapy against sold tumors has yet to be successful in most of the patients.
;   \                     
resulting in the loss of long-term survival capacity. These dysfunctional T cells possess epigenetic and transcriptional               \             *          \                  \  have identified that genetic ablation of PRDM1, which encodes Blimp1, efficiently supports the maintenance of anearly memory phenotype as well as cytokine polyfunctionality in repeatedly stimulated CAR-T cells. PRDM1-knockout
CAR-T cells displayed superior in vivo persistence and long-term antitumor response compared to the control CAR-T
cells in multiple adoptive immunotherapy models. Mechanistically, PRDM1 knockout globally altered epigenetic andtranscriptomic profiles of CAR-T cells towards those of early memory T cells. Intriguingly, PRDM1 knockout was            q\>%x                  \    >   >                   
antitumor T cell functions.
References
1. Yoshikawa T, Wu Z, Inoue S, Kasuya H, Matsushita H, Takahashi Y, Kuroda H, Hosoda W, Suzuki S, Kagoya Y. Genetic
/   {`     \       =          ]>~  ?*blood.2021012714
2. Kagoya Y, Tanaka S, Guo T, Anczurowski M, Wang CH, Saso K, Butler MO, Minden MD, Hirano N. A novel chimeric antigen receptor
     -;|<\;\               ` ?qx~ #?# q? x
3. Kagoya Y, Nakatsugawa M, Yamashita Y, Ochi T, Guo T, Anczurowski M, Saso K, Butler MO, Arrowsmith CH, Hirano N. BET
bromodomain inhibition enhances T cell persistence and function in adoptive immunotherapy models. J Clin Invest., 126(9): 34793494 (2016).

─ 24 ─

General Lectures 2

Development of sialic acid chemistry and its application
to glycan syntheses
Speaker

Naoko Komura

Affiliation

Institute for Glyco-core Research (iGCORE), Gifu University

Contact

komura@gifu-u.ac.jp

Sialic acid is biologically and therapeutically the most important sugar residue inglycoproteins and glycolipids. However, chemical synthesis of sialic acid–containing
glycans remains very challenging mainly due to the difficulty in the formation of     \   =             
sialylation method using a macro-bicyclic sialic acid donor, wherein the C1 and C5
positions were tethered with an alkyl linker.1) In the sialylation reactions of the macro-bicyclic sialic acid donor, the       /   /                        /     ]   "  
yields in a fully stereoselective manner. Importantly, the bicyclic sialoside moiety could be converted into the C5          ?? /         /"#       \           "# 
acid–containing glycolipids (gangliosides).1, 2) Furthermore, the sialylation method has been successfully applied for thesynthesis of sialic acid oligomer.
In conclusion, we have developed a reliable and powerful method for the stereoselective synthesis of diverse sialic
acid–containing compounds.
References
1. N. Komura et al. Science, 364, 677–680 (2019).
2. M. Takahashi et al. Org. Biomol. Chem., 18, 2902–2913 (2020).

─ 25 ─

General Lectures 3

Properties of 2'-5'-linked oligonucleotides with a conformationally
locked sugar conformation in an N-form.
Speaker

Masashi Sadaike

Affiliation

Division of Structural Molecular Pharmacology,
Nagoya University Graduate School of Pharmaceutical Sciences

Contactsadaike.masashi@k.mbox.nagoya-u.ac.jp

Recently, nucleic acid medicine has been attracting attention as a new pharmaceuticalmodality. We thought that 2'-5'-linked nucleic acids, which are relatively resistant to    #      ;*;  /       _       
2'-5'-linked nucleic acids, and their properties are not well understood. In particular,?#              /            
known at all, so we have been conducting research to elucidate their properties.
So far, we have designed and synthesized a 2'-5'-linked artificial nucleoside with an N-type sugar puckering, and       #  ; [  \           ?#        ?#[  q;x       \                   ;   /        /                # 
;   /           ; [           /          ;*; >                        /         >    ;     / _           /     ; [  \                            
I would like to use this knowledge to develop better nucleic acid materials.
References
1. Satoshi Obika et al. Tetrahedron, 58, 3039-3049 (2002).
2. Namrata Erande et al. Chem. Commun., 47, 4007-4009 (2011).
3. Osawa Takashi et al. Bioorg. Med. Chem., 26, 3875-3881 (2018).
4. Namrata Erande et al. Org. Biomol. Chem., 11, 746-757 (2013).

─ 26 ─

口頭発表抄録

Session A Room 11
Association between germline pathogenic variants
and breast cancer risk in Japanese women:
the HERPACC study.
【Presenter】 Yumiko Kasugai【 D e p t 】 Cancer Epidemiology and Prevention

Session A Room 12
Carbohydrate-binding properties of a novel sialic
acid binding site on Siglec-9【Presenter】 Hinano Komura【 D e p t 】 GlycoLife Science【Affiliation】 Nagoya University Graduate School of

Bioagricultural Sciences, iGCORE【Affiliation】 Aichi Cancer Center【Favorite Technique】 Genotyping【Favorite Technique】 Mammalian CellBased Protein Expression, Protein

Purification, ELISA【 C o n t a c t 】 ymaeda@aichicc.jp【 C o n t a c t 】 komura.hinano@b.mbox.nagoyau.ac.jp;  #10% of breast cancers are hereditary, caused by germline pathogenic variants (GPVs) in breast cancer predisposition
genes. Most studies of the prevalence of GPVs and risk of breast cancer for each gene based on cases and noncancer controls have been
conducted in Western countries, and little information from Japanese
populations is available. Furthermore, no studies considered con
founding by established environmental factors and single nucleotide
polymorphisms (SNPs) together in GPV evaluation. To evaluate theassociation between GPVs in nine established breast cancer predispo       ";*?   /     - 
women comprehensively, we conducted a casecontrol study within
the Hospitalbased Epidemiologic Research Program at Aichi Cancer
Center (629 cases and 1153 controls). The associations between GPVs
and the risk of breast cancer were assessed by odds ratios (OR) and#      q">x        
ed for potential confounders. A total of 25 GPVs were detected among
all cases (4.0%: 95%CI:2.65.9), whereas four individuals carried
GPVs in all controls (0.4%). OR for breast cancer by all GPVs includ  ";*?  ?? q34.0, P = 1.74E06). In conclusion, GPVs
increase the risk of breast cancer in Japanese women regardless of en
vironmental factors and SNPs.

Session A Room 13
Relationship between driving and gaze indicesusing a driving simulator

Sialic acidbinding immunoglobulinlike lectins (Siglecs) are pre              ter
minated glycolipids and glycoproteins. Recognition of glycans by Si      /      <  
been fully elucidated. Previously, we reported a novel sialic acidbind
ing region (site2) in addition to the wellknown primary ligandbind
ing region (site1) on Siglec7 based on in silico analysis and sitedi
rected mutagenesis1,2. Here, we report that Siglec9, which has 74 %[       <7, also has site2 and possibly uses two  /                 Siglec          / /   ligands, and it is important to clarify the mechanism, including ligand
binding, for its medical application. This report gives us new insights
into the ligandbinding properties of Siglec.
【References】

1. Yamakawa N et al. Sci Rep, 10, 8647 (2020)
2. Yoshimura et al. J. Biol. Chem, 296, 100477 (2021)

Session A Room 14
Radiosensitization effect of gold nanoparticles
on plasmid DNA damage inducedby therapeutic MV X-rays【Presenter】 Yoko Tanaka【 D e p t 】 Psychiatry【Presenter】 Katsunori Yogo
【 D e p t 】 Medical Quantum Science【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 cognitive brain function, Driving behavior【Affiliation】 Nagoya University Graduate School of of Medicine(Health Sciences)【 C o n t a c t 】 tanaka.yoko@c.mbox.nagoyau.ac.jp\      =   [     
drivers' driving skill problems causing the accidents. Furthermore, as
drivers must visually recognize pedestrians and surrounding vehicles
for driving safety, it is necessary to consider the driver's gaze charac
teristics. Thus, we measured healthy subjects' driving performance bya driving simulator and gaze to clarify their relationship. Three driving
tasks (roadtracking, carfollowing, and harshbraking) were con
ducted, and three gaze tasks (free        x performed in 36 healthy subjects. This study was approved by the Nagoya University Hospital Bioethics Review Committee, and written
informed consent was obtained from all study participants. As a result,the correlation analysis between driving and gaze showed that the in               tracking      /      /  
and the total distance of gaze in the freeviewing task of the gaze anal                 and speed gain and saccaderelated indicators in the smooth pursuittask. These results indicate that gaze function may predict driving abil
ity.

【Favorite Technique】 Analysis of DNA damage induced by radiation,

Imaging light emission induced by radiation【 C o n t a c t 】 yogo@met.nagoyau.ac.jp

Gold nanoparticles (AuNPs) can be used with megavolt (MV) Xrays                  
says and mice treatments. However, the detailed mechanisms are unclear; in addition to physical dose enhancement, several chemical andbiological processes have been proposed. Reducing the AuNP concen     =       
clinical application of AuNPs. Here, we used positively charged (+);{               ;{ / with MV X  ;     qx              ;{  ;      
species (ROS) generation. DNA damage was promoted by 1.4nm+AuNP with dose enhancement factors of 1.4 ± 0.2 for singlestranded breaks and 1.2 ± 0.1 for doublestranded breaks. +AuNPs combined with MV Xrays induced radiosensitization at the DNA level,            *    
biological. Although AuNPs induced similar ROS levels, they did notcause considerable DNA damage. Thus, dose enhancement by low
concentrations of +AuNPs may have occurred by increasing the local+AuNP concentration around DNA or via DNA binding. Further stud        ;{  /     applications for radiation therapy in MV ranges.
【Reference】

1. Yogo K et al. Int J Nanomed, 16, 359370 (2021)

─ 28 ─

Session A Room 15
Deficiency of orexin signaling during sleep isinvolved in abnormal REM sleep architecture in
narcolepsy

Session A Room 16
Dynamic changes and functions of orexin neurons
activities in motivative behavior【Presenter】 Dong Yutao【 D e p t 】 Neuropsychopharmacology and Hospital Pharmacy【Presenter】 Hiroto Ito【 D e p t 】 Neuroscience II【Affiliation】 Nagoya University Graduate School of Medicine【 C o n t a c t 】 dong.yutao@a.mbox.nagoyau.ac.jp【Affiliation】 Nagoya University Research Institute ofEnvironmental Medicine (RIEM)【Favorite Technique】 In vivo Ca imaging (nVista, fiberphotometry), in vivo

optogenetic experiment, EEG EMG measurement,
plasmid construction, AAV production. injection
surgery.
【 C o n t a c t 】 hiroto.ito.nagoya.uni.med@gmail.com
 q\ >x   /       q]neurons) considered as "wakeactive and wakepromoting neurons".
However, the neural mechanism is still unknown through which the              
sy; abnormal rapid eye movement (REM) sleep architecture, such as  _                  @`         
]             
synchronous activity during nonREM (NREM) sleep, and becamesilent during the transition from NREM to REM sleep. During REM
       /  /     >                @`  ]     /       
NREMREM sleep transitions in NREM sleep. REM sleep dependent /        /[ @`  >        /[  @` dependent in/           \                  abnormal REM sleep architecture of narcolepsy.

Session A Room 17
Elucidation of the functional significance of skeletal
muscle-specific splicing variant of glucosaminefructose-6-phosphate aminotransferase
isomerizing 1 (GFPT1)]             
including energy homeostasis and wakefulness, and are also related tomotivation and decision making. In this study, we investigated wheth                /      qx     based operant   /                       /     
ratio test. Under FR5 conditions in which rats were able to obtain a  /                           (after which food would be delivered). The activity peaked before rats
obtained reward, and then decreased after food intake. In addition, un ?              #     \                /    \   /                 /       /         
tation in taking behaviors.

Session A Room 21
Beneficial effects of Dimethyl Fumarate on theneuroinflammation in Alzheimer's disease mice【Presenter】 Ting Wang
【 D e p t 】 Neuroscience and Pathobiology【Presenter】 Paniz Farshadyeganeh【 D e p t 】 Neurogenetics【Affiliation】 Nagoya University Research Institute of【Affiliation】 Nagoya University Graduate School of Medicine【 C o n t a c t 】 panizfy@gmail.com【Favorite Technique】 we isolated astrocyte by MACs
【 C o n t a c t 】 wang.ting@j.mbox.nagoyau.ac.jp

Glutamine fructose6phosphate transferase 1 (GFPT1) is a ratelim         /    q_{x               /   cursors for N and Olinked glycosylation of proteins and lipid. A
novel GFPT1 splice variant (GFPT1L), containing a 54bp or 48bp                              
The addition of 18 or 16 amino acids at position 229 of the proteincauses less enzymatic activity for GFPT1L. However, why skeletal            Here, we generated a knock    }   9 toinvestigate the role of the GFPT1L variant in skeletal muscle.

      /          /[            in the pathologies of Alzheimerʼs disease (AD). Previous studies report
ed nuclear factor erythroid 2related factor 2 (Nfe2l2 or Nrf2) attenuated          
      _       
Nrf2               cortices of AppNLG*%GF (App|>x  / ; [  
To elucidate the mechanism of Nrf2mediated neuroprotection in AD,      ? /       q`x 
clinically available drug to activate Nrf2 pathway. We measured the;    ?        q;x     `        ;     _?d,
H2 ?   }/?         ?      
stream genes in primary astrocytes. Moreover, chronic oral administra  `            ;KI mice. DMFtreated App|>       
H2   "      ]        
DMF treatment also reduced amyloid       
App|>  \     `    mation by suppressing reactive astrocytes in AppKI mice through acti
vating Nrf2 pathway.

