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లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

特別講演
会長招待講演 シンポジウム

特別講演

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪇㪇㪇 䋭ĺ࠮ĳķ඾Ȫ࿐ȫġĲĴĻĳıȡĲĵĻĲıġġలˍٛાඅ༆࣒‫׵‬ġŔōĮĲɛ ŕũŦŰťŰųŦġŘįġŌŖœŕś
ŅŦűŢųŵŮŦůŵġŰŧġōŢţŰųŢŵŰųźġŎŦťŪŤŪůŦĭġŖůŪŷŦųŴŪŵźġŰŧġńŢŭŪŧŰųůŪŢĭġŔŢůġŇųŢůŤŪŴŤŰ

al holds that: 1) the initiation of salt-induced increases in blood pressure is commonly characterized
by increased net salt balance, increased cardiac output, and normal systemic vascular resistance,and 2) abnormal systemic vascular resistance appears only later in the course of hypertension after
the initial increase in blood pressure has occurred.

The conventional wisdom holds that abnormal

vascular resistance is merely a secondary phenomenon caused by autoregulatory changes in vascularfunction in response to primary increases in cardiac output and blood pressure.

However, it has

become increasingly clear that the sequence of events held by the conventional theory to berevision is required in the principal theory's "final common pathway" for the pathogenesis of saltinduced increases in blood pressure. In this presentation, I will present a corrected version of theprincipal theory for pathogenesis of salt-sensitive hypertension based on evidence showing that an

口頭発表

commonly responsible for the initiation of salt-sensitive hypertension is incorrect. Thus, a major

会長招待講演 シンポジウム

The principal unifying theory of salt-sensitive hypertension promoted by Guyton et al and Lifton et特別講演łġŎŢūŰųġœŦŷŪŴŪŰůġŰŧġŵũŦġőųŪůŤŪűŢŭġŖůŪŧźŪůŨġŕũŦŰųźġŰŧġŔŢŭŵĮŔŦůŴŪŵŪŷŦġŉźűŦųŵŦůŴŪŰůĻġ
ŏŦŸġņŮűũŢŴŪŴġŰůġŢġńŢŶŴŢŭġœŰŭŦġŧŰųġőųŪŮŢųźġłţůŰųŮŢŭŪŵŪŦŴġŪůġŗŢŴŤŶŭŢųġœŦŴŪŴŵŢůŤŦġ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

abnormality in vascular resistance is: 1) typically evident before the chronic phase of salt-sensitive

pressure.

2) commonly required for the initiation of salt-induced increases in blood

This analysis will show that, during the initiation of salt-sensitive essential hypertension,

it is the failure to effectively vasodilate in response to NaCl that is abnormal, not the magnitude of
the renal NaCl retention or the increased cardiac output.

Thus,

the revised theory for thepathogenesis of salt-sensitive hypertension places emphasis on a primary role for abnormalities invascular resistance in the initiation of salt-induced increases in blood pressure.

Potential

mechanisms that mediate the abnormal vascular response to NaCl will also be discussed.

This

correction of the principal unifying theory of salt-sensitive hypertension supports the need for
greater research emphasis on identifying and characterizing the mechanisms that give rise to䋭 㪋㪊 䋭

著者索引

abnormal vascular resistance during the initiation phase of hypertension in salt-sensitive individuals.

ポスター発表 ＹＩＡ選考発表

hypertension, andĺ࠮ĳĸ඾Ȫ߄ȫġĲĵĻııȡĲĵĻĶıġġలˍٛાඅ༆࣒‫׵‬ġŔōĮĳŎŰŭŦŤŶŭŢųġųŦŨŶŭŢŵŪŰůġŰŧġŢůŨŪŰŨŦůŦŴŪŴġŢůťġŷŦŴŴŦŭġŸŢŭŭġŢŴŴŦŮţŭźįɛ œŢŭŧġŉįġłŅłŎŔġŢůťġŤŰŭŭŦŢŨŶŦŴȁ
ŎŢŹġőŭŢůŤŬġŊůŴŵŪŵŶŵŦġŧŰųġŎŰŭŦŤŶŭŢųġŃŪŰŮŦťŪŤŪůŦĭġŅŦűŢųŵŮŦůŵġŕŪŴŴŶŦġŎŰųűũŰŨŦůŦŴŪŴĭġŢůťġŖůŪŷŦųŴŪŵźġŰŧġŎŶŦůŴŵŦųĭġ
ŇŢŤŶŭŵźġŰŧġŎŦťŪŤŪůŦĭġŎŶŦůŴŵŦųĭġňŦųŮŢůź

Angiogenesis is the main process mediating the expansion of the blood vessel network during
development, tissue regeneration or in pathological conditions such as cancer. The formation of new
endothelial sprouts, a key step in the angiogenic growth program, involves the selection ofendothelial tip cells, which lack a lumen, are highly motile, extend numerous filopodia, and lead
new sprouts. Angiogenic sprouting is induced by tissue-derived, pro-angiogenic signals such as
vascular endothelial growth factor (VEGF), which activates and triggers signaling by cognate
receptor tyrosine kinases in the endothelium. However, this response is strongly modulated byintrinsic signaling interactions between endothelial cells (ECs). For example, expression of theligand Delta-like 4 (Dll4) in tip cells activates Notch receptors in adjacent (stalk) ECs and is thought
to downregulate VEGF receptor expression in these cells. Thus, the tip cell phenotype is suppressedin stalk cells and a balance between sprouting and the necessary preservation of existing endothelial
tubes is established.
Our work is providing further insight into the regulation of sprouting angiogenesis. The Notch
ligand Jagged1 is a potent pro-angiogenic regulator with the opposite role as Dll4. In contrast to
current models, we found that Notch controls VEGFR2 only moderately whereas VEGFR3 isstrongly regulated. Moreover, blocking of Notch enables angiogenic growth even in mutant animals
lacking endothelial VEGFR2 expression.
We also found that endothelial sprouting and proliferation extension depend on VEGF receptor
endocytosis. Ephrin-B2, a ligand for Eph family receptor tyrosine kinases, is required forendothelial cell motility, VEGF receptor endocytosis and the activation of downstream signaltransduction cascades. More recently, we have identified Disabled 2, a clathrin-associated sorting
protein, and the cell polarity protein PAR-3 as novel interaction partners of ephrin-B2 and VEGF
receptors. These results establish that regional VEGF receptor endocytosis, which is controlled by acomplex containing Dab2, PAR-3 and ephrin-B2, play a key role in the spatial organization ofangiogenic growth.
Finally, we have started to address the role of endothelial cells in the regulation of tissuemorphogenesis and homeostasis. In the adult bone marrow, angiogenic signaling by the VEGF and
Notch pathways controls sinusoidal endothelial growth as well as endothelial-mesenchymal
interactions and tissue organization. Our work delineates a first structural and functional framework
for bone marrow homeostasis.
Acknowledgement: This study has been supported by the Max Planck Society, the University ofMuenster and the German Research Foundation.
䋭 㪋㪋 䋭

プログラムలĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

特別講演
会長招待講演 シンポジウム

会長招待講演

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪇㪇㪇 䋭ĺ࠮ĳĸ඾Ȫ߄ȫġĺĻııȡĲıĻ ııġġలˏٛાٛಿઉఞ࣒‫׵‬ȶ୆໤‫̥ͣݪࡄڠ‬ႉ઄͒ශ‫ͅة‬ജ‫̥̳ͥٳ‬ȉȷŊ ōĮĲɛ‫୼ئ‬ġࢤྶȁȁȁȁȁȁȁȁ
൐ཤఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬໦࿤ੀ͈‫ܥ‬੬ͬྶ̥̳ͣͥͅ࿒എ́Ȃ̴͘Ȃ൲໤κΟσ͈ैୋ৾ͤͅழ̺ͭȃ‫ۍ‬ᓕੀ̦ਅș͈೾ഽ͈‫ۍ‬൲ྤࣁ‫ا‬ພ་ͅࢡอ̳̭̥ͥ͂ͧͣȂηΣήῌΨσȜϋੱ‫ࣞ͂ٺ‬΋τΑΞυȜσ૙໅‫ۍͤ͢ͅك‬൲ྤࣁ‫ا‬ພ་ͬै଼̱൳໐͈ࠬ‫ۯ‬฽؊ͬ࠿൦̱̹̭͂ͧȂΓυΠΣϋȆΪΑΗηϋঁࠣͅచ̱̀ठ࡛଻̩͢
‫ۍ‬ᓕੀ̦ညอ̯̹ͦȃழ૕‫ڠ‬എͅ‫ۍ‬ᓕੀ໐պ͂‫ۍ‬൲ྤࣁ‫ا‬໐պ̦̩֚͢౿̱̹ȃষͅȂ‫׶྄͈ٸ‬છ଻་‫۾͈ا‬ဓͬ࠿൦̳ͥ࿒എ́ȂήΗ‫ۍ‬൲ྤͬ‫྄ٸ‬௰̥ͣ‫׶‬છ଻΍ͼΠ΃ͼϋ͞Ήκ΃ͼϋͬဥ̞̀ྕ଻
ঁ̱̹̭ࠣ͂ͧȂठ࡛଻̩͢‫ۍ‬ᓕੀ̦ညอ̯̹ͦȃ̭͈లˎ͈κΟσ͈ાࣣȂඤ๧‫ܥ‬ෝ͉‫أ‬ం̯ͦȂࠬ‫ۯ‬໹‫ً͈޼ڲ‬ਓੀͤ͢ͅ‫ۍ‬ᓕੀ̦୆̲̞̹̀ȃষͅȂࠬ‫ۯ‬໹‫ً͈޼ڲ‬ਓੀ͈໦ঊ‫࠿̞̀̾ͅࢹܥ‬൦̱̜̭ͥ͂ͬྶ̥̱̹ͣͅȃ̳̻̈́ͩȂ‫̹̯ͦا଻ڰ‬œũŰĮŬŪůŢŴŦ͉η΂Ώϋ౎ςϋॸ‫ࣖا‬ளͬဲଷ̳ͥ
̭͂ͤࠫ͢ͅ‫ض‬എͅη΂Ώϋࠚङ͈ςϋॸ‫̦ا‬ಠྶͅᄤૺ̱̞̭̀ͥ͂ͬྶ̥̱̹ͣͅȃ̹͘Ȃैဥ‫ܥ‬੬̦ະྶ͈͘͘·κ྄‫͈ࢃࠬ੄ئ‬ෞࠬ‫ۯ‬ᓕੀͅႉ઄؊ဥ̯̞̹ͦ̀ŧŢŴŶťŪŭ͈৽̈́࿪ၑैဥ̦஖఼

口頭発表̹̭͂ͧȂ໹‫޼ڲ‬ਓੀ͈໦ঊΑͼΛΙ͈࿨‫̞̱̹ͥ̀ضͬڬ‬œũŰĮŬŪůŢŴŦ͈อ࡛͞‫͈଻ڰ‬௩‫֦́৽̦ح‬会長招待講演 シンポジウム඾ུ૽͈‫଻ࠬݹ‬૤৖଼͈֦ۛͅ‫ۍ‬ᓕੀ̦ਹါ̈́࿨‫̩ࢩ͉̭̞̱̹͂ͥ̀ضͬڬ‬౶̞ͣͦ̀ͥȃ‫ۍ‬ᓕ

特別講演ࠬ‫ۯ‬ພ଼͈֦̤̫ͥͅ œũŰĮŬŪůŢŴŦ ͈փ݅ȁȽ‫ۍ‬ᓕੀκΟσ̥ͣႉ઄؊ဥ́͘Ƚ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineഎœũŰĮŬŪůŢŴŦஷ‫ैٺ‬ဥ̜̭́ͥ͂ͬྶ̥̱̹ͣͅȃ̷͈ࢃ͈ႉ઄ࡄ‫ͤ͢ͅݪ‬ȂŧŢŴŶťŪŭ̦ΪΠ̤̞̀ͅ‫ۍ‬൲ྤͅ୆̲ͥ‫ۍ‬ᓕੀ̈́̓ͅခ̜̭࢘́ͥ͂ͬྶ̥̱̹ͣͅȃ̹͘Ȃ‫ܖ‬யࡄ‫̞̤̀ͅݪ‬ȂŧŢŴŶťŪŭ͈ಿ‫ܢ‬ൎဓ̦‫ڎ‬ਅ͈൲ྤࣁ‫ا‬Ȇ૤ະ஠ȆࣞࠬգȆ෹ࣞࠬգ͈൲໤κΟσ̤̞̀ͅခ̜̭࢘́ͥ͂ͬྶ̥̱ͣͅ
̹ȃ࡛हȂŧŢŴŶťŪŭ୓ಕ࿪͉‫ۍ‬ᓕੀ͈΋ϋΠυȜσͅঀဥ̯ͦȂࠐ࢛࿪̦෹ࣞࠬգછͅచ̱̀হࡑಎ̜́
ͥȃ̯ͣͅड߃͈ࡄ‫͉́ݪ‬ȂœũŰĮŬŪůŢŴŦ̦ͼϋΑςϋ೷ࢯ଻Ȇ๬ྖȆࣞডࠬછ͈̈́̓య৫଻৖ۛ͜ͅ૬
̩‫۾‬ဓ̱̞̭̦̀ͥ͂ྶ̥̜ͣ̈́ͤ̾̾ͥͅȃ‫ۍ‬ᓕੀ͈ड੝͈ა໲ͬอນ̱̥̀ͣࣽා̻̠́̓͡Ĵıා̦̈́ͥͅȂ൲໤κΟσै଼̥ͣ໦ঊ‫͈ࢹܥ‬൳೰Ȃ࿪स͈‫ٳ‬อ̦̹֚̾̈́̽ͅ႕̱͂̀ત̱̹̞ٚȃ

ポスター発表 ＹＩＡ選考発表͜Ȃ‫ۍ‬ᓕੀ଻‫ޛ‬૤છȆ๷઀ࠬ‫ޛۯ‬૤છȆਔ੅‫͈ܢ‬ඳহ଻‫ۍ‬ᓕੀȆႻै‫ޛ‬૤છȆ෹ࣞࠬգછȆΑΞϋΠၣ౾

著者索引

䋭 㪋㪎 䋭

ĺ࠮ĳĸ඾Ȫ߄ȫġĺĻııȡĲıĻ ııġġలˏٛાٛಿઉఞ࣒‫׵‬ȶ୆໤‫̥ͣݪࡄڠ‬ႉ઄͒ශ‫ͅة‬ജ‫̥̳ͥٳ‬ȉȷŊ ōĮĳ஻࿪ດഎ̱͈͂̀ ŗņňŇ ਋ယఘ ļ ΣνȜυάςϋɛࣞോġ଼ඵȁȁȁȁȁȁȁȁ
ఱिఱ‫ڠ‬ఱ‫ڠا֓شݪࡄࠏڠ֭֓ڠ‬୆໤‫̥ͣݪࡄڠ‬஻࿪ດഎͬౝ॑Ȇ൳೰̱̀Ȃ̷͈ດഎͅచ̳ͥஷ‫ٺ‬स͞‫଻ڰ‬௯ૺसͬঀ̽̀৖ۛͬ
হၷ̳ͥȃ̭͉ͦȂ֓‫ݪࡄڠ‬৪̺̈́ͣͦ́͜ྪࡉͥ࿒ດ̜́ͥȃ੏۪‫ܕ‬ႀ֖͈ࡄ‫̥ͣ͜ݪ‬ఉ̩͈࿪स̦
‫ٳ‬อȂႉ઄؊ဥ̯̤ͦ̀ͤȂඅࠬͅ‫ͬۯ‬ດഎ̱̹͂࿪स͉੏۪‫ܕ‬৖̴͈͙ۛ̈́ͣ‫̞ࢩ̓̈́܈‬໦࿤͈৖ۛহၷͅঀဥ̯̞ͦ̀ͥȃ߃ා͉࿪स͈ਅ႒͜઀໦ঊ‫ࣣا‬໤̥ͣȂ଼ࣣβίΙΡȂ‫ॸړ‬Ȃࢯఘ̈́̓ఉ‫ܚ‬̷̹̠̺̫ͩͥ̈́ͤͦ͢ͅͅ஻࿪ດഎ͈໙͜ࢩ̦̜ͤ̾̾ͥȃ̾ͤ͘Ȃոஜ͉஻࿪ດഎ̱͂̀͏̯ͩ
̱̩̥̹͈̈́̽́͜͜ດഎ̳̭̦͂ͥ͂‫خ‬ෝ̜͂̈́ͤ̾̾ͥȃུ࣒‫͈૸ু͉́׵‬஻࿪ດഎౝ͈॑ࠐࡑ
ͬ͂ࣽ͜ͅࢃ͈஻࿪ດഎ͈ౝ༷̞ͤ̾̀ͅজࡉͬ੆͓̹̞ȃ䋭 㪋㪏 䋭

プログラムలĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

特別講演
会長招待講演 シンポジウム

シンポジウム

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪇㪇㪇 䋭㪌㪇‫ܖ‬யŔĮĲĮĲ

プログラム

ĺ࠮ĳķ඾Ȫ࿐ȫġĺĻııȡĲĲĻııġġలˍٛાΏϋεΐ;θġ‫ܖ‬ய ŔĮĲȶࠬ‫͈ݪࡄ଼ࠁۯ‬डஜ஌ȷ

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineΔήρέͻΛΏν͈ࠖ࢕ͼιȜΐϋΈٜଢ଼ͥࠬ͢ͅ‫଼ࠁۯ‬ι΃ΣΒθ͈ٜྶ
特別講演ɛ໛ࡔġ࿆༸Ȃབ࠮ġೄਏȁ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜळ༾୆໤‫ڠ‬໐̳ͥྤ‫଼ࠁۯ‬Ȃࡔইࠬ‫̥ͣۯ‬ඤ๧ळ༾̦੄ٔȂဋ௢̱૧̹̈́ࠬ‫ۯ‬࿌ͬࢹಃ̳ͥࠬ‫ۯ‬૧୆Ȃࠬ‫ۯ‬༃ळ༾͈ਬୟͥࠬ͢ͅ‫ا੃଼ۯ‬Ȃ̯͉ͣࠬͅ‫͈ۯ‬൲ྤȂ୓ྤ‫͈ا‬ίυΓΑͬࠐ̀ࠁ଼̯ͦͥȃ̭ͦ́ࠬ͘‫଼ࠁۯ‬ͬଷࢄ̳ͥ໦ঊ͉Ȃ֒ഥঊ٨་൲໤͈ٜଢ଼ͤ͢ͅ൳೰̧̯̹̦ͦ̀Ȃ̭ͦͣ໦ঊ̦শߗ‫ۼ‬എ͈̓͢ͅ
̠̈́໦ঊ‫଼ͬࠁۯࠬ́ࢹܥ‬ଷࢄ̱̞͈̥͉̀ͥྶ̥̯̞̞ͣͦ̀̈́ͅȃུࡄ‫͉́ݪ‬ȂΔήρέͻΛΏν
ͬκΟσ൲໤̱͂̀ဥ̞Ȃࠖ࢕ͼιȜΐϋΈٜଢ଼࣐̠̭ͬ͂́Ȃࠬ‫଼ࠁۯ‬Θͼ΢ηΒθ͈ٜྶͬদ͙̹ȃ৘ष͉ͅȂ๶͈૝ಿฺ̞ͅࠁ଼̯ͦͥ๶௰ࠬ‫ͅۯ‬಍࿒̱Ȃ๶௰ࠬ‫଼ًࠁۯ‬೾͈ྤ‫଼ࠁۯ‬Ȃࠬ‫ۯ‬૧୆‫͍ݞ‬ࠬ‫͈اྤ୓ۯ‬ίυΓἈ̦͈̠̈́͢໦ঊ‫ܥ‬੬́ଷࢄ̯̞͈̥ٜͦ̀ͥଢ଼̱̹ȃȺ༹༷͂ࠫ‫ض‬ȻĲįġ ྤ‫ࠁۯ‬έͻΛΏνͬဥ̞ٜ̀ଢ଼̱̹ȃ๶௰ࠬ‫଼͉ࠁۯྤ͈ۯ‬Ȃࠁ଼੝‫ܢ‬ȪĲĹȡĴıġũŰŶųġűŰŴŵĮŧŦųŵŪŭŪŻŢŵŪŰůĻġũűŧȫ͈ͺϋΐ΂ήρΑΠ͈อ୆͂௩૓Ȃࢃ‫ܢ‬ȪĴı ũűŧոࣛȫ͈ඤ๧ळ༾͈௩૓͂ࢃ༷͈͒ဋ௢ͅջం̳̭ͥ
̦͂໦̥̹̽ȃ̹͘ȂŔũũİŗŦŨŧΏΈ΢σ̦ࢃ‫͈ܢ‬ඤ๧ळ༾௩૓ͬଷࢄ̱̞̭̦̀ͥ͂ྶ̥̹ͣ̈́̽ͅȃġ

口頭発表଼͈ίυΓΑͬळ༾ਔ‫ܢ‬Ψͼ΂Γϋ΍ȜŇŶŤŤŪ‫࢕͍ݞ‬་۟߿ࠖ࢕౩ฒৗŏŭŴņŐŔͬඤ๧ळ༾́อ࡛̳ͥ

会長招待講演 シンポジウムȺࡄ‫͈ݪ‬෸ࠊ͂࿒എȻ஠૸ͅಫͤ੘̯̹ͣͦࠬ‫͉ۯ‬Ȃథ୆‫ͅܢ‬ͺϋΐ΂ήρΑΠ̦ࡔইࠬ‫ۯ‬஽ͬࠁ଼ĳįġ ࠬ‫ۯ‬૧୆ً೾͈ඤ๧ळ༾ࠁఠͬଷࢄ̳ͥ໦ঊ‫ܥ‬੬ͬྶ̥̳̹ͣͥ͛ͅȂͺ·Ιϋळ༾ࣸ‫͍ݞڒ‬œũŰٜଢ଼̱̹ȃńťŤĵĳ̦έ΁σηϋέ͹ηςȜͅ௺̳ͥŇŰųŮŪůĮŭŪŬŦ Ĵ̱ͬٚ̀έͻυεΟͻͺࠁ଼ͬည൵
̱Ȃ๶௰ࠬ‫ۯ͈ࠬۯ‬૧୆ͬଷࢄ̱̞̭̀ͥ͂ͬা̱̹ȃġ Ĵįġ ΃ΞΣϋഢৢ‫خ଻ڰ‬ণ‫ا‬ίυȜήͬඤ๧ळ༾́อ࡛̳ͥέͻΛΏνͬਏၛ̱Ȃ๶௰ࠬ‫଼̫̤ͥͅࠁۯ‬ϸ΃ΞΣϋ͈࿨‫ͬڬ‬ٜଢ଼̱̹ȃϸ΃ΞΣϋ͉ȂŃŎőΏΈ΢σ̽̀͢ͅ‫̯ͦا଻ڰ‬Ȃඤ๧ळ༾͈୆ంͬ֋঵̳̭ͥ͂́Ȃ๶௰୓ྤࠁ଼ͬଷࢄ̱̞̀ͥ
̭̦͂໦̥̹̽ȃȺࠫაȻ๶௰ࠬ‫଼̫̤ͥͅࠁۯ‬Ȃྤ‫଼ࠁۯ‬Ȃࠬ‫ۯ‬૧୆‫͈اྤ୓ۯ͍ࠬݞ‬໦ঊι΃ΣΒθ
͈֚໐ͬྶ̥̱̹ͣͅȃ

ポスター発表 ＹＩＡ選考発表έ͹ηςȜň౩ฒৗ‫خͬ଻ڰ‬ণ‫࢕̳ࠖͥا‬Ψͼ΂Γϋ΍Ȝͬඤ๧ळ༾́อ࡛̳ͥέͻΛΏνͬਏၛȆ

著者索引

䋭 㪌㪈 䋭

‫ܖ‬யŔĮĲĮĳ

ࠬ‫ۯ‬૧୆̤̫ͥࠬͅ‫ۯ‬ඤ๧ळ༾‫׋‬൲͈ଷࢄࠏ̱͈͂̀༃ळ༾͈࿨‫ڬ‬ɛୌ५ġ֚ࢗȂߪࡔġဉ‫ܖ‬൐‫ނ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬య৫୆ၑ‫ڠا‬ࠬ‫ۯ‬૧୆͉ȂȨ ̥̹̻ȩ̩ͬ̾ͥఉळ༾࡛ય͈֚႕͂௴̢̧̭̦ͥ͂́Ȃอ୆୆໤‫ڠ‬എ͙̀ͅޭ͛̀
‫ྙޟ‬૬̞ȃ̷̭͉ͅȂࠬ‫଼̳ͥࢹͬۯ‬ळ༾ో̷̦͈ంहા̤̞̀ͅအș̈́ĵষࡓഎ·υΑΠȜ·ͬ߫ͤ༐̳̭͂́ਏેࢹ௮̞̹͂̽ಉ੬̜ͥȨ̥̹̻ȩͬুၙഎ̩̾ͥͅȂুࡨழ૕‫࡛ا‬ય̦ంह̳ͥȃজ̹̻͉Ȃࠬ‫ۯ‬ळ༾̽̀͢ͅ૕̯ͤ̈́ͦͥুࡨழ૕‫͈͙̩̱͈ا‬ٜྶͅಯ͚̭͂́Ȃࠬ‫ۯ‬૧୆ͬ૧̱̞௰
࿂̥ͣၑٜ̳̭ͥ͂ͬ࿒ঐ̱̞̀ͥȃ̭ͦ́͘੄ٔഎࠬ‫ۯ‬૧୆ͬ࿅̳ழ૕෽ူ̀ͅȂࠬ‫ۯ‬ඤ๧ळ༾͈ĵষࡓ൲ఠͬ೰ၾഎٜͅଢ଼̧́ͥࠏͬࢹಃ̱࠿൦̧̱̹̀ȃ๤‫ڛ‬എౙ੗͂এ̢ͥࠬ‫ۯ‬အ͈Ȩ̥̹̻ȩً̩ͬ̾ͥ೾̤̞̀ͅȂ̷̱ͦͬ̈́ං̞̀ͥඤ๧ळ༾൲ఠ͉Ȃळ༾‫͈ۼ‬௖చഎպ౾ͬອ้ͅවͦఢ̢ͥ̈́̓Ȃ֚ࡉໝॠ̥̾൲എ࡛̈́ય̱͂̀௴̢̹ͣͦȃȨ̥̹̻ȩ̩ͬ̾ͥඤ๧ळ༾൲ఠ͉͈̠̓̈́͢ଷࢄͬ਋̫
̞͈̥̀ͥȉġ জ̹̻͉Ȃ̷͈ଷࢄࠏͬ౜̠͈֚̾࿨৪̱͂̀༃ळ༾ͅ಍࿒̱̹ȃ̭ͦ́͘༃ळ༾͉ࠬ
‫͈ۯ‬հ೰‫͞ا‬ςκΟςϋΈ̞̹͂̽ࠬ‫ۯ‬૧୆͈ࢃ฼໐໦͈́࿨‫༷̞̯֚́ͥ̀ͦ಺ޑ̦ڬ‬Ȃࠬ‫ۯ‬૧୆்‫͈ܢ‬Ȩ̥̹̻ȩ̩ͬ̾ͥष͈࿨‫͕͉̓ͭ͂ڬ‬ٜଢ଼̯̞̞ͦ̀̈́ȃ̭ͦ́͘ȂőŅňŇ਋ယఘϸಎგࢯఘੜ
ၑͤ͢ͅୃુ͈༃ळ༾͈๭ໞͬஷ‫̭̳́͂ͥٺ‬Ȃඤ๧ळ༾൲ఠ͈་‫ۯࠬ͂͂͜ͅا‬အࢹ௮͈૝͍̦՛
̩̭̈́ͥ͂ͬࡉ੄̱̹ȃ̹͘Ȃ૧୆ॾζ;Α࿌྄்̤̫ͥͅ‫͈ܢ‬૧୆ࠬ‫͈ۯ‬૝ಿ̦Ȃ൳အ̈́ੜၑ̳ͬͥ
̭͂́՛‫̹̱ا‬ȃ̭͈ͦͣࠫ‫͉ض‬Ȃ༃ळ༾͈ంह̦ࠬ‫ۯ‬૝ಿͬ୆͚ඤ๧ळ༾͈ਬ౬എ‫׋‬൲ͅచ̱̀௯
ૺഎͅ൱̞̞̭̀ͥ͂ͬাऐ̳ͥȃ̯ͣͅȂ༃ळ༾͈๭ໞஷ‫͙ͥͦͣ̀ͅٺ‬ඤ๧ळ༾൲ఠ་‫͈֚ا‬໐͉Ȃ‫خ‬ဣ߿ŕŪŦĳ਋ယఘੜၑ̀͜ͅ۷̹̭̥ͣͦ͂ͣȂ༃ळ༾̥ͣ໦๥̯ͦͥłůŨŪŰűŰŪŦŵŪů̱ͬٚ̀ଷࢄ̯
̞ͦ̀ͥ‫خ‬ෝ଻̦ࣉ̢̹ͣͦȃġུΏϋεΐ;θ͉́Ȃષ੆͈໦ଢ଼എ৘ࡑ਀༹͂໵̵̀Ȃࢹ଼എ৘ࡑ਀༹
Ȫड઀ࡠ͈ࢹ଼ါள̥ͣ੭șͅໝॠ͈̈́ͬ͜ैͤષ̷̬̞̩̭͈̱̩͙̀͂́ͬၑٜ̳ͥȫȂ̯ͣͅତၑ୆໤‫ڠ‬എ਀༹ͬဥ̞̀ං̧̞ͣͦ̀̀ͥड૧͈౶ࡉ͜࢐̢Ȃࠬ‫ۯ‬૧୆̤̫ͥͅඤ๧ळ༾‫׋‬൲͈ଷࢄࠏ̱͈͂̀༃ळ༾͈࿨‫ͬڬ‬ఉ‫ڙ‬എͅࣉख़̱̹̞ȃ䋭 㪌㪉 䋭

‫ܖ‬யŔĮĲĮĴ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineࠬ‫ۯ‬ඤ๧ळ༾‫۾‬Ⴒ֒ഥঊ͈࿌္എౝ॑ͥࠬ͢ͅ‫ܥ଼ࠁۯ‬੬͈ٜྶ
特別講演ɛջ෯ġୃষ
ಆ෨ఱ‫֓ڠ֓ڠ‬ၷࠏٜཎ‫ڠ‬Ȇอ୆‫ޗڠ‬৒‫ܖ‬๕͈஠ယ͉ྶ̥͉̞ͣ́̈́ȃِș͉ࠬ‫ۯ‬૧୆͈໦ঊι΃ΣΒθͬ༫‫گ‬എͅၑٜ̳̭ͥ͂ͬ࿒ດ̱͂
̀Ȃࠬ‫ۯ‬ඤ๧ळ༾͈ΠρϋΑ·ςίΠȜθͬ෤՜̳̭ͥ͂ͬদ͙̹ȃࠬ‫ۯ‬ඤ๧ळ༾ͬࠧఅ̳ͥŇŭŬĲΦΛ·ͺ;Πζ;Α᥷Ȫథ୆˔඾ȫ͂࿤୆߿᥷̤̫ͥ֒ͅഥঊอ࡛ͬ๤‫̱ڛ‬ȂΦΛ·ͺ;Πζ;Α᥷̤̞̀ͅࡘઁ̳̞̠ͥ͂ૄ࠯͂͂͜ͅȂ࿤୆߿᥷̥ͣ੗‫ۯ̹̱ࠬا‬ඤ๧ळ༾́ࣞഽͅอ࡛̳̞̠ͥ͂ૄ࠯͈
ழ̵͙ࣣͩͤ͢ͅȂĲĹı֒ഥঊͬ࢓༞֒ഥঊ̱͂̀൳೰̱̹ȃ̭͈ͦͣ֒ഥঊ߲͉ȂŗņĮŤŢťũŦųŪůȂ
őņńłŎĲȂ
ŇŭŬĲȂŇŭŵĲȂŕŪŦĲȂŕŪŦĳȂņůťŰŨŭŪů̈́̓Ȃࠬ‫ۯ‬ඤ๧ळ༾̤̞̜̀ͥͅ೾ഽ͈අ։଻ͬ̽̀͜อ࡛̱Ȃਹါ̈́࿨‫̳̹ضͬڬ‬ম̦‫ͅܡ‬༭̯̞࣬ͦ̀ͥ֒ഥঊ͈ఱ໐໦ͬ༫‫̹̞̱̀܄‬ȃ༷֚́Ȃ֒ഥঊྴ͉ంह̳

̞̈́ྚ౶֒ഥঊ߲ͬ‫̹̞́ͭ܄‬ȃࢃ৪͈΃ΞΌςȜͅ௺̳ͥ֒ഥঊ͈֚໐̞̾̀ͅȂΩͼυΛΠഎͅΪΠ෽ူࠬ‫ۯ‬ඤ๧ळ༾̤̫ͥͅΦΛ·Θ;ϋ࣐̹̭ͬ̽͂ͧȂŗņňŇջం଻͈ଫ࣌ࠁ଼ͬࡐಠͅஷ‫ٺ‬

口頭発表͈͈ͥࠬ͜‫ۯ‬ඤ๧ळ༾̤̞͈̀ͅ‫ܥ‬ෝ̞͉̾̀ͅྚ౶̜́ͥ֒ഥঊȂ̹֒͘ഥঊྴ̳ͣັဓ̯̞ͦ̀

会長招待講演 シンポジウムً‫ݲ‬ତ਱ා͈୶࣐ࡄ‫ͤ͢ͅݪ‬Ȃࠬ‫ۯ‬૧୆ͅ‫ܙ‬ဓ̳ͥତఉ̩͈֒ഥঊ̦൳೰̧̯̹̦ͦ̀Ȃྚ̺໦ঊ̳ͥ֒ഥঊȪķ֒ഥঊȫͬࡉ੄̱̹ȃˏ֒ഥঊ̞̾̀ͅΦΛ·ͺ;Πζ;Αͬैୋ̱Ȃˎ֒ഥঊ̞̾̀ͅ

‫ۯ‬૧୆ͅ‫ܙ‬ဓ̱ංͥ֒ഥঊ̦ౝ॑‫خ‬ෝ̜̭̦́ͥ͂া̯̹ͦȃ൳೰̯̹ͦ֒ഥঊ͉ͅȂΪΠਆន̤̞̀ࣞ͜ͅอ࡛̱̞͈̦̀ͥ͜‫̤ͤ̀ͦ͘܄‬Ȃ୆ၑഎࠬ‫ۯ‬૧୆̴͈͙̈́ͣພഎࠬ‫ۯ‬૧୆ͅ‫ܙ‬ဓ̳̥ͥ̓
̠̥ࣽࢃ͈‫ه‬ఴ͂̈́ͥ͂ࣉ̢ͣͦͥȃ

ポスター発表 ＹＩＡ選考発表࿌྄ࠬ‫ۯ‬૧୆͈հ೰‫ܙͅا‬ဓ̳̭ͥ͂ͬࡉ੄̱̹ȃոષ͈ম̥ͣȂِș͈਀༹ͤ͢ͅȂࡢఘτασ́ࠬ

著者索引䋭 㪌㪊 䋭

‫ܖ‬யŔĮĲĮĵ

œũŰŋġťŦŧŪůŦŴġŦůťŰŵũŦŭŪŢŭġŤŦŭŭġŮŰŵŪŭŪŵźġţźġŪůŵŦŨųŢŵŪůŨġŗņňŇġŢůťġŔŦŮŢĴņġ
ŴŪŨůŢŭŴ
ɛ૒ఆġྶ‫د‬૰࡫ఱ‫ڠ‬ఱ‫ۯࠬشݪࡄڠ֭֓ڠ‬୆໤‫ڠ‬໦࿤

In sprouting blood vessels, VEGF and Sema3E, and their receptors VEGFR2 and PlexinD1,
positively and negatively regulate endothelial cell (EC) motility, respectively. However, it is still
unclear how individual ECs integrate these opposite signals and cell-autonomously determine theirmigration. Here, we show that in angiogenic ECs, the small GTPase RhoJ plays pleiotropic roles tocontrol cytoskeletal rearrangements, receptor complex formation, and receptor degradation. By
regulating these activities, RhoJ orchestrates the dynamic cell movements during vascular patterning.
In cultured ECs, PlexinD1 sequesters GTP-RhoJ via its cytoplasmic Rho-binding domain. Sema3E
binding to PlexinD1 releases RhoJ from the receptor and enables RhoJ to induce actin
depolymerization and subsequent cell contraction. Upon VEGF stimulation, association of GTPRhoJ with PlexinD1 is a prerequisite for the formation of a receptor complex comprising VEGFR2,
PlexinD1, and neuropilin-1. This triplet holoreceptor decreases the degradation of internalized
VEGFR2, prolonging downstream signal transduction events. To terminate VEGFR2 signals, RhoJ
is converted to its GDP-bound state and dissociates from PlexinD1, which then facilitates VEGFR2
degradation. RhoJ deficiency, even in a single allele, affected the anterograde EC movements
toward the sprouting vascular tips, and led to variable morphogenetic defects in developing retinal
vasculature. Given the context-dependent effects of VEGF and Sema3E on ECs, neurons, and tumor
cells, the pleiotropic roles of endothelial RhoJ imply the existence of cell-intrinsic mechanisms tomodulate these signals. These insights may lead to the identification of novel therapeutic targets tomanipulate cell motility in disease or tissue regeneration.

䋭 㪌㪋 䋭

‫ܖ‬யŔĮĲĮĶ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine‫଼͈ࠁྤ୓ۍ‬໦ঊ‫ࢹܥ‬

Ĳ ఱिఱ‫شݪࡄࠏڠ֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ‫ނ‬സఱ‫ ڠ‬ŪőŔ ळ༾ࡄ‫ݪ‬ਫ਼Ȃۚळ༾໦‫ا‬ଷࢄ‫ڠ‬ȂĴ ൐‫ނ‬ఱ‫شݪࡄࠏڠ֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬͉ࠬ‫ۯ‬૧୆֦ঊ͈ŢůŨŪŰűŰŪŦŵŪůĮĲĩłůŨĲĪͅઙതͬ൚̀̀‫଼̫̤ͥͅࠁۯࠬۍ‬࿨‫࠿ͬڬ‬൦̱̹ȃłůŨĲŧŭŰŹζ;Α͂ŢŭűũŢĮŎŉńĮńųŦĮŕŨζ;Αͬ࢐෻̱̀૤޼අ։എłůŨĲࠧఅȪłůŨĲńŌŐȫζ;Αͬैୋ̱̹ȃłůŨĲńŌŐζ;Α͉ņĲĳįĶĮĲĵįĶ́థ୆౿ঘͬ೮̱Ȃ૤ඤ྄͂૤޼රಔ͈୪಍ະ஠ͬ೮̱̹ȃġ̯ͣͅłůŨĲńŌŐζ;Α͉ńŅĴĲ྾‫ע‬அ૗࣐̠ͬ͂Ȃథ୆‫ܢ‬૤௫́ࡉͣͦͥĳ௄͈‫̻̠͈ۯࠬۍ‬૤‫྄ٸ‬ೄ‫͈ئ‬ńŅĴĲု଻ඤ๧̦ࠧఅ̱̀Ȃ֚௄ඤ௰͈૤޼௄ඤ͈ńŅĴĲု଻ඤ๧͉࿤୆߿͂൳အͅ࠿੄̯̹ͦȃ̷͈ࠧఅ̳ͥńŅĴĲု଻ࠬ‫ۯ‬ඤ๧̦൲ྤȆ୓ྤඤ๧͈‫̥ͬͦة‬ٜྶ̳̹ͥ͛Ȃ୓ྤζȜ΃Ȝ͈ņűũŃĵု଻ळ༾́ŭŢŤśͬอ࡛̳ͥņűũŃĵĮŵŢŶŭŢŤśΦΛ·ͼϋζ;Α͂࢐෻̳ͥ͂ȂņűũŃĵု଻‫̦ྤ୓ۍ‬ņűũųŪůŃĳĮŵŢŶŭŢŤśΦΛ·ͼϋζ;Α͂࢐෻̳ͥ͂ȂņűũųŪůŃĳု଻‫ۍ‬൲ྤඤ๧͉࿤୆߿͂൳အͅ࠿੄
̯ͦ̀։ુ͉෇̥̹͛̈́̽ȃոષͤ͢łůŨĲ̦୓ྤ໦‫ྤ୓͂ا‬ඤ๧͈ဋ௢ͅ‫۾‬ဓ̳̭̦ͥ͂ထே̯̹ͦȃġ

口頭発表łůŨĲńŌŐζ;Ά͉ࠧఅ̱̀Ȃ‫ͅݙ‬൲ྤζȜ΃Ȝ̜́ͥņűũųŪůŃĳု଻ळ༾́ŭŢŤśͬอ࡛̳ͥ

会長招待講演 シンポジウム‫ۯࠬۍ‬ඤ๧̷͈࡙͈ܳ͂໦ঊ‫͈ࢹܥ‬ٜྶ͉ਹါ̈́‫ه‬ఴ̜̦́ͥȂྚ̺਱໦ٜͅྶ̯̞̞ͦ̀̈́ȃِș

特別講演ɛಎ‫ؖ‬ġၻგ ĲȂခനġု ĲȂઐ‫ז‬ġఊ֚ ĳȂ५‫ئ‬ġ੕ ĳȂ઀৒ġ଼֚ ĲĭĴ̷̭́łůŨĲ͈୓ྤ໦‫͂ا‬ဋ௢̤̫ͥͅ࿨‫࠿͈ڬ‬൦࣐̹ͬ̽ȃྚ໦‫̈́ا‬ņŔळ༾ဇြŇŭŬĲု଻ඤ๧ஜߐ

ဲଷ̯ͦȂ୓ྤ‫۾ͅا‬ဓ̳ͥഢৢ֦ঊńŐŖőĮŕŇŊŊ͈อ࡛̦ည൵̯̹ͦȃŕŪŦĳĮŭŢŤśΦΛ·ͼϋζ;Αဇြ͈୓ྤ൸͂૤པͬņĲıįĶ́ഊ੄̱̀Ȃ༷֚́࿤୆߿ྌ͉łůŨĲńŌŐζ;Αဇြ͈૤৒Ȇ૤‫྄ٸ‬໐໦ͬഊ੄̱̀Ȃၰ৪ͬ୪಍̵̯̀Ĵ඾‫ވۗܕۼ‬෽ူ̳ͥ͂Ȃ࿤୆߿͈૤৒͉́ŕŪŦĳု଻ඤ๧ळ༾͈୓ྤ൸͂
૤པ̥ͣ૤৒͈͒ૺව̦ࡉ̹̦ͣͦȂłůŨĲńŌŐζ;Α૤৒̷͉͈ͅૺව͉ࡉ̥̹ͣͦ̈́̽ȃġ ոષͤ͢Ȃ૤޼ဇြłůŨĲ͉‫଼ͅࠁྤ୓ۍ‬ຈଌ̜̭̦́ͥ͂ྶ̥̹ͣ͂̈́̽ȃ

ポスター発表 ＹＩＡ選考発表ळ༾͉ŗņňŇ͂ŤłŎőഞ‫́ح‬൲ྤඤ๧‫̦̭̳͂ͥا‬౶̦ͣͦͥȂ̭͈ࠏͅłůŨĲͬഞ‫̳͂ͥح‬൲ྤ‫͉ا‬

著者索引

䋭 㪌㪌 䋭

‫ܖ‬யŔĮĲĮķ

œŦŨŶŭŢŵŪŰůġŰŧġŷŢŴŤŶŭŢųġťŦŷŦŭŰűŮŦůŵġţźġŧŶůŤŵŪŰůŢŭġŮŰŭŦŤŶŭŦŴġťŰŸůŴŵųŦŢŮġ
ŰŧġŏŰŵŤũġŢůťġŃŎőġŴŪŨůŢŭŪůŨ
ɛಎ୼ġਘජၻࡇၛ֓‫ش‬ఱ‫୶ڠ‬౤֓‫ࢹܥݪࡄڠ‬੏۪‫ܕ‬ΏΑΞθ֓‫ݪࡄڠش‬৒ഐ୨̈́૤ࠬ‫͈ࠏۯ‬อ୆Ȇࠁఠࠁ଼͂Ȃ̷ͦͥ͢ͅ੏۪ࠏ͈‫ږ‬ၛ͉థ঱Ȫథॾȫ͈อ୆Ȇอ֗ͅຈଌ̜́
ͤȂ̷͈։ુͤ͢ͅథ঱Ȫథॾȫ͉౿ঘ͂̈́ͥȃ૤ࠬ‫͈ࠏۯ‬อ୆Ȇࠁఠࠁ଼͈໦ঊι΃ΣΒθ͉ໝॠ̥̾
ୈᣰͬޭ͛Ȃఉအ̈́ΏΈ΢σഥోࠏ̽̀͢ͅୈळ̈́ଷࢄ̦࣐̞ͩͦ̀ͥȃজ̹̻͉ոஜͤ͢ȂŏŰŵŤũૂ༭ഥోࠏ͈‫ئ‬ၠഢৢ಺୯֦ঊ̜́ͥŉŢŪųźĮųŦŭŢŵŦťġŵųŢůŴŤųŪűŵŪŰůġŧŢŤŵŰųȪŉųŵȫ
ȪŉŦźİŉŦŴųİŉŦųűİńŉŇ
͂͜ࡤ͊ͦͥȫ͈૤ࠬ‫̫̤ͥͅࠏۯ‬փ݅ͬ࠿൦̧̱̹̀ȃŉųŵĲ͂ŉųŵĳ͉อ୆‫ࠁ͈ܢ‬ఠࠁ଼̤̞̀ͅ௖
༞എ̥̾ਹါ̈́‫ܥ‬ෝͬခ̳̭̦ͥ͂༭̯̞̹̦࣬ͦ̀Ȃड߃জ̹̻͉ȂŤŰůťŪŵŪŰůŢŭġ ŌŐζ;Αͬဥ̞̹࠿൦ͤ͢ͅඤ๧ळ༾̤̫ͥͅŉųŵĲİŉųŵĳ͈‫ܥ‬ෝ̦ࠬ‫ۯ‬อ୆ͅຈଌ̜̭́ͥ͂ͬࡉ̞̺̱̹ȃ༷֚ȂŕňŇϸΑȜΩȜέ͹ηςȜ͈֥̜֚́ͥŃŎőĺİŃŎőĲı͉łōŌĲ਋ယఘ΋ϋίτΛ·Α͈‫͢ͅا଻ڰ‬ͤඤ๧ळ༾͈໦‫ࠁۯࠬ͂ا‬ఠࠁ଼ͅ൱̩̭̦͂౶ͣͦȂŏŰŵŤũૂ༭ഥోࠏ͂‫ފ‬൳̱̀ŉųŵ͈̈́̓ࠬ‫ࠏۯ‬ΏΈ΢σഥో֦ঊ͈อ࡛τασͬ಺୯̳̭ͥ͂͜༭̯̞࣬ͦ̀ͥȃड߃জ̹̻͉ȂłōŌĲ਋ယఘ͈‫଻ڰ‬‫̀̽͢ͅا‬อ࡛ଷࢄͬ਋̫ͥ૧̱̞ࠬ‫ۯ‬ඤ๧֒ഥঊŕŎņŎĲııͬ൳೰̱ȂŕŎņŎĲııࠧఅζ;Α̦łōŌĲ਋ယఘࠧఅζ;Α͂൳အ͈ਹඈ̈́ࠬ‫଼ࠁۯ‬։ુͤ͢ͅథ୆౿ঘ̭͂̈́ͥ͂ͬࡉ̞̺̱̹ȃ̭͈ࣽٝͦͣࡄ‫̮̞̀̾ͅضࠫݪ‬༭̱࣬Ȃ૤ࠬ‫͈ࠏۯ‬อ୆Ȇ໦‫ࠁ͂ا‬ఠࠁ଼ͬଷࢄ̳ͥΏΈ΢σഥో‫ࢹܥ‬̞̾̀ͅࣉख़̱̹̞ȃ䋭 㪌㪍 䋭

ĺ࠮ĳķ඾Ȫ࿐ȫġĲĶĻĲıȡĲĸĻĲıġġలˍٛાΏϋεΐ;θġ‫ܖ‬ய ŔĮĳȶࠬ‫଼ۚ͂ࠁۯ‬ळ༾ଷࢄȪŔŵŦŮġŤŦŭŭġţŪŰŭŰŨźġŪůġŵũŦġţŭŰŰťġŷŦŴŴŦŭġŧŰųŮŢŵŪŰůĪȷ‫ܖ‬யŔĮĳĮĲ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineࠬ‫͈ۚۯ‬ळ༾ΏΑΞθȽ΂ȜΨȜΫνȜ
特別講演ɛࣞாġ૝ࢨ
ఱिఱ‫ڠ‬๷୆໤ພࡄ‫ݪ‬ਫ਼ૂ༭ഥో໦࿤

会長招待講演 シンポジウム

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪌㪎 䋭

‫ܖ‬யŔĮĳĮĳ৖ۛ ŪőŔ ळ༾̥͈ͣࠬ‫ۯ‬ພκΟσࢹಃɛಿ஑ġ࠲ඵ
‫ނ‬സఱ‫ ڠ‬ŪőŔ ळ༾ࡄ‫ݪ‬ਫ਼߃ාȂळ༾֊૒ၷ༹Ȫ‫͈݅ޛ‬ठ୆֓ၷȫͅ‫̢̀ح‬ȂŪőŔळ༾ܿ੅ͬဥ̞̹ႉ઄؊ဥࡄ‫̱̀͂ݪ‬Ȃȶ৖ۛκΟσैୋࡄ‫ݪ‬ȪťŪŴŦŢŴŦġ ŮŰťŦŭŪůŨȫȷ̦େ࣐̞ͭͩͦ̀ͥͅȃ̷͉ͦȂඳহ଻৖͈ۛۛ৪ఘळ༾ͤ͢৖ۛ
͈อછͅ‫۾‬ဓ̳ͥ֒ഥૂ༭ͬခ̳ͥȶ৖ۛඅ։എŪőŔळ༾ȷͬਏၛ̱Ȃদࡑ‫ۯ‬ඤ́ᑋۛळ༾ਅ͒໦‫ا‬ည൵̳̭ͥ͂ͤ͢ͅພఠͬ࿅༩̳ͥ৖ۛκΟσͬैୋ̱Ȃພఠٜଢ଼͞হၷ࿪ౝ࣐̠॑ͬࡄ‫̜̭͈́͂ݪ‬ͥȃુஅ૗ఘ࿹଻ఉอ଻ෙ༾ଅȪłŅőŌŅȫ͉Ȃౙ֚֒ഥঊ͈ࡔ֦́୆̲ͥ৖̱ۛ͂̀डఉ͈̜̈́́ͤ͜Ȃଅ௫ͅఉତ͈ෙ༾ͬࠁ଼̱ྎ‫଻ྕܢ‬ଅະ஠ͅૺ࣐̱̠ͥඳহ଻৖̜ۛ́ͥȃ̹͘ȂłŅőŌŅ͈අಭ̱͂
̀Ȃ۴Ȇᦙෙ༾Ȃෞ൲ྤរȂ૤༕྄છȂఱಸࠆ৒̈́̓஠૸͈௫‫ࣣ̰̯̈́͘͘ͅܕ‬໵છͬ୆̲̭̦ͥ͂‫̬ݷ‬ͣͦͥȃ̭ͦ́͘৽ͅ൲໤κΟσͬဥ̞̹ພఠٜଢ଼ࡄ‫̧̦̹࣐̦̀ͦͩݪ‬Ȃۖ஠̈́ພఠ͈ٜྶ͉ͅঢ
̴ͣȂआহഎ̈́হၷ༹͜‫ږ‬ၛ̯̞̞ͦ̀̈́ȃ‫׵‬৪͉ͣȂłŅőŌŅ͈ພఠٜྶ̤͍͢হၷ༹‫ٳ‬อͅঀဥ‫خ‬ෝ̈́૧ܰদࡑ‫ۯ‬ඤ৖ۛκΟσͬ‫ٳ‬อ̳̹ͥ͛ͅȂłŅőŌŅۛ৪ĸ႕̥ͣ৖ۛඅ։എŪőŔळ༾ͬਏၛ̱̹ȃ̷̱̀ȂłŅőŌŅඅ։എŪőŔळ༾ͬဥ̞̹ଅෙ༾κΟσ͈ैୋࡄ‫̢̀حͅݪ‬Ȃࣣ໵છ͈ٜࠨͬ࿒ঐ̱Ȃ౿ঘၚ྄͈̞̩ࣞ͜‫̧̳̭ܳ֨ͬࠬ੄ئ‬ෞ൲ྤរ͈࿚ఴͅ಍࿒̱̹ȃłŅőŌŅඅ։എŪőŔळ༾̥ͣࠬ‫ۯ‬ඤ๧ळ༾͂ࠬ‫ۯ‬໹‫޼ڲ‬ळ༾͈͒໦‫ا‬ည൵࣐̞ͬȂ࠲ુ඾ུ૽ဇြŪőŔळ༾̥ͣैୋ̷̱̹͈ͦͣࠬ‫ۯ‬ळ༾͈͂୆ၑ‫ڠ‬എ‫ܥ‬ෝ͂֒ഥঊอ࡛͈๤‫ڛ‬ٜଢ଼Ȃ̯ͣͅȂෞ൲ྤរࣣͬ໵̳ͥłŅőŌŅĵછ႕͂๱ࣣ໵Ĵછ႕͈͂‫́ۼ‬൳အ͈๤‫ڛ‬ٜଢ଼࣐̹ͬ̽ȃ̷͈ࠫ‫ض‬Ȃෞ൲ྤរࣣͬ໵̳ͥłŅőŌŅۛ৪ဇြŪőŔळ༾̥ͣ໦
‫ا‬ည൵̱̹ࠬ‫ۯ‬ඤ๧̤̞̀ͅඅ։എͅอ࡛͈་‫̳֒ͥا‬ഥঊ̦൳೰̯ͦȂ৖ۛඅ։എŪőŔळ༾ͬဥ̞
̹ࠬ‫ۯ‬ພळ༾κΟσ͉Ȃ૧ܰພఠ‫۾‬Ⴒ໦ঊ͈ౝ॑ͅঀဥ̧́ͥ‫خ‬ෝ଻̦াऐ̯̹ͦȃոષȂུอນ̤ͅ
̞͉̀ȂŪőŔळ༾̥ͣࠬ‫଼ࢹۯ‬ळ༾͈͒໦‫ا‬ည൵ͬဥ̞̀ࠬ‫ۯ‬ພ͈ٜࠨͬ࿒ঐ̳৖ۛκΟσैୋࡄ‫ݪ‬͈࡛ે͂ࣽࢃ͈ജབ̞̾̀ͅ೹া̳ͥȃ䋭 㪌㪏 䋭

‫ܖ‬யŔĮĳĮĴ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineఉෝ଻ۚळ༾̥͈ͣඤ๧ळ༾໦‫̷͈͂ا‬؊ဥ
特別講演ɛ५‫ئ‬ġ੕‫ނ‬സఱ‫ ڠ‬ŪőŔ ळ༾ࡄ‫ݪ‬ਫ਼̻ȂņŔळ༾ͬဥ̞̀ࠏൡഎࠬͅ‫ۯ‬ळ༾͈໦‫ͬا‬ठ̧࡛́ͥ໦‫ا‬ည൵ࠏͬ‫ٳ‬อ̱ĩŏŢŵŶųŦĭġ ĳıııĪȂ൲ྤ୓ྤςϋΩ‫ˏ͈ۯ‬ਅ႒͈ඤ๧ळ༾ည൵଼̱̹ࢗ͜ͅĩłųŵŦųŪŰŴŤŭŦųġŕũųŰŮţġŗŢŴŤġŃŪŰŭĭġĳııķŢĭġĳııķţĪȃ
ड߃Ȃඤ๧ळ༾໦‫͈ا‬໦‫ا‬ఉအ‫̫̤ͥͅࢹܥا‬ŤłŎőΏΈ΢σ͈փ݅ͬষșͅྶ̥̱̹ͣͅȃˍȫŤłŎő͈‫ئ‬ၠ́őŊĮĴġŬŪůŢŴŦ̦ŏŰŵŤũĭġϸĮŤŢŵŦůŪů̱ͬٚ̀൲ྤඤ๧‫ͬا‬ည൵̱̞̀ͥĩŋġńŦŭŭġŃŪŰŭĭġĳıĲıĪȂ
ˎȫűųŰŵŦŪůġ ŬŪůŢŴŦġ łġ ĩőŌłĪ̦ࠬ‫ۯ‬ஜߐळ༾̤̫ͥͅŗņňŇ਋ယఘ߲͈อ࡛ͬᄤૺ̵̯Ȃඤ๧໦‫ͬا‬௯ૺ̱̞̀ͥĩŃŭŰŰťĭġ ĳııĺĪȂˏȫ൳ैဥ͉ńœņṈ̹́ͬٚņŵŴέ͹ηςȜഢৢ֦ঊņŵŷĳ͈อ࡛ည൵͢ͅ
ͥĩŔŵŦŮġ ńŦŭŭŴĭġ ĳıĲĳŢĪȃːȫŌŢűűŢ΂ά΂ͼΡ਋ယఘ̦ŇŭŬĲု଻ळ༾̤̞̀ࣞͅอ࡛̱ŤłŎőဲଷഎ̀ȂœŔŌġ ĩűĺıġ ųŪţŰŴŰŮŢŭġ Ŕķġ ŬŪůŢŴŦĪ̦ȂőŌłࣣ̱ࠫͅőŌł‫ͬ଻ڰ‬ஷ‫̭̳ͤ͂ͥ͢ͅٺ‬ඤ๧ळ༾͈੄
࡛ͬဲଷ̱̞̭̀ͥ͂ͬࡉ੄̱̞̀ͥȃ̭ͦͣ౶ࡉͬ؊ဥ̱Ȃ࡛हȂĺĺĦոષ͈੗ഽ́ȂŪőŔळ༾ˍࡢ̥

口頭発表ͅैဥ̱̀ඤ๧໦‫ဲ଼ͬࠁۯ͍ࠬݞا‬ଷ̳ͥĩŃŭŰŰťĭġ ĳıĲĲȈນঞĪȃ̹͘Ȃˑȫඤ๧ळ༾໦‫ًا‬೾̤̞ͅ

会長招待講演 シンポジウムِș͉ȂņŔळ༾‫͍ݞ‬ŪőŔळ༾ͬဥ̞̀૤ࠬ‫ۯ‬ळ༾͈໦‫͍ݞا‬ठ୆ͅ‫̧̹࣐̀̽ͬݪࡄ̳ͥ۾‬ȃ̳̈́ͩͣ࿩ķࡢ͈ඤ๧ळ༾ͬည൵̱̠ͥ੗ഽȆਓၾ͂͜ͅଲ‫ٮ‬डࣞτασ͈ΪΠŪőŔळ༾͈ඤ๧໦‫଼̱ࢗͅا‬എͅည൵̱̹૤ࠬ‫ۯ‬ळ༾ͬဥ̞̹ळ༾ΏȜΠȪ൐‫ނ‬੫ঊ֓ఱ͈͂‫ވ‬൳ࡄ‫ݪ‬ȫ͈ρΛΠՏ‫ܢ଻ݢ‬૤޼ࢸणκΟσȪࢸणĲ਩ࢃȫ͈͒֊૒৘ࡑ࣐̞ͬȂ֊૒ࢃĴώ࠮̤̞̀͜ͅခփ̈́૤ਓੀෝ٨஝ͬ෇̹͛ȃ૤‫ܥ‬ෝٝ໘͉ͅ֊૒૤޼͈ೄ୪എ࣓ࡃͤ͢͜֊૒૤޼ͥࠬ͢ͅ‫ۯ‬૧୆ͬಎ૤̱̹͂Ωρ·ρͼϋ࢘‫ض‬̦‫ܙ‬ဓ̱̞̹̀ġĩŔŵŦŮġŤŦŭŭŴĭġĳıĲĳţĪȃΏȜΠࢹ௮ࠁ଼͞Ωρ·ρͼϋैဥ௩‫ۯࠬͅޑ‬ळ༾̦‫۾‬ဓ̱̤̀ͤȂࠬ‫͍ݞۯ‬ਔսழ૕͈͂௖ࡽैဥ̦௫‫ܥܕ‬ෝ‫͍ݞ‬ळ༾হၷ࢘‫͈ض‬௩‫ͅޑ‬ਹါ͂ࣉ̢ͣͦͥȃ̭͈̠͢ͅအș̈́૤ࠬ‫ۯ‬໦‫ا‬ठ୆‫̧̤̥ͤ̀̀̽̈́͂ͣྶ̦ࢹܥ‬Ȃ̭ͦͣͬ؊ဥ̱̀૧̱̞ࠬ‫ۯ‬ດഎহၷ୽ၞ̦‫̢̹ͦͣࣉ̧͂ͥ́ఽٳ‬ȃ

ポスター発表 ＹＩＡ選考発表̞̀ͥȃඤ๧ळ༾ͬဥ̞̹হၷ؊ဥ͞৖ۛκΟσैͤ‫͍ݞ‬஻࿪ࡄ‫͈͒ݪ‬؊ဥ̦‫ܢ‬ఞ̯ͦͥȃ༷֚Ȃࠏൡ

著者索引

䋭 㪌㪐 䋭

‫ܖ‬யŔĮĳĮĵŪőŔ ळ༾ͬဥ̞̹ࠬ‫ۯ‬ພহၷ༹͈‫ٳ‬อɛড়നġႚȂ৒ࡔġཅྶྴࡣ‫ؚ‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬ࣞႢ‫ا‬২͈ٛൢြͤ͢ͅȂࠬ‫ۯ‬ພ͈ۛ৪ତ͉ࡐಠͅ௩‫̞̱ͥ̀ح‬ȃ̭͈̠̈́͢છ႕ͅచ̱Ȃࠬ‫ۯ‬૧୆ၷ༹͉૧̹̈́হၷ୽ၞ͈̱֚̾͂̀‫ږ‬ၛ̯̜ͦ̾̾ͥȃِș͉ȂŪőŔळ༾ဇြŧŦŵŢŭġŭŪŷŦųġŬŪůŢŴŦĮĲġȪŇŭŬĮ
Ĳȫု଻ळ༾֊૒̦Ȃζ;Α‫ئ‬ঠ‫ࠬݹ‬κΟσै଼ࢃ͈‫ئ‬ঠ͈ࠬၠͬ٨஝̱̠̭ͥ͂ͬࡉ̞̺̱̹ȃ̹͘Ȃळ༾֊૒͈হၷ࢘ၚ٨஝͈਀౲̱͂̀Ȃঽ‫ܨ‬ΏȜΠࢥ‫͂੅ܿڠ‬΋ρȜΊϋ༫ོ༹ͬழ̵͙ࣣ̭ͩͥ͂
ͤ͢ͅȂఉ௄ŪőŔळ༾ΏȜΠ͈ै଼଼̱̹ࢗͅȃΤȜΡζ;ᾼ‫ئ‬ঠ‫ࠬݹ‬κΟσͬै଼̱ȂŇŭŬĮĲု଻ळ༾ΏȜΠͬ֊૒̱̹̭͂ͧȂခփࠬͅၠ͈٨஝̦෇̹͛ͣͦȃŗņňŇ͞ţŇňŇ൝͈ࠬ‫ۯ‬૧୆֦ঊ͈อ࡛
͜௩‫̹̞̱̀ح‬ȃఉ௄ŪőŔळ༾ΏȜΠ͈ঀဥͤ͢ͅȂ֊૒ळ༾͈ळ༾ঘ̦ထཡ̯ͦȂ֊૒࢘ၚ͞୆಍ၚ
࢜͜ષ̱Ȃࠬ‫ۯ‬૧୆֦ঊ͈อ࡛̦௩‫ح‬Ȃͤ͢‫ޑ‬ႁ̈́ࠬ‫ۯ‬૧୆࢘‫ͬض‬อ‫خ̳ͥܞ‬ෝ଻̦াऐ̯̹ͦȃ̹͘Ȃِș͉Ȃζ;Αࠬ‫ٺੱۯ‬κΟσͬဥ̞̀ȂŪőŔळ༾ဇြŇŭŬĮĲု଻ळ༾͈ࠬ‫ۯ‬ςκΟςϋΈ̤̫ͥ࢘ͅ
‫࠿̞̀̾͜ͅض‬൦࣐̹ͬ̽ȃΤȜΡζ;ᾼࠬ‫ٺੱۯ‬κΟσͬै଼̱ȂŇŭŬĮĲု଻ळ༾ͬඤᴢ୓ྤ̥ͣ
ൎဓ̱Ȃ૧୆ඤ྄௩୆͈೾ഽͬບ‫̹̱ث‬ȃŇŭŬĮĲု଻ळ༾ൎဓ߲͉́Ȃࠬ‫͈ࢃٺੱۯ‬૧୆ඤ྄௩୆ͬခև
ͅဲଷ̱̹ȃ΀ΨϋΑήσȜஅ૗ͥ͢ͅठඤ๧‫ا‬ၚ͈௶೰࣐̹̭ͬ̽͂ͧȂŇŭŬĮĲု଻ळ༾ൎဓ߲́ခ
և̈́ठඤ๧‫͈ا‬௯ૺ̦෇̹͛ͣͦȃ̹͘Ȃൎဓ̱̹ŇŭŬĮĲု଻ळ༾͈֚໐͉Ȃੱ‫ͅۯࠬٺ‬ਬୟ̱̞̭̀ͥ
̦͂‫̹̯ͦ෇ږ‬ȃŪőŔळ༾ဇြŇŭŬĮĲု଻ळ༾͉Ȃńřńœĵ̦ࣞอ࡛̱̤̀ͤȂńřńœĵ͈ŭŪŨŢůť̜́ͥŔŅŇĮĲϷഞ‫ฺ̠ͅح‬ဋ௢ෝ͞୪಍ෝ̦ŇŭŬĮĲ֮଻ळ༾͂๤̱̀ಠྶ́Ȃ̭͈ͦͣैဥ͉ńřńœĵ͈ಎგࢯఘͥ͢ͅஜੜ౾ٜ́ੰ̯̹ͦȃŪőŔळ༾ဇြŇŭŬĮĲု଻ळ༾͉Ȃࠬ‫ۯ‬વ‫͈ࢃٺ‬ඤ๧ळ༾౎၂͈ਘ໘௯
ૺैဥͬခ̱Ȃࠬ‫ۯ‬ठ‫ޛ‬ॏ͈৽̹ͥࡔ֦̜́ͥඤ྄๬࢚ͬဲଷ̱̹ȃոષ͈̠͢ͅȂŪőŔळ༾͉Ȃࠬ‫ۯ‬ພ̤̞̀ͅခབ̈́হၷ࢓༞ळ༾̠̈́ͤͥ͂ͅࣉ̢̹ͣͦȃ䋭 㪍㪇 䋭

‫ܖ‬யŔĮĳĮĶ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine‫ܡ‬ంࠬ‫͈ۯ‬ඤ๧ۚळ༾͂ພఠ

ఱिఱ‫ڠ‬๷୆໤ພࡄ‫ݪ‬ਫ਼ૂ༭ഥో໦࿤

̞ͣͦ̀ͥȃࠬ‫ۯ͉ࠬ́ࠏۯ‬ಎ྄Ȃ‫྄ͅٸ‬ழ૕ۚळ༾̦ంह̳̭̦ͥ͂༭̯̞̦࣬ͦ̀ͥȂ͈̠̓͢ͅ
ࠬ‫ࢹ͈ۯ‬ಃͅ‫۾‬ဓ̳̥ͥྶ̥̞ͣ́̈́ȃ̹͘߃ා༭̯̹࣬ͦࣸଡဇြ͈ࠬ‫ۯ‬ඤ๧ஜߐळ༾Ȫņőńȫ̦૧ܰࠬ‫ࢹۯ‬ಃ͈̓ͅ೾ഽ࣓ࡃ̳̥ͥͅ‫͉̱̀۾‬Ȃ࡛ह݈͜ა̯̞̭̜ͦ̀ͥ͂ͧ́ͥȃࠬ‫ۯ‬૧୆͈ड੝
͈ΑΞΛί͉́ࠬ‫ۯ‬ඤ๧ळ༾̦௩૓̱࿉ळࠬ‫ࢹͬۯ‬ಃ̳̭̦ͥ͂ຈါ̜́ͥȃࠬ‫ۯ‬ඤ๧ळ༾͉ࠬ‫ݩ‬ळ༾͂‫ވ‬೒͈ळ༾̥ͣอ୆̳̭̦ͥ͂౶̞ͣͦ̀ͥȃࠬ‫ݩ‬ळ༾͉ࢭુ଻ͬ֋঵̳̹ͥ͛ͅ௮ࠬۚळ༾̦
ಎ૤͂̈́ͤळ༾͈ΗȜϋ΂ȜΨȜ࣐̞ͬȂ̹ࠬ͘‫͈ࠏݩ‬વ‫̧̦͂ͥܳٺ‬Ȃ͉ͤۚ͞ळ༾ͬಎ૤ࠬͅ‫ݩ‬ळ༾͈ठࢹಃ̦࣐ͩͦͥȃ༷֚́ྎઑͅంह̳ͥࠬ‫ۯ‬ඤळ༾͉‫ڎ‬ழ૕ͥ͢ͅࠁఠഎ̈́ఉအ଻͉౶ͣͦ

‫ۯ‬ඤ๧ळ༾̦͈̠̓͢ͅࢭુ଻ͬ֋঵̱Ȃ̹ࠬ͘‫ۯ‬૧୆শ͈̓ͅඤ๧ळ༾̦௩૓̱Ȃࠬ‫ͬۯ‬ठࢹಃ̳̥ͥમळ̈́࠿൦̦ຈါ̜́ͥȃِș͉̭ͦ́͘ྎઑࠬ‫ۯ‬ඤ๧ळ༾ۚͅळ༾̦ంह̱̞̥̈́Ȃΰ΅ΑΠ

口頭発表̞̦̀ͥȂ̳͓̀޳֚̈́ळ༾ਬ౬͙̯̤͂̈́ͦ̀ͤඤ๧ۚळ༾̦ంह̳̥ͥ๛̥͉ྶ̥̞ͣ́̈́ȃࠬ

会長招待講演 シンポジウム଼ఘ́ழ૕̦વ‫̧̹̯͂ͦٺ‬Ȃ̷͈ழ૕ͅంह̳ͥழ૕ۚळ༾̦‫̱ا଻ڰ‬ਘ໘‫ܥ‬ഢ̦൱̩̭̦͂౶

特別講演ɛඤ൥ġંൽȂ৹ႅġసȂ࿐࡫‫ؚ‬ġࢼࢫȂࣞாġ૝ࢨ૗ளͬ၌ဥ̱̹ŇłńŔٜଢ଼̧࣐̹ͬ̽̀ȃ̷̱̀Ȃྎઑࠬ‫͈ۯ‬ඤ๧ळ༾໦ْಎۚͅळ༾အ͈ඤ๧ळ༾̦

‫ࠬݹ‬শ͉ͅಿ‫֋̹̀̽ͩͅܢ‬঵̯ͦͥ‫ܥ‬ෝഎ̈́ࠬ‫ͬۯ‬ठࢹಃ̳̭ͥ͂ͬ༭̧̱̹࣬̀ȃུอນ͉̭́
͈ۚळ༾အࠬ‫ۯ‬ඤ๧ळ༾͈ۚळ༾଻ͅ‫ۯ̱ࠬ̀۾‬ඤ๧֊૒κΟσͬဥ̞̹મळٜ̈́ଢ଼Ȃ̯ͣͅਆន൝
͈ພഎࠬ‫ۯ‬૧୆̦୆̲ͥພఠ̤̫ͥͅȂ̭͈ۚळ༾အඤ๧ळ༾͈࿨‫̱̀۾ͅڬ‬อນ̱̹̞ȃ

ポスター発表 ＹＩＡ選考発表ంह̱Ȃ̭͈ۚळ༾အࠬ‫ۯ‬ඤ๧ळ༾͉Ȃࠬ‫ۯ‬ඤ๧ळ༾໦ْಎ͈ˍɓͬ୸͛Ȃඤ๧ळ༾ͬఉၾͅॲ୆̱Ȃ

著者索引

䋭 㪍㪈 䋭

ĺ࠮ĳĸ඾Ȫ߄ȫġĺĻııȡĲĲĻııġġలˍٛાΏϋεΐ;θġ‫ܖ‬ய ŔĮĴȶࠬ‫ܥۯ‬ෝͬଷࢄ̳ͥΏΈ΢ςϋΈ‫ࢹܥ‬ȷġ‫ܖ‬யŔĮĴĮĲͺΡτΦιΟνςϋ ĮœłŎő ΏΑΞθͥࠬ͢ͅ‫ܥۯ‬ෝଷࢄɛ૧൥ġၦ࣐
૞ਗఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪ພఠ‫࣒ڠ‬जͺΡτΦιΟνςϋĩłŎĪ͉Ȃࠬ‫̲͉͛ͬۯ‬Ȃ஠૸́ࢩํͅॲ୆̯ͦͥβίΙΡ̜́ͥȃłŎ͉ࠬ‫ڐۯ‬ಫ֦ঊ̱͂̀อࡉ̯̹̦ͦȂࢯॸ‫ैا‬ဥȂࢯ‫׶‬છैဥȂࢯ൲ྤࣁ‫ैا‬ဥ̈́̓ఉद̈́୆ၑ‫ͬ଻ڰ‬঵̭̦̾͂ྶ̧̥̹ͣ͂̈́̽̀ȃłŎ̷͈֚͂Ⴒ͈έ͹ηςȜ֦ঊ͉ȂˣΗϋΩ·‫ވ‬࿨߿਋ယఘńōœĩŤŢŭŤŪŵŰůŪůġ
ųŦŤŦűŵŰųĮŭŪŬŦġųŦŤŦűŵŰųĪͬ‫ވ‬ဥ̱̞̀ͥȃńōœ͉ͅȂ਋ယఘ‫಺଻ڰ‬୯ΗϋΩ·œłŎőġĩųŦŤŦűŵŰųġŢŤŵŪŷŪŵźĮ
ŮŰťŪŧźŪůŨġ űųŰŵŦŪůĪ ĲĭĳĭĴ ͈̠̻Ȃ̴̞̥ͦĲ̦ࣣ̱̾ࠫȂ਋ယఘ͂ς΄ϋΡ͈͂૶გ଻͞ळ༾ඤΏΈ΢σͬ಺୯̱̞̀ͥ͂ࣉ̢̞ͣͦ̀ͥȃłŎΦΛ·ͺ;Πζ;ΑĩłŎĮİĮĪ͉ࠬ‫͈ۯ‬อ୆։ુͤ͢ͅȂ຾ਆ͞੄ࠬͬ୆̲̀థ୆ಎ‫ͅܢ‬౿ঘ̦͂̈́ͥȂ̷͈ೄஜ͈ࠬ‫͉̞̤̀ͅۯ‬ȂœłŎőಎ́͜ȂඅͅœłŎőĳ͈ࣞอ࡛ͬ෇͛ͥȃِș͉Ȃࠬ‫̫̤ͥͅۯ‬łŎΏΈ΢σ͈ಎ૤̦œłŎőĳ̽̀͢ͅଷࢄ̯̞ͦ̀ͥ‫خ‬ෝ଻ͬࣉ̢ȂœłŎőĳΦΛ·ͺ;Πζ;ΑĩœłŎőĳĮİĮĪͬਏၛ̱̹ȃœłŎőĳĮİĮ͉́ȂłŎĮİĮ͈ນ࡛߿̦ठ࡛
̯ͦȂయੲ଻͈łŎอ࡛ᄤૺͬ෇̹̦͛Ȃ̷͈ఈ͈œłŎőอ࡛ͅ་‫̴͛෇ͬا‬ȂœłŎő΍ήͺͼΕέ΁Ȝθ͈‫ͅۼ‬௖༞଻̦̞̭̦̈́͂੝͛̀ྶ̥̹ͣ͂̈́̽ȃ௽ِ̞̀ș͉Ȃࠬ‫ۯ‬ඤ๧ळ༾අ։എœłŎőĳΦΛ·ͺ;Πζ;ΑĩņĮœłŎőĳĮİĮĪͬਏၛ̱̹ȃņĮœłŎőĳĮİĮ͉ȂœłŎőĳĮİĮ͂๤‫̱̀ڛ‬อ୆̦ૺ͚͈͈͜Ȃ཰͉̓੄୆ೄஜͅ౿ঘ̜̹́̽ȃ֚໐଼ఘ̹̈́̽ͅζ;Ά͉Ȃࠬ‫̲͉̥ͥͣ͘׶ۯ‬௫‫ܕ‬ඤ஌֋‫̦ا‬ুடอછ̱̹ȃষͅȂ଼ఘ̥̈́̽̀ͣͅœłŎőĳࠧఅͬည൵̳ͥ͂Ȃ଼ఘ̤̞̀ࠬ͜ͅ‫ۯ‬൫ً଻ᄤૺͅ
ฺ̠஠૸଻຾ਆ̦อછ̱̹ȃࠬ‫ۯ‬ඤ๧ळ༾͉́Ȃ೩໦ঊၾňΗϋΩ·͈಺୯։ુͤ͢ͅȂळ༾͈ࠁఠ։
ુ͞ญၗ̭̱̞ͬܳ̀ͥ͂ࣉ̢̹ͣͦȃ༷֚́ȂœłŎőĲ͂Ĵ͈ΦΛ·ͺ;Πζ;Ά͉Ȃอ୆͈։ુ͉
෇̥̹͛̈́̽ȃœłŎő΍ήͺͼΕέ΁Ȝθ‫ܥ̥̈́ͣྶͅۼ‬ෝ໦‫̦ا‬ంह̱ȂłŎ̷͈͂έ͹ηςȜ֦ঊ͈‫ܥ‬ෝ͈ఉအ଻ͅ‫۾‬ဓ̱̞̀ͥ͂ࣉ̢ͣͦͥȃ䋭 㪍㪉 䋭