Environmental Medicine (RIEM)【References】

1. Ting Wang et al. Liddelow SA, et al. Nature. 541 (7638): 481487 (2017).
2. Saito T, et al. Nat Neurosci. 17(5): 6613 (2014)─ 29 ─

Session A Room 22
Voluntary exercise of C57BL/6J male mice wasenhanced in the presence of both conspecific
C57BL/6J and heterospecific BALB/cCrSlc male mice.
【Presenter】 Kaichi Yoshizaki【 D e p t 】 Disease Model【Affiliation】 Aichi Developmental Disability Center Institute for

Session A Room 23
LGI1-ADAM22 levels to regulate seizure
thresholds in mice【Presenter】 Norihiko Yokoi【 D e p t 】 Membrane Physiology【Affiliation】 National Institute for Physiological Sciences (NIPS)【Favorite Technique】 Biochemical analysis of brain tissues to reveal andDevelopmental Research

quantify physiological protein complexes【 C o n t a c t 】 yosizaki@insthsc.jp【 C o n t a c t 】 nyokoi@nips.ac.jp

Social facilitation is a psychological phenomenon that an individualʼs    [                      /           "#$%*+- /    ;%*"<              /               /  self           ;%*"<  \                       /             "#$%*+-           /    "#$%*+-    
 ;%*"< /                 /   "#$%*+- /
server male mice was observed during the dark period, while that by  ;%*"< /    /        \       
"#$%*+-     ;%*"< /    
social facilitation, that is, self    ;%*"<    / >              ;%*"<             [   
       [       
transsynaptic LGI1;;`??    /   
tations or autoantibodies, cause epilepsy and amnesia. However, it re
mains unclear how LGI1ADAM22 levels are regulated and how much
LGI1;;`??     [ _     ;;`?? stoichiometrically phosphorylated in the mouse brain. In ADAM22
phosphorylation  in mice, the amounts of the ADAM22
and LGI1 proteins in the brain were decreased to about 40% and 55%,
respectively, compared to that in the wildtype mouse brain without seizures. Phosphorylation ;;`?? /  
tiondependent interaction with 1433 adaptor proteins, and subjected
to AP2mediated endocytosis for degradation. We demonstrated that[        ;;`?? /     ;(PKA) mediates high=   /    ;;`??    33
and forskolininduced PKA activation increases ADAM22 levels. Leveraging a series of ADAM22 and LGI1 hypomorphic mice, we found #  %}>     ;;`??   =        ;;`??     [  
citatory and inhibitory neurons. These results suggest strategies to in
crease LGI1;;`??    [  /   
PKA or 1433 for epilepsy treatment.
【References】

1. Yokoi et al. Nat. Med. 21, 1926 (2015).
2. Yokoi et al. Cell Reports. 37, 110107 (2021).

Session A Room 24
Molecular mechanism underlying cell deathtriggered adipose tissue fibrosis during thedevelopment of obesity

Session A Room 25
Molecular mechanisms of HCoV-229E coronavirus
entry【Presenter】 Miki Umeda【 D e p t 】 Virology【Presenter】 Hiro Kohda【 D e p t 】 Molecular Medicine and Metabolism【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Ultracentrifugal virus purification【Affiliation】 Nagoya University Research Institute ofEnvironmental Medicine (RIEM)【 C o n t a c t 】 m.umeda@med.nagoyau.ac.jp【 C o n t a c t 】 kouda.hiro@b.mbox.nagoyau.ac.jp

Obesity is considered as a state of chronic and low    
We have provided evidence on the molecular mechanisms of obesi
ty              
especially focusing on the crosstalk between adipocytes and macro       `induc
ible Ctype lectin (Mincle), a pathogen sensor for Mycobacterium tu
berculosis, is induced in adipose tissue macrophages during the  /  `          / / /           
lin resistance in the liver (ref.1). However, how Mincle     //       /   > 
study, we performed single ; [        
mal vascular fraction (SVF) in visceral adipose tissue from dietin
duced obese mice to analyze the cellcell interaction between Mincle        //        $ // /  "                `   
  >  `       
distinct macrophage clusters during the development of obesity. We ""          
cell communications, between Mincle    
obesity  //                         

Coronaviruses are RNA viruses that cause respiratory infections in hu
mans and infect cells via fusion with the host cell membrane or via
endocytosis. However, the mechanistic details of this infection path
way are still unknown, especially those involved in viral uncoating. In
this study, we try to analyse the molecular mechanisms of coronavirus
entry into host cells using the coronavirus strain, HCoV229E. Initial
ly, we established a HCoV??@     /     man hepatoma Huh7 cells to obtain a high titre virus. Using the puri _"!229E virus, we synchronised viral infection to earlyendosomes via ammonium chloride treatment, and then chased endo    /     ;      
the virus taken up into the endosomes colocalised with the early en
dosome marker, EEA1, and VCP (p97). It is reported that VCP inter    _;"+    /  /  /    /[  / \       /[   
are involved in the uncoating step of HCoV??@   >  
;  q>;!x     _  /[      
HCoV??@       >;!         of HCoV??@            other RNA viruses.

【Reference】

1. Tanaka M et al. Nat Commun, 5, 4982 (2014).

─ 30 ─

Session A Room 26
Spatially Variant Biases Considered Self-supervised
Depth Estimation Based on Laparoscopic Videos【Presenter】 Wenda Li【 D e p t 】 Mori Lab【Affiliation】 Nagoya University Graduate School of Informatics【Favorite Technique】 Depth estimation from laparoscopic images【 C o n t a c t 】 wdli@mori.m.is.nagoyau.ac.jp

Session A Room 27
Actin-binding protein filamin-A drives tau
aggregation and contributes to progressive
supranuclear palsy pathology【Presenter】 Koyo Tsujikawa【 D e p t 】 Neurology【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 clinical neurology, neuropathology and genetics

Depth estimation is an essential tool in obtaining depth information for
robotic surgery and augmented reality technology in the current lapa
roscopic surgery robot system. Since there is a lack of groundtruth fordepth values and laparoscope motions during operation, depth estima    =          
scopic images under the supervised strategy. It is challenging to gener               abdominal images. To tackle these problems, we propose a novel monocular selfsupervised depth estimation network with sparse nest ar
chitecture. We design a nonlocal block to capture broader and deeper             variant generaliza                `
we introduce an improved multimask feature in the loss function to
tackle the classical occlusion problem based on the timeseries infor
mation from stereo videos. We also use heteroscedastic aleatoric un                                          \        
model outperformed the stateofthe  [    [   

【 C o n t a c t 】 tsukoyo@med.nagoyau.ac.jp

Session A Room 31
Screening with in-vitro spheroids cultures identified
the efficacy of ibrutinib for IVLBCL

Session A Room 32
Identification of BLRF2 as a tegument network hub
via comprehensive analyses of intraviral EpsteinBarr virus protein-protein interactions【Presenter】 Mika Takai【 D e p t 】 Hematology and Oncology

While amyloid         ;  ease, key drivers for other tauopathies, including progressive supranu
clear palsy (PSP), are largely unknown. Various tau mutations are
known to facilitate tau aggregation, but how the nonmutated tau, whichmost cases with PSP share, increases its propensity to aggregate in          _             /     A in the PSP brains
without tau mutations. We provided in vivo biochemical evidence that   A levels enhance the phosphorylation and insolubil             ;    minA corrected aberrant tau levels in the culture cells from PSP cases.
`         A recapitulated tau      ]      A promotes            /   A
contributes to PSP pathology.

【Presenter】 Yuya Hara
【 D e p t 】 Virology【Affiliation】 Nagoya University Graduate School of Medicine【 C o n t a c t 】 takaim@med.nagoyau.ac.jp

Intravascular large Bcell lymphoma (IVLBCL) is a rare disease formof malignant lymphoma characterized by the lack of lymphadenopathy
and the selective proliferation of tumor cells within vessels of system
ic organs. The limited number of tumor cells from diagnostic speci
mens hinders the elucidation of underlying biology of IVLBCL. Although recent prospective trial revealed that immunochemotherapy
combined with central nervous system oriented therapy improves clin
ical outcomes of IVLBCL, a certain number of patients who develops                /
established for these patients. To overcome intractable diseases,preclinical evaluations using appropriate systems invitro and invi
vo are indispensable. To address these issues, we developed an invitro
spheroid culture system of IVLBCL tumor cells in addition to pa
tient   q{ x           
FDA     /  /   ʼs kinase inhib           \    /  /  validated in PDX model established from a patient who developed
relapsed disease after the current active treatment and it showed signif
icant antitumor activity. Our data demonstrates that spheroid culture
can be a useful tool in understanding the biology of IVLBCL.

【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Fluorescent immunostaining, FACS, WB, qPCR,

virus titer measurement【 C o n t a c t 】 yuya.hara0403@med.nagoyau.ac.jp

Proteinprotein interactions (PPIs) are crucial for various biologicalprocesses. Epstein  q@!x      
es, regulating the replication and persistence of the viral genome in  _    @!      
iological conditions remains unclear. In this study, we performed comprehensive analyses of EBV PPIs in living cells using the NanoBiT     # {{>       
been reported. Computational analyses of these PPIs revealed that
BLRF2, which is only found in gammaherpesviruses, is a central protein in the structural network of EBV tegument proteins. To characterize the role of BLRF2, we generated two BLRF2 knockout EBV clones  "><{*" %?                    / 
 %?   ]     %?   
network hub that plays essential roles in progeny virion maturation.

─ 31 ─

Session A Room 33
TBK selectively eliminates pathogenic monomeric
TDP-43 via humoral factors【Presenter】 Shohei Sakai【 D e p t 】 Neuroscience and Pathobiology【Affiliation】 Nagoya University Research Institute ofEnvironmental Medicine (RIEM)【Favorite Technique】 cell culture, molecular cloning, general DNA/RNA/
protein work
【 C o n t a c t 】 sakai.shohei@c.mbox.nagoyau.ac.jp
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the selective death of motor neurons. TDP43
pathology, which consists of cytosolic mislocalization, aggregation,and hyperphosphorylation of TDP43 protein in motor neurons, is acommon pathological feature in both sporadic and inherited cases of
ALS. TBK1 is one of notable ALScausative genes to study the mo
lecular basis of TDP43 pathology, because it is closely related to proteostasis. However, the molecular link between TBK1 and TDP43         =     \{43 pa          pression of monomeric form of TDP43 reproduces TDP43 pathology     q]   / x _       \|  \{43 protein level using its monomeric
TDP43 mutant cell model. Intriguingly, suppression of endogenous
TBK1 increased not wildtype (WT) but pathogenic monomeric TDP        ]       
TBK1 predominantly reduced monomeric TDP43 compared to WT.
These data suggested that TBK1 selectively eliminates pathogenic
TDP `         / \|             
TDP43. Elucidation of detailed molecular mechanism of TBK1me
diated protein clearance is underway.

Session A Room 34
Effect of a Rho-kinase inhibitor, fasudil,on cognitive impairments induced bymethamphetamine administration in mice carrying
mutations of the Arhgap10 gene【Presenter】 Rinako Tanaka【 D e p t 】 Neuropsychopharmacology and Hospital Pharmacy【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Golgi staining【 C o n t a c t 】 tanaka.rinako.k8@s.mail.nagoyau.ac.jp]       ;        -nese schizophrenia patients by the genomewide CNV analysis. ARHGAP10 belongs to the RhoGAP superfamily and regulates RhoA sig      ; <{*_@-                                q{"x q ?*x             (METH) in the visual discrimination (VD) task. In this research, toclarify a potential role of Rhokinase (ROCK) as a new therapeutictarget for schizophrenia, we investigated whether fasudil, a ROCK in/                 of cortical neurons and a higher sensitivity to METH in the VD task in; <{*_@-           {"after fasudil treatment using Golgi staining. Mice were administered`@\_ q * x   /    q? * x #min before the VD task. Fasudil ameliorated the decrease in spine density of cortical neurons in the mPFC and restored impairment of VD  / `@\_  ; <{*_@-  \ /
tions suggest that ROCK is a potential therapeutic target in schizo
phrenia.

Session A Room 35
Regulation of phosphorylation on a neuronal
adaptor protein by enzyme-linked receptors forglycosaminoglycans

Session A Room 36
Synthesis and Evaluation of (S)-5'-C-Aminopropyland (S)-5'-C-Aminopropyl-2'-arabinofluoromodified antisense oligonucleotides【Presenter】 Yuji Suzuki【 D e p t 】 Molecular Biology【Presenter】 Yujun Zhou
【 D e p t 】 Bioorganic Chemistry【Affiliation】 Nagoya University Graduate School of Medicine【 C o n t a c t 】 yjsuzuki@med.nagoyau.ac.jp【Affiliation】 Gifu University Graduate School of Natural Scienceand Technology, iGCORE【Background】 The damaged central nervous system does notregenerate again. Our group revealed that chondroitin sulfate (CS)         {\{¡ q type protein
tyrosine phosphatase), which dephosphorylates cortactin and disrupts            "  that the phosphorylation level of intracellular substrates seems          >    study revealed that heparan sulfate, which has a similar structure to CS,
activates ALK (receptortype protein tyrosine kinase)2. Our following    /       {\{¡   ;%|   
APBB1, which is known as an adaptor protein enriched in the brain.
【 *"  】APBB1 gene knockdown in cultured neurons /       ;{   /    ;%|*{\{¡   q/       /x ;%|         ;{             {\{¡      >       /  ;              {   
Apbb1 were observed in the wide region. These observations suggest        ;{ / ;%|   {\{¡
might be involved in the development of hypothalamus, probably bymodifying its adaptor capacity in the nucleus.
【References】

1. Sakamoto K et al. Nat Chem Biol, 15, 699709 (2019).
2. B. Phillip et al., Sci. Signal., 360, ra6 (2015).

【 C o n t a c t 】 zhou.yujun@i.mbox.nagoyau.ac.jp

Abstract: In our previous studies, inserting an aminoalkyl side chain
into the 5'           
resistance of the resulting oligonucleotides. Meanwhile, the siRNAs
with (S)5'Caminopropyl2'Omethyl   / 
thermal stability than (R)5'Caminopropyl2'Omethyl
ones. Here, (S)5'Caminopropylthymidine (5'APT) and (S)5'Caminopropyl2'/ thymidine(5'AP2'araFT)
were          ;     
"            ;*;     #;{2'araF\  =    /
while those containing 5'APT featured thermal destabilization.
Depending on the thermodynamic parameter, the thermal destabilization
was related to the unfavorable entropy. Meanwhile, the incorporation of               DNA oligomers. Moreover, the 5'AP2'araF ;*;    /       _mediatedcleavage compared to the 5'AP ;*;  _ 
the (S)5'Caminopropyl2'/ 
analogs might be potential candidates for the application of RNase
Hdependent antisense oligonucleotides as therapeutics, although theintroduction position should be optimized in further studies.
【References】

1. Kajino R. et al., J. Org. Chem., 84, 33883404 (2019).
2. Zhou Y. et al., RSC Adv., 10, 4190141914 (2020).

─ 32 ─

Session A Room 37
A novel device to evaluate upper limb ataxia
quantitatively

Session B Room 11
Sigma 1 receptor prevents ATAD3A dimerization tomaintain normal mitochondrial function【Presenter】 Yoshiyuki Kishimoto【 D e p t 】 Neurology【Presenter】 Mai Horiuchi【 D e p t 】 Neuroscience and Pathobiology【Affiliation】 Nagoya University Graduate School of Medicine【 C o n t a c t 】 kishimoto.yoshiyuki@j.mbox.nagoyau.ac.jp【Affiliation】 Nagoya University Research Institute ofEnvironmental Medicine (RIEM)【Objective】The aim of our study is to develop a novel device to as  /   [            /   q<";x         /        disease progression.【Methods】We recruited subjects with SCA and    q_"x  /         
vice that measures the threedimensional position every 10 ms. Partic
ipants were instructed to move a penlike part of the device iteratively
between two buttons. The trajectory length, time, velocity, and varia =                  [  </    ?     baseline evaluation.【Results】A total of 42 subjects with SCA and 33_"               ease duration and the total score of the Scale for the Assessment and    ;  q ¢ ?   ¢ #    ¢ +  £  
tively) and showed the largest standardized response mean (SRM) in
the longitudinal analysis (SRM = 0.57).【Conclusion】This new device    /   [           <";                 

Session B Room 12
Intranasal levels of lead as an exacerbation factor
for allergic rhinitis in humans and mice【Presenter】 Takumi Kagawa【 D e p t 】 Occupational and Environmental Health

Microarray, Epidemiological analysis, Animal study【 C o n t a c t 】 kagawa.takumi@j.mbox.nagoyau.ac.jp【Background】Allergic rhinitis (AR) has become a global healthproblem because of its high worldwide prevalence. Health disturbanc  /           have been recognized worldwide. However, there has been no clinical                 nasal cavity of patients with seasonal AR before the season (preseason)      q x `   /                    
pathological conditions of allergic rhinitis.【Result】Pb levels in epi     q@%x      ¤   from control subjects during the pollen season. Pb level in ELF was
positively associated with pollen counts for the latest 4 days before
visiting a hospital as well as severity of subjective symptoms. Intrana   {/ /         {/   /    {/   @%     
Pb        {/  allergic mice, despite intranasally challenging the same amount of Pb.
【Conclusion】>   {/   /  / 
symptoms of AR, indicating Pb as a novel hazardous air pollutant forAR.

1. Kagawa T et al. JACI,. 148(2), 655656 (2021).
2. Xu H et al. JACI,. 148(1), 139147.e10 (2021).

Oligodendrocyte isolation by magnetic cell sorting【 C o n t a c t 】 horiuchi.mai.u4@s.mail.nagoyau.ac.jp

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative diseasecharacterized by selective death of motor neurons. Dominant or reces
sive mutations in SOD1 or SIGMAR1 are causative for inherited ALS,
respectively. We have previously demonstrated that the collapse of mi
tochondriaassociated membranes (MAM), a contacting site of endo
plasmic reticulum (ER) with mitochondria, is a common mechanism of
ALS and that sigma 1 receptor (SigR1), a gene product of SIGMAR1,    `;`    _       
membrane protein, AAA ATPase domaincontaining protein 3A
q;\;;x        < ]  ;\;;      `;`      ;\;; 
deletion mutants, we revealed that two coiled   q""*?x
were crucial for interaction with SigR1 and the MAM induction by
ATAD3A. Intriguingly, depletion of SigR1 induced homodimeriza
tion of ATAD3A accompanied by mitochondrial fragmentation. The
ATAD3A dimerization was also observed in SOD1G93A ALS model
mice, in which SigR1 lost its physiological function. Combined with      ;\;;               <   ;\;; merization to prevent mitochondrial fragmentation. Thus, our study
implies that MAM impairment through SigR1 dysfunction in ALS may
compromise mitochondrial function via ATAD3Ainduced mitochon
drial fragmentation.

Session B Room 13
The effects of Cancer-associated fibroblasts
as components of the malignant lymphoma
microenvironment to Anti-CD20 antibody therapy【Presenter】 Yusuke Yamaga【 D e p t 】 Hematology and Oncology【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Bioinformatics, Nextgeneration sequencing,【References】【Favorite Technique】 Primary oligodendrocyte precursor cell culture,【Affiliation】 Nagoya University Graduate School of Medicine【 C o n t a c t 】 yusu55574@med.nagoyau.ac.jp

 /   CD20 antibody, has improved the outcome ofBcell lymphoma treatment. Recently, Obinutuzumab has been intro
duced, and has enhanced antibody     q;""x 1). On
the other hand, cancer  //  q";x       /            
on immunocompetent cells have attracted attention. We aimed to com         /   /   /                "; ;""   / " \Glo™ assay kit using NK cells collected from healthy
donor peripheral blood. The test was evaluated in monoculture and incoculture with CAFs. We evaluated 30 patients who underwent  / \  "?   #  ;""   /   /   /  ??  #?#q{¢£#x \            \  er, ADCC of NK cells monocultured or cocultured with CAFs was?$  # q{¢?+x   /   +   +$q{¢£#x /   / "    =    /      ";  |     \     \} / ";               cell regulation have been reported 2) and may contribute to our study.
【References】

1. Cartron G et al. Haematologica, 101(2), 226234 (2016).
2. Grauel LA et al. Nat Commun.,11, 6315 (2020).

─ 33 ─

Session B Room 14
Structural basis of local anesthetics binding tovoltage-gated sodium channels

Session B Room 15
Expression of CAR Targets on Solid Tumors byArmed Oncolytic virus has synergetic effecton CAR T cell therapy【Presenter】 Yoshinori Oda【 D e p t 】 Structural Biology【Presenter】 Mona Alhussein Aboalela【 D e p t 】 Cancer Immune Therapy Research Center【Affiliation】 Nagoya University Graduate School of

Pharmaceutical Sciences【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 flow cytometry, qPCR, Cloning, Virus generation,【Favorite Technique】 membrane protein purification, negative staining,
cryoEM, single particle analysis【 C o n t a c t 】 oda.yoshinori@g.mbox.nagoyau.ac.jp

mice tumor inoculation and TIL analysis【 C o n t a c t 】 aboalela.mona.al.hussein.mostafa@h.mbox.nagoyau.ac.jp

The nerve system is responsible for various actions such as sensing,memory, moving. Voltagegated sodium channels (Navs) are essential          \   /  
tential depolarization and open the ion gate. With the function, Navs      /        /      
trical signal reaches the synapse. Due to the responsibility on signaltransmission, Navs are the target of some drugs such as local anesthet
ic and antiarrhythmic agents. Local anesthetic drugs which target Navs
block the sodium current and shut the pain signal out. While somedrugs targeting Navs are in use, the detailed interactions are unclear.
Gamal ElDin T.M. et al. PNAS, 115, 1311113116 (2018) revealed
the crystal structures of a prokaryotic Nav (NavAb) with some drugs,
but detailed interactions between NavAb and drugs are still unclear
because of NavAb's fourfold structure and the characteristic of crystal
structure. Therefore we are trying to solve them with cryoEM single
particle analysis. We are now facing an issue that NavAb particles on
the cryoEM grid are very likely to be disordered, so we are searchingfor good conditions to make a better cryoEM grid for largescale datacollection.

Chimeric antigen receptor (CAR) T cell therapy showed limitation insolid tumors compared to hematological malignancies due to the het            
           ";T cell therapy. Furthermore, tumor cells may escape from CART by partial or complete       \       ";Ttherapy for solid cancer, we developed a combination therapy of
CAR\                  _              
virus1 (HSV1) by deletion of the neurovirulence viral genes ICP
34.5 and replacing it by insertion of mesothelin (MSLN) gene (HSVMSLN) to selectively deliver MSLN to malignant cells. Our virus
showed in vivo safety even after using a high dose (1 X 107 pfu) intumor/               >   _<!`<%           `<%   { ?
tumor cell line in a MOIdependent manner. HSVMSLNinfected{ ?             >  `<%"; \  ]           
combination of OVs and CART to trigger and improve CART cell
antitumor response in solid tumors in vivo.
【Reference】

1. Fesnak A et al. Nat. Rev. Cancer, 16, 566581 (2016).

Session B Room 16
3’-Sialyllactose on Notch: Notch1 functions as a
scaffold of O-linked, 3’-sialyllactosylated glycans

Session B Room 17
Metabolome and transcriptome analysis on muscleof sporadic inclusion body myositis【Presenter】 Yohei Tsukamoto【 D e p t 】 Molecular and Cellular Biology【Presenter】 Ayuka Murakami【 D e p t 】 Neurology【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Mass specrtrometry【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 muscle biopsy of human, staining of cryosectioned

human muscle【 C o n t a c t 】 tsukamoto.yohei.f8@s.mail.nagoyau.ac.jp

Notch signaling is important for the development and homeostasis ofmulticellular organisms. Dysregulation of Notch signaling leads tovarious human diseases. Genetic and biochemical studies have revealed that Olinked glycosylation on Notch receptors is essential forthe transduction of Notch signaling. However, it is not fully understood how Olinked glycans regulate the activity of Notch signaling.
To pursue this, we need to know the sites and structures of Olinked
glycans on Notch receptors. Our mass spectrometric analysis of pro       ]\"_   ?  
HEK293T cells revealed that many of the epidermal growth factorlikeq@}x    ]\"_   ?     ]glucose (Glc),Ofucose (Fuc), and O};        
<        ]Glc glycans     ]Glc site of EGF10 within the li
gandbinding region of NOTCH1. Further chemical analyses on?eliminationreleased glycans indicated that the structure of the novel OGlc glycans appeared to be Neu5Ac?23Gal?14GlcO. Genetic
deletion of both GXYLT1 and GXYLT2 in HEK293T cells increased
the ratio of the novel glycans on EGF10 in NOTCH1, suggesting the   /           
OGlc glycans. The novel glycans may confer a previously unknown     ]\"_【 C o n t a c t 】 murakamia@med.nagoyau.ac.jp【Objective】 Sporadic inclusion body myositis (sIBM) is the most [         #    >`is often steroidresistant, and its pathophysiology remains elusive. This             >`    
tify novel therapeutic targets using metabolomic and transcriptomic
analyses.【Methods】In this retrospective observational study, we ana  /     >`          /      /     
were used to measure metabolites with cation and anion modes of cap          q"@TOFMS).
We validated the metabolic pathway altered in muscles of sIBM patients ; [         【Results】A to    /     ` /           /     >`  
The pathways of histamine biosynthesis and certain glycosaminoglycan
biosynthesis were upregulated in sIBM patients, whereas those of carni
tine metabolism and creatine metabolism were downregulated. Histo               
tion of chondroitin sulfate in skeletal muscle samples, supporting theresults of metabolomic and transcriptomic analyses.【Conclusions】This
study suggest that mast cells, chondroitin sulfate biosynthesis, carnitine,and creatine play roles in sIBM pathophysiology.