‫ܖ‬யŔĮĴĮĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineŏŰŵŤũ ΏΈ΢σͥࠬ͢ͅ‫ۯ‬ळ༾͈໦‫ا‬ଷࢄ
特別講演

ɛ֙ġో࿟
߲෯ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬௫‫ܕ‬ພఠඤ‫ڠش‬ΪΠ̞̹ͥ́͘ͅఉळ༾୆໤́ૺ‫ا‬എͅ༗ం̯̞ͦ̀ͥȃሶ඿႒̤̞̀ͅ૤ࠬ‫̀͛܄ͬࠏۯ‬ତఉ̩͈௫‫ܕ‬Ȇळ༾͈໦‫ͅا‬ਹါ̈́࿨‫ͬڬ‬౜̠̭̦͂ྶ̧̥̯̹ͣͦ̀ͅȃळ༾໦‫͈ا‬ଷࢄ‫̱̀͂ࢹܥ‬Ȃ੝‫ͅܢ‬͉௰༷ဲଷȪ௰༷අ։଻ȫ̦೹੹̯ͦळ༾໦‫ဲͬا‬ଷ̳ͥΏΈ΢σ̱͂̀ࢩ̩෇౶̯̞̹̦ͦ̀Ȃ࡛ह͉́໦‫ا‬ည൵Ȃۚळ༾֋঵͈‫ܥ‬ෝ̦̜̭̥̞ͥ͂ͩ̽̀ͥ͜ȃŏŰŵŤũΏΈ΢σ̷̦͈ैဥͬอ‫̳ͥܞ‬ष͉ͅȂఉତ͈ါ֦Ȫळ༾ਅȂ໦‫ا‬౲‫ٴ‬Ȃఈ͈ΏΈ΢σ͈͂·υΑΠȜ·̈́̓ȫ̦‫۾‬ဓ̱Ȃ̷͈ͦͣ௙ࣣഎ
̈́ैဥͤ͢ͅळ༾͈डਞഎ̈́໦‫̦଻༷͈࢜ا‬։̩̈́̽̀ͥȃ̭͈̠̈́͢ŏŰŵŤũΏΈ΢σࡄ‫͈ݪ‬षͅࡉͣͦͥఉद̈́୆ၑैဥȪ֚ࡉठ࡛଻̦ྫ̞̠͢͜ͅࡉ̢ͥȫͬŤŰůŵŦŹŵġ ťŦűŦůťŦůŵ͂ࡤ͍ȂŏŰŵŤũΏΈ̓Ȃࠬ‫ۯ‬૧୆͈੝‫͈ܢ‬໦‫ا‬ଷࢄͬ౜̠ਹါ̈́‫̯̥ͦͣͅྶ̦̭̜͂ͥ́ࢹܥ‬Ȃਆនࠬ‫ۯ‬૧୆̤̞̀ͅ
͉Ņŭŭĵġ ţŭŰŤŬŢťŦ͈̈́̓ႉ઄؊ဥ̦࠿൦̯͕̹ͦͥ̓̈́̽ͅȃ̯ͣͅȂࠬ‫ۯ‬૧୆̴͈͙̈́ͣȂ൲ྤࣁ‫ا‬

口頭発表΢σͬၑٜ̳ͥષ́Ȃਹါ̈́‫ٽ‬ැ̞̈́̽̀ͥͅȃŏŰŵŤũΏΈ΢σ͉Ȃ൲୓ྤ໦‫ا‬ȆŵŪűġ ŤŦŭŭġ ŧŰųŮŢŵŪŰů̈́

会長招待講演 シンポジウムŏŰŵŤũΏΈ΢σ͉Ȃޫਫ਼എ̈́ळ༾‫ۼ‬௖ࡽैဥͬ೒̱̀ळ༾͈‫ྵ׋‬Ȫ໦‫ا‬ȫͬଷࢄ̳ͥ‫́ࢹܥ‬Ȃ஌ಖ̥͈ͣอછ͞൲ྤ୞‫͜ͅا٭‬ਹါ̈́࿨‫̧̹̥̦̭̠̀̽ͩ͂̈́ͬͅڬ‬ȃུ‫ڠ‬͉ٛ́Ȃࠬ‫ۯ‬ඤ๧ळ༾Ȇࠬ‫ۯ‬໹৒͈́࠿൦ͬ༭̳࣬ͥȃ

ポスター発表 ＹＩＡ選考発表‫޼ڲ‬ळ༾͈໦‫ۯࠬ͞ا‬୞‫଼͈ࠁا٭‬ष͈ŏŰŵŤũΏΈ΢σ͈࿨‫͂ڬ‬໦‫ا‬ଷࢄ͈໦ঊ‫ܥ‬੬̞̾̀ͅ൚ࡄ‫ݪ‬

著者索引

䋭 㪍㪊 䋭

‫ܖ‬யŔĮĴĮĴ

·ρΑ ŊŊϷ߿ őŊĴ ΅΢ȜΔ ĮńĳϷͥࠬ͢ͅ‫ۯ‬૧୆ȆΨςͺ‫ܥ‬ෝ಺୯ι΃ΣΒθɛ‫ؖ݌‬ġგࢴ ĲȂఉ‫ݛ‬გġങঊ ĲĭĳȂ‫ུؖ‬ġհဎ ĲȂఉ‫ݛ‬გġု Ĳ
Ĳ ߄ాఱ‫֓ڠ‬࿪༗࠲ࡄ‫ۯࠬࠏڠ֖֓ݪ‬໦ঊ୆ၑ‫ڠ‬Ȃĳ ୞୼ࡇၛۭࢌఱ‫ڠشࢫ࠲شڠࢌۭڠ‬ডৗςϋॸ‫ࣖا‬ள̜́ͥγΑέ͹ΙΐσͼΦΏΠȜσĮĴĮ΅΢ȜΔȪőŊĴŌȫ͉Ȃሶ඿႒̤̞̀ͅĹ͈̾ͺͼΕέ΁Ȝθ̦ంह̱Ȃ̷͈୆଼໤̜́ͥőŊĩĴĪőĭġ őŊĩĴĭĵĪőĳ‫͍ݞ‬őŊĩĴĭĵĭĶĪőĴ̱ͬٚ̀ఉ‫ͅܚ‬ളͥ୆ၑैဥͬอ‫̳ͥܞ‬ȃ·ρΑŊ߿ȪűĲĲıϷİϸİϹİϺȫ̤͍͢ŊŊŊ߿ȪŗűŴĴĵȫ͂։̈́ͤȂ·ρΑŊŊ߿őŊĴŌ͈୆ၑ‫ܥ‬ෝ͉̭ͦ́͘ະྶ̜̹́̽ȃ̷̭́Ȃ·ρΑŊŊϷ߿őŊĴŌĩńĳϷĪ֒ഥঊŌŐζ;Αͬैୋ̱ນ࡛߿͈ٜ
ଢ଼࣐̹ͬ̽ȃ஠૸߿ńĳϷŌŐζ;Α͉Ȃࠬ‫ۯ‬૧୆͈։ુͤ͢ͅอ୆ಎ‫̞̤̀ͅܢ‬థ୆౿ঘ̹͂̈́̽ȃࢵͅȂඤ๧ळ༾අ։എ΋ϋΟͻΏο΢σŌŐζ;Ὰ̤̞͜ͅȂࠬ‫ۯ‬૧୆ً೾̜́ͥȶอٔȆ໦‫ܚ‬ȷ଼͂੃̱̹ࠬ‫ࢹͬۯ‬ಃ̳ͥȶࠬ‫੃଼ۯ‬ȷ͈ၰίυΓΑ̦ಠ̱̩વ‫̹̞̯̀ͦٺ‬ȃඤ๧ळ༾͉́ńĳϷ͉৽ͅळ༾
ඤ઀༾Ȫ·ρΑςϋု଻઀༾Ȃ੝‫΀ܢ‬ϋΡΕȜθȂΠρϋΑȆΌσΐ௡౾ȫͅޫह̱̞̹̀ȃőŊĩĴĪőġ ĩńĳϷ‫ॲ଻ڰ‬໤Īġ ࠖ࢕ίυȜήġ ĩňŇőĮĳŹŇŚŗņĪͬဥ̞̹ٜଢ଼̥ͣȂńĳϷΦΛ·Θ;ϋŉŖŗņńळ༾̤̞̀ȂŇŚŗņု଻੝‫΀ܢ‬ϋΡΕȜθତ͈ಠ̱̞ࡘઁ͂઀༾‫׋‬൲଻Ȇ࿶௣͈ࡘ৻̦۷ख़̯̹ͦȃळ༾୪಍໦ঊ
ŗņ΃Ρΰςϋ͈ळ༾྄͈͒઀༾̱̹ͬٚ࿶௣͉ńĳϷΦΛ·Θ;ϋġ ळ༾̤̞̀ࡐಠͅ೩‫̱ئ‬Ȃඤ๧ळ༾‫̫̤ͥͅۼ‬ŗņ΃Ρΰςϋਬୟ̦વ‫̹̯ͦٺ‬ȃࢵͅńĳϷΦΛ·Θ;ϋळ༾͉́ȂŗņňŇঁࠣͥ͢ͅ
ŗņňŇ਋ယఘ͈ඤह‫ဲ̩ޑ̦ا‬ଷ̯ͦȂ΀ϋΡΕȜθષ͈́೩໦ঊňΗϋΩ·ৗœũŰł‫̦ا଻ڰ‬વ‫̯ٺ‬̹ͦȃ̭͈ͦͣࠫ‫ض‬ȂŗņňŇͥ͢ͅळ༾ဋ௢‫͍ݞ‬ζΠςΊσષ͈́‫଼̦ࠁ࣌ۯ‬ఈ͈őŊĴŌͺͼΕέ΁ȜθȆΦΛ·Θ;ϋळ༾͂๤͓ခփͅ೩‫̹̞̱̀ئ‬ȃ༷֚ȂńĳϷΰΞυŌŐζ;Α͉ୃુͅอ୆Ȇอ̳͈֗ͥ͜Ȃ୆ࢃ͈୆ၑഎ࿌྄ࠬ‫ۯ‬૧୆Ȇਆនࠬ‫ۯ‬૧୆͈ဲଷȂࠬ‫ۯ‬൫ً଻ᄤૺȂࠬ઀โ‫֦ا଻ڰ‬ঊȪőłŇȫͥ͢ͅͺ΢έͻρ΅ΏȜȆΏοΛ·͈ۜ਋଻ᄤૺȂ̯͉ͣͅͺϋΐ΂ΞϋΏϋŊŊྕ଻ൎဓٜͥ͢ͅၗ଻ఱ
൲ྤរ͈อછ̦۷ख़̯̹ͦȃոષ͈ࠫ‫̥ͣض‬ȂńĳϷ͉ඤ๧ळ༾྄̤̞̀ͅ઀༾࿶௣ĩιϋήτϋȆΠρέͻΛ
·Ī͈ଷࢄ̱ͬٚ̀Ȃඤ๧ळ༾‫ۼ‬୪಍ࢹ௮͈ࠁ଼Ȇհ೰‫͂ا‬ΏΈ΢σഥోͅຈଌ͈࿨‫̱̹ضͬڬ‬Ȃࠬ‫ۯ‬૧୆͂ࠬ‫࠲ۯ‬஠଻֋঵ͅਹါ̈́࿨‫ͬڬ‬౜̠őŊĴŌͺͼΕέ΁Ȝθ̜̭̦́ͥ͂ྶ̥̹ͣ͂̈́̽ȃ䋭 㪍㪋 䋭

‫ܖ‬யŔĮĴĮĵ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineࠬ‫ۯ‬Ⴧ‫ا‬ΏΈ΢σΥΛΠχȜ·ͥ͢ͅ੏۪య৫ଷࢄ
特別講演

ɛධ࿤ġഔ
૧‫ګ‬ఱ‫ڠ‬ఱ‫֭֓ڠ‬ভ‫ڠ‬௙ࣣࡄ‫شݪ‬੏۪‫ܕ‬ඤ‫ش‬ġႢ৪̤̞̀ͅ‫ވ‬೒ͅ෇̭̥͛ͣͦͥ͂ͣȂჇ‫ࠁ͈ا‬ৗ͈֚໐̱͂̀௴̢̧̭̦ͥ͂́ͥȃ̳̻̈́ͩȂ̭͈ͦͣ৖͈ۛ‫ޭݪ‬എ̈́হၷ͈ΗȜΊΛΠ͉Ȃ਍ྵͬ಺୯̳ͥॽழ̷͙͈͈̥̱̞ͦ̈́͜͜ȃ೒ુΪΠୃુఘळ༾͉Ȃ̜֚ͥ೰ٝତ͈໦Ⴈ௩૓ࢃȂळ༾Ⴧ‫ͥͦ͊͂͢ا‬໦Ⴈ೪গેఠ͂̈́ͥȃ̭͈̠̈́͢ळ༾
͈໦Ⴈ਍ྵͅਹါ֦̈́ঊ̦ȂΞυιͺ̜́ͥȃΞυιͺ͉Ȃஅ૗ఘ͈ၰ౤ͅంह̱Ȃ̷͈հ೰଻ͅ‫ܙ‬ဓ̳̦ͥȂŅŏłໝୋ̦ະۖ஠̜̹́ͥ͛Ȃळ༾໦Ⴈ͂͂͜ͅౣੀ̳ͥȃ̜֚ͥ೰͈ಿ̯́͘ౣੀ̱̹Ξυιͺ͉ȂŅŏłఅੱ̱͂̀෇ে̯ͦȂűĶĴջం଻ळ༾Ⴧ‫ا‬ΏΈ΢σ͈‫̀̽͢ͅا଻ڰ‬Ȃळ༾͉Ⴧ‫̳ͥا‬ȃड߃͉́Ȃॸ‫ا‬ΑΠτΑ͞ট‫ٸ‬஌͈̈́̓ΑΠτᾼ̽̀͢Ņŏłఅੱ̦୆̲ͥ͂ȂΞυιͺ͈ౣੀฺͬ

߲ۛ৪ͤ͢ං̹ͣͦळ༾͈਍ྵ͉ခփͅౣ̞̭̦͂̈́̓༭̯̞̭̥࣬ͦ̀ͥ͂ͣȂ‫ح‬Ⴂฺ̽̀ͅ୆̲
ͥழ૕̤̫ͥͅळ༾Ⴧ‫ا‬ΏΈ΢σ͈‫̦ا଻ڰ‬Ȃ਍ྵ͞‫ح‬Ⴂ‫۾‬Ⴒ৖͈ۛພఠ୆ၑͅ‫۾‬ဓ̳ͥ‫خ‬ෝ଻̦̜

口頭発表̴ͩͅळ༾͉Ⴧ‫̦̭̳͂ͥا‬౶̞ͣͦ̀ͥȃჇ‫̹̱ا‬ळ༾̦ࣞႢ৪͈ழ૕͒ਬୟ̳̭ͥ͂Ȃ்Ⴧછ࢓

会長招待講演 シンポジウム‫ح‬Ⴂฺ̽̀ͅȂൠෂພ͞൲ྤࣁ‫͈̓̈́ا‬୆‫ڰ‬ਠ‫۝‬ພ͈ᑋۛၚ̦௩‫̳ͥح‬ȃ̭͈ͦͣ৖͉ۛȂఉ̩͈ࣞͥȃ৘षȂ̭͈̠̈́͢űĶĴջం଻ळ༾Ⴧ‫ا‬ΏΈ΢σ̦‫ح‬Ⴂً͞૙͈̈́̓ΑΠτᾼ̽̀͢Ȃழ૕Ȫࠬ‫ۯ‬Ȇͅैဥ̱Ȃ୆‫ڰ‬ਠ‫۝‬ພ͈ພఠͅ‫۾‬ဓ̱̞̭̦̀ͥ͂Ȃड߃͈ࡄ‫̧̹̥̀̽̈́͂ͣྶ́ݪ‬ȃ̷ུ̭࣒́‫׵‬͉́Ȃࠬ‫ۯ‬Ⴧ‫ا‬ΏΈ΢σΥΛΠχȜ·̽̀͢ͅଷࢄ̯ͦͥ੏۪య৫ΏΑΞθ̞݈̾̀ͅა̱͙̹̞̀
͂এ̠ȃ

ポスター発表 ＹＩＡ選考発表૤௫Ȇডཛ̈́̓ȫ̤̞̀ͅ‫̯ͦا଻ڰ‬Ȃ̷͈ͦͣΏΈ΢σ̦ΥΛΠχȜ·ͬࠁ଼̳̭ͥ͂̽̀͢ͅࡽ̞

著者索引

䋭 㪍㪌 䋭

‫ܖ‬யŔĮĴĮĶ

ŃŎőȆŕňŇ ĮϸΏΈ΢σ
ɛള໐ġഔ჊
൐‫ނ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬໦ঊພၑ‫ڠ‬໦࿤ŵųŢůŴŧŰųŮŪůŨġŨųŰŸŵũġŧŢŤŵŰųġĩŕňŇĪĮϸ͉ͺ·ΙΫϋࣸ͞ࠁ଼֦ঊĩţŰůŦġŮŰųűũŰŨŦůŦŵŪŤġűųŰŵŦŪůŴȇ
ŃŎőŴĪͬ‫̹͛܄‬Ĵıոષ͈ΗϋΩ·ৗ̥ͣ̈́ͥΑȜΩȜέ͹ηςȜͬࠁ଼̱̤̀ͤȂอ୆଼͞ఘ‫͈ۗܕ‬ࢭુ଻֋঵ً͈̯̰̈́͘͘೾́ਹါ̈́࿨‫ͬڬ‬౜̞̽̀ͥȃ֒ഥ଻ࠬ‫ۯ‬৖͈ۛࡔ֦֒ഥঊ֒͞ഥঊ٨་
ζ;Α͈ٜଢ଼̥̈́̓ͣȂŕňŇĮϸΑȜΩȜέ͹ηςȜΏΈ΢σ͈։ુ̦ࠬ‫͈ۯ‬։ુ̧̭̳̭ͬ֨ܳ͂
̦ྶ̥̞ͣ͂̈́̽̀ͥȃِș͉ņŔळ༾ဇြ͈ࠬ‫ۯ‬ඤ๧ळ༾͞ࡢఘτασ͈৘ࡑࠏͬဥ̞̀Ȃ৽ͅŕňŇĮϸĳ̦ࠬ‫ۯ‬ඤ๧ळ༾͈௩૓͞ඤ๧ΏȜΠࠁ଼ͬဲଷ̱Ȃඤ๧‫ۼ‬ဩ֊࣐ĩŦůťŰŵũŦŭŪŢŭĮŵŰĮŮŦŴŦůŤũźŮŢŭġ
ŵųŢůŴŪŵŪŰů Ļ ņůťŎŕĪͬည൵̳̭ͥ͂ͤࠬ͢ͅ‫ۯ‬ඤ๧ळ༾͂̽̀ͅΥ΄ΞͻῄȂ̷̱̀ŃŎőĺ̦ࠬ‫ۯ‬ඤ๧ळ༾͈௩૓ͬᄤૺ̳̭ͥ͂ͤ͢ͅεΏΞͻῄ‫ܥ‬ෝ̳̭ͥ͂ͬࡉ੄̱̀ြ̹ȃ༷֚ȂςϋΩ‫ۯ‬ඤ๧ळ༾͉థ୆‫ۯࠬྤ୓ͅܢ‬ඤ๧ळ༾̤̞̀ͅőųŰŹĲഢৢ֦ঊ̦อ࡛̳̭ͥ͂ͤ͢ͅ໦‫଼̯ͦࠁ̱̀ا‬ͥȃ‫ྙޟ‬૬̞̭͂ͅςϋΩ‫ۯ‬ඤ๧ळ༾͈௩૓ͅచ̳ͥŕňŇĮϸĳ͂ŃŎőĺ͈࢘‫࠿ͬض‬൦̱̹̭͂ͧ‫ͅވ‬ဲଷഎͅ‫ܥ‬ෝ̳̭̦ͥ͂ࡉ੄̯ͦȂࠬ‫ۯ‬ඤ๧ळ༾͂ςϋΩ‫ۯ‬ඤ๧ळ༾͈ŕňŇĮϸέ͹ηςȜͅచ̳ͥ؊൞଻͈௖֑̦ྶ̥̹ͣ͂̈́̽ȃུอນ̤̞͉̭͈̀ͦͣͅ౶ࡉ͈મळ̈́໦ঊ‫ܥ‬੬̞̾̀ͅ༭̳࣬ͥȃ䋭 㪍㪍 䋭

ĺ࠮ĳĸ඾Ȫ߄ȫġĲĵĻĶıȡĲķĻĶıġġలˍٛાΏϋεΐ;θġ‫ܖ‬ய ŔĮĵȶळ༾య৫̦ଷࢄ̳ͥ൲എࢭુ଻̷͈͂෫౦ȡ૤ࠬ‫ۯ‬৖͈ۛଷգ̫͒࢜̀ȡȷ‫ܖ‬யŔĮĵĮĲ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine૤௫ພ̤̫ͥͅయ৫‫ܥ‬ෝႲ‫۾‬
特別講演ɛऎ࿤ġࡓ઎
ࠄᑄ݅ੂఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬ႁ‫ڠ‬എ̈́ΑΠτᾼచ؊̱̀Ȃࠬ‫੄ߐ͈ס‬ၾȪ૤ฏ੄ၾȫͬΘͼ΢ηΛ·ͅ་‫̵̜̭̯ͥ͂ͥͅا‬ȃ૤޼య৫͉Ȃ૤޼ਓੀͅຈါ̈́΀ΥσΆȜͬ‫̳ͥݯރ‬ȂτΡΛ·ΑଷࢄȂ΀άΐͿΥΞͻΛ·ଷࢄ̱ͬٚ
̀૤޼͈‫ܥ‬ෝ͂ྟ̥̥̞ͩ̽̀ͥͅȃड߃Ȃ૤޼య৫ͅಕ࿒̱̹ࡄ‫ڰ̦ݪ‬อ̞̈́̽̀ͥͅȃ̷͉ͦȂ૤޼య৫ࡄ‫ڟ੅ܿͅݪ‬૧̦̤̭ͤȂιΗδυȜθȆέρ·ΕȜθٜଢ଼Ȃৗၾ໦ଢ଼ͼιȜΐϋΈ༹̈́̓̽͢ͅ
̀Ȃ૤޼య৫ͬশߗ‫ۼ‬අ։എͅમळٜͅଢ଼̧̠̹̹̜́ͥ̈́̽͛́ͥ͢ͅȃུΏϋεΐ;θ͉́Ȃड૧͈ܿ੅ͬဥ̞̹૤޼య৫ࡄ‫ߓ̞̀̾ͅે࡛͈ݪ‬ఘ႕ͬဥ̞ٜ̀ଢ̵଼̯̞̹̺̩̀ȃ

会長招待講演 シンポジウム૤௫͈ड͜ਹါ̈́‫ܥ‬ෝ͉Ȃ֚඾ਔ‫͈ܢ‬་൲̳ͥྎઑழ૕͈ॸளຈါၾͅႲ൲̵̯̀Ȃ̜̞͉ͥȂ࣐ࠬ

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪍㪎 䋭

‫ܖ‬யŔĮĵĮĳ

ηΠ΋ϋΡςͺ‫ܥ‬ෝવ‫ͥ͢ͅٺ‬ळ༾௩૓ଷࢄ
ɛ֔‫ڈ‬ġో၍‫ނ‬സఱ‫ڠ‬ఱ‫֭ڠ‬୆ྵ‫شݪࡄڠش‬̦͈ͭอ୆Ȇૺജً೾̤̞̀ͅȂ̦ͭळ༾̷͈͂ਔ༏ळ༾͈௖ࡽैဥ͉ਹါ̈́࿨‫̳̹ضͬڬ‬ȃِș͉Ȃळ༾‫͈ۼ‬௖ࡽैဥ̱̹̦ͬٚͭଷࢄ‫ͬࢹܥ‬୆ఘτασ́ၑٜ̳̹ͥ͛ȂΏο;ΐο;Ψ΀ષ๧ͬκΟσ̱̹͂ਆន଼ಿȆ՛଻‫͈֒ࢹܥا‬ഥ‫ڠ‬എٜଢ଼ࠏͬࢹಃ̱Ȃ̷͈ٜଢ଼ͬૺ̧̹͛̀ȃΏο;ΐο;Ψ΀଼ಖࡔ‫͈ܖ‬ષ๧ழ૕̦ͭͅࡔ଻œŢŴȪ œŢŴŗĲĳȫͬอ࡛̳ͥఘळ༾·υȜϋͬည൵̳ͥ͂Ȃ̭͈ͦͣळ
༾઼ً߲͉ͅ௩૓̱̀ၻ଻ਆនͬࠁ଼̳ͥȃ̭͈ၻ଻ਆន̯ͣ̈́ͥͅඏட་։ͬ൵ව̱Ȃ་։ळ༾ু
૸̷͉̩͈́̈́ਔ༏͈ୃુळ༾͈௩૓̦‫̩ޑ‬௯ૺ̯֚ͦͥႲ͈ඏட་։ఘȪůŰůĮŢŶŵŰůŰŮŰŶŴġ
ŨųŰŸŵũ ļ ůŢŨ་։ఘȫͬౙၗ̱̹ȃ̭ͦͣůŢŨ་։ఘ͈ୣහ֒ഥঊٜͬଢ଼̱̹ࠫ‫ض‬ȂηΠ΋ϋΡςͺࡤ‫ݟ‬ङໝࣣఘ͈΋ϋεȜΥϋΠͬ΋ȜΡ̳֚ͥႲ͈֒ഥঊ߲̦൳೰̯̹ͦȃ̳̻̈́ͩȂœŢŴΏΈ΢σ͈‫ڰ‬଻‫͂ا‬ηΠ΋ϋΡςͺࡤ‫ݟ‬ङ͈‫ܥ‬ෝવ‫̦ٺ‬൳শ̭ܳͥ͂ͅȂ̷͈ਔ༏ळ༾͈௩૓̦௯ૺ̯̭̦ͦͥ͂
໦̥̹̽ȃ̯ͣͅȂ̭͈œŢŴ͈‫͂ا଻ڰ‬ηΠ΋ϋΡςͺ͈‫ܥ‬ෝવ‫ͬٺ‬൳শ̭̱̹ܳͅ་։ळ༾߲ͅ߃୪
̳ͥळ༾߲̦œŢŴͬ‫̹̱ا଻ڰ‬ၻ଻ਆន̜̹́̽ાࣣȂ̷͈ၻ଻ਆន͉՛଻‫̱̀ا‬૫੕Ȇഢ֊ෝͬ‫ڕ‬ං̳̭̦ͥ͂໦̥̹̽ȃ̭͈̠̈́͢ģळ༾๱ুၙഎģ̈́ਆន՛଻‫͈ا‬໦ঊ‫ͬࢹܥ‬ٜଢ଼̱̹ࠫ‫ض‬ȂœŢŴ͈‫଻ڰ‬‫͂ا‬ηΠ΋ϋΡςͺ͈‫ܥ‬ෝવ‫̹̱̭ܳͬٺ‬ळ༾͉‫ॸ଻ڰ‬ளਅͬఱၾͅॲ୆̱Ȃ̭ͦͤ͢ͅŋŏŌΏΈ΢σͬ‫̦̭̳͂ͥا଻ڰ‬໦̥̹̽ȃ̯ͣͅȂŋŏŌΏΈ΢σ͉œŢŴΏΈ΢σ͂‫ဲ̦̱ͭ̀಺ފ‬ଷࠐႹŉŪűűŰ
ࠐႹͬະ‫̱اڰ‬Ȃ‫׶‬છ଻΍ͼΠ΃ͼϋŖůűŢŪųŦťȪŊōĮķγκυΈȫ͈ॲ୆ͬည൵̳̭ͥ͂́Ȃਔ༏ழ૕͈
՛଻‫̹̥̽̈́͂ͣྶ̧̦̭̳̭͂ܳ֨ͬا‬ȃΪΠ͈̦ͭழ૕̤̞̀ͅηΠ΋ϋΡςͺ͈‫ܥ‬ෝવ‫̦ࣞٺ‬ອഽͅ෇̦͛ͣͦͥȂ̷͈փ͉̭͕݅ͦ́͂ͭ̓͘ະྶ̜̹́̽ȃոષ͈ࠫ‫͉ض‬ȂηΠ΋ϋΡςͺ͈‫ܥ‬ෝવ‫̦ٺ‬ळ༾‫ۼ‬΋ηνΣΉȜΏοϋ̱̦͈ͬٚ̀ͭૺജͬߐ൲̳ͥ‫خ‬ෝ଻ͬাऐ̱̞̀ͥȃ䋭 㪍㪏 䋭

‫ܖ‬யŔĮĵĮĴ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineΈυȜΨσ̈́ഢৢΘͼ΢ηΒθ͈ণത̥͙̹ͣ୆‫ڰ‬ਠ‫۝‬ພ͈໦ঊ‫ࢹܥ‬൐‫ش֓ނ‬ভ‫ش‬ఱ‫ڠ‬ඳহ৖ۛࡄ‫ݪ‬ਫ਼୶౤໦ঊ֓‫ݪࡄڠ‬໐࿝ळ༾໦ঊ֓‫ڠ‬໦࿤̭̦͂ͧȂྕ଻‫׶‬છ͉́Ȃ̶̈́‫׶‬છ฽؊̦ਓ௵̳̭̩ͥ͂̈́஗‫̥͈̳ͥװ‬Ȃ̷͈໦ঊ‫͉̈́́ږྶ͉ࢹܥ‬̞ȃ‫׶‬છ฽؊͉ͅအș̈́‫׶‬છळ༾̦‫۾‬ဓ̳̦ͥȂಎ́͜ζ·υέ͹Ȝΐ̦ఉद̈́‫ܥ‬ෝͬ‫ڕ‬ං̱‫׶‬છ͈ৼܳȆ௯ૺ͂ਓ௵͈ၰ࿂́ਹါ̈́࿨‫̦̭̳̹͂ضͬڬ‬ಕ࿒̯̞ͦ̀ͥȃ༷֚ȂςάΡη·Αٜଢ଼͈ૺ༜
ͤ͢ͅȂζ·υέ͹Ȝΐ̦ਅș͈ডཛॸ͞΋τΑΞυȜσయ৫ॲ໤ͬॲ୆Ȇ໦๥̳̭̦ͥ͂ྶ̥ͣ͂̈́̽
̞̀ͥȃུࡄ‫͉́ݪ‬Ȃ‫׶‬છ฽؊͉ळ༾య৫͂ྟ୪ͅ‫۾‬Ⴒ̱̞͈͉̞̥̀ͥ́̈́͂ࣉ̢Ȃ‫׶‬છ؊൞̤̫ͅ
ͥζ·υέ͹Ȝΐಎ͈ডཛॸͬςάΡη·ᾼͤ͢೰ၾٜଢ଼̱̹ȃ̷͈ࠫ‫ض‬Ȃňőœ̱ͬٚ̀ࢯ‫׶‬છैဥͬอ‫̳ͥܞ‬ЎĮĴಿङະ཈გডཛॸ଼͈ࣣ͉Ȃ‫׶‬છ੝‫ͅܢ‬೩‫̱ئ‬Ȃࢃ‫ͅܢ‬ಠ̱̩௩‫̹̱ح‬ȃ̭͈̠̈́͢

ͅœŏłĮŴŦŲͬဥ̞̀Ȃ‫׶‬છ؊൞̤̫ͥͅΈυȜΨσ̈́ഢৢ͂΀άΊΦθ͈൲ఠٜͬଢ଼̱̹ȃ‫׶‬છ‫଻ݢ‬‫͉ͅܢ‬ŏŇЀŃջం଻ͅ‫ړ‬ඤ਋ယఘōŪŷŦųġ řġ ųŦŤŦűŵŰųġ ĩōřœĪ͈‫ܥ‬ෝ̦௸̥͞ͅဲଷ̯ͦȂডཛॸ૝ಿࣖ

口頭発表ডཛॸ଼ࣣ಺୯͈໦ঊ‫ͬࢹܥ‬ٜྶ̳̹ͥ͛ͅȂ·υζΙϋ྾‫ע‬ೆࣛĮΏȜ·΀ϋΑ༹ĩńũŊőĮŴŦŲĪ͍̈́ͣ

会長招待講演 シンポジウム୆‫ڰ‬ਠ‫۝‬ພ͞‫܈‬Ȃ૰ࠐ་଻৖͈ۛ̈́̓ພఠͅ‫ވ‬೒̳ͥอછ‫ܖ‬๕̱͂̀Ȃྕ଻‫׶‬છ̦ಕ࿒̯̞ͦ̀ͥȃ

特別講演ɛനಎȪఱ୞ȫဇ๼ঊளņŭŰŷŭĶ͞ະ཈გ‫ࣖا‬ளŔńŅĳ͈อ࡛̦ࡘઁ̱Ȃࢯ‫׶‬છ଻ডཛॸ଼ً͈ࣣ̦֚଻ͅ೩‫̹̞̱̀ئ‬ȃ̭͂ĩŔœņŃőĪ̦ಁͦ̀‫̯ͦا଻ڰ‬Ȃōřœ͂‫׶ࢯ̱̀಺ފ‬છ଻ডཛॸ଼͈ࣣ̦ᄤૺ̱̹ȃ̭͈̠͢ͅȂōřœࠐႹ͂ŔœņŃőࠐႹ̦‫̱̀಺ފ‬ডཛॸ଼ࣣͬ಺୯̳̭ͥ͂̽̀͢ͅȂζ·υέ͹Ȝΐ͈հ೰‫͂ا‬ழ૕ࢭુ଻̦֋঵̯̞̭̦ͦ̀ͥ͂ྶ̥̹ͣ͂̈́̽ȃུ࠿൦ͤ͢ͅȂζ·υέ͹Ȝΐ̤̫ͥͅুၙഎ̈́ডཛॸ
଼ࣣ಺୯ٚͅව̱Ȃζ·υέ͹Ȝΐ‫ܥ‬ෝ͈հ೰‫ͬا‬ດഎ̱̹͂ࢯ๬ྖȆࢯ൲ྤࣁ‫ا‬হၷ͞ထཡ༹͈‫خ‬ෝ଻ͬ೹̱ܳȂ‫ٳ‬อ͈‫ܖ‬๕͂̈́ͥ౶েͬࢹಃ̱̹ȃ

ポスター発表 ＹＩＡ選考発表̦ͧȂ‫׶‬છࢃ‫͉ͅܢ‬Ȃ઀༾ఘ྄̥͈ͣίυΓΏϋΈͬࠐ̀ŔŵŦųŰŭġųŦŴűŰůŴŪŷŦġŦŭŦŮŦůŵġţŪůťŪůŨġűųŰŵŦŪůġ

著者索引

䋭 㪍㪐 䋭

‫ܖ‬யŔĮĵĮĵ

΀άΐͿΥΞͻ·Α‫΀ͥ͢ͅࢹܥ‬ΥσΆȜయ৫಺୯͂ພఠ
ɛಎ๶ġ࢕஝Ȃाࡓġࡐ‫ݛ‬Ȃ඾࿤ġ૞ষႿߧུఱ‫ڠ‬อ୆֓‫ݪࡄڠ‬ਫ਼΀άΐͿΥΞͻ·Α‫͉ࢹܥ‬ȂŅŏł͈ιΙσ‫ا‬ȂΪΑΠϋ͈‫ڠا‬ਘૐȂŅŏł͂ΗϋΩ·ৗ͈ໝࣣఘ́
̜ͥ·υζΙΰࠁ଼̯ͦͥ΀άΊΦθͬଷࢄ̳ͥॽழ͙̜́ͥȃ΀άΊΦθ͈ેఠ͉Ȃळ༾ඤ‫͈ٸ‬‫ͬޣג‬਋̫̦̈́ͣȂ̷͈ਘૐ͈་‫̱̀͂ا‬ಇୟ̯ͦͥȃఉ֦ঊ৖ۛȪ୆‫ڰ‬ਠ‫۝‬ພ͞‫̓̈́܈‬ȫ͈อછ͉ͅȂ֒ഥ֦ঊ۪͂‫֦ޏ‬ঊ̦௖ࡽैဥ̳ͥ‫خ‬ෝ଻̦̩ࣞȂ΀άΊΦθ͈ਘૐ͈་‫̦̭͂ͥͩ۾̦ا‬ထ‫̯ͦܢ‬̞̀ͥȃ΀ΥσΆȜయ৫͈΀άΐͿΥΞͻΛ·̈́ଷࢄȂ̫͂ͤͩȂ‫ူו‬Ȇ૙ম̦య৫ેఠ̠̓ͅ‫̥̳ͥͅޣג‬̞͉̾̀ະྶ͈ത̦ఉ̞ȃজ̹̻͉ȂέρΫϋջం଻͈ōŔŅĲςΐϋ౎ιΙσ‫ࣖا‬ள̦΀ΥσΆȜయ৫ͬଷࢄ̳ͥι΃ΣΒθͬྶ̥̱̹ͣͅȪŉŪůŰġŦŵġŢŭįġŏŢŵġńŰŮŮŶůĭġĳıĲĳȫȃōŔŅĲஷ‫͈ٺ‬ডཛळ༾̤ͅ
̞̀Ȃ΀ΥσΆȜક๯֒ഥঊ߲͈อ࡛̦ည൵̯ͦ̀Ȃ̷͈ࠫ‫ض‬ȂηΠ΋ϋΡςͺ͈ॸ‫ا‬എςϋॸ‫͂ا‬ডཛ໦ٜ̦௩‫̦̭̳͂ͥح‬໦̥̹̽ȃࣞডཛ໅‫ͥ͢ͅك‬๬ྖζ;Α͈ডཛழ૕͉́ȂōŔŅĲ͈ດഎ֒ഥঊ
߲͈อ࡛͉೩‫̤̱ͤ̀ئ‬Ȃఈ༷Ȃζ;ᾼōŔŅĲஷ‫ٺ‬࿪सͬൎဓ̳ͥ͂Ȃ̷͈֒ഥঊ߲̦ठ‫̯̀ͦا଻ڰ‬Ȃ๬ྖພఠ̦ಠ̱̩٨஝̱̹ȃ̯ͣͅȂ‫܈‬య৫͈͂‫۾‬Ⴒ଻ͬྶ̥̳̹ͣͥ͛ͅͅȂ۴௫‫܈‬ळ༾́ōŔŅĲͬஷ‫̳͂ͥٺ‬ȂηΠ΋ϋΡςͺ͈ॸ‫ا‬എςϋॸ‫ا‬ෝ̦௩‫̱ح‬Ȃٜൠࠏ͈‫̦଻ڰ‬೩‫̦̭̳͂ͥئ‬฻ྶ̱̹ȪŔŢŬŢŮŰŵŰġŦŵġ Ţŭįġ Ūůġ ųŦŷŪŴŪŰůȫȃ̭͈̠͢ͅȂōŔŅĲͥ͢ͅ΀άΊΦθଷࢄ̦Ȃ΀ΥσΆȜయ৫͈಺୯ͅྟ୪ͅ‫ͩ۾‬̭̦ͥ͂াऐ̯̹ͦȃུ࣒‫͉́׵‬Ȃ΀άΐͿΥΞͻ·Α‫͈ࢹܥ‬۷ത̥ͣȂ΀ΥσΆȜయ৫಺୯͂ພఠ̤̫ͥͅड߃͈౶ࡉ
ͬત̱ٚ̀Ȃ̷͈ै൲ࡔၑ͂փ̞݈݅̾̀ͅა̱̹̞ȃ䋭 㪎㪇 䋭

ĺ࠮ĳĹ඾ȪാȫġĺĻııȡĲĲĻııġġలˍٛાΏϋεΐ;θġ‫ܖ‬ய ŔĮĶȶਆនࠬ‫ۯ‬૧୆ȷġ‫ܖ‬யŔĮĶĮĲ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineਆនࠬ‫ۯ‬අ։എ̈́ࠬ‫ۯ‬૧୆໦ঊι΃ΣΒθ

Ĳ ࠄᑄ݅ੂఱ‫ڠ֓ڠ‬໐‫ܥ‬ෝࠁఠ‫ڠ‬໦࿤Ȃĳ ࠄᑄ݅ੂఱ‫ڠ֓ڠ‬໐ഩঊࡐ๷‫ݪࡄޢ‬৒ŗņňŇΏΈ΢σ͉Ȃ࠲ુࠬ‫֋଻ુࢭ͈ۯ‬঵͜ͅ‫ܙ‬ဓ̱Ȃ̷͈ஷ‫̦͉ͭٺ‬ո‫͈ٸ‬஠૸ࠬ‫͒͜ۯ‬๱අ։എͅ
ΘιȜΐ̤͖̳͜͢ȃ̹͘ΪΠ̦ͭͅచ̳ͥŗņňŇஷ‫ٺ‬स͈ಿ‫ܢ‬എ̈́ଷ̦ͭ࢘‫͉ض‬Ȃਆន͈ਅ႒̽͢ͅ
͉̥̀̈́ͤࡠ೰̯ͦȂ͈̭ࣽ͂ͧࠨ̱̀ྖ௷̞̩͈͉͂͜࡞̢̞̈́ȃ̱̥̱̦̈́ͣȂ֚শഎ́͜ͅਆន
ࠬ‫ۯ‬పੀȆਆន௩ఱ͈ဲଷࠠͅഎ̈́࢘‫ͬض‬อ‫̠̞̳͂ͥܞ‬ম৘͉Ȃষଲయ͈ࠬ‫̦ͭͥ͢ͅݪࡄۯ‬໦ঊດഎ֓ၷ͈๲࿬ͬ‫ܢ‬ఞ̵̯͉ͥͅ਱໦͈̜̈́́ͥ͂͜ࣉ̢ͥȃ࡛हŗņňŇஷ‫ٺ‬सͅయͩͥȂ̹͉͘໵ဥ
ͤ͢ͅଷ̦ͭ࢘‫ͥ͛ࣞͬض‬૧ܰ໦ঊດഎ͈ౝ̦॑ଲ‫ٮ‬എͅ‫ڰ‬อ‫̞̱ͥ̀ا‬ȃ̷͈ಎ͉ͅ࠲ુࠬ‫ࢭ͈ۯ‬ુ଻֋঵͉ͅ‫ܙ‬ဓ̱̞̈́Ȃ̦ͭࠬ‫ۯ‬අ։എ͈̈́͜͞ȂŗņňŇஷ‫ٺ‬स́ࡉ̠ͣͦͥ̈́͢ൎ࿪ಎ౯ࢃ͈ਆន

ਆនࠬ‫ۯ‬අ։എ̈́໦ঊι΃ΣΒθ̱͂̀Ȃॸ‫ا‬ΑΠτΑΏΈ΢σͅઙതͬ൚̀Ȃ̭͈ͦ́֒͘ഥঊ٨
་ζ;Αͬဥ̞̹ࡄ‫ضࠫݪ‬Ȃ̤͍͢ႉ઄എခဥ଻̧݈̾ͅა̱̹̞ȃ

口頭発表ठ଼ಿ̦ྶ̥ͣͅઁ̞͈̈́͜͜ࡉ੄̯̞ͦ̀ͥȃུ࣒‫͉́׵‬ȸεΑΠŗņňŇȹ͈ࠬ‫ۯ‬૧୆໦ঊດഎȂඅͅ

会長招待講演 シンポジウム൚੝Ȃอ୆‫ܢ‬Ȇਆន̤̫̈́̓ͥͅ‫ڰ‬อ̈́ࠬ‫ۯ‬ςκΟςϋΈ̱̥́ຈါ̯̞͂ͦ̈́͂ࣉ̢̧̹ͣͦ̀

特別講演ɛ‫ݛ‬༗നġ݅ࡐ Ĳĭĳ

ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪎㪈 䋭

‫ܖ‬யŔĮĶĮĳ

ਆនࠬ‫ۯ‬ଷࢄ̱̹ͬٚഢ֊ဲଷɛධġࠉ൐‫ނ‬ఱ‫୶ڠ‬౤‫ݪࡄ੅ܿڠش‬ΓϋΗȜࠬ‫ۯ‬୆໤‫ڠ‬̦ͭ௩૓Ȇഢ֊ཡগ̤̞̀ͅȂ̦ͭ๷઀۪‫ޏ‬Ȃࠬ‫ۯ‬൲ఠࡄ‫̦ݪ‬ະ‫̜ͥ́ࠧخ‬ȃِș͉̭ͦ́ࠬ͘ͅ‫ۯ‬ࢹಃ͈‫ܖ‬ய̳ͬ̈́ඤ๧ळ༾̤̞̀ͅ௩૓֦ঊġ ĩŗņňŇĪġ ͞‫׶‬છȆާࡥঁࠣġ ĩŵũųŰŮţŪůĪġ ́ည൵̯֦ͦͥ
ঊͬΏΑΞθഎٜͅଢ଼̱̹ࠫ‫ض‬Ȃ்‫ͅܢ‬Θ;ϋછ‫۾‬Ⴒ֦ঊġĩŅŔńœĪĮĲȂഢৢ֦ঊġņŨųĮĴġ̦‫ވ‬೒̱̀डఱ
ͅષઌ̱̩̭̀ͥ͂ͬࡉ੄̱̹ȃඅͅ΃σΏΣνȜςϋĮŏŇłŕ ΏΈ΢σ͈κΐντȜΗȜ̜́ͥġŅŔńœĮĲ ͉อ୆‫׶͍ݞܢ‬છȂਆន۪‫ۯ͈ࠬ́ئޏ‬ඤ๧ळ༾ͅ஖఼എࣞͅอ࡛̱ཡࢌഎͅैဥ̳̭ͥ͂Ȃ̹͘Θ;ϋછۛ৪̤̫ͥͅࡥࠁ̦ͭᑋۛၚࡘઁ̧̭̳ͬ֨ܳ৽ါ֦ঊ̜̭́ͥ͂ͬྶ̧̥̱̹ͣ̀ͅȃ̷̭́ġ ŅŔńœĮĲ ඤ๧հ೰อ࡛ζ;Α͞ΦΛ·ͺ;Πζ;Αͬဥ̞̀Ȃਆន௩૓͞ഢ֊͈͒‫ܙ‬ဓͬౝ̱̹̭॑͂ͧȂŅŔńœĮĲ ඤ๧հ೰อ࡛͉̦ͭ௩૓͞෹͈̦͒ͭഢ֊ͬ‫ޑ‬ႁͅဲଷ̱̠̭̦ͥ͂ྶ̥ͣ͂
̹̈́̽ȃ༷֚ Dscr-1-/- ζ;ᾼ̤̫ͥࡔอਆន۪‫͉́ئޏ‬Ȃඤ๧ྟഽͅచ઼ً̱̈́௩૓֦ঊ͈ঁ̦ࠣ
ව̭ͥ͂́ήτȜ΅࿨ͬ৐̹̽ඤ๧̦ະհ೰‫ࡔ̱ا‬อਆន͈௩૓̦ಁ‫༷̳֚ͥװ‬Ȃ෹͈̦͒ͭഢ֊̦
்‫଼ͅܢ‬ၛ̳̭̦ͥ͂ࡉ੄̯̹ͦȃ෹͉ࠬ‫ྟۯ‬ഽ̦डఱ͈௫‫̜ͤ́ܕ‬ȂDscr-1 -/- ζ;Ά͉අͅűųŦĮŮŦŵŢŴŵŢŵŪŤġ ůŪŤũŦ ۪‫ ̢ͥͦͣࣉ̱̀͂ޏ‬ŗņňŇ ̦‫̩ޑ‬ည൵̯ͦȂ̷͈ࠫ‫ض‬๷઀۪‫ޏ‬අ։എͅ ŏŇłŕġ
ջం଻͈ ŗņňŇĮŗņňŇœĳġ ůŪŤũŦ ࠁ଼்̦‫ͅܢ‬୆̲̭̦̭͈ͥ͂ഢ֊଼ၛͅ‫۾‬ဓ̱̞̹̀ȃ̯ͣͅ෹๷઀۪‫͈ޏ‬༫‫گ‬എͺτͼ‫͍ݞ‬෹ഢ֊ႉ઄࠿ఘ̥ͣ ŗņňŇĮŏŇłŕĮłůŨŪŰűŰŪŦŵŪůĮĳ ͬ৊̱̹͂΍ͼΠ΃ͼϋ͈ષઌ̦ ŅŔńœĮĲ ͈ခྫͅୃ௖‫̤̱ͤ̀۾‬ȂDscr-1-/-ζ;ᾼ̤̫ͥ‫׶̞ޑ‬છ૫੕̦͂ͭഢ֊͉ġŴŰŭŶţŭŦĮŕŪŦĳ ͈ൎဓͤ࢘͢ͅၚഎͅဲଷ̯ͦͥࠫ‫̹̽̈́͂ض‬ȃ̷ུ̤̞͉͈ٛ̀ͅૺೃ݈ͬა̱̹̞ȃ䋭 㪎㪉 䋭

‫ܖ‬யŔĮĶĮĴ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineŗŢŴŰũŪţŪůĮĳġŢŴġŢġůŰŷŦŭġŵŢųŨŦŵġŧŰųġŤŢůŤŦųġŵųŦŢŵŮŦůŵ
特別講演ɛऎ൥ġ࿭ঃ
൐ཤఱ‫حڠ‬Ⴂ֓‫ݪࡄڠ‬ਫ਼

neo-vessels. This process, known as angiogenesis, occurs in various pathologic conditions including
cancers. We have isolated vasohibin-1 (VASH1) as a novel VEGF-inducible endothelium-derived
angiogenesis inhibitor, and vasohibin-2 (VASH2) as its homologue. We found that VASH1 andVASH2 are highly conserved between species, and their roles in the regulation of angiogenesis are
distinct and perhaps contradictory. Our subsequent analyses indicated that VASH1 is expressed inendothelial cells and negatively regulates the course of angiogenesis. In contrast, VASH2 isexpressed mainly in cancer cells and promotes tumor growth by stimulating angiogenesis.

human cancers including serous ovarian adenocarcinoma and hepatocellular carcinoma. This
expression of VASH2 in cancer cells is mediated not by hypoxia but by the alteration of miR-200b
expression. We then used 2 representative human serous adenocarcinoma cell lines, and examinedof cancer cells in vitro, but notably inhibited tumor growth, peritoneal dissemination, and tumor
angiogenesis in a murine xenograft model. Thus, VASH2 can be a potential target for cancer
treatment.

ポスター発表 ＹＩＡ選考発表

the role of VASH2 in the tumor. The knockdown of VASH2 showed little effect on the proliferation

口頭発表

Immunohistological analysis revealed that VASH2 protein was preferentially detected in various

会長招待講演 シンポジウム

The vascular system is one of the most quiescent organs in the body, but has the capacity to form

著者索引䋭 㪎㪊 䋭

‫ܖ‬யŔĮĶĮĵ

ਆនࠬ‫ۯ‬ඤ๧ळ༾͈࿪स೷ࢯ଻
ɛ๳നġ‫ނ‬ঊཤ٬ൽఱ‫ڠ‬ఱ‫֭ڠ‬ভ‫ۯࠬشݪࡄڠ‬୆໤‫ޗڠ‬৒ࠬ‫ۯ‬૧୆ஷ‫ٺ‬ၷ༹͉஠͈̦̀ͭͅ‫ވ‬೒̳ͥࠬ‫ۯ‬૧୆ͬດഎ̱̞̹͂̀ͥ͛ĭġ ఉ̩͈‫܈‬ਆ́ࢯ‫܈‬स͈͂໵ဥ́হၷ࢘‫̞ͥ̀ͦͣ͛෇̦ض‬įಿාȄࠬ‫ۯ‬ඤ๧ळ༾ͬດഎ̳͂ͥࠬ‫ۯ‬૧୆ஷ‫ٺ‬ၷ༹͉ͅ࿪स೷ࢯ
଻̦୆̲̞̈́͂૞̧̲̹̦ͣͦ̀ĭġ ड߃ĭġ ̭ͦͣͅచ̱̀͜࿪स೷ࢯ଻̦୆̲̭̦ͥ͂༭̯̞࣬ͦ̀
ͥį̷͈ι΃ΣΒθ̱͉͂̀߃ා́͘ȶਆនळ༾ͥ͢ͅࠁৗ་‫ا‬ȷ̦‫ܥ‬੬̱͂̀ࣉ̢̞̹ͣͦ̀ḙ͉̏ͦ́ͩͦͩͦ͘ਆនࠬ‫ۯ‬ඤ๧ळ༾ȪŕŶŮŰųġ ŦůťŰŵũŦŭŪŢŭġ ŤŦŭŭ Ļ ŕņńȫ̦ŨųŰŸŵũġ ŧŢŤŵŰų͞࿪स͈͒ۜ਋଻
֒͞ഥঊอ࡛Ȅ௩૓ෝȄဋ௢ෝ̦̈́̓ୃુࠬ‫ۯ‬ඤ๧ȪŏŰųŮŢŭġŦůťŰŵũŦŭŪŢŭġŤŦŭŭ Ļġŏņńȫ͉͂։̭̈́ͥ͂
ͬ༭̧̱̹࣬̀įġ ̯ͣͅȄஅ૗ఘ։ુ̦෇̹̭̥͛ͣͦ͂ͣȄŕņń̦֒ഥঊະհ೰଻ͬ̾͜‫خ‬ෝ଻̦াऐ̯̹ͦȅड߃Ȅ͉ͩͦͩͦŕņń̦ŏņńͅ๤‫̱̀ڛ‬ŎŶŭŵŪťųŶŨġ ųŦŴŪŴŵŢůŤŦġ ŨŦůŦĮĲ ĩŎŅœĲĪ İ űĮŨŭźŤŰűųŰŵŦŪůġĩűĮŨűĪ͈อ࡛̦̩ࣞȄࢯ̦ͭसġűŢŤŭŪŵŢŹŦŭͅచ̱̀೷ࢯ଻̦̜̭ͥ͂ͬࡉ੄̱̹ȅ̯ͣͅȄ̦ͭळ༾ဇြŗņňŇ̽̀͢ͅȄŏņń̤̞̀͜ͅűĮŨű͈อฺ࡛̠ͬ࿪स೷ࢯ଻̧̦̭̯֨ܳͦͥ
̭̥̹͂ͩ̽͜ġĩłŬŪźŢŮŢġŦŵġŢįĭġłŮġŋġőŢŵũŰŭġĳıĲĳĪġȅġŪůġŷŪŷŰġਆនκΟσ̤̫ͥͅΩ·ςΗ΅Γσͥ͢ͅহၷ৘ࡑ͈षͅűĮŨű͈ஷ‫ٺ‬सαρΩησͬ໵ဥ̳ͥ͂Ω·ςΗ΅Γσ͈হၷ࢘‫̦ض‬௩‫̱ޑ‬̹ȅոષ͈ࠫ‫ͤ͢ض‬Ȅŕņń͈අ଻ͅ಍࿒̳̭ͥ͂ͤ͢ͅ‫ܡ‬ం͈࿪सͬ૧̱̞̦͈ͭহၷ༹ͅ؊ဥ̧́
̭̦ͥ͂াऐ̯̹ͦȅ༷֚Ȅ͉ͩͦͩͦഢ֊ෝ̦։̈́ͥਆនဇြ͈ࠬ‫ۯ‬ඤ๧ळ༾‫̞̤̀ͅۼ‬ŕņń͈࿪सۜ਋଻͜։̭̈́ͥ͂Ȅਆន͈՛଻ഽ͈֑̞̽̀͢ͅĭŕņń͉ͅఉအ̈́଻ৗ̦̜̭ͥ͂ͬࡉ੄̱̞̀ͥ
ĩŐũŨŢġŦŵġŢŭįĭġłŮġŋġőŢŵũŰŭġĳıĲĳĪȅġ̭͈̠̈́͢ŕņń͈ఉအ଻͈ၑٜ̦ࠬ‫ۯ‬૧୆ஷ‫ٺ‬ၷ༹͈ࡢ༆‫ا‬হၷ͈͒؊ဥ͉ͅਹါ͂এͩͦͥȅġȁȁ䋭 㪎㪋 䋭

‫ܖ‬யŔĮĶĮĶ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine̦ͭ๷઀۪‫·΀ޏ‬ΕΕȜθ͂ਆនࠬ‫ۯ‬૧୆ඊၛ࣐ଽ༹૽࣭ၛ̦ͭࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼໦ঊळ༾হၷࡄ‫ݪ‬໦࿤̱̹̦ͭ๷઀۪‫͈ޏ‬අ։଻ͬ͜୆͙੄̱̞̀ͥȃ̭͈๷઀۪‫͈ޏ‬අ։଻ͬࢹ଼̳ͥ૧̱̞৽࿨͈ంह
̦ĳııĸාͅΑ;ͿȜΟϋ͈ΈσȜί̽̀͢ͅඏශྶ̥̯̹ͣͦͅȃ๞̦ͣা̱̹͈͉Ȃळ༾઀༾ᴧၥ
ȪņŹŰŴŰŮŦĻ΀·ΕΕȜθȫಎͅζͼ·υœŏł̦༫ོ̯̤ͦ̀ͤȂ΀·ΕΕȜθ̱̹ͬٚळ༾‫ۼ‬ζͼ·υœŏł֊௣ͥ͢ͅྚ౶͈ૂ༭ഥో‫͈ࢹܥ‬ంह̜̹́̽ȃ̭ͦͬ๧୨ͤͅळ༾‫ͅٸ‬༶੄̯ͦͥ໦๥߿ζͼ·υœŏł͞΢Φ΍ͼΒ͈΀·ΕΕȜθ̷͈͈͈͜୆໤‫ڠ‬എփ͈ٜ݅ྶ̫̹࢜ͅಯ୽̦ଲ‫ٮ‬ಎ́ΑΗȜΠ̱̹ȃ̷̱̀Ȃ̭͈΀·ΕΕȜθͥ͢ͅ୆ྵ࡛ય͈ζͼ·υζΥȜΐιϋΠ͈৘ఠ̦ĭ̦ͭͬই̳͛͂ͥఉ̩͈֓‫ڠ‬୆໤‫͈ڠ‬໦࿤́ྶ̥̜ͣ̈́ͤ̾̾ͥͅȃ̦ͭळ༾͉ౙඊ́ంह̳͈͉̩ͥ́̈́Ȃ઀۪‫̦ͭͅޏ‬ळ༾̦ഐ؊̱ু͈ͣ୆ྵͬ֋঵̳̹ͥ͛ͅȄೄ୪എ̈́ळ༾‫ۼ‬௖ࡽैဥ͞ȂΩρ·ρͼϋഎ̈́ΗϋΩ·ৗ͈༶੄ͥ͢ͅਔս͈ळ༾͈ଷࢄ‫̩͉̫̺̈́́ࢹܥ‬Ȃ΀·ΕΕȜθͅඤ༫̵̯̹අ೰͈

口頭発表ਔս͈အș̈́ळ༾͞ζΠςΛ·Α͂௖ࡽैဥ̱̦ͬ̈́ͣਬ౬଼̱͂̀ಿ̳ͥȃ̭̠̱̹୆ఘޫਫ਼͈๷

会長招待講演 シンポジウム̦͈ͭহၷ೷ࢯ଻ͬయນ̳̦ͥͭۚळ༾͈ంह͉Ḁ͈̑ͭ‫ٴ‬௄଻̴͈͙̈́ͣȂ̦ͭۚळ༾ͬೀത͂

特別講演ɛ၂౓ġࢣࢩ

‫ܥ‬ෝͬခ̳ͥζͼ·υœŏłͬȂ႕̢͊Ȃ૫੕ഢ֊ͅຈါ̈́ਔս͈ࠬ‫ۯ‬ඤ๧͞ςϋΩ‫ۯ‬ळ༾ͅັဓ̳ͥ

௯ૺ̳̠ͥ̈́͢ζͼ·υœŏł͞ࢯਆនͅ൱̩྾‫ע‬ळ༾ͬဲଷ̳ͥζͼ·υœŏł̦̈́̓΀·ΕΕȜθͅంह̳ͥম͞Ȃ࿪सఛ଻ͅ‫۾‬ဓ̳ͥłŃńΠρϋΑεȜΗȜ൝͜΀·ΕΕȜθ̽̀͢ͅȂ࿪सۜ਋଻͈
ळ༾͒͂එ̫ͣͦͥম̈́̓͜બྶ̯̞ͦ̀ͥȃਲ̽̀Ȃ΀·ΕΕȜθ໦๥͂࿶௣Ȃًࣺ͙͈৾ͤ೾ͬ৭
౯̳̭̦ͥ͂Ȃ૧̱̞̦ͭহၷ୽ၞ͜ͅೄ̳ࠫͥȃུ࣒‫͉́׵‬Ḙ̠̱̹̏΀·ΕΕȜθ̦ٚह̳ͥζͼ·υœŏłͥ͢ͅਆនࠬ‫ۯ‬૧୆͈৘ఠ͞‫ڞ׿‬௫‫͈͒ܕ‬ഢ֊ι΃ΣΒθ̞̾̀ͅ૧̱̞౶ࡉͬત̳ٚͥȃ

ポスター発表 ＹＩＡ選考発表ম́Ȃ̦ͭळ༾ু૸͈ၛાͬခ၌ͅ൵̩̠̈́͢ΏθΞθ̦ͭ͜ळ༾͉ैͤષ̬̹ȃ৘षͅȂࠬ‫ۯ‬૧୆ͬ

著者索引

䋭 㪎㪌 䋭

ĺ࠮ĳķ඾Ȫ࿐ȫġĺĻııȡĲĲĻııġġలˎٛાΏϋεΐ;θġႉ઄ ŔĮĲȶ‫ۍ‬൲ྤ৖ۛ͂‫׶‬છȷႉ઄ŔĮĲĮĲ

൲ྤࣁ‫͈ا‬อછȆૺജ̤̫ͥͅ‫׶‬છ‫ܥ‬ഢ͂τΣϋȆͺϋΐ΂ΞϋΏϋࠏɛ५നġࢼ෗
‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬൲ྤࣁ‫͈ا‬อછૺജͅτΣϋȆͺϋΐ΂ΞϋΏϋࠏȪœłࠏȫ̦ਹါ̈́࿨‫ྶ͉̭̞̱̹͂ͥ̀ضͬڬ‬̥̜̦ͣ́ͥȂ̷͈મळ̈́ι΃ΣΒθ͉਱໦ٜྶ̯̞̞ͦ̀̈́ȃœłࠏ͈৽ါ̈́୆ၑ‫଻ڰ‬໤ৗ̜́ͥͺϋΐ΂ΞϋΏϋŊŊȪłůŨŊŊȫ͉ȂΗͼίˍȪłŕĲȫ਋ယఘ̱ͬٚ̀୆ఠ͈γι΂ΑΗΏΑͬ֋঵̱̞̦̀ͥȂழ૕œłࠏ̱ͬٚ̀൲ྤࣁ‫ۯ଼ࠬ͞ࠁا‬ςκΟςϋΈ̤̞̀͜ͅಎ૤എ࿨‫ͬڬ‬౜̞̽̀ͥȃΪΠ൲ྤࣁ‫ا‬ພ་̤̫ͥͅœłࠏ͈࿨‫̞̀̾ͅڬ‬ȂˍȫΪΠࠬ‫ۯ‬ழ૕̤̫ͥͅœłࠏ͈อ࡛အ৆ȂˎȫΪΠ͈൲ྤࣁ‫ܥ଼ࠁا‬੬̤̫ͥͅœłࠏ͈‫۾‬ဓȂˏȫłńņஷ‫ٺ‬࿪̤͍͢łœŃ͈ະհ೰ίρȜ·ͅచ̳ͥैဥȂͬಎ૤̭͈ͦ́͘ͅ౶ࡉͬାၑ̱̹̞ȃষͅȂ‫ۍ‬൲ྤ৖͈ۛພఠ୆ၑ͉ͅౙ‫ݩ‬Ȇζ·υέ͹Ȝΐ͉̲ͬ͛͂
̱̹ࠬ‫ࠏݩ‬ळ༾ͥ͢ͅ‫׶‬છ͈ৼ̦ܳ༭̯̞࣬ͦ̀ͥȃজ̹̻͈ΈσȜί͉ȂࣸଡłŕĲ਋ယఘ̦ࠬ‫ੱۯ‬‫ۯ͈ࠬࢃٺ‬ஜߐळ༾͈൲ఠͅ‫ै̳͖ݞ‬ဥͬྶ̥̱ͣͅ૧୆ඤ྄௩୆̷̤̫͈ͥͅփ̞݅̾̀ͅ༭࣬
̧̱̹̀ȃ̹͘Ȃ൲ྤࣁ‫଼̫̤ࣸͥͅࠁا‬ଡłŕĲ਋ယఘ͈࿨‫̧̹̱̥̀ͣͅྶ̭̞́ͦ̀̾͘͜ͅڬ‬ȃ̯ͣࣸͅଡłŕĳ਋ယఘ͈ζ·υέ͹Ȝΐࠁৗ་‫ͬا‬̱̹ٚࢯ൲ྤࣁ‫ैا‬ဥ̞̾̀͜ͅત̱̹̞ٚȃ߃ාȂ‫ۍ‬൲ྤ৖͈ۛ‫׶‬છ‫ܥ‬ഢ̤̫ͥࠬͅ‫ۯ‬ਔսডཛழ૕͈࿨‫̦ڬ‬ಕ࿒̯̞ͦ̀ͥȃ‫ۍ଻ݢ‬છ࢓߲ۛ৪͈
ࠬ‫ۯ‬ਔսডཛழ૕̤̫ͥͅζ·υέ͹Ȝΐ͈ಠྶ̈́ਬୟ͂‫׶‬છ଻΍ͼΠ΃ͼϋ͈อ࡛௩ఱ̦༭̯࣬
̞ͦ̀ͥȃࠬ‫ۯ‬ਔսডཛழ૕͉ඤ௫ฒ૗ডཛ͂։̈́ͤ‫ڴ‬૗ডཛအ͈ࠁৗͬা̳̦Ȃࣞডཛİࣞ΋τΑΞυȜσ૙໅‫ͬك‬ဓ̢̹൲ྤࣁ‫ا‬κΟσζ;Ά͉Ȃࠬ‫ۯ‬ਔսডཛழ૕͈͒‫׶‬છ଻ࠬ‫ݩ‬ळ༾͈ਬୟ͂‫׶‬છ଻΍ͼΠ΃ͼϋ͈อ࡛ᄤૺ̦‫̞̯ͥ̀ͦ෇ږ‬ȃ̯ͣͅȂ̭̠̱̹ࠬ‫ۯ‬ਔսডཛழ૕ͬ֊૒̯̹ͦζ;Ά͉Ȃ֊૒໐պ͂‫ͅވ‬஠૸͈൲ྤࣁ‫ૺ଼͜ࠁا‬ജ̱̞̭̦̀ͥ͂‫̹̯ͦ෇ږ‬ȃࠬ‫ۯ‬ਔսডཛழ૕
̤̫ͥͅ‫׶‬છৼܳ͂œłࠏ͈͂‫ࡑু̞̀̾ͤͩ͜ͅ۾‬႕ͬ‫͛܄‬ત̱̹̞ٚȃ䋭 㪎㪍 䋭

ႉ઄ŔĮĲĮĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine‫ۍ଻ݢ‬છ࢓߲̤̫ͥͅ ŮźŦŭŰŪťĮųŦŭŢŵŦťġűųŰŵŦŪůĮĹİĲĵġĩŎœőĮĹİĲĵĪ
特別講演ɛऎ‫ۼݛ‬ġၑ၍Ȃ࿤੄ġࢣ֚ऎٖఱ‫ڠ֓ڠ‬໐੏۪‫ܕ‬ඤ‫ش‬ͼ·υͺτͼͬဥ̞̀Ȃ‫଻ݢ‬૤޼ࢸणۛ৪߲͂Ⴛै଻‫ޛ‬૤છ߲͈ࠬ઀โȪ‫ݩړݴ‬ȫ֒ഥঊͬίυέ͹ͼ
ςϋΈ̱̹ȃ̳ͥ͂‫଻ݢ‬૤޼ࢸण߲́อ࡛̦̞ࣞ౩ฒ̱͂̀ŮźŦŭŰŪťĮųŦŭŢŵŦťġűųŰŵŦŪůĩŎœőĪĮĲĵ̦൳೰̯̹ͦȃŎœőĮĲĵ͉΃σΏ;θͼ΂ϋ಺୯౩ฒ͈ŔĲıı౩ฒͅ௺̱Ȃࠬಎ͉́ŎœőĮĹİĲĵΰΞυΘͼζȜ̱͂̀ంह̱̞̀ͥȃŎœőĮĹİĲĵ͈৽ါॲ୆ळ༾͉ᴧၥ‫ݩ‬Ȃඅͅࢡಎ‫̦̜ͥ́ݩ‬Ȃౙ‫ݩ‬Ȃζ·υέ͹Ȝΐ̥ͣ͜ॲ୆̯̞ͦ̀ͥȃུࡄ‫͈ݪ‬࿒എ͉‫ۍ଻ݢ‬છ࢓߲̤̫ͥͅŎœőĮĹİĲĵ௶೰͈ႉ઄എփ݅Ȃພఠ୆ၑ‫ڠ‬എփٜ݅ͬྶ̳̭̜ͥ͂ͥͅȃŎœőĮĹİĲĵͬ‫׶͚܄‬છζȜ΃Ȝͬ௶೰̱Ȃ‫ۍ଻ݢ‬છ࢓߲ĩĳĲ႕Ī̤͍͢Ⴛै଻‫ޛ‬૤છ߲ĩĲı႕Ī͈ĳ߲‫̞̤̀ͅۼ‬ȂŎœőĮĹİĲĵͬ‫׶͚܄‬છΨͼ΂ζȜ΃Ȝͬ‫ۍ‬൲ྤ௮‫ג‬শͅ௶೰ٜଢ଼͉́ŎœőĹİĲĵࣞ౵̦‫ۍ଻ݢ‬છ࢓߲͈ඊၛ̱̹‫֦ࡏܓ‬ঊ̹͂̈́̽ȃষͅႲ௽ĴĹછ႕͈‫ۍ଻ݢ‬છ࢓߲ۛ৪̤̞̀ͅȂ‫߲̹ͦͣ͛෇̦஀ࠬ֨ݟ‬ĩ‫஀ࠬ֨ݟ‬ȪĬȫĻĳĴ႕Ī͂ࠬ஀̦෇̥̹߲͛ͣͦ̈́̽ĩ‫஀ࠬ֨ݟ‬口頭発表̱๤‫࠿ڛ‬൦̱̹ȃ‫ۍ଻ݢ‬છ࢓߲ĩĳĲ႕Ī́ŎœőĮĹİĲĵ͉ခփ̩ࣞͅĩĲıįĸ ŷŴ ķįĵЂŨİŮŭĭġ űľıįıĴĴĪȂఉ་ၾ

会長招待講演 シンポジウムِș͉Ȃ‫଻ݢ‬૤޼ࢸण͈ࡔ֦̦ίρȜ·෫౦̷̧͂ͦ֨ͅ௽̧୆̲ͥࠬ஀໾ण̭̥ͥ͂ͣ͢ͅȂζĩȽĪ ĻĲĶ႕Ī͈ĳ߲‫̞̤̀ͅۼ‬ŎœőĮĹİĲĵ౵ͬ๤‫࠿ڛ‬൦̱̹ȃ‫ྙޟ‬૬̞̭͂ͅ‫ۍ̫̤߲ͥͅ஀ࠬ֨ݟ‬൲ྤ‫̞̤߲̀ͅ஀ࠬ֨ݟ‬ŎœőĮĹİĲĵ͉η΀υβσ΂΅ΏΘȜΔ͂ခփ̈́௖‫̹͛෇ͬ۾‬ȃ̹ࠬ͘஀͈྾‫ע‬அ૗͉́ȂŎœőĮĹİĲĵ͉ńŅĲĲţု଻͈ฒࠬ‫ݩ‬ષͅ‫ވ‬அ૗ု଻̱͂̀෇̹̦͛ȂŎœőĹİĲĵ͂ńŅĵĳ˽͈͂‫ވ‬அ૗ု଻ळ༾͉෇̥̹͛̈́̽ȃոષ̥ͣฒࠬ‫ݩ‬Ȃඅͅࢡಎ‫ݩ‬İౙ‫ۍ଻ݢ̦ݩ‬છ࢓߲ୣහພ་̤̫ͥͅ
ŎœőĹİĲĵ৽ါॲ୆࡙͂ࣉ̢̹ͣͦȃŎœőĮĹİĲĵ͉Ȃࠬ઀โĮฒࠬ‫ݩ‬௖ࡽैဥͅ‫۾‬ဓ̱ȂίρȜ·ະհ೰‫ا‬ȂίρȜ·෫౦ࠬ͞஀ࠁ଼͈ພఠͬນ̳Ψͼ΂ζȜ΃Ȝ଼̠ͤͥͅ‫خ‬ෝ଻̦াऐ̯̹ͦȃ