─ 34 ─

Session B Room 21
Tumor-specific glutamine metabolism inhibition
may promote CD8+ TILs activation and enhance theefficacy of immunotherapy

Session B Room 22
Testosterone regulates the neuroinflammation
through glial androgen receptor in
Alzheimer’s disease mice【Presenter】 Kazuhiro Kumagai【 D e p t 】 Immunology【Presenter】 Kasumi Maekawa【 D e p t 】 Neuroscience and Pathobiology【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Cell metabolic analysis, Flow cytometry for various【Affiliation】 Nagoya University Research Institute ofprotein expression, Tumor bearing mice making【 C o n t a c t 】 kumagai.kazuhiro@e.mbox.nagoyau.ac.jp【Favorite Technique】 Primary cell culture, Cell isolation using MACS
【 C o n t a c t 】 maekawa.kasumi@h.mbox.nagoyau.ac.jp

Cancer immunotherapy by targeting to PD*{L1 and CTLA4 has
been approved for several cancer types, and its clinical application is   _           
are limited. Various factors are associated with this limitation, one ofwhich is cancer immune escape. Recently, many researchers reported
that the reprogramming of tumormetabolism derived from gene mutation and copy number variations (CNVs) build immunesuppressive
environment in tumor. Here, we show that Notch1 signaling in cancer                    q] {_]<x*    /  de               caused metabolic reprogramming by glutamine addiction. As a result,glutamine concentration was decreased in tumor. In turn, the glutamine           *    " 
TILs by inhibiting glycolytic metabolism through mTORC1 signaling,  /          \>% \  mine metabolism inhibition using glutamine transporter targeting shRNA may improve CD8+ TILs metabolic condition and promote prolif  *          =    

      /          
cytes with secreted humoral factors, is deeply involved in the patho   ;   q;x ]   ; [             q;x 
decreased in the human precuneus with early AD pathology and isolat
ed microglia and astrocytes from AppNLG*%GF (AppKI)
mice, the new generation AD model. Previous studies have demon
strated that testosterone is associated with AD pathologies, but the de
tails of correlation between glial AR and AD pathology are still un \              
glial AR on AD pathology using castratedAppKI male mice. In isolatedmicroglia of aged castratedAppKI mice, mRNA levels ofpro    q"   "#x    /  
Meanwhile, mRNA level of Socs3, critical for cytokine secretion              
astrocytes. Moreover, in Barnes maze test for evaluating spatial learning and memory, aged wild   /           /   /     /      by castration was slight in aged AppKI mice. These results suggested
that testosterone may regulate pro*    
  ;             
dysfunction.

Session B

Session B Room 24
Acquisition of Anti-SARS-CoV-2 Spike Human
Monoclonal Antibody from Single B Cells of
COVID-19 Infected Patients Using Cell-free Protein
Synthesis System

Room 23Functions of FUT8 stem region【Presenter】 Seita Tomida【 D e p t 】 Glycobiochemistry【Affiliation】 Gifu University Graduate School of Natural Scienceand Technology, iGCORE

Environmental Medicine(RIEM)【Presenter】 Monami Kihara【 D e p t 】 Molecular Biotechnology【Favorite Technique】 Assay of glycosyltransferase activity【 C o n t a c t 】 z4521055@edu.gifuu.ac.jp【Affiliation】 Nagoya University Graduate School of\ q+fucosyltransferase) transfers fucose to the innermost GlcNAc residues in Nglycans and is a typeII membrane protein having
a stem region between an Nterminal cytosolic region and a large
Cterminal catalytic domain. In general, it is considered that the stem
region of glycosyltransferases is involved in the regulation of Golgi
localization, however, the functions of the FUT8 stem region are still
unclear. Here, we revealed that the FUT8 stem region is essential forthe enzyme oligomerization. FUT8Δstem mutants in which the stem      *      
HEK293 FUT8 KO cells, and the western blotting, lectin blotting and
HPLC analysis showed that the enzymatic activity of the mutants wasalmost the same as that of FUT8 wild type. However, the immunopre
cipitation and nativePAGE analysis showed that FUT8Δstem mu
tants impaired multimer formation in cells, whereas FUT8 WT forms a
multimer. Furthermore, FUT8Δ        pression levels, the more ER localization and the shorter protein half
lives than FUT8 WT, suggesting that the loss of the stem region causes  /    \    ]        
FUT8 stem region is critical for the multimer formation.

Bioagricultural Sciences【Favorite Technique】 Antibody screening, DNA immunization【 C o n t a c t 】 kihara.monami@e.mbox.nagoyau.ac.jp]          / [ 
method (named Ecobody technology), in which antibody genes fromisolated single B cells from peripheral blood or tissues of animals are /  cell reverse transcription and several rounds of
PCR, followed by cell free protein synthesis, resulting in a generationof Fab fragment in a very highthroughput manner. In this study, anti
bodies were conducted against spike proteins, which are membraneproteins of novel coronaviruses and are attracting attention as targets
for antibodies to be used in diagnosis and vaccines. B cells were col
lected from patients infected with human novel coronaviruses, and B
cells presenting antigen  /       
genbinding beads. After isolation of each cell, the antibody gene wasobtained by reverse transcription PCR and twostep PCR. In addition,using a cellfree protein synthesis system, the binding ability to Spike    / @%<;              / @%><;        [    ─ 35 ─

Session B Room 25
Analysis of bst1+ that regulates lifespanin fission yeast

Session B Room 26
Role of NPY-CRH neural axis in the PVH incarbohydrate selection in mice【Presenter】 Masataka Kusano【 D e p t 】 Molecular Microbiology【Presenter】 Nawarat Rattanajearakul【 D e p t 】 Endocrinology and Metabolism【Affiliation】 Nagoya University Graduate School of【Affiliation】 National Institute for Physiological Sciences (NIPS)【Favorite Technique】 DREADD technique, Food selection assay

Pharmaceutical Sciences【 C o n t a c t 】 kusano.masataka@d.mbox.nagoyau.ac.jp【 C o n t a c t 】 nawarat@nips.ac.jp

Fission yeast, Schizosaccharomyces pombe is a powerful tool forstudying lifespan at the cellular level, because it is easy to analyze
genetically. In a previous study, screening was conducted to obtainlong                 
sites. Among these strains, a number of particularly longlived strains
were found to contain independent mutations in bst1 + gene. We found           /      of bst1 +. We also found that deletion of the bst1+ caused abnormal
cell morphology and worsened growth in a medium with glycerol as  /  \      /      derstanding of cell life span.

Our lab revealed a subpopulation of corticotropin releasing hormone(CRH) neurons in the paraventricular nucleus of the hypothalamus(PVH), is necessary for a high carbohydrate diet (HCD) selection overa high fat diet (HFD). Neuropeptide Y (NPY) injection into the intra
cerebroventricular (ICV) also increases an HCD intake. However, therelationship between PVH CRH neurons and NPY is poorly understood. Here, I investigated their functional connection in mice. Injec
tion of NPY into ICV or intraPVH increased HCD selection over
HFD. In contrast, chemogenetic inhibition of CRH neurons in the PVH
by introduction of AAV encoding Credependent hM4Dimcherry into
the PVH of CRHires"       {in
duced increase in HCD intake without a change in HFD intake. To
study the physiological relevance of the NPY"_   _"    >   _"   _          2Dglucose (2DG) that induces a wholebody glucopenia.
2DG injection largely increased HCD selection, and this increase was    /  /   {!_ "_    more, injection of NPY receptor antagonists (Y1R and Y5R) in the
PVH suppressed the 2DGinduced HCD selection. These results suggest that NPY"_    {!_       
glucoprivationinduced carbohydrate selection.

Session B Room 27
FIB/SEM analyses for mitochondrial in the axon
initial segments (AIS) and microglial activation
around AIS after nerve injury

Session B Room 31
Exercise-induced changes in the hypothalamicneural circuits controlling energy metabolism【Presenter】 Hirotake Misu
【 D e p t 】 Endocrinology and Metabolism【Presenter】 Hiromi Tamada【 D e p t 】 Functional Anatomy and Neuroscience【Affiliation】 National Institute for Physiological Sciences (NIPS)【Favorite Technique】 Injection to soleus or brown adipose tissue,【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Electron Microscopy

stereotaxic injection of the mouse brain, etc.

【 C o n t a c t 】 tamada@med.nagoyau.ac.jp【 C o n t a c t 】 hiromisu@nips.ac.jp\ _   >          /        q;><x §            ;><           
In this study, the mitochondrial localization in AIS and the activation    ;><         > *<   @  ` q>*<@`x !    were observed in the normal AIS, although abundant mitochondria       ;><     \     that drastically alternations of mitochondrial sorting system in AIS al              >*<@` showed that microglia adhered directly to AIS membrane along thewhole length without insertion of any other elements. Some microglia
whose processes were attached to AIS were also adhering to other distinct nerve       / \  [ braneassociated proteins of the AIS would be lost after injury because
the microglia could not distinguish between somatic and AIS membrane under the condition. In conclusion, the precise threedimension
al ultrastructural analysis revealed the drastic changes of AIS in both              /crucial responses for injured neuron to survive and regenerate.

        /     \ pothalamus in the brain detects the energy status in the body and con
trols the energy metabolism of peripheral tissues through the autonom
ic nervous system. This neural circuit connecting the hypothalamus
and peripheral tissues could play an important role in the changes in   /  /  /       
mains less clear. In this study, we investigated whether regular volun              
eral tissues, thereby altering energy metabolism. We used a retrograde
viral tracer, pseudorabies virus (PRV) to identify hypothalamic neurons projecting to skeletal muscle and brown adipose tissue (BAT). We   {!         ;\   non        /  infected cells in
the hypothalamus. We found that the number of virusinfected cells in          \  
included the lateral hypothalamic area and dorsomedial hypothalamic >          /       \     /    
increase the number of hypothalamic neurons that control skeletal
muscle and BAT and induce changes in energy metabolism.

─ 36 ─

Session B Room 32
Comprehensive Analysis of Pathways Involved in
Liposomal Gene Transfer【Presenter】 Shurui Chen
【 D e p t 】 Immunology【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 flow cytometry and data analysis, gene transfection

to modify certain cells, isolation of different kinds ofcells from human blood, etc.
【 C o n t a c t 】 csr960928@hotmail.com

Session B Room 33
Asteltoxin suppresses extaracellular vesicle
secretion though AMPK/mTOR-mediated activationof lysosome function【Presenter】 Fumie Mitani【 D e p t 】 Cancer Cell Regulation【Affiliation】 Aichi Cancer Center【Favorite Technique】 Isolation and analysis of cancerderived extracellular

vesicles. Immunostaining. Isolation of lipid raft.
【 C o n t a c t 】 fmitani@aichicc.jp

Liposome is a nonviral carrier composed of a bilayer of lipid amphi
pathic molecules, and usually used to encapsulate the active substancesuch as drug, DNA, mRNA within the lipid bilayer or inside the lipo
some. The great success in COVID19 vaccine proved the possibilityof the liposome technology. The susceptibility of cells to liposomal
gene transduction is various depending on cell types. Although most              \   =       >     \cells becomes feasible, repeated treatment with gene \ 
will be promising option devoid of viral vectors. To enhance the lipo  =           tosis or phagocytosis and other critical intracellular molecules during
lipofection process. We hypothesized that could determine candidate
genes critical for liposomalbased gene transfection by screening de
letion mutants that have become resistant to lipofection. After concen                      /     [   ]       molecules, now we may search for methods such as small molecule               
= @     @   q@!x       
luminal vesicles (ILVs) within multivesicular bodies (MVBs). When`!      /  >%!       
tracellular space as an EV. Conversely, fusion of MVB with lysosome
leads to ILV degradation. EVs were demonstrated to play a crucial rolein cancer progression. Therefore, cancerderived EVs are attractive
therapeutic targets. To date, several EV inhibitors have been are re    =         /             /          /      ;\{      @!
 /          /  @!     
ing mitochondrial damage at low concentrations. We also found that     ;\{        ;`{|*mTOR pathway signaling, which is a major regulator of lysosome
function, resulting in promotion of lysosome activity. Furthermore,              /   `! / \           [ @!  /     `!   ;`{|*\]mediated activation of lysosome function.

Session B Room 34
Graphical Extraction of Intra-acinar Airways fromMicro-CT Volumes of Resected Human Lungs

Session B Room 35
Secondhand aerosol exposure from heated tobacco
products and its socioeconomic inequalities inJapan: The JASTIS study 2017-2020【Presenter】 Takeru Shiina【 D e p t 】 Mori Lab【Affiliation】 Nagoya University Graduate School of Informatics【Favorite Technique】 medical image processing, artificial intelligence【 C o n t a c t 】 tshiina@mori.m.is.nagoyau.ac.jp

              from lung microfocus X "\ q¨"\x  _resolution CT   ¨"\  /          human lung. However, observation of the intraacinar airways (i.e., the  /       x    ¨"\          /         
crostructures. Visualization of the intraacinar airways is desirable tofacilitate observation for physicians. We combine a tubular structural                 like structure of these ducts. Our method consists of two stages. In
stage 1, we obtain the intraacinar airway skeletons from a downsam   ¨"\  /   < ʼ       tance map of the lumen regions. In stage 2, we convert an intraacinar
airway skeleton into the treelike structure of the intraacinar airways.
We applied our method to two specimens of the human lungs. The re  /                  /                \         
ising toward accurate segmentation of the intraacinar airways.

【Presenter】 Yudai Tamada【 D e p t 】 Preventive Medicine【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Study design【 C o n t a c t 】 ytamada@med.nagoyau.ac.jp【Introduction】The growing use of heated tobacco products (HTPs)

has raised concerns about secondhand aerosol (SHA) from HTPs, but
few studies have been reported on it. This study aimed to investigate    <_;        [  
Japan.【Methods】\    <_;   ?$  ??was estimated using longitudinal internet survey data of 5,221 partici
pants, aged 20+   ?$ q/ x ` / 
{          /       q         [  x  /    <_;   ??         【Results】\       <_; 
has consistently increased from 4.5% in 2017 to 10.8% in 2020. Lower educational attainment was associated with a higher risk of SHA q    ¢ x \  adjusted risks of SHA        education and middleeducationlevel were 1.57 and 1.34 times higher, respectively, than in those witha high   _   [     <_;  [       /
【Conclusions】]         <_;            [   <_; 

─ 37 ─

Session B Room 36
A hydrophobic residue is critical for speciesspecific aggregation of canine SOD1 with E40K
mutation in canine degenerative myelopathy

Session B Room 37
A Novel Antibody Drug Conjugate Targeting CCR8+
Tumor-infiltrating Regulatory T Cells Induces aStrong Antitumor Immunity【Presenter】 Kei Hashimoto【 D e p t 】 Neuroscience and Pathobiology【Presenter】 He Zhang【 D e p t 】 Immunology【Affiliation】 Nagoya University Research Institute of【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 establish experimental tumor metastasis model

Environmental Medicine (RIEM)【Favorite Technique】 DNA handling, Immunoblotting【 C o n t a c t 】 hashimoto.kei@k.mbox.nagoyau.ac.jp
Canine degenerative myelopathy (DM), an inherited fatal neurodegen
erative disease characterized by progressive motor neuron loss of the     /        "* 
dismutase (SOD1) in similar to amyotrophic lateral sclerosis (ALS).
Canine SOD1 with E40K mutation (cSOD1E40K), the most common
mutation in DM, aggregates in the canine spinal cords and cultured
cells. On the other hand, human SOD1 with E40K (hSOD1E40K) does
not form aggregates. To elucidate responsible residues for the spe
cies    <]@|       <]@|         <] 
found that M117L mutation inhibited the aggregation by increasing thestability of cSOD1E40K and also improved the cell viability. Our datasuggest that the Leu117 in hSOD1 plays a key role in stabilization of
the hydrophobic region, and thus Met117 in cSOD1 can contribute to
the vulnerability for E40K mutation due to the less stable hydrophobic
interactions. Enhancing the stability of hydrophobic region in canine
SOD1 provides a clue for developing novel therapeutic strategies forDM.

by intravenous injection, prepare antibody by
hybridoma cell
【 C o n t a c t 】 zhang.he@h.mbox.nagoyau.ac.jp
Regulatory T (Treg) cells, an immunosuppressive subset of CD4+ T cells
are known to play a key role in the maintenance of selftolerance. In tu
mor immunity, Treg cells suppress antitumor immune responses, thereby
promoting the tumor development and progression. It has been shownthat CCR8 discriminate Treg cells within tumor from those in PBMCs at
individual RNA level. Moreover, antiCCR8 monoclonal antibody
q;/x              vival in mouse models. Thus, CCR8 could be an attractive target to de
plete tumor     \            >    ""  /     microenvironment and peripheral blood of cancer patients were analyzed      >    ""      guished feature of tumor     \    in      \      \  >    >      =    "" targeted reagent (antiCCR8
antibody drug conjugate: CCR8300460) as a Treg celltarget therapy.
CCR8+    ""   \                  ""   _     =      \  
tumor                【References】

1. Yosuke Togashi et al, Nat Rev Clin Oncol, 16, 356371 (2019).
2. George et al, Immunity, 45, 11221134 (2016).

Session C Room 11
Genome-wide CRISPR screen in human CAR-T cells
identifies CUL5 as negative regulator of CAR-T cells
effector function【Presenter】 Yoshitaka Adachi【 D e p t 】 Hematology and Oncology

Session C Room 12
Biochemical analysis of molecular mechanisms
dealing with AP site-HMCES cross-link【Presenter】 Yohei Sugimoto【 D e p t 】 Genome Dynamics【Affiliation】 Nagoya University Research Institute of【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Genetic engineering and various assay using primary

Environmental Medicine (RIEM)【Favorite Technique】 Protein purification and in vitro reconstitution assay

with purified components.

human T cell
【 C o n t a c t 】 adachiy0216@med.nagoyau.ac.jp【 C o n t a c t 】 sugimoto.yohei@f.mbox.nagoyau.ac.jp>       term maintenance are the hallmark oftreatment success after CD19 CAR\  \   
candidate genes which can regulate CART cell function, we utilized
genomewide CRISPRCas9 knockout screening in human CART
cells. We transduced human CD8 positive T cells with genomewide
;   /   " ";   [   
also electroporated Cas9 protein into them for gene knockout. Genome       "%#                   "%#    cell division of CART cells. CUL5 knockout also increased the fre[        /     > 
Ag stimulation. RNA[     "%#    hanced the activity of JAKSTAT pathway. Consistent with the resultof RNA[            
revealed that CUL5 knockout enhanced phosphoSTAT5 and phos
phoSTAT3 signals compared with control CD19 CART cells. Intro
duction of CUL5 knockout CD19CAR\       
prolonged survival of NOG mice with Raji tumors compared with re
sults from controls. In conclusion, these results suggested that genomewide CRISPRCas9 knockout screening is the promising meth
od to identify genes regulating human CART cells function anddevelop clinically relevant geneedited CART cells.

;  *  q;{x          ; 
     \ /     ;{      [/   /                       / ;   [  
this instability, DNA containing AP sites is prone to strand scission.
HMCES (embryonic stem cell #  sinebinding protein) covalently binds to an aldehyde form of AP site
in singlestranded DNA, and forms a stable HMCES crosslink via astable thiazolidine ring (thiaHMCES) to shield AP sites from the     </[   HMCES can be dissolved proteolytically, passively leaving peptide chain with thiazolidine ring
(thiapep). Although the mechanism of the thiaHMCES formation
has been well analyzed, it remains unknown how cellular function
deals with the thiaHMCES and thia \     
ploration of molecular mechanisms dealing with the thiaHMCES andthiapep using model substrates of thiaHMCES and thiapep. In thispresentation, I discuss the replication mechanisms of thiaHMCES
and thiapep, and the repair mechanisms of thiapep.

─ 38 ─

Session C Room 13
Elucidation of the pathogenesis of Alzheimer's
disease focusing on the white matter function

Session C Room 14
Structure of glycyrrhizin binding to the scaffolding
protein ZO1-PDZ1 domain of tight junctions
and its function【Presenter】 Yuki Aoyama【 D e p t 】 Molecular Cell Biology【Presenter】 Emi Hibino【 D e p t 】 Structural Molecular Pharmacology【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 twophoton microscopy, open skull【Affiliation】 Nagoya University Graduate School of

Pharmaceutical Sciences【 C o n t a c t 】 ykaoyama@med.nagoyau.ac.jp

Alzheimerʼs disease (AD) is a neurodegenerative disorder character
ized by shortterm memory impairment. The pathological feature of
AD is the accumulation of amyloid                >        
pathological changes in white matter (WM) detected by MRI correlatewith cognitive decline. However, the mechanism of WM pathology inAD remains unclear. Here, we focused on the myelin, the componentof WM, to understand the pathological mechanism of WM in APP
knockin mice (AD mice). To evaluate the myelin structure and pro      /     \   ;   ?   +     <       
was detected by electron microscopy at 4 and 6 months of age in AD \     related proteins did not change
at 4 months, but increased in 6 months AD mice, suggesting their re
modeling caused by myelin damage. Furthermore, spatial learning was
impaired in 6 months AD mice, correlating with the time dependent
myelin damages. We now visualize the Ca²+ responses of oligodendro                
conduction velocity to verify the regulatory mechanisms of WM func
tions that contribute to learning.

【Favorite Technique】 Detection and analysis of proteinprotein interactions and ligand

protein interactions by multidimensional NMR measurement ofproteins, largescale synthesis of recombinant proteins using an
E. coli expression system, and largescale synthesis of 15N and
13Clabeled proteins for multidimensional NMR measurements.
【 C o n t a c t 】 hibino.emi@b.mbox.nagoyau.ac.jp
Glycyrrhizin (GA) is the principal active ingredient of a medicinal herb
licorice, and has been reported to have various pharmacological activi
ties including anti    };                q\-x       //        _`} _   
targets of the various activities of GA are still unclear. Recently, we   };   /     {   ]1 (ZO1
PDZ1), one of the component molecules of TJs. We also calculated the      ]@   "<{       
ty of the structure by NMR measurements using structural analogues ofGA as well as ZO1{    \      of GA on TJs against the epithelial cell monolayer, transepithelial electrical resistance (TEER) of the cultured Caco?    }; assessed. We succeeded in reproduce the results reported previously(1),in which highdose GA could prolong the TJ       
cholate. Our results suggest that GA blocks the interaction of TJs throughZO1, and that the function of GA depends on the condition since GA   \-        【Reference】

1. Sakai M et al. J Pharm Pharmacol, 51(1), 2733 (1999).

Session C Room 15
Characterization of compound heterozygous
mutation derived from DOK7-related-CMS patient

Session C Room 16
AI-based live-cell-image analysis for spinal andbulbar muscular atrophy pathology【Presenter】 Shaochuan Zhang【 D e p t 】 Neurogenetics【Presenter】 Kenji Sakakibara【 D e p t 】 Neurology【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 gene editing【Affiliation】 Nagoya University Graduate School of Medicine【 C o n t a c t 】 keng19850411@yahoo.co.jp【 C o n t a c t 】 zhangsc@med.nagoyau.ac.jp【Objective】Spinal and bulbar muscular atrophy (SBMA) is a neuroCongenital myasthenic syndromes (CMS) are a group of heteroge
neous diseases characterized by fatigue and weakness. These inherited
diseases are responsible for a specialized structure neuromuscular   q`-x              /
tween motoneuron and skeleton muscle. Up to date, overpass 30 kinds    /      "`<    
cules, the downstream of tyrosine kinase 7 (DOK7) contribute to themost prevalent form of limbgirdle myasthenia. Dozens of mutations
 ]|$  /           ?$
However, just part of mutations are characterized. The role of DOK7  /  `-                 >  /            
(c.653}¤"§ }¤;x   ]|$CMS patient, and these two         -  ]       two mutations.

   / ";}        
receptor gene. We demonstrate an AIbased cellmorphologic analysis
               
SBMA.【Methods】We used a muscular C2C12 cell model of SBMA
(97Q cells) and control (24Q cells). We administered 5 alphadihydro
testosterone (DHT) which is known to aggravate the pathogenesis of
SBMA, and pioglitazone (PG) which is reported to increase the viabil
ity of 97Q cells, and evaluated whether the image analysis could re             
to identify genes that were dysregulated in 97Q cells. Based on the
results, we selected drugs that target the signaling pathway associated              
analysis. 【Results】The clustering of DHTtreated 97Q cells moved
away from that of 24Q cells. In contrast, the clustering of PGtreated$©       ?©       
ysis, we selected naratriptan (NRT), p38 inhibitor, NFkB inhibitor,Nacetylcystein and nifedipine. NRT and p38 inhibitortreated 97Q
cells shifted toward 24Q cells. All others make no change. 【Conclu
sions】We develop an AI platform for evaluating living cells to deter   =  

─ 39 ─

Session C Room 17
Prediction of the Splicing Effects of Single-Nucleotide
Variants (SNVs) at 1st nucleotide of an exon
【Presenter】 Atefeh Joudaki【 D e p t 】 Neurogenetics

Session C Room 21
Neuroinflammation in Toll-like receptor 7
agonist-induced mouse model for systemic lupus
erythematosus【Presenter】 Ritsuko Shimogawa【 D e p t 】 Neuroscience and Pathobiology【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Machine learning, Prediction the splicing, SNV,

【Affiliation】 Nagoya University Research Institute ofmRNA Splicing【 C o n t a c t 】 atefeh.joudaki@med.nagoyau.ac.jp

Environmental Medicine (RIEM)【 C o n t a c t 】 shimogawa.ritsuko.g8@s.mail.nagoyau.ac.jp【Objective】Various tools have been developed in recent years to pre     <!    _    /            <!      }    !       /         <!      }         ;}de
pendence of the 3ʼ splice site (ss) and interaction with U2AF35. Also,
there is not enough information about the functional study of splicing
in the recent databases.【Methods】Around 380 Papers reporting a totalof 130 SNVs were individually scrutinized.We employed 124 featuresand considered both linear and nonlinear models, including Gradient          < !  " q<!"x \models were generated by 65 splicing    <!   _
Gene Mutation Database (HGMD) and 94 neutral SNVs with a minor [    ª `; £ #   /<{  / }
Search optimizes hyperparameters. Crossvalidation was performed     【Results】Gradient Boosting had thebest model evaluation, the area under the receiver operating character
istic curve (AUROC) and the area under the precisionrecall curve(AUPR) were on average 0.88 and 0.86, respectively.【Conclusions】
The performance of our model is higher than other available tools. We
will generate a web service that accepts a genomic coordinate accord     }"$*  }" *  \    
cally will generate three possible SNVs at the coordinate and predicts
a probability of aberrant splicing.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease                 tem (CNS) involvement. Previous studies have reported a higher riskof developing dementia in the patients with SLE. However, the mech
anisms of systemic and central immune system crosstalk in SLE are    >          in the brains of Tolllike receptor 7 (TLR7) agonistinduced SLEmodel mice, which are established by the chronic skin administration [ q>`©x       "#$%*+   +                 elevated level of antinuclear antibody in serum of IMQtreated miceas a hallmark of SLE. IMQinduced SLE mice also showed increases
 " ;   microglia and astrocytes. In addition, activated (A1) astrocyte markers such as H2d and Fkbp5 were upregu
lated in the isolated astrocytes from IMQinduced SLE mice. These    <%@        
chemokines in CNS through peripheral TLR7induced systemic in                             \%$   induced model      <%@  +* 

Session C Room 22
Epstein-Barr Virus BBLF1 is Involved in Efficient
Virus Egress

Session C Room 23
Analysis of Dynamic Postural Control Related to
Trunk-Lower Extremity Coordination on Gait Initiation【Presenter】 Md. Kamal Uddin【 D e p t 】 Virology【Presenter】 Masahiro Nishimura【 D e p t 】 Creative Physical Therapy【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Fluorescence microscopy, gene knockout in BAC【Affiliation】 Nagoya University Graduate School of of Medicine

system.
【 C o n t a c t 】 kamal@med.nagoyau.ac.jp【Favorite Technique】 Gait analysis using a wearable device (accelerometer)(Health Sciences)

Viral particles of all herpesviruses contain a proteinaceous tegument
between the nucleocapsid and envelope of the virus particle. Tegument
proteins play multiple roles in virus lifecycle, including modulation ofcell environment in primary infection, virion morphogenesis, and immune evasion, but their functions are not fully understood. EpsteinBarr Virus (EBV), a herpesvirus family member, causes several
cancers, including lymphoma and gastric carcinoma. The EBV BBLF1
is one of the tegument proteins conserved across all herpesvirus sub
families. To analyze the biological function of BBLF1, we generated a%       /      ing the entire EBV genome and established stably infected cell lines.
%             ;         /             ]           creased intracellular virion production and then accumulated virion
was observed by transmission electron microscopy. These data
demonstrate the role of BBLF1 to achieve the optimal release of virus
particles.