ポスター発表 ＹＩＡ選考発表ŎœőĹİĲĵෛഽ͉Ȃ‫߲̱͂̈́஀ࠬ֨ݟ‬๤͓ခփࣞͅ౵ͬা̱̹ȃ̷̭́ŎœőĮĹİĲĵ͈ॲ୆࡙ͬ࠿൦̱̹ȃ

著者索引

䋭 㪎㪎 䋭

ႉ઄ŔĮĲĮĴ

ίρȜ·ະհ೰‫͂ا‬κΦ΍ͼΠ İ ζ·υέ͹Ȝΐ΍ήΓΛΠ
ɛࣽୌġຮဎȂ୤िġၦঃგ‫ظ‬५ࡇၛ֓‫ش‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬‫ۍ଻ݢ‬છ࢓߲͈৽ພ֦͉‫ۍ‬൲ྤίρȜ·͈ະհ೰‫̧֨ͅا‬௽̩ίρȜ·෫Ⴈ̜́ͥȃِș͉̭͈֚Ⴒً͈೾̤̫ͥͅౙ‫ݩ‬΍ήΓΛΠ͈‫۾‬ဓ̞̾̀ͅ࠿൦̧̱̹̀ȃ୶̴Ȃհ೰‫ޛ‬૤છۛ৪ķĲྴͬచયͅȂྎઑࠬౙ‫ݩ‬΍ήΓΛΠ͈໦ືအ৆͂ŮŶŭŵŪĮťŦŵŦŤŵŰųġŤŰŮűŶŵŦťġŵŰŮŰŨųŢűũźġĩŎŅńŕĪ࠿औͤ͢ͅ൳೰
̯̹ͦະհ೰ίρȜ·ĩίρȜ·ńŕ౵͈೩‫͍̤͢ئ‬İ̹͉͘ု଻ςκΟςϋΈͬྖ̹̳͈͜Ī͈͂‫۾‬Ⴒͬ࠿൦̱̹ȃ̷͈ࠫ‫ض‬Ȃ੏۪ࠬಎńŅĲĵĬńŅĲķĬౙ‫ݩ‬ତ͈௖చഎ௩‫ۍ͉ح‬൲ྤະհ೰ίρȜ·͈ంह̤͍͢ତ͂ခփͅ‫۾‬Ⴒ̳̭ͥ͂ͬྶ̥̱̹ͣͅȃষͅະհ೰‫ޛ‬૤છۛ৪ĵķྴͬచયͅȂౙ‫ݩ‬΍ήΓΛΠ
͈ఉအ଻͂‫ۍ‬൲ྤίρȜ·଻ે͈͂‫۾‬Ⴒ͙̹ͬȃ‫ۍ‬൲ྤίρȜ·͈଻ેບ‫͉ͅث‬ŰűŵŪŤŢŭġ ŤŰũŦųŦůŤŦġ
ŵŰŮŰŨųŢűũźġ ĩŐńŕĪͬဥ̞̹ȃίρȜ·෫Ⴈ߲͂๱෫Ⴈ߲ͅ໦႒̱̹̭͂ͧȂίρȜ·෫Ⴈ߲͉ĳĸྴȪĶĺĦȫȂ๱෫Ⴈ߲͉ĲĺྴĩĵĲĦĪ͙̹ͣͦͅȃౙ‫ݩ‬΍ήΓΛΠ͈͂‫۾‬Ⴒ͙̹ͬࠫ‫ض‬ȂίρȜ·෫Ⴈ߲͉๱
෫Ⴈ߲ͅ๤̱ȂခփͅńŅĲĵĬńŅĲķĬౙ‫ݩ‬ତ̦ࣞ౵̜̹́̽ȃ༷֚ȂńŅĲĵĬ ńŅĲķȽౙ‫ݩ‬ତ͉ίρȜ·෫Ⴈ͈ခྫ͂ခփ̈́‫۾‬Ⴒͬ෇̥̹͛̈́̽ȃِș͉̹͘Ȃ
ౙ‫۾ͅا଻ڰ͈ݩ‬ဓ̳ͥŕŰŭŭĮŭŪŬŦġ ųŦŤŦűŵŰųġ ĵ͈อ࡛τασ̦‫଻ݢ‬૤޼ࢸणۛ৪ဇြ͈ńŅĲĵĬńŅĲķĬౙ‫ݩ‬ळ༾ນ࿂́ࡐಠͅ௩‫̹̱̥ͣͅྶ̭̞̱ͬ͂ͥ̀ޑ‬ȃ̹͘Ȃ࿪໤ٚව͈۷ത̥ͣȂະհ೰‫ޛ‬૤છۛ৪́‫ۍͅܢ଻ݢ‬൲ྤࠁ଼੅ĩőńŊĪͬঔ࣐̱Ȃठᚇၠ଼̱ࢗͅ
̹ĵıછ႕ͬచયͅȂΑΗΙϋࠏ࿪सൎဓͥ͢ͅྎઑࠬౙ‫ݩ‬΍ήΓΛΠ̤͍͢‫ۍ‬൲ྤ͈஌֋଻๭྄࢚
ĩŐńŕͬဥ̞̀௶೰Īͅ‫࠿ͬض̳͖࢘ݞ‬൦̱̹ȃ̷͈ࠫ‫ض‬ȂΑΗΙϋࠏ࿪स͈ൎဓ͉ńŅĲĵĬńŅĲķĬౙ‫ݩ‬ͬခփͅ೩‫̵̹̯ئ‬ȃ̹͘Ȃ஌֋଻๭྄࢚͈་‫͉ا‬ńŅĲĵĬńŅĲķĬౙ‫͂ݩ‬ခփ̈́໅͈௖‫̹͛෇ͬ߸۾۾‬ȃոષͤ͢Ȃྎઑࠬౙ‫ݩ‬΍ήΓΛΠȂඅͅńŅĲĵĬńŅĲķĬౙ‫͉ݩ‬Ȃະհ೰ίρȜ·͈൳೰̤͍͢࿪໤হၷ
͈࢘‫ض‬฻೰ͅ‫̱̀۾‬Ȃ࿹̹ͦΨͼ΂ζȜ΃Ȝ̈́ͤͅංͥ‫خ‬ෝ଻̦াऐ̯̹ͦȃ䋭 㪎㪏 䋭

ႉ઄ŔĮĲĮĵ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

ŎœŊ ͥ͢ͅະհ೰ίρȜ·͈ບ‫ث‬

Ĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬Ȃĳ ૧ࡣٖພ֭੏۪‫ܕ‬ඤ‫ش‬ΐϋΈ̥ͣอജ̱̹ȃŕĲ‫ْ಺ޑ‬௨Ȃŕĳ‫ْ಺ޑ‬௨̱̩͉͜ίυΠϋྟഽ‫ْ಺ޑ‬௨ͅŅŰŶţŭŦġ ŊůŷŦųŴŪŰůġ
œŦŤŰŷŦųźġ őŶŭŴŦͬঀဥ̳ͥȪţŭŢŤŬġ ţŭŰŰť༹ȫ̭͂́Ȃᴢ൲ྤࠬ‫ۯ‬༃̦ࣞ૞࣢ͅຝ੄̯ͦͥȃŎŰŰťź͉ͣᴢ൲ྤඤ྄ญၗ੅ஜ͈છ႕ͬ๱௮‫ג‬ŕĲ‫༹́಺ޑ‬ज़௨̱Ȃ̷͈ࣞ૞࣢͈ంह͉łŉł ĩłŮŦųŪŤŢůġ
ũŦŢųŵġ łŴŴŰŤŪŢŵŪŰůĪġ ŵźűŦġ ŗŊȪŤŰŮűŭŪŤŢŵŦťġ ŢŵũŦųŰŮŢȫͅచ؊̱Ḁ̑̾ड߃͈ෞ‫ࠬݹ‬છછે͂‫̩ޑ‬௖‫۾‬̳̭ͥ͂ͬা̱̹ˍĪȃ‫ۍ‬൲ྤ̤̞̀͜ͅᴢ൲ྤ͂൳̲ΏȜΉϋΑ̦ဥ̞ͣͦȂ૧ࡣٖພ͈֭ΈσȜί̦ไဥĲįĶŕġ ŎœŊͬဥ̞̀ĳııķාͅĴŅĮ๱௮‫ג‬ŕĲ‫ْ಺ޑ‬௨ͥ͢ͅ‫ۍ‬൲ྤίρȜ·ͼιȜΐϋΈ଼̱̹ࢗͅȃ̷̱̀Ȃ̭͈๱௮‫ג‬ŕĲ‫ْ಺ޑ‬௨́ࣞܵഽͅຝ੄̯ͦͥίρȜ·ͬŉźűŦųĮŪůŵŦůŴŦġ őŭŢŲŶŦġ ĩŉŊőĪ

ု଻ςκΟςϋΈȪűŰŴŪŵŪŷŦġ ųŦŮŰťŦŭŪůŨȫȂ೩̞ńŕ౵ȪĴıġŉŖྚྖȫȂŊŗŖŔ́‫ࡘ̞ޑ‬ଚ΀΋Ȝͬ೮̳ͥ̈́̓ȂŎŅńŕ͈ࡄ‫́ݪ‬ະհ೰ίρȜ·ͬাऐ̳ͥਫ਼ࡉ֚͂໐ਹໝ̳ͥඅಭͬခ̱̞̹̀ĳȫȃ೒ુȂ൲ྤ

口頭発表͂ઠ̱̞̀ͥȃ̯ͣͅ‫ۍ‬൲ྤ͈ŉŊő͈අಭ͉ո‫ͅئ‬া̳ਫ਼ࡉ͂‫۾̩ޑ‬Ⴒ̳̭̦ͥ͂฻ྶ̱̹ȃ̳̻̈́ͩȂ

会長招待講演 シンポジウムŎœŊͬဥ̞̹൲ྤࣁ‫ْ͈ا‬௨૷౯͉Ȃߗ‫ۼ‬໦ٜෝ͞చયࠬ‫͈ۯ‬අಭ̥ͣȂᴢ൲ྤ͈ίρȜ·ͼιȜ

特別講演ɛ࿤࢛ġᔐຳ ĲȂ୼ॄġ࿻ဉ ĳȂ୞ࡔġୃহ ĲȂ઀୼ġ‫ݛ‬ဎ ĲȂհനġ௛ Ĳ

ࣁ‫ا‬ίρȜ·͉ζ·υέ͹Ȝΐ͞‫׶‬છळ༾ฺ̠ͬডৗȪডৗ΋ͺȫ̷͂ͦͬໞ̠஌֋଻๭྄Ȃ̯ͣͅ୞ȪŅŕŊȫ͂ࡤ͍Ȃࣞ૞࣢̦๤‫ڛ‬എ૧̱̞ࠬ஀̜̞͉ͥࠬਆͬນ̳̱̞ͩ͂̀ͥȃ൚ΓϋΗȜ͈ࠐࡑ͉́Ȅࠛ൲ྤίρȜ·̤̞̀ࣞͅ૞࣢ͬা̳͈͉ডৗ͂੄̦ࠬईह̳ͥાࣣ̦ఉ̩Ȃຈ̴̱ࠬ͜஀ࠬ͞ਆ̦ం
ह̱̩̈́̀ࣞ͜૞࣢ͬা̳ાࣣ͜ࠐࡑ̱̤̀ͤŕĲ‫༹̫̤ࣞͥͅ಺ޑ‬૞࣢͈૯͈ࡔ֦͉ྚٜࠨ̜́ͥȃࣽࢃȂ‫ۍ‬൲ྤŉŊő̦ະհ೰ίρȜ·͈‫ޑ‬ႁ̈́ŴŶųųŰŨŢŵŦȁŮŢųŬŦų̠̥̯̈́ͤͥͣ̈́ͥͅࡄ‫̦ݪ‬ຈါ̜́ͥȃུΓΛΏοΰ͉ȂŎœŊͬဥ̞̹‫ۍ‬൲ྤίρȜ·ບ‫̞̀̾ͅث‬ᴢ൲ྤίρȜ·͈౶ࡉͬ‫ٽ̀͛܄‬୰̧̱̞̹̞̀ȃ

ポスター発表 ＹＩＡ選考発表‫̦஀ࠬ͞ا٭‬ईह̳ͥࠁ́ంह̳ͥȃŎŰŰťź͉ͣȂ๞̦ͣဥ̞̹ŕĲ‫༹ͬ಺ޑ‬ťŪųŦŤŵġŵũųŰŮţŶŴġŪŮŢŨŪůŨ

著者索引

䋭 㪎㪐 䋭

ႉ઄ŔĮĲĮĶ

ΑΞϋΠࢃ͈ੱ‫ۯࠬٺ‬༃͈‫׶‬છ͂ਘ໘‫ܥ‬ഢɛՒ໐ġ্჊
ᜥ‫ش֓ފ‬ఱ‫ڠ‬૤௫Ȇࠬ‫ۯ‬ඤ‫ش‬࿪सဣ੄଻ΑΞϋΠĩŅņŔĪ͉ठ‫ޛ‬ॏͬಠ̱̩ࡘઁ̱̹̦ಿ‫ܢ‬ထࢃͬຈ̴̱͜٨஝̱͉̞̞̀̈́ȃठ‫ޛ‬ॏ͈‫ܥ‬੬͉৽̱͂̀ࠬ‫ۯ‬໹‫޼ڲ‬ळ༾͈௩૓͞ळ༾‫ٸ‬ζΠςΛ·Α͈௩୆ͥ͢ͅ૧୆ඤ྄௩૓̜́ͤȂ‫׶଻ݢ‬છ฽؊̧̦֨߄̭͂̈́̽̀ܳͥੱ‫઼ً͈ۯࠬٺ‬ਘ໘฽؊̜́ͥȃੱ‫͈ۯࠬٺ‬ਘ໘ً೾̤̞̀ͅठඤ๧‫ا‬Ȃ̳̻̈́ͩࠬ‫ۯ‬ඤ๧͈ठ୆͉ୃુਘ໘ͅຈଌ͈ίυΓΆ̜ͥȃठ୆ࠬ‫ۯ‬ඤ๧ळ༾͈֚໐͉
ࣸଡဇြ͈ඤ๧ஜߐळ༾͈໦‫̢̞ͥ̀ͦͣࣉ͈͂ͥ͜͢ͅا‬ȃ༷֚ठ‫ޛ‬ॏ̤̫ͥͅ௩૓໹‫޼ڲ‬ळ༾̷͈֚͜໐͉໹‫޼ڲ‬ஜߐळ༾ဇြ̜́ͥȃŅņŔ̷͉͈ນ࿂͈࿪໤̦໹‫޼ڲ‬ळ༾௩૓ͬဲ̢̭ͥ͂́ठ‫ޛ‬ॏͬထཡ̳̦ͥȂ‫׶͈ܢ଻ݢ‬છ฽؊ဲଷ͜ठ‫ޛ‬ॏထཡ֚ͅ࿨ͬ౜̠ȃ̱̥̱‫ޑ‬ႁ̈́‫׶‬છဲଷ࢘‫̷͉ض‬͈ࢃ͈ठඤ๧‫ا‬ည൵ͬ͜ဲ̢Ȃ୆ၑഎࠬ‫ۯ‬ਘ໘ͬఅ̠̹̈́͛Ȃ‫׶͉ͅܢڞ׿‬છ̦ठී̳ͥ‫خ‬ෝ଻̦ࣉ̢ͣͦͥȃ̹͘ŅņŔ̤̫ͥͅ‫׶‬છ͈ठී͉ͅΑΞϋΠນ࿂ͅ࿪स̵ࣣ̯̹͈ͬࠫͥ͛εςζȜ͈ంह͜‫̳ͥ߸۾‬ȃِș͉‫ۍ‬൲ྤΑΞϋΠࢃ‫ޫۯࠬٺੱ͈ܢ଻ݢ‬ਫ਼͈‫׶‬છ‫ܥ‬ഢ͂ࣸଡۚळ༾͈൲֥̤͍͢ၰ
৪͈‫ͬ߸۾‬۷ख़̱Ȃ‫̫̤ͥͅܢڞ׿‬ठඤ๧‫ا‬Ȇ૧୆ඤ྄௩૓͈໦ঊ‫࠿ͬࢹܥ‬൦̱̹ȃ̷͈ࠫ‫ض‬αͺιΗσΑΞϋΠĩŃŎŔĪၣ౾ࢃ͉ͅ‫ۍ‬੏۪ඤ́ĳ඾ࢃͬάȜ·̳͂ͥࢡಎ‫ݩ‬ນ࿂ષ͈ͼϋΞΈςϋŎŢŤĮĲ͈‫̦ا଻ڰ‬Ȃྎઑ͉ࠬ́ĸ඾ࢃͬάȜ·̳͂ͥńŅĴĵု଻ࣸଡۚळ༾͈௩‫̦ح‬۷ख़̯̹̦ͦȂΏυςθΑ
ဣ੄଻ΑΞϋΠĩŔņŔĪၣ౾ࢃ̴͉̞́ͦ͜ಠ̱̩ဲଷ̯̹ͦȃ̹͘ŃŎŔၣ౾ࢃͅ۷ख़̯̹ͦĸ඾ࢃ͈ྎઑࠬۚळ༾͈ńŅĴĲု଻ඤ๧အळ༾͈͒໦‫ا‬ȂϷĮŔŎłု଻໹‫޼ڲ‬အळ༾͈͒໦‫̦ا‬ŔņŔၣ౾ࢃ̴͉̞
ͦ͜ဲଷ̯̞̹ͦ̀ȃষͅŔņŔၣ౾Ĳාࢃ͈ठ‫ޛ‬ॏ႕̤̞̀ͅͺΞτ·ΠηȜĩŅńłĪ́ං̹ͣͦழ૕ͬ
ŃŎŔၣ౾฼ාࢃ̷͈ͦ͂๤‫̭̹̱ͧ͂ڛ‬ȂńŅĵĶု଻ŕςϋΩ‫ݩ‬ȂńŅķĹု଻ζ·υέ͹Ȝΐ͈૫੕̦ခփͅ‫ͬض̠̞̞ࠫ͂ޑ‬ං̹ȃ̹͘లඵଲయ͈ŅņŔ̜́ͥΖΗυςθΑဣ੄଻ΑΞϋΠĩśņŔĪၣ౾ĵ΃࠮ࢃ͈ཎ࠿႕̤̞̀͜ͅΑΠρΛΠͅ୪̱̀ࣞഽ͈‫׶‬છ฽؊̦۷ख़̯̹ͦȃ̭͈ͦͣࠫ‫̥ͣض‬ŅņŔၣ౾ࢃ͉ੱ‫͈ۯࠬٺ‬ਘ໘ً೾͈ಁ‫װ‬Ȃ̱̩͉͜ະۖ஠হ࿴̥ͣ‫׶‬છ฽؊̦‫ͅܢڞ׿‬ठීȂ஗‫̭̳ͥاװ‬̦͂াऐ̯̹ͦȃ䋭 㪏㪇 䋭

ႉ઄ŔĮĲĮķ

ɛനࡔġ୹ࢩȂനࡔġකঊȂུఉġၮฎȂ૧നġၻგȂ঱ޮġ‫ܮ‬ဢȂࢾ࢛ġηΦςȂࣽஂġ༓Ȃ
໛ུġ݅ࢬ

特別講演

ŇŅňĮőņŕİńŕġͬဥ̞̹൲ྤࣁ‫̫̤ͥͅا‬໦ঊພఠ͈ບ‫ث‬ġȽ‫ۍ‬൲ྤ͈͒؊ဥ͈‫خ‬ෝ଻Ƚ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine‫ݛ‬ၣༀఱ‫ڠ֓ڠ‬໐ඤ‫࣒ڠش‬ज૤௫Ȇࠬ‫ۯ‬ඤ‫ش‬໐࿝ŦŮŪŴŴŪŰůġ ŵŰŮŰŨųŢűũźĻġ őņŕĪ͉Ȃ૤޼ŷŪŢţŪŭŪŵź͈ບ‫̴ͣ̓͂͘ͅث‬Ȃະհ೰ίρȜ·ͬຝ੄̳̭ͥ͂
̦‫خ‬ෝ̈́૧̱̞໦ঊͼιȜΐϋΈ̱͂̀อജ̱̞̀ͥȃِș͉ȂŇŅňĮőņŕ͂ńŕ͈ဏْࣣ௨ͬဥ̞̀
ᴢ൲ྤ͞ఱ൲ྤ̤̫ͥͅίρȜ·͈‫׶‬છ‫ڰ‬൲଻ͬ๱۷ࠬഎͅຝ੄Ȃ̷͈‫ڰ‬൲଻ͬ೰ၾ‫̱ا‬ȂΑΗΙϋ͞ͼϋΑςϋ೷ࢯ଻٨஝࿪ͥ͢ͅ࿪໤ၷ༹͈࢘‫خͬض‬ণ‫̱̀ا‬ບ‫خ̦̭̳͂ͥث‬ෝ̜̭́ͥ͂ͬ༭
̧̱̹࣬̀ġĩŋġłŮġńŰŭŭġńŢųťŪŰŭĭġŋłńńġńŢųťŪŰŷŢŴŤġŊŮŢŨŪůŨĭġņŶųġŉŦŢųŵġŋĭġŋġŏŶŤŭġŎŦťĪȃ̱̥̱̦̈́
ͣȂŇŅňĮőņŕ͈‫ۍ‬൲ྤພ་͈͒؊ဥ͉૤޼͈ŇŅňਬୟ͞ߗ‫ۼ‬໦ٜෝ͈̈́̓࿚ఴͤ͢ͅ؊ဥ̦ଷࡠ̯
̧̹ͦ̀ȃུΓΛΏοΰ͉ȂĲįஜੜ౾ͤ͢ͅ૤޼͈ŇŅňਬୟͬဲଷ̳̭̦ͥ͂‫خ‬ෝ̥ŀ ĳį ŇŅňĮພ་ͅచ̳ͥ࿪໤ၷ༹͈࢘‫ض‬฻೰̦‫خ‬ෝ̥ŀ ĵį ࣽࢃ͈࿚ఴത͞ജབ̞̾̀ͅ࠿൦̳ͥȃུࡄ‫͉ݪ‬Ȃ̭ͦ́͘ͅ‫ۍ‬൲ྤພ་ͅଷࡠ̧̯̹ͦ̀ŇŅňĮőņŕ͈؊ဥͬஜૺ̵̯ͥ‫خ‬ෝ଻̦̜ͥ͂ࣉ̢ͣͦͥȃ̯ͣͅȂ

口頭発表őņŕİńŕͬဥ̞̀‫ۍ‬൲ྤພ་͈ŇŅňਬୟͬບ‫خ̦̭̳͂ͥث‬ෝ̥ŀ Ĵį ŇŅňĮőņŕİńŕͬဥ̞̀‫ۍ‬൲ྤ

会長招待講演 シンポジウム߃ාȂĲĹŇດেŧŭŶŰųŰťŦŰŹźŨŭŶŤŰŴŦġ ĩŇŅňĪġ ͬΠτȜ΍Ȝ̱̹͂εΐΠυϋ౯௄ज़‫ג‬ġ ĩűŰŴŪŵųŰůġ

߃ා͈őņŕġŵŦŤũůŰŭŰŨź͈อജ̞̾̀͜ͅ༭̳࣬ͥȃ

ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪏㪈 䋭

ĺ࠮ĳķ඾Ȫ࿐ȫġĲĶĻĲıȡĲĸĻĲıġġలˎٛાΏϋεΐ;θġႉ઄ ŔĮĳȶࢯࠬ஀ၷ༹͈ΠάΛ·Αȷġġႉ઄ŔĮĳĮĲ

๱༕྄છ଻૤པळ൲ۛ৪ͅచ̳ͥ૧̱̞ࢯާࡥ࿪͈պ౾̫̿
ɛୄକġખ඾ུ֓‫ش‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬૤པळ൲͈࿪໤হၷ͉ͅȂอैͬထཡ̱൸಺ၙ֋঵̰̳ͬ͛ςΒθ΋ϋΠυȜσ͂Ȃ૤པळ൲͉ယ
෇̱૤ฏତ಺୯͉̥ͬͥτȜΠ΋ϋΠυȜσহၷ̦̜ͥȃ༷֚́Ȃ૤པळ൲࿪໤হၷ͈̠͈֚̾͜ಔ͉Ȃऒཔඤࠬ஀ͥ͢ͅ૤ࡔ଻ण஀છͬထཡ̳̭̜ͥ͂́ͥȃඅͅ૤ࡔ଻ෞࢸणͬอછ̳ͥ͂୆ྵ̥̥ͩͅ
ͥ‫̜̦ͤࡏܓ‬Ȃ̹͘ŒŐō̦ಠ̱̩೩‫̳ͥئ‬ȃ̭ͦ́͘฼ଲ‫͈ܮ‬ಿ̧ͅളͤ૤པळ൲ۛ৪͈૤ࡔ଻ෞࢸ
णထཡ͉ͅχσέ͹ςϋ̦ဥ̞ͣͦȂఱܰ࿅ࡄ‫଼ͥ͢ͅݪ‬ୡ͉́Ȃχσέ͹ςϋ͉૤ࡔ଻ෞࢸणͬĲİĴͅࡘ̳̭̦ͣ͂બྶ̯̞ͦ̀ͥȃ̱̥̱Ȃ೰‫ܢ‬എ̈́őŕĮŊŏœΙͿΛ·͈ຈါ଻͞Ȃ૙মଷࡠȂఈ͈࿪स͂
͈௖ࡽैဥ͈̈́̓‫ۯ‬ၑ͈๏ॠ̯̦̜ͤȂ૤པळ൲ۛ৪̤̞̀ͅχσέ͹ςϋͥ͢ͅࢯާࡥၷ༹̦਱໦
ͅຽ‫̞࡞͉̞̱͂ͥ̀ݞ‬ඳ̥̹̽ȃ̭͈̠̈́͢ે‫̥͈̈́ޙ‬Ȃ૧̱̞ैဥ‫ܥ‬੬͈ࢯާࡥ࿪̱͂̀ೄ୪ΠυϋΫϋஷ‫ٺ‬स͈ΘΫ΄ΠρϋȂలřŢ֦ঊஷ‫ٺ‬࿪͈ςΨȜυ΅΍Ψῧͺά΅΍Ψϋ̦̦࣭̤̞ͩͅ
̀ႉ઄ঀဥ੄ြ̠ͥ̈́ͤ͢ͅȂୟޭഎ̈́ࢯާࡥၷ༹̦৘ঔ̯͈ͦͥ͂͜‫ܢ‬ఞ̯̞ͦ̀ͥȃ̱̥̱Ȃ૧ܰࢯާࡥ࿪̦ঀဥ̧̠́ͥ̈́̽̀͢ͅĳාဒ̦ͤࠐً̱̹̦Ȃ૧ܰࢯާࡥ࿪̢̞͂̓͜ȂාႢȂఘਹȂଅ‫ܥ‬ෝ͈̈́̓ςΑ·ͬࣉၪ̱̹૥ਹ̈́ঀဥ̦ຈါ̧̜̞̠̭̥̹́ͥ͂͂ͩ̽̀͜ȃ૧ܰࢯާࡥ࿪͈ಎ́
͈ঀ̞໦̫̞͉̾̀ͅȂœņĮōŚȂœŐńŌņŕĮłŇȂłœŊŔŕŐŕōņদࡑ͈ࠫ‫ͬض‬਱໦ͅ࠿બ̳ͥ͂͂͜ͅȂ̭͈ͦͣςΑ·ͬ‫ې‬մ̱̹ঀဥ̧̭̭̦̫͓̜ͬͧͥ́ͥȃ̹͘Ȃ฼ࡘ‫̴͈̞̦ͦܢ‬૧ܰࢯާࡥ࿪͜Ĳĳশ‫ۼ‬ஜࢃ͕͖͂൝̴̱̞̥̥ͩͣ͜ͅȂ໚ဥ̦Ĳ඾Ĳٝ͂ĳ̦̜͈֑̞ٝͥ̈́̓͜ࣉၪ̳ͥຈါ̦̜
ͥȃ̭͈ͦͣ૧ܰࢯާࡥ࿪ͬͤ͢ఉ̩͈ႉ઄֓ͅഐୃͅຽ‫̵͉̹̩̞̯͛̀ͅݞ‬Ȃ୺࿝̦̭͈֓࿪स
̞̾̀ͅ౶ͤȂঀ̞༷ͬࣉ̢Ȃഥ̢̞̩̭̦̀͂ਹါ͂এͩͦͥȃུ࣒‫͉́׵‬Ȃ̭͈̠ͦ́̓̈́ۛ͘͢
৪ͅ૧ܰࢯާࡥ࿪ͬൎဓ̱Ȃ͈̠̓̈́͢തͬಕփ̱̞͈̥̀ͥȂ̞̹͂̽തͬત̳ٚͥ͂͂͜ͅȂ૧̱̞শయ̢ͬࠞͥࢯާࡥၷ༹͈͒‫ܢ‬ఞ͂ࣽࢃ͈‫ه‬ఴ̞̾̀ͅત̱̹̞ٚȃ䋭 㪏㪉 䋭

ႉ઄ŔĮĳĮĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine૤ࡔ଻ෞण஀છ͈‫ܢ଻ݢ‬হၷ͂ठอထཡ
特別講演ɛ໹࿤ġચ෗
ఱ໦ఱ‫ڠ֓ڠ‬໐૰ࠐඤ‫࣒ڠش‬जͥࢯࠬ஀ၷ༹͈ΠάΛ·Α͉ȂĩĲĪġ ųŵĮőł୓ಕၷ༹ȪŊŗġ ųŵĮőłȫ͈হၷ‫ٳ‬ই‫خ‬ෝশ‫ۼ‬ȪŕŕŘȫ̦ĵįĶশ‫͘ۼ‬́‫װ‬ಿ̯̹̭ͦ͂ȂĩĳĪġ ठอထཡ͈΂ίΏοϋͅ૧ܰࠐ࢛ࢯާࡥ࿪ȪŏŐłńȫ̦‫ˎ͈̭̹͂̽ͩح‬തͅਬ࿩̯ͦͥȃ
Ⱥ‫ܢ଻ݢ‬হၷȻ൚੝ȂŊŗġųŵĮőł͈ŕŕŘ͉ŏŊŏŅŔদࡑȪĲĺĺĶȫͅ‫̧̿ܖ‬Ĵশ‫ͅۼ‬୭೰̯̹̦ͦȂņńłŔŔĴȪĳııĹȫ́ĴȡĵįĶশ‫͈ۼ‬ෞࢸण͈͒ခ࢘଻̦া̯ͦȂ؎ਗ͉́ĳııĺා͈΄ͼΡρͼϋ٨ഁ̥ͣŕŕŘġ ĵįĶশ‫ུ͈́ۼ‬ၷ༹ͬଔ੻̱̞̀ͥȃ඾ུ͉́ŋĮłńŕȪĳııķȫ͈ࠫ‫̀̽ͬ͜ض‬Ŋŗġ ųŵĮőł̦෇‫خ‬̯ͦȂঌ์ࢃႉ઄দࡑġ ŋĮłńŕġ ŊŊȪĳıĲıȫ͞ঌ์ࢃ஠࣭಺औġ ŋĮŎłœŔȪĳıĲıȫ̷͈̽̀͢ͅခ࢘଻Ȇհ஠଻̦‫̞̯ͥ̀ͦ෇ږ‬ȃ̷͈ࢃȂĳııĺාͅ඾ུෞ௾ಎ‫ڠ‬͉࢚ٛႻજͅచ̱ŕŕŘġ ĵįĶশ‫͈͒ۼ‬་ࢵփࡉͬ

లඵๅȷ̦࢖ນ̯ͦȂ૧̹̈́শ‫ۼ‬იͅ௱̹̽ഐୃঀဥͬ߼อ̱̞̀ͥȃȺठอထཡȻ‫͈ܢ଻ݢ‬ठอဲଷͬ
࿒എ̱͂̀ࢯާࡥၷ༹̦৘ঔ̯̞ͦ̀ͥȃĲ඾ĶĭıııȡĲıĭıııౙպ͈ΰΩςϋ঵௽ൎဓ࣐̞ͬȂχσέ͹

口頭発表೹੄̱ȂĴා಼͈ૣ݈ͬࠐ̀ĳıĲĳාĹ࠮ͅŕŕŘ‫װ‬ಿ͈࢖౶૭୏̦෇̹͛ͣͦȃĲı࠮͉ͅȶഐୃহၷঐૻ

会長招待講演 シンポジウム૤ࡔ଻ෞण஀છ͉Ȃෞࢸण஠ఘ͈࿩ĲİĴͬ୸͛Ȃఉ̩͉๱༕྄છ଻૤པळ൲֦̳ܳͥͅȃུછ̤̫ͅ

ςϋͬே೰֋঵ၾ̥ͣ‫ٳ‬ইȂဥၾ΋ϋΠυȜσ࣐̞ͬȂőŕĮŊŏœ̦হၷ‫֖ͅࡠئ‬ව̹̭̽͂ͬ‫̹̱෇ږ‬ͣତশ‫͉ͅࢃۼ‬਱໦̈́࢘‫ͬض‬อ‫̳ͥܞ‬ȃ̱̹̦̽̀ඤ໚‫خ‬ෝ̜́ͦ͊ΰΩςϋͬঀဥ̳̭̩ͥ͂̈́‫ݢ‬଻‫̥ͣܢ‬ठอထཡͅ֊̧࣐́Ȃह֭඾ତౣੀ்͞‫ܢ‬ςΧΫς͈͒໛‫̞ͥ̀̽̈́͂إ‬ȃ̱̥̱œņĮōŚ͞œŐńŌņŕĮłŇ͉́อછĲĵ඾ոඤȂłœŊŔŕŐŕōņ͉́อછĸ඾ոඤ͈‫ܢ଻ݢ‬છ႕͉చય̥ͣੰ‫̯̀ͦٸ‬̤ͤȂ඾ུ͈́ঀဥࠐࡑͬ೒̱̀հ஠଻Ȇခ࢘଻ͬ࠿બ̱̞̩̭̦̀͂‫̞ͥ̀ͦͣ͛ݥ‬ȃ

ポスター発表 ＹＩＡ選考発表শത́ΰΩςϋਞၭ๊̳͈̦֚͂ͥഎ̜́ͥȃĳıĲĲා̥ͣષঌ̯̹ͦŏŐłń͉Ȃ̴̞ͦ͜੝ٝඤ໚̥

著者索引

䋭 㪏㪊 䋭

ႉ઄ŔĮĳĮĴ

๱૤ࡔ଻ෞࢸण͈͒ࢯࠬ஀ၷ༹
ɛ்୼ġۚ૽
࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜෞࠬ‫ۯ‬ඤ‫ش‬ෞ௾ಎহၷ΄ͼΡρͼϋĳııĺ͉́Ȃ๱૤ࡔ଻ෞࢸणȪͺΞυȜθࠬ஀଻ෞࢸणȂρ·΢ࢸणȫठอထཡ̱͂̀ȂͺΑάςϋȂ·υάΡΈτσȪΙ·υάΐϋȫȂΏυΑΗΖȜσͥ͢ͅࢯࠬ઀โၷ༹̦ଔ੻̯
̞̦ͦ̀ͥȂͺΑάςϋౙसၷ༹‫͈ئ‬છ࢓଻ࠛ൲ྤ̹͉͘൮‫ڀ‬ඤ൲ྤࣞഽ‫ޛ‬ॏ̤̫ͥͅठอၚ͉‫ڎ‬ĳķįĲĦİĳාġ ĩŏłŔńņŕĪȂĲĹĦİාĩŘłŔŊŅĪ͂ࠨ̱̀೩ၚ͉̩́̈́Ȃෞࢸण‫͈ܢ଻ݢ‬ͺΑάςϋൎဓ͜ခ͈͈࢘̈́͜ŏŏŕġĲĲĲ͂Ȃ̷͈࢘‫̢̧̞̞͉͈̈́͂ͥ́͜௷ྖ͉ض‬ȃ̷͈̹͛Ȃ‫ࣞ͞ܢ଻ݢ‬ഽ‫ޛ‬ॏພ་൝͈ठอࣞςΑ·႕̤̫ͥͅఉस໵ဥࢯࠬ઀โၷ༹͈ခ࢘଻̦ౝ̧̯̹॑ͦ̀ȃͺΑάςῧ·υάΡΈτσ͈໵ဥȪŅłőŕȫͬͺΑάςῧ๤‫̹̱ڛ‬ńłœņŔŔȪછ࢓଻ࠛ൲ྤ‫ޛ‬ॏછ̦చયȫ̜̞͉ͥńōłŊœȪછ࢓଻൮‫ڀ‬ඤ൲ྤ‫ޛ‬ॏ̦చયȫ͉́ȂŅłőŕͥ͢ͅࠐ൮‫ڀ‬Ρίρ̤̫ͥͅ๷઀஀ঊΏΈ΢σ͈ခփ̈́೩ࡘͬ෇͛Ȃછ࢓଻൮‫ڀ‬ඤ൲ྤࣞഽ‫ޛ‬ॏͅచ̱Ņłőŕͬ‫͚܄‬ඤ‫ش‬হၷ͂ࠬ‫ۯ‬ඤহၷͬ๤‫̹̱ڛ‬ŔłŎŎőœŊŔ͉́Ȃඤ‫ش‬হၷͥ͢ͅෞ௾ಎİঘཌၚĲĳĦİා͂ŘłŔŊŅͤ͢ၻࢡ̈́Ȫ̥̾ࠬ‫ۯ‬ඤহၷͅ࿹ͥȫ଼ୡ̜̹́̽ȃŇłŔŕņœ͉́อછĳĵশ‫ۼ‬ոඤ͈ࠚછෞࢸणİŕŊł̤̞̀ͅȂĺı඾‫ͼ଻஀͈ࠬۼ‬αϋΠİঘཌၚ͉Ņłőŕ́೩ၚ̈́߹̜̹࢜́̽ȃͺΑάςῧΏυΑΗΖȜσ͈໵ဥ̞͉̾̀ͅȂછ࢓଻൮‫ڀ‬ඤ൲ྤ‫ޛ‬ॏͬచય̱̹͂ŕŐŔŔȪͺΑάςῧ͈๤‫ڛ‬ȫȂŕŐŔŔĮĳȪŅłőŕ͈͂๤‫ڛ‬ȫͤ͢ͅΏυΑΗΖȜσ͈‫ޛ‬ॏૺ࣐ဲଷİ٨஝࢘‫̦ض‬াऐ̯̹̦ͦȂŎœŊͥ͢ͅ૧ܰ‫ࠬݹ‬ພ་͈੄࡛͉Ņłőŕ́ͤ͢೩ၚ̈́߹࢜
̜̹́̽ȃ༷֚́Ȃࢯࠬ઀โၷ༹ͅ‫۾‬Ⴒ̱̹ෞ੄͉̦࣭ࠬͩ́஠ෞ੄͈ࠬĲȡĳ‫̤ͤ̀͛୸ͬڬ‬Ȃྫণ̧̞́̈́ͼϋΩ·Πͬခ̱̞̀ͥȃŎłŕńŉ͉ෞࢸणȆŕŊłͬచયͅ·υάΡΈτσ͂Ņłőŕͬ๤‫̹̱ڛ‬œńŕ̺̦ȂŅłőŕ͈ࠬ஀଻ͼαϋΠٝ๰͈࿹պ଻͉া̴̯ͦȂ൮‫ڀ‬ඤ੄ࠬ൝͈੄ࠬ଻ͼαϋΠ͉ခփͅ௩‫̹̱ح‬ȃŔőŔĴ͉ρ·΢ࢸण̤̫ͥͅŅłőŕ͈ठอထཡ࢘‫ͬض‬ͺΑάςῧ๤‫̹̱ڛ‬œńŕ̜̦́ͥȂ͉ͤ͞࿹պ଻ͬা̵̴੄ࠬ଻ͼαϋΠİঘཌ̦௩‫̹̽̈́͂ض̳ࠫͥح‬ȃུ࣒‫͉́׵‬Ȃ๱૤ࡔ଻ෞࢸणͅ
చ̳ͥࢯࠬ஀ၷ༹̞̾̀ͅȂඅͅఉस໵ဥࢯࠬ઀โၷ༹͈ࢗऻͅઙത̜̦ͬ̀̈́ͣ‫ٽ‬୰̱̹̞ȃ䋭 㪏㪋 䋭

ႉ઄ŔĮĳĮĵ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine෹ࠬ஀ण஀છͅచ̳ͥࢯࠬ஀ၷ༹
特別講演ɛ५നġങ֚
२ਹఱ‫ڠ‬ఱ‫֭ڠ‬੏۪‫ܕ‬Ȇଅ௫ඤ‫ڠش‬࿪͉ྚ໦ْ͒Ωςῧχσέ͹ςΰ͈͙̜̹̽ȃၰ࿪स͂͜ͅ਱໦̈́হၷ࢘‫ͬض‬ං̹ͥ͛ͅອ͈ٝ
ࠬ‫࠿ס‬औͥ͢ͅൎဓၾ಺୯ͬါ̱̹ȃ̱̥̱ȂĳıĲĲාͅ૧̹̈́ࢯާࡥ࿪̱͂̀ঀဥ‫خ‬ෝ̹͂̈́̽έ΁ϋΘΩςΤ·Α͉୆໤‫ڠ‬എ၌ဥၚ̦̩ࣞȂఘਹͅਲ̹֚̽೰ၾ͈ൎဓ́਱໦̈́࢘‫̦ض‬ංͣͦȂࠬ‫࠿ס‬औͥ͢ͅဥၾ಺୯ͬຈါ̱̞̈́ȃ̹͘Ȃ૙ম͞ఈ͈࿪स͈‫͜ޣג‬਋̫̩̞̞̠͂ͅ၌തͬခ̱̞̀ͥ
̹͛Ȃུ৖͈ۛ‫ܢ଻ݢ‬হၷͬ۰༒‫̱ا‬ခ࢘̈́হၷ࿪̹͂̈́̽ȃొ̱Ȃ݃૷౲‫́ٴ‬ൎ࿪̳ͥાࣣ͞ଇ௸̈́
ࢯާࡥ࢘‫ͬض‬ါ̳ͥਹછ෹ࠬ஀ण஀છ͈ાࣣ͉ͅȂਲြ೒͈ͤྚ໦ْ͒Ωςϋ͈‫୓௸ݢ‬ಕ̦ഐ̱̞̀
ͥȃ̯ͣࠬͅ஀ဣٜၷ༹ͬຈါ̳̠͂ͥ̈́͢ਹછ෹ࠬ஀ण஀છͅచ̱͈̀࢘‫͞ض‬հ஠଻͉‫ږ‬ၛ̯ͦ̀ςΑ·ͬٝ๰̳̹͉ͥ͛ͅଅ‫ܥ‬ෝવ‫ࣞ͞ٺ‬Ⴂ৪ͅచ̳ͥࡘၾȆಎগ͜ਹါ̜́ͥȃ̯ͣͅಕ࿒̯ͦ̀
̞͈͉ͥ෹ࠬ஀ण஀છ͈হၷ࿪̱͂̀͜‫ٳ‬อಎ̜́ͥ૧ܰࠐ࢛ࢯřŢ࿪͈ςΨȜυ΅΍ΨϋȂ΀Ρ΅΍

口頭発表̴̤ͣȂ฼ࡘ‫̦ܢ‬ಿ̞̭͂͞ಎგस̦̞̭̈́͂ͤ͢Ȃൎဓஜ͈੄͈ࠬςΑ·ບ‫͜ث‬ਹါ̜́ͥȃ੄͈ࠬ

会長招待講演 シンポジウム෹ࠬ஀ण஀છͅచ̳ͥࢯࠬ஀ၷ༹͈ಎ૤͉ࢯާࡥၷ༹̜́ͤȂུཆ͉́ಿ̞‫ۼ‬Ȃঀဥ‫خ‬ෝ̈́ࢯާࡥΨϋȂͺά΅΍Ψΰ̜ͥȃ̭͈ͦͣ૧࿪̦ઇ෇̯ͦͦ͊Ȃ‫͈ܢ଻ྕ̥ͣܢ଻ݢ‬ठอထཡ́͘ࠑ௽ঀဥ

ण஀છ͈ࠚછ႕ͅచ̱͉̀ౣ‫ܢ‬ව֭Ȃ̱̩͉͜೩໦ঊၾ͒ΩςϋȪ෹ࠬ஀ण஀છ͈হၷ࿪ུ̱͉͂̀
ཆྚઇ෇ȫ͞έ΁ϋΘΩςΤ·Α͈ুࡨ๧‫ئ‬ಕৣͥ͢ͅ‫ٸ‬ြহၷ̦দ͙̞ͣͦ̀ͥȃထࢃၻࢡ̈́ࠚછ
෹ࠬ஀ण஀છ͈ಒ੄༹͈‫ږ‬ၛ̦‫ه‬ఴ͉̜͈͈́ͥ͜Ȃஜ੆̱̹‫ٳ‬อಎ͈૧ܰࠐ࢛ࢯާࡥ࿪̦ঀဥ‫خ‬ෝ͂̈́ͦ͊Ȃུཆ̤̞̀͜ͅౣ‫ܢ‬ව֭͞‫ٸ‬ြহၷ̦‫خ‬ෝ͂̈́ͥȃਹછ෹ࠬ஀ण஀છͅచ̱̀Ȃ்‫஀ࠬܢ‬ဣٜȂ࣐ࠬ൲ఠ٨஝ͬ࿒എ̱͂̀ဥ̞ͣͦͥࠬ஀ဣٜၷ༹͈ঀဥອഽུ͉ཆ́͜೩‫̜̱ͥ̾̾ئ‬ȃඅͅՏࢩํ߿છ႕ͅచ̳ͥࠬ஀ဣٜၷ༹͈ଵ๱̞͉݈̾̀ͅა̦໦̥̞ͦ̀ͥȃ̭̠̱̹ࣽࢃ͈‫ه‬ఴ͜‫܄‬̹͛෹ࠬ஀ण஀છͅచ̳ͥࢯࠬ஀ၷ༹͈ΠάΛ·ᾼ̧̾‫ٽ‬୰̱̹̞ȃ

ポスター発表 ＹＩＡ選考発表‫خ‬ෝ͂̈́ͤȂ෹ࠬ஀ण஀છ͈হၷ୽ၞ̦ఱ̧̩་‫ܢ̦̭̳͂ͥا‬ఞ̯̞ͦ̀ͥȃ‫؎ͅܡ‬ༀ͉́Ȃ෹ࠬ஀

著者索引

䋭 㪏㪌 䋭

ႉ઄ŔĮĳĮĶ

࿪໤ဣ੄଻ΑΞϋΠশయ̤̫ͥͅࢯࠬ஀ၷ༹
ɛ઀ോġ੓ߧུఱ‫ڠ֓ڠ‬໐້௺ພ֭ࣞഽ֓ၷ‫ٳ‬อΓϋΗȜ૤ະ஠୶౤֓ၷ‫້࣒ܙ‬ज૧͈ܰࢯާࡥ࿪ȪŏŐłńȫ̦ड߃̈́ͤͅষș͂ഴા̧̱̤̀̀ͤȂ૧͈ܰࢯࠬ઀โ࿪͜߃̞੿ြȂ඾ུ̞̩̥́̾͜ഴા̳̭̦ͥ͂ࠨ೰̱̞̀ͥȃ࿪໤ဣ੄଻ΑΞϋΠͬຈါ̳͂ͥ‫଻ࠬݹ‬૤৖ۛۛ৪ͅ
చ̱̀Ȃਲြ͈ࢯࠬ஀࿪͜‫͛܄‬Ȃࣽࢃ͈̠̓̈́͢ঀ̧̞༷̱̞̩͓̜͈̥ͬ̀́ͥȂේ̱̞͘࿚ఴ̦຾
ષ̱̞̀ͥȃχȜέ͹ςϋ͉̭ͦ́͘ࠐ࢛ࢯާࡥ࿪้̱͂̀ဥ̧̯̹ͦ̀యນഎ̈́࿪̜́ͥȃŏŐłń
͈ഴાͤ͢ͅȂ૙ম͈ଷࡠ͞ळ̥͛̈́őŕĮŊŏœ͈ΙͿΛ·͉ະါ̹̈́̽ͅȃ༷֚Ȃ‫଻ࠬݹ‬૤৖̤̞ۛ̀ͅȂ૤པळ൲ࣣ໵ۛ৪ͅచ̳ͥ‫ۍ‬൲ྤͼϋΗȜαϋΏοϋঔ࣐̤̫ͥͅࢯࠬ஀࿪͈ঀ̞༷̞̾̀ͅȂ඾ུ͉֚́೰̱̹΋ϋΓϋ΍Α̦ං̞̞͈̦࡛ͣͦ̀̈́ે̜́ͥȃ؎ༀ͈΄ͼΡρͼΰ͉Ȃ‫خ‬ෝ̈́ࡠͤȂχȜέ͹ςϋͅ‫઀ࠬࢯ̢ͥح‬โ࿪ĳस͈໵ဥ‫ͬۼܢ‬ౣ̩̱Ȃ̷͈ࢃࢯࠬ઀โ࿪Ĳस̱ͅȂडਞഎ͉ͅχȜέ͹ςϋ̺̫̳ͥ͂ͅা̱̞̀ͥȃඅͅࢯࠬ઀โ࿪ĳस໵ဥ‫ۼܢ‬ಎ͈őŕĮŊŏœ͉৻̳̠ܱ͛ͥ͢ͅͅश
̦̜ͥȃ̱̥̱‫΀̹ͥࡥږ‬ΫΟϋΑ͉̩̈́Ȃ࡛ह͈඾ུ͉́؎ༀ͈΄ͼΡρͼϋ͈ඤယ̳͓ͬ̀਋̫
ව̭͉ͦͥ͂ඳ̱̞ȃ̹͘Ι·υάΐϋ̥ͩͥͅࢯࠬ઀โ࿪̱͂̀·υάΡΈτσ̦ഴા̱Ȃ஠૸͈൲ྤࣁ‫ا‬৖ۛۛ৪ͅచ̱ခဥ଻̦া̯̞ͦ̀ͥȃ̱̥̱·υάΡΈτσ͉య৫ͬ਋̫̀‫̯ͥͦا଻ڰ‬ίυΡρΛΈ̜́ͤȂඅͅͺΐͺ૽͉́࿪໤య৫ࣖள̜́ͥńŚőĳńĲĺ͈֒ഥঊఉ߿͈࿚ఴ̦৾ͤષ
̬ͣͦȂ૤ࠬ‫ͼۯ‬αϋΠ͈͂‫̦߸۾‬ճা̯̞ͦ̀ͥȃड߃Ȃ٬‫͉́ٸ‬૧̹̈́ࢯࠬ઀โ࿪̜́ͥίρΑΈτσ͞Ι΃Έτυσ͈లĴ௖দࡑ̦࣐ͩͦȂ̷͈ခဥ଻̦া̯̹͈͈ͦ͜Ȃ੄ࠬͅ‫̳ͥ۾‬հ஠଻͈࿚ఴ
͜ઁ̴̥̈́ͣࣉၪ̯̞ͦ̀ͥȃ๊̭֚ͦ́͘എͅȂ‫ۍ‬൲ྤ৖ۛͅచ̳ͥͺΑάςϋൎဓȂ૤པळ൲ͅచ
̳ͥχȜέ͹ςϋൎဓ͉΄ͼΡρͼΰ͜·ρΑĲ̱͂̀ࠇ̬̤ͣͦ̀ͤȂ̭͈ͦͣ࿪सͬൎဓ̳ͥ
̭͉͂൚ட͈̭̱͂͂̀ࣉ̢̧̹ͣͦ̀ȃ̱̥̱ŏŐłń͞૧͈ܰࢯࠬ઀โ࿪̦߃̞੿ြȂ৘ႉ઄̤ͅ
̞̀ర൮̱̩̭͉̀ͥ͂‫̢̹͛ͥͦͣࣉ̩̞֑̈́ۼ‬Ȃ‫ܡ‬ం͈࿪स͜‫͛܄‬Ȃ૧͈ܰࢯࠬ஀࿪͈ခ࢘଻͞
հ஠଻͈̈́̓අಭͬ਱໦ͅၑٜ̱̀Ḁ̥̑ͥۛ৪ͅঀ̞໦̫ͥশయͅြ̞̀ͥ͂ࣉ̢ͥȃ䋭 㪏㪍 䋭

ĺ࠮ĳĸ඾Ȫ߄ȫġĺĻııȡĲĲĻııġġలˎٛાΏϋεΐ;θġႉ઄ ŔĮĴȶఱ൲ྤ৖̤̫ۛͥͅ ťŢůŨŦųġŴŪŨůŢŭ ͂‫׶‬છȷġႉ઄ŔĮĴĮĲ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineఱ൲ྤ৖̤̫ۛͥͅ ťŢůŨŦųġŴŪŨůŢŭ
特別講演ɛऎ൥ġ࢖ဎȂ‫୼ئ‬ġࢤྶ൐ཤఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬ΠτΑͬ਋̫̹ळ༾ͤ͢༶੄̯ͦͥඤ֦଻ς΄ϋΡ͂ζ·υέ͹Ȝΐ͈̈́̓‫׶‬છळ༾ͅอ࡛̳ͥΓϋ΍Ȝ͈௖ࡽैဥͤ͢ͅྕ଻എ̈́‫׶‬છ฽؊̧̭̱ͬ֨ܳȂ૤ࠬ‫ۯ‬ςκΟςϋΈͬ௯ૺ̳ͥȃ೒ુ͉ळ༾ඤͅంह̳ͥ౩ฒ଼໦̦Ȃ۪‫ޏ‬ΑΠτΑ͞ळ༾ঘ́ळ༾‫ͅٸ‬༶੄̯ͦͥ͂Ȃ̷ͦͬΓϋ΍Ȝ̦ŅŢůŨŦųġ ŔŪŨůŢŭ̱͂̀ۜ౶̱Ȃ‫׶‬છ฽؊̦ည൵̯̭̦ͦͥ͂໦̧̥̹̽̀ȃġ ̷̠̱̹‫׶‬છৼ଼ܳ໦͉
ŅłŎőŴȪťŢŮŢŨŦĮŢŴŴŰŤŪŢŵŦťġŮŰŭŦŤŶŭŢųġűŢŵŵŦųůŴȫ͂ࡤ̞͊ͦ̀ͥȃŅłŎőŴ͉྾‫ע‬ळ༾͈ΩΗȜϋ෇ে਋ယఘ͞ŅłŎőŴ਋ယఘࣣ̱ࠫͅȂ‫׶‬છ଻΍ͼΠ΃ͼϋ͈໦๥௯ૺȂழ૕͈͒‫׶‬છळ༾૫੕Ȃ̯͉ͣͅ૤ࠬ‫ۯ‬κΟςϋΈͬ௯ૺ̳ͥ͂ࣉ̢̞ͣͦ̀ͥȃུΏϋεΐ;θ͉ͅȂఱ൲ྤរ͞ఱ൲ྤٜၗ̤ͅ

͈ۛอછ‫͂ࢹܥ‬ພఠ͈ၑٜͬ૬̭͛ͥ͂́Ȃ்‫ܢ‬อࡉ͞૧̱̞হၷ୽ၞ͈͒‫ܢ̭ͬ͂ͥ̈́ͅޘ̫ط‬ఞ
̱̹̞ȃ

口頭発表

̫ͥŅŢůŨŦųġ ŔŪŨůŢŭ͞‫׶‬છ͈࿨‫̞̀̾ͅڬ‬Ȃ඾ུอ͈ड୶౤͈ࡄ‫̦ض଼ݪ‬େࣺ̞ͤͦ̀ͥ͘ȃఱ൲ྤ৖

会長招待講演 シンポジウム૤ࠬ‫ۯ‬৖͈ۛૺ࣐ͅ‫ވ‬೒̳ͥ‫ܖ‬๕̱͂̀ȂŅŢůŨŦųġ ŔŪŨůŢŭ̦ಕ࿒̯̞ͦ̀ͥȃŅŢůŨŦųġ ŔŪŨůŢŭ͉ȂΑ

ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪏㪎 䋭

ႉ઄ŔĮĴĮĳ

ŉŎňŃĲ ͂ఱ൲ྤរ
ɛհ୔ġੇ‫ ݛ‬ĲȂ‫ع‬࿤ġၦ঎ ĳ
Ĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬Ȃĳ ࠄᑄ݅ੂఱ‫ڠ֓ڠ‬໐੏۪‫ܕ‬ඤ‫ش‬‫ړ‬ඤ๱ΪΑΠϋ౩ฒ̜́ͥŉŎňŃĲ͉Ȃळ༾ٟঘฺ̽̀ͅळ༾‫͒ٸ‬༶੄̯ͦȂŕŰŭŭĮōŪŬŦġœŦŤŦűŵŰųġĩŕōœĪ
͞œŦŤŦűŵŰųġ ŧŰųġ łťŷŢůŤŦġ ňŭźŤŢŵŪŰůġ ņůťĮűųŰťŶŤŵŴġ ĩœłňņĪ̱ͬٚ̀ȂŏŇĮЀŃͬ‫ޑ̵̯ا଻ڰ‬ႁ̈́‫׶‬છ฽؊ͬৼ̱ܳȂłœŅŔȂ‫଻ݢ‬෹વ‫ࠬݹ͞ٺ‬ठᚇၠવ‫͈ٺ‬ພఠͅ‫۾‬ဓ̳̭̦ͥ͂౶̞ͣͦ̀ͥȃِș͉Ȃໜ໐ఱ൲ྤរ̀ͅ਀੅̦ঔ࣐̯̹ͦછ႕͈୨ੰດུͬဥ̞̀࠿൦࣐̹ͬ̽ȃ̷͈ࠫ‫ض‬Ȃఱ൲ྤរ༃
͈‫׶‬છळ༾Ȃ໹‫޼ڲ‬ळ༾Ȃࠬ‫ۯ‬ඤ๧ळ༾̤̞̀ͅŉŎňŃĲ͈ࣞഽ̈́อ࡛̦෇̹͛ͣͦȃఱ൲ྤរࠁ଼ً
೾̤̫ͥͅŉŎňŃĲ͈࿨‫̹̳̥͛ͥͣͅྶͬڬ‬Ȃ‫΃ا؂‬σΏ;θঁࠣͥ͢ͅζ;Αఱ൲ྤរκΟσͬဥ̞̀࠿൦࣐̹ͬ̽ȃ୆ࢃĹ਩͈࿤୆߿ζ;ᾼచ̱̀ȂβϋΠΨσΫΗȜσཻଜ‫ٳͅئ‬ໜ̱Ȃଅ൲ྤ̥ͣಸࣸ൲ྤ໦‫ܚ‬໐ͅıįĶŎġńŢńŭĳͬ૫̱̹ĴřĶŮŮ͈΄ȜΔͬĲĶ໦‫ۼ‬ၣ౾̱Ȃ̷͈ࢃ୆૙́஄૆̳ͥ
łłł߲͂୆૙͈͙͈ੜ౾࣐̠ͬŔũŢŮ߲ͬै଼̱̹ȃłłł߲̤̞͉̀ͅȂ΋ϋΠυȜσŊŨŚࢯఘൎဓ߲ȪłłłİńŐŏȫ͂ŉŎňŃĲಎგࢯఘൎဓ߲ȪĲıŮŨİŬŨİťŢźͬĴ඾ྀķ਩‫ۼ‬ĭġ łłłİŢůŵŪĮŉȫ͈ĳ߲ͬै଼̱̹ȃķ਩ࢃͅఱ൲ྤͬഊ੄̱Ȃఱ൲ྤរࠂͬ௶೰ࢃȂũŦŮŢŵŰŹźŭŪůĮŦŰŴŪůȪŉņȫஅ૗͍̈́ͣͅŦŭŢŴŵŪŤŢġ
ŷŢůġňŪŦŴŰůȪņŗňȫஅ૗ͤ͢ͅȂழ૕‫ڠ‬എ࠿൦࣐̹ͬ̽ȃ̷͈ࠫ‫ض‬ȂłłłİńŐŏ߲͉́ȂŔũŢŮ߲ͅ๤͓Ȃခփͅໜ໐ఱ൲ྤរࠂ̦‫ڐ‬ఱ̱ȂłłłİŢůŵŪĮŉ߲͉́ȂłłłİńŐŏ߲ͅ๤‫̱ڛ‬ခփͅໜ໐ఱ൲ྤរࠂ
͈ੀ઀ͬ෇̹͛ȃŉņஅ૗͉́ȂłłłİńŐŏ߲̤̞̀ͅȂŔũŢŮ߲ͅ๤‫׶̱ڛ‬છळ༾૫੕͈௩‫̹͛෇ͬح‬̦ȂłłłİŢůŵŪĮŉ߲͉́ȂłłłİńŐŏ߲ͅ๤‫׶̱ڛ‬છळ༾૫੕͈ခփ̈́ࠚࡘͬ෇̹͛ȃņŗňஅ૗͉́ȂłłłİńŐŏ߲́ఱ൲ྤಎ྄௄͈ᨉถ‫΀͂ا‬ρΑΙϋ͈෨ેࢹ௮͈෫ٟ̦෇͈͛ͣͦͥͅచ̱̀ȂłłłİŢůŵŪĮŉ߲͉́Ȃ̷̦ͦࠚࡘ̯̤ͦ̀ͤȂŉŎňŃĲಎგࢯఘൎဓͥ͢ͅໜ໐ఱ൲ྤរࠁ଼͈ဲଷ࢘
‫̦ض‬াऐ̯̹ͦȃࠫࢊȇŉŎňŃĲ͉Ȃ‫׶‬છ͈‫ڐ‬ఱ̱ͬٚ̀ఱ൲ྤរࠁ଼ً೾̤̫ͥࠬͅ‫ۯ‬ςκΟςϋΈ
ͅਹါ̈́࿨‫خ̞̱̹ͥ̀ضͬڬ‬ෝ଻̦ࣉ̢ͣͦͥȃ䋭 㪏㪏 䋭

ႉ઄ŔĮĴĮĴ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineழ૕ਘ໘֦ঊ łůŨűŵŭĳ ͂ఱ൲ྤរ

ߧུఱ‫ڠ‬ఱ‫֭ڠ‬୆ྵ‫ݪࡄڠش‬໐Ȇ֓‫ࠏڠ‬Ȇ໦ঊ֒ഥ‫ڠ‬୆ఘඤ͈‫ڎ‬ழ૕͉ͅȂ‫ܥ‬ෝഎȂࢹ௮എͅ๷઀̈́అੱ̦୆̲̞̀ͥȃ̭͈అੱͬਘ໘̳ͥ୆ఘ͈ࢭુ଻֋
঵؊൞‫̱̀͂ࢹܥ‬Ȃ‫ڎ‬ழ૕̤̫ͥͅ৘ৗळ༾͂‫ۼ‬ৗळ༾͈͂ळ༾‫ۼ‬୪಍͞‫֦଻ס‬ঊ̱̹ͬٚ௖ࡽैဥȂ‫̱̀͂ض̷͈͍ࠫݞ‬ည൵̯ͦͥ‫ݙخ‬എ̈́ழ૕͈ςκΟςϋΈ̦ਹါ̜́ͥȃ̱̥̱Ȅಿ‫ܢ‬എ̜̞͉ͥ
ًഽ͈ΑΠτᾼཕႺ̯̭ͦͥ͂́Ȃ୆ఘ͈ࢭુ଻֋঵؊൞‫͈ࢹܥ‬؊൞ະ஠઼ً͞؊൞̦୆̲ͥȃඅͅȂ઼ً؊൞ͤ͢ͅழ૕̤̞̀ͅᛞ̹̠̽̈́͢೩τασ͈Ȩྕ଻‫׶‬છȩ̦̹̯ͣͦ͜Ȃະ‫ݙخ‬എ̈́ழ૕͈ςκΟςϋΈ̦୆̲Ȃਅș͈୆‫ڰ‬ਠ‫۾۝‬Ⴒ৖ۛอછȂჇ‫ا‬௯ૺȂ࠲ࢫಿ਍͈ஷ‫ͅٺ‬อജ̳̭̦ͥ͂ಕ࿒̯
̞ͦ̀ͥȃ̭͈̭͉͂ȂȨྕ଻‫׶‬છȩ͈ࡎ֦͂̈́ͥঊͬ൳೰̳̭̦ͥ͂Ȃྕ଻‫׶‬છ‫۾‬Ⴒ৖͈ۛ໦ঊພఠ͈

ͥȃུΏϋεΐ;θ͉́Ȃِș̦൳೰̱̹ͺϋΐ΂ε΀Ιϋအ֦ঊĳȪłůŨűŵŭĳȫ͈۷ത̥ͣ୆ఘ͈ࢭુ
଻֋঵‫ࢹܥ‬Ȃ̷͈෫౦̹̯̽̀ͣͦͥ͢͜ͅྕ଻‫׶‬છȂະ‫ݙخ‬എழ૕ςκΟςϋΈȂ৖͈ۛอછ͞ૺജ

口頭発表ٜྶ̴͈͙̈́ͣȂ૧ܰহၷ୽ၞͥ͢ͅ࠲ࢫಿ਍২ٛ৘࡛ͬࣉ̢̢̠ͥ́ਹါ̜̭́ͥ͂ͬাऐ̱̞̀

会長招待講演 シンポジウム߃ා͈୆‫ڰ‬ਠ‫͈۝‬ఉအ‫ͤ͢ͅا‬Ȃ୆ఘ͉အș̈́ඤഎȆ‫ٸ‬എΑΠτᾼુͅཕႺ̯̤ͦ̀ͤȂ̷͈ࠫ‫ض‬Ȃ

特別講演ɛ๶౻ġဎ֚

̞̾̀ͅఱ൲ྤរ͈໦ঊພఠ͈͒‫ͤͩͅ۾‬ઙത̱ड߃ِ͈ș͈ΟȜΗ̮ͬત̱݈ٚა̱̹̞ȃ

ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪏㪐 䋭

ႉ઄ŔĮĴĮĵ

ͼϋέρζΕȜθ͂ఱ൲ྤរ
ɛࣞ‫ޘ‬ġ੿໲ুহ֓‫ش‬ఱ‫ڠ‬໦ঊພఠহၷࡄ‫ݪ‬ΓϋΗȜ‫׶‬છȆ྾‫ݪࡄע‬໐ఱ൲ྤរ͉̲̱̹ͬ͛͂૤ࠬ‫ۯ‬৖̤̫ۛͥͅ‫׶‬છ฽؊͈ਹါ଻̦া̯̞ͦ̀ͥȃ૤ࠬ‫ۯ‬৖̤̫ۛͅ
ͥ‫׶‬છ͉Ȃພࡔఘ͈‫۾‬ဓ̦̞̭̥̈́͂ͣྫ޿଻‫׶‬છȪŴŵŦųŪŭŦġ ŪůŧŭŢŮŮŢŵŪŰůȫ͂ࡤ̞̦͊ͦ̀ͥȂ̷͈‫׶‬છৼܳ‫ܥ‬੬͉̭̥̞̥̹ͦ́ͩ̽̀̈́̽͘ȃ߃ාȂ̞̩̥͈̾ພఠ̤̫ͥͅྫ޿଻‫׶‬છ̦ͼϋέρζΕȜθȪŪůŧŭŢŮŮŢŴŰŮŦȫ̞̠͂૧̹̈́ুட‫׶‬છࠐႹ̱ͬٚ̀ည൵̯̩̭̦ͦ̀ͥ͂༭̯̤࣬ͦ̀ͤȂ૤ࠬ‫ۯ‬৖͈ۛ́ྫ޿଻‫׶‬છ̤̞̀͜ͅͼϋέρζΕȜθ͈‫۾‬ဓ̦ྶ̥̜ͣ͂̈́ͤ̾̾ͥȃͼϋέρζΕȜθ͉͂Ȃ‫ࡏܓ‬ΏΈ΢σͤ͢ͅळ༾ඤͅࠁ଼̯ͦͥ໦ঊໝࣣఘ̜́ͤȂ΃ΑΩȜΔĮĲ͈‫׶ͤ͢ͅا଻ڰ‬છ଻΍ͼΠ΃ͼΰ̜ͥͼϋΗȜυͼ΅ϋĮĲϸȪŊōĮĲϸȫ଼͈੃‫ͬا‬ည൵̱̀‫׶‬છͬৼ̳ܳͥȃِș͉Ȃ̭ͦ́͘૤‫ࠬݹ‬ठᚇၠࠬ͞‫͈ࢃٺੱۯ‬ඤ྄๬࢚Ȃ൲ྤࣁ‫͈̓̈́ا‬ພఠ̤̫ͥͅͼϋέρζΕȜθ͈ਹါ଻ͬ༭̧̱̹࣬̀ȃఱ൲ྤរ̤̞̀͜ͅພ་໐պ́ͼϋέρζΕȜθࢹ଼໦ঊ͈อ࡛ᄤૺͬ෇͛ȂͼϋέρζΕȜθࢹ଼໦ঊ̜́ͥŏōœőĴ͞łŔńȂ΃ΑΩȜΔĮĲͬࠧఅ̵̯̹ζ;Ά͉Ȃ‫׶‬છ฽؊͈ࡘ
৻͂͂͜ͅఱ൲ྤរ͈ࠁ଼̦ဲଷ̯̭ͦͥ͂ͬࡉ੄̱̞̀ͥȃ̭͈̭̥͂ͣȂͼϋέρζΕȜθ̦ఱ൲ྤរ͈ພఠ̤̞̀ͅਹါ̈́࿨‫̤̱̹ͤ̀ضͬڬ‬Ȃུ৖ۛͅచ̳ͥ૧̹̈́হၷດഎ̢̭̦͂̈́ͤͥ͂
াऐ̯ͦͥȃ䋭 㪐㪇 䋭

ႉ઄ŔĮĴĮĶ

ɛ߄५ġਁၖȂဿġ઀༰Ȃခനġ࿆ঊȂ‫ॄݠ‬ġఽ჊Ȃ‫ॄݠ‬ġડ઎გఱ‫ڠ֓ڠ‬໐୆‫ڠا‬elderly individuals and is responsible for a significant number of deaths in western countries1.
Oxidative stress, generated by excessive reactive oxygen species (ROS) represented by hydrogen
peroxide (H 2 O 2 ), has been shown to play causal roles in AAA. Hydrogen peroxide-inducible clone
5 (Hic-5), originally identified as a gene induced by H 2 O 2 as well as transforming growth factor-ϸ1(TGF-ϸ1), serves as a focal adhesion protein that belongs to the paxillin family. Using theangiotensin II (AngII)-induced AAA model in Apoe-/- mice, we showed that Apoe-/- Hic-5-/- mice
were completely protected from AAA formation and rupture while Apoe-/- mice were not.

Suppression of the JNK2 pathway by Hic-5 loss resulted in the limited secretion of proMMP2 and
MMP2 and expression of MT1-MMP, which led to protection from elastin degradation andsubsequent AAA formation and rupture. This study not only identified Hic-5 as a downstream

specific scaffold between MKK4 and JNK2 in VSMCs.

ポスター発表 ＹＩＡ選考発表

molecule of ROS, which promotes AAA formation, but also suggested that Hic-5 can serve as a

口頭発表

Mechanistically, Hic-5 can bind to both JNK2 and its upstream regulatory molecule, MKK4.