Visualization of time series data, waveform analysis,
multiple (MATLAB)
Stability research related to dynamic postural control【 C o n t a c t 】 nishimura.masahiro@g.mbox.nagoyau.ac.jp
A walking process from gait initiation (GI) to steadystate gait was
repeated in daily living. COP"]`     q">x   
the stability of voluntary movement in stair climbing and standing po
sition, however, itʼs unknown to be applied for GI. The aim of thisstudy is to clarify whether CI can evaluate stability on GI. 11 young
people and 23 elderly people aged 65 years or older walked 5 times on
a 10m walking path at comfortable speed. A foot pressure distribution
sensor and motion capture were used to obtain COP and COM trajec
tory respectively. Main outcome were CI in ML and AP direction (CI_ML, CI_AP), other outcomes were gait parameters, movement perfor  [   /    ;     starting movement to 3rd heel contact. Elderly people were divided
into two groups (elder (H), elder (L)) based on balance ability. Signif    /   q%x          ">¬;{ ;   /     ">           ">       ">¬`%           ">¬;{       ?       \   
indicate that CI can evaluate gait stability on GI related to coordinationof the trunk and lower limbs.

─ 40 ─

Session C Room 24
Synaptic inputs from motor cortex do not have arole in motor-related membrane potential dynamics
in mouse somatosensory cortex

Session C Room 25
Matrix remodeling-associated protein 8 is a marker
of a subset of cancer-associated fibroblasts inpancreatic cancer【Presenter】 Masahiro Kawatani【 D e p t 】 Neuroscience II【Presenter】 Ryosuke Ichihara【 D e p t 】 Tumor Pathology【Affiliation】 Nagoya University Research Institute of【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 RNA in situ hybridization, immunohistochemistry

Environmental Medicine(RIEM)【Favorite Technique】 Electrophysiology (In vivo/ vitro patchclamp
recording, silicone probe recording), AAV injection【 C o n t a c t 】 s4014528@gmail.com

staining and transplantation of mouse PDAC cells
into mice, etc.
【 C o n t a c t 】 ichihara.r1@med.nagoyau.ac.jp               _
ever, the underlying cellular and circuit mechanisms remain unclear. In      q<x /     q!x          /       q`x      q`x       `  /        < _   vivo wholecell patchclamp or nanoelectrode intracellular recordings
in awake behaving mice, we investigated the contribution of wM1→S1
inputs to WMinduced Vm changes in S1 neurons. A brief (12 ms)
optogenetic stimulation of wM1 typically induced triphasic responses
 <  ~         /     /     
We analyzed the correlation among the amplitudes of these responses
and WMinduced Vm changes in S1 neurons. However, we did not                   itive correlation found in intracellular recordings were not reproducedin patchclamp recordings. Thus, even with the rich innervation fromwM1 that is activated at the onset of WMs, wM1 activity may not be amajor cause of WMinduced Vm dynamics in S1 neurons. We are currently testing this hypothesis by directly inhibiting wM1→S1 synaptic
inputs by optogenetics.

Cancer  //  q";x      microenvironment, were previously thought to be a uniform cell population that promotes cancer progression. However, recent studies
have shown that CAFs are heterogeneous and that there are at least two
types of CAFs, i.e., cancerpromoting and restraining CAFs. We pre   `         restraining
CAFs (rCAFs) in pancreatic ductal adenocarcinoma (PDAC). The precise nature of rCAFs, however, has remained elusive owing to a lack ofunderstanding of their comprehensive gene signatures. Here, we          `   cell         ;            associated protein 8 (MXRA8),
which encodes a type I transmembrane protein with unknown molec     ;   ` ;    {;"    ` ;         
CAF markers. Moreover, in patients with PDAC or syngeneic tumors
developed in MXRA8   ` ;        ";         /     ` ;  ";      ]   MXRA8 as a new CAF marker; further studies are needed to determine
the relevance of this marker.

Session C Room 26
The downregulation of PTBP1 promotes alternative
splicing of AGRN mRNA essential for AChR
clustering

Session C Room 27
A central oxytocin neural pathway that
regulates metabolism【Presenter】 Bushra Samira【 D e p t 】 Neurogenetics【Presenter】 Akihiro Fukushima【 D e p t 】 Integrative Physiology【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Brain slice patchclamp recording, In vivo

【Affiliation】 Nagoya University Graduate School of Medicine【 C o n t a c t 】 twinbushra@gmail.com;   /[       
isoforms that are involved in a variety of biological processes. Howev
er, only the neuron  q   x             [       q`-x \             “ ” “  ” and “ ” induces neural agrin, but theunderlying mechanism is unknown. The search for ciselements in thehuman AGRN gene revealed that binding sites for polypyrimidine tract
binding protein 1, a splicing repressor, are enriched near the Y and Z  <   {\{   ;       /              `    {\{ /                    
/ {\{     q{x            /        ;   
in vitro binding assay demonstrated that PTBP1 competes with
?;+#  /       ʼs PY tract, thereby inhibiting its             
{\{         /        
increase. We propose that downregulation of PTBP1 in mature neurons [  `-   /      ;}mRNA splicing.

physiological experiments, Nanoinjection into thebrain.
【 C o n t a c t 】 akifuku@med.nagoyau.ac.jp]  q] \x         pothalamic nucleus (PVH), contributes to a variety of behaviors, such        / ] \       /            central nervous system, and dysfunction of the OXT neural network
has been linked to PraderWilli syndrome, a condition in which severe
obesity develops. However, it is unknown how the OXT neural network contributes to the regulation of energy homeostasis. We developed a new adeno   q;;!x   /         ] \        ] \
neurons in the PVH project to the rostral medullary raphe region(rMR), which harbors sympathetic premotor neurons that control met
abolic heat production in brown adipose tissue (BAT). In vivo optoge
netic stimulation of the PVH→rMR OXTergic neural pathway not only
elicits BAT thermogenic and cardiac responses, but also potentiates
sympathetic responses evoked by glutamatergic transmission in the` \       ] \     
hypothalamus to the medulla oblongata, through which emotionallydriven OXT signaling enhances metabolic functions and thereby im
pacts wholebody energy balance.

─ 41 ─

Session C Room 28
Exercise-induced Ampk activation ameliorates
polyglutamine-mediated neuromusculardegeneration in SBMA mice

Session C Room 31
Analysis of mechanism to control the expressionof NOTCH receptors by detecting abnormal
O-glycosylation【Presenter】 Tomoki Hirunagi【 D e p t 】 Neurology【Presenter】 Yuko Tashima【 D e p t 】 Molecular and Cellular Biology【Affiliation】 Nagoya University Graduate School of Medicine【 C o n t a c t 】 hirunagi.tomoki@med.nagoyau.ac.jp【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Flow cytometry, cell sorting, glycobiology,【Objective】Spinal and bulbar muscular atrophy (SBMA) is a hered【 C o n t a c t 】 tashima@med.nagoyau.ac.jp

     /   ";}    
androgen receptor (AR) gene. The aim of this study is to investigate                
muscular degeneration in a mouse model of SBMA.【Methods】We
assigned SBMA model mice (AR97Q mice) to three groups: 1) the     q@{x~ ?x        q@{ x~ x       q<@x @Pre  @Post mice received 1hour forced wheelrunning 5 days aweek for 4 weeks.【Results】@{  /  @Post mice,
showed improvement in motor function and survival with ameliorationof neuronal and muscular histopathology. Especially, nuclear accumu
lation of polyglutamine (polyQ)  ;             @Pre mice compared to that in<@              ;signaling and inhibited mTOR pathway that regulates protein synthesisin the skeletal muscle. Correspondingly, pharmacological activation of
Ampk inhibited protein synthesis and downregulated polyQ 
AR protein in C2C12 skeletal muscle cells.【Conclusions】Early phys    ;     /     <`;    
er neuromuscular disorders caused by abnormal protein accumulation.

NOTCH signaling is important for the cell fate decision. NOTCH re
ceptors are heavily glycosylated with three kinds of Oglycans in their    ]\"_     /   ]glycosylation sites in each molecule. Some sites for Oglycosylation are            ]\"_   >       [    ]glycosylation            
anism is not known. Our purpose is to reveal how to distinguish unma
tured NOTCH receptors or abnormally Oglycosylated NOTCH re
ceptors and how to lead abnormal NOTCH receptors into thedegradation pathway. First, we made a NOTCH1 mutant with several
mutations of Oglycosylation sites near the transmembrane region andanalyzed it. Flow cytometric analysis showed that the NOTCH1 mu        \ ]\"_   
observed in the ER resulted in accumulation. We investigated whether  /    ]glycosylation sites was important for the
]\"_         /       [ /          /  
identify proteins nearby the NOTCH1 mutant. Weʼll discuss candidate
proteins interacting with the NOTCH1 mutant.

Session C Room 32
Visualizing neuronal circuit activity underling
sensory abnormalities of ASD

Session C Room 33
Exploring RhoGEFs involved in Cdc42 activation in
excitatory synapses【Presenter】 Midori Shibushita【 D e p t 】 Molecular Cell Biology【Presenter】 Yutaro Nagasawa【 D e p t 】 Center for Brain Research【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 In vivo twophoton imaging of mouse brain【Affiliation】 National Institute for Physiological Sciences (NIPS)【 C o n t a c t 】 yutaron@nips.ac.jp【 C o n t a c t 】 shibushita@med.nagoyau.ac.jp{                    
neurons, known as structural longterm potentiation (sLTP), are be
lieved to be the basis of learning and memory. Previous studies foundthat Cdc42, a member of the Rho family small GTPase, is activatedduring sLTP triggered by singlespine glutamate stimulation, and it
plays an essential role in sLTP. However, the molecules that activate"?              _    "?           change factor (RhoGEF) and monitor their recruitment into stimulated
spines. RhoGEFs fused to BrUSLEE (a mutant of EGFP with a short  x     @}{     
hippocampal slices by gene gun. The recruitment of BrUSLEEGEF
was monitored by 2        
scope. Among RhoGEFs, FGD1 and ARHGEF15 were recruited into
the stimulated spines, implying that they activate Cdc42 in spines. We
also investigated their functions by lossoffunction assay using shR;      }    [               ;_}@#  [          \     }*ARHGEF15 are Cdc42 activators involved in sLTP.

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder    /   ;       connectivity of thalamus         /
sis of neuronal circuitry that causes sensory abnormalities remains unknown. Furthermore, the pathological reciprocal interaction between
sensory abnormalities and impaired social behavior has not been
demonstrated. In this study, we used previously known maternal im
mune activation (MIA) with Poly(I:C) mouse as ASD model. To study
the functional sensory evoked response of neuronal population andtheir contribution on functional local circuit connectivity in ASD model mice, we visualized neuronal activities with whisker stimulation orwith holographic single cell stimulation in the primary somatosensory  /  q<x     photon holographic mi /                     correlation withwhisker stimuli as whiskerresponse cells. Whiskerresponse cell
population in S1BF of MIA mice showed lower synchrony, and highfailure response rate for 10 serial stimuli, compared to WT mice. The
results suggest the variance of neuronal responses to whisker stimuli,      /      
brain functions in ASD. This study provides the pathological perspective of sensory abnormalities and their abnormal circuitrybasis ofASD.