会長招待講演 シンポジウム

Abdominal aortic aneurysm (AAA) is an age-associated disease that affects approximately 5% of

特別講演ŉŪŤĮĶġťŦŧŪŤŪŦůŤźġţŭŰŤŬŴġŵũŦġťŦŷŦŭŰűŮŦůŵġŰŧġŢţťŰŮŪůŢŭġŢŰųŵŪŤġŢůŦŶųźŴŮŴġţźġ
ŪůũŪţŪŵŪůŨġŤĮŋŶůġŏĮŵŦųŮŪůŢŭġŬŪůŢŴŦġĳġŪůġŮŪŤŦ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

著者索引䋭 㪐㪈 䋭

ႉ઄ŔĮĴĮķ

ࢡಎ‫ݩ‬ဇြ ŎŎőĺ ̱̹ͬٚ‫଻ݢ‬ఱ൲ྤٜၗ͈อછ‫ࢹܥ‬ɛୄକġၻঊ ĲȂߪࡔġ౺ࢤ ĳȂ‫ئ‬നġ੿෗ ĴȂչ൥ġဉ ĲȂཱġૺࢅ ĳȂ‫ؖ‬നġ༗ങ Ĵ
Ĳ ࠄᑄ݅ੂఱ‫ڠ֓ڠ‬໐ଅ௫ඤ໦๥య৫ඤ‫ش‬Ȃĳ ࠄᑄ݅ੂఱ‫ڠ֓ڠ‬໐‫ޗڠ֓ݢݣ‬৒ȂĴ ࠄᑄ݅ੂఱ‫ڠ֓ڠ‬໐ພၑ‫ޗڠ‬৒‫଻ݢ‬ఱ൲ྤٜၗĩłłŅĪ͉౿ঘၚ͈̞ࣞ੏۪‫ݢݣܕ‬৖̜ۛ́ͤȂခဥ̈́૷౯ζȜ΃Ȝ͞࿪໤হၷ༹̦
̩̈́Ȃ̹̭ͦ́͘͘ഐ୨̈́൲໤κΟσ̦̞̭̥̈́͂ͣȂอછ‫ܥ‬੬͈ࡄ‫̞̞̈́́ͭૺ̦ݪ‬ȃζΠςΛ·ΑιΗυίυΞͺȜΔȪŎŎőȫ̦ྕ଻ࠬ‫ۯ‬ພ་͈ࠁ଼ͅਹါ̜̭͉̩́ͥ͂͢౶̞̦ͣͦ̀ͥȂ˝˝ˠ͈̠̈́͢‫଻ݢ‬৖̷̤̫͈ۛͥͅ࿨‫͞ڬ‬મळ̈́‫ܥ‬੬̞͉̾̀ͅະྶ̜́ͥȃłłŅ̤̫ͥͅŎŎő͈࿨‫ͬڬ‬ྶ̥̳̹ͣͥ͛ͅͅȂ̴ِ͘ș͉‫ٸݢݣ‬ြͬ਋૷̱̹łłŅۛ৪͈ࠬಎŎŎőෛഽͬ௶೰̱̹ȃྚ෫Ⴈఱ൲ྤរۛ৪̤͍͢࠲ુ૽͂๤‫̱̀ڛ‬łłŅ͉́ࠬಎŎŎő˕ෛഽ̦࿹պͅષઌ̱̤̀ͤȂ̯͉ͣͅయນ
എ̈́૤ࠬ‫ۯ‬γσκΰ̜ͥͺϋΐ΂ΞϋΏϋ˥˥ĩłůŨŊŊĪෛഽ͜࿹պͅષઌͬ෇̹͛ȃ̭͈ࠫ‫̧̿ܖͅض‬Ȃِș͉΋ρȜΊϋȆ΀ρΑΙϋ͈‫ࣖޘط‬ள̜́ͥŭźŴźŭġ ŰŹŪťŢŴŦ͈ஷ‫ٺ‬सŃłőŏͬဘ৻ζ;ᾼஜൎဓ̳̭ͥ͂́ఱ൲ྤ༃ୖ৻‫ͥ͢ͅا‬ఱ൲ྤរͬࠁ଼̱Ȃ̭ͦͅłůŨŊŊ͈ൎဓ࣐̠̭ͬ͂́ȂłůŨŊŊൎဓࢃķশ‫̥ͣࢃۼ‬łłŅ̦อછ̱ই͛ȂĲĳশ‫͉ͅࢃۼ‬ĲııĦ͈‫ږ‬ၚ́łłŅͬอછ̳ͥ૧̹̈́łłŅ൲໤κΟσ͈‫ږ‬ၛ଼̱̹ࢗͅȃΦσ΀άΥέςϋ͈ൎဓ͉́łłŅ͈อછͬ෇̥̹͛̈́̽ȃষͅłłŅอછ͈͒ŎŎő˕͈‫ܥ‬ෝഎ̈́‫۾‬ဓͬ࠿൦̳̹ͥ͛ΪΠłłŅ̤͍͢łłŅκΟσζ;Α͈ࠬ‫ۯ‬ພ་̤̫ٜͥͅଢ଼
̥ͣȂࠬ‫ۯ‬ඤ྄͈͒ࢡಎ‫ݩ‬૫੕͂ࢡಎ‫֚ͅݩ‬౿̱̹ŎŎőĺ͈อ࡛ષઌ̤͍͢‫ͬا଻ڰ‬łłŅۛ໐ࠬ‫́ۯ‬෇̹͛ȃζ;ΑκΟσ͈͒ŎŎőஷ‫ٺ‬सൎဓ̤͍͢ŎŎő˕ΦΛ·ͺ;Πζ;Ά͉łłŅ͈อછ̦࿹պ
ͅဲଷ̯ͦȂ̹͘ňųĲࢯఘൎဓͥ͢ͅࢡಎ‫́͜ݲੰݩ‬łłŅ͈อછၚ͉ဲଷ̯̹ͦȃոષ̥ͣࠬ‫ۯ‬ඤ྄͒૫੕̱̹ࢡಎ‫͈̥ͣݩ‬łůŨŊŊঁࠣ؊൞଻ͅ༶੄̱̹ŎŎőĺ̦łłŅ͈อછͅ‫۾‬ဓ̱̞̀ͥ͂ࣉ̢̹ͣͦȃ䋭 㪐㪉 䋭

ĺ࠮ĳĸ඾Ȫ߄ȫġĲĵĻĶıȡĲķĻĶıġġలˎٛાΏϋεΐ;θġႉ઄ ŔĮĵȶ‫ۍ‬൲ྤίρȜ·ْ͈௨૷౯ġȡႉ઄֓‫ْ̫̤ͥͅڠ‬௨૷౯͈ૺ༜͂੿ြജབȡȷႉ઄ŔĮĵĮĲ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineŗŶŭůŦųŢţŭŦġűŭŢŲŶŦ ͉͂ȡພၑͤ͢
特別講演ɛֵ๶ġဉ෗
໶ࡩ֓‫ش‬ఱ‫ڠ‬ພ֭ພၑ໐

ඤ੄͈ࠬ̈́̓ίρȜ·͈ழ૕ࢹ଼଼໦͈໦ື̽̀͢ͅࠨ೰̯ͦȂίρȜ·͈෫Ⴈ͉ͅழ૕଻ે͂͂͜
ࠬͅၠͥࠬ͢ͅ‫ۯ‬༃ͅచ̴̳ͥͤ؊ႁ͞ίρȜ·͈ඤգ̈́̓ႁ‫ڠ‬എါ֦̦‫۾‬ဓ̱̞̀ͥȃίρȜ·͈෫Ⴈ͉‫ۇ‬ਆͬ๭ໞ̱ࠬ‫ۯ‬ඤ͈࣌͂‫ٮޏ‬໐ͅࡉͣͦͥ஌֋଻๭྄͈౯Ⴈ̭̽̀ܳͥ͢ͅȃِș͈࠿൦͉́ȂίρȜ·͈෫Ⴈછ႕͈̠̻࿩ĸıĦ̦ίρȜ·͈ၛ̻ષ̦͈ͤ໐໦ġĩűŭŢŲŶŦġŴũŰŶŭťŦųĪġ́஌֋଻๭྄
̦౯Ⴈ̱̞̹̀ȃழ૕‫ڠ‬എͅ űŭŢŲŶŦġ ŴũŰŶŭťŦų ͉஌֋଻๭྄͂ୃુͅ߃̞ࠬ‫ۯ‬༃̦࢐ए̱ழ૕଻ે̦
་‫̳ͥا‬໐պ́Ȃࠬၠ̱̩͉͜ίρȜ·ඤ̥͈ͣ໅‫̥̥̦͂ͥك‬ΑΠτΑͬ਋̫̳̞͂͞ࣉ̢ͣͦ
ͥȃ̹͘൳໐͉‫׶‬છळ༾૫੕̦࿒ၛ̻Ȃ஌֋଻๭྄̦ಠྶͅᨉถ‫̦̭̞̱͂ͥ̀ا‬ఉ̞ȃ̭͈ͦͣ‫׶‬ͥȃŗŶŭůŦųŢţŭŦġ űŭŢŲŶŦ͈ழ૕‫ڠ‬എඅಭ̱͂̀ఱ̧̈́ ůŦŤųŰŵŪŤġ ŤŰųŦ ̦‫̬ͥͦͣݷ‬ȃůŦŤųŰŵŪŤġ ŤŰųŦ͉ٟͅঘ໤͞΋τΑΞςϋࠫએ͈ೆ಍̦ࡉͣͦͥȃ̯ͣͅίρȜ·ඤ੄͉ࠬίρȜ·͈ୖ৻଻ͬࠨ͛ͥਹ

口頭発表છळ༾̽̀͢ͅॲ୆̯ͦͥळ༾‫ܖٸ‬ৗ͈໦ٜࣖள̽̀͢ͅ ŧŪţųŰŶŴġŤŢű ͉෫ٟ̯ͦȂষలͅᨉถ‫̳ا‬

会長招待講演 シンポジウムίρȜ·͈ୖ৻଻͉ळ༾‫ܖٸ‬ৗȂডৗȂٟঘॲ໤Ȃ‫׶‬છळ༾Ȃࠬ‫ۯ‬໹‫޼ڲ‬ळ༾Ȃࠬ஀Ȃ୞‫ا٭‬ȂίρȜ·ါ̈́ါ֦͈̠̻͈̜͌͂̾́ͥȃ੄̦ࠬ ůŦŤųŰŵŪŤġ ŤŰųŦ ඤ̭ܳͥ͂ͅȂίρȜ·͈ඤգ̦‫ࠣͅݢ‬ષઌ̱ळ༾྄ͅ‫ͥͦ͘܄‬ডৗ଼໦̦΋τΑΞςϋࠫએ̱͂̀ೆ಍̱ȂůŦŤųŰŵŪŤġ ŤŰųŦ͈௩ఱͅίρȜ·ඤ੄̦ࠬ‫۾‬ဓ̱̞̭̦̀ͥ͂౶̞ͣͦ̀ͥȃ̹͘ŗŶŭůŦųŢţŭŦġ űŭŢŲŶŦ͉́໹‫޼ڲ‬ळ༾͞ζ·υέ͹Ȝΐ͈ͺεΠȜΏΑ̦̭̞ܳ̽̀ͥȃζ·υέ͹Ȝΐ͈ͺεΠȜΏΑ͉ ůŦŤųŰŵŪŤġ ŤŰųŦ ͈௩ఱͅ‫۾‬ဓ̱Ȃ໹‫޼ڲ‬ळ༾͈ͺεΠȜΏΑ͉஌֋଻๭྄͈ᨉถ‫ྟ͂ا‬୪̈́‫̜̦ͥ߸۾‬ȃ̭͈ͦͣळ༾଼໦͈ͺεΠȜΏΑ̦ίρȜ·͈ୖ৻଻ͅਹါ̈́࿨‫̞̱̹ͥ̀ضͬڬ‬ȃ

ポスター発表 ＹＩＡ選考発表ίρȜ·͈෫Ⴈ͈ည֦̠͂̈́ͤͥȃ̹͘੄ࠬࢃͅίρȜ·ඤ́୤ࠬ‫̦ݩ‬་଻Ȃ‫ݟ‬ਓ̯ͦͥ͂୤ࠬ‫͈ݩ‬

著者索引

䋭 㪐㪊 䋭

ႉ઄ŔĮĵĮĳ

ŗŶŭůŦųŢţŭŦġűŭŢŲŶŦ ૷౯̤̫ͥͅ ńŕ ͈ૺ༜͂੿ြജབ
ɛ઀ઐġ୍Ȃ঱ޮġგ‫ݛ‬බॄಎ؇ພ֭૤௫ࠬ‫ۯ‬ΓϋΗȜड߃૤௫ńŕ͈́‫ۍ‬൲ྤज़‫̦ג‬ຽ‫̱ݞ‬Ȃ‫ۍ‬൲ྤ‫ޛ‬ॏͬ‫ٸ‬ြτασ́૷౯̧̠̹́ͥ̈́̽͢ͅȃ૟ਥഎ‫ۍ‬൲ྤ௮‫಼̢ͥͬג‬εΞϋΏλσͬńŕ̦঵̞̽̀ͥ͂ࣉ̢͈͉ͣͦͥȂńŕ́‫ۍ‬൲ྤίρȜ·ͬ๱૟ਥഎͅບ‫̧̜̭ͥ́͂ͥ́ث‬ȃକͬˌŉŖȂߗ‫ͬܨ‬ĮĲıııŉŖͬ೰̱̹݅ńŕ౵́൚੝อജ̱̹ȃńŕ́έ΁υȜͺΛί̳ͦ͊ȂίρȜ·͜‫ۍ̀͛܄‬൲ྤ͈ૺ࣐̦฻೰̧́ͥ͂ࣉ̢ͣͦͥȃ୞‫͉ا٭‬ńŕ౵̦̩ࣞȂ೩ńŕ౵͉ডৗ଼໦̦ཅີȂ஌֋଼໦̦ఉ̞͕̓ńŕ౵̦ષઌ̳ͥȃ̱̥̱̞̞ͧͧ̈́࿚ఴത̦̥ͩ̽̀
̧̹ȃ௮‫ג‬ෛഽ̦ถ̞͂ίρȜ·͈ńŕ౵͜೩̩̈́ͤȂ௮‫ג‬ෛഽ̦ෛ̞͂ȂίρȜ·͈ńŕ౵͉̩ࣞ̈́ͥȃίρȜ·͈அ͉ͤ͘‫ۍ‬൲ྤ͈அͤ̽̀͘͢ͅ‫̯ͥͦ͜ޣג‬Ȃ‫ۍ‬൲ྤ͈அ͉ͤ͘ͅ൳֚ۛ৪́͊ͣ̾͜
̧̦̜ͤஅ֚ͤͬ͘೰Ȫஜٝ͂൳೾ഽȫ̳̭͉ͥ͂ࣾͅඳ̜̹́̽ȃ̱̹̦̽̀ȂĲٝ࿒͂ĳٝ࿒͈ńŕ౵̦๤‫̧̞̈́́ڛ‬ȃȶ‫ة‬ŉŖո‫̦ئ‬řřίρȜ·͂౯࡞̳ͥȷ̭̦͂࡞̢̞̈́Ȃ̭͈̹͛ͅȂńŕ౵͉૞ဥ́
̧̞̈́̈́̓͂࡞̠̹ͩͦͥ̈́̽͢ͅȃ̭ͦͬ࣪໚̱̞̈́͂೰ၾ͜૞ှ଻̫ࠧͥͅȃ͉ͩͦͩͦȂ௮‫ג‬सၾͬड೩ࡠ̱̦͂̈́ͣ‫ۍ‬൲ྤ͈அ͈ͤ͘໙ͬਲြͤ͢઀̯̩̳ͥńŕ ŏŶŮţŦųĮŤŰůŵųŰŭŭŪůŨġ ŔźŴŵŦŮ
ȪŌŰŮŢŵŴŶġ Ŧŵġ Ţŭįġ ŋġ ńŢųťŪŰŭĭġ ĳıĲĳĭġ ŦűŶţȫͬ‫ٳ‬อ̱̹ȃ̭̻̞ͦͬ̀͜Ȃέ΁υȜͺΛίńŕ́ȶஜٝ͂൳ၾ͈௮‫ג‬सၾȷȂȶఘਹ൚̹͈ͤ௮‫ג‬ġ सၾȷͬൎဓ̳ͥͤ͢͜ஜ͈ٝ‫ۍ‬൲ྤ͈அͤͬ͘ड͜ୃ‫̷ͅږ‬̢̭̦ͧͥ͂‫خ‬ෝ̜́ͥȪŌŰŮŢŵŴŶġŦŵġŢŭįġŋġńŢųťŪŰŭĭġĳıĲĴȫȃġུ༹͈ႉ઄എခဥ଻Ȃඅ̷͈ͅૄ࠯‫́ئ‬͈ίρȜ·͈་‫̞̀̾ͅا‬Ȃജབͬ੆͓ͥȃ䋭 㪐㪋 䋭

ႉ઄ŔĮĵĮĴ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

૤௫ ŎœŊ ͥ͢ͅະհ೰ίρȜ·ͼιȜΐϋΈ͈͒ಯ୽

Ĳ
ĳ
Ȫ২֓ȫ
ഛ૰ٛ૧ࡣٖພ֭૤௫ࠬ‫ۯ‬ΓϋΗȜȂȪ২֓ȫഛ૰ٛࡣٖພ֭ ĳĲ ႉ઄༶ৣ஌໐ȂĴ ࣭ၛ੏۪‫ܕ‬ພΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬໐ழ૕໦ٜෝͬ঵̭̥̾͂ͣίρȜ·Ȃඅͅະհ೰ίρȜ·͈ৗഎ૷౯ͅఱ̧̈́‫ܢ‬ఞ̦‫̵̞̀ͦͣܙ‬ͥȅŎœŊͬဥ̞̹ະհ೰ίρȜ·ͼιȜΐϋΈ̞͉̾̀ͅȄᴢ൲ྤ͈ႀ்֖͉̩̥́ͣႉ઄؊ဥ̯ͦȄ̷͈ခဥ଻͉ࢩ̩෇ে̯̞ͦ̀ͥȅ༷֚Ȅ‫ۍ‬൲ྤ͈ະհ೰ίρȜ·ͼιȜΐϋΈͅ‫̱̀͜۾‬ĳıııා̥ࣼͣ༭̦࣬८ࡉ̯ͦȄِș͈ঔ୭்́͜‫͈̭̥ͣܢ‬ŎœŊͥ͢ͅ‫ۍ‬൲ྤ͈ະհ೰ίρȜ·ͼιȜΐϋΈ৾ͤͅழ̧̹ͭ́ȅȁίρȜ·ͼιȜΐϋΈ͉ไဥĲįĶŕġŎœŊͬဥ̞̀Ȅ๱௮‫ג‬ĴŅĮŕĲ‫ْ಺ޑ‬௨ͅţŭŢŤŬġ
ţŭŰŰť༹ͬঀဥ̱࣐̠ȅίρȜ·͈൳೰͈̹͛ŘũŰŭŦġŉŦŢųŵġńŰųŰůŢųźġŎœłͥ͢ͅŢŹŪŢŭْ௨͈͂ŧŶŴŪŰůġ
ŪŮŢŨŦͬै଼̳ͥȅίρȜ·͈൳೰ࢃ͉ίρȜ·ඤ͈૞࣢‫ޑ‬ഽĩűŭŢŲŶŦġŵŰġŮŶŴŤŭŦġųŢŵŪŰ ļġőŎœȄ
߃ཌྷ͈૤೰̱̹݅ḙ͈̏ŉŊő͉໲ࡃഎࣉख़̥ͣίρȜ·ඤ͈੄ࠬ͞ডৗͬ฽‫خ̞̱ͥ̀ד‬ෝ଻̦‫̩ޑ‬ȄůŰůĮŉŊő
ͅ๤̱૤௫ńŕ͈͂చ๤̥ͣະհ೰ίρȜ·͈අಭ̯͂ͦͥűŰŴŪŵŪŷŦġ ųŦŮŰťŦŭŪůŨȄŭŰŸġ ńŕġ ťŦůŴŪŵź

口頭発表޼͈͂૞࣢‫ޑ‬ഽ͈๤ၚĪͬॳ੄̱Ȅ૞࣢‫ޑ‬ഽ͈̞ࣞ౵ͬ঵̾ίρȜ·ͬ ũŪŨũġŪůŵŦůŴŪŵźġűŭŢŲŶŦ ĩŉŊőĪ ͂

会長招待講演 シンポジウムŎœŊ͉༶ৣ஌๭ธ̦ྫ̩௮‫ג‬स͜ঀဥ̱̞̹̈́͛Ȅ૯͈փྙ́๱૟ਥഎْ௨૷౯༹̜́ͤȄࣞഽ̈́඲

特別講演ɛ୼ॄġ࿻ဉ ĲȂ࿐஑ġ౺ং ĳȂ࿤࢛ġܵຳ ĴȂࡣٖġ૝຃ Ĳ

ɃĴıŉŖͬఉ̩ခ̱Ȅ̹͘ŊŗŖŔષ͉‫ࡘ̞ޑ‬ଚ΀΋Ȝਫ਼ࡉͬခ̳ͥ̈́̓Ȅະհ೰ίρȜ·ͬাऐ̳ͥ͂

ŤŶŵġ Űŧ౵͉Ĳįĵ́Ȅ̷͈ࢃ͈೏୥಺औ͉́ŉŊőછ႕̥ͣခփͅఉ̩͈ͼαϋΠĩłńŔȄłőĪ̦อછ̳̭ͥ
̧̦ٜ̹͂̽̀ȅ͉ࣽٝŉŊő̞͈̾̀ͅ૧̱̞౶ࡉͬ൩̢̦̈́ͣ͘૤௫ŎœŊ͈ະհ೰ίρȜ·࠿੄͈‫خ‬ෝ଻̞̾̀ͅ੆͓ͥȅ

ポスター発表 ＹＩＡ選考発表̯ͦͥਫ਼ࡉ͈අಭͬခ̧̱̞̭̦̥̹̀ͥ͂ͩ̽̀ȅ੿ြഎͅͼαϋΠͬ୆̲ͥ‫خ‬ෝ଻ͬ঵̾őŎœ͈

著者索引

䋭 㪐㪌 䋭

ႉ઄ŔĮĵĮĵ

ŗŶŭůŦųŢţŭŦġűŭŢŲŶŦġ૷౯̤̫ͥͅġŊŗŖŔġ͈ૺ༜͂੿ြജབ
ɛࣞ५ġ಑ܵȂᎢġ‫ގ‬ঃȂ๳࢛ġ݅হȂ᠟൥ġ‫כ‬Ȃ໹५ġඈ঎඾ུఱ‫ڠ֓ڠ‬໐੏۪‫ܕ‬ඤ‫ش‬ŊŗŖŔͥٝ͢ͅ໘‫ܢ‬૤޼ࢸणۛ৪̤̫ͥͅୣහࠬ‫ۯ‬Ȇ๱ୣහࠬ‫ͬۯ‬۷ख़̱̹ȃ̹͘Ȃະհ೰ίρȜ·͉ඤণ‫ޢ‬ਫ਼ࡉ͈ؕ૗ίρȜ·͂ŊŗŖŔ͈ࠗ௶ࠫ‫ͬض‬ဥ̞̀࠿൦̱̹ȃ‫ۍ଻ݢ‬છ࢓߲ۛ৪͈ࢸणୣහࠬ
‫́͂ۯ‬๱ୣහࠬ‫̞̀̾͜ͅۯ‬ŊŗŖŔͥ͢ͅ۷ख़̱Ȃؕ૗ίρȜ·ͬŊŗŖŔ͈ਔ෨ତٜଢ଼࣐̹ͬ̽ȃ̹͘Ȃൠෂພۛ৪̤̫ͥͅίρȜ·଻ે̞̾̀͜ͅ࠿൦̱̹ȃŊŗŖŔͥ͢ͅ࠿൦ࣜ࿒͉೰ၾഎບ‫ث‬Ȃࠁఠഎບ‫ث‬ĩ༊૤଻ȆίρȜ·଻ેȆయੲ଻‫ڐ‬ఱ͈ခྫȆ୞‫͈ا٭‬ခྫȂޫहĪ࣐̞ͬ๤‫࠿ڛ‬൦̱̹ȃ̯ͣͅȂŊŗŖŔ
ષ͈ίρȜ·͂ඤণ‫̹̯ؕͦ੄࠿́ޢ‬૗ίρȜ·̦֚౿̱̹ພ་́ਔ෨ତٜଢ଼࣐̹ͬ̽ȃ‫ۍ଻ݢ‬છ࢓߲ۛ৪͉́Ȃ༊૤଻ίρȜ·Ȃ೩ܵഽίρȜ·Ȃయੲ଻‫ڐ‬ఱȂ೟នࠁ଼ͬȶࣞອഽͅ෇̹͛ȃŭŪűŪťġ
űŰŰŭ͉ĳıĦȂ୞‫͉ا٭‬ĶĸĦͅ෇̹̦͛ͣͦ૬ह଻̦ఉ̥̹̽ȃ̹͘Ȃࠬ‫ۯ‬ඤণ‫ͥ͢ͅޢ‬۷ख़͉́Ȃؕ૗ίρȜ·͂ŊŗŖŔਫ਼ࡉ͈͂๤‫͉́ڛ‬Ȃؕ૗ίρȜ·͈ؕ૗ഽ̦̫ࣞͦ͊ਔ෨ତٜଢ଼͉́ȂŏŦŤųŰŵŪŤġ
ńŰųŦ͈‫̦ࣣڬ‬ခփͅ௩‫̹̞̱̀ح‬ȃ̹͘Ȃൠෂພࣣ໵ۛ৪͈ίρȜ·͉ȂťŪŧŧŶŴŦġ ŭŰůŨ̈́ພ་̜́ͤȂűŰŴŪŵŪŷŦġ ųŦŮŰťŦŭŪůŨ͈ອഽ̦ઁ̞̭̦̈́͂අಭ̜̹́̽ȃŊŗŖŔ͉́Ȃࢸणୣහࠬ‫͍̤͢ۯ‬๱ୣහࠬ‫̞̤̀͜ͅۯ‬యੲ଻‫ڐ‬ఱฺ̠ͬ༊૤଻͈ΕέΠίρȜ·̦෇̹͛ͣͦȃൠෂພ̈́̓ۛ৪‫ܖ‬ய৖ۛ͢ͅ
ͤίρȜ·͈଻ે͉։̈́ͥ͂͜ࣉ̢ͣͦȂࠬ‫ۯ‬ඤহၷ̢̳̠ͥ́͜ίρȜ·଻ેͬ౶̭͉ͥ͂ਹါ͂
̤ͩͦͥ͜ȃŊŗŖŔͥ͢ͅະհ೰ίρȜ·͈Α·ςȜΣϋΈ͉ࣽࢃŐŎŕ͉ͅຈါະ‫͂ͥ̈́͂ࠧخ‬এͩͦͥȃඅͅȂίρȜ·հ೰‫ا‬হၷ͈ΑΗΙϋহၷո‫ॼ͈ٸ‬ဒςΑ·͈͒చ؊ͬ‫̀͛܄‬ਹါ̜͂̈́ͥ́
̠ͧȃ̹͘ȂίρȜ·հ೰‫ا‬Ȃపੀͬ‫͈̺̹֚̾ે̧࡛ͥ́෇ږ‬κΘςΞͻȜ̜́ͤȂࣽࢃ͉ͤ͢৘க
എͅႉ઄͈ા́ঀဥ̯ͦͥ͂এͩͦͥȃ䋭 㪐㪍 䋭

ႉ઄ŔĮĵĮĶ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineŗŶŭůŦųŢţŭŦġűŭŢŲŶŦ ૷౯̤̫ͥͅ Őńŕ ͈ૺ༜͂੿ြജབ

Ĳ ඾ུ֓‫ش‬ఱ‫୷ڠ‬ဩཤ௙ພ֭੏۪‫ܕ‬ΓϋΗȜȂĳ २‫࢚ק‬୆মު౬ખͬ၌ဥْ̱௨‫̳ͥا‬૧̱̞૷౯༹́Ȃ߃ා‫ۍ‬൲ྤ͈ͼιȜΐϋΈΏΑΞθ̱͂̀ႉ઄ঀဥ̯̞ͦ̀ͥȃŐńŕ͉ٜ௨ഽĲĶĮĳı ŮŪŤųŰŮŦŵŦų͈ࣞ໦ٜෝْ௨ͬ೹‫̭̳ͬ͂ͥރ‬डఱ͈අಿ̳͂ͥȃ̯ͣͅඅಭഎ̈́ΏΈ΢σΩΗȜϋ̥ͣডৗȂ஌֋Ȃ୞‫଼ا٭‬໦̞̹͂̽ίρȜ·͈ࢹ଼଼໦Ȃࠬ஀͈ୃ‫̈́ږ‬ழ૕૷౯ͬ‫خ‬ෝ̳ͥͅȃ‫׶‬છ଻ळ༾૫੕̦ཅີ́Ȃถ̞஌֋଻๭྄̦ডৗ΋ͺͬໞ̠ŵũŪůĮŤŢűġŧŪţųŰŢŵũŦųŰŮŢ
ȪŕńŇłȫ
͈෫Ⴈ͂ࠚ๷̈́ඤ྄વ‫͍̜ͬͭͣͥ́ٺ‬௙ઠ̱̹ίρȜ·෫౦͉‫ۍ଻ݢ‬છ࢓̧߲̭̳ͬ֨ܳ৽֦͂̈́ͥȃŐńŕْ͈௨අ଻ͬ၌ဥ̱̀ŕńŇł͞‫׶‬છळ༾̜́ͥζ·υέ͹Ȝΐਬᢎ͈൳೰̧࣐̠̭̦ͬ̈́͂́ȂŷŶŭůŦųŢţŭŦġ űŭŢŲŶŦ ͈අಭ͈֚໐ͬࠁఠ‫ڠ‬എͅ૷౯̳̭̦ͥ͂‫خ‬ෝ̈́ͥͅȃ૧̱̞ܿ੅ͬ؊ဥ̱̹ষଲ

口頭発表యŐńŕ̞̾̀͜ͅ੆͓ͥထ೰̜́ͥȃ

会長招待講演 シンポジウム࢕ۙખ౯௄༹ȪŰűŵŪŤŢŭġ ŤŰũŦųŦůŤŦġ ŵŰŮŰŨųŢűũź Ļ Őńŕȫ͉߃୤‫ٸ‬஌ͬழ૕ͅચৣ̳̭ͥ͂́୆̲ͥۙ

特別講演ɛࣞ࿤ġٗਰ ĲȂୄ࿤ġୈ຃ ĲȂକ࿤ġշ֚ ĳ

ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪐㪎 䋭

ႉ઄ŔĮĵĮķ

ŗŶŭůŦųŢţŭŦġűŭŢŲŶŦ ૷౯̤̫ͥࠬͅ‫ۯ‬ඤণ‫ૺ͈ޢ‬༜͂੿ြജབ
ɛષനġ‫ࠉޕ‬ఱि࠙ख़ພ֭੏۪‫ܕ‬ඤ‫ش‬ࠬ‫ۯ‬ඤণ‫͉́ޢ‬Ȃୃુࠬ‫ۯ‬༃͉ฒ૗ͅࡉ̢ȂŷŶŭůŦųŢţŭŦġ űŭŢŲŶŦġ ĩŗőĪ͉ؕ૗ພ་̱͂̀࠿੄̯ͦͥȃŐńŕ́૷౯‫خ‬ෝ̈́ŵũŪůĮŤŢűġ ŧŪţųŰŢŵũŦųŰŮŢġ ĩŕńŇłĪ͈஌֋଻๧྄͈࢚͙͂ؕ૗಺͈೾ഽ͉ͅၻࢡ̈́
௖‫̥̭̜̦ͣ͂ͥ۾‬Ȃࠬ‫ۯ‬ඤণ‫̀̽͢ͅޢ‬ŕńŇłͬ૷౯̧́ͥȃ̯ͣͅȂ‫଻ݢ‬૤޼ࢸणୣහພ་͈ĺıɓոષ̤̞̀ؕͅ૗ίρȜ·ͬ෇̭̥͛ͥ͂ͣȂ࿩ĸıɓͬ୸̞͛ͥ͂ͩͦͥίρȜ·෫Ⴈ̴͈͙̈́ͣȂ࿩Ĵıɓͬ୸̞͛ͥ͂ͩͦͥίρȜ·͍͈ͣͭພ་͜Ȃඤণ‫ޢ‬എ͉ؕͅ૗ίρȜ·͂ࣉ̢ͣͦͥȃ̳̻̈́ͩȂίρȜ·෫Ⴈ̧̹̳ͬ‫خ‬ෝ଻͈̞ࣞŗő̜́ͥŕńŇł̴͈͙̈́ͣȂίρȜ·̧͍̹̳ͣͭͬ‫خ‬ෝ଻͈̞ࣞŗőؕ͜૗ίρȜ·̱͂̀૷౯̧́ͥ͂ࣉ̢ͣͦͥȃ̹͘Ȃ͈֚̾ؕ૗ίρȜ·̥ͣ‫ۍ଻ݢ‬છ࢓߲̦อછ̳ͥອഽ͉๱ુͅ೩̞̦Ȃ‫ۍ‬൲ྤඤͅంह̳ͥؕ૗ίρȜ·̦ఉ̞͕̓੿ြ‫ۍ଻ݢ‬છ࢓߲ͬอછ̳ͥ‫خ‬ෝ଻̞̭̦ࣞ͂͜া̯̞ͦ̀ͥȃńŌŅۛ৪͉ͤ͢ఉ̩͈ؕ૗ίρȜ·ͬ঵̞̭̽̀ͥ͂
̦া̯̤ͦ̀ͤȂ‫ۍ଻ݢ‬છ࢓߲อછςΑ·̦̞ࣞ‫ܥ‬੬͈֚̾͂ࣉ̢ͣͦͥȃ̹͘‫ͅݙ‬ȂΑΗΙϋহၷ̽̀ؕ͢ͅ૗ίρȜ·͈ؕ૗಺͉ప૗̱ȂίρȜ·͈հ೰‫ͬا‬ඤণ‫ޢ‬എͅ૷౯̧́ͥȃ̱̥̱Ȃࠬ‫ۯ‬ඤণ‫̀̽͢ͅޢ‬Ȃ‫ۍ଻ݢ‬છ࢓߲ͬอછ̱̞̞̀̈́ྫછ࢓଻ίρȜ·෫౦̦ఉ̩ంह̳̭̦ͥ͂ྶ̥̯ͣͅ
̞ͦ̀ͥȃ̳̻̈́ͩȂŗő͉෫౦̱̀͜Ȃ̷͈̮̩֚໐̱̥‫ۍ଻ݢ‬છ࢓߲ͬอછ̵̴Ȃఉ̩͉ྫછ࢓଻ͅ
হ࿴̱̞̩̀͂ࣉ̢ͣͦͥȃ̷͈̹͛Ȃŗő૷౯͈डఱ͈࿚ఴ͉Ȃ̷͈૷౯̦ୃ̱̥̹̥̽๛̥ͬႉ઄എ
ͅ౶༹༷ͥȂ̳̻̈́ͩ෫౦̱̹̥๛̥ͬ౶༹༷̦ͥంह̱̞̭̜̈́͂́ͥȃ̯ͣͅȂ෫౦̱̹ίρȜ·̦‫ۍ଻ݢ‬છ࢓߲ͬอછ̳̹ͥ͛ͅຈါ̈́ૄ࠯̦ٜྶ̴̯̤ͦ̀ͣȂ̷͈ٜྶ̦ŗő͈૷౯ոષͅਹါ́
̜ͥȃࠬ‫ޛ͞଻࡙஀͈ࠬס‬ॏഽ̦࢓༞̱͂̀ࣉ̢̞ͣͦ̀ͥȃະհ೰‫ޛ‬૤છ̥ͣ‫଻ݢ‬૤޼ࢸण͈͒ૺ
ജထཡ͉ͅΑΞϋΠၣ౾̦ခဥ̜̦́ͥȂŗő̜̞͉ͥ෫౦ίρȜ·ͬ̾͜ಎ൝ഽ‫ޛ‬ॏພ་ͅచ̱̀͜ȂΑΞϋΠၣ౾̦‫଻ݢ‬૤޼ࢸणอછထཡ͈̹͛ͅခဥ̈́‫خ‬ෝ଻̦̜ͥȃ̭̞͉ͦ̾̀ͅȂࣽࢃ͈ఱܰ࿅
ႉ઄দࡑͥ͢ͅ࠿൦̦‫ܢ‬ఞ̯ͦͥȃ䋭 㪐㪏 䋭

ĺ࠮ĳĹ඾ȪാȫġĺĻııȡĲĲĻııġġలˎٛાΏϋεΐ;θġႉ઄ ŔĮĶȶࣞࠬգࣣ໵છ̪ͬ̾̈́ࠬ‫ۯ‬୆໤‫ڠ‬ȷġႉ઄ŔĮĶĮĲ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineࣞࠬգ͂শࠗ֒ഥঊ
特別講演ɛ࿤੄ġࢣ֚
ऎٖఱ‫ڠ֓ڠ‬໐੏۪‫ܕ‬ඤ‫ش‬·σȜί̱̹ͬٚ໦ঊι΃ΣΒθ̽̀͢ͅȂ̷̤͢ĳĵশ‫ۼ‬ਔ‫́ܢ‬་൲̳̭ͥ͂́୆͙੄̯ͦͥ‫ٽ‬඾ςΒθ͈̭̜͂́ͥȃࠬ‫ܥۯ‬ෝ͜඾ඤ་൲̦̜ͤȂ̷ͦͬଷࢄ̳ͥఘඤশࠗ֒ഥঊ͈୆ၑഎփ̦ٜ݅ྶ
̯̜ͦ̾̾ͥȃሶ඿႒͉́஠͈̀ळ༾ͅশࠗ֒ഥঊ̦ంह̱Ȃ૤޼Ȃࠬ‫ۯ‬໹‫޼ڲ‬Ȃࠬ‫ۯ‬ඤ๧ळ༾Ȃ஍֋ٔळ༾ͅশࠗ֒ഥঊ̦อ࡛̱̞̀ͥȃ࡛हȂőņœĲĭġőņœĳĭġńœŚĲĭġńœŚĳĭġńōŐńŌĭġŃŎłōĲ̦̈́̓‫ٽ‬඾ςΒθͬैͤ੄̳৽ါ̈́শࠗ֒ഥঊ͂ࣉ̢̞ͣͦ̀ͥȃŃŎłōĲࠧఅζ;Ά͉ࠬգ͈඾ඤ་൲͉ક৐̱Ȃ΃Ξ΋ρηϋ͈ॲ୆೩‫̵ࣣ̀ͩ͂ئ‬೩ࠬգͬ೮̳ȃ༷֚ȂńœŚĲİĳġ ࠧఅζ;Ά͉Ȃ໗ଅ͈ͺσΡΑΞυϋॲ୆̦ᄤૺ̱̀૙‫ۜ؂‬਋଻ࣞࠬգͬ೮̳̭̦ͥ͂ྶ̥̯̹ͣͦͅȃőņœĳࠧఅζ;Α͉ȂͺΓΙσࣸଡ̥͈ͣࠬ‫ۯ‬ඤ๧ஜߐळ༾Ȫņőńȫ͈൲֥̦ࡘઁ̳̭̦ͥ͂̈́̓౶̞ͣͦ̀ͥȃಎଥ͂ྎઑশࠗ֒ഥ
ঊ̦ఘඤশࠗͬ΋ϋΠυȜσ̱̞̦̀ͥȂ̷͈ͦͣশࠗ֒ഥঊ͉ΥΛΠχȜ·ͬैͤȂႲࠈ͂൳಺Ώ

口頭発表΋ςϋঁࠣͥࠬ͢ͅ‫ۯ‬౸۱฽؊̦೩‫̭̳͂ͥ͞ئ‬Ȃ‫ۯ͉̹ࠬࠬ͘ݹ‬ඤ๧௩૓֦ঊĩŗņňŇĪঁࠣͥ͢ͅ

会長招待講演 シンポジウムఘඤশ͉ࠗ͂ȂȨশࠗ֒ഥঊȩ͂ࡤ͊ͦͥ֒ഥঊ߲͈ഢৢ‫̦଻ڰ‬ȂεΐΞͻήȆΥ΄ΞͻήέͻȜΡΨΛΑΞθͬခ̱̞̀ͥȃণ࢐एષ‫ͅړ‬ంह̳ͥಎଥশࠗ֒ഥঊ͉Ȃ࢕̲ͬۜ‫̯ͦا଻ڰ‬Ȃઐ‫ض‬ఘͅैဥ̱

͈ςΒθͬ಺୯̱̞̀ͥȃőņœĳ͉Ŏłő΅΢ȜΔ͞ńŌĳͤ͢ͅςϋॸ‫̭̯́͂ͥͦا‬Ȃ‫଻ڰ‬་൲̦಺୯̯̞ͦ̀ͥȃႉ઄͈́শࠗ֒ഥঊ‫͈଻ڰ‬༭͉࣬ઁ̥̹̦̈́̽Ȃِș͉࿉༫ळ༾ͬဥ̞̹শࠗ֒ഥঊ
‫௶଻ڰ‬೰ͬ༭̱̹࣬ȃ༹̭͈༷́ȂΏέΠχȜ΃Ȝ͈শࠗ֒ഥঊ‫௶ͬ଻ڰ‬೰̱̹̭͂ͧȂΟͼχȜ΃Ȝͅ๤‫̱̀ڛ‬๱‫ͅ଻ݙخ‬་‫̥̭̞̱ͣ͂ͥ̀ا‬Ȃ‫ٸ‬എ̈́ςΒθ։ુ̦ඤഎ̈́শࠗ֒ഥঊͬ་‫̵̯ͥا‬ম̦াऐ̯̹ͦȃ૤ࠬ‫ۯ‬Ȇඤ໦๥ࠏ͈௫‫͈ܕ‬শࠗ֒ഥঊ͈‫಺଻ڰ‬୯ι΃ΣΒθͬ࠿൦̳ͥম́Ȃࣞࠬգ͈ພఠٜྶ͈͈֚̾ͺίυȜΙ͂̈́ͥম̦‫ܢ‬ఞ̯ͦͥȃ

ポスター発表 ＹＩＡ選考発表ιρΠΣϋ໦๥ͬଷࢄ̱ȂଗྨȆ‫୑ژ‬Ȇૂ൲ͬ঑෻̳ͥȃྎઑশ͉ࠗ࢕๱ۜ਋଻́Ȃయ৫ȆࠬգȆඤ໦๥ࠏ

著者索引

䋭 㪐㪐 䋭

ႉ઄ŔĮĶĮĳŅŏł χ·Ιϋͬဥ̞̹ࣞࠬգ૧ܰহၷ
ɛಎ૰ġ߼ඃ ĲȂ૩‫ئ‬ġၧ֚ ĳ
Ĳ ఱिఱ‫ڠ‬ఱ‫֭ڠ‬Ⴒࣣ઀঱อో‫ࢫ࠲شݪࡄڠ‬อో֓‫້࣒ܙڠ‬जȂĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬ႉ઄֒ഥঊহၷ‫ڠ‬಼ࣞႢ‫ا‬২͈ٛ́୆‫ڰ‬ਠ‫۝‬ພͅచ̳ͥ૧̱̞হၷ༹̱͂̀χ·Ιϋ͈‫ٳ‬อͅಯ୽̱̞̀ͥȃࣞࠬգ͉ոஜ̥ͣχ·Ιϋ͈‫ٳ‬อ͈ࡄ‫̧̹̯̦̀ͦݪ‬৖̜ۛ́ͤȂඅͅτΣϋȆͺϋΐ΂ΞϋΏϋࠏͬດഎ̱̹͂χ·Ιϋ͈‫ܖ‬யȆ؊ဥࡄ‫̧̹࣐̦̀ͦͩݪ‬ȃ̭͈ͦ́͘‫ܖ‬யࡄ‫́ݪ‬Ȃͺϋΐ΂ΞϋΏϋŊȂͺϋΐ΂ΞϋΏϋŊŊ ĩłůŨŊŊĪ ̤͍͢ͺϋΐ΂ΞϋΏϋ਋ယఘͅచ̳ͥβίΙΡχ·Ιϋ͉ুடࣞࠬգอછρΛΠĩŔŉœĪ́ခփ̈́ࢯఘ‫͈ث‬ષઌ͂ࠬգ೩‫͛෇ͬئ‬Ȃ̯ͣͅĳııĹා͉ͅႉ઄দࡑ́łůŨŊŊχ·Ιϋൎဓͥࠬ͢ͅգ͈ခփ̈́೩‫̦ئ‬༭̯̹̦࣬ͦȪōŢůŤŦŵȫȂਰ໦̈́ࣛգͅຈါ̈́ࢯఘ‫͈ث‬ષઌ͉ౣ‫෇̥̱ۼܢ‬̴͛ͣͦȂࢵ̈́ͥ٨஝̦‫̞ͥ̀ͦͣ͛ݥ‬ȃ̷̭́Ȃِș͉ࣞࠬգͬই̱̹͛͂୆‫ڰ‬ਠ‫۝‬ພͅచ̳ͥχ·Ιῧ̱̀Ȃুࡨ྾‫ע‬৖ۛͬٝ๰̱̦̞̈́ͣࣞ͜ခ࢘଻ͬ৘࡛̳̹͈ͥ͛‫଻ס‬྾‫৽ע‬൵χ·Ιϋͬ‫ٳ‬อ̱̹ȃࣞࠬգͬచય̱̹͂χ·Ιΰ͉Ȃχ·Ιϋ͈ࢯࡔ̱͂̀৽̱͂̀ळ༾‫ͅٸ‬ంह̱ࠬಎෛഽ
͈೩̞łůŨŊŊͬ஖఼̱ȂβίΙΡ͂Ņŏłχ·Ιϋ͈ၰ༹༷͈༷ͬদ͙̹ȃβίΙΡχ·Ιΰ͉ȂłůŨŊŊĮŌōŉͬࢯࡔ̱͂ȂͺΐνΨϋΠ̱͂̀ŇųŦŶůťĨŴġ ŢťūŶŷŢůŵͬဥ̞̀ńĶĸŃŭİķζ;ᾼĳ਩ྀͅĴٝൎဓ̱̹̭͂ͧȂłůŨŊŊͅచ̳ͥࢯఘ‫͉ث‬ခփͅષઌ̱̹ȃ̭͈ࢯఘ‫͈ث‬ષઌ͉ෛഽջం଻̜́ͤȂͺϋΐ΂ΞϋΏϋŊ ͞ͺϋΐ΂ΞϋΏΦȜΊϋͅచ̳ͥࢯఘ͉ॲ୆̯̥̹ͦ̈́̽ȃ̯ͣͅȂłůŨŊŊͬດഎ̱̹͂Ņŏłχ·Ιῢ̤̞͉ͅȂࢯࡔ೹াෝ̹ͬࣞ͛ͥ͛ͅŃ߿۴‫ͼ;׶‬σΑ͈΋ͺ౩ฒ͂łůŨŊŊ
ͬဏ̵ࣣ̯̹ίρΑηΡŅŏłͬဥ̞̀ȂুடࣞࠬգอછρΛΠͅૻ̱̈́ಕৣ‫ͬܕ‬ဥ̞̀๧ඤͅĳ਩ྀͅĴٝ֒ഥঊ൵ව࣐̹ͬ̽ȃࠫ‫ض‬ȂłůŨŊŊͅచ̳ͥࢯఘ‫͈ث‬ခփ̈́ષઌ̷ฺ̠͂ͦࠬͅգ͈೩‫͛෇ͬئ‬Ȃൎဓࢃķ̥࠮‫ۼ‬ոષ঵௽̱̞̹̀ȃոષ͈ࠫ‫ͤ͢ض‬ȂłůŨŊŊͬດഎ̱̹͂χ·Ιϋহၷ͉̞́ࣞհ஠଻
ͬ౜༗̱̦̈́ͣခ࢘଻̞̫ͬࣞ͛̀ͥ‫خ‬ෝ଻̦̜ͤȂࣽࢃ͈อജ̦‫ܢ‬ఞ̧́ͥ͂ࣉ̢̹ͣͦȃ䋭 㪈㪇㪇 䋭ႉ઄ŔĮĶĮĴ

ɛ५ུġࢼ֚
ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬ჇාȆଅ௫ඤ‫ڠش‬৽ఘ͉ͺϋΐ΂ΞϋΏϋŊŊͥ͢ͅň౩ฒ‫ވ‬࿨߿ͺϋΐ΂ΞϋΏϋŊŊ Ĳ߿਋ယఘĩłŕĲĪ͈‫̜ͥ́ا଻ڰ‬ȃłŕĲ͈‫ۯ͉ࠬا଻ڰ‬ਓੀ͞ͺσΡΑΞυϋॲ୆ͥ͢ͅఘ‫ס‬ಡၣ̧̭̳̭ͬ֨ܳ͂́ࣞࠬգ଼͈֦͂
̺̫̩̈́ͥ́̈́Ȃఘழ૕ͅೄ୪എ̈́ੱ‫̳̭ܳͬٺ‬ম́൲ྤࣁ‫͞ا‬ńŌŅ൝ఉ̩͈ࣞࠬգࣣ໵છ͈ૺജͅ
ਹါ̈́࿨‫̞̥ͥ̀̽̈́ͣͅྶ̥ͣݪࡄ͈̭̦̭̳̹́ͦ͂͘ضͬڬ‬ȃ༷֚Ȃࣞࠬգۛ৪͉́ॸ‫ا‬ΑΠτΑ̦ᄤૺ̱̤̀ͤࠬಎ͈ŭŰŸġ ťŦůŴŪŵźġ ŭŪűŰűųŰŵŦŪůĩōŅōĪ̦ॸ‫ે̞̳̯ͦ͞ا‬ఠ̜̭̦ͥ͂ͅࡣ̩̥
ͣ༭̯̞࣬ͦ̀ͥȃॸ‫ا‬ōŅō͉ζ·υέ͹Ȝΐͅ᭻૙̯ͦࠬ‫׶ۯ‬છ̧̭̳̦ͬ֨ܳȂ̷ͦո‫ۯࠬͅٸ‬༃ͅంह̳ͥτ·Ιϋအॸ‫ا‬ōŅō਋ယఘĩōŐřĮĲĪࣣ̱ࠫ̀ͅ൲ྤࣁ‫ͬا‬௯ૺ̳̭̦ͥ͂ྶ̥ͣ̈́̽ͅ

ЀŃ൝ఉ̩͈ळ༾ඤΏΈ΢σഥోࠏͬ‫̦̭̳͂ͥا଻ڰ‬༭̯̞̦࣬ͦ̀ͥȂōŐřĮĲ̦ॸ‫ا‬ōŅōࣣ̱̹͂ࠫࢃ͈̠̓͢ͅळ༾ඤΏΈ΢σͬഥో̳̥͈ͥમळ̞͉̭̾̀ͦ́͘ͅྶ̥̥̹ͣ́̈́̽ȃِș͉

口頭発表̞̀ͥȃࠬ‫ۯ‬ඤ๧ळ༾̤̞̀ͅॸ‫ا‬ōŅō͉ōŐřĮĲ̱ͬٚ̀ŏłŅőŉ΂΅ΏΘȜΔȂŎłő΅΢ȜΔȂŏŇĮ

会長招待講演 シンポジウムτΣϋĮͺϋΐ΂ΞϋΏϋࠏ͉୆ఘ̤̞̀ࠬͅգ֋঵ͅಎ૤എ̈́࿨‫̳̹ضͬڬ‬ઌգࠏ̜̦́ͥȂ̷͈

特別講演ͺϋΐ΂ΞϋΏϋ ŊŊ ๱ջం଻ͺϋΐ΂ΞϋΏϋ ŊŊ ਋ယఘ‫ͥ͢ͅا଻ڰ‬૧̹̈́ࣞࠬգࣣ໵છૺജ‫ࢹܥ‬プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineōŐřĮĲ͈ळ༾ඤΏΈ΢σഥోι΃ΣΒθͅłŕĲ̦‫۾‬ဓ̱̞̞̠̀ͥ͂‫ب‬୰ͬၛ̀ࡄ‫̧̹࣐̀̽ͬݪ‬ȃ̳̭ͥ͂ͬळ༾৘ࡑ́ࡉ੄̱̹ȃ̹͘ ŦŹ ŷŪŷŰ ͈࠿൦̤̞̀ͅॸ‫ا‬ōŅōͥࠬ͢ͅ‫ۯ‬ඤ๧‫ܥ‬ෝવ‫̦ٺ‬łŕĲջం଻̜̭́ͥ͂ͬাऐ̳ͥࠫ‫ͬض‬ං̞̀ͥȃͺϋΐ΂ΞϋΏϋŊŊͤ͢ͅōŐřĮĲ͈อ࡛̦ષઌ̱
ॸ‫ا‬ōŅōͤ͢ͅłŕĲ͈อ࡛̦ષઌ̳̭̦ͥ͂༭̯̞̭̥࣬ͦ̀ͥ͂ͣȂōŐřĮĲ͂łŕĲ͉ഢৢ಺୯͂
ΏΈ΢σഥో‫͈ࢹܥ‬ၰ࿂́‫಺ފ‬എͅैဥ̱̞̭̦̀ͥ͂াऐ̯ͦͥȃၰ৪͈ྟ୪̈́·υΑΠȜ·͉ඊၛ̱̹‫֦ࡏܓ‬ঊ͂ࣉ̢̧̹ͣͦ̀ࣞࠬգ͂ডৗ։ુછ̦ΏΈ΢σഥోࠐႹͬ‫ވ‬ခ̳̭ͥ͂ͬা̳͜
͈̜́ͤȂࣽࢃ͈ࣞࠬգࣣ໵છহၷ୽ၞͬࣉ̢ͥષ́‫ྙޟ‬૬̞ȃ

ポスター発表 ＹＩＡ選考発表࡛ह́͘ͅōŐřĮĲ͉ळ༾྄ષ́łŕĲࣣ̱̤͂ࠫ̀ͤॸ‫ا‬ōŅō͉ōŐřĮĲ͈ࣣ͂ࠫͤ͢ͅłŕĲͬ‫ا଻ڰ‬

著者索引

䋭 㪈㪇㪈 䋭ႉ઄ŔĮĶĮĵ

ŊůŵŦŨųŢŵŪŷŦġųŰŭŦġŰŧġůŰůĮŮźŰŤźŵŦŴġŪůġŭŦŧŵġŷŦůŵųŪŤŶŭŢųġųŦŮŰťŦŭŪůŨġŢŧŵŦųġ
ŮźŰŤŢųťŪŢŭġŪůŧŢųŤŵŪŰůġŤŰŮűŭŪŤŢŵŦťġţźġũźűŦųŵŦůŴŪŰů
ɛ୤ᚧġࢤ ĲȂ઀৒ġ଼֚ ĳ
Ĳ ൐‫ނ‬ఱ‫ڠ‬ఱ‫୶شݪࡄࠏڠ֭֓ڠ‬౤ႉ઄֓‫ٳڠ‬อ࣒जȂĳ ൐‫ނ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ش‬The heart is the most important target organ of hypertension. In addition to the systemic effects including
elevation of blood pressure, sodium and water retention, the renin-angiotensin system has direct
deleterious effects on the hearts through a local activation system in tissues. Clinical benefits ofangiotensin II type 1 (AT1) receptor blockers in patients with myocardial infarction (MI) have been
established by a number of clinical studies. Although left ventricular (LV) dysfunction and remodeling is
a complicated process involving numerous interactions between cardiac myocytes and non-myocytes
including fibroblasts and vascular cells, the cell type-specific role of AT1 receptor remains unknown in
post-MI hearts. To elucidate the role of AT1 receptor in cardiac fibroblasts, we produced MI in cardiac
fibroblast-specific AT1 receptor-deficient (AT1-CKO) mice, homozygous for floxed Agtr1a allele andharboring Cre recombinase under the control of the Postn promoter. AT1-CKO mice showed a significant
improvement in survival rate after MI, as compared with control mice. At 2 weeks after MI, AT1-CKO
mice exhibited smaller heart-to-body-weight ratios, and less left ventricular end-diastolic dimension andbetter fractional shortening. Histologically, the infarct area was significantly smaller, and interstitial
fibrosis in the peri-infarct zone was milder in AT1-CKO mice than in control mice. Immunofluorescencerevealed that the number of infiltrating CD68-positive macrophages in the peri-infarct zone wassignificantly smaller in in AT1-CKO mice than in control mice. Real-time RT-PCR analysis indicatedthat mRNA expressions of fibrosis-related effectors (Tgfb1, Col1a1) and inflammatory cytokines(Tnf, Il6) in FACS-sorted cardiac fibroblasts were significantly lower in AT1-CKO than in control mice.
These results define an unexpected integrative role for AT1 receptor in cardiac fibroblasts to promote LV
remodeling after MI by exaggerating fibrotic and inflammatory processes.

䋭 㪈㪇㪉 䋭ႉ઄ŔĮĶĮĶ

ɛಅനġ଺হȂષఆġঃႿȂઐ֔ġੳȂઐུġܲਏȂཽ๶ġժঊȂષനġ࿻ढȂल൥ġෝ຃ජၻࡇၛ֓‫ش‬ఱ‫ڠ‬లˍඤ‫ش‬৖͈ۛᑋۛၚ̤͍͢ঘཌၚ̦ಠྶ̞̦ࣞͅȄ̷͈‫ܥ‬੬͉ྶ̥̞ͣ́̈́ȅ͉̭͈ͩͦͩͦͦ́͘࠿൦́Ȃ൲ྤࣁ‫ا‬௯ૺഎͅैဥ̳̯ͥ͂ͦͥőŭňŇȪథ๕ဇြ௩૓֦ঊȫ͞ŗņňŇȪࠬ‫ۯ‬ඤ๧௩૓֦ঊȫ͈ඤ֦଻ஷ‫ٺ‬໤ৗ̜́ͥ‫خ‬ဣ଻ŇŭŵĮĲȪŴŇŭŵĮĲȫ̦ńŌŅۛ৪́೩‫̭̞̱ͬ͂ͥ̀ئ‬อࡉ̱̹ȅĶİķଅ௫ഊ੄ζ;Α͈࠿൦͉́ଅ௫͂෹́ŴŇŭŵĮĲ͈อ࡛̦೩‫̭̞̱͂ͥ̀ئ‬ȂńŌŅۛ৪ࠬୄͬΪΠඤ๧ळ༾ͅൎဓ̳ͥ͂ȂŴŇŭŵĮĲอ࡛ၾ͈೩‫͂ئ‬ඤ๧ळ༾વ‫ٺ‬ζȜ΃͂ॸ‫ا‬ΑΠτΑζȜ΃͈อ࡛ၾ̦௩‫̥̭̹̱ͣ͂ح‬ȂńŌŅۛ৪͈ࠬ‫ۯ‬ඤ๧ळ༾́ŴŇŭŵĮĲॲ୆̦೩‫̦̭̞̱͂ͥ̀ئ‬াऐ̯̹ͦȃ̯ͣͅࢯॸ‫ا‬स̜́ͥΫΗηϋņൎဓ́ŴŇŭŵĮĲ౵͈೩‫ဲ̦ئ‬ଷ̯̹ͦȃ̹͘ŴŇŭŵĮĲ͉͒Ωςϋൎဓ́౵̦ఱ̧̩་൲̳̯̦ͥ͂ͦͥȂ͒ςϋȪıįĵġŊŖİŌŨȫͬൎဓ̳ͥ͂ൎဓࢃͅ࿹պͅŴŇŭŵĮĲ౵̦ષઌ̱Ȃ̷͈౵͉ଅ‫ܥ‬ෝ͂ခփ̈́ୃ௖‫ͬ۾‬া̱̹ȃΪΠࠬ‫ۯ‬ඤ๧ळ༾ͬဥ̞̹࠿൦͉́Ȃ͒ΩςϋൎဓĲı໦ࢃͅ෽ူષୄಎ͈ŴŇŭŵĮĲ̦ࣞ౵̜́ͤȂ

口頭発表Ωςϋൎဓࢃ͈౵̦൲ྤࣁ‫ဲا‬ଷͅ‫۾‬Ⴒ̳̥̠̥̞ͥ̓̾̀ͅ࠿൦̱̹ȃńŌŅછ႕̮̩ͅઁၾ͈ΰΩ

会長招待講演 シンポジウムࣞࠬգ͈ࣣ໵છ̱͂̀ଅવ‫̜̦ͤٺ‬Ȃ̯ͣͅྕ଻ଅ௫ພȪńŌŅȫ͉́൲ྤࣁ‫ا‬છ͈ࣣ໵ͤ͢ͅ૤ࠬ‫ۯ‬

特別講演ࣞࠬգࣣ໵છ̱͈͂̀ଅȆࠬ‫ۯ‬Ⴒ‫۾‬Ȫ‫خ‬ဣ߿ ŇŭŵĮĲ ̱̹ͬٚ ńŌŅ ࣣ໵൲ྤࣁ‫ا‬છ͈‫ܥ‬੬ٜྶ͂হၷ؊ဥȫプログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineࠬ‫ۯ‬ඤ๧ळ༾྄ષ͈ŴŇŭŵĮĲ̦͒Ωςΰࠬಎͅဋ੄̱Ȃ̷͈౵̦ŴŇŭŵĮĲ͈௙ၾͬা̳̭͂ȂńŌŅۛ৪͈́ૺ࣐̹͉͘૤ࠬ‫ͼۯ‬αϋΠ͈௩‫̹͛෇ͬح‬ȃŴŇŭŵĮĲȆłűŰņΘήσΦΛ·ͺ;Πζ;Α͈࠿൦͉́ȂΘήσΦΛ·ͺ;Πζ;Ά߲͉΋ϋΠυȜσ߲ͅ๤̱̀൲ྤࣁ‫ا‬ພ་̦ૺ࣐̱̤̀ͤȂς΋ϋΫ΢ϋ
ΠŴŇŭŵĮĲ͈ൎဓ́Ķİķଅ௫ഊ੄ζ;Α͈൲ྤࣁ‫ا‬ພ་͈ૺജ̦ဲଷ̯̹ͦȃ̭͈̭̥͂ͣȂńŌŅۛ৪͉́ॸ‫ا‬ΑΠτᾼͥ͢ඤ๧વ‫̦ٺ‬ŴŇŭŵĮĲ͈อ࡛೩‫̱ܳৼͬئ‬ȂőŭňŇ͈൲ྤࣁ‫ا‬௯ૺΏΈ΢σ̦௖చഎͅᄤૺ̳̭ͥ͂́൲ྤࣁ‫ૺ̦ا‬ജ̳̭ͥ͂ȂŴŇŭŵĮĲ͈༞ਰ̦൲ྤࣁ‫ૺ͈ا‬ജͬဲଷ̱̠̭̦ͥ͂াऐ
̯̹ͦȃ

ポスター発表 ＹＩＡ選考発表̷͉͈௙ၾ̦೩‫̦̭̳͂ͥئ‬ଔ௶̯̹ͦȃ৘षͅΰΩςϋൎဓࢃ͈őŭňŇİŴŇŭŵĮĲࣞ౵႕͉‫ۍ‬൲ྤພ་

著者索引

䋭 㪈㪇㪊 䋭ႉ઄ŔĮĶĮķ

ࣞࠬգࣣ໵છ͂ͺΟͻε΍ͼΠ΃ͼϋ͈‫۾‬Ⴒɛఱඤġ઺ခ ĲȂড়നġႚ ĳȂఱ‫ޘ‬ġࢼඵ ĲȂ৒ࡔġཅྶ ĳ
Ĳ ྴࡣ‫ؚ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬໦ঊ੏۪‫ڠܕ‬Ȃĳ ྴࡣ‫ؚ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬ِ̦࣭̤̞̀ͅȂ୆‫ڰ‬ਠ‫͈۝‬་‫ฺ̹̽ͅا‬๬ྖȂඅͅඤ௫ডཛಇୟͬ‫ܖ‬๕̱̹͂ࣞࠬգȂൠయ৫։ુȂডৗయ৫։ુͬࣞၚࣣͅ໵̳ͥιΗδςΛ·ΏϋΡυȜθ̷͈͂ਞྎ௨̜́ͥ૤ࠬ‫ۯ‬ພ͈௩‫͉ح‬ఱ̧̈́࿚ఴ̞͂̈́̽̀ͥȃডཛழ૕͉ͺΟͻε΍ͼΠ΃ͼῧ௙ઠ̯ͦͥ୆ၑ‫଻ڰ‬βίΙΡͬ‫ڰ‬อͅ໦๥̳ͥ௫‫̜ͤ́ܕ‬ȂͺΟͻε΍ͼΠ΃ͼϋ͈ॲ୆։ુȆैဥ։ુ̦๬ྖࣣ໵છ͈อછȆૺജͅ‫۾‬ဓ̳̭̦ͥ͂ྶ̧̥̹ͣ͂̈́̽̀ȃఉ̩͈ͺΟͻε΍ͼΠ΃ͼϋ͉๬ྖࣣ໵છͅ௯ૺഎͅैဥ̳̦ͥȂ๬ྖࣣ໵છͅచ̱̀ཡࢄഎͅैဥ̳ͥͺΟͻε΍ͼΠ΃ͼϋ͜ంह̳ͥȃ̷͈యນഎ̈́ͺΟͻε΍ͼΠ΃ͼϋ͉ͺΟͻεΥ·Ιΰ̜ͤȂࠬգષઌͬဲଷ̱Ȃ૤ࠬ‫ͅࠏۯ‬༗ࢌഎͅैဥ̳ͥȃِș͉Ȃ‫ܥ‬ෝ̦ྚ౶̜́ͥ૧ܰͺΟͻε΍ͼΠ΃ͼϋ͈Α·ςȜΣϋΈً೾́ͺΟͻεΥ·ΙϋΩρυΈ̜́ͥńŕœőĺͅ಍࿒̱Ȃńŕœőĺ̦૤޼‫ࠬݹ‬વ‫ۯࠬ͞ٺ‬વ‫ͅٺ‬చ̱̀ཡࢄैဥͬခ̳̭ͥ͂ͬྶ̥̱̹ͣͅȃུ࣒‫͉́׵‬Ȃ૧ܰͺΟͻε΍ͼΠ΃ͼϋ͈ࣞࠬգࣣ໵છ̤̫ͥͅ࿨‫͈̞̀̾ͅڬ‬ड߃͈౶ࡉͬત̱̹̞ٚȃ䋭 㪈㪇㪋 䋭ႉ઄ŔĮķĮĲ

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ĺ࠮ĳĹ඾ȪാȫġĲĴĻĲıȡĲĶĻĲıġġలˍٛાΏϋεΐ;θġႉ઄ ŔĮķȶయ৫։ુ͂૤ࠬ‫ۯ‬ພȷ

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

łŕő య৫͂૤ࠬ‫ۯ‬ພ
特別講演ɛࣞോġ଼ඵ
ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬໦ঊ૤ࠬ‫ڠ֓ۯ‬̱̥̱‫ͅݙ‬Ȃ‫֦ࠬ́ࡔ͈̥ͣة‬ၠ̦ࡘઁ̜̞͉ͥ৭౯̯ͦͥ͂ਹඈ̈́௫‫ܕ‬ະ஠ͅ‫ͥۿ‬ȃࠬၠ͈৭౯ͅ
ͥ̽͂͢͜͜ఱ̧̈́࿚ఴ͉ॸள‫͈ݯރ‬৭౯̜́ͥȃ̷ͦͤ͢ͅηΠ΋ϋΡςͺ̤̫ͥͅॸ‫ا‬എςϋॸ
‫ا‬฽؊̦೪গ̱Ȃ௫‫͉ܕ‬਱໦̈́łŕőͬॲ୆̳̭̦ͥ͂ະ‫خ‬ෝ͂̈́ͥȃ௫‫͈ܕ‬ಎ́͜ड͜ఉ̩͈ηΠ΋ϋΡςͺͬခ̱ఱၾ͈łŕőͬॲ୆̳ͥ૤௫̤̞͉̀ͅඅࠬͅၠ͈৭౯̦ਹඈ̈́௫‫ܥܕ‬ෝະ஠̧ͬ֨
̭̳ܳȃ༷̭͈֚́ͦͣ೩ॸளેఠͅచ̱̀Ȃ୆ఘ͉ఉ̩͈ഐ؊‫ܥ‬੬ͬခ̱̞̀ͥȃ೩ॸளͅచ̱͉̀Ȃࠬ‫ڐۯ‬ಫ໤ৗ͈ຮ௸̈́໦๥͞௫‫͈ܕ‬య৫ဲଷͥ͢ͅłŕőક๯͈ဲଷ̦̭̈́̓ܳͥȃඅͅίτ΋ϋΟͻ
ΏοΣϋΈ࡛ય͂ࡤً֚͊ͦͥ଻͈೩ॸளঁ͈ࠣࢃͅ୆ఘ̦‫ڕ‬ං̳ͥ೩ॸளͅచ̳ͥ‫̞ޑ‬ఛ଻‫ڕ‬ංॸள̦ພఠͅ‫۾‬ဓ̳ͥఉ̩͈৖͈ۛ஻࿪ດഎ͂̈́ͥ‫خ‬ෝ଻̦̞ࣞȃম৘Ȃ೩ॸள́ည൵̯ͦͥŗņňŇ͞΀ςΑυεͼ΀Ιϋ͈̈́̓ΗϋΩ·ৗͬດഎ̱̹͂‫ࣣا‬໤͉̳́ͅႉ઄؊ဥ̯̞ͦ̀ͥȃ̭͈ͦͣ೩

口頭発表࡛ય͉Ȃ̯̰֦̈́͘͘ঊ̷̦̭ͅ‫۾‬ဓ̳̭̦ͥ͂౶ͣͦͥȃ̯̭͈֦ͣͦͣͅঊͬ൳೰̳̭͉ͥ͂೩

会長招待講演 シンポジウムୢ್൲໤͉ࣞഽ̈́໾ङࠬ‫̭͉ͤ͂̾͢͜ͅࠏۯ‬ໝॠ̈́௫‫ܕ‬ໝࣣఘͬࠁ଼̳̭̦ͥ͂‫خ‬ෝ̹͂̈́̽ȃॸளͅచ̱̀Ȃ୆ఘ͉ळ༾ඤ͉́łŕőક๯ͬဲଷ̳ͥయ৫ࠐႹͬ͂ͥ͂ࣉ̢̢ͣͥȃ̱̥̱Ȃ൳শͅ௩‫̵̯ͥح‬ΗϋΩ·ৗͬΑ·ςȜΣϋΈ̱൳೰̱̹ȃ̹̭͈͘ࡄ‫ً͈ݪ‬೾́łŕőॲ୆ෝ̦௫‫ܥ͈ܕ‬ෝ͂๱ુ̩͢ͅ௖‫̹̱੄ࡉ̭̳ͬ͂ͥ۾‬ȃ̭͈Ώϋεΐ;θ͉́Ȃ൳೰̯̹ͦłŕőయ৫‫۾‬ႲΗϋΩ·ৗ͈஻࿪ΏȜΒ̱͈͂̀‫خ‬ෝ଻ͬা̳͂͂͜ͅȂłŕőॲ୆ෝͬ௶೰̳̭ͥ͂ͥ͢ͅ௫‫ܥܕ‬ෝບ‫͈ث‬૧̱̞ࣉ̢༷ͬ೹੹̱̹̞ȃ

ポスター発表 ＹＩＡ選考発表łŕőͬ௩‫̵̠̯̈́ͥ͢ح‬య৫‫ب̴̠̞͉̭͂ͥܳ͜଻ڰ‬୰͈͂͜Ȃड߃ِș͉૧̱̞łŕőॲ୆௸ഽͬ

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䋭 㪈㪇㪌 䋭ႉ઄ŔĮķĮĳ

൲ྤࣁ‫̫̤ͥͅا‬ͺΟͻεΥ·Ιϋ İġͺΟͻεΥ·Ιϋ਋ယఘ͈࿨‫ڬ‬ɛ‫܊‬໐ġ๼‫ܮ‬Ȃ५ඤġຮୃȂ‫܊‬໐ġ૯૽Ȃ࿝ზġࢣ൐‫ނ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬ൠෂພȆయ৫ඤ‫ش‬ِ̦࣭͈ঘ֦͈ષպͬ୸͛ͥ૤ࠬ‫ۯ‬৖͈ۛ৽ါ̈́ࡔ֦̜́ͥιΗδςΛ·ΏϋΡυȜθȆĳ߿ൠෂພ͉Ȃଲ‫ٮ‬ಎ́ࠣ௩̱̤̀ͤȂ̷͈৽֦̦๬ྖฺ̠ͅͺΟͻεΥ·ΙϋȪłťȫİͺΟͻεΥ·Ιϋ਋ယఘȪłťŪűŰœȫΏΈ΢σ͈ैဥ೩‫̧̹̱̥̀ͣͅྶ̭̜ͬ͂ͥ́ئ‬ȃ༷֚́Ȃłťࠧఅζ;Ὰ̤̞͉ͅȂ࿤୆߿ζ;Α͂๤‫̱ڛ‬Ȃ΃έવ‫ͅٺ‬చ̱̀Ȃඤ྄๬࢚̦ĳ෼೾ഽခփͅ௩‫̭̳͂ͥح‬Ȃ̹͘Ȃłť઼ًอ࡛łűŰņࠧఅζ;Ὰ̤̞͉ͅȂłűŰņࠧఅζ;Ά෇͛ͣͦͥ൲ྤࣁ‫ا‬ພ་̦ࠚࡘ̳̭ͥ͂̈́̓Ȃłț̌ࢯ൲ྤࣁ‫֦ا‬ঊ̱͂̀ैဥ̱̞̭̀ͥ͂ͬ༭̧̱̹࣬̀ȃ̱̥̱̦̈́ͣȂłť͈ࢯ൲ྤࣁ‫ैا‬ဥ̤̫ͥͅ਋ယఘȪłťŪűŰœȫ͈փ݅‫̷͈͍ݞ‬મळ̈́ι΃ΣΒθ̞͉̾̀ͅȂྶ̥̞̞ͣ͂̈́̽̀̈́ȃ൲ྤࣁ‫̫̤ͥͅا‬łťŪűŰœ͈ࡢఘτασ͈́փ݅͞࿨‫ڬ‬Ȃ̯ͣͅ൲ྤࣁ‫ا‬อછͅਹါ̈́ழ૕̜́ͥ
ࠬ‫͍ݞۯ‬ζ·υέ͹Ȝΐ̤̫̈́̓ͥͅłťİłťŪűŰœ͈ळ༾ඤΏΈ΢σ̈́̓Ȃłť͈ࢯ൲ྤࣁ‫ैا‬ဥι΃ΣΒθ͈ٜྶͬ࿒എ̱͂Ȃ஠૸‫ۯ͍ࠬݞ‬ඤ๧අ։എłťŪűŰœࠧఅζ;Α̈́̓ͬဥ̞Ȃ൲ྤࣁ‫ͅا‬చ̳ͥ‫࠿̞̀̾ͅޣג‬൦̱̹ȃ৘षͅȂ๬ྖȆĳ߿ൠෂພκΟσζ;Α‫͍ݞ‬൲ྤࣁ‫ا‬κΟσ̈́̓ພఠ̤̫ͥࠬͅ‫͉́ۯ‬ȂłťŪűŰœĳ͈อ࡛̦೩‫̹̞̱̀ئ‬ȃ̯ͣͅȂ஠૸‫ۯ͍ࠬݞ‬ඤ๧අ։എłťŪűŰœࠧఅζ;Α̈́̓ͬဥ̞Ȃ̹͘Ȃࣸଡ֊૒࣐̞͜Ȃ΃έવ‫ͅٺ‬చ̳ͥඤ྄๬࢚ͬບ‫́ࠏ̳ͥث‬ȂłťŪűŰœ͈࿨‫̞̀̾ͅڬ‬ٜଢ଼࣐̹ͬ̽ࠫ‫ض‬ȂłťŪűŰœĲ͈ࢯ൲ྤࣁ‫ैا‬ဥ̤̞̀ͅȂઁ̩̈́͂ࣸ͜ଡ͈́࿨‫̦ڬ‬Ȃ̹͘ȂłťŪűŰœĳ̞͉̾̀ͅȂઁ̩̈́͂ࠬ͜‫ۯ‬ඤ๧͈́࿨‫̦ڬ‬ਹါ̜̭̦́ͥ͂াऐ̯̹ͦȃ̹͘ȂłťŪűŰœĳ͈ͺΟΦ;ͼσᾼͥ͢ޫਫ਼
઼ً͈́อ࡛ͤ͢ͅȂඤ྄๬࢚̦ဲଷ̯ͦȂ̷͈ι΃ΣΒθ͈̱֚̾͂̀ȂőőłœϹͬࡐಠͅ௩‫̵̯ح‬̞̀ͥ‫خ‬ෝ଻̦া̯̹ͦȃ̱̹̦̽̀ȂłťİłťŪűŰœΏΈ΢σ͈௩‫͍ݞޑ‬łťŪűŰœͺΌΣΑΠ̦ȂͼϋΑςϋ೷ࢯ଻͞ൠෂພȆডৗ։ુછͬ٨஝̴̳͈͙ͥ̈́ͣȂ൲ྤࣁ‫ͅا‬చ̳ͥೄ୪ैဥ͜‫ܢ‬ఞ̧́Ȃࣽࢃ͈হၷ࿪‫ٳ‬อͅࠒ̦ͥ
‫خ‬ෝ଻̦াऐ̯̹ͦȃ䋭 㪈㪇㪍 䋭ႉ઄ŔĮķĮĴ

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లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineডৗ͈ৗͅণതͬ౾̞̹య৫։ુ͂૤ࠬ‫ۯ‬ພহၷ୽ၞ
特別講演

ɛോ࿤ġ૾
ಆ෨ఱ‫֓ڠ֓ڠ‬ၷࠏඤ໦๥య৫ൠෂພඤ‫ش‬‫ͅۯࠬ͞ܕ‬ಇୟ̳ͥডৗ͈ৗഎ་൲̞͉̜̾̀ͤ͘ͅ‫۾‬૤̦໡̞̥̹ͩͦ̀̈́̽ȃਲြȂ཈გডཛॸ
͉൲ྤࣁ‫ا‬௯ૺ̱Ȃఉ‫ث‬ະ཈გডཛॸȪőŖŇłȫ͉ࢯ൲ྤࣁ‫ैا‬ဥͬခ̳̭̦ͥ͂౶̞ͣͦ̀ͥȃőŖŇł
͉Ȃෞ૤ࠬ‫ۯ‬৖͈֚ۛষඵষထཡ̞̾̀ͅ΀ΫΟϋΑ̦ਬୟ̧̯̹ͦ̀ȃ̷͈ι΃ΣΒθ͉৽ͅőŖŇł͈ࢯࠬ઀โȄࢯࠬ஀଻ैဥ̯ͣͅड߃͉́‫׶‬છ͈͒ैဥͅ‫̢̞ͥ̀ͦͣࣉ̩͂̿ܖ‬ȃඅͅůĮ˒ͺρ΅Ρϋॸࠏ̦‫׶‬છৼܳ଻ͅ൱̩༷֚ȂůĮĴġņőłĭġŅŉłࠏ͉ࢯ‫׶‬છैဥͅ൱̧Ȃࢯ൲ྤࣁ‫ैا‬ဥͬ୰ྶ̳ͥ૧
̹̈́ैဥത̱͂̀ಕ࿒̯̞ͦ̀ͥȃ༷֚ոஜͤ͢őŖŇł͉۴௫ΠςΈςΓςΡ଼ࣣဲଷȂࠬಎΠςΈςΓςΡ೩‫ैئ‬ဥͬခ̳̭̦ͥ͂౶̞̹̦ͣͦ̀Ȃ̷͈ι΃ඵΒθ͉ডཛॸ଼ࣣഢৢ֦ঊŔœņŃőĮĲŤ͈ͥȃőŖŇł̦ŔœņŃőĮĲŤͬఉ࿂എͅဲଷ̳ͥι΃ΣΒθ̞̾̀ͅŪůġ ŷŪŷŰĭġ Ūůġ ŷŪŵųŰ́࠿൦̱̹౶ࡉ̾ͅ
̞̀ა̴ͥȃ๬ྖൠෂພ‫۾‬Ⴒ৖ۛȂྕ଻‫׶‬છ͈ܳത̱͂̀ডཛॸ͈အș̈́୆ၑ͂ພఠ̦াऐ̯̦ͦͥġ

口頭発表ဲଷ̱̞ͬٚ̀ͥȃ཈૙֒ഥঊŔœņŃőĮĲŤ͉΀ΥσΆȜ઼ًેఠͅ؊̲̀ςεΐͿΥΏΑͬ‫̳ا଻ڰ‬会長招待講演 シンポジウム̭ͦ́͘൲ྤࣁ‫ا‬ထཡ୽ၞ͉ōŅō΋τΑΞυȜσͬ৽ࠬͅಎডৗಇୟ͈ၾഎ‫ۯ‬ၑ̦ণത͂̈́ͤȂ௫τΓίΗȜ̱̹ͬٚΏΈ΢σ͈̥ͥ͢ͅळ༾ඤ͈య৫͈ࠫ‫̀͛܄̥͈ͬ̈́ض‬őŖŇłैဥ͂ພఠ͈ࡄ‫ݪ‬ςϋۜ਋଻͞အș̈́୆໤‫ڠ‬എैဥͅਹါ̈́‫ͬޣג‬ဓ̢ͥȃŔœņŃőĮĲ͈ດഎ֒ഥঊ̱͂̀อࡉ̯̹ͦড
ཛॸ‫װ‬ಿࣖளņŭŰŷŭķ͈ࠧఅζ;Ά͉ࣞ΀ΥσΆȜ૙́๬ྖȂডཛ۴̱̹̦ͬȂփ‫̈́ٸ‬মͅͼϋΑςϋ೷ࢯ଻̦ཡ̦̹ͦȃ̹͘۴વ‫ٺ‬ȂœŐŔȂ஌֋‫̓̈́ا‬ŏłŔŉਫ਼ࡉ͜ཡ̦̹ͦȃζ·υȜέ͹Ȝΐ͈ņŰŷŭķ
ࠧఅ͉Ȃ༺ྏ‫۾ͅا‬ဓ̱̀൲ྤࣁ‫ဲͬا‬ଷ̱̹ȃņŭŰŷŭķͬ৊̱̹ͅङಿͬণത̱̹͂ডཛॸழ଼͈ਘ
ૐ͉Ȃయ৫଻ྕ଻‫׶‬છພఠ̯ͣͅෞ‫ܥ‬ෝଷࢄ̈́̓૧̹̈́ႀ֖͈͒ͺίυȜΙ̦‫ܢ‬ఞ̯ͦͥȃডཛॸ͈ৗഎ‫ۯ‬ၑͥ͢ͅ௫‫ܕ‬વ‫ٺ‬ཡࢄ୽ၞ͈ജ‫݈̞̀̾ͅٳ‬ა̱̹̞ȃডཛॸ͈ৗഎ‫ۯ‬ၑͥ͢ͅ௫‫ܕ‬વ‫ٺ‬ཡࢄ୽ၞ͈ജ‫݈̞̀̾ͅٳ‬ა̱̹̞ȃ

ポスター発表 ＹＩＡ選考発表͉౤੣̞̹̥̜̾͊ͤ́ͥͅȃডཛॸ͈ະ཈გഽ̴̞͈͙̾̀̈́ͣͅङಿ͜΀ΥσΆȜయ৫ȂͼϋΑ

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䋭 㪈㪇㪎 䋭ႉ઄ŔĮķĮĵ

ŎźŴŵŦųŪů ͂͜͜͞͞ພ
ɛ૽ࡉġຮྶȂ઀ႅġ‫ض‬Ȃ઀ஂġ઎ຳ‫ނ‬സఱ‫ڠ‬ఱ‫מޏ۪شݪࡄڠ֭֓ڠ‬୆‫ڠ‬໦࿤͜͜͞͞ພ͉Ȃඤᴢ൲ྤਞྎ໐͈໾ण̷ฺ̠͂ͦࠬ͜͜͞͞ͅ‫ͥͦ͊ࡤ͂ۯ‬։ુ̈́ࠬ‫ۯ‬࿌͈ࠁ଼ͬ
අಭ̳͂ͥ৖̜ۛ́ͤȂ৹ා଻ෞ௾ಎ͈৽ါ̈́ࡔ֦͈̜֚̾́ͥȃ඾ུͬ‫͚܄‬൐ͺΐͺ́ఉอ̳ͥതȂۛ৪͈࿩ĲĶĦͅ‫ز‬௼Ⴄͬ෇͛ͥത̥ͣ֒ഥါ֦͈‫̦ޣג‬ே೰̯̞̹̦ͦ̀Ȃ‫۾‬ဓ̳ͥ֒ഥঊ͉ಿ̩ະ
ྶ̜̹́̽ȃ
߃ාȂِș͉ુஅ૗ఘ࿹଻ࠁৗͬা̳͜͜͞͞ພ‫ͬࠏز‬చયͅ஠ΊΦθႲङٜଢ଼̤͍͢΀·ΕȜθٜଢ଼࣐̞ͬȂĲĸ๔அ૗ఘષ͈ȫ
mysterinȪRNF213ȫ֒ഥঊ̦͜͜͞͞ພۜ਋଻֒ഥঊ̜̭́ͥ͂ȂűįœĵĹĲıŌ
ఉ߿̦඾ಎ‫͈ۛ܀‬৪ͅ‫ވ‬೒̳ͥۜ਋଻ఉ߿̜̭́ͥ͂ͬྶ̥̱̹ͣͅ
ȪPLoS ONE, ĳıĲĲȫȃ̹͘୆‫ڠا‬എٜଢ଼ͤ͢ͅŮźŴŵŦųŪů͉łŕőŢŴŦ‫͂଻ڰ‬ξΫ΅Ιϋς΄ȜΔ‫֚ͬ଻ڰ‬໦ঊඤ́໵̵঵̾๱ુͅξΣȜ
·̈́ΗϋΩ·ৗ̜̭́ͥ͂ͬྶ̥̱̹ͣͅȃࢵࠬͅ‫ۯ‬κΟσ൲໤ΔήρέͻΛΏνͬဥ̞̀Ȃκσέ΁ςΦ΂ςΌͥ͢ͅŮźŴŵŦųŪůอ࡛ဲଷ৘ࡑ࣐̹ͬ̽ȃ̷͈ࠫ‫ض‬Ȃ൮໐ႀ֖́ಠྶ̈́ࠬ‫଼ࠁٔۯ‬։ુȂඅͅ‫܉‬༾͈ඤ୓ྤႊ̥͈ͣࠬ‫଼̦ࠁٔۯ‬௩‫̳ͥح‬๱ુͅඅಭഎ̈́ນ࡛߿ͬ෇͛ȂŮźŴŵŦųŪů̦൮໐ࠬ‫ۯ‬อ୆ͅਹါ̈́࿨‫̦̭̳̹͂ضͬڬ‬াऐ̯̹ͦȃষͅŮźŴŵŦųŪů͈‫ܥ‬ෝͬྶ̥̳̹ͣͥ͛ͅͅȂmysterin ŌŐζ;Αĩmysterin -/- Ī͈ै଼࣐̹ͬ̽ȃ̞̩̥͈̾֒ഥພ͉́͜͜͞͞ພ͂ൠෂພ͈ࣣ໵̦༭̯̞࣬ͦ̀ͥത̥ͣȂِș͉ mysterinġ ŌŐ ζ;Αͬᦙϸळ༾͈઀༾ఘΑΠτᾼͥ͢ൠෂພκΟσ̜́ͥłŬŪŵŢζ;Αĩ ŊůŴĳġ ńĺķŚİŘŕĪ͂࢐෻̱Ȃ
mysterinġ
ŌŐİłŬŪŵŢζ;Αĩmysterin -/-ĭ Ins2 C96Y/WT Īͬං̀ນ࡛߿ͬ࠿൦̱̹ȃ̷͈ࠫ‫ض‬Ȃ
mysterinࠧఅ͉łŬŪŵŢζ;Α͈ࠬୄ̤͍͢ᦙോͼϋΑςϋၾͬ௩‫̵̭̯́͂ͥح‬ൠෂພͬ٨஝̳̭̦ͥ͂া̯̹ͦ
ȪBBRC, ĳıĲĴȫȃ
łŬŪŵŢζ;Α͈ᦙϸळ༾͉́઀༾ఘ‫۾‬Ⴒ໦ٜȪņœłŅȫͤ͢ͅ։ુίυͼϋΑςϋ̴͈͙̈́ͣୃુίυͼϋΑςϋ͈໦ٜ͜௯ૺ̱̞̭̦̀ͥ͂ൠෂພอ୆ͅਹါ̈́࿨‫̢̞ͥ̀ͦͣࣉ̳̹͂ضͬڬ‬ȃུࡄ‫ݪ‬͉Ȃmysterin̦ņœłŅͅਹါ̈́࿨‫خ̳̹ضͬڬ‬ෝ଻ͬাऐ̱̞̀ͥȃࣽࢃ͉Ȃ̯ͣͅમळͅmysterin͈‫ܥ‬ෝͬྶ̥̳ͣͥ͂͂͜ͅͅȂ͜͜͞͞ພུ͈ఠ̜́ͥඤᴢ൲ྤ໾
णͅ‫̳̹ض‬mysterin͈࿨‫͈ڬ‬ٜྶ̰̳ͬ͛ȃ䋭 㪈㪇㪏 䋭ĺ࠮ĳĹ඾ȪാȫġĲĴĻĲıȡĲĶĻĲıġġలˎٛાΏϋεΐ;θġႉ઄ ŔĮĸȶࠬ‫ۯ‬ठ୆ࡄ‫͈ݪ‬डஜ஌ȷȁȁȁȁȁȁȁȁġġġġ‫ވ‬टȇŏőŐ༹૽ࠬ‫ݪࡄڠ֓ۯ‬ଔૺ‫ࢹܥ‬ႉ઄ŔĮĸĮĲ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine૽ࢥఉෝ଻ۚ ĩŪőŔĪ ळ༾ͬဥ̞̹ࠬ‫ۯ‬ςκΟςϋΈૺജထཡ͈দ͙
特別講演ɛ৒ࡔġཅྶȂ५ུġଢ෗Ȃড়നġႚྴࡣ‫ؚ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬‫ૺ͈ا‬ജࠬ͞‫ͥ͢ͅٺੱۯ‬ठ‫ޛ‬ॏ͉࡛ह͜‫ه‬ఴ̱͂̀ॼ̞̽̀ͥȃ૽ࢥఉෝ଻ۚȪŪőŔȫळ༾͉Ȃࠬ‫ۯ‬ඤ๧ळ༾͒໦‫̱ا‬ං̭̦ͥ͂༭̯̞̦࣬ͦ̀ͥȂŪőŔळ༾͈൲ྤࣁ‫ۯࠬ͞ا‬ςκΟςϋΈͅచ̳ͥ‫͉ޣג‬ྚ̺࠿൦̯̞̞ͦ̀̈́ȃ͉ࣽٝͩͦͩͦȂζ;Αࠬ‫ٺੱۯ‬κΟσͬဥ̞̀ȂŪőŔळ༾ဇြŇŭŬĮĲု଻ळ༾Ȫࠬ‫ۯ‬ஜߐळ༾ȫ͈ࠬ‫ۯ‬ςκΟςϋΈ̤̫ͥ࢘ͅ‫࠿̞̀̾ͅض‬൦࣐̹ͬ̽ȃȺ༹༷Ȼζ;Αࠬ‫ٺੱۯ‬κΟσ͉ȂıįĴĹŮŮ͈ΑΙȜσχͼμȜͬဥ̞̀ȂŌŔŏΤȜΡζ;Α͈ఱద൲ྤ
ඤ๧ͅੱ‫ͬٺ‬ဓ̢̭ͥ͂ͤ͢ͅै଼̱̹ȃ̭͈ͦͣζ;ᾼȂĲȿĲıķࡢ͈ζ;ΑŪőŔळ༾ဇြŇŭŬĮĲု଻ळ༾͞ŪőŔळ༾ဇြŇŭŬĮĲ֮଻ळ༾Ȃ΋ϋΠυȜσ̱͂̀őŃŔͬඤᴢ୓ྤ̥ͣൎဓ̱Ȃ̷͈ࢃ͈૧୆ඤ྄

Ⱥࠫ‫ض‬ȻŇŭŬĮĲု଻ळ༾ൎဓ߲͉́ȂŇŭŬĮĲ֮଻ळ༾ൎဓ͞őŃŔൎဓ߲ͅ๤̱̀Ȃ੅ࢃĳĲ඾࿒͈૧୆ඤ྄௩
୆ͬခփͅဲଷ̱̞̹̀ȃ੅ࢃĸ඾࿒͈ੱ‫ͬۯࠬٺ‬ဥ̞̀Ȃ΀ΨϋΑήσȜஅ૗ͥ͢ͅठඤ๧‫ا‬ၚ͈௶

口頭発表௩୆ͬບ‫̹̱ث‬ȃ

会長招待講演 シンポジウムȺ෸ࠊȻ૤ࠬ‫ۯ‬৖͉ۛ‫شٸ‬എ਀੅Ȃ΃ΞȜΞσহၷ̞̹͂̽হၷ͈ૺ༜͉෇͈͈͛ͥ͜Ȃ̷͈ࢃ͈൲ྤࣁ

೰࣐̹̭ͬ̽͂ͧȂŇŭŬĮĲု଻ळ༾ൎဓ߲́ခև̈́ठඤ๧‫͈ا‬௯ૺ̦෇̹͛ͣͦȃőŌŉĳķ́ρασ̯ͦńřńœĵ̦ࣞอ࡛̱̤̀ͤȂŪůġ ŷŪŵųŰ͈ࠏ͉́Ȃńřńœĵ͈ŭŪŨŢůť̜́ͥŔŅŇĮĲϷ͈ഞ‫ฺ̠ͅح‬ဋ௢ෝ͞୪
಍ෝ̦ŇŭŬĮĲ֮଻ळ༾͂๤̱̀ಠྶ́Ȃ̭͈ͦͣैဥ͉ńřńœĵ͈ಎგࢯఘͥ͢ͅஜੜ౾ٜ́ੰ̯̹ͦȃȺࠫაȻŪőŔळ༾ဇြŇŭŬĮĲု଻ळ༾͈ൎဓ͉Ȃζ;Αࠬ‫ۯ‬વ‫͈ࢃٺ‬ඤ๧ळ༾౎၂͈ਘ໘௯ૺैဥͬခ̱Ȃ̭͈ࠫ‫ض‬Ȃࠬ‫ۯ‬ठ‫ޛ‬ॏ͈৽̹ͥࡔ֦̜́ͥඤ྄๬࢚ͬဲଷ̱̹ȃŪőŔळ༾͉Ȃࠬ‫ۯ‬হၷࢃ͈ठ‫ޛ‬ॏထཡ̤̞̀ͅȂခབ̈́হၷ࢓༞ळ༾̠̈́ͤͥ͂ͅࣉ̢ͣͦͥȃ

ポスター発表 ＹＩＡ選考発表̹ŇŭŬĮĲု଻ळ༾͉Ȃੱ‫ͅۯࠬٺ‬ਬୟ̳̭̦ͥ͂‫̹̯ͦ෇ږ‬ȃ̹͘ȂŪőŔळ༾ဇြŇŭŬĮĲု଻ळ༾͉Ȃ

著者索引

䋭 㪈㪇㪐 䋭ႉ઄ŔĮĸĮĳ

௫‫ܕ‬ठ୆۪‫ۯ̫̤ࠬͥͅޏ‬ठ୆ι΃ΣΒθࡄ‫ݪ‬ɛஃࡔġࢣ෗Ȃ௩നġহঃ൐٬ఱ‫ڠ֓ڠ‬໐ठ୆֓ၷ‫ڠش‬ۚळ༾୆໤‫͈ݪࡄڠ‬อജ͂‫ͅވ‬Ȃठ୆֓ၷ৘ဥ‫ߓ̦ا‬ఘഎ̧̞̈́̽̀̀ͥͅȃ̱̥̱Ȃহၷ͈చય͂
̈́ͥठ୆ະ஠͈৖ۛ௫‫͉̞̤̀ͅܕ‬Ȃু͈ͣठ୆฽؊ͬཐ‫֦̳ͥٺ‬ঊ̦ఉਹͅ‫̞ͥ̀̽ͩ۾‬ȃအș͈৖ۛ௫‫͉́ܕ‬Ȃྕ଻‫ࠬݹ‬Ȇ‫׶‬છ྾‫ע‬฽؊Ȇ஌֋‫̦ا‬ພఠͬ՛‫̵̞̯ͥ̀ا‬ȃ̾ͤ͘௫‫ܕ‬ठ୆଼͈๛͉Ȃ௫‫ܕ‬ۚळ༾͈ठ୆ෝႁ͂͂͜ͅȂठ୆۪‫ેࠬݹ͈ޏ‬ఠȆ‫׶‬છȆ྾‫ע‬฽؊ͬශ‫࣪ͅة‬໚̳̥̥̥̞ͥ̽̀ͥͅ
͂ࣉ̢ͣͦͥȃུࡄ‫ݪ‬৒͉́ȂĲĺĺĸාࠬͅ‫ס‬ಎ͈ࣸଡဇြࠬ‫ۯ‬ठ୆ळ༾Ȫņőńȫͬอࡉ̱̹ȃ̭͈ࣸଡဇ
ြ͈ळ༾͉ྎઑࠬಎͬ੘̱ٝȂ୆ၑȆພၑ‫ڠ‬എࠬ‫ۯ‬ठ୆ͬ௯ૺ̵̯̞̭̦̀ͥ͂฻ྶ̱Ȃ௫‫ܕ‬ठ୆۪‫ޏ‬̤̫ͥࠬͅ‫ۯ‬ठ୆ι΃ΣΒθ͈ਹါ଻̦ಕ࿒̯̹ͦȃ̵̭ࣣͦͩ̀ͅȂ௫‫ܕ‬ठ୆হၷ͈̹͈͛ࠬ‫ۯ‬ठ୆ၷ༹͈΋ϋΓίΠ͜‫ږ‬ၛ̯ͦȂ࡛ह͉ņőńͬဥ̞̹‫ئ‬ঠ‫ۛࠬݹ‬৪Ȃ૤޼ࢸणۛ৪͈̈́̓͒ႉ઄ࡄ‫ݪ‬Ȇহࡑ́࢘‫͂ض‬հ஠଻̦༭̯̜࣬ͦ̾̾ͥȃ̱̥̱Ȃņőń͈ၾ͂ৗͬ‫ږ‬༗̳͈̦ͥ۰ౙ̞̭́̈́͂͜฻ྶ̱
̜̾̾ͥȃఉ̩͈ۛ৪́ȂࣞႢȆ୆‫ڰ‬ਠ‫۝‬ພȆ‫ܖ‬ய৖͈ۛ‫́ޣג‬ņőń͈ၾ̦ࡘઁ̱Ȃळ༾‫ܥ‬ෝ͈೩‫ږ͜ئ‬෇̯̞ͦ̀ͥȃ̷̭́Ȃུࡄ‫ݪ‬৒͉́ņőń෽ူ༹ͬ‫ږ‬ၛ̧̱̹̀ȃ̭͈ࠬ‫ۯ‬ठ୆΋ϋΟͻΏοΣϋΈ෽ူͤ͢ͅȂņőńͬĵı෼ոષͅ௩໙̵̯Ȃࠬ‫ۯ‬ठ୆ෝႁ͜௯ૺ̧̭̦́ͥ͂‫੄෇ږ‬ြ̹ȃ̹̺̱Ȃņőń໦ၗ͈̹͛ͅńŅĴĵİńŅĲĴĴု଻ळ༾ͬ໦ၗ̱̥̀ͣ෽ူ̳̹ͥ͛ͅȂไဥ଻Ȇࠐफ଻́Ⴆ̹ͥ͛Ȃྎઑࠬౙ‫ۯ͈ࠬ͒ݩړ‬ठ୆΋ϋΟͻΏοΣϋΈ෽ူ͜দ͙̞ͣͦ̀ͥȃ‫ྙޟ‬૬̞̭͂ͅȂౙ‫̠̞͂ݩړ‬ņőńȆౙ‫ݩ‬ζ·υέ͹ȜΐȆςϋΩ‫͈ݩ‬ईࣣळ༾߲ͬࠬ‫ۯ‬ठ୆΋ϋΟͻΏοΣϋΈ̳ͥ͂Ȃņőń͈௩໙ͤࠬ͢ͅ
‫ۯ‬ठ୆ෝႁ̦௯ૺ̯ͦͥ͂͂͜ͅȂȶठ୆߿ȷ͈ŎĳĮζ·υέ͹ȜΐȆŕũĳĮŕळ༾Ȇଷࢄ଻ŕळ༾̦ည൵̯
ͦȂࢯ‫׶‬છȆ྾‫ۘע‬ယȆठ୆ည൵ͅ൱̧Ȃ௫‫ܕ‬ठ୆̦ૺജ̳̭̦ͥ͂฻ྶ̱̹ȃ̭͈ळ༾߲͉Ȃౙ‫ݩړ‬ळ༾߲ͅठ୆ΏΈ΢σͬ‫̱̀ݯރ‬ංͣͦͥठ୆۪‫͈̹͈͛ޏ‬ळ༾߲̜̭̥́ͥ͂ͣȂठ୆ͺΕΏ΀ͼΠळ༾͂ྵྴ̯ͦȂࠬ‫ۯ‬ठ୆͂‫׶‬છȆ྾‫ע‬฽؊͈௙ࣣഎठ୆۪‫ޏ‬ι΃ΣΒθࡄ‫̷͈͍̤͢ݪ‬হၷࡄ‫̱̀͂ݪ‬ಕ࿒̯ͦͥȃ䋭 㪈㪈㪇 䋭ႉ઄ŔĮĸĮĴ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineŉňŇ ֒ഥঊͬဥ̞̹ࠬ‫ۯ‬ठ୆হၷ͈࡛ે͂੿ြ
特別講演ɛ૩‫ئ‬ġၧ֚ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬Α·ͬ೩‫ږ̵̯ͥئ‬৘̈́਀౲͉ంह̱̞̈́ȃ̷͈̠̈́͢ພఠͅచ̱Ȃِș͉඾ུ́อࡉ̯̹ͦ۴ळ༾
௩૓֦ঊȪŉňŇȫͅ಍࿒̱Ȃ̷͈ࠬ‫ۯ‬૧୆ैဥͬ၌ဥ̱̹֒ഥঊহၷ͈ႉ઄ࡄ‫ͬݪ‬ĳııĲා̥ͣఱिఱ
‫͛ૺ̞̤̀ͅڠ‬Ȃĳĳ႕͈໾ण଻൲ྤࣁ‫ا‬છ̜̞͉ͥΫνσ΄Ȝພۛ৪̤̞̀ͅȂķ‫ڬ‬ոષ͈ۛ৪́ྶ
̥ͣ̈́છે͈٨஝̦෇̹̭͛ͣͦ͂ͬা̱̹ȃࢵͅȂਹછ‫ࠬݹ‬ঠۛ৪ͬచય̱̹͂ίρΓδచચྫैև‫ا‬ඵਹ࿋࠿๤‫ڛ‬দࡑ͈ࠫ‫ض‬Ȃ‫଻ࠬݹ‬೟ន̜̞͉ͥհ୓শគ೑͈٨஝̤̞̀ͅȂŉňŇ֒ഥঊহၷ͈ίρΓδͅచ̳ͥ࿹‫̯ͦ෇ږ̦଻ק‬ȪűľıįıĲĵȫȂհ஠଻͜ͅఱ̧̈́࿚ఴ͉෇̥̹̭͛ͣͦ̈́̽͂ͬྶͣ
̥̱̹ͅȪňŦůŦġ ŕũŦųŢűźġ ĳıĲıȫȃĲාࢃ͈ఱ୨౯อ୆ၚȇĶįĴĦȂঘཌၚȇĳįķĦ଼̞̠͂ୡ̦ං̤ͣͦ̀

଼̈́ୡ̜́ͥȃ̹͘Ȃఱिఱ‫ڠ‬૤௫ࠬ‫͉́شٸۯ‬Ȃਹછ૤ະ஠ۛ৪ͅచ̳ͥŉňŇ֒ഥঊͬဥ̞̹֓঍
৽൵͈ႉ઄হࡑ͈੔๵࣐̞ͬ̽̀ͥȃ͈ࣽٝ࿪ম༹٨ୃͤ͢ͅȂठ୆֓ၷȆ֒ഥঊহၷ͉Ȃ்‫ܢ‬ઇ෇చ

口頭発表ͤȂ̭͉ͦŕłŔńŊŊ́༭̯̞࣬ͦ̀ͥĲාࢃ͈ఱ୨౯อ୆ၚȇĴıĦȂঘཌၚȇĳĶɓ̈́̓͂๤‫̳͂ͥڛ‬ၻࢡ

会長招待講演 シンポジウムਹછ‫ࠬݹ‬ঠ͉Ȃ‫଻ࠬݹ‬೟ន͞հ୓শគ೑ͬ೮̳ͥྕ଻൲ྤ໾णછ͈ਹඈ̈́ພఠ̜́ͤȂ‫ئ‬ঠ୨౯ςય͂̈́ͥထ೰̜́ͤȂࣽࢃࠬ‫ۯ‬ठ୆֒ഥঊহၷ͉Ȃఱ̧̩৘ဥ‫ܢ̦̭̳͂ͥا‬ఞ̯ͦͥȃ

ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪈㪈㪈 䋭ႉ઄ŔĮĸĮĵ

ࠬ‫ۯ‬ठ୆হၷ͉ őłŅ ͈ ŤŭŪůŪŤŢŭġŦůťűŰŪůŵ ͬో଼̧̥́ͥȉɛༀྖġ‫݌‬გ߇ਗఱ‫ڠ‬ఱ‫֭ڠ‬࿪‫֭ݪࡄڠ‬Ψͼ΂֓࿪஻଼‫ڠ‬ŊŴůŦų̦ͣĲĺĺĵාͅ੝͛̀৘ࡑഎͅȶহၷഎࠬ‫ۯ‬૧୆Ȇठ୆ŵũŦųŢűŦŶŵŪŤġ ŢůŨŪŰŨŦůŦŴŪŴȷ͈΋ϋΓίΠ
ͬอນ̱̀‫̩̈́͜ۼ‬ĳıා̦ࠐً̱̠̱̞͂̀ͥ͢ȃ̭͈‫ۼ‬Ȃழ̢۟ΗϋΩ·Ȃ֒ഥঊȂळ༾̈́̓ͬဥ̞̹
ႉ઄দࡑ̦ଲ‫ٮ‬ಎ́ૺ̹̦͛ͣͦȂ̤ࣽ̈́ࠬ‫ۯ‬ठ୆হၷ͉ດ੔হၷ͉ͅঢ̞̞̽̀̈́ȃ̶̜̠̥̈́́ͧȉࠬ‫ۯ‬ठ୆হၷ͈ႉ઄দࡑ͈ఉ̩͉Ȃ੝‫ܢ‬ȪలŊĮŊŊŢ௖ȫ଼͈ୡ͉࣐́ࠬ൲ఠ͈٨஝̦̈́̓ࡉ̞͈ͣͦ̀ͥ͜
͈Ȃఉঔ୭ඵਹ࿋࠿দࡑȪలŊŊţĮŊŊŊ௖ȫ̤̞̀ͅ৽ါບ‫ࣜث‬࿒ͬో଼̱̹༭͉͕̞࣬͂ͭ̓̈́ȃ̷͈ၑဇ̱͂̀ȂȪˍȫ‫ۼ‬ᗰ଻ᮢ࣐ȪŊńȫ͂ਹછ‫ࠬݹ‬ঠȪńōŊȫ͉Ȃ̷͈ພఠ͜ႉ઄എαΥέͻΛΠȪɁ৽ါບ‫ࣜث‬࿒ȫ͜দࡑ༹༷͜஠̩։̈́ͥ͜ͅ‫̴ͣͩ۾‬Ȃࠬ‫ۯ‬ठ୆হၷ̦͈̠̓̈́͢ႉ઄છ࢓ͅαΥέͻΛΠ̦̜͈̥ͥȂ̞̾̀ͅ౶ࡉ͈ਬୟ̦ૺ̞̞̭ͭ́̈́͂ȂȪˎȫőłŅ͈ႉ઄ບ‫͉ͅث‬ίρΓδ࢘‫̭͂ͥͦͣࡉ̩̦ࣞض‬ȂȪˏȫႉ઄ບ‫༹͉֓ث‬঍͈৽۷എ฻౯ͅջం̱̹Ȫ႕ȇńōŊ̤̫ͥͅŢŮűŶŵŢŵŪŰůশ‫͈ܢ‬฻౯ȫȂ̜̞͉ͥ୆
ၑ‫ڠ‬എ̈́࠿औȪŊń̤̫ͥͅΠτΛΡησ൝ȫ̦ఉ̩Ȃদࡑ΍ͼΠ̮͈͂ΨρΜ΅̦ఱ̧̞̭͂Ȃ̦৽ါ̈́࿚ఴത̱͂̀‫̬ͥͦͣݷ‬ȃȪˍȫ̞͉̾̀ͅȂĲĺĺĺා̞ͩͥ͠ͅΨȜΔσ݈̤̞ٛ̀ͅȂ࢘ෝບ‫༹༷͂ث‬ΟΎͼϋ͈೹մ̦࣭षഎࣣͅփ̯ͦȪńŪųŤŶŭŢŵŪŰůį Ĳĺĺĺ ļĲıı Ļ ŦĸĶĮŦĹĲȫȂ࡛हༀ࣭ŇŅł͉‫ུܖ‬എ̭͈ͅ΄ͼΡρͼϋͅ‫̩࢘̿ܖ‬ෝບ‫ͬث‬৘ঔ̱̞̀ͥȃȪˎȫ̤͍͢Ȫˏȫ̞͉̾̀ͅȂ΋υρΡఱ‫͈ڠ‬ŉŪŢŵŵ‫ޗ‬਎͉ͣņŒŶŊő
ȪņůťűŰŪůŵġŒŶŢŭŪŵźġŊůŵŦųŷŦůŵŪŰůġőųŰŨųŢŮȫͬ‫ٳ‬อ̱ȂίρΓδ࢘‫͂ض‬΍ͼΠ̮͈͂௶೰౵
͈ήτ͈೩ࡘͬ৘࡛̱̞̭̀ͥ͂ͅಕ࿒Ȃ߇ਗఱ‫͉́ڠ‬൳ఱ͈஠࿂‫ފ‬ႁ͈͂͜Ȃˎා‫̹ͥͩͅۼ‬ņŒŶŊő
͈ܿ੅ΠρϋΑέ͹Ȝͬ৘ঔȂ࣭ष‫ވ‬൳হࡑͬ৘ঔ̳ͥள౷ͬ‫ږ‬ၛ̱̹ȃུΏϋεΐ;θ͉́ȂőłŅ̤̫ͥͅ࿪໤ၷ༹ບ‫ͬે࡛͈ث‬௙‫̱گ‬Ȃոષͅ‫ِ̳ͥ۾‬ș͈দ͙̮ͬત̳ٚͥȃ䋭 㪈㪈㪉 䋭ႉ઄ŔĮĸĮĶ

ɛ౻നġࢤඵ
‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬

vasculature, while postnatal vasculogenesis occurs by mobilization of bone marrow-resident
endothelial progenitors into the peripheral blood circulation and their homing to sites ofneovascularization. We previously identified a novel gene, termed ARIA that is highly andpreferentially expressed in EC and endothelial progenitor cells (EPC). ARIA is a membrane proteinwith a single transmembrane domain, and no specific domain was found by the analysis of its aminoacid sequence. Gene silencing of ARIA substantially enhanced EC and EPC angiogenic functions suchas migration and tube formation, while it reduced their apoptosis in association with enhanced

inhibitor of PI3K, at its intracellular domain to anchor PTEN at plasma membrane. Thus, loss of ARIA
reduced the membrane-association of PTEN, which leads to the reduced PTEN function, andconsequently enhanced PI3K/Akt signaling in EC. Accordingly, ARIA-KO mice showed substantiallyinhibition of PI3K. Studies of bone marrow-chimeric mice showed that ARIA in both EC and bonemarrow cells plays a significant role in the regulation of the ischemia-induced neovascularization.
These indicate that ARIA is a new pharmacotherapeutic target, and therefore we conducted to identify
a small compound that inhibits ARIA functions. By using a computational modeling for ARIA-PTEN
association and an in sillico screening, we identified a compound that inhibits the interaction between
ARIA and PTEN in vitro. This compound would be a lead compound of the ARIA inhibitor that is apotential new drug to treat ischemic diseases.

ポスター発表 ＹＩＡ選考発表

enhanced angiogenesis and blood flow recovery in an ischemic limb, which was cancelled by the

口頭発表

PI3K/Akt signaling. Mechanistically, we found that ARIA associates with PTEN, an endogenous

会長招待講演 シンポジウム

Angiogenesis occurs via the proliferation and sprouting of endothelial cells (EC) from an existing

特別講演łġųŰŭŦġŰŧġłœŊłġŪůġŢůŨŪŰŨŦůŦŴŪŴļġŢġűŰŵŦůŵŪŢŭġŵŢųŨŦŵġŧŰųġŵũŦġŵũŦųŢűŦŶŵŪŤġ
ŢůŨŪŰŨŦůŦŴŪŴ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

著者索引䋭 㪈㪈㪊 䋭䋭 㪈㪈㪊 䋭

プログラムలĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

特別講演
会長招待講演 シンポジウム

口頭発表

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪈㪈㪎 䋭ĺ࠮ĳķ඾Ȫ࿐ȫġĺĻııȡĲĲĻııġġలˏٛા࢛൮ġႉ઄ ŐńĲȶ૤৖ۛȟ෹ࠬ‫ۯ‬৖ۛȟࠬ‫ۯ‬૧୆Ȇठ୆হၷȷ

ŐńĲĮĲŊŮűŢŤŵġŰŧġŅŰůŰųĮŵųŢůŴŮŪŵŵŦťġōŦŴŪŰůŴġŰůġŗŢŴŤŶŭŢųġœŦŮŰťŦŭŪůŨġŢůťġŊůŵŪŮŢŭġŕũŪŤŬŦůŪůŨġ
ŪůġńŰųŰůŢųźġłųŵŦųźġŢŧŵŦųġŉŦŢųŵġŕųŢůŴűŭŢůŵŢŵŪŰů

࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜńŭŪůŪŤŢŭġŔŪŨůŪŧŪŤŢůŤŦġŰŧġņŢųŭźġňŢťŰŭŪůŪŶŮġņůũŢůŤŦŮŦůŵġŧŰųġŅŦŵŦŤŵŪůŨġŎźŰŤŢųťŪŢŭġ
ŅŢŮŢŨŦġŪůġőŢŵŪŦůŵŴġŸŪŵũġŕŢŬŰŵŴŶţŰġńŢųťŪŰŮźŰűŢŵũź

口頭発表

ŐńĲĮĳ

会長招待講演 シンポジウム

Objectives; The objective of present study was to evaluate the relationship of vessel remodeling and donor transmitted
lesions after heart transplantation.
Background; Vessel remodeling is known to play an important role in influencing luminal narrowing in cardiac
allograft vasculopathy. However the influence of donor transmitted lesion on plaque progression and vessel
remodeling remains unclear.
Methods; Seventy-four patients who underwent heart transplantation from May 1999 to March 2013 were followed at
our institution, of whom 16 were obtained annually intravascular ultrasounds studied from baseline to 4 years. Vessel,
lumen and plaque volume in the first 50mm of the left anterior descending artery were calculated using Simpson's
method. On the basis of maximum intimal thickening at baseline, recipients were divided into donor-transmitted lesion
group (DL+ group, n=9) or non donor-transmitted lesion group (DL- group, n=7).
Results; Plaque volume in DL- group didn't change during 4 years, vessel volume significantly decreased. Thesechanges resulted in a significant decrease of lumen volume. On the other hand, plaque volume in DL+ group increased
during first 2 years and lumen volume didn't significantly decrease due to compensatory vessel dilatation. There wereno significant differences in lumen volume at 4 years in both groups.
Conclusions; The presence or absence of donor transmitted lesions influenced vessel remodeling and plaqueprogression during 4 years after heart transplantation. Donor transmitted lesions were associated with significant
plaque progression and compensatory vessel dilatation. Vessel constrictive changes were observed in only DL- group.

特別講演ɛളᰧġీ࿟Ȃఆനġ޷ဢȂଳ࢛ġၑȂᢒଳġୃ૝Ȃऎ൥ġీ૯Ȃ‫ڙ‬ධġ੉ਏȂ૱ġࢩਏȂ൥നġ౶෗Ȃ઀ႅġਜ਼ඵ჊Ȃಎ౓ġ໌঄

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛ௖୼ġࢨ୆Ȃ࿤࢛ġᔐຳȂ୞ࡔġୃহȂ઀୼ġ‫ݛ‬ဎȂհനġ௛䋭 㪈㪈㪎 䋭著者索引

Background: T2-weighted imaging (T2WI) on cardiovascular magnetic resonance (CMR) allows for identification of
acute inflammation and myocardial edema. We have previously shown that early gadolinium enhancement (EGE) is analternative technique for identifying myocardial edema in patients with Takotsubo cardiomyopathy (TCM). The
present study investigates whether EGE can identify impaired myocardial regions in patients with TCM. Methods: We
studied 60 consecutive patients with TCM (7 males and 53 females, mean age 70Ⱦ12 [SD] years) who underwent
gadolinium (Gd)-enhanced CMR using a 1.5 T scanner to determine the myocardium to ventricular lumen signal
intensity ratio (M/L ratio). CMR images were acquired 2, 5, 10, and 20 minutes after injection of gadolinium (0.15mmol/kg body weight). The EGE phase was defined as 2 to 5 minutes after Gd administration. The inversion delay
time was fixed at 300 msec. Follow-up cine CMR was also performed to evaluate myocardial wall motion recovery 14
and 30 days after the onset of TCM. Results: EGE was detected in 43 patients (72%) (Figure, yellow arrows), and highsignal intensity on T2WI was seen in 39 patients (65%) in the region with abnormal wall motion. The M/L ratio 5
minutes after Gd administration in impaired regions was significantly higher than at baseline (0.5Ⱦ0.1 vs. 2.5Ⱦ0.4,
p<0.01). Furthermore, there was good agreement between regions with EGE and regions with high intensity signals on
T2WI (r=0.79, p<0.01). There was only one (1.7%) patient with conventional late GE. Follow-up CMR demonstrated
that recovery of regions with abnormal wall motion was delayed in EGE-positive patients compared with EGEnegative patients (28Ⱦ5 vs.14ȾConclusion: In TCM, EGE could delineate a greater extent of myocardial damage thatis associated with delayed recovery of wall motion abnormalities.

ポスター発表 ＹＩＡ選考発表࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬ŐńĲĮĴ

ńŭŪůŪŤŢŭġńũŢųŢŤŵŦųŪŴŵŪŤŴġŢůťġőųŰŨůŰŴŪŴġŰŧġŔűŰůŵŢůŦŰŶŴġńŰųŰůŢųźġłųŵŦųźġŅŪŴŴŦŤŵŪŰůġŪůġ
źŰŶůŨġŧŦŮŢŭŦļġŇųŰŮġŢġĳıĮźŦŢųġŅŢŵŢţŢŴŦġŰŧġłŤŶŵŦġńŰųŰůŢųźġŔźůťųŰŮŦ
ɛಎോġ߼ဉȂ࿤࢛ġᔐຳȂ൥࿤ġٗঃȂाུġဉਏȂ߄౓ġ౺ྶȂߧाġႛ‫إ‬Ȃ࣏୼ġഘဎȂ५आġଢঃȂ‫֔ז‬ġ၌ࢨȂஃ٬ġణ‫ו‬Ȃ‫ݠ‬ઽġ࿷ၻȂࢃ൥ġဩ֚Ȃ୞ࡔġୃহȂ઀୼ġ‫ݛ‬ဎȂհനġ௛࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬

Background; Spontaneous coronary artery dissection (SCAD) is an unusual cause of acute coronary sydrome (ACS)and very rare. Despite of a recent report studying the US patients with spontaneous coronary artery dissection (SCAD),
clinical features and prognosis are not fully investigated in Japanese patients, especially younger, female populations.
Methods; By using a 20-year database from 1991 to 2011 including 6129 patients with acute coronary syndrome, we
performed a retrospective, single-center study. From this database, we selected 29 female ACS patients with age lessthan 50-year-old female, and categorized into SCAD-group (n=5) and Non-SCAD group (n=24), angiographically.
Results; In SCAD-group, mean age was 36 years and overall and prevalence was very low (0.8 per thousand). Acutemyocardial Infarction developed following physical or emotional stress in 3 patients, and during pregnancy in 1
patient, respectively. Differently from the US study, particular collagen disease was not found in any patients of thepresent study. The left anterior descending artery was involved in 4 patients, among whom 3 patients had multi-vessel
SCAD. However, only 2 patients underwent revascularization therapy. Regarding with younger female population,
SCAD is not rare as cause of ACS. The number of coronary risk factor, peak CK level and prevalence of anterior AMI
were comparable between SCAD-group and Non SCAD-group. SCAD-group had lower LDL, lower LVEF comparedwith Non SCAD-group. Importantly, during a median follow-up of 424 (61 - 7682) days, 2 patients experienced reinfarction due to recurrent SCAD and 1 patient died suddenly. In Kaplan-Meier analysis, ACS patients with SCAD
showed significantly higher rate of cardiac event (death, myocardial infarction and heart failure) in compatison withthose without SCAD (with SCAD, 60% vs without SCAD, 17%; p=0.004). Conclusions; Patients with SCAD, even inyounger population, seem to be prone to cardiac events.

ŐńĲĮĵņŢųŭźġŢŴġńŰŮűŢųŦťġŵŰġōŢŵŦġŅŦŷŦŭŰűŮŦůŵġŰŧġłŤŶŵŦġŌŪťůŦźġŊůūŶųźġŪŴġŢġŔŵųŰůŨġőųŦťŪŤŵŰųġ
ŰŧġŎŰųŵŢŭŪŵźġŪůġłŤŶŵŦġŎźŰŤŢųťŪŢŭġŊůŧŢųŤŵŪŰů
ɛ૩५ġങࢴȂ୞ࡔġୃহȂ࿤࢛ġᔐຳȂाུġဉਏȂಎୌġൽ჊Ȃ࣏୼ġഘဎȂߧाġႛ‫إ‬Ȃ߄౓ġ౺ྶȂ‫ݠ‬ઽġ࿷ၻȂஃ٬ġణ‫ו‬Ȃ‫֔ז‬ġ၌ࢨȂ५आġଢঃȂ൥࿤ġٗঃȂࢃ൥ġဩ֚Ȃհനġ௛࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬

Background Acute kidney injury (AKI) often occurs in patients with acute myocardial infarction (AMI) and isassociated with unfavorable outcomes. However, the impact of timing of AKI development on prognosis after AMI
remains unclear.
Method This study consisted of 760 patients with AMI who admitted to the National Cerebral and CardiovascularCenter of Japan within 48 hours after symptom onset. Blood sample was obtained on admission and repeated every day
for the first 3 days, and then at least every one or two days during the first week. AKI was diagnosed by AKI network
criteria: increase in serum creatinine level >0.3mg/dl or >50% within 48 hours. Patients were divided into 2 groups
according to the timing of AKI development: early AKI (within 48 hours after admission) and late AKI (>48 hours).
Results AKI developed in 95 patients (13%), who had higher in-hospital mortality than those without AKI (25.3% vs
3.0%, p<0.001). There were 63 patients with early AKI (66.3%), and 32 patients with late AKI (33.7%). Patients withearly AKI had higher in-hospital mortality than those with late AKI (34.9% vs 6.3%, p=0.002). Recovery from early
AKI was observed in 69.8% of the patients. Among patients with early AKI, recovery from AKI was observed in 69%,
and was associated with lower mortality than those without recovery from AKI (18% vs 74%, p<0.001). However,mortality of patients with recovery from early AKI was still higher than those without AKI (p<0.001) and those withlate AKI (p=0.12)
Conclusion These findings suggested that early AKI was associated with higher in-hospital mortality after AMI as
compared to late AKI. Patients with persistent renal dysfunction after early AKI had the worst outcome, but patientswith early AKI were at high risk of mortality even if renal function was once returned to baseline level.
䋭 㪈㪈㪏 䋭ŐńĲĮĶ

ŕũŦġńũŢůŨŦġŪůġŵũŦġōŶŮŪůŢŭġŔŵŦůŰŴŪŴġŢŵġŵũŦġŔŪŵŦġŰŧġŔŪŭŦůŵġőŭŢŲŶŦġŅŪŴųŶűŵŪŰůġŪůġŵũŦġņųŢġ
ŰŧġŐűŵŪŮŢŭġŎŦťŪŤŢŭġŕũŦųŢűź

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineɛआུġܲટȂઐ๶ġࢼ঎Ȃ଩ࡔġၦఊȂୌུġဉඵȂષനġ‫ࠉޕ‬ōŰůŨĮŵŦųŮġŴŢŧŦŵźġŢůťġűųŰŨůŰŴŵŪŤġŪŮűŢŤŵġŰŧġŮŦŴŦůŤũźŮŢŭġŴŵŦŮġŤŦŭŭŴġŵųŢůŴűŭŢůŵŢŵŪŰůġ
ŪůġűŢŵŪŦůŵŴġŸŪŵũġůŰůĮŪŴŤũŦŮŪŤİŪŴŤũŦŮŪŤġŤŢųťŪŰŮźŰűŢŵũź

Ĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬໐࿝Ȃĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼䋭 㪈㪈㪐 䋭著者索引

Background: Despite advanced pharmacological and non-pharmacological therapies for patients with cardiomyopathy,
their prognosis has been limited. Since mesenchymal stem cells(MSCs) are multipotent cells that can differentiate into
cardiomyocytes and vascular endothelial cells, those implantation into severely depressed myocardium may havebeneficial effects in part via myogenesis and angiogenesis. The present study therefore aimed to investigate the longterm safety and prognostic impact of intramyocardial MSCs implantation in patients with ischemic/non-ischemic
cardiomyopathy. Methods: Eight patients with advanced heart failure even on maximal therapy(age;52+/-11[SD]years,
left ventricular ejection fraction(LVEF);25+/-7%, ischemic/non-ischemic cardiomyopathy;3/5) were included in MSCs
group and were compared with 54 patients of the control group that was matched by age and cardiac function(age;52+/13 years, LVEF;22+/-7%). Results: 3.7x107 MSCs[mean] were injected into endocardium with transcatheter method.
Left ventricular diastolic dimension, %-fractional shortening evaluated by echocardiography and serum brain
natriuretic peptide(sBNP) did not significantly change 5 years after MSCs implantation(-1.0+/-6.1mm, +1.3+/-4.6%,+8+/-182pg/ml). 1 patient led to heart transplantation and 1 patient was re-hospitalized due to worsening heart failurein 5 years after MSCs implantation. Whereas, in the control group, major cardiac events including cardiac death orheart transplantation(n=6) and worsening heart failure(n=20) occurred in 54 patients. There were no patientsdeveloping cancer or fatal arrhythmias after MSCs implantation in the follow-up period.Conclusion: These findings
indicate that MSCs implantation into depressed myocardium may have long-term prognostic impact in patients withischemic and non-ischemic cardiomyopathy without reference to improvement of cardiac function and malignancy
development.

ポスター発表 ＹＩＡ選考発表ɛ࿮୆ġ࣠ ĲȂࣞᚰġฎࢨ ĲȂஃ٬ġణ‫ ו‬ĲȂ‫౓ז‬ġ࠻प ĳȂ࿤࢛ġᔐຳ ĲȂ୞ࡔġୃহ ĲȂհ୔ġੇ‫ ݛ‬ĲȂཤ໓ġଽঃ ĲȂ઀୼ġ‫ݛ‬ဎ ĲȂ‫୼ێ‬ġࡋহ ĳȂհനġ௛ Ĳ

口頭発表

ŐńĲĮķ

会長招待講演 シンポジウム

Background: Plaque disruption followed by its healing process is supposed one of major mechanisms foratherosclerosis progression. Indeed, there is a pathological evidence of repeated plaque rupture and healing at the siteof significant stenosis. We examine the change in the luminal stenosis at the site of silent plaque disruption and analyze
its associated factors in the Era of optimal medical therapy.Methods: Among 144 consecutive patients who received
coronary angiography and angioscopy that identified silent plaque disruption from August 2007 to December 2010(baseline), 36 patients who had repeated coronary angiography later (follow-up) were included for analysis. Silent
plaque disruption was defined as the plaque with thrombus detected by angioscopy in the non-culprit segments ofcoronary arteries. Diameter stenosis of the site with silent plaque disruption was angiographically measured at baseline
and that of the same site at follow-up was also measured; and their difference was defined as stenosis change.Results:
Statin was used in 89% of study patients, and serum low-density lipoprotein cholesterol level was 91Ⱦ21mg/dL. The
diameter stenosis at silent plaque disruption decreased significantly from baseline to follow-up (32Ⱦ14 vs. 27Ⱦ14,
p<0.001); and the stenosis change was -5.6Ⱦ7.9%. High-density lipoprotein cholesterol was significantly associatedwith stenosis change (r=-0.51, p=0.001) and was the only factor significantly associated with stenosis change bymultivariate linear regression analysis (B=-0.34, p=0.001). Conclusion: In the era of optimal medical therapy withstatin, the site of silent plaque disruption showed significant regression of luminal stenosis. However, the serum levelof high-density lipoprotein cholesterol was negatively associated with the stenosis change at the site of silent plaquedisruption.

特別講演ఱि࠙ख़ພ֭੏۪‫ܕ‬ඤ‫ش‬ŐńĲĮĸ

ńŰůŦġĮġţŦŢŮġńŰŮűŶŵŦťġŕŰŮŰŨųŢűũźġņůŢţŭŦŴġŔŢŧŦġŢůťġņŧŧŦŤŵŪŷŦġŃŢŭŭŰŰůġőŶŭŮŰůŢųźġ
łůŨŪŰűŭŢŴŵźġŪůġńũųŰůŪŤġŕũųŰŮţŰŦŮţŰŭŪŤġőŶŭŮŰůŢųźġŉźűŦųŵŦůŴŪŰůġőŢŵŪŦůŵŴį
ɛ೚ġྶࢤ ĲȂఱ‫ޡ‬ġ࣠ ĲȂ໛֔ġਹ໲ ĲȂ๶ॄġ࢖๼ ĳȂ२നġટۘ ĳȂ૩നġ‫ ࢤج‬ĳȂ໛നġഓ࿟ ĳȂಎୌġ୹໲ Ĳ
Ĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬໐࿝෹੏۪‫ش‬Ȃĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ༶ৣ஌‫ش‬

Background: Balloon pulmonary angioplasty(BPA) is an alternative interventional therapy for patients with inoperable
chronic chronic thromboembolic pulmonary hypertension(CTEPH). However, reported complications such as
reperfusion pulmonary edema(60%) and pulmonary bleeding, resulting in severe respiratory failure, are the major
issues that need to be solved. In our center, we often used to experience reperfusion pulmonary edema (5 of 10
procedures), involving the need of invasive mechanical ventilation in one procedure. Recently cone-beam computed
tomography (CBCT) has been found to reveal the precise information of peripheral target lesions in the pulmonary
artery. Detailed intervention strategy involving CBCT prior to BPA could reduce the rate of complications. Methods
and Results: 25patients(mean age, 64.4years) with inoperable CTEPH underwent BPA(76procedures in total).We
evaluated the positions, length, and vessel diameters of target lesions in the pulmonary arteries using CBCT or
multidetector CT(MDCT)before perfoming BPA.Target region and balloon size were determined by
CBCT/MDCT.After BPA, pulmonary artery mean pressures significantly decreased from 44.6mmHg to
30.4mmHg(p=0.0001).The cardiac index tended to improve from 2.4L/min/m2 to 2.5L/min/m2. Localized reperfusion
pulmonary edema occurred during 6 out of 76 procedures(7.9%). Conclusions Evaluation with CBCT before BPA
reduces the incidence of pulmonary edema and enables effective therapy for CTEPH patients.

ŐńĲĮĹডཛဇြۚळ༾ȪłŅœńŴȫ
ͬဥ̞̹ळ༾֊૒ၷ༹͈෹൲ྤ଻෹ࣞࠬգછκΟσρΛ
Π͈͒ခ࢘଻͈࠿൦̷͈͂ι΃ΣΒθ͈ٜྶɛࢺ࢛ġୃႃȂ౻നġ௛ংȂऎ൥ġఱ༟Ȃ઀੄ġ࿹ঃȂ‫ع‬࿤ġࢼડȂஜఆġࢼඵಿॄఱ‫ڠ‬ພ֭੏۪‫ܕ‬ඤ‫ش‬Ⱥ࿒എȻ෹൲ྤ଻෹ࣞࠬգછĩőłŉĪ͉ထࢃະၻ͈৖ۛ́Ȃ߃ාহၷ࿪̦‫ٳ‬อ̧̯̹͈͈ͦ̀͜হၷ೷ࢯ଻͈ۛ৪͜ఉ̩
૧̹̈́হၷ༹͈‫ٳ‬อ̦བ̞ͦ̀ͥ͘ȃłŅœńŴ͉Ȃুࡨ̥ͣཅີͅन̧̹৾́ͥ͛Ȃ̷͈ठ୆֓ၷ͈͒؊ဥ̦ࢩ̽̀͘
̞ͥȃőłŉ͈ພఠ͉ͅ‫׶‬છ̦‫۾‬ဓ̳̭̦ͥ͂౶ͣͦȂłŅœń͉ͅࢯ‫׶‬છैဥ̦̜̭ͥ͂ͤ͢őłŉ͈হၷͅ؊ဥ̧́
ͥ‫خ‬ෝ଻̦̜ͥȃུࡄ‫͉́ݪ‬őłŉͅచ̳ͥłŅœń͈হၷ࢘‫͂ض‬Ȃ̷͈ι΃ΣΒθͬ࠿൦̱̹ȃȺ༹༷ȻŘŪŴŵŢųġ œłŕͅŎŰůŰŤųŰŵŢŭŪůĩŎńŕĪġ ĶıŮŨİŬŨͬൎဓ̱ġ őłŉκΟσρΛΠͬै଼̱̹ȃŎńŕͬൎဓ̱̀ˍ਩
‫ࢃۼ‬ȂőłŉκΟσρΛΠ͉łŅœńŴൎဓ߲ĩŎİłĪ͂ȂŅŎņŎൎဓ߲ĩŎĶıĪͅ໦̫ͣͦȂłŅœńŴ߲͉ͅĸȿĲıķࡢ͈ळ༾̦๶୓ྤ̥ͣൎဓ̯̹ͦȃ֚໐ŅŪŊ́அ૗̱̹łŅœńŴͬൎဓ̱̹ȃ෹൲ྤգ͉૤΀΋Ȝ́෹൲ྤࠬၠ͈łŤŤŦŭŦųŢŵŪŰůġ
ŵŪŮŦĩłŕĪ͂ŅŦŤŦŭŦųŢŵŪŰůĩŅŤŵĪͬࠗ௶̱๱۷ࠬഎͅບ‫̱ث‬ȂŎńŕൎဓࢃĵ਩࿒Ȃழ૕ͬन̱৾ພၑ‫ڠ‬എບ‫̹࣐̽ͬث‬ȃ̹͘Ŏńŕൎဓࢃˎ਩࿒Ȃ෹ழ૕̥ͣŮœŏłಒ੄̱Ȃਅș͈֒ഥঊ͈อ࡛ͬųŦŢŭġŵŪŮŦġőńœͬဥ̞̀࠿൦̱̹ȃȺࠫ‫ض‬ȻŅŪŊ́அ૗̯̹ͦłŅœńŴ̦෹ழ૕ͅంह̳̭̦ͥ͂‫̧̹́෇ږ‬ȃ૤΀΋ȜષȂłŅœńŴൎဓ߲͉́ŅŎņŎൎဓ߲͂๤‫̱̀ڛ‬Ȃ෹൲ྤգ͈೩‫̹ͦͣ͛෇̦ئ‬Ȫłŕġ ťŢźĳĹġ ŎĶıġ ŷŴġ Ŏİłġ ĳıįĵġ Ⱦġ ĴįĲġ ŷŴġ ĳĵįıġ Ⱦġ ĵįıġ űɃıįıĶġ ŅŤŵġťŢźĳĹġ ŎĶıġ ŷŴġ Ŏİłġ Ĳĵĸĵįıġ Ⱦġ ĵķĸįĺġ ŷŴġ ĹĺĹįķġ Ⱦġ ĳĴĹįĴġ űɃıįııĶġ ŏľĺȫȃ
ழ૕‫ڠ‬എ͜ͅ෹൲ྤ͈๬࢚̦ဲଷ̯ͦ
ĩŗŦŴŴŦŭġŸŢŭŭġŵũŪŤŬůŦŴŴġŎĶıġŷŴġŎİłġıįĵĵġȾġıįıĵġŷŴġıįĴĲġȾġıįıĵġűɃıįııĲġŏľĺĪȂ෹൲ྤ͈ςκΟςϋΈͬဲ̢̧̭̦̹ͥ͂́ȃ̹͘ņůťŰŵũŦŭŪůĩņŕĪġ ġ ųŦŤŦűŵŰųĮłġ ĩŎĶıġ ŷŴġ Ŏİłġ ĲįĸĴġ ŷŴġ ĲįĲĲġ űɃıįıĶġ ŏľķĪȂņŕġ ųŦŤŦűŵŰųĮŃġ ĩŎĶıġŷŴġ Ŏİłġ ĳįĸĸġ ŷŴġ ĲįĲĴġ űɃıįıĶġ ŏľķĪĭġ ņŕĮĲġ ĩŎĶıġ ŷŴġ Ŏİłġ ĴįıĹġ ŷŴġ ĲįĵĲġ űɃıįıĶġ ŏľķĪ͞ŕňŇĮţŦŵŢĩŎĶıġ ŷŴġ ŎİłġĴįĴĺġŷŴġĳįıĴġűɃıįıĶġŏľķĪ͈֒ഥঊอ࡛ͬဲ̢̞̹̀ȃȺࠫࢊȻłŅœńŴळ༾֊૒ၷ༹͉‫׶‬છ଻΍ͼΠ΃ͼΰ̜ͥŕňŇĮţŦŵŢ͈อ࡛ͅ་‫̱̭ܳͬا‬ȂņŕĲ͞ņŕġ ųŦŤŦűŵŰųĮłġņŕġ ųŦŤŦűŵŰųĮŃ͈อ̢࡛̤̯ͬȂŎńŕͥ͢ͅőŉ͈ૺ࣐ͬဲ̢̹ȃ̭͈̭͉͂łŅœńŴळ༾֊૒ၷ༹̦෹൲ྤ଻෹ࣞࠬ
գછ͈૧̹̈́হၷ༹༷̠̭̦̈́ͤͥ͂ͅাऐ̯̹ͦȃ䋭 㪈㪉㪇 䋭ŐńĲĮĺ

֊૒૤‫ۍ‬൲ྤພ་̤̫ͥͅ ŪůŵŪŮŢ ඤ͈ࠬ‫ۯ‬૧୆ͅ‫࠿̳ͥ۾‬൦ġȡ࢕ۙખ౯௄༹Ȃࠬ‫ۯ‬ඤ಼‫إ‬෨ͥ͢ͅ۷ख़ȡ

Ĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬૤௫ࠬ‫ڠشٸۯ‬Ⱥ෸ࠊȻ֊૒૤͉Ȃ྾‫ڠע‬എȂ๱྾‫ڠע‬എါ֦ͤ͢ͅȂᛀྗ଻͈ŪůŵŪŮŢ๬࢚ͬඅಭ̱̹͂֊૒૤‫ۍ‬൲ྤພ་ȪńŢųťŪŢŤġ
łŭŭŰŨųŢŧŵġŗŢŴŤŶŭŰűŢŵũźĻġńłŗȫ
ͬ୆̲ͥȃ૤௫֊૒ࢃ͈৽ါ̈́ထࢃܰ೰֦ঊ̜́ͤȂૺ࣐‫ܥ‬੬͈ٜྶ͉ਹါ̈́‫ه‬ఴ͂

特別講演ɛঌཱġణဉ ĲȂ઀౓ġਜ਼֚ ĲȂࢾ਀ġ࿺ ĲȂఱ౓ġ༸૾ ĲȂߧനġ஠ဉ ĲȂ‫ݐ‬ġ࢖֚ ĲȂाനġణঃ ĲȂ໛፜ġ‫ޗ‬ռ ĳȂᚧġ༿ਏ ĳȂධസġ૝ٚ ĲȂ઀৒ġ଼֚ Ĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine̯̞ͦ̀ͥȃρΛΠͬဥ̞̹൲໤κΟσ́ȂŪůŵŪŮŢඤ͈ࠬ‫ۯ‬૧୆̱̹ͬٚńłŗ͈ૺജ̦༭̯̞࣬ͦ̀ͥȃ࢕ۙખ౯௄
൲ྤບ‫ۯ̹͈ࠬ͛ث‬ඤ಼‫إ‬෨ȪŊŗŖŔȫ͂Őńŕၰ༷ͬঔ࣐̱̹Ⴒ௽ĴĴ႕Ȫ֊૒ࢃĲȡĲķාĭ໹޳ĶįĲාȫ̤̞̀ͅȂŎń͈ອഽȂŎń͂ŪůŵŪŮŢŭġ ŷŰŭŶŮŦ͈͂‫࠿ͬ߸۾‬൦̱̹ȃȺ༹༷Ȼऒஜ‫࣐ئ‬খĴĲখȂ
ऒٝஉখĳĵখȂֲ‫ۍ‬൲ྤĳķখ͈ࠗĹĲখͬ࠿൦̱̹ȃŐńŕષ͈Ŏń͉ŪůŵŪŮŢඤ͈ůŰůĮŴŪŨůŢŭ̈́‫ࢹે࣌ۯ‬௮ġ ĩႲ௽ĴŧųŢŮŦոષĪ͂೰̱݅Ȃड͜Ŏń͈ఉ̞ŧųŢŮŦ́ତͬତ̢̹ȃŊŗŖŔͬဥ̞̀ŷŦŴŴŦŭȂ
ŭŶŮŦůȂ
ŪůŵŪŮŢ͈ŷŰŭŶŮŦ
ȪŮŮĴȫ
ͬࠗ௶̱Ȃ
̷̸͈ͦͦ۷ख़‫ݻ‬ၗȪŮŮȫ́ੰ̱̹ŪůťŦŹ
ȪŮŮĴİŮŮȫ
ͬॳ੄̱̹ȃ
ŗŦŴŴŦŭġ ŷŰŭŶŮŦͅచ̳ͥŪůŵŪŮŢŭġ ŷŰŭŶŮŦ͈୸͛ͥ‫ࣣڬ‬ȂŪůŵŪŮŢŭġ ţŶųťŦůĩĦĪ͜ॳ੄̱̹ȃȺࠫ‫ض‬Ȼ
Ŏń͉Ĳķ႕ȪĵĹĦȫ
ȂĳĶখ
ȪĴĲĦȫ
ͅ෇͛Ȃ
ŤũŢůůŦŭତ͉໹޳ĵįĹࡢȪųŢůŨŦġ ĲȡĲĶࡢȫ̜̹́̽ȃŎńĩĬĪ߲
ȪĲĸ႕ȫ͂ŎńĩĮĪ߲ȪĲķ႕ȫ͈෸ࠊͬ๤‫̭̹̱ͧ͂ڛ‬Ȃ֊૒ࢃࠐًාତ͞Ρ΢ȜාႢȂ‫୲ݵ‬฽؊Ȃ‫֦ࡏܓۍ‬ঊ̈́̓ͅओ͉෇̥̹͛̈́̽ȃ̱̥̱ȂŎńͬ෇̹͛‫ۍ‬൲ྤ͉Ȃ෇̞͈͛̈́͜ͅ๤͓̀ȂŪůŵŪŮŢŭġ ŷŰŭŶŮŦġ ŪůťŦŹȪĵįĸķġ Ⱦġ ĲįĵĲġ ŮŮĴİŮŮġ ŷŴįġ ĴįĲĳġ Ⱦġ ĲįĴĴġ
ŮŮĴİŮŮĭġűɃıįııĲȫ͂ŪůŵŪŮŢŭġţŶųťŦůĩĴıġȾġķĦġŷŴįġĳĴġȾġĸĦĭġűɃıįııĲĪġ̦ခփͅ௩ఱ̱̞̹̀ȃ̹͘ȂŤũŢůůŦŭତ͂ŪůŵŪŮŢŭġŷŰŭŶŮŦġŪůťŦŹ͈‫͉ͅۼ‬ခփ̈́ୃ͈௖‫̹̜̦̽߸۾۾‬ĩųľıįķĭġűľıįııĴĪȃ
ȺࠫაȻńłŗ̤̞̀ͅŪůŵŪŮŢඤ͈Ŏń͉࿩Ĵ໦͈Ĳ͈ࠬ‫͛෇ͅۯ‬ȂŪůŵŪŮŢŭġ ŷŰŭŶŮŦ͈௩ఱ͂‫̹̞̱̀߸۾‬ȃŊůŵŪŮŢඤ͈ŢůŨŪŰŨŦůŦŴŪŴ̦ńłŗ͈ૺജͅ‫ܙ‬ဓ̱

会長招待講演 シンポジウム༹ȪŐńŕȫ͉ŪůŵŪŮŢඤ͈ࠬ‫ۯ‬૧୆ͬŮŪŤųŰŤũŢůůŦŭȪŎńȫ̱͂̀۷ख़̧̳̭̦ͥ͂́ͥȃ̷ِ̭́ș͉Ȃ൚֭́֊૒૤‫ۍ‬̞̀ͥ͂ࣉ̢̹ͣͦȃɛᚧനġ࿾ ĲȂඤ൥ġဇႿ ĲȂֵ๶ġဉ෗ ĳȂᎢ౓ġ૞֚ ĲȂ‫܊‬෫ġੇฎ ĲȂ؈ࡔġટܲ ĲȂ૩ᚧġఱဈ ĲȂࢺ࢛ġྶଲ ĲȂఱିġ૯ܲঊ ĲȂ‫ུݠ‬ġဉহ ĴȂᎢനġ୍֚ ĳȂ௩५ġၑ Ĳ

Ⱥ෸ࠊȻഘ͉୆ఘ͈ࢭુ଻ͬ֋঵̳̹ͥ͛ͅຈါະ‫༷̜֚ͥ́ࠧخ‬Ȃ઼ً̈́ഘ͉ॸ‫ا‬ΑΠτΑ͞‫׶‬છͬৼ̱ܳȂழ૕વ‫̧̳̭ܳ֨ͬٺ‬ȃໜ໐ఱ൲ྤរȪłłłȫ͈ພఠࠁ଼ͅॸ‫ا‬ΑΠτΑ͞‫׶‬છ͈‫۾‬ဓ̦༭̯̞̦࣬ͦ̀ͥȂłłł̤̫ͥͅഘ͈‫۾‬ဓͬ࠿൦̱̹༭͉̞࣬̈́ȃ̷̭́Ȃഘ͉łłł͈ພఠࠁ଼ͅ‫۾‬ဓ̳ͥ͂‫ب‬୰̹ͬ̀Ȃłłł༃̤̫ͥͅഘ‫܄‬ခၾ̤͍͢ഘೆ಍ͬ࠿൦̱Ȃॸ‫ا‬ΑΠτΑ̤͍͢‫׶‬છ͈͂‫࠿ͬ߸۾‬൦̱̹ȃ
Ⱥ༹༷ȻĳıĲĳාĵ࠮̥ͣĳıĲĴාĴ࠮͈́͘Ĳා‫ۼ‬́൚֭̀ͅ૤௫ࠬ‫̦੅਀شٸۯ‬ঔ࣐̯̹ͦĶĴ႕ͬచયͅ࠿൦࣐̹ͬ̽ȃłłłͅచ̱̀ఱ൲ྤ౾۟੅̦ঔ࣐̯̹ͦછ
႕ͬłłł߲ȪůľĲĺȫ̱͂̀Ȃఱ൲ྤ༕‫ޛ‬ॏછ̹͉͘ఱ൲ྤ༕‫ݙ‬ၠછͅచ̱̀ఱ൲ྤ༕౾۟੅̦ঔ࣐̯̹ͦછ႕ͬ๱
łłł߲ȪůľĴĵȫ̱͂̀ဥ̞̹ȃఱ൲ྤழ૕͉Ȃఱ൲ྤ౾۟੅̹͉͘ఱ൲ྤ༕౾۟੅ঔ࣐শͅन̱̹৾ȃࡔঊ‫༹̤͢࢕ݟ‬͍ασςϋ୒அ૗ͬဥ̞̀Ȃఱ൲ྤழ૕̤̫ͥͅഘ‫܄‬ခၾ͍̈́ͣͅഘೆ಍ͅ‫̱̀۾‬ບ‫̹࣐̽ͬث‬ȃ̹͘ࢯĹĮŐŉťň̤͍͢ńŅķĹࢯఘͬဥ̞̹྾‫ע‬ழ૕அ૗̀ͅȂॸ‫ا‬ΑΠτΑ̤͍͢‫׶‬છͅ‫࠿̱̀͜۾‬൦࣐̹ͬ̽ȃȺࠫ‫ض‬Ȼłłł߲̤̞̀ͅ౳଻̤͍͢‫׸ݎ‬ၚ̦ࣞ౵̜̹̦́̽Ȃ‫ܖ‬ய৖ۛȆඤ໚ͅ‫͉̱̀۾‬ၰ߲‫ͅۼ‬ခփओͬ෇̥̹͛̈́̽ȃఱ൲ྤഘ‫܄‬ခၾ͉๱łłł༃͂๤̱̀łłł༃́ခփͅ௩‫̤̱ͤ̀ح‬Ȃασςϋ୒அ૗̤̞̀͜ͅłłł༃̀ͅഘೆ಍͈ᄤૺͬ෇̹͛ȃഘೆ಍ႀ֖͂߃୪̱̀ంह̱̤̀ͤȂĹĮŐŉťň̤͍͢ńŅķĹ͈อ࡛ၾ͉ഘೆ಍ၾ͂ୃ͈௖‫ͬ۾‬া̱̞̹̀ȃȺ ࠫࢊȻłłł͈ພఠࠁ଼̤̞̀ͅȂഘ͈‫۾‬ဓ̦াऐ̯̹ͦȃ䋭 㪈㪉㪈 䋭著者索引

ĹĮŐŉťň̤͍͢ńŅķĹอ࡛͉Ȃഘೆ಍͈ࠫ‫͂ض‬൳အͅȂłłł༃́ᄤૺ̱̞̹̀ȃࢵͅȂĹĮŐŉťň̤͍͢ńŅķĹอ࡛ႀ֖͉

ポスター発表 ＹＩＡ選考発表

Ĳ ໶ࡩ֓‫ش‬ఱ‫ڠ‬ඤ‫ڠش‬੏۪‫ܕ‬ඤ‫ش‬Ȃĳ ໶ࡩ֓‫ش‬ఱ‫ڠ‬ພ֭ພၑ໐ȂĴ ໶ࡩ֓‫ش‬ఱ‫ڠ‬૤௫ࠬ‫شٸۯ‬

口頭発表ŐńĲĮĲı ໜ໐ఱ൲ྤរ͈ພఠ̤̫ͥͅഘ͈‫۾‬ဓ̞̾̀ͅ

ŐńĲĮĲĲ ‫ح‬Ⴂؕแ་଻̤̫ͥͅ œŐńŌġͺͼΕέ΁Ȝθඅ։എ ŮŢŤųŰűũŢŨŦġŦťŶŤŢŵŪŰůġŵũŦųŢűź
ɛಎ๶ġ૧ఊ჊ ĲȂśŢůťŪġŔŰŶŴŬŢ ĴȂ୞୼ġࠋඵ჊ ĲȂ‫݌‬നġ࿆୆ ĲȂऎș࿐ġ໲෗ ĳȂ‫ࢾ؍‬ġ‫ڡ‬຃ ĳȂŉŢŧŦŻŪĮŎŰŨũŢťŢŮġłŭŪ ĴȂ୞‫ޘ‬ġోႿ Ĳ
Ĳ ߇ਗఱ‫ڠ֓ڠ‬໐‫ش܉‬Ȃĳ ߇ਗఱ‫ڠ֓ڠ‬໐֓‫ڠا‬ȂĴ ŅŦűŢųŵŮŦůŵġŰŧġœŢťŪŰŭŰŨźĭġŉŢųŷŢųťġŎŦťŪŤŢŭġŔŤũŰŰŭĭġŃŰŴŵŰůĭġŎł