─ 42 ─

Session C Room 34
Effects of sialic acid synthesis and degradation
deficiency on medaka development

Session C Room 35
CD83 marks progenitor exhausted T cell population【Presenter】 Zhiwen Wu【 D e p t 】 Immune Response【Presenter】 Takahiro Nakagawa【 D e p t 】 Animal Cell Function【Affiliation】 Aichi Cancer Center【 C o n t a c t 】 z.wu@aichicc.jp【Affiliation】 Nagoya University Graduate School of

Bioagricultural Sciences, iGCORE【Favorite Technique】 biochemical analysis of glycans【 C o n t a c t 】 nakagawa.takahiro@d.mbox.nagoyau.ac.jp

Sialic acid (Sia) is a group of acidic sugars with a ninecarbon back
bone. Sias are present at nonreducing termini of glycan, and their /    /    /  >    mutations of Sia synthetic and degradative enzyme genes cause vari
ous symptoms such as intellectual development disorders, skeletal     _       embryogenesis and development is still unknown. Thus, in this study,    /           <{<
and a degradative enzyme, SPL in medaka model. First, we analyzed   <{<   <{%   ;                 / <{< or
SPL  q|]x  / "><{*"       the SPSKO medaka was lethal in young fry, while the SPLKO medaka could survive although some of them showed cardiac abnormal
ity. Finally, we measured Sia amount of the SPS and SPLKO meda
ka, and found that Sia amount was decreased in the SPSKO medaka,
although it was unchanged in the SPLKO medaka. These results sug  <{<   <{%        / and development.

\             \      /      @  \   /          \                    \                  \           \              / _             \    /     _                  
 \            / 
antigen receptor (CAR)engineered human T cells. Among the candi            \    /
available RNA[       "    pressed in the CCR7+ PD1+ tumor     ";T cell populationcompared with the CCR7 and PD1 T cells. While CD83 was robust
ly induced in T cells with an early memory phenotype, its upregulation
 /      \       ]     "              \        \          
T cell population.

Session C Room 36
Calcium transients control a morphogenetic cycle
underlying neuronal migratory movement

Session C Room 37
Elucidation of the mechanism of reduced ICB
treatment efficacy in advanced-stage cancer【Presenter】 Shinichiro Horigane【 D e p t 】 Neuroscience I【Presenter】 Kaori Fujimaki【 D e p t 】 Immunology【Affiliation】 Nagoya University Research Institute of【Affiliation】 Nagoya University Graduate School of Medicine【Favorite Technique】 Flow Cytometry, Subcutaneous injection of cancer

Environmental Medicine (RIEM)【Favorite Technique】 Ca2+ imaging, brain slice preparation, in utero
electroporation【 C o n t a c t 】 horigane@riem.nagoyau.ac.jp

cells into mice
【 C o n t a c t 】 fujimaki.kaori@f.mbox.nagoyau.ac.jp

In spite of the critical importance of neuronal migration in the construction of brain architecture and neuronal circuits, morphogenetic rules
operating neuronal migration during cortical layer formation have re   >        [ 
migrate in succession in a timeorchestrated manner within a limited
space remains unsolved. We previously showed that migrating neurons           "2+   
voltage gated Ca2+ channels (VGCCs), and further discovered a potential
role for VGCCdriven spontaneous regenerative Ca2+ transients in neuronal migration. In keeping with this, we here found that radially migrat      /   /       "2+transients, while they underwent a characteristic, transient nuclear de
formation or ʻroundingʼ. Furthermore, an evoked sustained Ca2+ eleva
tion was able to trigger such nucleus deformation and maintained it
throughout the duration of its transients. Intriguingly, the Ca2+ elevation        * 
changes during a migratory movement: an initial acceleration followed
by a halt in nucleus movement, a retraction in the trailing process, as   /         \ "2+ elevation regu
lated three key morphogenetic components of neuronal migration.
Mechanistically, Ca2+    %type VGCC was essential for nucleus        "        Ltype VGCC gainoffunction mutation, associated with a syndromic              
perturbed cell migration. Together, our results shed light on the funda
mental role of Ca2+ transients in orchestrating multistep morphogenetic
cycles underlying neuronal radial migration.

Recently, it has been shown that antitumor immune responses can be
rescued by removing immunosuppressive factors, such as PD1, andsuch immune checkpoint blockade (ICB) is becoming established as        /      _ >"              stage cancer withresponse rates of only 1530%. Therefore, elucidation of the mecha
nism of resistance to ICB in patients with advancedstage cancer is anurgent issue.
In this study, using a MC38bearing mouse model, we investigated theimpact of the timing of ICB administration on antitumor immune responses. We found that the group early administration of ICB resulted
in complete, tumors regressed completely, whereas the group later ad
ministration failed to contain tumor growth. Immunological analysis
showed that the advancedstage tumor was enriched with more regu  \        \     lystage tumor. We also analyzed the function of dendritic cells (DCs)            "   
was lower in advancedstage cancer compared to earlystage cancer.
Taken together, our results indicate that the function of T cells and DCs
     =        stage
cancer.

─ 43 ─

第 3 回 CIBoG リトリート参加者一覧
No.

Name

氏 名

1 Fumie Mitani

三谷

2 Yumiko Kasugai

春日井

3 Yuki Kagoya

籠谷

4 Zhiwen Wu䬗

5 Yuta Adachi

足立

6 Masahiro Aoki

文美絵

Department, Section, or Division

Institute, University, or Company

Cancer Cell Regulation

Aichi Cancer Center

Cancer Epidemiology and Prevention

Aichi Cancer Center

Immune Response

Aichi Cancer Center

Immune Response

Aichi Cancer Center

雄太

Molecular Therapeutics

Aichi Cancer Center

青木正博

Pathophysiology

Aichi Cancer Center7 Kaichi Yoshizaki

吉崎嘉一

Disease Model

Aichi Developmental Disability Center
Institute for Developmental Research

8 Masato Asai浅井真人

Disease Model

Aichi Developmental Disability Center
Institute for Developmental Research

9 Saki Murofushi

室伏紗希

Disease Model

Aichi Developmental Disability Center
Institute for Developmental Research

10 Yujin Zhou

Yujin Zhou

Bioorganic Chemistry

Gifu University Graduate Schoolof Natural Science and Technology,
iGCORE

11 Ryota Hiratsuka

平塚

Bioactive Molecule Science

Gifu University Graduate Schoolof Natural Science and Technology,
iGCORE

12 Toshiki Mori

森

Cell Biophysics

Gifu University Graduate Schoolof Natural Science and Technology,
iGCORE

13 Reina F Osuka

大須賀

Glycobiochemistry

Gifu University Graduate Schoolof Natural Science and Technology,
iGCORE

14 Seita Tomida富田晟太

Glycobiochemistry

Gifu University Graduate Schoolof Natural Science and Technology,
iGCORE

15 Naoko Komura

河村

奈緒子

Bioactive Molecule Science

Gifu University Institute for Glycocore
Research (iGCORE)

16 Monami Kihara

木原

もなみ

Molecular Biotechnology

Nagoya University Graduate School of
Bioagricultural Sciences

17 Rio Okuda

奥田理央

Molecular Biotechnology

Nagoya University Graduate School of
Bioagricultural Sciences

18 Takahiro Nakagawa

中川貴博

Animal Cell Function

Nagoya University Graduate School of
Bioagricultural Sciences, iGCORE

19 Ayane Naramura

奈良村

GlycoLife Science

Nagoya University Graduate School of
Bioagricultural Sciences, iGCORE

20 Hinano Komura

古村雛乃

GlycoLife Science

Nagoya University Graduate School of
Bioagricultural Sciences, iGCORE

21 Masaya Hane羽根

正弥

GlycoLife Science

Nagoya University Graduate School of
Bioagricultural Sciences, iGCORE

22 Rina Hatanaka

畑中理菜

GlycoLife Science

Nagoya University Graduate School of
Bioagricultural Sciences, iGCORE

由美子
勇紀

智聞

諒大

俊貴

玲奈

文音

─ 44 ─

No.

Name

氏 名

Department, Section, or Division

Institute, University, or Company

GlycoLife Science

Nagoya University Graduate School of
Bioagricultural Sciences, iGCORE

少翔

Kudo Lab

Nagoya University Graduate School ofInformatics

冬平

Mori Lab

Nagoya University Graduate School ofInformatics

健Mori Lab

Nagoya University Graduate School ofInformatics

李文達

Mori Lab

Nagoya University Graduate School ofInformatics

28 Yunheng Wu

呉運恒Mori Lab

Nagoya University Graduate School ofInformatics

29 Zhongyang Lu魯仲陽Mori Lab

Nagoya University Graduate School ofInformatics

30 Shogo Tamura

田村彰吾

Cellular and Genetic Sciences

Nagoya University Graduate School of
Medicine (Health Sciences)

31 Reiko Kurokawa

黒川玲子">} ]=Nagoya University Graduate School of
Medicine (Health Sciences)

32 Kohei Uno

宇野光平

Integrated Health Sciences

Nagoya University Graduate School of
Medicine (Health Sciences)

33 Masahiro Nishimura

西村匡弘

Creative Physical Therapy

Nagoya University Graduate School of
Medicine (Health Sciences)

34 Mitsuo Sato佐藤光夫

Host Defense Sciences

Nagoya University Graduate School of
Medicine (Health Sciences)

35 Nozomi Kawabe

川邉

のぞみ

Host Defense Sciences

Nagoya University Graduate School of
Medicine (Health Sciences)

36 Katsunori Yogo

余語

克紀

Medical Quantum Science

Nagoya University Graduate School of
Medicine (Health Sciences)

37 Hikari Isaji

伊佐次

Occupational Therapy Science

Nagoya University Graduate School of
Medicine (Health Sciences)

38 Yuga Takeda

武田悠我

Occupational Therapy Science

Nagoya University Graduate School of
Medicine (Health Sciences)

39 Yutaka Kondo

近藤豊

Cancer Biology

Nagoya University Graduate School of
Medicine

40 Mona Alhussein Aboalela Mona Alhussein Aboalela

Cancer Immune Therapy Research Center

Nagoya University Graduate School of
Medicine

41 Tsukasa Shimamura

島村司

Cell Biology

Nagoya University Graduate School of
Medicine

42 Keisuke Kuroda

黒田啓介">} ]=Nagoya University Graduate School of
Medicine

43 Takashi Murate

村手隆司">} ]=Nagoya University Graduate School of
Medicine

44 Tomoko Hattori服部智子">} ]=Nagoya University Graduate School of
Medicine

45 Aoi Ebata㻮䟠ᇫ圄

Dermatology

Nagoya University Graduate School of
Medicine

46 Yuya Murase

村瀬友哉

Dermatology

Nagoya University Graduate School of
Medicine

47 Hidetaka Suga

須賀英隆

Endocrinology and Diabetes

Nagoya University Graduate School of
Medicine

23 Sayo Morishita森下

24 Shaoxiang Dang

党

25 DongPing Pan

潘

26 Takeru Shiina

椎名

27 Wenda Li

沙世

光莉

─ 45 ─

No.

Name

氏 名

Department, Section, or Division

Institute, University, or Company

48 Shintaro Iwama

岩間

信太郎

Endocrinology and Diabetes

Nagoya University Graduate School of
Medicine

49 Tomoko Kobayashi

小林

朋子

Endocrinology and Diabetes

Nagoya University Graduate School of
Medicine

50 Yoshinori Yasuda

安田康紀

Endocrinology and Diabetes

Nagoya University Graduate School of
Medicine

51 Hiromi Tamada

玉田宏美

Functional Anatomy and Neuroscience

Nagoya University Graduate School of
Medicine

52 Hiroshi Kiyama

木山博資

Functional Anatomy and Neuroscience

Nagoya University Graduate School of
Medicine

53 Hiroyuki Konishi

小西博之

Functional Anatomy and Neuroscience

Nagoya University Graduate School of
Medicine

54 Kenichi Nagata

永田健一

Functional Anatomy and Neuroscience

Nagoya University Graduate School of
Medicine

55 Hidekazu Takahashi髙橋

秀和

Gastroenterology

Nagoya University Graduate School of
Medicine

56 Marie Ohbiki

大引

真理恵

Hematology and Oncology

Nagoya University Graduate School of
Medicine

57 Mika Takai

高井美佳

Hematology and Oncology

Nagoya University Graduate School of
Medicine

58 Seitaro Terakura

寺倉

精太郎

Hematology and Oncology

Nagoya University Graduate School of
Medicine

59 Yoshitaka Adachi

安達慶高

Hematology and Oncology

Nagoya University Graduate School of
Medicine

60 Yusuke Yamaga

山家佑介

Hematology and Oncology

Nagoya University Graduate School of
Medicine

61 He Zhang

張Immunology

Nagoya University Graduate School of
Medicine

62 Kaori Fujimaki

藤巻

加於梨

Immunology

Nagoya University Graduate School of
Medicine

63 Kazuhiro Kumagai熊谷和裕

Immunology

Nagoya University Graduate School of
Medicine

64 Naoki Yuri

由利

直樹

Immunology

Nagoya University Graduate School of
Medicine

65 Shurui Chen

陳

Immunology

Nagoya University Graduate School of
Medicine

66 Akihiro Fukushima

福島章紘

Integrative Physiology

Nagoya University Graduate School of
Medicine

67 Yohei Tsukamoto

塚本庸平

Molecular and Cellular Biology

Nagoya University Graduate School of
Medicine

68 Yuji Kondo

近藤裕史

Molecular and Cellular Biology

Nagoya University Graduate School of
Medicine

69 Yuko Tashima田嶌優子

Molecular and Cellular Biology

Nagoya University Graduate School of
Medicine

70 Kazuma Sakamoto

坂元

一真

Molecular Biology

Nagoya University Graduate School of
Medicine

71 Kenji Kadomatsu

門松健治

Molecular Biology

Nagoya University Graduate School of
Medicine

72 Shiori Go

郷

Molecular Biology

Nagoya University Graduate School of
Medicine

鶴

書蕊

詩織

─ 46 ─

No.