‫ح‬Ⴂؕแ་଻͉‫ۯࠬ܉‬૧୆ພ͈యນ̜́ͤȂ৐ྶ̦̾̈́ͥͅਹါ̈́৖̜ۛ́ͥȃड߃Ȃ‫̞̤̀̓̈́ͅ܈‬ພఠջంഎ
ζ·υέ͹Ȝΐ໦‫̦ا‬ٜྶ̯ͦȂ‫׶‬છͅ‫۾‬ဓ̳ͥŎĲζ·υέ͹Ȝΐ͂ழ૕ਘ໘ͅ‫۾‬ဓ̳ͥŎĳζ·υέ͹Ȝΐ̦ంह̳̭̦ͥ͂༭̯̞࣬ͦ̀ͥȃ̱̥̱Ȃ‫ح‬Ⴂؕแ་଻̤̫ͥͅྤ၁྄ࠬ‫ۯ‬૧୆͈͒ŎĲĭġŎĳζ·υέ͹Ȝΐ͈‫۾‬ဓ͉ະྶ̜́ͥȃ̹͘ळ༾ࣸ‫͈ڒ‬ठࢹ଼ࠬ͞‫ۯ‬૧୆ͅ‫۾‬ဓ̳ͥœŐńŌ͉ͅȂœŐńŌĲȆœŐńŌĳ̞̠͂ˎ͈̾ͺͼΕέ΁Ȝθ̦౶̞̦ͣͦ̀ͥȂྤ၁྄ࠬ‫ۯ‬૧୆͈͒‫۾‬ဓȂ̯ͣͅœŐńŌ͈ζ·υέ͹Ȝΐ໦‫۾͈͒ا‬ဓ͉࡛ह͈̭͂ͧະྶ̜́ͥȃࣽٝȂ͉ͩͦͩͦྤ၁྄ࠬ‫ۯ‬૧୆͈͒ŎĲĭġ Ŏĳζ·υέ͹Ȝΐ‫۾‬ဓȂ̯ͣͅœŐńŌ͈ພఠ͈͒‫۾‬ဓ̞̾̀ͅ࠿൦̱̹ȃΪΠୃુ࿌྄͉ͅġ œŐńŌอ࡛͉۷ख़̯̥̹̦ͦ̈́̽Ȅഊ੄ΪΠྤ၁྄ࠬ‫ۯ‬૧୆โ̤̞̀ͅœŐńŌĲ͂œŐńŌĳ͂͜ͅอ࡛̦۷ख़̯̹ͦȃ̹͘΍σȂζ;ΑτȜΎȜည൵ྤ၁྄ࠬ‫ۯ‬૧୆κΟσ̤̞̀͜ͅ൳အ̜̹́̽ȃζ;ΑκΟσ̤̞̀ͅȂœŐńŌĲĬİĮŕŪŦĲńųŦζ;Ὰ̤̞ࠬͅ‫ۯ‬૧୆ည൵̦۷ख़̯̹̦ͦȂœŐńŌஷ‫ٺ‬स̜́ͥέ͹ΑΐσȂœŐńŌĳ
අ։എஷ‫ٺ‬सȂ͂͜ͅခփࠬͅ‫ۯ‬૧୆ͬဲଷ̱̹ȃ‫ྙޟ‬૬̞̭͂ͅέ͹Αΐσ͉́૫੕ζ·υέ͹Ȝΐତ͉ခփͅဲ
ଷ̯̹̦ͦȂœŐńŌĳඅ։എஷ‫ٺ‬सൎဓ߲͉́૫੕ζ·υέ͹Ȝΐତ͉΋ϋΠυȜσ߲͂൳൝̜̹́̽ȃষͅŇłńŔͬဥ̞̀ྤ၁྄͈͒ŎĲĭġŎĳζ·υέ͹Ȝΐ૫੕ͬ࠿൦̳ͥ͂ȂťŢźĲ̥ͣġŎĲζ·υέ͹Ȝΐ૫੕ͬ෇͛ȂġťŢźĸͅခփ̈́Ŏĳζ·υέ͹Ȝΐ૫੕ͬ෇̹͛ȃœŐńŌĳඅ։എஷ‫ٺ‬सൎဓ߲̤̞͉̀ͅခփͅŎĳζ·υέ͹Ȝΐ૫੕̦ဲଷ̯
̹ͦȃ̹͘ζ;Αྤ၁྄ࠬ‫ۯ‬κΟσ̤̞̀ͅġ ŎĲζ·υέ͹Ȝΐ‫܉‬ඤൎဓͤࠬ͢ͅ‫ۯ‬૧୆̦ဲଷ̯̹͈ͦͅచ̱ȂġŎĳζ·υέ͹Ȝΐൎဓ߲͉́ခփࠬͅ‫ۯ‬૧୆͉௩‫̹̱ح‬ȃ̯ͣͅŪůġ ŷŪŵųṲ̞̋̀ͅœŐńŌĳஷ‫ͤ͢ͅٺ‬ŎĲ‫۾‬Ⴒ֦ঊŊŇŏĮϹĭġńŅĹıळ༾௩‫͛෇ͬح‬ȂŎĳ‫۾‬Ⴒ֦ঊŊōĮĲıĭġńŅĳıķळ༾ࡘઁͬ෇̹͛ȃࣽٝȂ‫ح‬Ⴂؕแ་଻̤̫ͥͅྤ၁྄ࠬ‫ۯ‬૧୆͈ພఠœŐńŌĳջంഎŎĳζ·υέ͹Ȝΐ໦‫̦ا‬ਹါ̜̭̦́ͥ͂াऐ̯̹ͦȃġ œŐńŌĳஷ‫ͥ͢ͅٺ‬ŮŢŤųŰűũŢŨŦġ
ŦťŶŤŢŵŪŰůġŵũŦųŢűź͉‫ح‬Ⴂؕแ་଻͈૧̹̈́হၷ͂̈́ͥ‫خ‬ෝ଻̦̜ͥȃŐńĲĮĲĳ ‫ح‬Ⴂͥ͢ͅ૤‫ܥ‬ෝ೩‫͉ئ‬૤௫ۚळ༾‫ܥ‬ෝ೩‫۾͂ئ‬Ⴒ̳ͥɛ៍നġ໲ฎȂ౓५ġ݅ྶȂ൐ġ੗ढȂ૩‫ئ‬ġၧ֚ఱिఱ‫شݪࡄࠏڠ֓ڠ‬ႉ઄֒ഥঊহၷ‫࣒ڠ‬ज‫ح‬Ⴂ͉૤ະ஠͈ඊၛ̱̹‫֦ࡏܓ‬ঊ̜́ͤȂ‫ح‬Ⴂ͂‫ͅވ‬૤ະ஠อછၚ̦௩̢̭͉ͥ͂Ȃέρηϋ΄θࡄ‫͞ݪ‬ńŉłœŕ
ࡄ‫́ݪ‬া̯̞ͦ̀ͥȃࡔ֦̱͂̀૤޼͈๬ఱ͞஌֋‫̀̽̓̈́͢ͅا‬Ȃ૤௫஠ఘ͈‫ܥ‬ෝ̦೩‫̢̦̞ͥ̀ͦͣࣉ̳͂ͥئ‬Ȃ̷͈ι΃ΣΒθ͉͕͂ͭ̓໦̥̞̞̽̀̈́ȃজ̹̻͉Ȃ‫ح‬Ⴂ̽̀͢ͅࡘઁ̳ͥऒ৒࿉ळࠬ‫ۯ‬ତͅ಍࿒̱Ȃ೩ॸளႀ֖
ͅంह̳ͥ૤௫ۚळ༾ͬĴȂĳĵȂĴıώ࠮Ⴂ͈ζ;Ά࠿બ̱̹ȃ೩ॸளζȜ΃Ȝ̜́ͥőŪŮŰůŪťŢŻŰŭŦĩőŪŮŰĪု଻ȂŤŬŪŵ
ု଻૤௫ۚळ༾͉‫ح‬Ⴂ͂‫ͅވ‬Ȃಠྴͅ௩‫̱ح‬Ȃࢵͅ‫ྙޟ‬૬̞̭͂ͅȂőŪŮŰ֮଻૤௫ۚळ༾͈͙̦໦ႨĩŌŪķĸု଻ĪȂ໦‫ا‬ĩŏŬŹĳįĶȂňłŕłĵု଻Ī̱̞̹̀ȃ̹͘ȂőŪŮŰ֮଻૤௫ۚळ༾͉Ȃု଻૤௫ۚळ༾ͅ๤͓̀Ȃͤࠬ͢‫̞߃ͅۯ‬պ౾ͅంह ̱ ̀ ̞ ͥ ̭ ͂ ̦ ྶ ͣ ̥ ͂ ̈́ ̽ ̹ ȃষ ͅ ೩ ॸ ள ळ ༾ ĩ Ĳ ı Ů Ů ŉ Ũ ո ‫ ئ‬Ī ͬ ஖ ఼ എ ͅ ͺ ε Π Ȝ Ώ Α ͅ ည ൵ ̳ ͥ ȂŕŪųŢűŢŻŢŮŪůĩŕőśĪͬဥ̞̀࠿൦̱̹̭͂ͧȂŕőśൎဓࢃĲ඾́ȂőŪŮŰု଻૤௫ۚळ༾͉͕͖ક৐̱̹̦ȂőŪŮŰ֮଻૤௫ۚळ༾̦ŴźŮŮŦŵųŪŤͅ໦Ⴈ̱ۚळ༾ତͬ௩‫̵̯ح‬ȂൎဓĹ඾ࢃ͉ͅőŪŮŰု଻૤௫ۚळ༾ତ͉αȜΑρͼϋͅ࿗̞̹̽̀ȃ̭͈̭͉͂ȂőŪŮŰု଻Ȃ֮଻૤௫ۚळ༾ΣΛΙ͉‫ܥ‬ෝഎͅႲ̱̞̭ࠫ̀ͥ͂ͬাऐ̱̞̹̀ȃ̹͘ȂΞυιͺಿ͉೩ॸள૤௫ۚळ༾Ȃୃુॸள૤௫ۚळ༾Ȃ૤޼͈ਜ਼ͅౣ̩̞̹̦̈́̽̀ȂࣞႢζ;Ά͉৹̞ζ;Α͂๤‫̱ڛ‬̀ಠྴͅୃુ૤௫ۚळ༾͈Ξυιͺ̦ౣ̩̤̈́̽̀ͤȂ̭ͦͤࣞ͢ͅႢζ;Α૤޼͈Ξυιͺಿ̦ౣੀ̱̞̀͂ࣉ
̢̹ͣͦȃ̭ͦ́͘ͅȂজ̹̻͉ȂΞυιͺಿ͂૤޼ਓੀෝ̦ୃ௖‫̭̳ͬ͂ͥ۾‬બྶ̱̞̀ͥȃΞυιͺ͈ౣ̞૤௫
ۚळ༾̥ͣ໦‫̹̱ا‬૤޼͉൳အͅΞυιͺ̦ౣ̩Ȃ૤޼ਓੀႁ̦৻̞ȃ̭͈ι΃ΣΒθ̦‫ح‬Ⴂͥ͢ͅ૤ະ஠̧ͬ֨
̭̳ܳ͂ထே̯̹ͦȃ೩ॸள૤௫ۚळ༾͉‫ح‬Ⴂ͂‫ͅވ‬௩‫̳ͥح‬ȃ̱̥̱ȂࣞႢζ;Α૤௫ඤ͈೩ॸளႀ֖ͅ໦ື̳ͥ
૤௫ۚळ༾͉ͅාయഎͅȨࡣ̞ȩ̦‫ܥ‬ෝഎ͉ͅȨ৹̞ȩۚळ༾̦ంह̱Ȃ̭͈ळ༾ͬΗȜΊΛΠ̱̹ͅȂ૤ະ஠͈૧̹
̈́হၷ༹̦͈̾̈́ͥ͂͜ͅࣉ̢̞̀ͥȃ䋭 㪈㪉㪉 䋭ĺ࠮ĳĸ඾Ȫ߄ȫġĲĵĻĶıȡĲķĻĶıġġలˏٛા࢛൮ġႉ઄ Őńĳȶ‫ۯࠬ଻ࠬݹ‬৖ۛȟ̷͈ఈȷŐńĳĮĲĴ ల ĳ ଲయ࿪सဣ੄ΑΞϋΠၣ౾ࢃ͈‫ۍ‬൲ྤ͈ພၑ‫ڠ‬എඅಭɛ୼ષġ̥ͤ ĲȂ૒നġ੝ࢺ ĳȂֵ๶ġဉ෗ Ĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

Ĳ ໶ࡩ֓‫ش‬ఱ‫ڠ‬ພ֭ພၑ໐Ȃĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜႉ઄ພၑ‫ش‬ŅņŔȫ͈΀αυςθΑဣ੄଻ΑΞϋΠȪņŷŦųŰŭŪŮŶŴĮŦŭŶŵŪůŨġ ŴŵŦůŵȈġ ņņŔȫ͞Ψͼ΂ςθΑဣ੄଻ΑΞϋΠȪŃŪŰŭŪŮŶŴĮ
ŦŭŶŵŪůŨġ ŴŵŦůŵȈŃņŔȫ͈ႉ઄എခဥ଻͂հ஠଻͉‫ږ‬ၛ̯̞ͦ̀ͥȅ̱̥̱ȄΪΠ‫ۍ‬൲ྤ̤̫ͥͅĳůťġ ŅņŔၣ౾ࢃ͈ພၑ
‫ڠ‬എਫ਼ࡉ͉ྶ̥͉̞ͣ́̈́ȅུࡄ‫͉ݪ‬ȄĳůťġŅņŔၣ౾ࢃ͈ழ૕฽؊ͬພၑ‫ڠ‬എͅྶ̥̳̭̜ͣͥ͂́ͥͅȅ

特別講演Ⱥ࿒എȻలĲଲయ࿪सဣ੄଻ΑΞϋΠȪŧŪųŴŵġ ŨŦůŦųŢŵŪŰůġ ťųŶŨĮŦŭŶŵŪůŨġ ŴŵŦůŵȈĲŔŕ ŅņŔȫͅ๤‫̱̀ڛ‬ȄలĳଲయŅņŔȪĳůťġ

Ⱥ༹༷Ȼ໶ࡩ֓‫ش‬ఱ‫࣭͂ڠ‬ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ͈ཎ࠿છ႕ͤ͢ං̹ͣͦȄĳůťġ ŅņŔၣ౾ࢃĲාոඤ͈ĸછ႕Ĳĳພ་૧୆ඤ྄ͥ͢ͅΑΞϋΠΑΠρΛΠ͈๭ໞၚ͂͂͜ͅȄْ௨ٜଢ଼ΕέΠͬဥ̞̀ΑΠρΛΠਔս͈έͻήςϋ͈࿂ୟͬ೰ၾ̱̹ȅȺࠫ‫ض‬ȻΑΞϋΠΑΠρΛΠ͈૧୆ඤ྄ͥ͢ͅ๭ໞၚȄέͻήςϋ͈࿂ୟ̷̸͉ͦͦȄņņŔ͉́ ķĺįĲ Ⱦ ĴĴįĺ ɓȄĸĲĶįĵȾġĲĳĲĳįĲЂŮĳȄĲŔŕġŅņŔ͉́ġĴĵįıġȾġĲĲįĸġɓȄġĸĸķĶĴįĴġȾġĳĸĵĶĴįĹġЂŮĳ̜̹́̽ȅȁȺ௙‫گ‬Ȼ
ĲŔŕġ ŅņŔͅ๤‫̱̀ڛ‬Ȅġĳůťġ ŅņŔၣ౾ࢃ͈‫ۍ‬൲ྤ͉Ȅခփͅ૧୆ඤ྄ͥ͢ͅΑΠρΛΠ͈๭ໞၚ̦̩ࣞȄΑΞϋΠΑΠρΛΠਔս͈έͻήςϋ͈ଢ଼੄̦ઁ̥̹̈́̽ḙ͈̏ͦͣழ૕฽؊͉ȄĲŔŕġ ŅņŔġ ͂ĳůťġ ŅņŔၣ౾ࢃ͈ਘ໘‫ܥ‬ത͈֑̞ͬນ̱̞̀ͥ͂ࣉ̢ͣͦȄĳůťġŅņŔ͈ႉ઄എခဥ଻ͅ‫۾‬ဓ̱̞̀ͥ‫خ‬ෝ଻̦াऐ̯̹ͦȅ

Ĳ ‫۾‬ୌႻबພ֭੏۪‫ܕ‬ඤ‫ش‬Ȃĳ ఱिఱ‫ڠ‬ఱ‫ૺ୶֭ڠ‬૤ࠬ‫ۯ‬হၷ‫ڠ‬Ⱥ෸ࠊȻġ ພၑ‫ڠ‬എ࠿൦̀ͅȂ‫ۍ‬൲ྤΑΞϋΠၣ౾໐໦ͅ෇͛ͣͦͥࠬ஀ັ಍͂ठඤ๧‫ا‬ະ஠͈‫۾‬Ⴒ̦ঐഊ̯̞ͦ̀ͥįȺ࿒എȻġ ࠬ‫ۯ‬ඤণ‫ͬޢ‬ဥ̞̀հ೰‫ޛ‬૤છۛ৪ͅၣ౾̯̹ͦ‫ڎ‬ਅ࿪सဣ੄଻ΑΞϋΠၣ౾ࢃĹ΃࠮শത͈ࠬ஀ັ಍໐໦
͈૧୆ඤ྄๭ໞ଻ેͬບ‫̱ث‬Ȃ૧୆ඤ྄๭ໞ଻ે͂ठඤ๧‫ا‬ະ஠͈‫۾‬Ⴒͬ࠿൦̳̭ͥ͂įġȺ༹༷ȻġĲĶĵུ͈࿪सဣ੄଻
ΑΞϋΠȪ΀αυςθΑဣ੄଻ΑΞϋΠġ ĴĹུȂΏυςθΑဣ੄଻ΑΞϋΠġ ĵķུȂΩ·ςΗ΅Γσဣ੄଻ΑΞϋΠġ ĴĶུȂΖΗυςθΑဣ੄଻ΑΞϋΠġ ĳıུȂΨͼ΂ςθΑဣ੄଻ΑΞϋΠġ ĲĶུȫͅచ̱̀ࠬ‫ۯ‬ඤণ‫ޢ‬۷ख़ͬঔ࣐̱̹įġ ۷ख़చય̱̹͂ΑΞϋΠ͉Ȃհ೰‫ޛ‬૤છ͈ୣහພ་̜́ͥࡥခ‫ۍ‬൲ྤ͈੝ٝພ་ͅၣ౾̯̹͈͈͙̱̹ͦ͂͜įġ ૧୆ඤ྄๭ໞࠁఠ͉ȂΑΞϋΠ̦૧୆ඤ྄‫̥̞̱ͥ̀཯ོͅئ‬๛̥́ĳ౲‫ͅٴ‬໦႒̱Ȃࠬ஀͈ັ಍໐໦͈૧୆ඤ྄๭ໞഽͬ
ບ‫̹̱ث‬ȃȺࠫ‫ض‬Ȼġ ĲĶĵུ͈࿪सဣ੄଻ΑΞϋΠ͈̠̻Ȃࠬ஀͈ັ಍͉ĴķΑΞϋΠͅ෇̹͛ͣͦįġ ۷ख़̯̹ͦࠬ஀͉Ȃ
Ĳ
ུ͈ΏυςθΑဣ੄଻ΑΞϋΠͅັ಍̱̞̹̀ฒ૗ࠬ஀ͬੰ̧Ȃ̳͓̀୤૗͈༃हࠬ஀̜̹́̽įġ ஠ĲĶĵུ͈ΑΞϋΠ̤̞̀ͅȂ૧୆ඤ྄‫̞̞̱̈́̀཯ོͅئ‬ΑΠρΛΠ໐໦͉Ȃོ཯̱̞̀ͥ໐պͅ๤͓ခփࠬͅ஀͈ັ಍̦ఉ̩Ȫۖ஀ັ಍ͬ෇̹͈͉͛Ω·ςΗ΅Γσဣ੄଻ΑΞϋΠˎུ͈͙̜̹́̽įġȺࠫࢊȻġΑΞϋΠ͈ਅ႒ͅ‫̴ͣͩ۾‬ĭġࠬ஀͉૧୆ඤ྄‫̞̞̱̈́̀཯ོͅئ‬ΑΠρΛΠͅັ಍̱̞̹̀įġ ΑΠρΛΠ̦૧୆ඤ྄‫̥̞̱ͥ̀཯ོͅئ‬๛̥͉ĭġ ΑΞϋΠၣ౾ࢃ͈ठඤ๧‫ͬا‬ບ‫̢̠̳́ͥث‬ခဥ̈́ࠁఠ‫ڠ‬എඅಭ̜́ͥ͂ࣉ̢̹ͣͦį䋭 㪈㪉㪊 䋭著者索引

஠๭ໞ໐໦ͅັ಍ĻġĺĵĦġŷŦųŴŶŴġະۖ஠๭ໞ໐໦ĻġķĦĭġőɃıįıııĲȫ
Ȃ૧୆ඤ྄‫ͅئ‬ΑΠρΛΠོ̦཯̱̞̀ͥ໐໦ࠬͅ

ポスター発表 ＹＩＡ選考発表ɛծനġଽਏ ĲȂ୞ࡔġၦ࣐ ĲȂ൥നġٗঃ ĲȂള໐ġഔ࿟ ĲȂ๑നġਘ ĲȂ‫ུؖ‬ġ૥ ĲȂକષġୱࣝ ĲȂධസġୄํ ĲȂ๑നġస෯ ĲȂฒܱġో࿟ ĲȂ૰നġܲঃ ĲȂ೚ఆġస࿟ ĲȂ؈࿤ġ߽ဈ ĲȂධസġ૝ٚ ĳȂષઐġୃႿ Ĳĭĳ

口頭発表ŐńĳĮĲĵ ࿪सဣ੄଻ΑΞϋΠၣ౾ࢃ͈૧୆ඤ྄๭ໞ଻ે͂ठඤ๧‫۾͈ا‬Ⴒ଻̞͈̾̀ͅ࠿൦ȇࠬ‫ۯ‬ඤণ‫ݪࡄޢ‬

会長招待講演 シンポジウム͈‫ۍ‬൲ྤ͂ĲŔŕġŅņŔၣ౾ࢃķછ႕Ĺພ་͈‫ۍ‬൲ྤ̞̾̀ͅ๤‫࠿ڛ‬൦̱̹ȅΑΞϋΠၣ౾໐͉ਏড༫ོ̀ͅ୨༌ͬैୋ̱ȄŐńĳĮĲĶ ņųźŵũųŰűŰŪŦŵŪůĮŢťŮŪůŪŴŵųŢŵŪŰůġŧŰųġŵũŦġŕųŦŢŵŮŦůŵġŰŧġłŤŶŵŦġŎźŰŤŢųťŪŢŭġŊůŧŢųŤŵŪŰůġĩņőŐĮ
łŎŊĮŊŊġŔŵŶťźĪĻġłġŃųŪťŨŦġŧųŰŮġŃŦůŤũġŵŰġńŭŪůŪŤŢŭġőųŢŤŵŪŤŦ
ɛ๬ࢃġਘ֚Ⴟ ĲȂධ࿤ġഓ౳ ĲȂುֵġ࠲ ĳȂ઀ᚧġఽ࿟ ĴȂ௖ᚧġ݅པ ĳȂ઀৒ġ଼֚ Ĳĭĵ
Ĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ၛ୼௙ࣣພ֭ȂĴ ૧‫ګ‬ఱ‫֓ڠ‬ভ‫ڠ‬௙ࣣພ֭Ȃĵ ൐‫ނ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬

Purpose: The development of novel pharmaceutical interventions to improve the clinical outcomes of patients withacute ST-segment elevation myocardial infarction (STEMI) is an inadequate medical need. In animal models, a single
intravenous administration of erythropoietin (EPO) during reperfusion improves left ventricular (LV) function in thechronic stage. However, the results of recent proof-of-concept trials using high-dose EPO in patients with STEMI are
inconsistent. In our pilot study, low-dose EPO after successful percutaneous coronary intervention (PCI) improved theLV ejection fraction (EF) and did not trigger severe adverse clinical events in patients with STEMI. One possible
reason for this discrepancy is the dose of EPO used.Study Design: To clarify the safety and efficacy of low-dose EPO
in patients with STEMI, we have conducted a double-blind, placebo-controlled, randomized, multicenter clinical trial(EPO-AMI-II). STEMI patients who have a low LVEF (less than 50%) will be randomly assigned to intravenous
administration of placebo or EPO (6,000 or 12,000 IU) within 6 hours after successful PCI. The primary endpoint isthe difference in LVEF between the acute and chronic phases (6 months), as measured by single-photon emission
computed tomography. This study has been approved by the Evaluation System of Investigational Medical Care. The
clinical trial is currently in progress since December, 2011, and totally 77 patients have been enrolled.Conclusions:
EPO-AMI-II will clarify the safety and efficacy of low-dose EPO in STEMI patients with LV dysfunction in a doubleblind, placebo-controlled, multicenter study.

ŐńĳĮĲķ ‫ۍ‬൲ྤ ńŕ ̀ͅ ŷŶŭůŦųŢţŭŦġűŭŢŲŶŦ ͂૷౯̯̹ͦພ་ͅచ̳ͥ ŐűŵŪŤŢŭġńŰũŦųŦůŤŦġ
ŕŰŮŰŨųŢűũźġĩŐńŕĪġͬဥ̞̹ٜଢ଼
ɛೞུġࠃ௱Ȃ‫ع‬ఆġࢼ໹Ȃ౓‫ڈ‬ġഔȂࡼ਱ദġࢬඵȂा౓ġ౶຃Ȃ࿐ఆġ૨२Ȃઐ๶ģ̜̭̇Ȃ֔ષġ߼ংȂ൥നġฎ‫ނ‬സలඵ୤਱লພ֭੏۪‫ܕ‬ඤ‫ش‬෸ࠊĻġ߃ාĭġ‫ۍ‬൲ྤńŕ̤̫ͥͅ൲ྤࣁ‫ا‬ພ་͈ಎ́͜ĭġűŰŴŪŵŪŷŦġųŦŮŰťŦŭŪůŨġĩųŦŮŰťŦŭŪůŨġŪůťŦŹɄĲįĲĪġฺ̠ͬĭġńŕ౵ĴıŉŖո‫͈ئ‬ŭŰŸġ ŢŵŵŦůŶŢŵŪŰůġ űŭŢŲŶŦ͉੿ြ‫ۍ଻ݢ‬છ࢓߲ġ ĩłńŔĪġ ͅ֊࣐̳ͥ‫خ‬ෝ଻͈̞ࣞŷŶŭůŦųŢţŭŦġ űŭŢŲŶŦ̜́ͥ͂༭̯̞࣬ͦ̀ͥįġ̹͘ĭġŇųŢŮŪůŨũŢŮġųŪŴŬġŴŤŰųŦŴġĩŇœŔĪġ̦ࣞ౵̜́ͥછ႕͉́ĭġ‫ۍ‬൲ྤńŕ̤̞̀ͅĭġ̭͈̠̈́͢
ŷŶŭůŦųŢţŭŦġűŭŢŲŶŦͬ෇͛ͥອഽ̦̞ࣞ͂༭̯̞࣬ͦ̀ͥįġུࡄ‫͈ݪ‬࿒എ͉ĭġ‫ۍ‬൲ྤńŕ̤̞̀ͅŷŶŭůŦųŢţŭŦġűŭŢŲŶŦ͂૷౯̯̹ͦພ་ͬĭġ ŐűŵŪŤŢŭġ ńŰũŦųŦůŤŦġ ŕŰŮŰŨųŢűũźġ ĩŐńŕĪġ ͬဥ̞ٜ̀ଢ଼̳̭̜ͥ͂́ͥį༹༷Ļġ ൚֭̀ͅĳıĲĲාĴ
࠮ſĳıĲĳාĲĳ࠮ͅ‫ۍ‬൲ྤŐńŕͬဥ̞̀‫ۍ‬൲ྤͼϋΗȜαϋΏοϋĩőńŊĪͬ৘ঔ̱̹છ႕͈̠̻ĭġ ੅ஜĴ΃࠮ոඤͅ‫ۍ‬൲ྤńŕͬज़௨̱̹Ĳĳછ႕Ĳĳພ་ͬచય̱̹͂įġ ‫ۍ‬൲ྤńŕ௡౾͉ĭġ ŕŰŴũŪţŢġ ŎŦťŪŤŢŭġ ŔźŴŵŦŮŴ২ୋ͈ķĵႥζσΙΑρͼΑńŕͬঀဥ̱̹įġ ‫ۍ‬൲ྤńŕ̤̞̀ͅĭġ ພ་໐͈ࠬ‫̦ࠂۯ‬చચࠬ‫ͅࠂۯ‬చ̱ĲıĦոષ͈‫ڐ‬ఱ̦̜ͤĭġ ̤̥̈́̾ńŕ౵̦ĴıŉŖྚྖ͈ŭŰŸġŢŵŵŦůŶŢŵŪŰůġűŭŢŲŶŦͬခ̳͈ͥͬ͜ġńŕĮŗŶŭůŦųŢţŭŦġőŭŢŲŶŦġĩńŕĮŗőĪ͂೰̱̹݅įġńŕĮŗő͈ခྫͥ͢ͅŐńŕਫ਼ࡉ͈௖֑̞̾̀ͅ࠿൦࣐̹ͬ̽įࠫ‫ض‬Ļġ ńŕĮŗő͉Ĳĳພ་ಎĸພ་ĩĶĹįĴĦĪͅ෇̹͛ͣͦįġ ‫ۍ଻ݢ‬છ࢓߲̤͍͢ডৗయ৫։ુછ͈ອഽ͉ĭġ ńŕĮŗő߲̤̞̀ͅůŰůġ ńŕĮŗő߲ͅ๤̱ࣞၚ̜̹́̽ĩĸĲįĵĦġ ŷŴįġ ıįıĦĭġ űľıįııĭġ
ĹĶįĸĦġ ŷŴįġ ĵıįıĦĭġ űľıįıĳĭġ ųŦŴűŦŤŵŪŷŦŭźĪįġ ‫ۍ‬൲ྤŐńŕġ ਫ਼ࡉ͉́ĭġ ńŕĮŗő߲̤̞̀ͅůŰůġ ńŕĮŗő߲ͅ๤̱ŭŪűŪťĮųŪŤũġ
űŭŢŲŶŦ̤͍͢ŮŢŤųŰűũŢŨŦ͈ਬୟ̦ࣞၚͅ෇̹͛ͣͦĩĲııĦġ ŷŴįġ ĵıįıĦĭġ űľıįııĭġ ĲııĦġ ŷŴįġ ĹıįıĦĭġ űľıįııĭġ
ųŦŴűŦŤŵŪŷŦŭźĪįġ༷֚́ĭġŵũŪůĮŤŢűġŧŪţųŰŢŵũŦųŰŮŢġĩŕńŇłĪ͞ŵũųŰŮţŶŴͬ෇͛ͥອഽ͉ńŕĮŗő߲̞́ࣞ߹̜̹̦࢜̽ͅ
ခփओ͉̥̹̈́̽įࠫაĻġ ‫ۍ‬൲ྤńŕͥ͢ͅŷŶŭůŦųŢţŭŦġ űŭŢŲŶŦ͉ĭġ Őńŕ̤̞̀ͅĭġ ࣞອഽͅŎŢŤųŰűũŢŨŦ͈ਬୟฺ̠ͬĭġōŪűŪťġųŪŤũġűŭŢŲŶŦ̜́ͤĭġłńŔ͈͂௖‫̦۾‬াऐ̯̹ͦį䋭 㪈㪉㪋 䋭ŐńĳĮĲĸ ൚಼̤̫֭ͥͅಁอ଻ΑΞϋΠඤࠬ஀છͅచ̳ͥࠬ‫ۯ‬ඤণ‫࠿͈̥ͣޢ‬൦ɛ൥നġࢴ༟Ȃષ࿤ġٗঃȂ୆നġ૧֚჊Ȃ५ུġࢩ෗ȂհനġઍგȂ౻നġ౺෗Ȃଫġၧ࿟Ȃ५হġ࠻ඵȂ઀ຳ‫ز‬ġგࢤȂ‫ז܊‬ġ஝ၦȂ‫ॄݠ‬ġੇ֚෸ࠊȇ಼ಁอ଻ΑΞϋΠࠬ஀છȪŷŦųźġŭŢŵŦġŴŵŦůŵġŵũųŰŮţŰŴŪŴĻġŗōŔŕȫ
͈ι΃ΣΒθͅ‫͉̱̀۾‬਱໦͉ٜͅྶ̯̤ͦ̀
̴ͣȂໝࣣഎ̈́ါள̦ࡔ֦̱͂̀ࣉ̢̞ͣͦ̀ͥȃࣽٝȂِș͉ŗōŔŕછ႕ͅచ̱̀Ȃࡢș͈છ႕͈ႉ઄എඅಭ͂ࠬ‫ۯ‬ඤণ‫͈஀ࠬ֨ݟ͞ޢ‬ພၑழ૕ਫ਼ࡉ͈͂‫࠿͈̞̀̾ͅ߸۾‬൦࣐̹ͬ̽ȃ༹༷͂ࠫ‫ض‬Ļ൚͉֭́ȂĳıĲĲාĳ࠮̥ͣĳıĲĴාĲ

特別講演߃‫ܪ‬ఱ‫ڠ֓ڠ‬໐້௺ພ֭੏۪‫ܕ‬ඤ‫ش‬プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine࠮͈́͘‫́ۼܢ‬ȂĹ႕͈ΑΞϋΠࠬ஀છͬࠐࡑ̷̱͈̠̻ĸ႕̦ŗōŔŕ̜̹́̽ȃ஠͈̀ŗōŔŕછ႕ͅచ̱̀ࠬ‫ۯ‬ඤণ̀࠿൦࣐̹ͬ̽ȃࠫ‫ض‬ȂΑΞϋΠၣ౾ࢃͅŗōŔŕ̦୆̲͈ͥ́͘໹޳‫͉ۼܢ‬ĶĹįĸώ࠮̜̹́̽ȃࠬ‫ۯ‬ඤণ‫͉́ޢ‬ůŦŰŢŵũŦųŰŴŤŭŦųŰŴŪŴฺ̠ͅછ႕̦ĵ႕ȂŶůŤŰŷŦųŦťġ ŴŵŦůŵġ ŴŵųŶŵ͈છ႕̦Ĵ႕۷ख़̯̹ͦȃ̷̸͈ͦͦΑΞϋΠਅ႒ͅ‫۾‬̱̀ĭůŦŰŢŵũŦųŰŴŤŭŦųŰŴŪŴ͉ŃŢųŦġŮŦŵŢŭġŴŵŦůŵġĩŃŎŔĪ̦ˍ႕ȂŴŪųŰŭŪŮŶŴġŦŭŶŵŪůŨġŴŵŦůŵġĩŔņŔĪ̦ˏ႕̜́ͤȂŶůŤŰŷŦųŦťġ
ŴŵŦůŵġ ŴŵųŶŵ͉́ŃŎŔ̦ˍ႕ȂŔņŔ̦ˎ႕̜̹́̽ȃඤ໚࿪ͅ‫࠿̳ͥ۾‬൦͉́ȂůŦŰŢŵũŦųŰŴŤŭŦųŰŴŪŴ͉́ĵ႕͂͜ࢯࠬ઀
โ࿪ĳस̱̩͉͜Ĳस̦ࠑ௽̯̤ͦ̀ͤȂŶůŤŰŷŦųŦťġ ŴŵŦůŵġ ŴŵųŶŵ͉́Ĵ႕͂͜ࢯࠬ઀โ࿪̦ಎগ̯̞̹ͦ̀ȃພၑழ૕ਫ਼ࡉ̥͉ͣȂ
ůŦŰŢŵũŦųŰŴŤŭŦųŰŴŪŴ͈͉ͥ́͢͜ͅĵ႕ಎĳ႕́ডৗ଼໦ฺ̠ͬࠬ஀ͬ࠿੄̱ȂŶůŤŰŷŦųŦťġ ŴŵŦůŵġ ŴŵųŶŵ͉́ ࠬ ઀ โ ࠬ ஀ ̦ ఉ ̞ ߹ ࢜ ́ ̜ ̽ ̹ ȃࠫ აȇΑ Ξ ϋ Π ࠬ ஀ છ ͉ Ȃࠬ ‫ ۯ‬ඤ ণ ‫ ޢ‬ਫ਼ ࡉ ̥ ͣ ͉ ĳ ̾ ͅ ఱ ༆ ́ ̧ ȂůŦŰŢŵũŦųŰŴŤŭŦųŰŴŪŴฺ̠ͅΑΞϋΠࠬ஀છͅ‫͉̱̀۾‬ພၑழ૕ਫ਼ࡉ́ডৗ଼໦ͬ෇̹̭̥͛͂̈́̓ͣίρȜ·෫Ⴈͥ͢ͅ‫̦ޣג‬াऐ̯̹ͦȃ

Ĳ ఱिఱ‫شݪࡄࠏڠ֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ఱिఱ‫شݪࡄࠏڠ֓ڠ‬྾‫ע‬ͺτσΆȜඤ‫ڠش‬ȂĴ ఱिఱ‫ڠ‬྾‫ڠע‬έυϋΞͻͺࡄ‫ݪ‬ΓϋΗȜ྾‫ܥע‬ෝଷࢄ‫ڠ‬Ȃĵ ൐‫ނ‬ఱ‫شݪࡄࠏڠ֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬䋭 㪈㪉㪌 䋭著者索引

Background Takayasu arteritis (TA) is a chronic inflammatory vasculitis of unknown pathogenesis affecting large
vessels, predominantly the aorta and its main branches. Treatment of refractory TA remains an unresolved clinicalissue. Patients usually respond to glucocorticoid (GC) therapy, but often relapse on tapering of GC dose. We aimed toassess the safety and efficacy of the interleukin-6 (IL-6) receptor antibody tocilizumab (TCZ) in the patients with TA
refractory to the conventional therapies including GC.Methods and Results Four patients with TA who had shown
GC resistance received TCZ infusions (8 mg/kg) every four weeks for at least 24 times (range: 24 to 51). Clinicalsymptoms, the serum levels of acute phase proteins and IL-6, GC dosage necessary to maintain remission, and crosssectional imaging by enhanced CT and MRI were assessed. All patients achieved good clinical response and rapid
normalization of the acute phase proteins such as C-reactive protein and serum amyloid A during the therapy with
TCZ. The mean dosage of prednisolone could be reduced from 21.3 mg/day to 1.5 mg/day. Although the serum IL-6
level was transiently elevated in all patients after several times of TCZ infusion, it gradually recovered to the initiallevel. Along with the decrease of serum IL-6, two patients exhibited significant reduction in the thickened arterial
lesions. No drug-related adverse effects were noted. Conclusions In this small group of patients with refractory TA,
TCZ therapy was effective and well-tolerated. Further larger studies should be conducted to confirm this finding.

ポスター発表 ＹＩＡ選考発表ɛಎ‫ؖ‬ġၻგ ĲȂ๳࢛ġࣝ૕ ĲȂခനġု ĲȂ༌‫ؖ‬ġଢࢬ ĲȂհ‫ݳ‬ġీ ĲȂ౻‫ؖ‬ġཆణ ĲȂషࡔġ߽ঊ ĲȂനಎġຮ჊ ĳȂ‫ུ܅‬ġ಑२ ĴȂ઀৒ġ଼֚ Ĳĭĵ

口頭発表ŐńĳĮĲĹ ŕŰŤŪŭŪŻŶŮŢţġłŮŦŭŪŰųŢŵŦŴġŗŢŴŤŶŭŢųġŊůŧŭŢŮŮŢŵŪŰůġŢůťġńŭŪůŪŤŢŭġŔźŮűŵŰŮŴġŪůġŵũŦġőŢŵŪŦůŵŴġ
ŸŪŵũġŕŢŬŢźŢŴŶġłųŵŦųŪŵŪŴġœŦŧųŢŤŵŰųźġŵŰġňŭŶŤŰŤŰųŵŪŤŰŪťŴ

会長招待講演 シンポジウム‫ͬޢ‬ဥ̞ȂΑΞϋΠඤ૧୆ඤ྄͈๭ໞેఠȂ૗಺̈́̓ͅ‫̱̀۾‬۷ख़࣐̞ͬȂ̹͘‫̱̀͜۾ͅ஀̹̱ࠬ֨ݟ‬ພၑழ૕ͅ

ŐńĳĮĲĺ ŕũŦġœŦŭŢŵŪŰůŴũŪűġţŦŵŸŦŦůġŃŪŧŶųŤŢŵŪŰůġłůŨŭŦġŢůťġłŵũŦųŰŴŤŭŦųŰŵŪŤġőŭŢŲŶŦġŅŪŴŵųŪţŶŵŪŰůġŪůġ
ńŰųŰůŢųźġłųŵŦųŪŦŴĻġłůġŐűŵŪŤŢŭġńŰũŦųŦůŤŦġŕŰŮŰŨųŢűũźġŔŵŶťź
ɛളᰧġ૯࡞ȂષఆġঃႿȂଫࡔġဉȂષനġ࿻ढȂഞനġࢭခȂಅനġ଺হȂ୼നġ߼෗Ȃ୼ષġ၌ࣝȂल൥ġෝ຃ජၻࡇၛ֓‫ش‬ఱ‫ڠ‬లˍඤ‫ش‬

Background: Atherosclerotic plaques in the arterial bifurcation are prone to develop in the opposite side of flow
divider where wall shear stress (WSS) is low, but take various forms of distribution in reality. Previous experimental
studies indicated that bifurcation angle (BA) influences the local flow turbulence and WSS. The purpose of this study
was to investigate the relation between BA and plaque distribution at coronary bifurcation lesions in patients withpercutaneous coronary intervention (PCI) by using frequency domain optical coherence tomography (FD-OCT).
Method: Forty-seven lesions with Medina classification (1,0,0), (0,1,0), (1,1,0) of were studied in 44 patients with FDOCT guided PCI (70.5Ⱦ9.1 y/o). FD-OCT was performed on the main vessel (MV) before PCI. Plaque distribution
was evaluated within 3mm distal MV to carina tip. The eccentric plaque oriented toward the opposite side of SB was
defined as typical plaque distribution. BA was measured based on the longitudinal reconstruction images of FD-OCT.
Results: Typical plaque distribution was more frequently observed in 25 lesions (53.2%), and non-typical plaquedistribution was in 22 lesions (46.8%). The frequency of medina (1,0,0), (0,1,0), and (1,1,0) were 32%, 52%, and 16%
in typical plaque distribution and 23%, 50%, and 27% in non-typical plaque distribution. BA was significantly greaterin non-typical plaque distribution compared to typical plaque distribution (72.2Ⱦ24.3 vs. 44.1Ⱦ27.0 degree, p<0.01).
ROC analysis indicated BA>59 degree (AUC=0.812, sensitivity 77.3%, specificity 80.0%) as the best cutoff values for
non-typical plaque distribution at coronary bifurcation lesions.
Conclusions: FD-OCT is useful to identify the plaque distribution of coronary bifurcation lesions. Wide BA wasassociated with the high incidence of non-typical plaque distribution. Baseline BA may predict the future morphology
of atherosclerotic plaque around coronary bifurcation.

ŐńĳĮĳı ૤௫ະାྤহၷဥˑέτϋΙ΃ΞȜΞσ͈́ଅ൲ྤඤͺήτȜΏοϋͅ‫̳ͥ۾‬‫ܖ‬யഎ࠿൦
ɛ؈५ġဉংȂಎ౓ġఱैȂධ࢛ġ૾Ȃ૰ॄġྔ౺ঊȂ຃ெġੇࢁȂाനġణঃȂධ࿤ġഓ౳Ȃධസġ૝ٚȂ઀৒ġ଼֚ఱिఱ‫ڠ‬ఱ‫֭ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬ਹછ૤ະ஠Ȇ౿ঘഎະାྤͬই͛ఉ̩͈੏۪‫ܕ‬৖ۛ́࢐ۜ૰ࠐ‫͈଻ڰ‬ᄤૺ̦ਹါ̈́࿨‫̞̱̹ͥ̀ضͬڬ‬ȃ̹͘ඳহ଻ࣞࠬգ̤̞̀͜ͅଅ࢐ۜ૰ࠐࠏً͈‫ڰ‬൲̦૬̩‫۾‬ဓ̳̭̦ͥ͂༭̯̤࣬ͦ̀ͤȂŌųŶŮ͉ͣଅ൲ྤඤ́ࣞਔ෨೒ഩ
࣐̠̭ͬ͂́঵௽എࣛգ̦ංͣͦȂ̷͈‫ܥ‬੬̱͂̀ଅ൲ྤਔսͅ໦ື̳ͥଅ૰ࠐȪ౶‫ژ‬૰ࠐ͂࢐ۜ૰ࠐȫ̦ੱ‫̯ͦٺ‬̹̹̜̠͛́ͧ͂༭̱̞࣬̀ͥȃଅ౶‫ژ‬૰ࠐ͈ੱ‫ۜ࢐̀̽͢ͅٺ‬૰ࠐಎଥ͈͒වႁ૞࣢̦ࡘͤȂ஠૸എ̈́࢐ۜ૰ࠐ‫ڰ‬଻̦೩‫خ̳ͥئ‬ෝ଻̦̜̭̥ͤ͂ͣȂଅ൲ྤඤͺήτȜΏοϋ̦ਹછ૤ະ஠͞౿ঘഎະାྤ͈হၷ̱͈͂̀ခ࢘଻
̦‫ܢ‬ఞ̯ͦͥȃଅ൲ྤඤ࣌͂ଅ૰ࠐ͈‫ݻ‬ၗ͉ତŮŮոඤ̜́ͤȂ΃ΞȜΞσ̱̹ͬٚࣞਔ෨೒ഩ́ယօͅ૰ࠐ͈ੱ‫ٺ‬̦ංͣͦͥ͂ଔ೰̯̦ͦͥȂ͈̓೾ഽ͈੄ႁȂ೒ഩশ‫̦ۼ‬ຈါ̜͈̥͉́ͥࡢș͈΃ΞȜΞσ̽̀͢ͅ։̈́ͥ‫خ‬ෝ଻̦̜ͥȃ̷ِ̭́șུ͉ཆ́ව਀‫خ‬ෝ̈́૤௫ະାྤহၷဥ͈ഩޭ΃ΞȜΞσȪĶέτϋΙȂĶ̉̉ഩޭಿȫͬဥ̞̀ଅ൲ྤͺήτȜΏοϋ࣐̹ͬ̽ાࣣ͈ࠬ‫ޛۯ‬ॏȆࠬ஀͈ࣣ̈́̓໵છ͈‫͂଻ࡏܓ‬ઘ৴ํս̞̾̀ͅȂගͬঀဥ̱̹‫଻ݢ‬৘ࡑ́࠿બ̱̹ȃࠬ‫ޛۯ‬ॏ͉஖఼എ௮‫ג‬Ȃࠬ஀̞͉̾̀ͅഐܽŐńŕͬဥ̞̀ບ‫̹̱ث‬ȃઘ৴ํս̞͉̾̀ͅ৘ࡑࢃͅଅ൲
ྤͬ୨ͤ੄̱Ȃழ૕அ૗࣐̹ͬ̽ȃ੝‫͈ܢ‬৘ࡑ́Ĳķ˳ոષ͈੄ႁ́ࣞഽ‫ޛ‬ॏ͈੄࡛ͬ෇̹̹͛͛ȂĵȂĹŘȂĲȡĵ໦‫͈ۼ‬೒ഩ̞̾̀ͅમळͅ࠿൦̱̹ȃ̷͈ࠫ‫ض‬ȂĹ˳͈೒ഩ͉̱̱́͊͊ࢩ̞ํս́‫྄́͘ͅٸ‬ઘ৴̦‫̹̞́ͭݞ‬ȃ༷֚ĵ˳Ȃ
Ĳ໦͈೒ഩ͉́‫̞ޑ྄́͘ٸ‬་଻̦͙̭͉ͣͦͥ͂‫̹̜̽́ܭ‬ȃոષͤ͢Ȃ‫ܡ‬ం͈ĶέτϋΙͺήτȜΏοϋ΃ΞȜΞσͬဥ̞̹ાࣣȂĵ˳೾ഽ̥ͣ‫྄ͅٸ‬໼௢̳ͥଅ૰ࠐ஌֋ͬੱ‫خ̧ͥ́ٺ‬ෝ଻̦̜̭ͥ͂Ȃ̤͍͢೒ഩ੄ႁ͉Ĺ˳೾ഽ́͘ͅဲଷ̧̳͓̜́ͥ͂ࣉ̢̹ͣͦȃ䋭 㪈㪉㪍 䋭ŐńĳĮĳĲ ŕųŢůŴŤŢŵũŦŵŦųġłųŵŦųŪŢŭġņŮţŰŭŪŻŢŵŪŰůġŧŰųġŕŦůťŪůŰűŢŵũźġŢůťġņůŵũŦŴŰűŢŵũźġœŦŧųŢŤŵŰųźġŵŰġ
ŏŰůĮŴŶųŨŪŤŢŭġŎŢůŢŨŦŮŦůŵ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛ؈࿤ġဈষ

ɛಎఆġഓ໹ ĲȂࢬനġౌ຃ ĲȂಱாġୃ‫ ܮ‬ĳȂఱ࿐ġࢼং ĲȂཤ໓ġଽঃ ĳ

口頭発表ŐńĳĮĳĳ ඿ဇြβίΙΡ ŗŢŭĮőųŰĮőųŰĭġŊŭŦĮőųŰĮőųŰ ͈ࠬ‫ۯ‬ඤ๧‫ܥ‬ෝͅ‫ޣג̳͖ݞ‬会長招待講演 シンポジウム

Aims; The pathophysiology of tendinopathy and enthesopathy has not been defined. Abnormal neovessels andaccompanying nerves have been recently identified as possible sources of pain associated with tendinopathy andenthesopathy. This study evaluates the feasibility and effects of transcatheter arterial embolization using
imipenem/cilastatin sodium (IPM/CS) to treat tendinopathy and enthesopathy that are refractory to traditional nonsurgical management.material and methods; Transcatheter arterial embolization using IPM/CS as an embolic agent
proceeded in seven patients (male, n = 5; mean age 51.7 y) with tendinopathy and enthesopathy (patellar tendinopathy(n = 1), rotator cuff tendinopathy (n = 2), plantar fasciitis (n = 1), lateral epicondylitis (n = 1), iliotibial band syndrome(n = 1), and Achilles insertion tendinopathy (n = 1). All patients had unrelenting pain at the site of tendinopathy andenthesopathy before the procedure. Technical success, adverse events and changes in Visual Analog Scale (VAS)
scores were assessed.Results; All procedures were technically successful, and no major adverse events developed.
Abnormal neovessels were located at the pathological site in all cases. Compared with before the procedure, mean
VAS scores significantly decreased at 1 day, 1, 4, and 10 months after the procedure. The effects lasted for 10 months
except for one case that obviously had recurrent pain at 6 months after procedure.Conclusion; Transcatheter arterial
embolization using IPM/CS for tendinopathy and enthesopathy was feasible and the effect lasted for 10 months in mostcases.

特別講演

ࢺ࡫୼ພ֭

Ĳ ΃σάΑ‫ڼ‬৆ٛ২อࣖ؊ဥࡄ‫ݪ‬ਫ਼Ȃĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬ထཡͅခဥ͂ࣉ̢ͣͦͥȃ඿ဇြβίΙΡŗŢŭĮőųŰĮőųŰȪŗőőȫĭġ ŊŭŦĮőųŰĮőųŰȪŊőőȫ͉ͺϋΐ΂ΞϋΏϋ་۟ࣖள͈ஷ‫ٺ‬‫ͬ଻ڰ‬ခ̱Ȃ̭͈ͦͣβίΙΡͬ‫͚܄‬૙຦͈ࣛգैဥ̞̾̀ͅఉତ༭̦̜࣬ͥȃ̱̥̱Ȃŗőőĭġ Ŋőő͈ࠬ‫ۯ‬ඤ๧‫ܥ‬ෝͅ‫̞̀̾ͅޣג̳͖ݞ‬ະྶ̈́ത̦ఉ̞ȃȺ༹༷ȻĩĲĪ Ūůġ ŷŪŷŰ দࡑȇྚহၷ͈ࠚછࣞࠬգ౳଻ĳĵྴȪාႢĶĵįĲȾĹįĲपȫȪ໹޳ȾŔŅȫͅŗőőĭġ Ŋőőͬ‫͚܄‬඿ΗϋΩ·ৗ‫ح‬କ໦ٜ໤̹͉͘ίρΓδ͈΃ίΓσͬĲ਩‫ۼ‬୫̵̯৾ȂίρΓδచચΘήσήρͼϋΡ·υΑ΂ȜΨȜদࡑͬ৘ঔ̱̹ȃࠬ‫ۯ‬ඤ๧‫ܥ‬ෝ͉Ķ໦‫ۼ‬ષუߐࠬࢃȂίτΙΑκΈρέͻȪņńĮķĭġ
ŅįņįŉŰŬŢůŴŰů২ȫ́ບ‫̹̱ث‬ȃĩĳĪ Ūůġ ŷŪŵųŰ দࡑȇΪΠဇြࠬ‫ۯ‬ඤ๧ळ༾ŉŖŗņńͅŗőőĭġ Ŋőőͬഞ‫̱ح‬Ȃ෽ူષୄಎ͈
ůŪŵųŪŤġŰŹŪťŦ
ȪŏŐřľġŏŐĳġĬġŏŐĴȫ
ͬ௶೰̱̹ȃ
̹͘ȂŘŪŴŵŢųࠏρΛΠȪĹĮĺ਩ႢȂဎȫ̥ͣഊ੄̱̹‫ޝ‬໐ఱ൲ྤͤࠬ͢‫ۯ‬ςϋΈͬै଼̱Ȃࠬ‫ڐۯ‬ಫ฽؊ͬζΈΤΆ༹ບ‫̹̱ث‬ȃȺࠫ‫ض‬ȻĩĲĪίρΓδ߲͈ߐٜࠬ༶ࢃडఱࠬၠၾ͉ĳıįĹȾķįĸġŮŭİŮŪůİĲııŮōͅచ̱Ȃͺ·Ξͻή߲͉́ĴıįıȾĲıįĵġ ŮōİŮŪůİĲııŮō͂ခփࣞͅ౵ͬা̱̹ȃ༷֚Ȃષუࠬգ͞
ΣΠυΈςΓςϋͥࠬ͢ͅ‫ڐۯ‬ಫ฽؊̤̞߲̀ͅ‫ۼ‬ओ͉͙̥̹ͣͦ̈́̽ȃĩĳĪŉŖŗņńͅŗőőĭġŊőőͬഞ‫ض̹̱ࠫح‬ȂŏŐřෛഽ͈ခփ̈́ષઌ̦͙̹ͣͦȃ̹͘Ȃࠬ‫ۯ‬ςϋΈͅŗőőĭġ Ŋőőͬഞ‫̹̱ح‬ાࣣ͉‫ڐ‬ಫ฽؊̦͙̹̦ͣͦȂඤ๧ŢůŵŢŨŰůŪŴŵȪŉŐņĮĲĵıȫ͈ഞ‫ͤ͢ͅح‬Ȃŗőőĭġ Ŋőő͈ࠬ‫ڐۯ‬ಫैဥ̦΅λϋΓσ̯̹ͦȃȺࠫაȻŗőőĭġ Ŋőő͉ࠚછࣞࠬգ৪͈ࠬ‫ۯ‬ඤ๧‫ܥ‬ෝͬ٨஝̱Ȃ̷͈ι΃ΣΒθ̱͂̀ࠬ‫ۯ‬ඤ๧ळ༾͈ŏŐॲ୆ည൵̦‫۾‬ဓ̱̞̀ͥ‫خ‬ෝ଻̦াऐ̯̹ͦȃ䋭 㪈㪉㪎 䋭著者索引

ळ༾ੰ‫ڐͤ͢ͅݲ‬ಫ฽؊̦ခփͅဲଷ̯̹ͦȃ̹͘ȂŏŐ଼ࣣࣖளஷ‫ٺ‬सȪōĮŏłŎņȫ͞ ţųŢťźŬŪůŪůġ Ńĳġ ųŦŤŦűŵŰųġ

ポスター発表 ＹＩＡ選考発表Ⱥ෸ࠊȻࠬ‫ۯ‬ඤ๧‫ܥ‬ෝ͈೩‫͉ئ‬൲ྤࣁ‫͞ا‬੏۪‫ܕ‬ພͬৼ̳̭̥ܳͥ͂ͣȂࠬ‫ۯ‬ඤ๧‫ܥ‬ෝͬ٨஝̳̭͉ͥ͂੏۪‫ܕ‬ພ͈ŐńĳĮĳĴ ૤௫ζ·υέ͹Ȝΐ͉૤௫գ໅‫ͅك‬చ̱̀༗ࢌഎͅैဥ̳ͥ
ɛড়നġਕ຃ ĲȂ૯ණġ֚჊ ĲȂ‫֔ז‬ġၻ२ ĳȂ઀৒ġ଼֚ Ĳ
Ĳ ൐‫ނ‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬Ȃĳ ুহ֓‫ش‬ఱ‫ڠ‬ྕ଻‫׶‬છ͉૤ະ஠ͬ‫̹͛܄‬૤ࠬ‫ۯ‬৖ۛͅ‫۾‬ဓ̳ͥ͂ࣉ̢̞ͣͦ̀ͥȃ৘षȂ૤ະ஠ۛ৪͉́‫׶‬છ଻΍ͼΠ΃ͼϋ͈τασ̦ષઌ̱̞̀ͥȃ̱̥̱̦̈́ͣ૤ະ஠̤̫ͥͅ‫׶‬છ͈ୃ‫̈́ږ‬࿨‫͉ڬ‬໦̥̞̞̽̀̈́ȃ༷֚́૤‫ܥ‬ෝ͉૤޼ळ༾
̴͈͙̈́ͣȂ‫ۼ‬ৗळ༾̽̀͢͜ͅଷࢄ̯̞̭̦ͦ̀ͥ͂ྶ̥̜ͣ͂̈́ͤ̾̾ͥȃࣽٝȂِș͉૤৖̤̫ۛͥͅ૤޼ळ
༾͂‫׶‬છळ༾͈͂௖ࡽैဥͅ಍࿒̱̹ȃ͉̲͛ͅέυȜ΍ͼΠιΠςȜͬဥ̞̀૤௫ಎͅంह̳ͥ྾‫ע‬ळ༾ٜͬଢ଼
̱̹ȃ̷͈ࠫ‫ض‬Ȃ૤௫ಎ͉ͅ೰ુેఠ̤̞̀͜ͅఉତ͈ζ·υέ͹Ȝΐ̦ంह̳̭̦ͥ͂ྶ̥ͣ͂̈́ͤȂ̷͈ତ͉૤
௫գ໅‫ك‬ĩŕłńĪͤ͢ͅ௩‫̹̱ح‬ȃ̭ͦͣζ·υέ͹Ȝΐ͈‫ܥ‬ෝٜͬଢ଼̳̹ͥ͛Ȃِș͉࿪सͬဥ̞̀ζ;Ὰ̤̞ͅζ·υέ͹Ȝΐͬવ‫̹̱ٺ‬ષ́ŕłń࣐̹ͬ̽ȃ̳ͥ͂գ໅‫͉ك‬ζ·υέ͹Ȝΐવ‫ٺ‬ζ;Ὰ̤̞ͅಠྶ̈́૤‫ܥ‬ෝ೩‫̱̹ͣͬ͜ئ‬Ȃ‫଻ݢ‬૤ະ஠ͥ͢ͅঘཌ̧̭̱̹ͬ֨ܳȃ̭͈̭̥͂ͣζ·υέ͹Ȝΐ͉૤௫գ໅‫̞̤̀ͅك‬༗ࢌഎ̈́ैဥͬခ̱̞̀ͥ͂ࣉ̢̹ͣͦȃιΗδυȜθٜଢ଼͈ࠫ‫ض‬Ȃζ·υέ͹Ȝΐ͉૤޼͈ٜൠࠏ̤͍͢ŕńłٝႹͬଷࢄ̱
̞̭̦̀ͥ͂াऐ̯̹ͦȃ૤௫ζ·υέ͹Ȝΐ͉ນ࿂ζȜ΃Ȝٜଢ଼͈ࠫ‫ض‬ȂŎĳ߿ζ·υέ͹Ȝΐ̜̭̦́ͥ͂ྶͣ
̥̹͂̈́̽ȃഢৢ֦ঊŔŕłŕķ̦Ŏĳ߿ζ·υέ͹Ȝΐ͈͒໦‫ͅا‬ຈଌ̜̭̦́ͥ͂౶̞̹ͣͦ̀ͥ͛Ȃِș͉ࣸଡ֊૒ͤࣸ͢ͅଡळ༾͈͙́Ŕŕłŕķͬࠧఅ̳ͥζ;Αͬैୋ̱̹ȃࣸଡळ༾͈͙́Ŕŕłŕķͬࠧఅ̳ͥζ;Ὰ̤̞͜ͅ૤޼͈ٜൠࠏయ৫͉વ‫̯ͦٺ‬Ȃζ·υέ͹Ȝΐ̦૤޼య৫ͬଷࢄ̱̞̭̦̀ͥ͂ၔັ̫̹ͣͦȃِ̯ͣͅș͉ζ·υέ͹Ȝΐ̥ͣ໦๥̯ͦȂ૤޼ͅैဥ̳֦ͥঊͬ൳೰̱̹ȃ̭͈֦ঊ͉૤௫ζ·υέ͹Ȝΐ͈͙ͅอ࡛̱Ȃໜ࣌͞۴௫͈ζ·υέ͹Ȝΐ́อ࡛͉͙̥̹ͣͦ̈́̽ȃζ·υέ͹Ȝΐવ‫ٺ‬ζ;Α̭͈֦͒ঊͬൎဓ̳̭ͥ͂ͤ͢ͅ૤޼͈
య৫વ‫͉ٺ‬௖फ़̯ͦȂ૤௫գ໅‫ͥ͢ͅك‬૤ະ஠͉‫ݣ‬੩̯̹ͦȃոષ͈ࠫ‫ض‬Ȃ૤௫ζ·υέ͹Ȝΐ͉૤޼య৫ͬଷࢄ̳
̭ͥ͂ͤ͢ͅ૤޼͈ࢭુ଻֋঵ͅຈଌ͈࿨‫̢̹ͦͣࣉ̞̱̹͂ͥ̀ضͬڬ‬ȃŐńĳĮĳĵ ͺϋΐ΂ΞϋΏϋ ŊŊġŅŏł χ·Ιϋͥࣞࠬ͢ͅգછ͈૧ܰহၷ༹͈‫ٳ‬อɛߴ५ġࢬ ĲȂಎ૰ġ߼ඃ ĲȂോఆġਕં ĲȂੳ౓ġ࿻ࢤ ĳȂ‫ڢ‬࿐ġࢤ৘ ĴȂ૩‫ئ‬ġၧ֚ ĳ
Ĳ ఱिఱ‫ڠ‬ఱ‫֭ڠ‬Ⴒࣣ઀঱อో‫ࢫ࠲شݪࡄڠ‬อో֓‫້࣒ܙڠ‬जȂĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬ႉ઄֒ഥঊহၷ‫້࣒ܙڠ‬जȂĴ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬ჇාȆଅ௫ඤ‫࣒ڠش‬जŜ࿒എŞχ·Ιϋহၷ͉߃ාۜஅછ̥ͣ‫͞܈‬୆‫ڰ‬ਠ‫۝‬ພ̷͈͒͂ഐ؊છͬࢩ̬ͥ‫ٳ‬อࡄ‫̞ͥ̀ͦͣ͛ૺ̦ݪ‬ȃུࡄ‫͉ݪ‬łůŨŪŰŵŦůŴŪůġ ŊŊġ ĩłůŨġŊŊĪͅచ̳ͥŅŏłχ·Ιϋͬैୋ̱ȂࣞࠬգুடอછρΛΠĩŔŉœĪ͈́‫ܖ‬ய৘ࡑ࣐̠̭ͬ͂́Ȃ੿ြഎ̈́ႉ઄؊ဥͬ࿒ঐ̳̭͂ͬ࿒എ̱̹͂ȃŜ༹༷̤͍ࠫ͢‫ض‬Şġ łůŨġŊŊͬࢯࡔ̱͂̀෇ে̯ͦօ̩̳̹ͥ͛Ȃ̞ࣞࢯࡔ଻ͬັဓ̳̭̦ͥ͂༭̯࣬ͦȂႉ઄হࡑͅဥ̞̞ͣͦ̀ͥŉŦűŢŵŪŵŪŴġ Ńġ ŤŰųŦġ ĩŉŃŤĪ౩ฒ͈͂ဏࣣ౩ฒ̱͂̀อ࡛̯
̵ͥα·ΗȜͬैୋ̱̹ȃŔŉœͬŉŃŤĮłůŨġŊŊα·ΗȜൎဓ߲ȪłůŨŊŊ߲ȫȂ΋ϋΠυȜσα·ΗȜȪŉŃŤα·ΗȜȫൎဓ߲Ȃ୆ၑ૙‫؂‬କൎဓ߲ͅ໦̫̹ĩ‫߲ڎ‬ůľķĮĹĪȃ‫̱̈́ૻ߲͂͜ڎ‬ಕৣ‫ܕ‬ĩΏζΐͿΛΠĪͬဥ̞̀෸໐ͅˎ਩‫ˏ́ڞۼ‬ٝ๧ඤൎဓ̱̹ȃ
ࢯఘ‫ͬث‬ņōŊŔł́௶೰̱̹̭͂ͧȂ੝ٝൎဓˎ਩ࢃ̥ͣłůŨ ŊŊ߲́ࢯłůŨġ ŊŊࢯఘ͈ॲ୆̦෇͛ͣͦȂൎဓĳĵ਩ࢃ͜঵௽̱̹ȃॲ୆̯̹ͦࢯఘ͉ȂłůŨŊŊȂłůŨŊࣣ̱̹̦ࠫͅłňŕȂłůŨĲĮĸ̵̴͉͕ࣣ͂͂ͭ̓ࠫȂඅ։଻͈ࣞ
̞͈̦͜ॲ୆̯̹ͦ͂ࣉ̢̹ͣͦȃࠬգ௶೰͉́ൎဓː਩ࢃ̥ͣłůŨŊŊ߲́ŔŃő͈೩‫ͦͣ͛෇̦࢜߹ئ‬Ȃൎဓ˔਩ࢃ
ͤ͢ઁ̩̈́͂͜ൎဓˎː਩ࢃ́͘ခփ̈́ŔŃő೩‫̦ئ‬঵௽̱̹ȃ̹͘łůŨŊŊ߲͉́ࠬಎłůŨġ ŊŊෛഽ̦ခփͅ೩‫̞̱̀ئ‬̹ȃոષ̥ͣχ·Ιϋൎဓͤ͢ͅ୆଼̱̹ࢯఘ̦łůŨġ ŊŊ ಎგࢯఘ̱͂̀ैဥ̱Ȃࠬգࣛ‫ͬئ‬୆̵̲̯̹͈͂͜ࣉ̢ͣ
̹ͦȃଅ௫Ȃ
૤௫Ȃఱ൲ྤȂ۴௫͈ழ૕அ૗̀ͅພၑ‫ڠ‬എਫ਼ࡉ͉෇̥̹͛̈́̽ȃ૤௫ழ૕͈ŎŢŴŴŰůġŵųŪŤũųŰŮŦஅ૗࣐ͬ̽
̹̭͂ͧȂłůŨŊŊ߲́ࠬ‫ۯ‬ਔս͈஌֋‫̦ا‬ခփͅဲଷ̯̞̹ͦ̀ȃ̭͈ͦͣࠫ‫ུ༹͉̥ͣض‬๤‫ڛ‬എհ஠଻̦̩ࣞȂ௫‫ܕ‬༗ࢌ࢘‫ܢ͜ض‬ఞ̧́ͥ͂ࣉ̢̹ͣͦȃŜࠫࢊŞġ ŔŉœͅłůŨġ ŊŊġ Ņŏłχ·Ιϋͬൎဓ̳̭ͥ͂́ࢯłůŨġ ŊŊࢯఘ̦ॲ୆̯
ͦȂઁ̩̈́͂͜฼ාոષࠬգࣛ‫̦ئ‬঵௽̳̭̦ͥ͂ྶ̥̹ͣ͂̈́̽ȃࣽࢃࢵ̈́ͥ‫ٳ‬อͤࣞࠬ͢ͅգછহၷ༹͈૧̹̈́
஖఼ঠ̭̦͂̈́ͥ͂‫ܢ‬ఞ̯ͦͥȃ䋭 㪈㪉㪏 䋭ĺ࠮ĳķ඾Ȫ࿐ȫġĲĶĻĲıȡĲĸĻĲıġġలˏٛા࢛൮ġ‫ܖ‬ய ŐŃĲŐŃĲĮĲͺΘίΗȜ໦ঊͺέ͹Οͻϋͥ͢ͅౙၾఘ ňŕő ͺȜΔ œũŰł ̱̹ͬٚςϋΩ‫ࠁۯ‬଼͈ଷࢄ‫ࢹܥ‬プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛ૯ോġଢ ĲȂ୾നġ‫ݛ‬გ ĳࠬ‫଼͞ࠁۯ‬ςϋΩ‫଼̞̤̀ͅࠁۯྤ଼͈̓̈́ࠁۯ‬Ȃඤ๧ळ༾൳আ͈ळ༾‫ۼ‬୪಍͉ਹါ̜́ͥȃͺέ͹Οͻϋ͉Ȃ྄֚ٝ۹೒߿ळ༾‫ۼ‬୪಍໦ঊΥ·Ιϋ͈ळ༾ඤႀ֖ࣣ̳ࠫͥͅͺΘίΗȜ໦ঊ̜́ͤȂळ༾‫ۼ‬୪಍͈ࠁ଼ͅఱ̧̈́࿨
‫̞̱̹ͥ̀ضͬڬ‬ȃ̹͘Ȃͺέ͹Οͻϋ͉ळ༾‫ۼ‬୪಍͈ࠁ଼ͅ‫̢ح‬Ȃळ༾୆ం͞ळ༾‫׋‬൲͈ଷࢄ͈̈́̓ఉအ̈́ळ༾‫ܥ‬

特別講演

Ĳ ؈ֵఱ‫ڠ‬࿪‫ڠ‬໐Ȃĳ সٖ֓‫ش‬ఱ‫ڠ‬໦ঊພఠ୆‫ڠا‬ෝͬ঵̞̽̀ͥȃ̱̥̱Ȃඤ๧ळ༾̤̫ͥͅͺέ͹Οͻϋ͈ैဥ‫͉̞̀̾ͅࢹܥ‬ະྶ̈́ത͜ॼ̯̞ͦ̀ͥȃ̷̭́Ȃͺ༾අ։എͅͺέ͹Οͻϋͬࠧ৐̵̯̹΋ϋΟͻΏο΢σΦΛ·ͺ;ΠȪŤŌŐȫζ;Αͬैୋ̱Ȃٜଢ଼࣐̹ͬ̽ȃͺέ͹ΟͻϋŤŌŐζ;Α͉థ঱‫ͅܢ‬ಠྶ̈́຾ਆͬြ̹̱Ȃ͕̦͂ͭ̓థ୆౿ঘ̹͂̈́̽ȃͺέ͹ΟͻϋŤŌŐζ;ᾼ̤̫ͥྤ‫ࠁ͈ࠏۯ‬ఠ͉́ȂςϋΩ‫͈ۯ‬ඤ๧ळ༾‫ۼ‬୪಍͉෫౦̱ȂςϋΩ‫଼ͅࠁۯ‬ఱ̧̈́։ુ̦ࡉ̹͈͈ͣͦ͜Ȃࠬ‫଼͉ࠁۯ‬͕͖ୃુ̜̹́̽ȃͺέ͹Οͻϋ͈ࠧ৐̦ࠬ‫ۯ‬ඤ๧ळ༾͉̩́̈́ȂςϋΩ‫ۯ‬ඤ๧ळ༾࿹պͅ‫̳͖ݞͬޣג‬ι΃ΣΒθ
ͬྶ̥̳̹ͣͥ͛ͅȂΪΠ૧୆঱๷઀ࠬ‫ۯ‬ඤ๧ळ༾ȪŉŎŗņńĮŃȫ͂ΪΠ૧୆঱๷઀ςϋΩ‫ۯ‬ඤ๧ळ༾ȪŉŎŗņńĮōȫͬဥ̞̯̀ͣͅ࠿൦࣐̹ͬ̽ȃ̭͈ͦͣळ༾̤̞̀ͅΦΛ·Θ;ϋͤ͢ͅͺέ͹Οͻϋ͈อ࡛ͬஷ‫̳͂ͥٺ‬ȂŉŎŗņńĮ
ō͈͙ͅळ༾͈֎ੀ͂ळ༾‫ۼ‬୪಍͈෫౦̦ࡉͣͦȂळ༾‫ۼ‬୪಍ζȜ΃Ȝ̜́ͥŗņĮ΃Ρΰςϋ͈அ૗ΏΈ΢σ͜ࡘ৻̱̞̹̀ȃ̹͘Ȃͺέ͹ΟͻϋͬΦΛ·Θ;ϋ̱̹ŉŎŗņńĮṓ͉Ȃळ༾͈֎ੀͅ‫ͥͩ۾‬ळ༾ਔս͈ͺ·Ιϋ஌֋௵̦௩ఱ̱̤̀ͤȂౙၾఘňŕőͺȜΔœũŰł͈‫͉଻ڰ‬Ȃͺέ͹ΟͻϋͬΦΛ·Θ;ϋ̱̹ŉŎŗņńĮŃ͂๤‫̱̀ڛ‬Ȃಠྶͅ௩‫̹̞̱̀ح‬ȃ‫ͅݙ‬Ȃͺέ͹ΟͻϋͬΦΛ·Θ;ϋ̱̹ŉŎŗņńĮōͅΡη΢ϋΠΥ΄ΞͻήœũŰłͬ൵ව̱̀œũŰł‫଻ڰ‬ͬஷ‫̳͂ͥٺ‬Ȃळ༾͈ࠁఠ̦ୃુ‫̹̱ا‬ȃոષ͈ࠫ‫ͤ͢ض‬Ȃͺέ͹Οͻϋ͉ȂςϋΩ‫ۯ‬ඤ๧ळ༾͈œũŰł͈‫଻ڰ‬τασŐŃĲĮĳņĴ ξΫ΅Ιϋς΄ȜΔ ńŖōĴ ͉ळ༾ࣸ‫಺ڒ‬୯̽̀ࠬ͢ͅ‫ۯ‬૧୆ͬଷࢄ̳ͥ
ɛाષġႃ‫ݛ‬Ȃ֔ષġฎ໲Ȃ൐५ġ้ਏ

口頭発表ͬࡕྟͅ಺୯̳̭ͥ͂ͤ͢ͅథ঱‫͈ܢ‬ςϋΩ‫଼ͬࠁۯ‬ଷࢄ̱̞̀ͥ͂ࣉ̢̹ͣͦȃ

会長招待講演 シンポジウムέ͹Οͻϋ͈ඤ๧ळ༾̤̫ͥͅैဥ‫଼̫̤ͥͅࠁۯྤ͂ࢹܥ‬࿨‫ͬڬ‬મ̱̩಺͓̹ͥ͛ȂńųŦİŭŰŹőࠏͬဥ̞̀ඤ๧ळ

Քຎఱ‫ڠ‬ίυΞ΂΍ͼ΀ϋΑΓϋΗȜळ༾௩૓ਆនଷࢄ໐࿝

૧୆ͬဲଷ̳ͥŏŰŵŤũΏΈ΢σ‫ئ‬ၠָഢৢ֦ঊńŃŇĮĲͬ໦ٜ̳̭ͥ͂́ࠬ‫ۯ‬૧୆ͬୃͅଷࢄ̳̭ͥ͂ͬা̧̱̹̀
ȪŃŭŰŰťĭġ ĳıĲĳȫȃ̱̥̱ȂŃłśŇΦΛ·ͺ;Πζ;Α࿌྄̤̞̀ͅńŖōĴͬΦΛ·Θ;ϋ̳ͥ͂Ȃ̯ͣͤ͢ͅਹඈ̈́ࠬ
‫ۯ‬૧୆͈෫౦ͬ୆̲̭̥ͥ͂ͣȂńŖōĴ͉ȂŃłśṈ̹̌ͬٚࠬ‫ۯ‬૧୆ଷࢄ‫͉͂ࢹܥ‬༆͈ΏΈ΢σഥోࠐႹ̱ͬٚ̀Ȃࠬ‫ۯ‬૧୆ͬଷࢄ̳ͥ‫خ‬ෝ଻̦ࣉ̢̹ͣͦȃ̷ِ̭́ș͉̭͈ࡔ֦ͬྶ̥̳̹ͣͥ͛ͅȂ̞̩̥͈̾৘ࡑ࣐̞ͬȂո‫͈ئ‬ࠫ‫ͬض‬ං̹ȃ̴͘ȂńŖōĴͬΦΛ·Θ;ϋ̳ͥ͂ȂŗņňŇĮł̴͈͙̈́ͣȂţŇňŇ͞ŕőł͈̈́̓ఉအ̈́ࠬ‫ۯ‬૧୆֦ঊ̽͢ͅ
̀ည൵̯ͦͥŵŶţŦġ ŧŰųŮŢŵŪŰů̦ஷ‫̹̯ͦٺ‬ȃ̯ͣͅȂΗͼθρίΑͼιȜΐϋΈͥ͢ͅમळٜ̈́ଢ଼͈ࠫ‫ض‬ȂńŖōĴͬΦΛ·Θ;ϋ̱̹ŉŖŗņń͉Ȃळ༾૝ಿ̦‫ဲ̩ޑ‬ଷ̯̭̦ͦͥ͂฻ྶ̱̹ȃ̷ِ̭́ș͉Ȃ̭͈ळ༾૝ಿஷ‫͉֦ࡔ͈ٺ‬Ȃळ༾‫ܖٸ‬ৗ͈͒୪಍ஷ‫͞ٺ‬ळ༾ࣸ‫͈ڒ‬։ુ̜́ͥ͂ࣉ̢ȂŊůŵŦŨųŪṳ͍̊͢œũŰέ͹ηςȜ͈อ࡛ͬŘŃͬဥ̞ٜ̀ଢ଼
̱̹ȃ̷͈ࠫ‫ض‬ȂńŖōĴΦΛ·Θ;ΰ߲͉२ষࡓ෽ူඅ։എͅϸĲĮŪůŵŦŨųŪů͈อ࡛̦೩‫̭̳͂ͥئ‬Ȃ̹͘œũŰέ͹ηςȜ͈ಎ́͜œũŰłĭġœũŰŃĭġœũŰń͈ΗϋΩ·อ࡛ၾ̦ࡐಠͅષઌ̳̭̦ͥ͂̈́̓໦̥̹̽ȃ̯ͣͅͺ·Ιϋਹࣣͬ‫خ‬ণ‫̧ͥ́ا‬ōŪŧŦŢŤŵίυȜήͬဥ̞̀ΗͼθρίΑͼιȜΐϋΈٜଢ଼࣐̹̭ͬ̽͂ͧȂ΋ϋΠυȜσ߲͉́ਹࣣ̱̹
̭̞̭̦̽̀ͥ͂‫̹̯ͦ෇ږ‬ȃ̷̭́ȂœũŰͅచ̳ͥŴŪœŏł͞ȂœŐńŌஷ‫ٺ‬स̜́ͥŚĮĳĸķĴĳͬဥ̞̀œũŰĮŬŪůŢŴŦ‫ڰ‬଻ͬஷ‫̭̹̱ͧ͂ٺ‬Ȃͺ·Ιϋً͈ਹࣣ̦ક৐̳ͥ͂൳শͅϸĲĮŪŵŦŨųŪů͈อ࡛̦ٝ໘̳͕̥ͥȂࠬ‫ۯ‬૝ಿ̦͕͖ۖ஠
ٝͅ໘̳̭̦ͥ͂໦̥̹̽ȃոષ͈ࠫ‫̥ͣض‬ȂńŖōĴ͉ࠬ‫ۯ‬૧୆̤̞̀ͅȂξΫ΅ΙϋĮίυΞͺΕȜθࠏ̱̹ͬٚ
œũŰέ͹ηςȜΗϋΩ·ৗ͈ॲ୆ၾͬଷࢄ̳̭ͥ͂́ࠬ‫ۯ‬૝ಿ͞ȂϸĲĮŪůŵŦŨųŪů̱̹ͬٚळ༾‫ܖٸ‬ৗ͈͒୪಍ͬଷࢄ
̳ͥ‫ܥ‬ෝͬခ̳̭̦ͥ͂ྶ̥̹ͣ͂̈́̽ȃ䋭 㪈㪉㪐 䋭著者索引