Name

氏 名

Department, Section, or Division

Institute, University, or Company

73 Shoma Tsubota

坪田

庄真

Molecular Biology

Nagoya University Graduate School of
Medicine

74 Tomoya Ozaki尾崎智也

Molecular Biology

Nagoya University Graduate School of
Medicine

75 Yuji Suzuki

鈴木佑治

Molecular Biology

Nagoya University Graduate School of
Medicine

76 Hiroaki Wake和氣

弘明

Molecular Cell Biology

Nagoya University Graduate School of
Medicine

77 Ikuko Takeda

竹田育子

Molecular Cell Biology

Nagoya University Graduate School of
Medicine

78 Midori Shibushita

渋下碧

Molecular Cell Biology

Nagoya University Graduate School of
Medicine

79 Yuki Aoyama

青山友紀

Molecular Cell Biology

Nagoya University Graduate School of
Medicine

80 Reiko Muto武藤玲子

Nephrology

Nagoya University Graduate School of
Medicine

81 Atefeh Joudaki

Atefeh Joudaki

Neurogenetics

Nagoya University Graduate School of
Medicine

82 Bushra Samira

Bushra Samira

Neurogenetics

Nagoya University Graduate School of
Medicine

83 Kinji Ohno

大野

Neurogenetics

Nagoya University Graduate School of
Medicine

84 Paniz Farshadyeganeh

Paniz Farshadyeganeh Neurogenetics

Nagoya University Graduate School of
Medicine

85 Shaochuan Zhang

張Neurogenetics

Nagoya University Graduate School of
Medicine

86 Tomonari Hamaguchi濵口

知成

Neurogenetics

Nagoya University Graduate School of
Medicine

87 Toshihiko Kawachi

河地利彦

Neurogenetics

Nagoya University Graduate School of
Medicine

88 Ayuka Murakami

村上

あゆ香

Neurology

Nagoya University Graduate School of
Medicine

89 Kenji Sakakibara

榊原健二

Neurology

Nagoya University Graduate School of
Medicine

90 Koyo Tsujikawa

辻河高陽

Neurology

Nagoya University Graduate School of
Medicine

91 Satoshi Yokoi

横井聡

Neurology

Nagoya University Graduate School of
Medicine

92 Takashi Uematsu

植松高史

Neurology

Nagoya University Graduate School of
Medicine

93 Tomoki Hirunagi蛭薙智紀

Neurology

Nagoya University Graduate School of
Medicine

94 Yoshiyuki Kishimoto

岸本祥之

Neurology

Nagoya University Graduate School of
Medicine

95 Yosuke Ogura

小椋

陽介

Neurology

Nagoya University Graduate School of
Medicine

96 Dong Yutao

Dong Yutao

Neuropsychopharmacology and Hospital Nagoya University Graduate School of
Pharmacy
Medicine

97 Rinako Tanaka

田中

Neuropsychopharmacology and Hospital Nagoya University Graduate School of
Pharmacy
Medicine

欽司

少川

里奈子

─ 47 ─

No.

Name

氏 名

Department, Section, or Division

Institute, University, or Company

Occupational and Environmental Health

Nagoya University Graduate School of
Medicine

Pathology and Biological Responses

Nagoya University Graduate School of
Medicine

98 Takumi Kagawa

香川99 Hao Zheng

鄭100 Satoshi Nakano

仲野聡

Pediatric Surgery

Nagoya University Graduate School of
Medicine

101 Yudai Tamada

玉田雄大

Preventive Medicine

Nagoya University Graduate School of
Medicine

102 Yoko Tanaka

田中

陽子

Psychiatry

Nagoya University Graduate School of
Medicine

103 Koji Sakamoto

阪本考司

Respiratory Medicine

Nagoya University Graduate School of
Medicine

104 Taichi Hibi

日比太智

Systems Biology

Nagoya University Graduate School of
Medicine

105 Atsushi Enomoto

榎本篤Tumor Pathology

Nagoya University Graduate School of
Medicine

106 Ryosuke Ichihara

市原亮介

Tumor Pathology

Nagoya University Graduate School of
Medicine

107 Atzin BolanosCeron

Atzin BolanosCeron

Virology

Nagoya University Graduate School of
Medicine

108 Hiroshi Kimura

木村宏

Virology

Nagoya University Graduate School of
Medicine

109 Md. Kamal Uddin

Md. Kamal Uddin

Virology

Nagoya University Graduate School of
Medicine

110 Miki Umeda

梅田実希

Virology

Nagoya University Graduate School of
Medicine

111 Yasuyuki Miyake

三宅康之

Virology

Nagoya University Graduate School of
Medicine

112 Yoshitaka Sato佐藤好隆

Virology

Nagoya University Graduate School of
Medicine

113 Yuya Hara

原

Virology

Nagoya University Graduate School of
Medicine

114 Kazue Kimura

木村和恵

Cell and Molecular Bioengineering

Nagoya University Graduate School of
Pharmaceutical Sciences

115 Ryuji Kato加藤

竜司

Cell and Molecular Bioengineering

Nagoya University Graduate School of
Pharmaceutical Sciences

116 Hideki Tatsukawa

辰川

英樹

Cellular Biochemistry

Nagoya University Graduate School of
Pharmaceutical Sciences

117 Kiyotaka Hitomi

人見清隆

Cellular Biochemistry

Nagoya University Graduate School of
Pharmaceutical Sciences

118 Fumitaka Osakada

小坂田

Cellular Pharmacology

Nagoya University Graduate School of
Pharmaceutical Sciences

119 Tomoki Kodera

小寺知輝

Cellular Pharmacology

Nagoya University Graduate School of
Pharmaceutical Sciences

120 Hirofumi Aiba

饗場

浩文

Molecular Microbiology

Nagoya University Graduate School of
Pharmaceutical Sciences

121 Masataka Kusano

草野雅貴

Molecular Microbiology

Nagoya University Graduate School of
Pharmaceutical Sciences

122 Emi Hibino

日比野

Structural Molecular Pharmacology

Nagoya University Graduate School of
Pharmaceutical Sciences

匠
好

優矢

文隆

絵美

─ 48 ─

No.

Name

氏 名

Department, Section, or Division

Institute, University, or Company

123 Masashi Sadaike

定池雅司

Structural Molecular Pharmacology

Nagoya University Graduate School of
Pharmaceutical Sciences

124 Tetsuya Kodama兒玉哲也

Structural Molecular Pharmacology

Nagoya University Graduate School of
Pharmaceutical Sciences

125 Shota Suzuki

鈴木翔大Structural Physiology

Nagoya University Graduate School of
Pharmaceutical Sciences

126 Yoshinori Oda

織田祥徳

Structural Physiology

Nagoya University Graduate School of
Pharmaceutical Sciences

127 Yoshitaka Hayashi

林

Endocrinology

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

128 Yohei Sugimoto

杉本

陽平

Genome Dynamics

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

129 Hiro Kohda

神田容

Molecular Medicine and Metabolism

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

130 Akira Sobue

祖父江顕

Neuroscience and Pathobiology

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

131 Kasumi Maekawa

前川華澄

Neuroscience and Pathobiology

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

132 Kei Hashimoto

橋本慶

Neuroscience and Pathobiology

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

133 Koji Yamanaka

山中宏二

Neuroscience and Pathobiology

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

134 Mai Horiuchi

堀内麻衣

Neuroscience and Pathobiology

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

135 Ritsuko Shimogawa

下川

梨津子

Neuroscience and Pathobiology

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

136 Shohei Sakai

酒井昭平

Neuroscience and Pathobiology

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

137 Ting Wang

王 䆾

Neuroscience and Pathobiology

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

138 Yukako Kinoshita

木下 裕香子Neuroscience and Pathobiology

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

139 Shinichiro Horigane

堀金

慎一郎

Neuroscience I

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

140 Shuhei Ueda

上田修平

Neuroscience I

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

141 Akinobu Ohba

大庭彰展

Neuroscience II

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

142 Hiroto Ito伊藤洋人

Neuroscience II

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

143 Masahiro Kawatani

河谷昌泰

Neuroscience II

Nagoya University Research Institute ofEnvironmental Medicine (RIEM)

144 Mitsuru Shinohara

篠原充

Aging Neurobiology

National Center for Geriatrics andGerontology (NCGG)

145 Akihiko Nishikimi

錦見昭彦

Biosafety Division

National Center for Geriatrics andGerontology (NCGG)

146 Hirotake Misu

三須宏武

Endocrinology and metabolism

National Institute for Physiological
Sciences (NIPS)

147 Nawarat Rattanajearakul

Nawarat Rattanajearakul Endocrinology and metabolism

National Institute for Physiological
Sciences (NIPS)

良敬

─ 49 ─

No.

Name

氏 名

Department, Section, or Division

Institute, University, or Company

148 Norihiko Yokoi

横井紀彦

Membrane Physiology

National Institute for Physiological
Sciences (NIPS)

149 Yutaro Nagasawa

長澤

裕太郎

Supportive Center for Brain Research

National Institute for Physiological
Sciences (NIPS)

150 Kenta Kobayashi

小林憲太

Viral Vector Development

National Institute for Physiological
Sciences (NIPS)

Innate Immune Systems

Osaka University Graduate School of
Medicine
RIKEN Center for Integrative Medical
Sciences (IMS)151 Kazuyo Moro

茂呂和世

─ 50 ─

第 3 回 CIBoG リトリート実行委員
氏

名

実行委員長

尾崎

智也

名古屋大学医学系研究科 分子生物学・CIBoG 教員

特任助教

副 委 員 長羽根正弥

名古屋大学生命農学研究科 糖鎖生命コア研究所（統合生命医科学糖鎖研究センター）・CIBoG 教員

助

宇野

光平

名古屋大学医学系研究科

特任助教

岩間

信太郎

名古屋大学医学系研究科 糖尿病・内分泌内科学

講

小西

博之

名古屋大学医学系研究科 機能組織学

准教授

阪本

考司

名古屋大学医学系研究科 呼吸器内科学

病院助教

坪田

庄真

名古屋大学医学系研究科 分子生物学

助

教

西岡

朋生

名古屋大学医学系研究科 神経情報薬理学

助

教

田村

彰吾

名古屋大学医学系研究科（保健）分子病態解析学

講

師

篠原

充

国立長寿医療研究センター 認知症先進医療開発センター
分子基盤研究部

副部長

小林

憲太

生理学研究所 ウィルスベクター開発室

准教授

足立

雄太

愛知県がんセンター がん標的治療 TR 分野

主任研究員

吉崎

嘉一

医療療育総合センター発達障害研究所 障害モデル研究部門

主任研究員

濵口

知成

名古屋大学医学系研究科 神経遺伝情報学・CIBoG 教員

特任助教

永田

健一

名古屋大学医学系研究科 機能組織学・CIBoG 教員

特任助教

横井

聡

名古屋大学医学系研究科 神経内科学・CIBoG 教員

特任助教

実 行 委 員事

問務

総合保健・CIBoG 教員

職名

教

師

祖父江

顕

名古屋大学環境医学研究所 病態神経科学・CIBoG 教員

特任助教

日比野

絵美

名古屋大学創薬科学研究科 構造分子薬理学・CIBoG 教員

特任助教

河村

奈緒子

岐阜大学糖鎖生命コア研究所（iGCORE）・CIBoG 教員

助

酒井

昭平

名古屋大学環境医学研究所 病態神経科学・CIBoG 履修生

大学院生

藤巻

加於梨

名古屋大学医学系研究科 分子細胞免疫学・CIBoG 履修生

大学院生

名古屋大学医学系研究科（保健）リハビリテーション療法
学・CIBoG 履修生

大学院生

伊佐次

顧

講座名

光莉

教

畑中

理菜

名古屋大学生命農学研究科 糖鎖生命科学・CIBoG 履修生

大学院生

神田

容

名古屋大学環境医学研究所 分子代謝医学・CIBoG 履修生

大学院生

鈴木

佑治

名古屋大学医学系研究科 分子生物学・CIBoG 履修生

大学院生

植松

高史

名古屋大学医学系研究科 神経内科学・CIBoG 履修生

大学院生

河谷

昌泰

名古屋大学環境医学研究所 神経系分野Ⅱ・CIBoG 履修生

大学院生

髙橋

秀和

名古屋大学医学系研究科 消化器内科学・CIBoG 履修生

大学院生

大野

欽司

名古屋大学医学系研究科 神経遺伝情報学

教

授

木山

博資

名古屋大学医学系研究科 機能組織学

教

授

木村

宏

名古屋大学医学系研究科 ウイルス学

教

授

黒田

啓介

名古屋大学医学系研究科 CIBoG 卓越大学院推進室

特任准教授

服部

智子

名古屋大学医学系研究科 CIBoG 卓越大学院推進室

事務員

村手

隆司

名古屋大学医学系研究科 CIBoG 卓越大学院推進室

事務員

黒川

玲子

名古屋大学医学系研究科（保健）CIBoG 卓越大学院推進室

事務員

─ 51 ─