ͺ·Ιϋ஌֋̦͕͂ͭ̓ࡉ̥̹͈ͣͦ̈́̽ͅచ̱̀ȂńŖōĴͬΦΛ·Θ;ϋ̱̹ŉŖŗņń͉́ͺ·Ιϋً͈ਹࣣ̦ܳ

ポスター発表 ＹＩＡ選考発表ِ̭ͦ́͘ș͉ņĴξΫ΅Ιϋς΄ȜΔńŖōĴ̦ȂŗņňŇΏΈ΢σ͈‫ئ‬ၠͅպ౾̳ͥŃłśŇ͂ໝࣣఘͬࠁ଼̱Ȃࠬ‫ۯ‬ŐŃĲĮĴ

ŏŦŤŭĮĵ ͥࠬ͢ͅ‫ۯ‬ඤ๧ळ༾͈‫׋‬൲͂‫଼͈ࠁ࣌ۯ‬ଷࢄɛ५ྴġટఊ ĲȂႁ໌ġၻ࣐ ĲĭĳȂࣞ֔ġ݅๼ ĴȂ໹നġ࠲֚ Ĳ
Ĳ ૰࡫ఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ش‬Ȃĳ ૰࡫ఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬ΏΈ΢σഥో‫ڠ‬ȂĴ ૰࡫ఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬ພఠΏΈ΢σ‫ڠ‬෸ࠊȇࠬ‫ۯ‬૧୆̤̫ͥͅਹါً̈́೾̜́ͥࠬ‫ۯ‬ඤ๧ळ༾͈‫׋‬൲͂‫଼͉ࠁ࣌ۯ‬Ȃ௩૓֦ঊ਋ယఘ͂ͼϋΞΈςϋ̥͈ͣळ༾ඤΏΈ΢σͅ؊൞̱̹ͺ·ΙϋΘͼ΢η·ᾼ̽̀͢ଷࢄ̯̞ͦ̀ͥȃΥ·Ιϋအ໦ঊȪŏŦŤŵŪůĮŭŪŬŦġŮŰŭŦŤŶŭŦȇ
ŏŦŤŭȫ͉ळ༾‫ٸ‬ႀ֖ͅ྾‫ע‬ΈυήςϋအσȜίͬခ̳ͥˍ྄ٝ۹೒߿͈ळ༾୪಍໦ঊ̜́ͤȂŏŦŤŭĮĲ̥ͣĮĶ͈Ķ͈̾ιϋΨȜ̥ͣ̈́ͥȃজ͉̓͜ŏŦŤŭĮĶ̦ŗņňŇ਋ယఘ͂ͼϋΞΈςῧ͈௖ࡽैဥͬଷࢄ̱̀ŗņňŇͥ͢ͅळ༾ඤΏΈ΢σ͈‫ͬا଻ڰ‬௯ૺ̳̭ͥ͂́ࠬ‫ۯ‬૧୆ͬ಺୯̱̞̭̀ͥ͂ͬ༭̱̹࣬ȃ̱̥̱ȂŏŦŤŭĮĶո‫͈ٸ‬ιϋΨȜ͈ŏŦŤŭ͈ࠬ‫ۯ‬ඤ๧ळ༾̤̫ͥͅอ࡛͞‫ܥ‬ෝ͉ະྶ͈̜́ͥ͘͘ȃ༹༷Ȇࠫ‫ض‬ȇজ͉̓͜྾‫ע‬ழ૕அ૗̀ͅȂζ;Α͈ఱ൲ྤȂ‫ۍ‬൲୓ྤȂ‫ئ‬ঠ࿉ळࠬ‫ۯ͈ࠬۯ‬ඤ๧ͅŏŦŤŭĮĵ̦อ࡛̱̞̭̀ͥ͂ͬࡉ੄̱̹ȃအș̈́ࠬ‫ۯ‬઄ဇြ͈෽ူΪΠࠬ‫ۯ‬ඤ๧ळ༾̤̞̀͜ͅŏŦŤŭĮĵ̦อ࡛̱̞̭̀ͥ͂ͬ;΀ΑΗϋήυΛΠ̀ͅ‫̹̱෇ږ‬ȃ෽ူΪΠࠬ‫ۯ‬ඤ๧ळ༾̤̫ͥͅŏŦŤŭĮĵ
͈อ࡛͉ळ༾ྟഽջం଻ͅ௩‫̹̱ح‬ȃࠬ‫ۯ‬ඤ๧ळ༾̤̫ͥͅŏŦŤŭĮĵ͈‫ܥ‬ෝͬྶ̥̳̹ͣͥ͛ͅͅȂŴŪœŏłͬဥ̞̀ŏŦŤŭĮĵͬΦΛ·Θ;ϋ̱̹ȃŏŦŤŭĮĵ͈ΦΛ·Θ;ϋͤ͢ͅȂŗņňŇͥ͢ͅ‫׋‬൲͂‫ဲ଼͉ࠁ࣌ۯ‬ଷ̯̹ͦȃ̯ͣͅȂΑΠτΑέ͹ͼΨȜ͂έ΁Ȝ΃σͺΡΪȜΐοϋ͈ࠁ଼̤͍͢η΂ΏϋγΑέ͹ΗȜΔ಺୯΍ήξΣΛΠĲġ ĩŎŚőŕĲĪ͈ςϋॸ‫̦ا‬ᄤૺ̱ȂœŐńŌ͈‫̦ا଻ڰ‬া̯̹ͦȃΑΠτΑέ͹ͼΨȜ̤͍͢έ΁Ȝ΃σͺΡΪȜΐοϋ͈ࠁ଼͉œŐńŌஷ‫ٺ‬स̜́ͥŚĮĳĸķĴĳġ ͂ŧŢŴŶťŪŭͤ͢ͅဲଷ̯̹ͦȃ൳အͅȂŏŦŤŭĮĵ͈ΦΛ·Θ;ϋͥ͢ͅळ༾͈‫׋‬൲͂‫࣌ۯ‬ࠁ଼͈೩‫͜ئ‬ŚĮĳĸķĴĳ͂ŧŢŴŶťŪŭͤ͢ͅ໐໦എٝͅ໘̱̹ȃࠫࢊȇոષͤ͢ȂŏŦŤŭĮĵ͉œŐńŌ‫಺ͬ଻ڰ‬୯̱̀Ȃࠬ‫ۯ‬ඤ๧ळ༾͈‫׋‬൲͂‫଼ͬࠁ࣌ۯ‬௯ૺ̳̭̦ͥ͂ྶ̥̹ͣ͂̈́̽ȃŐŃĲĮĵőŅōŊŎĶġŪŴġŢġůŦŸġŴŶţŴŵųŢŵŦġŰŧġłŎőŌġŢůťġűŭŢźŴġŢġŬŦźġųŰŭŦġŪůġłŎőŌĮŪůťŶŤŦťġŪůũŪţŪŵŪŰůġ
ŰŧġťŪųŦŤŵŪŰůŢŭġŤŦŭŭġŮŪŨųŢŵŪŰůɛ ŚŢůġŚŪ ĲȂ೓ུġ௬ ĲȂ࿐‫ؖ‬ġਜၦ ĲȂཤ໓ġଽঃ ĳȂࣞോġ଼ඵ Ĳ
Ĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬໦ঊ૤ࠬ‫ڠ֓ۯ‬Ȃĳ ࣭ၛ੏۪‫ܕ‬ພΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬Cell migration contributes to numerous diseases including cancer and cardiovascular diseases such as atherosclerosis.
AMP-activated protein kinase (AMPK), a highly conserved Ser/Thr kinase, plays a key role not only in the regulationof energy homeostasis but also in cell polarity and motility. We previously reported that inhibition of AMPK impairs
microtubule stabilization and perturbs directional cell migration. However, we found that activation of AMPK also
inhibited cell migration although its mechanism remains unknown. Here, we identified a new substrate of AMPK thatmediates its effect on cell migration. In the course of investigation of AMPK activation using C2C12 cells, we
incidentally discovered a strong, reproducible and evidently specific protein that cross-react with antibody against
phosphorylated ACC (pACC), and identified it as PDZ and LIM domain 5 (PDLIM5) by a unique three-step column
chromatography followed by LC/MS/MS analysis. Furthermore, the experiments with deletion mutants and sitedirected mutagenesis of PDLIM5 identified Ser177 as a responsible residue of the cross-reactivity. Next, we madespecific polyclonal antibodies against phospho-Ser177 of PDLIM5 and performed in-vitro phosphorylation assay,
which demonstrated that GST-tagged wild-type PDLIM5, but not GST-tagged S177A PDLIM5, was phosphorylated
directly by purified AMPK. To investigate the effect of Ser177 phosphorylation of PDLIM5 on cell migration, siRNAresistant wild-type-, non-phosphorylatable (S177A) - or phosphomimetic (S177D)-PDLIM5 mutant proteins wereexpressed in mouse smooth muscle cells whose endogenous PDLIM5 was knocked down by siRNA. Interestingly,
both scratch assay and cell migration assay demonstrated that only S177D mutant perturbed directional cell
migration without affecting cell proliferation even in the absence of AMPK stimulators. In conclusion, PDLIM5
is a new direct substrate of AMPK and a key player in the inhibition of cell migration in response to AMPK activation.
PDLIM5 may be a potential target of novel treatment of cancer and cardiovascular diseases.
䋭 㪈㪊㪇 䋭ŐŃĲĮĶ

łġœŢűĲġŴŮŢŭŭġňŕőŢŴŦġűŰŵŦůŵŪŢŵŦŴġŦůťŰŵũŦŭŪŢŭġţŢųųŪŦųġŧŶůŤŵŪŰůġţźġŴűŢŵŪŢŭŭźġŤŰůŵųŰŭŭŪůŨġ
ŮźŰŴŪůġŊŊġŢŤŵŪŷŪŵź

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛհ൥ġࢫঃ ĲĭĳȂ໛ࡔġ࿆༸ ĲȂ৿‫ؚ‬ġࢣဢ ĳȂབ࠮ġೄਏ Ĳ

ඤ๧ळ༾໦‫ ̫̤ͥͅا‬œŔŌĵ ͈࿨‫ڬ‬ɛઐ‫ז‬ġఊ֚ ĲĭĳȂ५କġࢫ໹ ĴȂ઀ড়ġგঊ ĵĭĶȂ઀ോġଠయ ĵȂಅඤġ੗ ĵĭĶĭķȂ५‫ئ‬ġ੕ Ĳĭĳ

口頭発表

ŐŃĲĮķ

会長招待講演 シンポジウム

Endothelial cell-cell junctions regulate vascular barrier function, which restricts the passage of plasma proteins andcirculating cells across the endothelium. The endothelial cell-cell adhesion-regulated barrier function largely depends
on where the actin cytoskeleton is formed. Circumferential actin bundles (CAB) aligned along the cell-cell contacts
potentiate endothelial barrier function, whereas formation of radial stress fibers (RSF) originating from cell-cell
contacts leads to cell contraction and barrier disruption. Previously, we have reported that a small GTPase, Rap1,
induces disruption of RSF and formation of CAB to potentiate endothelial barrier function. However, the mechanism
by which Rap1 induces reorganization of actin cytoskeleton remains unknown. Here, we show that Rap1 reorganizes
the actin cytoskeleton by spatially regulating the activity of non-muscle myosin II (NM-II), a key regulator of actin
cytoskeleton, to potentiate endothelial barrier function.
NM-II was activated in the RSF in unstimulated human umbilical vein endothelial cells (HUVECs) and in the CAB in
Rap1 signal-activated cells. In unsitimulated HUVECs, NM-II was activated downstream of a Rho-ROCK pathway to
induce RSF formation. However, Rap1 suppressed the NM-II activity stimulated by the Rho-ROCK pathway, leading
to disassembly of RSF. Interestingly, we also showed that myotonic dystrophy kinase-related CDC42-binding kinase(MRCK)-mediated activation of NM-II at the cell-cell contacts was essential for Rap1-induced CAB formation.
Through FGD5, a guanine nucleotide exchange factor for Cdc42, Rap1 activated Cdc42 at the cell-cell junctions,whereby stimulating the NM-II activity by localizing MRCK and subsequently inducing CAB formation. Furthermore,
we found that Rap1-induced CAB formation through the FGD5-Cdc42-MRCK-NM-II signaling axis potentiatedendothelial barrier function.
Collectively, these findings indicate that Rap1 signal induces CAB formation by locally stimulating the Cdc42MRCK-NM-II pathway at the cell-cell junctions, whereas Rap1 simultaneously induces RSF disassembly throughsuppression of the Rho-ROCK-NM-II pathway. Thus, Rap1 potentiates endothelial cell-cell junctions by spatiallycontrolling the NM-II activity.

特別講演

Ĳ ࣭੏ΓࡄȆळ༾୆໤Ȃĳ ൐ཤఱ֭Ȇ࿪Ȇळ༾ૂ༭

Ĳ ‫ނ‬സఱ‫ڠ‬ġŪőŔ ळ༾ࡄ‫ݪ‬ਫ਼௩૓໦‫ݪࡄࢹܥا‬໐࿝Ȃĳ ‫ނ‬സఱ‫ڠ‬ठ୆֓‫ݪࡄڠش‬ਫ਼ۚळ༾໦‫ا‬ଷࢄࡄ‫ݪ‬໦࿤Ȃĵ ൐‫ނ‬ఱ‫΀ڠ‬άΊΦθ৖ۛࡄ‫ݪ‬ΓϋΗȜ૤੏۪‫ܕ‬ठ୆ࡄ‫ݪ‬໦࿤ȂĶ ൐‫ނ‬ఱ‫ڠ‬ఱ‫֭ڠ‬ၑ‫شݪࡄࠏڠ‬Ȃķ ŋŔŕġőœņŔŕŐ

ࠬ‫ۯ‬ඤ๧ळ༾͈໦‫ۯ͉ࠬا‬อ୆͈ड்͜‫ͼ͈ܢ‬αϋΠ͈̜֚̾́ͥȃِș͉Ȃඵষࡓ෽ူ‫ྚ̀ͅئ‬໦‫ا‬ņŔळ༾̥ͣಎ᥷ဩζȜ΃Ȝ̜́ͥŇŭŬĲု଻ळ༾ͬࠐ̀ࠬ‫ۯ‬ळ༾ĩඤ๧ळ༾͂༃ळ༾Īͬည൵̧́ͥ໦‫ا‬ΏΑΞθͬࢹಃ̱̹
ĩŏŢŵŶųŦĭġĳıııĪȃ
ड߃ِș͉Ȃ
ŢťųŦůŰŮŦťŶŭŭŪůġĩłŎĪ൝ͥ͢ͅġŤźŤŭŪŤġŢťŦůŰŴŪůŦġŮŰůŰűũŰŴűũŢŵŦġĩŤłŎőĪİőŌłΏΈ΢σ͈‫̦ا଻ڰ‬ġņŵŴġŷŢųŪŢůŵġĳġĩņŵŷĳĪ อฺ࡛̠ͅŗņňŇ਋ယఘĩŇŭŬĲ̤͍͢ůŦŶųŰűŪŭŪůĲĪ͈อ࡛ည൵̱ͬٚȂඤ๧ळ༾͈໦‫ͬا‬௯ૺ̳̭ͥ͂ͬࡉ੄̱̹
ȪłŕŗŃĭĳııķļġŃŭŰŰťĭġĳııĺļġŔŵŦŮġŤŦŭŭŴĭġĳıĲĳĪȃ
ུࡄ‫͉́ݪ‬ඤ๧ळ༾͈໦‫͈ࢹܥا‬ٜྶ͈̹͛Ȃ૧ܰଷࢄ໦ঊ͈൳೰͂‫ܥ‬ෝٜଢ଼ͬ࿒എ̳͂ͥȃඤ๧ळ༾໦‫ًا‬೾̤̞̀ͅอ࡛̦་‫̞̱֒ͥ̀ا‬ഥঊ߲ͬౝ̱̹॑ࠫ‫ض‬ȂΓςϋİΑτ΂Σϋ΅΢ȜΔ̜́ͥœŔŌĵġ ĩųŪţŰŴŰŮŢŭġ űųŰŵŦŪůġ Ŕķġ ŬŪůŢŴŦġ ĵĪ̦ŇŭŬĲု଻͈ಎ᥷ဩळ
༾́ࣞอ࡛̱Ȃඤ๧ळ༾͈͒໦‫ًا‬೾ͅอ࡛̦ࡘઁ̳ͥমͬࡉ੄̱̹ȃœŔŌ͉ȂœŢŴĮŎłőŌΏΈ΢σ͈‫ئ‬ၠ֦ঊ̜́
ͤȂळ༾௩૓͞ဋ௢Ȃ୆ంͅ‫۾‬ဓ̳ͥম̦༭̯̞̦࣬ͦ̀ͥȂࠬ‫ۯ‬อ୆̤̫ͥͅœŔŌĵ͈࿨‫͉ڬ‬ະྶ̜́ͥȃœŔŌஷ‫ٺ‬स̜́ͥŔōıĲıĲͬಎ᥷ဩळ༾ͅൎဓ̳ͥমͤ͢ͅȂņŵŷĳ̤͍͢ŇŭŬĲอ࡛̦ᄤૺ̱Ȃඤ๧ळ༾໦‫̦ا‬ခփͅ௯ૺ̱
̽̀͢ક৐̱̹ȃ൳အͅȂœŔŌĵġ Ŵũœŏł̽̀͢ͅȂņŵŷĳ̤͍͢ŇŭŬĲอ࡛͈ᄤૺ͂ඤ๧ळ༾໦‫͈ا‬௯ૺͬ෇̹͛ȃ̹͘ȂœŔŌĵ઼ًͬอ࡛̱̹ࠫ‫ض‬ȂœŔŌĵ̦ೄ୪őŌłŤࣣ̱ࠫͅȂőŌł‫ဲͬ଻ڰ‬ଷ̱̹ȃ̯ͣͅȂņĹġŦŮţųźŰͬŦŹġŷŪŷŰ̀ͅŔōıĲıĲంह‫́ئ‬෽ူ̱̹̭͂ͧȂźŰŭŬġ ŴŢŤષ͈ńŅĴĲု଻͈ࠬ‫ۯ‬ႀ֖̦։ુͅ௩‫̹̱ح‬ȃոષ͈ࠫ‫ͤ͢ض‬ȂœŔŌĵ
͉ȂŤłŎőİőŌłΏΈ΢σ̱̹ͬٚņŵŷĳ̤͍͢ŇŭŬĲอ࡛ͬೄ୪ဲଷ̱Ȃඤ๧ळ༾໦‫ͬا‬໅ͅଷࢄ̳ͥ૧̱̞಺୯֦
ঊ̜́ͥম̦াऐ̯̹ͦȃ̭ͦ́͘ȂŇŭŬĲอ࡛ͬ಺୯̳ͥ໦ঊ͉Ȃ৽ͅୃ͈಺୯֦ঊ̜̹̦́̽Ȃུࡄ‫̹̱੄ࡉ̦ݪ‬໅͈ଷࢄ֦ঊ̜́ͥœŔŌĵ‫ܥ‬ෝͅ‫̳ͥ۾‬౶ࡉ͉Ȃඤ๧ळ༾͈໦‫ا‬ଷࢄ‫͈ࢹܥ‬ٜྶ͂ࠬ‫ͬۯ‬ດഎ̱̹͂হၷ༹‫ٳ‬อ࣓ͅࡃ̧́ͥ‫خ‬ෝ଻̦̜ͥȃ䋭 㪈㪊㪈 䋭著者索引

̹ȃ̭͈ͦͣ࢘‫͉ض‬ŤłŎőΏΈ΢σջంഎ̜́ͤȂŴũœŏłͬဥ̞̹őŌłŤġ ĩŤŢŵŢŭźŵŪŤġ ŴŶţŶůŪŵġ ŢŭűũŢĪ͈อ࡛ဲଷͅ

ポスター発表 ＹＩＡ選考発表Ĵ ōŢţŰųŢŵŰųźġŰŧġňŦůŦŵŪŤŴĭġŏŢŵŪŰůŢŭġŊůŴŵŪŵŶŵŦġŰůġłŨŪůŨġĩŏŊłĪĭġŏŢŵŪŰůŢŭġŊůŴŵŪŵŶŵŦŴġŰŧġŉŦŢŭŵũġĩŏŊŉĪĭġŖůŪŵŦťġŔŵŢŵŦŴȂ

ŐŃĲĮĸ

ŊŮűŭŪŤŢŵŪŰůġŰŧġŕňŇĮϸġŴŪŨůŢŭŪůŨġŪůġŵŶŮŰųġŢůŨŪŰŨŦůŦŴŪŴġŢůťġŭźŮűũŢůŨŪŰŨŦůŦŴŪŴ
ɛչ൐ġঃঊ ĲȂࣞ࿐ġఄఱ ĲȂঌ୼ġ߽ ĲȂŇųŶŵŵŪŨŦųġŎŢųŤŶŴ ĳȂňŶŪŭŭŦųŮŰġŐŭŪŷŦų ĴȂչ൐ġૺ ĵȂള໐ġీ࿟ Ĳ
Ĳ ൐‫ނ‬࿪‫ش‬ఱ‫ڠ‬୆ྵ‫ڠش‬໐Ȃĳ ŖńōġŊůŴŵŪŵŶŵŦġŰŧġŐűũŵũŢŭŮŰŭŰŨźȂĴ ŅŦűŢųŵŮŦůŵġŰŧġňŦůŦŵŪŤŴĭġŔŵġŋŶťŦġńũŪŭťųŦůĨŴġœŦŴŦŢųŤũġŉŰŴűŪŵŢŭȂĵ ઎გ࿪‫ش‬ఱ‫ڠ‬୆‫ݪࡄڠا‬৒TGF-ϸ signaling is involved in the normal vascular development and maintenance via type I and type II receptors.
Our previous studies have demonstrated major insights into the role of TGF-ϸ and its downstream Smad proteins inembryonic angiogenesis and the maintenance of blood vessel integrity. Contrary to the well-documented to the actionof TGF-ϸ signaling in angiogenesis in embryos, it is not clear how TGF-ϸ signaling affects vascular formation in
postnatal mice because of the embryonic lethality in most of genetically modified mice lacking TGF-ϸ receptors or
Smads. To address this issue, TGF-ϸ type II receptor (TϸRII) conditional knockout mice; TϸRIIF/F, were crossedwith Pdgfb-icreER and Prox1-CreER T2 mice in which Cre recombinase is induced in blood (BECs) and lymphatic
vascular endothelial cells (LECs) by tamoxifen (Tx), respectively. This allows us to analyze the role of TGF-ϸ
signaling in the blood and lymphantic vasculature using tumor model mice. When Lewis lung carcinoma cells were
subcutaneously injected into control and TϸRIIF/F; Pdgfb-icreER (TϸRIIBEC-CKO) mice after administration of Tx, we
were not able to find any difference of tumor size between them in 12 days. However, tumors in TϸRIIBEC-CKO mice
showed much gory morphology. Supporting this phenomenon, we confirmed the increased area of blood vessel intumors by staining with an anti-PECAM-1 antibody. Interestingly, metastases were increased in TϸRIIBEC-CKO mice.
Furthermore, when we deleted TϸRII genes in LECs, TϸRIIF/F;Prox1-CreERT2 (TϸRI LEC-CKO) mice revealed more
LYVE-1 positive cells in the tumor area than the control mice. These results indicated that TGF-ϸ signaling inhibits
tumor angiogenesis and lymphangiogenesis in adults.

ŐŃĲĮĹਆនࠬ‫ۯ‬૧୆͂ഢ֊̤̫ͥͅͺΡτΦιΟνςϋȽ œłŎőĳ ࠏ͈փ݅ɛനಎġՔ ĲȂ઀५ġࢴ‫ ם‬ĳȂ॓֔ġࠉ෗ ĲȂ૰‫݌‬ġ઎ঊ ĲȂဠġ᠇ ĲȂ૒ಅġၨ֚ ĲȂ५ඤġ߼ࢬ ĲȂࡼ਱၆ġ‫ޕ‬ঊ ĲȂು५ġ࿸֚ ĲȂ૧൥ġၦ࣐ Ĳ
Ĳ ૞ਗఱ‫شݪࡄࠏڠ֓ڠ‬੏۪ພఠ‫࣒ڠ‬जȂĳ ࣭ष֓ၷ໛ছఱ‫࠿ڠ֓ڠ‬औ‫شڠ‬ͺΡτΦιΟνςϋĩłŎĪ͉Ȃఉद̈́୆ၑ‫ͬ଻ڰ‬ခ̳ͥඤ֦଻βίΙΡ̜́ͥȃِș͉ȂłŎΦΛ·ͺ;Πζ;Α
ĩłŎĮİĮĪ̤͍͢ȂłŎ͈਋ယఘ‫಺଻ڰ‬୯ΗϋΩ·̜́ͥœłŎőĳ͈ΦΛ·ͺ;Πζ;ΑĩœłŎőĳĮİĮĪ̦Ȃ‫ͅވ‬థ଻ಎ‫ͅܢ‬຾ਆ͞੄ࠬͤ͢ͅ౿ঘ̭̥͂̈́ͥ͂ͣȂłŎĮœłŎőĳࠏ̦ࠬ‫͈ۯ‬อ୆ͅຈଌ̜̭́ͥ͂ͬ༭̧̱̹࣬̀ȃ༷֚ȂłŎȂœłŎőĳ͉Ȃအș̈́ਆន̤̞̀ࣞ͜ͅอ࡛ͬ෇͛ͥȃུࡄ‫͉́ݪ‬ȂłŎĮœłŎőĳࠏ͈ਆន௩૓͂ഢ֊̤̫ͥͅພఠ‫ڠ‬എփ̞݅̾̀ͅ࠿൦࣐̹ͬ̽ȃœłŎőĳĮİĮ͉థ଻౿ঘ̹͂̈́ͥ͛Ȃ଼ఘ̥̈́̽̀ͣࠬͅ‫ۯ‬ඤ๧ळ༾͈œłŎőĳࠧఅͬ΂ϋΟζϋΡͅည൵̧́ͥζ;ΑĩŅųŶŨġ ŪůťŶŤŦťĮŦůťŰŵũŦŭŪŢŭĮœłŎőĳĮİĮ ļ ŅŊĮņĮœłŎőĳĮİĮĪͬ૧̹ͅਏၛ̱̹ȃœłŎőĳࠧఅည൵ࢃȂŔĲĹıζ;Αරਆळ༾͂ŃĲķŇĲıιρΦȜζळ༾͈๧‫֊ئ‬૒৘ࡑ࣐̹ͬ̽ȃŅŊĮņĮœłŎőĳĮİĮ͉́Ȃ΋ϋΠυȜσͅ๤‫̱̀ڛ‬ȂŔĲĹıਆន௩૓͉ဲଷ̯ͦȂਆនࠬ‫ۯ‬૧୆͞Ȃࠬ‫ۯ‬૧୆֦ঊ߲͈อ࡛̦೩‫̹̞̱̀ئ‬ȃ༷֚ȂŃĲķŇĲı͉́Ȃࠬ‫ۯ‬૧୆ࡘ৻͂‫ͅވ‬Ȃਆនழ૕͈ুٟ̦අಭഎͅ෇̹͛ͣͦȃষͅŃĲķŃōķιρΦȜζळ༾ͬဥ̞̀Ȃ෹͈͒ਆន
ഢ֊͈࠿൦࣐̹ͬ̽ȃ̷͈ࠫ‫ض‬ȂŅŊĮņĮœłŎőĳĮİĮ͉́Ȃ΋ϋΠυȜσͅ๤‫̱̀ڛ‬ഢ֊ၚȂഢ֊ତ̦ᄤૺ̱̞̹̀ȃŅŊĮņĮ
œłŎőĳĮİĮ͉́ȂœłŎőĳࠧఅည൵ࢃȂഢ֊ͬ୆̲ͥஜ͈౲‫͈ٴ‬෹̤̞̀ͅȂŗņĮ΃Ρΰςϋ͈̈́̓ඤ๧ळ༾୪಍֦ঊ
͈อ࡛೩‫͂ئ‬Ȃࠬ‫ۯ‬ඤ๧ळ༾͈ࠁఠ։ુͬ෇͛ȂŕŏŇĮϷ͈̈́̓‫׶‬છ଻΍ͼΠ΃ͼϋอ࡛̦ષઌ̱̞̹̀ȃࢵͅਆនळ
༾͈ഢ֊௏͈͒ဋ௢ͬ௯̳ŔĲııłĹĭ ĺ͈อ࡛ᄤૺͬ෇͛Ȃഢ֊ஜാિ̦ࠁ଼̯̞ͦ̀ͥ‫خ‬ෝ଻̦ࣉ̢̹ͣͦȃոષ̥ͣȂࠬ‫͈ۯ‬œłŎőĳࠧఅည൵ͤ͢ͅȂࠬ‫ۯ‬૧୆̦ဲଷ̯ͦȂਆន௩૓͉ဲଷ̯͈ͦͥͅచ̱Ȃഢ֊୶௫‫͉̞̤̀ͅܕ‬Ȃࠬ‫͈ۯ‬ະհ೰‫׶͂ا‬છ̦ৼ̯ܳͦȂഢ֊̦௯ૺ̯ͦͥ͂ࣉ̢̹ͣͦȃłŎĮœłŎőĳࠏ͉Ȃޫਫ਼͈ਆន௩૓͂ഢ֊̤̞̀ͅȂ௖฽എ̈́ພఠ‫ڠ‬എփ݅ͬခ̳ͥ‫خ‬ෝ଻̦াऐ̯ͦͥȃ䋭 㪈㪊㪉 䋭ŐŃĲĮĺ

ŇňŇİŎņŌġŴŪŨůŢŭŴġŮŢŪůŵŢŪůġŵũŦġŪťŦůŵŪŵźġŰŧġŵŶŮŰųġŦůťŰŵũŦŭŪŢŭġŤŦŭŭŴġŵũųŰŶŨũġůŦŨŢŵŪŷŦġ
ųŦŨŶŭŢŵŪŰůġŰŧġŕňŇĮϸ ĮŪůťŶŤŦťġŦůťŰŵũŦŭŪŢŭĮŵŰĮŮŦŴŦůŤũźŮŢŭġŵųŢůŴŪŵŪŰůġĩņůťŎŕĪġĲ ൐‫ނ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬໦ঊພၑ‫ڠ‬໦࿤Ȃĳ ཤ٬ൽఱ‫ڠ‬ఱ‫֭ڠ‬ভ‫ۯࠬشݪࡄࠏڠ‬୆໤‫ޗڠ‬৒

Ĳ ཤ٬ൽఱ‫ڠ‬ఱ‫֭ڠ‬ভ‫ۯࠬشݪࡄڠ‬୆໤‫ڠ‬Ȃĳ ཤ٬ൽఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬ଅ๥ෂ‫شٸܕ‬ȂĴ ཤ٬ൽఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬ક‫ شٸܕا‬Ĳ Ȃĵ ཤ٬ൽఱ‫شݪࡄڠ֓ڠ‬੏۪‫ܕ‬Ȇࡤ‫ڠشٸܕݟ‬䋭 㪈㪊㪊 䋭著者索引

Molecules specifically expressed in tumor endothelial cell (TEC) are important to target tumor angiogenesis. We foundthat Suprabasin (SBSN) is upregulated in TEC compared to normal endothelial cell (NEC) by DNA microarray. SBSN
was discovered as a gene that is highly expressed in suprabasal layers of the epithelia of various organ. SBSN is
involved in the process of epidermal differentiation. Recent study showed that SBSN plays an important role inmaintaining invasive / metastatic potential in adenoid cystic carcinoma. However, the role of SBSN on tumor
angiogenesis has not been reported.
In this study, we investigated the function of SBSN in TEC. Both mRNA and protein of SBSN was upregulated in
TEC compared to NEC. We next examined the role of SBSN in TEC using SBSN RNAi. SBSN siRNA significantly
inhibited the cell migration and tube formation in TEC. Additionally, we revealed that SBSN activated AKT in TEC.
Furthermore, immunostaining showed that SBSN was highly expressed in tumor blood vessels of resected clinicalhuman renal and colon cancer tissues compared to normal counterpart.
These findings suggest that SBSN is a novel TEC-specific marker and might be useful for antiangiogenic purposes.

ポスター発表 ＹＩＡ選考発表ɛ‫ז‬๶ġਕঊ ĲȂŎŰũŢŮŮŢťġłŭŢŮġįŕ ĲȂఱٖġ௱ࢣ ĲȂਝ५ġᎢ༟ ĲȂ‫ۼ‬୞ġජ࡮ ĲȂ୼ུġణ༟ ĲȂ৚ࡔġ૞ဎ ĳȂ໌ຶġત૞ ĴȂ๳നġణࢼ ĵ

口頭発表ŐŃĲĮĲı ŔŃŔŏġŪŴġŢġůŰŷŦŭġŕŶŮŰųġņůťŰŵũŦŭŪŢŭġńŦŭŭġŮŢųŬŦų

会長招待講演 シンポジウム

Tumor microenvironment consists of various components including tumor cells, tumor vessels and cancer associatedfibroblasts (CAFs). Recent studies have shown that a part of CAFs is originated from tumor endothelial cells (TEC) via
endothelial-to-mesenchymal transition (EndMT). During EndMT, endothelial cells lose their characteristics such ascell-cell contact and the expression of endothelial markers including VE-cadherin, and acquire mesenchymal
phenotypes including migratory ability and the expression of mesenchymal markers including smooth muscle Ϸ-actin(Ϸ-SMA). Since multiple lines of evidence have shown that CAFs support the growth and progression of cancer cells,
EndMT is expected to be a novel target of cancer therapy. While signals mediated by transforming growth factor(TGF)-ϸ have been implicated in EndMT, the molecular mechanisms underlying it remain to be fully elucidated. In
the present study, we identified fibroblast growth factor (FGF) -2 as a negative regulator of TGF-ϸ-induced EndMT.
FGF-2 significantly suppressed the TGF-ϸ2-induced expression of various mesenchymal markers in MS-1 pancreatic
endothelial cells and normal endothelial cells (NEC: primarily cultured dermal endothelial cells). FGF-2 preferentiallybinds FGF receptor (FGFR) 1IIIc and activates intracellular signaling cascades consisting of mitogen-activated protein
kinase/extracellular signal-regulated kinase kinase (MEK). In accordance with the effects of FGF-2, PD325901, an
inhibitor of MEK1/2, enhanced the expression of mesenchymal markers induced by TGF-ϸ2. Furthermore, we foundthat the expression levels of FGF-2 and FGFR1IIIc in TEC are significantly higher than those in NEC, and areincreased by the treatment of TGF-ϸ2. Taken together with the previous reports that TGF-ϸ is abundantly present intumor microenvironment, these results suggest that FGF-2 produced by TEC protects themselves from TGF-ϸ2induced EndMT in an autocrine fashion.

特別講演ɛ୤ೋġဉ֚ ĲȂࠋġઆࢤ ĲȂႝ࿐ġဢ ĲȂ‫݌‬ઐġࢫဉ ĲȂఱٖġ௱ࢣ ĳȂ๳നġ‫ނ‬ঊ ĳȂ‫׬ݠ‬ġࢼ໹ ĲȂള໐ġഔ჊ Ĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineŐŃĲĮĲĲ ̦ͭഢ֊̤̫ͥͅਆនࠬ‫ۯ‬ඤ๧ळ༾͈࿨‫ڬ‬ɛ‫ۼ‬୞ġජ࡮ ĲȂఱાġဎٚ ĳȂఱٖġ௱ࢣ ĲĭĴȂਝ५ġᎢ༟ ĲȂ५ུġგࢨ ĲȂຩനġ੓֚ ĵȂ୼ུġణ༟ ĲȂłŭŢŮġŎŰũŢŮŮŢťġŕįĲȂ๳നġణࢼ ĲȂ๳നġ‫ނ‬ঊ Ĳ
Ĳ ཤ٬ൽఱ‫ڠ‬ఱ‫֭ڠ‬ভ‫ۯࠬشݪࡄڠ‬୆໤‫ڠ‬Ȃĳ ཤ٬ൽఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬ळ༾୆ၑ‫ڠ‬ȂĴ ཤ٬ൽఱ‫ڠ‬ఱ‫֭ڠ‬ভ‫૷࢛࣌شݪࡄڠ‬౯ඤ‫ڠش‬Ȃĵ ཤ٬ൽఱ‫֒ڠ‬ഥঊພଷࢄࡄ‫ݪ‬ਫ਼ۚळ༾୆໤‫ڠ‬໦࿤ȂĶ ཤ٬ൽఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬Ȇࡤ‫ڠشٸܕݟ‬̦͈࣐ͭࠬ଻ഢ֊̤̞̀ͅȄਆនळ༾͉ࠬ‫ۯ‬ඤ๧ळ༾Ȫņńȫ͂௖ࡽͅैဥ̱Ȅࠬ‫ۯ‬ඤ๧ळ༾‫ͬۼ‬೒ً̱̀ࠬ‫ס‬੏۪ͅවͥȅ͉̭ͩͦͩͦͦ́͘ਆនࠬ‫ۯ‬ඤ๧ळ༾Ȫŕņńȫ͈໦ၗ෽ူ࣐̞ͬȄ̷̦ͦͣୃુࠬ‫ۯ‬ඤ๧ळ༾Ȫŏņńȫ͂๤‫ڛ‬̱̀အș̈́ओ։̦̜̭ͥ͂Ȅ̯͉ͣͅ՛଻ഽ̦։̈́ͥਆនဇြ͈ŕņń‫́͜ۼ‬အș֑̞̦̜̭̈́ͥ͂ͬྶ̥̱ͣ̀ͅ
̧̹ȅུࡄ‫͉́ݪ‬Ȅࣞഢ֊଻ਆនඤ́։ુ଻ͬ‫ڕ‬ං̱̹ŕņń̦Ȅਆនळ༾͒൱̧̥̫̦͈̀ͭഢ֊ͬ௯ૺ̳ͥ‫خ‬ෝ଻̞̾̀ͅ࠿൦̱̹ȅΤȜΡζ;Α͈ΪΠ๧‫֊ئ‬૒ਆនȪࣞഢ֊଻ਆនȄ೩ഢ֊଻ਆនȫ̥ͣĳਅ႒͈ŕņńȪࣞഢ֊଻ਆ
នဇြņńȇŉŎĮŕņńȄ
೩ഢ֊଻ਆនဇြņńȇōŎĮŕņńȫ
ͬȄ΋ϋΠυȜσ̱͂̀ୃુζ;Α̥ͣୃુ๧ໂဇြņńȪŏņńȫͬ໦ၗ෽ူ̱̹ȅ̴͘ȄŉŎĮŕņń̦೩ഢ֊଻ਆនळ༾͈ഢ֊ͬ௯ૺ̳͈̥̠̥ٜͥ̓ͬଢ଼̳̹ͥ͛Ȅਆនळ༾͂‫ڎ‬ņńͬζ;ᾼ‫֊ވ‬૒̱Ȅྎઑ੏۪ਆនळ༾Ȫńŕńȫ͂෹ഢ֊͈ခྫٜͬଢ଼̱̹ȅŉŎĮŕņń͈͂‫֊ވ‬૒ͤ͢ͅȄńŕńତ͈௩‫͂ح‬෹ഢ֊͈௯ૺ̦෇̹͛ͣͦḙ̷̏́ȄŉŎĮŕņń̦ਆនळ༾͈ࠬ‫ۯ‬ඤ૟වً͈͈̓೾ͅ‫۾‬ဓ̳̥ͥȄਆនळ༾͈ņń͈͒ဋ௢Ȅ୪಍Ȅࠬ‫ۯ‬ඤ๧‫ࠤۼ‬ဋ௢̷̸̞̾̀ͦͦͅ Ūůġ ŷŪŵųŰ ٜ́ଢ଼̱̹ȅਆនळ༾͉ŉŎĮŕņńͅచ̱̀डࣞ͜
̞௢‫଻ا‬Ȅ୪಍ෝͬা̱ȄŉŎĮŕņń‫ͬۼ‬೒ً̱̹ḙ͈࡛̏ͦͣયͅచ̱ȄŉŎĮŕņń̤̞̀ͅอ࡛̦ᄤૺ̱̞̀ͥ໦๥
ΗϋΩ·ŃŪŨŭźŤŢůͅ಍࿒̱̹ȅŉŎĮŕņń͈ŃŪŨŭźŤŢůͬŴŪœŏłͤ͢ͅΦΛ·Θ;ϋ̳ͥ͂ȄŉŎĮŕņńͅచ̱̀ਆនळ
༾͈௢‫̦଻ا‬೩‫̹̱ئ‬ȅ̯ͣͅŴũŃŪŨŭźŤŢůġ ŉŎĮŕņńͬਆនळ༾͂‫֊ވ‬૒̳ͥ͂Ȅਆនळ༾͈ࠬ‫ۯ‬ඤ૟ව̤͍͢෹ഢ
֊̦ဲଷ̯̹ͦȅոષͤ͢Ȅࣞഢ֊଻ਆនඤ́ࠬ‫ۯ‬ඤ๧ळ༾͉ŃŪŨŭźŤŢů͈໦๥ͬᄤૺ̵̯Ȅ̦͈ͭഢ֊ͬ௯ૺ̵̯̠
̭̦ͥ͂াऐ̯̹ͦȅŐŃĲĮĲĳ ਆនࠬ‫ۯ‬૧୆ஷ‫ٺ‬सͥ͢ͅςϋΩ࣐଻ഢ֊௯ૺैဥ͈͒ ŤĮŎŦŵ ͈‫۾‬ဓɛఱઔġੇྴ ĲȂŎŤŅŰůŢŭťġŅŰůŢŭť ĳ
Ĳ Քຎఱ‫ڠ‬௙ࣣ‫ݪࡄڠش‬঑‫׳‬ΓϋΗȜ୆໤঩࡙໦࿤Ȃĳ ŖůŪŷŦųŴŪŵźġŰŧġńŢŭŪŧŰųůŪŢĭġŔŢůġŇųŢůŤŪŴŤŰ

Ⱥ෸ࠊȻਆន͈ࠬ‫ۯ‬૧୆ͬດഎ̳͂ͥŗŢŴŤŶŭŢųġŦůťŰŵũŦŭŪŢŭġŨųŰŸŵũġŧŢŤŵŰųġĩŗņňŇ ļġࠬ‫ۯ‬ඤ๧଼ಿ֦ঊĪஷ‫ٺ‬ၷ༹͉ਆន͈૧̹̈́হၷ༹̱͂̀‫ܢ‬ఞ̯̤ͦ̀ͤȂఉ̩͈ŗņňŇஷ‫ٺ‬स̦ႉ઄؊ဥ̯̞ͦ̀ͥȃ̷͈̠̥̈́̈́͢ȂŗņňŇஷ‫ٺ‬स̦࣐ࠬ଻ഢ֊ͬ௯ૺ̳̭ͥ͂Ȃ̯ͣͅȂ̷͉ͦͅŤĮŎŦŵ̦‫۾‬ဓ̱̞̭̦̀ͥ͂া̯̹ͦȃ̳̻̈́ͩȂŗņňŇஷ‫ٺ‬स̦ਆនඤ͈ࠬ‫ྟۯ‬ഽͬࡘઁ̵̯̭ͥ͂́ॸள཈გഽ̦೩‫̱ئ‬Ȃ̷͈ࠫ‫ض‬ȂŤĮŎŦŵ͈‫̦଻ڰ‬ᄤૺ̱̀ਆន͈૫੕଻͞
ഢ֊଻̦௩‫̹̥̽̈́͂ͣྶ̦̭̯͂ͥͦޑ‬ȃ̱̥̱̦̈́ͣȂŗņňŇஷ‫ٺ‬स͈ςϋΩ࣐଻ഢ֊͈͒‫͉ޣג‬ະྶ̜́ͥȃȺ࿒എȻུࡄ‫͉́ݪ‬ȂŗņňŇஷ‫ٺ‬स̦ςϋΩ࣐଻ഢ֊ͬ௯ૺ̳̥ͥȂ̹͘Ȃ̷̭ͅŤĮŎŦŵ̦‫۾‬ဓ̱̞̥̀ͥͬྶ̥ͣͅ
̳̭ͥ͂ͬ࿒എ̱̹͂ȃȺ ऺၳ༹༷͂ȻਆនκΟσζ;ᾼ࿪सͬĴ਩‫ۼ‬ൎဓ̱̹ࢃȂ۪ၠࡥ೰̱ழ૕‫ڠ‬എٜଢ଼ͅ‫ރ‬̱̹ȃဣ෾చચ߲ȂŗņňŇஷ‫ٺ‬सൎဓ߲ȂŗņňŇஷ‫ٺ‬स͂ŤĮŎŦŵஷ‫ٺ‬स͈‫ވ‬ൎဓ߲͈ࠗĴ߲ͬ୭೰̱̹ȃਆនळ༾͈ςϋΩ‫ۯ‬ඤ͈͒૫੕͂ςϋΩ୯ഢ֊Ȃ̯ͣͅςϋΩ‫ۯ‬ඤ๧ळ༾̤̫ͥͅŤĮŎŦŵ͈อ࡛ͬ಺͓̹ȃȺࠫ‫ض‬Ȼచચ߲ͅ๤͓ȂŗņňŇஷ‫ٺ‬सൎဓ߲͉́ਆនळ༾͈ςϋΩ‫ۯ‬ඤ૫੕͂ςϋΩ୯ഢ֊̦௩‫̹̞̱̀ح‬ȃ̹͘ȂŗņňŇஷ‫ٺ‬सൎဓ߲́
͉ਆនळ༾ȂςϋΩ‫ۯ‬ඤ๧͂͜ͅȂŤĮŎŦŵ͂‫߿ا଻ڰ‬ŤĮŎŦŵ̦‫̹̜̽́଻ုޑ‬ȃŗņňŇஷ‫ٺ‬सൎဓ߲ͅ๤͓ȂŗņňŇஷ‫ٺ‬स͂ŤĮŎŦŵஷ‫ٺ‬स͈‫ވ‬सൎဓ߲͉́Ȃਆនळ༾͈ςϋΩ‫ۯ‬ඤ͈͒૫੕͂ςϋΩ୯ഢ֊̦ဲଷ̯̹ͦȃȺ ࠫაȻոષ
ͤ͢ȂŗņňŇஷ‫ٺ‬स͉ςϋΩ࣐଻ഢ֊ͬ௯ૺ̳̭ͥ͂Ȃ̷̭ͅŤĮŎŦŵ̦‫۾‬ဓ̱̞̭̀ͥ͂ȂŗņňŇஷ‫ٺ‬सൎဓশͅŤĮŎŦŵஷ‫ٺ‬सͬ‫ވ‬ൎဓ̳̭ͥ͂́ȂŗņňŇஷ‫ٺ‬सͥ͢ͅςϋΩ୯ഢ֊͈௯ૺͬဲଷ̧̭́ͥ͂ͬྶ̥̱̹ͣͅȃ䋭 㪈㪊㪋 䋭ĺ࠮ĳĸ඾Ȫ߄ȫġĲıĻııȡĲĲĻııġġలˏٛા࢛൮ġ‫ܖ‬ய ŐŃĳŐŃĳĮĲĴ ࠬ‫ۯ‬ඤ๧ळ༾ͬ‫خ‬ণ‫ ͈̹̳͛ͥا‬ŇŭŬĲĮňŇő ̤͍͢ ŇŭŵĲĮŵťŴœŦťġŃłń ΠρϋΑΐͿ
ΣΛ·ζ;Α͈ैୋプログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛઐུġ࠲Ȃୌࢺġ࿻๼Ȃջ෯ġୃষŜ෸ࠊȂ࿒എȂ༹༷Ş࡛हȂࠬ‫ͬࠏۯ‬ଷࢄ̳ͥΏΈ΢σഥోࠏ̱͂̀ȂŗņňŇȂŇňŇȂŕňŇĮϸȂͺϋΐ΂ε΀Ιϋ̈́̓Ȃఉ̩͈໦ঊ̦༭̯࣬
̞ͦ̀ͥȃ̷͈ಎ́ŗņňŇĮł̷͈͂਋ယఘȪŇŭŬĲĭġ ŇŭŵĲȫ̱̹ͬٚഥోࠏ͉Ȃอ୆ً೾ͅ‫ۯ̞ࠬ̀؃‬ඤ๧ळ༾͈อ୆̤

特別講演ಆ෨ఱ‫֓ڠ֓ڠ‬ၷࠏ୆ྵΏΑΞθ֓‫ࢲ୺ڠ‬ٜཎ‫ڠ‬อ୆‫ݪࡄڠ‬৒͍͢໦‫ͅا‬ຈါ̜̺̫̩́ͥ́̈́Ȃਆនࠬ‫ۯ‬૧୆൝͈ພഎࠬ‫ۯ‬૧୆̤̞̀͜ͅਹါ̈́࿨‫̦̭̳̹͂ضͬڬ‬౶̜ͣͦ̀́ͥ͂ࣉ̢ͣͦͥȃུࡄ‫ِ̞̤̀ͅݪ‬ș͉Ȃอ୆ً೾̤͍͢ພഎࠬ‫ۯ‬૧୆̤̫ͥͅŇŭŬĲȂŇŭŵĲ͈อ࡛ͬκΣΗȜ̳̹͈ͥ͛ŇŭŬĲĮňŇő̤͍͢ŇŭŵĮĲĮŵťŴœŦťġŃłńΠρϋΑΐͿΣΛ·ζ;Αͬਏၛ̱̹͈́༭̳࣬ͥȃŜࠫ‫ض‬Ȃࣉख़Şِș͉ȂŇŭŬĲĮňŇő̤͍͢ŇŭŵĲĮŵťŴœŦťġ ŃłńΠρϋΑΐͿΣΛ·ζ;Αͬဥ̞̭ͥ͂́Ȃథ঱଼̤͍͢਷͈ࠬ‫ۯ‬ඤ๧ळ༾̤̫ͥͅŇŭŬĲȂ
ŇŭŵĲ̷̸͈ͦͦอ࡛ͬȂňŇő̤͍͢ŵťŴœŦť́κΣΗȜ੄ြ̭ͥ͂ͬা̱̹ȃ྾‫ע‬அ૗༹ͤ͢ͅȂňŇőȂŵťŴœŦť̷̸͈ͦͦอ࡛̦ඤह଻ŇŭŬĲȂŇŭŵĲ͈อ࡛͂཰̓ठ࡛̱̞̭̀ͥ͂ͬ෇̹͛ȃ̹͘Ȃอ୆ً೾̤̞̀ͅňŇőȂŵťŴœŦť͈อ࡛̦ȂĹįĶġ ඾᥷̷͂ͦո̤̞ࣛ̀ͅ཰͈̓ࠬ‫ۯ‬ඤ๧ळ༾́෇̭̦͛ͣͦͥ͂۷ख़̯̹ͦȃ‫̢̀ح‬Ȃ̭ͦͣζ;Α͉Ȃਆនळ༾๧‫֊ئ‬૒κΟσ̤̞̀ͅਆនඤ໐ͅည൵̯ͦͥࠬ‫ۯ‬ඤ๧ळ༾ͬκΣΗȜ੄ြ̭ͥ͂ͬ෇̹͛ȃ̭͈ͦͣࠫ‫ͤ͢ض‬Ȃࣽٝਏၛ̱̹ŇŭŬĲĮňŇő̤͍͢ŇŭŵĲĮŵťŴœŦťġ ŃłńΠρϋΑΐͿΣΛ·ζ;Α͉ࠬ‫͈ۯ‬อ୆͞ພഎࠬ
‫ۯ‬૧୆͈ࡄ‫ͅݪ‬ခ‫̈́ף‬κΟσ൲໤̜̭̦́ͥ͂‫̩ޑ‬াऐ̯̹ͦȃɛฐനġ࠺ ĲĭĳȂ঳֔ġ࠲ఊ ĴȂ໛ࡔġ࿆༸ ĲȂࡗ‫ۼ‬ġ઎຃ ĳȂབ࠮ġೄਏ Ĳ
Ĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼ळ༾୆໤‫ڠ‬໐Ȃĳ ඾ུ֓‫ش‬ఱ‫ڠ‬ඤ‫࣒ڠش‬जȪࡤ‫ܕݟ‬ȆۜஅછȆਆន໐࿝ȫȂĴ ൐‫ނ‬ఱ‫ڠ‬໦ঊळ༾୆໤‫ݪࡄڠ‬ਫ਼໦ঊ‫ܥ‬ෝࠁఠࡄ‫ݪ‬໦࿤ࠬ‫଼ͅࠁۯ‬ϸńŵůͥ֒͢ͅഥঊอ࡛ଷࢄ͉ຈଌ͂ࣉ̢̞ͣͦ̀ͥȃ̱̥̱Ȃ୆ఘ͈ࠬ‫ۯ‬ඤ๧ळ༾́ϸńŵůջంഎഢৢ̦ශ
‫಺ͅة‬୯̯ͦȂࠬ‫଼ͬࠁۯ‬ශ‫ͅة‬ଷࢄ̳̥͉ͥະྶ̜́ͥȃ̭͈݃࿚ٜͬྶ̳̹ͥ͛ȂΔήρέͻΛΏνͬဥ̞̹ࠖ࢕ͼιȜΐϋΈܿ੅ͤ͢ͅȂ୆̧̹ࡢఘ́ࠬ‫ۯ‬ඤ๧ळ༾̤̫ͥͅϸńŵů͈ഢৢ಺୯‫خͬ଻ڰ‬ণ‫̳ͥا‬ΏΑΞθͬࢹಃ̱Ȃϸńŵů͈࿨‫ͬڬ‬ٜଢ଼̱̹ȃࠬ‫ۯ‬ඤ๧අ։എίυκȜΗȜଷࢄ‫́ئ‬ȶ‫ړ‬ඤഢৢ֦ঊŕńŇ͈ϸńŵůࣣࠫႀ֖ȷ
͂ȶňłōĵഢৢ֦ঊ͈Ņŏłࣣࠫႀ֖ȷ
͈ဏࣣ౩ฒৗͬอ࡛̳ͥ֒ഥঊ٨་έͻΛΏνͬਏၛ̱̹ȃ̷̱̀Ȃňłōĵഢৢ֦ঊ͈෇ে෻Ⴅ͈‫ئ‬ၠ́ࠖ࢕౩ฒৗņňŇőͬอ࡛̳ͥέͻΛΏν͂࢐෻̳ͥম́Ȃࠬ‫ۯ‬ඤ๧̤̫ͥͅϸńŵů͈ഢৢ‫ͬ଻ڰ‬ȂņňŇőࠖ࢕́‫خ‬ণ‫଼̹̱̭̳ࢗ͂ͥͅا‬ȃ̭͈ࠏͬဥ̞Ȃࠬ‫ۯ‬อ୆ً೾͈ϸńŵů‫ͬ଻ڰ‬ٜଢ଼̱̹̭͂ͧȂ૤ඤ྄Ȃ൮໐ࠬ‫ۯ‬Ȃ๶௰୓ྤ͈ඤ๧ळ༾́ϸńŵů‫̦଻ڰ‬ᄤૺ̱̞̹̀ȃ
̷̭́Ȃ๶௰୓ྤࠁ଼̤̫ͥͅϸńŵů͈࿨‫ͬڬ‬ٜଢ଼̱̹̭͂ͧȂϸńŵů͉ඤ๧ळ༾͈୆ంͬ֋঵̳̭ͥ͂́Ȃ๶௰୓ྤࠁ଼ͬଷࢄ̳̭̦ͥ͂া̯̹ͦȃ̭ͦ́͘๶௰୓ྤࠁ଼̤̫ͥͅŃŰůŦġ ŮŰųűũŰŨŦůŦŵŪŤġ űųŰŵŦŪůġ ĩŃŮűĪ͈‫۾‬ဓ̦༭̯̞࣬ͦ̀ͥȃ̷̭́ȂŃŮű̦ϸńŵů
‫ͬ଻ڰ‬ଷࢄ̳̥ͥ࠿൦̱̹ȃŃŮű઼ًอ࡛ͤ͢ͅ։ਫ਼଻͈୓ྤࠬ‫଼̯ͦࠁ̦ۯ‬Ȃϸńŵů‫̦଻ڰ‬ᄤૺȂ‫ͅݙ‬ŃŮűͺϋΗΌΣ̯ͣͅȂŃŮűͥ͢ͅϸńŵů‫֒ͥͩ۾ͅا଻ڰ‬ഥঊ̱͂̀Ȃ୓ྤȆ࿉ळࠬ‫ࠁܗۯ‬Ȃࣸ඲໐ழ૕ًࠁ଼ͬ৽ಭ̳͂ͥŌŭŪűűŦŭĮ
ŕųŦůŢŶůŢźછ࢓߲͈ࡔ֦֒ഥঊȂłŨŨŧĲͅ಍࿒̱̹ȃŃŮű઼ًอ࡛ͤ͢ͅłŨŨĲอ࡛̦ᄤૺ̱ȂŏŰŨŨŪů઼ً͈อ࡛͢ͅ
ͤ೩‫̹̱ئ‬ȃ̹͘ȂłŨŨ̂Ĳ͈ΦΛ·Θ;ϋͤ͢ͅȂϸńŵů‫̦଻ڰ‬೩‫̱ئ‬Ȃ๶௰୓ྤࠁ଼̦ஷ‫̹̯ͦٺ‬ȃ
ոષ̥ͣȂ
ŃŮű͉
łŨŨŧĲ͈อ࡛̱ͬٚ̀ϸńŵů͈ഢৢ‫ͬ଻ڰ‬௩‫̭̳͂ͥޑ‬Ȃ̯̭͈ͣͅϸńŵů‫̦଻ڰ‬๶௰୓ྤࠁ଼ً೾͈ඤ๧ळ༾͈୆ంͬ
ଷࢄ̱̞̭̦̀ͥ͂া̯̹ͦȃ䋭 㪈㪊㪌 䋭著者索引

ΑΠĩŏŰŨŨŪůĪ઼ً͈อ࡛ͤ͢ͅȂϸńŵů‫̦଻ڰ‬೩‫̱ئ‬Ȃ๶௰୓ྤࠁ଼̦ஷ‫̹̯ͦٺ‬ȃ̭͈̭̥͂ͣŃŮű̦๶௰୓ྤࠁ଼ً
೾͈ϸńŵů‫ͬ଻ڰ‬ଷࢄ̱̞̭̦̀ͥ͂া̯̹ͦȃ

ポスター発表 ＹＩＡ選考発表ϸĮŤŢŵŦůŪů
Ȫϸńŵůȫ
͉ळ༾͈௩૓Ȇ໦‫ا‬Ȇ଼ಿͅ‫۾‬Ⴒ̳ͥഢৢ಺୯֦ঊ̜́ͥȃϸńŵůࠧఅȆ઼ًอ࡛ζ;Α͈༭̥࣬ͣȂ

口頭発表ŐŃĳĮĲĵ ࠬ‫ۯ‬ඤ๧අ։എ̈́ϸĮŤŢŵŦůŪů ջంഎഢৢ಺୯͈ࠖ࢕୆ఘͼιȜΐϋΈ

会長招待講演 シンポジウム̞ͥȃ̭͈̠̈́͢อ୆ષȂႉ઄ષ͈ਹါ଻̥ͣȂŇŭŬĲ̤͍͢ŇŭŵĲ͈อ࡛ͬκΣΗȜ̳̹͈ͥ͛൲໤κΟσ͉ఱ་ခ‫ף‬ŐŃĳĮĲĶ ඤࠛ൲ྤࠏ್͂ࣸ൲ྤࠏ͉อ୆ً೾̤̞̞̥̱̀̀ͅͅႲ̯͈̥ࠫͦͥ
ɛ࿐ఆġ‫ם‬ඵȂ֙‫ٵ‬ġ੗ຳȂ૽ࡉġষ჊‫ش֓਀܊‬ఱ‫ڠ‬ٜཎ‫࣒ڠ‬ज૽ఘอ୆‫ڠ‬໦࿤ࠬ‫͉ࠏۯ‬Ȃอ୆͈੝‫ًܢ‬೾́ࠨ̹̽͘Ηͼθ΋Ȝᾼਲ̞Ȃհ೰̱̹ࠁఠͬࠁ଼̳ͥȃ̭͈ࠁ଼ً೾͉Ȃ࡛हġఱ̧̩ྤ‫ۯ଼ࠬ͂ࠁۯ‬૧୆ͅ໦̫̀ࣉ̢̤ͣͦ̀ͤȂྤ‫଼͉́ࠁۯ‬ġ ̴͘ྚ໦‫ۯࠬ̈́ا‬࿌̦ࠁ଼̯ͦȂ̷͈̥̥̈́ͣࠬၠͅ
̽̀͢൲ྤ͂୓ྤ̦஖̞̠͊ͦͥ͂ĲııාஜͅŕũŰŮŢ͞ņŷŢůŴ̦ͣ೹੹̱̹ΥΛΠχȜ·κΟσ̦नဥ̯̞ͦ̀ͥȃ̭͈‫ب‬୰͈आ‫͉͈̞ͥ̀̽̈́͂ݶ‬ȂႲ௽୨༌͈ठࢹಃ༹ͥ͢ͅ۷ख़ࠬ͞‫ۯ‬૗ளಕව༹̥ͣං̹ͣͦ౶ࡉ́Ȃሶ඿႒ͬဥ̞̹ٜଢ଼͉́൳֚ࡢఘ͈อ୆ً೾ͬႲ௽̱̀۷ख़̧̞́̈́ത̦৘ष͈ࠁ଼ً೾ͬၑٜ̳ͥષ́ఱ̧̈́વ‫̜̽́ٺ‬̹ȃ̭͈વ‫࣪ͬٺ‬໚̳ͥκΟσ୆໤̱͂̀Ȃِș͉ġ ΔήρέͻΛΏνġ ĩŅŢůŪŰġ ųŦųŪŰĪġ ͅ಍࿒̱̹ȃΔήρέͻΛΏν
͉Ȃঊ‫ٸݠ‬อ୆̱Ȃఉॲ́Ȃ᥷̦൫ྶ́Ȃ๤‫ڛ‬എ۰༒֒ͅഥঊௌै̢̦࣐ͥ̈́̓֒ഥ‫ڠ‬Ȃ৘ࡑอ୆‫ͅڠ‬ഐ̱̹අ଻ͬခ
̱̞̀ͥȃ̯ͣࠖͅ࢕૗ளͥࠬ͢ͅ‫ۯ‬௮‫༹ͥ͢ͅג‬อ୆ͺΠρΑ͜ै଼̯ͦȂࠬ‫଼ࠁۯ‬ι΃ΣΒθ͈ٜଢ଼κΟσ̱͂̀ਹဥ̯̞ͦ̀ͥȃࠬ‫ۯ‬ඤ๧́අ։എࠖͅ࢕ͬอ̳ͥΠρϋΑΐͿΣΛ·ȆΔήρέͻΛΏν͈ΗͼθρίΑȆͼιȜΐϋΈ༹ͥ͢ͅ۷ख़̥ͣȂࠬ‫ۯ‬࿌ࠬ͞ၠͅ‫̞̈́ͣݶ‬ఘۚ໐͈ࠬ‫଼ًࠁࠏۯ‬೾̦༭̯࣬ͦȂِș͈ΈσȜί͜ġ ߃ාġ ൮໐ࠬ‫ͬࠏۯ‬చયͅȂ൳အ͈ٜଢ଼ࠫ‫ͬض‬ං଼̭̱̹ͥ͂ࢗͅȃ͉́Ȃ̞̥̱̀ͅෞ͈ࠬ‫͂ࠏۯ‬ୢଡ͈ࠬ‫͉ࠏۯ‬ൡࣣ̯͈̥ͦͥȃඤᴢȆఱ൲ྤႊȆෞೲȆ್ࣸ൲ྤ̥ͣ̈́ͥࠬ‫͉ࠏۯ‬ġ ෞ̦ୃુͅ‫ܥ‬ෝ̳ͥષ́ޭ͛̀ਹါ̜́ͤȂ̷͈ٜཎ‫ڠ‬എࢹ௮͉ୢ್൲໤ͬ೒̲֚̀೰̱̞̀ͥȃِș͉Ȃ൳အ͈਀༹ͬဥ̞̀ġ లˍ୯‫ۼ‬൲ྤဇြ͈ඤ๧ळ༾̦ġ ෞୢଡࠬ‫ࠏۯ‬͈Ⴒًࠫ೾́৽ါ̈́࿨‫̭̳̹ͬ͂ضͬڬ‬อࡉ̱̹ȃ̹͘ŴŪŭŦůŵġ ũŦŢųŵ֒ഥঊ͈อ࡛ͬဲଷ̱̀ࠬၠ̦୆̲̞̈́᥷́͜Ȃ਋ୈࢃĴ඾࿒́͘Ⴒࠫ໐պ͈ඤ๧ळ༾͈ߗ‫ۼ‬എ̈́෻౾̦֋঵̯̞̭̥ͦ̀ͥ͂ͣȂ̭͈Ⴒࠫ੝‫ًܢ‬೾ࠬ͜ၠͅ‫̈́ͣݶ‬̞֒ഥഎ̈́ι΃ΣΒθͤ͢ͅଷࢄ̯̞̭̦ͦ̀ͥ͂฻ྶ̱̹ȃ̭͈̠̱̀͢ͅࠁ଼̯̹ͦႲ͉ࠫȂ̷͈ࢃ͈ςκΟςϋΈͬࠐ್̀ࣸ൲ྤࠏ͂Ⴒ̳ࠫͥȃུอນ͉́Ȃෞ͂ୢଡ͈ࠬ‫̱̥̞̦̀ͅࠏۯ‬Ⴒ̯͈̥ࠫͦͥͬȂࠁఠ‫ڠ‬എٜ̈́ଢ଼ࠫ‫ͬض‬ಎ૤ͅ༭̳࣬ͥȃŐŃĳĮĲķ ͺϋΆ΂εͼ΀Ιϋ Ĳ ͉୓ྤ൸͈ྚ໦‫ۯࠬا‬ඤ๧ळ༾ͬဋ௢Ȇ໦‫ࠁྤ୓ۍ̵̯ا‬଼ͅຈଌ͈֦ঊ̜́ͥ
ɛခനġု ĲȂಎ‫ؖ‬ġၻგ ĲȂઐ‫ז‬ġఊ֚ ĳȂ࿐࡫‫ؚ‬ġࢼࢫ ĴȂ‫ུޘ‬ġଢࢬ ĲȂ౻‫ؖ‬ġཆణ ĲȂࣞாġ૝ࢨ ĴȂབ࠮ġೄਏ ĵȂ५‫ئ‬ġ੕ ĳȂ઀৒ġ଼֚ ĲĭĶ
Ĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ‫ނ‬സఱ‫ڠ‬ठ୆֓‫ݪࡄڠش‬ਫ਼ۚळ༾໦‫ا‬ଷࢄࡄ‫ݪ‬ႀ֖ȂĴ ఱिఱ‫ڠ‬๷୆໤ພࡄ‫ݪ‬ਫ਼ૂ༭ഥో໦࿤Ȃĵ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼ळ༾୆໤‫ڠ‬໐ȂĶ ൐‫ނ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ⱥ෸ࠊ͂࿒എȻ‫ۯࠬۍ‬ඤ๧ळ༾̷͈࡙͈ܳ͂໦‫۾ͅا‬ဓ̳֦ͥঊͅ‫͉̱̀۾‬ະྶ̈́ത̦ఉ̞ȃौාུ͈‫ڠ‬ٛ́Ȃِș͉૤௫අ։എͺϋΆ΂εͼ΀ΙϋĲĩłůŨĲĪΦΛ·ͺ;ΠĩłůŨĲńŌŐĪζ;Α̦‫ࠧͬྤ୓ۍ‬అ̱Ȃ૤޼ဇြłůŨĲ̦‫୓ۍ‬ྤࠁ଼ͅຈଌ̜̭́ͥ͂ͬ༭̱̹࣬ȃ̹͘Tie2-lacZτεȜΗȜζ;Αဇြ͈୓ྤ൸͂૤པͬņĲıįĶ́ഊ੄̱Ȃ༷֚́΋ϋΠυȜσྌ͉łůŨĲńŌŐζ;Αဇြ͈૤৒Ȇ૤‫྄ٸ‬໐໦ͬഊ੄̱̀Ȃၰ৪ͬ୪಍̵̯Ĵ඾‫ވۗܕۼ‬෽ူ̳ͥ͂Ȃ΋ϋΠυȜσ͈૤৒͉ͅŕŪŦĳု଻ඤ๧ळ༾͈ૺව̦ࡉ̹̦ͣͦłůŨĲńŌŐζ;Α͈૤৒͉ͅૺව͉ࡉ̴ͣͦȂłůŨĲ
̦૤৒͈͒ŕŪŦĳု଻ඤ๧͈ဋ௢ͬଷࢄ̳̭ͥ͂͜༭̱̹࣬ȃ͉ࣽٝ୓ྤ൸͈ඤ๧ळ༾ͅઙതͬ൚̀Ȃ͈̠̓̈́͢ඤ
๧ळ༾̦łůŨĲ͈ैဥ́‫࠿̥ͬͥͩ۾଼ͅࠁྤ୓ۍ‬൦̱̹ȃȺ༹༷͂ࠫ‫ض‬Ȼ‫଼̯ͥͦࠁ̦ۯࠬۍ‬ஜ͈ņĲıįĶ͈୓ྤ൸ͅ
͉Ȃ୓ྤζȜ΃Ȝ͈Ĳ̾łőŋ͉ńŅĴĲု଻ࠬ‫ۯ‬ඤ๧ळ༾͈֚໐ͅࡠޫอ࡛̱Ȃ୓ྤ൸͉łőŋု଻‫͍ݞ‬łőŋ֮଻ඤ๧ळ༾
͈ˎਅ႒͈ळ༾ਬ౬̥ͣࢹ଼̯̞̹ͦ̀ȃ૤པ͒‫ૺ͈ۯࠬۍ‬ව̦ইͥ͘ņĲĲįĶ͉́Ȃ΋ϋΠυȜσ͂łůŨĲńŌŐζ;Α͈૤པ͂͜ͅłőŋု଻ඤ๧ळ༾͉෇̴͛Ȃłőŋ֮଻ඤ๧ळ༾͈͙̦ૺව̱̞̹̀ȃņĲĳįĶ͉́΋ϋΠυȜσ͈૤པ͉́łőŋု଻ඤ๧ळ༾̦੄࡛̱̹̦ȂłůŨĲńŌŐζ;Ά͉łőŋု଻ඤ๧ळ༾͉ࡉ̥̹ͣͦ̈́̽ȃņĲĴįĶ͈૤৒͉́Ȃ΋ϋΠυȜσ͉́łőŋု଻‫ྤ୓ۍ‬ඤ๧ळ༾̦ࡉ̹̦ͣͦȂłůŨĲńŌŐζ;Ά͉ࡉ̥̹ͣͦ̈́̽ȃոષͤ͢Ȃ‫ྤ୓ۍ‬͉ྚ໦‫̈́ا‬łőŋ֮଻ඤ๧ळ༾̦łůŨĲ͈ैဥ́୓ྤ൸̥ͣဋ௢̱Ȃ૤޼௄ඤ͈́ဋ௢ً೾́łůŨĲͅธ̯̭ͦͥ͂́
łőŋု଻ඤ๧ळ༾͒໦‫̦̭̳͂ͥا‬াऐ̯̹ͦȃ̹͘ζ;ΑņŔळ༾ဇြ͈ŇŭŬĲု଻ࠬ‫ۯ‬ඤ๧ஜߐळ༾ͅŗņňŇͅłůŨĲͬഞ‫̱̀ح‬෽ူ̳ͥ͂łőŋ͈อ࡛̦ည൵̯̹̭̥ͦ͂ͣȂłůŨĲ͉ྚ໦‫ا‬ඤ๧́łőŋͬอ࡛ည൵̧̭̦́ͥ͂
াऐ̯̹ͦȃ
ȺࠫࢊȻ૤޼ဇြłůŨĲ͉୓ྤ൸͈ྚ໦‫ۯࠬا‬ඤ๧ळ༾ͬဋ௢Ȇ໦‫଼ͅࠁྤ୓ۍ̵̯̀ا‬ຈଌͅຈଌ͈࿨
‫̳̹ضͬڬ‬ȃ䋭 㪈㪊㪍 䋭ŐŃĳĮĲĸ őŪŨűŦůĭġŢġůŶŤŭŦŢųġŤŰŪŭŦťġţŰťźġŤŰŮűŰůŦůŵġűųŰŵŦŪůĭġŪŴġŪůŷŰŭŷŦťġŪůġŦůťŰŵũŦŭŪŢŭġ
ťŪŧŧŦųŦůŵŪŢŵŪŰů

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛհ໐ġ͙͘͠ ĲȂऎ൥ġ࿭ঃ ĳȂ૩നġ֗౳ ĴȂᚗ౓ġୃঃ Ĳ
Ĵ ൐‫ش֓ނ‬ভ‫ش‬ఱ‫ڠ‬ఱ‫֭ڠ‬໦ঊळ༾‫ܥ‬ෝ‫ڠ‬໦࿤

口頭発表ŐŃĳĮĲĹ ೰ၾഎպ௖ࡐ๷‫ͬޢ‬ဥ̞̹ࠬ‫ۯ‬ඤ๧ळ༾ບ‫ث‬

会長招待講演 シンポジウム

We previously reported that puromycin-insensitive leucyl-specific aminopeptidase (PILSAP) is required forangiogenesis and for endothelial differentiation from embryonic stem (ES) cells via the aminopeptidase activity of
PILSAP. To search for molecules that function during angiogenesis in cooperation with PILSAP, we performed
proteome analysis of nuclear extracts from embryoid bodies (EBs) made from ES cells transfected with mutant
PILSAP lacking aminopeptidase activity (mtPILSAP-EB) and mock EBs (Mock-EB). Pigpen, a 67-kDa nuclear coiled
body component protein was identified. We demonstrated that pigpen is involved in postnatal angiogenesis in vitro andin vivo. In this study, we examined whether pigpen affects endothelial differentiation by using an EBs culture system.
Flk-1 showed two peaks in this in vitro ES culture system, days 4 and 10. The first peak represents mesoderm
expansion with increase in brachyury, but no other endothelial markers such as VE-cadherin, CD34, CD31, and Tie2.
The second peak comes with these endothelial markers, suggesting the fraction of endothelial precursors. Inhibition of
pigpen expression by siRNA (siPigpen) decreased levels of vascular lineage markers including Flk-1, VE-cadherin,
CD34, CD31, and Tie2. Moreover, siPigpen treatment reduced the markers of successive lineages from Flk-1 positive
mesoderm, ϷSMA (smooth muscle actin) and CD45, but did not the ectodermal marker, GFAP (glial fibrillary acidic
protein). PILSAP is localized mainly in cytosol, whereas pigpen is in nucleus in EBs as well as in endothelial cells.
Binding of PILSAP and pigpen was decreased in mtPILSAP-EB compared with Mock-EB. These results suggest that
pigpen plays a role in growth of vascular, hematopoietic, and muscular lineage population from Flk-1 positive
mesodermal precursors in cooperation with PILSAP.ȁ

特別講演

Ĳ ષ໌ఱ‫ڠ֓ڠ‬୆ၑ‫ݪࡄڠ‬ਫ਼Ȃĳ ൐ཤఱ‫حڠ‬Ⴂ֓‫ݪࡄڠ‬ਫ਼ਆន੏۪ࡄ‫ݪ‬໦࿤Ȃɛ໹୼ġ௛ঃ ĲȂ५ඤġཅ຃ ĳȂ࡫ாġ૧ਏ Ĳ

෽ူळ༾͈ࠁఠ་‫ͬا‬೰ၾഎͅ௶೰̳̭͉ͥ͂Ȃ୆ఘ‫ܥ‬ෝ͈ࢭુ଻͂෫౦ͬບ‫̳ͥث‬ષ́ခဥ̜́ͥȃ೰ၾഎպ௖
ࡐ๷‫͉ޢ‬Ȃ୆ळ༾͈ࠁఠ་‫ͬا‬२ষࡓ́ບ‫̧ͥ́ث‬૧̹̈́ບ‫̜ͥ́ࠏث‬ȃࣽٝȂ೰ၾഎպ௖ࡐ๷‫ͬޢ‬ဥ̞̀୆ၑ‫଻ڰ‬໤ৗ͂࿪स࢘‫ͬض‬ບ‫̳ͥث‬૧̹̈́ίυΠ΋σͬ‫ږ‬ၛ̱̹͈́༭̳࣬ͥȃᨽཻ૮͉Ȃ๧ໂ๷઀ࠬ‫́ۯ‬ΪΑΗηϋ̦ࠬ‫ۯ‬ඤ๧ळ༾ͅैဥ̳̭ͥ͂ͤ͢ͅ୆̲ͥȃ̱̥̱Ȃࠬ‫ۯ‬ඤ๧ळ༾྄̤̫ͥͅ౩ฒ་‫͞ا‬ΏΈ΢σഥో͉ະྶ̈́ത̦ఉ̞ȃ̷̭́Ȃ෽ူ๧ໂဇြࠬ‫ۯ‬ඤ๧ळ༾ͅΪΑΗηϋͬഞ‫̱ح‬Ȃ೰ၾഎպ௖ࡐ๷‫́ޢ‬ळ༾͈̯ࣞͬບ‫̹̱ث‬ȃ̭͈ࠫ‫ض‬ȂΪΑΗηϋ͈ैဥ́ࠬ‫ۯ‬ඤ๧ळ༾͉̯̦ࣞಠ̱̩௩̳̭̦͂ྶ̥̹ͣ̈́̽ͅȃ̯ͣͅࠐশഎͅ۷ख़̳̭ͥ͂ͤ͢ͅȂ̯͈ࣞ་‫͈̾ˎ͉ͅا‬ΑΞΛί̦̜̭ͥ͂ͬࡉ੄̱̹ȃड੝͈་‫͉ا‬ळ༾ࣸ‫͈ڒ‬་‫̭͂ͥ͢ͅا‬Ȃĳ͈̾͛་‫྄͉ا‬౩ฒ͈ક‫ͤ͢ͅا‬ळ༾͈̯̦ࣞᄤૺ̳̭̦ͥ͂ଔख़̯̹ͦȃΪΑΗηϋഞ‫ࢃح‬Ȃࠬ‫ۯ‬ඤ๧ळ༾྄͈ນ࿂͉́ŗņĮŤŢťũŦųŪů͈ŴũŦťťŪůŨ̦୆̲Ȃळ༾‫ۼ‬୪಍̦ࡘ৻̳̭̦ͥ͂ࡉ੄̯̹ͦȃ̯ͣͅȂ̭͈‫ڠا‬എίυΓΑ͉ȂłŅłŎĲĸ̜̞͉ͥłŅłŎĲıͅջం̳̭̦ͥ͂ྶ̥̹ͣ͂̈́̽ȃ༷֚ȂࢯΪΑΗηϋस̜́ͥŭŦŷŰŤŦŵŪųŪŻŪůŦͬഞ‫̳͂ͥح‬Ȃ྄ນ࿂̤̫ͥͅŗņĮŤŢťũŦųŪů͈୨౯͉ဲଷ̯̹ͦȃ೰ၾഎպ௖ࡐ๷‫ࠐ́ޢ‬শഎͅ۷ख़̳ͥ͂ȂŭŦŷŰŤŦŵŪųŪŻŪůŦഞ‫͉߲́ح‬ΪΑ಍ळ༾͈ࠁఠ་‫נͬا‬ຮͅ௴̢̭̦ͥ͂‫خ‬ෝ̜́ͤȂࣽࢃအș̈́ळ༾ບ‫́ࠏث‬ไဥ̯̭̦ͦͥ͂‫ܢ‬ఞ̯ͦͥȃ䋭 㪈㪊㪎 䋭著者索引

Ηηϋঁࠣͬ‫̢̀͜ح‬ळ༾͈̯͉ࣞ་‫̴̵ا‬Ȃळ༾‫ۼ‬୪಍͜֋঵̯̹ͦȃոષ͈ࠫ‫ͤ͢ض‬Ȃ೰ၾഎպ௖ࡐ๷‫͉ޢ‬୆ၑ‫଻ڰ‬໤ৗ͂࿪स࢘‫ͬض‬ບ‫̳ͥث‬ષ́Ȃޭ͛̀ခဥ̈́௶೰ܿ੅̜̭̦́ͥ͂ྶ̥̹ͣ͂̈́̽ȃ೰ၾഎպ௖ࡐ๷‫͉ޢ‬Ȃ୪

ポスター発表 ＹＩＡ選考発表

Ĳ ຩઐ֓‫ش‬ఱ‫ڠ֓ڠ‬໐๧ໂ‫࣒ڠش‬जȂĳ ຩઐγΠΣ·Αĺ࠮ĳĹ඾ȪാȫġĺĻııȡĲĲĻııġġలˏٛા࢛൮ġ‫ܖ‬ய ŐŃĴŐŃĴĮĲĺ ŕňŇϸĲĮŔŮŢťĳİĴ ΏΈ΢σഥోࠏ̱̹ͬٚࠬ‫ۯ‬૧୆಺୯̤̫ͥͅ·ρΑ ŊŊϷ߿ őŊĴ΅΢ȜΔ őŊĴŌĮńĳϷ͈‫ܥ‬ෝഎ࿨‫ڬ‬ɛհᩖġ᥈ ĲȂ‫ؖ݌‬ġგࢴ ĲȂ‫ུؖ‬ġհဎ ĲȂఉ‫ݛ‬გġങঊ ĲĭĳȂఉ‫ݛ‬გġု Ĳ
Ĳ ߄ాఱ‫ڠ‬ఱ‫ۯࠬشݪࡄࠏڠ֭֓ڠ‬໦ঊ୆ၑ‫ڠ‬Ȃĳ ୞୼ࡇၛۭࢌఱ‫ڠشࢫ࠲شڠࢌۭڠ‬γΑέ͹ΙΐσͼΦΏΠȜσĩőŊĪĮĴ΅΢ȜΔġ ĩőŊĴŌĪġ ͉Ȃ͕඿႒̤̞̀ͅĴ͈̾·ρΑġ Ŋĭġ ŊŊĭġ ŊŊŊġ ͅ௺̳ͥĹ͈̾ͺͼΕέ΁Ȝθ̦ంह̱Ȃಎ́͜·ρΑŊϷ߿ġőŊĴŌġĩűĲĲıϷĪġ͉ŗņňŇġͤ͢ͅည൵̯ͦͥࠬ‫ۯ‬૧୆ͅຈଌ̜́ͥȃ༷֚Ȃ̭ͦ́͘୆ၑ‫ܥ‬ෝ̦ະྶ̜̹́̽·ρΑġ ŊŊϷ߿ġ őŊĴŌġ ĩńĳϷĪġ ͈஠૸߿‫͍ݞ‬ඤ๧අ։എ΋ϋΟͻΏο΢σŌŐζ;Α͉อ୆ಎ‫̞̤̀ͅܢ‬౿ঘ͂̈́ͤȂ̷͈ঘ֦͉อٔഎࠬ‫ۯ‬૧୆଼͂੃ً೾͈։ુ̜̭̭́ͥ͂ͬͦ́͘ͅྶ̥̱̹ͣͅȃ̱̥̱Ȃඤ๧ळ༾̤̫ͥͅńĳϷͥࠬ͢ͅ‫ۯ‬૧୆಺୯͈໦ঊ‫͉ࢹܥ‬ະྶ̈́ത̦ఉ̞ȃུࡄ‫͉́ݪ‬Ȃ৽ါ̈́ࠬ‫ۯ‬૧୆֦ঊ͈ˍ̜̾́ͥΠρϋΑέ΁ȜηϋΈ଼ಿ֦ঊϸĲ ĩŕňŇϸĲĪ ͈ඤ๧ळ༾ैဥ̤̫ͥͅńĳϷ͈‫ܥ‬ෝഎ࿨‫ͬڬ‬ٜଢ଼̱̹ȃ૽ᦡఝ୓ྤඤ๧ळ༾ġ ĩŉŖŗņńĪġ ̤̞̀ͅȂœŏłۙખ༹ͬဥ̞̀ńĳϷͬΦΛ·Θ;ϋġ ĩńĳϷȽŌŅĪġ ̱ȂŕňŇϸĲ͈̯
̰̈́ࠬ͘͘‫ۯ‬ඤ๧ळ༾ैဥ͈ńĳϷջం଻ͬ࠿൦̱̹ȃńĳϷȽŌŅळ༾͉́ȂŕňŇϸĲ ͥ͢ͅġ ŔŮŢťĳİĴ͈ςϋॸ‫ݞا‬͍‫ࡐ̦࣐֊ړ‬ಠͅ೩‫̹̞̱̀ئ‬ȃ‫ྙޟ‬૬̞̭͂ͅȂ΀ϋΡΕȜθષ͈́ŔŮŢťĳİĴςϋॸ‫ͅا‬ຈଌ̈́௷ાΗϋΩ·ŔŮŢťġ ŢůŤũŰųġ ŧŰųġ ųŦŤŦűŵŰųġ ŢŤŵŪŷŢŵŪŰůġ ĩŔłœłĪġ ͈ळ༾ඤޫह͈་‫ا‬Ȃ‫΀͍ݞ‬ϋΡΕȜθષ͈́őŊĩĴĪőġ ĩńĳϷ‫ॲ଻ڰ‬໤Ī̱̹ͬٚŔŮŢťĳİĴ͂Ŕłœł͈͂ໝࣣఘࠁ଼̦ȂńĳϷȽŌŅळ༾̤̞̀ͅಠ̱̩೩‫̤̱ͤ̀ئ‬ȂńĳϷ̷͈͂ॲ໤
őŊĩĴĪő͉΀ϋΡΕȜθષ͈́ŔłœłĮŔŮŢťĳİĴໝࣣఘࠁ଼ͅ‫۾‬ဓ̳̭̦ͥ͂াऐ̯̹ͦȃ̹͘ȂńĳϷȽŌŅġ ळ༾̤̞̀ͅȂŕňŇϸĲĮŔŮŢťĳİĴࠏ̱̹ͬٚŗņňŇĮłġ ॲ୆̦೩‫̤̱ͤ̀ئ‬Ȃ̭͈ࠫ‫ض‬ġ ŕňŇϸĲͤ͢ͅည൵̯ͦͥळ༾ဋ௢‫ݞ‬͍ζΠςΊσષġŪůġŷŪŵųŰġ‫଼ࠁ࣌ۯ‬ෝ̦ಠ̱̩વ‫̹̯ͦٺ‬ȃ̯ͣͅȂζΠςΊσίρΈȆŪůġŷŪŷŰġࠬ‫ۯ‬૧୆ͺΛΓͼ̤̞̀ͅȂ࿤୆߿ζ;Α‫͍ݞ‬໹‫޼ڲ‬අ։എńĳϷĮŌŐζ;Ά͉ŕňŇϸĲ͉ζΠςΊσඤ͈๷઀ࠬ‫ۯ‬ତͬಠ̱̩௩‫̵̹̯ح‬͈ͅచ̱Ȃඤ๧අ։എńĳϷĮŌŐζ;Ὰ̤̞ͅ๷઀ࠬ‫ۯ‬ତ͈௩‫̹̥̽̈́ͦͣࡉ͉ح‬ȃոષ͈ࠫ‫̥ͣض‬Ȃඤ๧ळ༾ࣞͅ
อ࡛̳ͥńĳϷ͉Ȃ΀ϋΡΕȜθષ́őŊĩĴĪőॲ୆̱ͬٚ̀ŔłœłĮŔŮŢťĳİĴġ ໝࣣఘࠁ଼͂ŔŮŢť‫ͬا଻ڰ‬ଷࢄ̳̭ͥ͂ͤ͢ͅȂŕňŇϸĲĮŔŮŢťĳİĴΏΈ΢σഥోࠏͥࠬ͢ͅ‫ۯ‬૧୆಺୯ͅຈଌ̜̭̦́ͥ͂ྶ̥̹ͣ̈́̽ͅȃŐŃĴĮĳı ŊůũŪţŪŵŪŰůġŰŧġŵũŦġŢűŦŭŪůĮłőŋġŴŪŨůŢŭġŴŸŪŵŤũŦŴġŦůťŰŵũŦŭŪŢŭġŤŦŭŭŴġŧųŰŮġűųŰŭŪŧŦųŢŵŪŷŦġŵŰġ
ŮŢŵŶųŦġŴŵŢŵŦġŪůġűŢŵũŰŭŰŨŪŤŢŭġųŦŵŪůŢŭġŢůŨŪŰŨŦůŦŴŪŴ
ɛ‫֔ڦ‬ġ੓ং ĲĭĳȂ୞‫܃‬ġᅀ‫ ܛ‬ĴȂஜനġ೰ਝ Ĵ
Ĳ ఱिఱ‫ྚڠ‬ြ୽ၞ‫ࢹܥ‬Ȃĳ ఱिఱ‫ڠ‬ఱ‫֭ڠ‬࿪‫شݪࡄڠ‬૰ࠐ࿪ၑ‫ڠ‬ȂĴ ୫ධఱ‫ڠ‬࿪‫ڠ‬໐࿪໤হၷ‫ڠ‬The recruitment of mural cells such as pericytes to patent vessels with an endothelial lumen is a key factor for thematuration of blood vessels and the prevention of hemorrhage in pathological angiogenesis. To date, our understandingof the specific trigger underlying the transition from cell growth to the maturation phase remains incomplete. Since
rapid endothelial cell growth causes pericyte loss, we hypothesized that suppression of endothelial growth factors
would both promote pericyte recruitment, in addition to inhibiting pathological angiogenesis. Here, we demonstratethat targeted knockdown of apelin in endothelial cells using siRNA induced the expression of monocyte
chemoattractant protein-1 (MCP-1) through activation of Smad3, via suppression of the PI3K/Akt pathway. The
conditioned medium of endothelial cells treated with apelin siRNA enhanced the migration of vascular smooth muscle
cells, through MCP-1 and its receptor pathway. Moreover, in vivo delivery of siRNA targeting apelin, which causes
exuberant endothelial cell proliferation and pathological angiogenesis through its receptor APJ, led to increased
pericyte coverage and suppressed pathological angiogenesis in an oxygen-induced retinopathy model. These data
demonstrate that apelin is not only a potent endothelial growth factor, but also restricts pericyte recruitment,
establishing a new connection between endothelial cell proliferation signaling and a trigger of mural recruitment.

䋭 㪈㪊㪏 䋭ŐŃĴĮĳĲ ŉŪŴŵŢŮŪůŦġŪůťŶŤŦŴġŷŢŴŤŶŭŢųġũźűŦųĮűŦųŮŦŢţŪŭŪŵźġţźġŪůŤųŦŢŴŪůŨġţŭŰŰťġŧŭŰŸ
ɛՠྴġࢗ໹ ĲȂೡिġܱ݅ ĲĭĳȂఱ૩ġ߼ٚ ĲȂཱġୃຮ ĲȂ๶ॄġฎ ĲȂఆനġࢨ‫ ݛ‬Ĳĭĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

Ĳ ൐‫ނ‬ఱ‫ڠ‬ఱ‫֭ڠ‬෠‫ڠ‬୆ྵ‫شݪࡄڠش‬਷֓࿪ၑ‫ޗڠ‬৒Ȃĳ ൐‫ނ‬ఱ‫ڠ‬ఱ‫֭ڠ‬෠‫ڠ‬୆ྵ‫شݪࡄڠش‬༶ৣ஌൲໤‫ޗڠش‬৒

会長招待講演 シンポジウム

口頭発表ŐŃĴĮĳĳ ňŭŶŤŰŴŦġťŦűŭŦŵŪŰůġŪŴġŦŴŴŦůŵŪŢŭġŧŰųġŵũŦġńœĮŮŦťŪŢŵŦťġŢŤŵŪŷŢŵŪŰůġŰŧġŤŢųťŪŢŤġŢůŨŪŰŨŦůŦŴŪŴġ
ŢůťġŢŶŵŰűũŢŨź

特別講演[Objective]Histamine is a major mediator of allergic inflammation which is released from mast cells. Although
histamine is well-known to increase vascular permeability, its precise mechanism remains unknown. In this study, weinvestigated the mechanism of histamine-induced vascular hyper-permeability both in vivo and in vitro. [Methods andresults] Administration of histamine to mouse ears induced tissue swelling and increased vascular permeability indexed
as a leakage of intravenously injected dye. Pretreatment with a H1 receptor antagonist diphenhydramine but not a H2
receptor antagonist cimetidine inhibited the histamine-induced hyper-permeability. Intravital imaging showed that
histamine or a H1 agonist pyridylethylamine relaxed ear artery and vein, increased blood flow and induced hyperpermeability. Consistently, pretreatment with a nitric oxide synthesis inhibitor L-NAME or a vasoconstricting
substance phenylephrine abolished the histamine-induced blood flow increase and vascular hyper-permeability. In
isolated rat mesenteric artery, histamine dose-dependently induced endothelium-dependent relaxation. Pretreatment
with diphenhydramine or L-NAME blocked this relaxation suggesting that histamine stimulates NO production by
activating endothelial H1 receptor. We next examined the effect of histamine on endothelial barrier formation. In
isolated bovine aortic endothelial cells, histamine enhanced barrier formation indexed as an increase in transendothelial
electrical resistance. Pretreatment with cimetidine, or a protein kinase A (PKA) inhibitor blocked the histamineinduced endothelial barrier enhancement.[Conclusion] We here revealed that H1 receptor-mediated NO production inendothelial cells and subsequent blood flow increase are responsible for histamine-induced vascular hyperpermeability. We also showed that histamine-H2 signaling enhances endothelial barrier function via PKA-activationand thus partially inhibits histamine-induced vascular hyper-permeability.[Footnote] This work is supported by
Programme for Promotion of Basic and Applied Researches for Innovations in Bio-oriented Industry.

ɛ໲লġ઎ဎȂा൐ġణঊȂେ຃ġ୒५Ȃ୼ଳġহढȂ२֔ġൡঊȂ৒ࡔġཅྶ䋭 㪈㪊㪐 䋭著者索引

[BACKGROUND] Calorie restriction (CR) has been demonstrated to exert various cardioprotective effects; however,it remains unclear whether #1 CR may modulate cardiac angiogenesis in response to heart failure, #2 which may be theessential nutrient factor(s) that is responsible for the CR-mediated enhanced cardiac angiogenesis, and #3 theunderlying molecular mechanism(s). [METHODS] Pressure overload (2 weeks)-induced heart failure model was
generated by transaortic constriction (TAC) in mice and randomly allocated to a 4-week CR (TAC-CR and sham-CR)
and ad libitum (TAC-AL and sham-AL) groups, and analyzed at the age of 18 week-old. Cultured endothelial cells(ECs) were divided into 4 groups that exposed to culture media of control, glucose-depleted, amino acid-depleted, andserum-depleted condition, respectively. [RESULTS] Immunohistochemical analyses revealed that CR enhanced
cardiac angiogenesis in TAC mice. CR promoted increased in myocardial cyclic AMP concentration with concomitant
PKA/AMPK/eNOS activation and the simultaneous increase in autophagic activity both in TAC hearts. Of note,cardiac Akt activity remains unchanged by CR. In vitro analysis revealed that glucose depletion, as well as forskolin(10ЂM) and 8-bromo-cyclic AMP (1 mM), activated PKA/AMPK axis thereby facilitated angiogenesis and autophagy
assessed by LC3 turnover assay and changes in autophagy markers (p62, Beclin1) in ECs. The enhanced in vitro
angiogenesis induced by glucose depletion and PKA enhancers was abrogated by autophagy inhibitor 3-MA treatment.
PKA inhibitors (H89 and RP-cAMP) abrogated the increase in AMPK/eNOS phosphorylation levels induced by glucose
depletion. Neither amino acid- nor serum-depletion had no effect on angiogenesis and autophagy.[CONCLUSIONS]
Glucose depletion is essential for the CR-mediated activation of cardiac angiogenesis and autophagy in acAMP/PKA/AMPK-dependent fashion.

ポスター発表 ＹＩＡ選考発表ྴࡣ‫ؚ‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬ŐŃĴĮĳĴ œŦŨŶŭŢŵŪŰůġŰŧġŦŏŐŔġŮœŏłġŴŵŢţŪŭŪŵźġŷŪŢġœŐńŌĳĮŮŦťŪŢŵŦťġŦņŇĲłĲġűũŰŴűũŰųźŭŢŵŪŰů
ɛ࿤‫ۼ‬ġ࡚ආ ĲȂᎢ֔ġ൫ဎ ĳȂōŪŢŰġŋŢŮŦŴ ĴȂ൐ġࢨ૾ Ĳ
Ĳ ࢩോఱ‫ࡔڠ‬บ༶ৣ஌֓‫ݪࡄڠش‬ਫ਼ΊΦθવ‫ٺ‬ພၑࡄ‫ݪ‬໦࿤Ȃĳ ࣭ၛ࣭ष֓ၷΓϋΗȜພ֭੏۪‫ܕ‬ඤ‫ش‬ȂĴ ŔŦŤŵŪŰůġŰŧġńŢųťŪŰŭŰŨźĭġŖůŪŷŦųŴŪŵźġŰŧġńũŪŤŢŨŰġŎŦťŪŤŢŭġńŦůŵŦų

Ⱥ෸ࠊȆ࿒എȻࠬ‫ۯ‬ඤ๧‫ܥ‬ෝવ‫ٺ‬Ȃ̳̻̈́ͩඤ๧ळ༾̤̫ͥͅŦŏŐŔͥ͢ͅŏŐॲ୆͈೩‫̀̽͢ͅئ‬ෞ૤ࠬ‫ۯ‬৖͉ۛอછȂૺജ̳̭̦ͥ͂౶̞ͣͦ̀ͥȃ༷֚ȂœŐńŌͥ͢ͅŦŏŐŔġ Ůœŏłġ ŴŵŢţŪŭŪŵź͈೩‫ͬئ‬̱̹ٚŦŏŐŔอ࡛ଷࢄ͈મळ
̈́‫ܥ‬੬͉ྶ̥͉̞ͣ́̈́ȃड߃ȂŦŶŬŢųźŰŵŪŤġ ŦŭŰůŨŢŵŪŰůġ ŧŢŤŵŰųġ ĲĮϷĲġ ĩŦņŇĲłĲĪ̦ŦŏŐŔġ Ůœŏł͈ĴĨĮŖŕœࣣ̳̭͂ࠫͥ͂̽̀͢ͅŦŏŐŔġ Ůœŏłġ ŴŵŢţŪŭŪŵźͬ೩‫̵̦̭̯͂ͥئ‬༭̯̹࣬ͦȃِࣽٝș͉Ȃ
œŐńŌĲ̹͉͘œŐńŌĳͥ͢ͅŦņŇĲłĲ͈‫ͬا଻ڰ‬̱̹ٚŦŏŐŔġŮœŏłġŴŵŢţŪŭŪŵź͈ଷࢄ̞̾̀ͅ࠿൦̱Ȃ̹֒͘ഥঊ٨་ζ;Αͬဥ̞̹ŪůġŷŪŷṲ̫̋ͥͅœŐńŌͺͼΕέ΁ȜθĩœŐńŌĲ̤͍͢œŐńŌĳĪ͈࿨‫࠿̞̀̾ͅڬ‬൦̱̹ȃȺ༹༷Ȇࠫ‫ض‬ȻńłĮœŐńŌĲ̤͍͢ńłĮœŐńŌĳͤ͢ͅňŔŕĮŦņŇĲłĲ͉ςϋॸ‫̯ͦا‬ȂńłĮœŐńŌĳͥ͢ͅςϋॸ‫͈ا‬೾ഽ̦ခփ̥̹ࣞ̽ͅȃŦŏŐŔġ Ůœŏł͈ĴĨĮŖŕœ̤̫ͥͅŦņŇĲłĲ͈૶გ଻͉ńłĮœŐńŌĳͤ͢ͅ௩‫̹̯ͦޑ‬ȃŉŖŗņń̤̫ͥͅœŐńŌஷ‫ٺ‬सέ͹Αΐσ
͈ൎဓ͉́ȂŦņŇĲłĲ͈อ࡛ͅ་‫̦̹̥͉̽̈́ا‬ȂŦņŇĲłĲ͈ςϋॸ‫͉ا‬ஷ‫̹̯ͦٺ‬ȃœŐńŌĲĬİĮ̤͍͢œŐńŌĳĬİĮ
ζ;Αͤ͢෽ူ̯̹ͦඤ๧ळ༾̤̞̀ͅȂœŐńŌĳĬİĮ̦œŐńŌĲĬİĮ͂๤̱̀ȂœŐńŌĲĬİĮ̦Řŕ͂๤̱̀ခփͅ
ŦŏŐŔอ࡛͈௩‫̹͛෇ͬح‬ȃ̹͘ȂœŐńŌĳĬİĮ̤̫ͥͅŦŏŐŔġ Ůœŏłġ ŴŵŢţŪŭŪŵź̦Řŕ͂๤̱̀ခփ̥̹ࣞ̽ͅȃً֚଻ಎఱෞ൲ྤ໾णκΟσ̤̫ͥͅ࠿൦͉́ȂŘŕ͂๤̱̀œŐńŌĳĬİĮ̤̞̀ͅࢸणႀ֖͈೩‫̦̹͛෇ͬئ‬ȂŦŏŐŔĮİĮ
͂ŦŏŐŔĮİĮœŐńŌĳĬİĮ‫͉́ۼ‬ခփओ͉෇̥̹͛̈́̽ȃȁȺࠫაȻœŐńŌĳͥ͢ͅŦņŇĲłĲ͈ςϋॸ‫ͬا‬̱̹ٚŦŏŐŔġ
Ůœŏłġ ŴŵŢţŪŭŪŵź͈ଷࢄ̦া̯̹ͦȃඤ๧‫ܥ‬ෝવ‫֦ࡏܓۍ̳ͥܳৼͬٺ‬ঊȂࢩไ̈́૤ࠬ‫ۯ‬৖ۛͅచ̱̀œŐńŌĳ̦૧̹̈́হၷດഎ̈́ͤͅංͥ‫خ‬ෝ଻̦াऐ̯̹ͦȃŐŃĴĮĳĵ ྫࠬୄඵষࡓౙ௄෽ူͥ͢ͅΪΠ ŪőŔ ळ༾̥͈ͣࣞ࢘ၚࣞਓၾ̈́ඤ๧ळ༾໦‫ا‬ည൵༹ɛ‫ܜ‬࿤ġ‫ ܧ‬ĲĭĳȂੵུġ‫ם‬၌ ĲĭĳȂ‫֔܃‬ġࢴ ĳȂධ༷ġࡊඵ ĳȂ౻നġ݅ ĳȂाനġၦ௮ ĳȂ५‫ئ‬ġ੕ Ĳ
Ĳ ńŦůŵŦųġŧŰųġŪőŔġńŦŭŭġœŦŴŦŢųŤũġŢůťġłűűŭŪŤŢŵŪŰůġĩńŪœłĪȂ‫ނ‬സఱ‫ڠ‬Ȃ‫ނ‬സȂ
ĳ ૤௫ࠬ‫شٸۯ‬Ȃ‫ނ‬സఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬Ȃ‫ނ‬സȺ෸ࠊȻΪΠ૽ࢥఉෝ଻ۚĩŪőŔĪळ༾ͬठ୆֓ၷ͞৖ۛκΟσͅ؊ဥ̳̹ͥ͛࢘ͅၚഎ̈́໦‫ا‬ည൵̵༹͉̥̞ࠧ̈́ȃِș͉̭ͦ́͘ͅȂζ;Αఉෝ଻ۚळ༾̤̞̀ࠬͅ‫ۯ‬ඤ๧ळ༾௩૓֦ঊȪŗņňŇȫ਋ယఘĮˎု଻͈ಎ᥷ဩळ༾ͬ‫ވ‬೒͈ஜߐळ༾̱̹͂૤ࠬ‫ࠏۯ‬ळ༾͈ࠏൡഎ໦‫ا‬ည൵༹̞̾̀ͅ༭̧̱̹࣬̀ȃŗņňŇ͉ඤ๧ळ༾͈໦‫ͅا‬ຈଌ̜́ͤȂĹĮţųŰŮŰġ ŤźŤŭŪŤġ ŢťŦůŰŴŪůŦġ ŮŰůŰűũŰŴűũŢŵŦġ ĩŤłŎőĪ̷͉͈࢘‫ͬض‬௩‫̭̳͂ͥ͜ޑ‬া̱̹ĩŃŭŰŰťĭġ ĳııĺఈĪȃ̹͘ȂΪΠŪőŔळ༾̤̞͉̀ͅōŢŧŭŢŮŮŦ͈ͣඵষࡓౙ௄ࣞྟഽ૤޼ည൵༹ͬ͂͜ͅȂ࢘ၚ͂ਓၾͬ٨஝̱̹૤޼ည൵༹ͬ༭࣬
̧̱̹̀ġ ĩőōŰŔġ ŐůŦĭġ ĳıĲĲĪȃ஼༷͈ࠫ‫̞̀̿ܖͅض‬ȂΪΠŪőŔळ༾ဇြಎ᥷ဩळ༾ͅŗņňŇ͂ŤłŎőͬैဥ̵̯̭ͥ
͂ͤ͢ͅȂඤ๧ळ༾໦‫͈࢘ا‬ၚ‫ͬا‬দ͙̹ȃȺ༹༷ȻΪΠŪőŔळ༾͈ඵষࡓౙ௄෽ူࠏ̤̫ͥͅಎ᥷ဩळ༾ည൵‫ͅܢ‬ȂŗņňŇ͂ŤłŎőͬෛഽ‫಺ͬۼܢ͍ݞ‬୯̱̾̾ैဥ̵̯Ȃ໦‫ا‬ည൵˕඾࿒ͅŇłńŔͬဥ̞̀ࠬ‫ۯ‬ඤ๧΃ΡΰςϋĩŗņĮńŢťũŦųŪůĪု଻ळ༾ͬ௶೰̱ඤ๧ळ༾̱̹͂ȃȺࠫ‫ض‬Ȼ
໦‫ا‬ည൵ː඾࿒ͤ͢ŗņňŇġȪĲııůŨİŮŭȫͬȂːȽ˒඾࿒ͅŤłŎőġ
ȪĲŮŎȫͬ‫̢̦߲̹ح‬ड࢘͜ၚഎ̜́ͤȂŗņňŇౙඊൎဓ߲͞๱ൎဓ߲͂๤‫̱̀ڛ‬ඤ๧ळ༾ည൵ၚ͉ࣞ౵̜̹́̽
ȪĶķįĳȾĲĳįĶĦġ ŷŴġ ĲĲįĹȾĸįĳĦȪŗņňŇౙඊȫġ ŷŴġ ĳįĴȾĳįĵĦȪ๱ൎဓȫȂőľıįııııĲĸȂůľĵȫȃည൵ඤ๧ळ༾ତ͜൳အ͈ࠫ‫́ض‬̜̹̽ȪĲįĸķȾıįĸıȿĲı ĶġŷŴġĵįĺȾĴįĴȿĲı ĵġŷŴġĺįĹȾĲıįĵȿĲıĴġळ༾ İ ŤŮĳĭġőľıįııĳĳĭġůľĵȫȃུ໦‫ا‬ည൵˕඾࿒ͅŗņĮńŢťũŦųŪůု଻ळ༾ͬŇłńŔ੗‫̱ا‬Ȃ੗ഽĺĺĦոષ͈ඤ๧ळ༾̦ං̹ͣͦĩıįĸĺȾıįĴĶĭġˍŪőŔळ༾̥͈ͣඤ๧ळ༾ତĭġůľķĪȃ
̯ͣͅȂķ඾࿒ͅŗņňŇ਋ယఘĮˎု଻ಎ᥷ဩळ༾ͬŇłńŔ੗‫ا‬Ȇठ෽ူً̳ͥ೾ͬ‫̢̭ͤ͂ͥ͢ͅح‬Ȃ੗ഽĺĺĦոષ́ĺ඾࿒͈ਓၾ̦࿩ĵ෼٨஝̱̹ĩĴįĲĳȾıįĵĹĭˍŪőŔळ༾̥͈ͣඤ๧ळ༾ତĭġůľĵĪġĩőľıįıııĺķĪȃ
ȺࠫࢊȻΪΠŪőŔळ༾ͬဥ̞
̹ྫࠬୄౙ௄ඵষࡓ෽ူͥ࢘͢ͅၚഎ́ࣞਓၾ̈́ඤ๧ळ༾ည൵༹ͬ‫ږ‬ၛ̱̹ȃࠬ‫ͬۯ‬ດഎ̱̹͂ठ୆֓ၷ͞৖ۛκΟσͬဥ̞̹஻࿪ࡄ‫̫̤ͥͅݪ‬ခབ̈́ܿ੅‫ܖ‬๕̈́ͥ͂ͅࣉ̢ͣͦͥȃ䋭 㪈㪋㪇 䋭ŐŃĴĮĳĶ ŊůũŪţŪŵŪŰůġŰŧġőĳřĸġųŦŤŦűŵŰųġŴŪŨůŢŭŪůŨġűųŰŮŰŵŦŴġŢťŷŦųŴŦġŤŢųťŪŢŤġųŦŮŰťŦŭŪůŨġŢŧŵŦųġ
ŮźŰŤŢųťŪŢŭġŪůŧŢųŤŵŪŰůġŵũųŰŶŨũġŦůũŢůŤŦťġŤŢųťŪŢŤġŧŪţųŰţŭŢŴŵġŮŪŨųŢŵŪŰů

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛߧ౓ġખ໹Ȃಎ५ġฎ෗Ȃ‫ݠ‬ზġ઎࢕Ȃ࿉၌ġ࿻๼Ȃ൥๶ġ঴

口頭発表ŐŃĴĮĳķ ŎŖœńġųŦŨŶŭŢŵŦŴġœũŰİœŐńŌġŴŪŨůŢŭŪůŨġŪůġŷŢŴŤŶŭŢųġŴŮŰŰŵũġŮŶŴŤŭŦġŤŦŭŭŴġŢůťġŮŦťŪŢŵŦŴġ
ŵũŦġťŦŷŦŭŰűŮŦůŵġŰŧġűŶŭŮŰůŢųźġŢųŵŦųŪŢŭġũźűŦųŵŦůŴŪŰů

会長招待講演 シンポジウム

Background: P2X7 receptor (P2X7R) is a member of the P2X receptor family which is comprised of ligand-gated ionchannels. P2X7R is mainly expressed on macrophages and monocytes and activated by ATP and cathelicidin
antimicrobial peptide (CAMP). ATP/P2X7R has been thought to be involved in proinflammatory signaling throughinflammasome activation. However, the long-term effects of P2X7R signaling inhibition on cardiac remodeling after
myocardial infarction (MI) remain to be elucidated. Objective: To identify the physiological role of P2X7R signaling
in progression of cardiac remodeling after MI. Methods and Results: MI was generated by ligating the left coronary
artery in mice. P2X7R expression was upregulated in hearts from day 4 to day 14 after MI. To determine the functionalrole of P2X7R in heart, we generated MI in control or P2X7R knockout (KO) mice. Importantly, deficiency of P2X7R
aggravated fibrosis (control; 32.4Ⱦ11.0%, P2X7R KO; 57.4Ⱦ9.6%, n=6-7, p<0.01) and cardiac dysfunction(fractional shortening: control; 37.6Ⱦ8.3%, P2X7R KO; 24.8Ⱦ11.4%, n=6-7, p<0.05) at day 14 after MI. To
elucidate the underlying mechanism of protective effect caused by P2X7R after MI, we investigated the inflammasome
activation in P2X7R null mice. However, there were no differences in ASC expression, caspase-1 activity and IL-1ϸ
expression after MI between control and P2X7R KO mice. On the other hand, we observed sustained upregulation of
CAMP, a well-known agonist of P2X7R, in hearts after MI. In vitro experiments revealed that treatment with LL37, ahuman homologue of CAMP, decreased migration distances of cardiac fibroblasts assessed by wound healing assay.
Moreover, ablation of P2X7R abrogated LL37-mediated inhibition of cardiac fibroblast migration. Conclusion:
CAMP-P2X7R signaling plays cardioprotective roles in the suppression of cardiac remodeling after MI via inhibitionof cardiac fibroblast migration. Thus, CAMP-P2X7R signaling could be a novel therapeutic target for heart failure
after MI.

特別講演ఱिఱ‫ڠ‬ఱ‫֭ڠ‬࿪‫شݪࡄڠ‬ႉ઄࿪ٜ࢘ଢ଼‫ڠ‬໦࿤ɛಎୌġೄ຃Ȃ઀ࠁġ‫ۘڡ‬Ȃ‫୼ݠ‬ġࢼఊ჊Ȃᚰ‫ؖ‬ġഓ჊Ȃ‫܃‬५ġંਏȂષ५ġ౶ࡨ䋭 㪈㪋㪈 䋭著者索引

[Background] Pulmonary arterial hypertension (PAH) is a progressive disease associated with a poor prognosis. The
Rho/ROCK pathway has been suggested to be associated with PAH. Deficiency of caveolin-1 (Cav1) enhances RhoA activity
and causes PAH. Mutations in Cav1 are also associated with PAH. MURC/Cavin-4, a fourth member of the cavin family which
regulates caveolar formation and function together with caveolins, regulates the Rho/ROCK pathway in cardiomyocytes.
However, the role of MURC in RhoA signaling in vascular smooth muscle cells (VSMCs) and the development of PAH
remains unknown.
[Methods and Results] In a model of chronic normobaric hypoxia, MURC-knockout (MURC-/-) mice exhibited attenuation of
hypoxia-induced PAH and vascular remodeling compared with wild-type (WT) mice. VSMCs isolated from MURC-/- mice had
reduced RhoA activity, proliferation and migration, while MURC overexpression in VSMCs enhanced them. MURC-induced
proliferation and migration were inhibited by a ROCK inhibitor. We further examined the relationship between MURC andCav1 on RhoA signaling. Overexpression of Cav1 suppressed RhoA activity in VSMCs and Cav1 was associated with theactive form of GϷ13 (GϷ13-GTP), suggesting that the association of Cav1 with GϷ13 inhibits GϷ13-mediated RhoA
signaling. Cav1-mediated suppression of RhoA activity was reversed by MURC overexpression. MURC bound to Cav1 anddecreased the binding of Cav1 to GϷ13-GTP, which facilitated the association of GϷ13-GTP with p115RhoGEF. Furthermore,both of MURC and GϷ13 were associated with the scaffolding domain of Cav1. These findings suggest that MURC
competitively inhibits the interaction of Cav1 with GϷ13, thereby activating RhoA signaling.
[Conclusions] Absence of MURC attenuates PAH with suppressed vascular remodeling. MURC regulates proliferation andmigration through the Rho/ROCK pathway in VSMCs. MURC is associated with Cav1, which induces GϷ13-mediatedactivation of Rho signaling. Our findings provide novel insight into the mechanisms of caveola-mediated Rho/ROCK signaling
in the development of PAH.

ポスター発表 ＹＩＡ選考発表‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬ŐŃĴĮĳĸ ŎŖœńİŤŢŷŪůĮĵġũŢŴġŢġűųŰŵŦŤŵŪŷŦġųŰŭŦġŪůġŵũŦġűųŰŨųŦŴŴŪŰůġŰŧġŢţťŰŮŪůŢŭġŢŰųŵŪŤġŢůŦŶųźŴŮ
ɛ‫୼ݠ‬ġࢼఊ჊Ȃ઀ࠁġ‫ۘڡ‬Ȃಎୌġೄ຃Ȃᚰ‫ؖ‬ġഓ჊Ȃ‫܃‬५ġંਏȂષ५ġ౶ࡨ‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬[Background] Abdominal aortic aneurysm (AAA) is a relatively common disease in the elderly population. MURC
(muscle-restricted coiled-coil protein)/cavin-4 is localized to caveolae in muscle cells. Deficiency of caveolin-1, a
critical component of caveolae, has been shown to be protective against atherosclerosis. Although mutations in MURC
have been identified in patients with dilated cardiomyopathy, a role of MURC in vascular smooth muscle cells(VSMCs) and AAA remain unknown.
[Methods & Results] To examine the role of MURC in AAA, we subjected wild-type (WT) and MURC knockout(MURC-/-) mice to a model of AAA induced by periaortic application of CaCl2. After 6 weeks of CaCl2 treatment, theinternal aortic diameter was significantly increased in MURC-/- mice compared with WT mice. Measurement of theexternal aortic diameter after perfusion fixation also showed an increase in MURC-/- mice compared with WT mice.
Fibrosis and cell infiltration of the tunica media were increased in CaCl2-treated MURC-/- mice compared with CaCl2treated WT mice. The dilation of the aorta in CaCl2-treated MURC-/- mice was accompanied by disruption of the elastic
lamellae. The activation of JNK was suppressed in CaCl2-treated MURC-/- mice compared with CaCl2-treated WT
mice. Since MURC is expressed only VSMCs in the aorta, we then examined the role of MURC in VSMCs. MURC-/VSMCs showed suppression of fetal bovine serum (FBS)-induced proliferation and migration, which wereaccompanied by reduced RhoA activity. Furthermore, MURC knockdown in VSMCs suppressed TNF-Ϸ-induced JNK
activation and FBS-induced proliferation and migration. Overexpression of MURC in VSMCs induced RhoA activation,
proliferation, and migration. MURC-induced proliferation and migration were inhibited by a ROCK inhibitor.
[Conclusion] Deficiency of MURC deteriorates AAA accompanied by disruption of the elastic lamellae, which islikely attributable to reduced proliferation and migration of VSMCs. Our findings indicate that MURC plays aprotective role in the progression of AAA.

ŐŃĴĮĳĹ ๬ྖζ;Α͈ࣸ‫׶͉́޼ڒ‬છ଻ౙ‫̦ݩ‬௩‫ۯ̱ࠬح‬൫ً଻̦ᄤૺ̱̞̀ͥ
ɛ଩നġ੗֚ ĲȂୌఆġ౺ ĲĭĳȂ઀৒ġ଼֚ Ĳ
Ĳ ൐‫ނ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ش‬Ȃĳ ΏΑΞθ৖ۛ୆ྵ‫୶ͥ͢ͅڠش‬౤֓ၷܿ੅‫ٳ‬อ‫ݶ‬തȺ࿒എȻͼϋΑςϋ͈৽ါດഎ௫‫̱̀͂ܕ‬۴௫͂ࣸ‫̬ͥͦͣݷ̦޼ڒ‬ȃِș͉Έσ΋ȜΑ͈डఱક๯௫‫ڒ̜ࣸͥ́ܕ‬޼ͅಕ࿒̱̀ພఠٜྶͬૺ̹͛ȃ๬ྖ͞ˎ߿ൠෂພ̤̞͉̀ͅȂͼϋΑςϋͥ͢ͅ࿉ळࠬ‫ۯ‬ນ࿂ୟ͈௩‫͍ࠬݞح‬ಎ̥ͣࣸ‫ۼ޼ڒ‬ৗ͈͒ͼϋΑςϋ֊࣐̦વ‫̦̭̞̯͂ͥ̀ͦٺ‬ঐഊ̯̞ͦ̀ͥȃ̷̭́Ȃِș͉ඵ࢕ঊτȜΎȜࡐ๷‫ͬޢ‬ဥ̞̀ࣸ‫ܥ޼ڒ‬ෝ։ુ͂ͼϋΑςϋ೷ࢯ଻͈‫ͬ߸۾‬ٜଢ଼̱̹ȃȺ༹༷Ȼඵ࢕ঊτȜΎȜࡐ๷‫ͬޢ‬ဥ̞̹୆ఘͼιȜΐϋΈͤ͢ͅຽ೒૙ζ;Α͂ࣞডཛ૙໅‫ك‬ζ;Α͈୆ఘඤ͈޼ර௨ͬ۷ख़̱̹ȃࣸ‫޼ڒ‬ಎ͈ࠬ‫ۯ‬ඤ͂‫ۼ‬ৗಎ͈ŇŊŕń͈ܵഽͬ๤‫̭̳̀̽͂ͥ͢ͅڛ‬Ο΅ΑΠρϋ͈֊࣐ͬບ‫̹̱ث‬ȃষͅȂࠬ‫ۯ‬൫ً଻ͅచ̳ͥ‫׶‬છ͈‫۾‬ဓͬ࠿൦̳̹ͥ͛ȂŕŏŇĮϷ‫͍ݞ‬ŊōĮķͬൎဓ̱̀ࠬ‫ۯ‬൫ً଻ͬບ‫̹̱ث‬ȃ๬ྖພఠ̤̞̀ͅডཛழ૕͂൳အࣸͅ‫ॸ଻ڰ́͜޼ڒ‬ளਅ͈ॲ୆ᄤૺ̦෇̥͛ͣͦͥͬ಺͓̹ͥ͛Ȃ‫ॸ଻ڰ‬ளਅͼϋΟͻΉȜΗȜͬဥ̞̀ࣸ‫ۼ޼ڒ‬ৗಎ͈‫ॸ଻ڰ‬ளਅ͈ॲ୆ၾͬ
ບ‫̹̱ث‬ȃ̯ͣͅȂࣸ‫̫̤ͥͅ޼ڒ‬྾‫ע‬Ȇ‫׶‬છ଻ळ༾͈‫۾‬ဓͬζσΙ΃ρȜ͈έυȜ΍ͼΠιΠςȜٜͤ͢ͅଢ଼̱̹ȃȺࠫ‫ض‬Ȼࣸ‫ۼ̞̤̀ͅ޼ڒ‬ৗ̦‫خ‬ণ‫̯ͦا‬Ȃࠬಎ̥ͣ‫ۼ‬ৗ͈͒ŇŊŕńດেΟ΅ΑΠρϋ͈֊࣐̦۷ख़̯̹ͦȃࣞডཛ૙໅
‫ك‬ζ;Α͈࠿൦͉́Ȃຽ೒૙ζ;ᾼ๤͓̀‫ۼ‬ৗ͈͒Ο΅ΑΠρϋ͈֊࣐̦ᄤૺ̱̞̹̀ȃ̹͘ȂŕŏŇĮϷͬൎဓ̳ͥ
̭͂̽̀͢ͅခփͅΟ΅ΑΠρϋ͈֊࣐͈ᄤૺ̦۷ख़̯̹ͦĩűɃıįıĶĪȃࣞডཛ૙໅‫ك‬ζ;Ά͉Ȃຽ೒૙ζ;ᾼ๤͓̀ࣸ‫ۼ޼ڒ‬ৗಎ͈‫ॸ଻ڰ‬ளਅ͈ॲ୆ᄤૺ̦෇̹͛ͣͦȃέυȜ΍ͼΠιΠςȜ͈ࠫ‫ض‬Ȃࣞডཛ૙໅‫ك‬ζ;Ά͉ࣸ‫޼ڒ‬ಎͅౙ‫͈ݩ‬௩‫ͦͣ͛෇̦ح‬Ȃळ༾ນ࿂ζȜ΃Ȝٜͬଢ଼̱̹̭͂ͧȂńŅĲĲţĩĬĪōźķňĩĬĪōźķńĩĬĪ͈‫׶‬છ଻ζ·υέ͹Ȝΐ̜̹́̽ȃȺࠫაȻࣸ‫ۼ͈޼ڒ‬ৗ͈‫خ‬ণ‫ͤ͢ͅا‬୆ఘඤ́‫ۼ‬ৗ‫ܥ‬ෝͬບ‫خ̦̭̳͂ͥث‬ෝ̹̈́̽ͅȃ๬ྖພఠ͉́ࣸ‫޼ڒ‬ಎ͈ࠬ‫ۯ‬൫ً଻̦ᄤૺ̱̤̀ͤȂ‫׶‬છ଻ळ༾͈௩‫ܥ̷͈̦ح‬੬ͅ‫۾‬ဓ̳ͥ͂ࣉ̢̹ͣͦȃ๬ྖພఠ͉́ͼϋΑςϋͥࣸ͢ͅ‫޼ڒ‬ಎ͈࿉ळࠬ‫ۯ‬ນ࿂ୟ௩‫̦ح‬વ‫̤̯ͤ̀ͦٺ‬Ȃయੲഎࠬͅ‫ۯ‬൫ً଻̦ᄤૺ̱̞̀ͥ͂ࣉ̢̹ͣͦȃ䋭 㪈㪋㪉 䋭ŐŃĴĮĳĺ œŰŭŦġŰŧġűŢŵũŰŨŦůġųŦŤŦűŵŰųĮŮŦťŪŢŵŦťġůŰůĮŪůŧŦŤŵŪŰŶŴġŪůŧŭŢŮŮŢŵŪŰůġŪůġŤŢųťŪŢŤġŢťŢűŵŪŷŦġ
ųŦŴűŰůŴŦġŵŰġűųŦŴŴŶųŦġŰŷŦųŭŰŢť

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛ൐ཆġࢫ౺ ĲȂऎനġଽၦ ĳȂ઀৒ġ଼֚ Ĳ

会長招待講演 シンポジウム

口頭発表

Background: Inflammation is induced in the heart during the development of cardiac hypertrophy. The initiating
mechanisms and the role of inflammation in cardiac hypertrophy, however, remain unclear. This study was performed
to clarify the role of non-infectious inflammation mediated by pathogen receptors in cardiac hypertrophy.
Methods AND Results: At 2 weeks after transverse aortic constriction (TAC), Toll-like receptor-2 knockout(TLR2KO) mice showed reduced cardiac hypertrophy and fibrosis with more left ventricular dilatation and impaired
systolic function compared with wild-type mice, which indicated impaired cardiac adaptation in response to pressure
overload in TLR2KO mice. Inflammatory responses were suppressed in TLR2-deleted hearts compared with those inwild-type hearts after TAC. Bone marrow transplantation experiment revealed that TLR2 expressed in the heart, but
not in bone marrow-derived cells, is important for cardiac adaptive response to pressure overload. In vitro experiments
demonstrated that TLR2 signaling can induce cardiomyocyte hypertrophy, and fibroblast and vascular endothelial cellproliferation through nuclear factor ЀB (NF-ЀB) activation and interleukin-1ϸ (IL-1ϸ) upregulation. Systemic
administration of an NF-ЀB inhibitor or anti-IL-1ϸ antibodies to wild-type mice resulted in impaired adaptive
cardiac hypertrophy after TAC. Besides, genetic disruption of NLRP3, which is one of pathogen receptors and plays animportant role in the generation of active IL-1ϸ through the catalytic activation of caspase-1, resulted in impaired
cardiac adaptive response to pressure overload. We also found that heat shock protein 70 (HSP70), which wasincreased in murine plasma after TAC, can activate TLR2 signaling in vitro and in vivo. Systemic administration ofanti-HSP70 antibodies to wild-type mice suppressed inflammatory responses in the heart and impaired adaptive cardiac
hypertrophy after TAC.
Conclusions: Pathogen receptor-mediated inflammation contributes to adaptive cardiac hypertrophy in response topressure overload. Thus, modulation of signaling pathway of pathogen receptors may provide a novel strategy fortreating cardiac hypertrophy and heart failure.

特別講演

Ĳ ൐‫ނ‬ఱ‫ڠ֓ڠ‬໐້௺ພ֭੏۪‫ܕ‬ඤ‫ش‬Ȃĳ ඃോఱ‫ڠ‬ఱ‫֭ڠ‬ΰσΑΨͼ΂΍ͼ΀ϋΑࡄ‫ݪ‬໐੏۪‫ܕ‬ඤ‫ڠش‬

ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪈㪋㪊 䋭䋭 㪈㪋㪊 䋭

プログラムలĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

特別講演
会長招待講演 シンポジウム

ポスター発表口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪇㪇㪇 䋭ĺ࠮ĳķ඾Ȫ࿐ȫġĲĲĻĲıȡĲĲĻĴĶġġεΑΗȜٛાεΑΗȜġႉ઄ őńĲȶࠬ‫ۯ‬૧୆Ȇठ୆হၷȟൠෂພࣣ͂໵છȷ

őńĲĮĲอో‫ܢ‬෹༾๷઀੏۪ࠏવ‫̷͈͂ٺ‬ٝ໘ً೾̤̫ͥ֒ͅഥঊอ࡛͈་‫ا‬ȡłůŨŪŰűŰŪŦŵŪůĮĲ ͉อో‫͈ܢ‬෹༾๷઀੏۪ࠏવ‫ͬٺ‬٨஝̵̯ͥȡプログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛಎୌġਜ຃ ĲȂཤࡔġਜহ ĳȂ‫֔݌‬ġྶ඾ࣝ ĳȂ֔ષġ࣠ ĴȂఱᚧġ‫ ܧ‬ĴĴ ൐‫ނ‬ఱ‫୶ڠ‬౤‫ݪࡄ੅ܿڠش‬ΓϋΗȜȺ࿒എȻࣞෛഽॸளൎဓ֚ͤ͢ͅ౞ੱ‫ͬٺ‬਋̫̹อో‫͈ܢ‬෹͉Ȃಿ‫̹ͤͩͅܢ‬෹༾๷઀੏۪ࠏ͈։ુͬ෇̭͛ͥ͂ͬ
లĲĺٝࠬ‫ۯ‬୆໤‫ڠ‬ٛȪ൐‫ނ‬ȫ́༭̱̹࣬ȃ̷͈ࣽٝੱ‫͍̤͢ٺ‬ٝ໘ً೾ͅ‫֒ͥͩ۾‬ഥঊอ࡛̞̾̀ͅζͼ·υͺτͼ

特別講演

Ĳ ൐‫ނ‬੫ঊ֓‫ش‬ఱ‫ڠ‬༦ঊ௙ࣣ֓ၷΓϋΗȜ૧୆঱໐࿝Ȃĳ ൐‫ނ‬੫ঊ֓‫ش‬ఱ‫ڠ֓ڠ‬໐ٜཎ‫ڠ‬Ȇอ୆୆໤‫࣒ڠ‬जȂͤ͢ͅ࿌္എٜͅଢ଼̱Ȃࠬ‫ۯ‬૧୆Ȇࠁ଼ͅਹါ̈́࿨‫ͬڬ‬঵̾֒ഥঊͬ࠿൦̱̹ȃȺऺၳ༹༷͂ȻŊńœζ;Αͬ୆ೄࢃͤ͢
ĲĵťȂĳĲťȫȂࣞෛഽॸளĲĵ඾߲ȪŐĳ ĮĲĵťȫȂࣞෛഽॸளٝ໘߲ȪŐĳĮłŪųĮĳĲťȫ͈෹ழ૕̥ͣœŏłͬಒ੄̱Ȃอ࡛๤Ʉĳįı͈͈ͬ͜ခփ̈́อ࡛̱͂̀Ȃζͼ·υͺτͼٜଢ଼ͤ͢ͅ࿌္എͅ‫۾‬Ⴒ֒ഥঊ͈ಒ੄࣐̹ͬ̽ȃ̹͘űųŦŭŪŮŪůŢųźġ ŴŵŶťź
̱͂̀łůŨŪŰűŰŪŦŵŪůĮĲȪłůŨĮĲȫൎဓ̦Ȃ̭͈ͦͣ։ુͬ٨஝̵̯ͥ͂ࣉ̢Ȃࣞෛഽॸளၗ౎ೄࢃȪ඾ႢĲĵȫ͂඾ႢĲĸͅȪŐĳ ĮłŪųĮőŃŔȫͬໜ࣌ඤൎဓ̱Ȃ̷͈ൎဓ࢘‫ڎ̞̀̾ͅض‬ਅζȜłůŨĮĲȪŐĳ ĮłŪųĮłůŨĲȫ̱̩͉͜ςϋॸ۱઩‫ס‬ȪőŃŔȫ
΃Ȝͬဥ̞̹ఉਹࠖ࢕྾‫ע‬அ૗͂ഩঊࡐ๷‫಼ͥ͢ͅޢ‬๷ࠁఠ۷ख़ٜͤ͢ͅଢ଼̱̹ȃȺࠫ‫ࣉ͂ض‬ख़ȻŐĳ ĮĲĵť͂łŪųĮĲĵť
͂๤‫̱̀ڛ‬อ࡛๤͈୲చ౵̦ĳįıոષ̜̹́̽֒ഥঊ߲ȪŽŐĳ ĮĲĵťİłŪųĮĲĵťŽɄĳįıȫ͉Ȃ଼ಿͤ͢ͅ་‫̳͂ͥا‬এͩͦͥ֒ഥঊȪŽłŪųĮĳĲťİłŪųĮĲĵťŽɄĳįıȫͬੰ‫̱̀͜ٸ‬ĲĶĳĺࡢ൳೰̯ͦȂུવ‫ٺ‬κΟσ͉́ఉ̩͈őŢŵũŸŢź̦‫۾‬ဓ̱̞̭̀ͥ
̦͂াऐ̯̹ͦȃ̷̯͈ͣͅࢃ͈ٝ໘ً೾́อ࡛๤ͅ་‫̹̜̦֒̽ا‬ഥঊ߲ȪŽŐĳ ĮłŪųĮĳĲťİŐĳ ĮĲĵťŽɄĳįıȫ͉ĸĸĴࡢ̦൳೰̯̹ͦȃ̷͈ಎ̥ͣłůŨĮĲͬဥ̞̹őųŦŭŪŮŪůŢųźġ ŴŵŶťź͉́ȂŐĳ ĮłŪųĮłůŨĲ͉Őĳ ĮĲĵť͂๤‫̱̀ڛ‬Ȃ෹༾ࢹ௮͈ྶ
̥ͣ̈́٨஝͉෇̥̹̦͛ͣͦ̈́̽ȂࢯńŅĴĲࢯఘͥࠖ͢ͅ࢕྾‫ע‬அ૗̤̞̀ͅ࿉ळࠬ‫ۯ‬ତ͈ષઌ̷͈͂அ૗ΩΗȜϋ͈٨஝ͬ෇̹͛ȃ಼๷ࠁఠ۷ख़̤̞̀͜ͅȂŐĳ ĮłŪųġ łůŨĮĲ͉́ȂŐĳ ĮłŪųġ őŃŔ͂๤‫̷͈̱̀ڛ‬་‫͉ا‬٨஝̱̞̹̀ȃอ

会長招待講演 シンポジウムĹĶɓॸளȪŐĳȫ̱̩͉͜σȜθ΀ͺȪłŪųȫ‫ͅئ‬Ĳĵ඾‫ۼ‬ཕႺ̵̯̹ࢃȂٝ໘‫̱̀͂ܢ‬łŪų‫ͅئ‬ĸ඾‫ۼ‬ব̱̹֗ȃłŪų߲ȪłŪųĮ

ో‫ܢ‬෹વ‫ͥͩ۾ͅٺ‬ఉ̩͈ΏΈ΢σࠐႹ͈ಎ́ȂłůŨĲ͉૧̱̞হၷ୽ၞ̭̦͂̈́ͥ͂াऐ̯̹̦ͦȂ࡛हȂζͼ·υ
̜ͧ́ͥȃ

őńĲĮĳ

૧ܰ֒ഥঊ ŇłŎĲĳĵŃ ͈ඤ๧අ։എอ࡛ଷࢄ‫ࢹܥ‬ٜଢ଼

口頭発表ͺτͼٜଢ଼̽̀͢ͅ൳೰̯̹ͦ֒ഥঊ߲͈ಎ̥ͣহၷດഎ͂̈́ͥ֒ഥঊ߲̞̯̾̀ͣ̈́ͥͅ࠿॑ͬૺ̞̭͛̀ͥ͂

ɛࣞ‫ޘ‬ġ୹ක ĲĭĳȂ૰‫݌‬ġࢫୀ ĳȂྎࢬġ੓֚ ĳȂఱᚧġ‫ ܧ‬ĳȂչ൐ġঃঊ ĲȂධġࠉ ĳŇŢŮŪŭźġ ŸŪŵũġ ŴŦŲŶŦůŤŦġ ŴŪŮŪŭŢųŪŵźġ ĲĳĵŃ ĩŇłŎĲĳĵŃĪ ͉Ȃࠬ‫ݩ‬Ȃࠬ‫͈ࠏۯ‬໦‫ͅا‬ਹါ̈́࿨‫̳̹ضͬڬ‬ഢৢ֦ঊňłŕłĳ͈‫ئ‬ၠ֦ঊ̱͂̀ńũŊőĮŴŦŲŶŦůŤŦ‫͍ݞ‬ζͼ·υͺτͼٜଢ଼̥ͣ൳೰̯̹ͦ૧ܰ֒ഥঊ̜́ͥȃȪŌŢůŬŪġ Śġ ŦŵġŢŭġ ĳıĲĲĭġ ņŎŃŐġ ŋȫ̷̭́ŇłŎĲĳĵŃ͈୆ၑ‫ܥ‬ෝ͞อ࡛ଷࢄͬྶ̥̳̹ͣͥ͛ͅͅȂζ;Α͈‫ڎ‬௫‫̥ͣܕ‬Fam124bġŮœŏł͈೰ၾٜଢ଼࣐̹ͬ̽ȃFam124bġ Ůœŏłอ࡛͉‫ڎ‬௫‫̦̹ͦͣ͛෇ͅܕ‬Ȃඅͅ෹͞۴௫́ࣞอ࡛̱̤̀ͤȂ̷͈อ࡛ΩΗȜϋ͉‫ڎ‬௫‫ۯ͈ࠬܕ‬ඤ๧ྟഽ͂‫̞ޑ‬௖‫̢̹ͦͣࣉ̦۾‬ȃ̷̭́෹Ȃ۴௫̥ͣࠬ‫ۯ‬ඤ๧ळ༾ͬౙၗ̱ġŇŢŮĲĳĵŃ͈อ࡛ٜͬଢ଼̱̹̭͂ͧȂඅͅ‫̞ޑ‬อ࡛ͬা̱̹ȃষͅȂୃુΪΠᦡఝ୓ྤඤ๧ळ༾ȪŉŖŗņńȫȂୃુΪΠ๧ໂ๷઀ࠬ‫ۯ‬ඤ๧ळ༾ȪŉŎŗņńȫȂΪΠ஍֋ٔळ༾ȪŇŪţųŰţŭŢŴŵȫȂΪΠథ঱ଅळ༾ȪŉŦŬĳĺĴȫ̤̫ͥͅอ࡛ٜଢ଼࣐̹̭ͬ̽͂ͧȂࠬ‫ۯ‬ඤ๧ळ༾̤̞͈͙̀ͅ‫̞ޑ‬อ࡛̦‫̯ͦ෇ږ‬Ȃ̯ͣͅΪΠŇŢŮĲĳĵţġίυκȜΗȜͬဥ̞̹̥ͣτεȜΗȜͺΛΓͼ́͜൳အ͈ඤ๧අ։଻ͬা̱̹ȃ̭͈ŇłŎĲĳĵŃίυκȜΗȜႀ֖͉ͅໝତ͈ňłŕłĳࣣࠫႀ֖̦ంह̱̀
̤ͤȂඅͅ΀ϋΧϋ΍Ȝႀ֖ͅంह̳ͥňłŕłĳႀ֖ͅത་։̞ͬͦͥ͂ŇłŎĲĳĵŃ͈อ࡛̦ࡐಠͅဲଷ̯̹ͦȃոષ͈̭̥͂ͣȂŇłŎĲĳĵŃ̦ňłŕłĳ͈ଷࢄ‫́ئ‬Ȃࠬ‫ۯ‬ඤ๧අ։എͅอ࡛̱̞̭̦̀ͥ͂‫̩ޑ‬াऐ̯̹ͦȃȁ̯ͣͅ
CX37͈̈́̓֒ഥঊ̦ŇłŎĲĳĵŃ͈ດഎ̜́ͥ‫خ‬ෝ଻̦াऐ̯̹ͦȃ̭͈ͦͣ౶ࡉ͉ȂŇłŎĲĳĵŃ̦ࠬ‫ۯ‬ඤ๧ळ༾͈ζȜ΃Ȝ̺̫̩́̈́Ȃਹါ̈́ࠬ‫ۯ‬ȂςϋΩ‫ܥۯ‬ෝͅ‫۾‬ဓ̱̞̀ͥ‫خ‬ෝ଻̦াऐ̯ͦͥȃ䋭 㪈㪋㪎 䋭著者索引

ŇłŎĲĳĵŃġŴŪœŏłͥ͢ͅġŬůŰŤŬťŰŸůġ۪‫ئޏ‬Ȃζͼ·υͺτͼͬဥ̞̹࿌္എ֒ഥঊอ࡛ٜଢ଼࣐̹̭ͬ̽͂ͧȂ
LYVE1Ȃ

ポスター発表 ＹＩＡ選考発表

Ĳ ൐‫ނ‬࿪‫ش‬ఱ‫ڠ‬ఱ‫֭ڠ‬୆ྵ‫شݪࡄڠش‬Ȃĳ ൐‫ނ‬ఱ‫୶ڠ‬౤‫ݪࡄ੅ܿڠش‬ΓϋΗȜȁőńĲĮĴ

ࠬ‫ۯ‬ඤহၷࢃͅठී̱̹‫ئ‬ঠඳহ଻೟នͅచ̱̀ࣸଡౙ‫ݩړ‬ळ༾֊૒ͥࠬ͢ͅ‫ۯ‬ठ୆֓ၷͬদ͙̹ᦑࡔພۛ৪͈֚႕
ɛུ५ġ૨֚჊Ȃ஠ġۖȂչ൥ġ෗ࢫȂऎ໦၌ġ୍ȂგനġೄຮȂୌġ૯ࢤȂ५ུġ߼ఊȂ५࢛ġ૯֚჊Ȃષႅġఱ༟Ȃၛ୼ġࢬࢣȂྂġࠏ߃ࢺสฦঌၛ௙ࣣ֓ၷΓϋΗȜ੏۪‫ܕ‬ඤ‫ش‬ĸıपȂ੫଻ȃĳıĲıාĹ࠮ֲࣼͤ͢లĲᮜͅ೟នࠁ଼ȃŔőőֲ̦௰́ခփͅ೩౵ȃńŕ̀ͅຄ‫ئ‬൲ྤႀ֖͈ᛀྗ଻‫ޛ‬ॏȆ໾णͬঐഊȃĳıĲıාĲĲ࠮‫ئ‬ঠ൲ྤ௮‫࠿ג‬औĩŢůŨŪŰĪঔ࣐Ȃஜ᥼ࣸ൲ྤ͈ۖ஠໾ण̤͍͢ᦄࣸ൲ྤȆࢃ᥼ࣸ൲ྤ͈໾णͬ
‫෇ږ‬ȃ௰໗࣐ࠬႹ̀ͅྎઑࠬ‫خ෇ږۯ‬ෝ̈́ࢃ᥼ࣸ൲ྤͅచ̱ࠐ๧എࠬ‫੅଼ࠁۯ‬ĩőŕłĪঔ࣐Ȃྎઑ͈́͘ၻࢡ̈́ࠬၠठ
‫෇ږͬٳ‬ȃ̷͈ࢃȂ೟ន͜੭șͅ٨஝̱ࠐًၻࢡ̜̹̦́̽ȂĳıĲĲාĲĳ࠮ࣼͤ͢ठഽŔőő͈೩‫͛෇ͬئ‬ȂĳıĲĲාĴ࠮͉ͅ೟ន͜௩՛ȃŢůŨŪŰ̀ͅठ໾णͬ෇̹̹͛͛ठഽőŕłঔ࣐͜ȂŸŪųŦġ ŤųŰŴŴະ‫̹͈͛خ‬ġ ŧŢŪŭŶųŦȃĳıĲĲාĵ࠮ࣸଡౙ‫ړ‬‫ݩ‬ळ༾֊૒੅ͥ͢ͅ‫ئ‬ঠࠬ‫ۯ‬ठ୆֓ၷঔ࣐ȃ੅ࢃࠐًਜ਼಺́Ȃၻࢡ̈́රٔࠁ଼͜෇̹͛ȃਹછ‫ئ‬ঠ‫ࠬݹ‬႕ͅచ̳ͥőŕłȆࠬ‫ۯ‬ठ୆֓ၷ൝ͥ͢ͅহၷ༷ૻͬ࠿൦̳ͥȃőńĲĮĵĳ ߿ൠෂພ̤̫ͥͅఱ઀ࠬ‫ࣣۯ‬໵છૺജ͈ঐດ̱͈͂̀ࠬಎౙ‫ݩ‬ତ͈ခဥ଻
ɛ໛നġ֚ܳȂઐఆġ࣠Ȃ୞֔ġܰຳȂ࿐‫ئ‬ġฎ෗Ȃ५നġकၐࠃȂଳΦ࢛ġၦ໲Ȃ࣏࿐ġ‫֚ו‬ߧུఱ‫ڠ‬ఱ‫֭ڠ‬୆ྵ‫ݪࡄڠش‬໐య৫ඤ‫ڠش‬Ⱥ࿒എȻౙ‫͚֚܄ͬݩ‬໐͈ฒࠬ‫ࠏݩ‬ळ༾͉൲ྤࣁ‫ا‬છอછૺജͅ‫۾‬ဓ̳̭̦ͥ͂౶̞ͣͦ̀ͥȃ߃ා൲ྤࣁ‫ا‬છ͈ࣞςΑ·߲̤̞̀ͅȂฒࠬ‫ݩ‬ତ͞ౙ‫ݩ‬ତ̦ᴢ൲ྤඤಎ྄๬࢚ഽĩńńłĮŊŎŕĪ͂ୃ௖‫̦̭̳͂ͥ۾‬༭̯̞࣬ͦ̀ͥȃ̱̥̱‫ڎ‬ਅฒࠬ‫ݩ‬໦ْ͂ൠෂພఱࠬ‫ࣣۯ‬໵છ̜̞͉ͥळ઀ࠬ‫ࣣۯ‬໵છ͈͂‫۾‬Ⴒ଻͉ྚ̺ະྶ̜́ͥȃ̷̭́ࣽٝĳ߿ൠෂພ̤̞̀ͅȂฒࠬ‫ݩ‬໦ْ͂ఱࠬ‫ࣣۯ‬໵છ‫͍ݞ‬ळ઀ࠬ‫ࣣۯ‬໵છ͈ૺജ͈͂‫۾‬Ⴒ଻ͬ࠿൦̱̹ȃȺ༹༷Ȼ൚‫ش‬ව֭ĳ߿ൠෂພۛ৪ĵĹĵྴͅచ̱Ȃ‫ܖ‬ய಺औ‫͍ݞ‬ฒࠬ‫ݩ‬໦ْ࠿औȂ‫ڎ‬ਅ୆‫࠿ڠا‬औȂŉţłĲŤĩŏňŔő౵ĪȂਓੀ‫ࠬܢ‬գĩŔŃőĪȂ‫ڐ‬ಫ‫ࠬܢ‬գĩŅŃőĪȂńńłĮŊŎŕȂྤ෨௸ഽĩţŢőŘŗĪͬ௶೰̱Ȃ‫ڎ‬་ତ‫͈ۼ‬௖‫࠿ͬ଻۾‬൦̱̹ȃ̯ͣͅńńłĮŊŎŕȂଅછ͈‫ܡ‬؉Ȃౙ‫ݩ‬ତ͈୰ྶ་ତͬΑΞΛίχͼΒਹٝ‫ܦ‬໦ଢ଼́࠿൦̱̹ȃȺ଼ୡȻ஠႕ٜଢ଼̀ͅȂńńłĮŊŎŕ͉ාႢĩųľıįĳĹĹĭġ űɃıįııĲĪȂ
ţŢőŘŗĩųľıįĳĸĴĭġ űɃıįııĲĪȂ
ŔŃőĩųľıįĲĵıĭġ űľıįııĳĪȂᑋພ‫ۼܢ‬ĩųľıįĲĸķĭġ űɃıįııĲĪȂฒࠬ‫ݩ‬ତĩųľıįĲĲĴĭġ űľıįıĲĵĪȂ
ౙ‫ݩ‬ତĩųľıįĴĴĹĭġűɃıįııĲĪȂࢡಎ‫ݩ‬ତĩųľıįĲĴıĭġűľıįııĵĪ͈͂ခփ̈́ୃ͈௖‫ͬ۾‬ȂŅŃőĩųľĮıįĲıĳĭġűľıįıĳķĪ͈͂໅͈௖‫෇ͬ۾‬̹͛ȃ̹͘౳଻ĩųľĮıįĲĲĺĭġ űľıįııĺĪ‫͍ࠬࣞݞ‬գĩųľıįĲĵĹĭġ űľıįııĲĪȂ
‫଻ࠬݹ‬૤৖ۛĩųľıįĲķĵĭġ űɃıįııĲĪȂ໾ण଻൲ྤࣁ‫ا‬છĩųľıįĲıĲĭġ űľıįıĳĸĪȂ࿌྄છĩųľıįĲĺĲĭġ űɃıįııĲĪȂ૰ࠐવ‫ٺ‬ĩųľıįĲķĳĭġ űɃıįııĲĪ͈‫ܡ‬؉͂ခփ̈́௖‫̹͛෇ͬ଻۾‬ȃఱࠬ‫ࣣۯ‬໵છͅచ̱͉̀Ȃฒࠬ‫ݩ‬໦ْ͈ಎ́ౙ‫ݩ‬ତ͈͙̦‫଻ࠬݹ‬૤৖͈ۛ‫ܡ‬؉ĩųľıįĲĳĶĭġ űľıįııķĪ͂ခփ̈́௖‫͛෇ͬ଻۾‬̹ȃ༷֚Ȃळ઀ࠬ‫ࣣۯ‬໵છͅచ̱͉̀Ȃౙ‫ݩ‬ତ͉ଅછĩųľıįĲĴĲĭġ űľıįııĵĪ͈‫ܡ‬؉͂ခփ̈́௖‫̹͛෇ͬ଻۾‬ȃΑΞΛίχͼ
Βਹٝ‫ܦ‬໦ଢ଼͉́ȂńńłĮŊŎŕͅచ̱͉̀ාႢȂౙ‫ݩ‬ତȂţŢőŘŗ̦Ȃଅછ͈‫ܡ‬؉ͅచ̱͉̀ෂಎͺσήηϋၾȂŔŃőȂౙ‫ݩ‬ତ̦Ȃౙ‫ݩ‬ତͅచ̱͉̀ńńłĮŊŎŕȂࣞۜഽńœőȂ‫ܡ͈׸ݎ‬؉ȂŃŎŊ̦ခփ̈́୰ྶ་ତ̜̹́̽ȃȺࠫაȻĳ߿ൠෂພۛ
৪̤̞̀ͅȂౙ‫ݩ‬ତ͉ńńłĮŊŎŕ́ນ࡛̯ͦͥఱࠬ‫ࣣۯ‬໵છ͈ૺജഽͬນ̳ခ‫̈́ף‬ζȜ΃Ȝ̈́ͥͅ‫خ‬ෝ଻̦াऐ̯ͦ
̹ȃ̯ͣͅౙ‫ݩ‬ତ͉Ȃळ઀ࠬ‫ࣣۯ‬໵છ̞͉̾̀ͅଅછ͈ζȜ΃Ȝ̱͂̀ခဥ଻̦̞ࣞ‫خ‬ෝ଻̦াऐ̯̹ͦȃ䋭 㪈㪋㪏 䋭őńĲĮĶ

‫଻ݢ‬૤޼ࢸण̤̫ͥͅ‫ࠬࣞܢ଻ݢ‬ൠȂྕ଻ࣞࠬൠ̦ౣ‫ܢ‬ထࢃͅဓ̢ͥ‫ޣג‬ɛ൥࿤ġٗঃȂ୞ࡔġୃহȂಎୌġൽ჊ȂाུġဉਏȂ࿤࢛ġܵຳȂ௜࿤ġ࠲ࢁȂհ୔ġੇ‫ݛ‬Ȃࢃ൥ġဩ֚Ȃհനġ௛Ȃ઀୼ġ‫ݛ‬ဎȺ෸ࠊȻ‫଻ݢ‬૤޼ࢸणĩłŎŊĪ̤̞̀ͅൠయ৫։ુ͉ထࢃͅਹါ̈́‫ͬޣג‬ဓ̢֦ͥঊ̜́ͥȃਲြȂྕ଻ࣞࠬൠ͈ঐດ́
̜ͥŉţłĲȚ̌ထࢃ͈ঐດ̱͂̀ဥ̧̞̹̦ͣͦ̀Ȃ߃ාȂ‫ࠬࣞܢ଻ݢ‬ൠ͈ਹါ଻̦෇ে̯̠̹ͦͥ̈́̽͢ͅȃȺ༹༷Ȼĳııĸා̥ͣĳıĲĳා͈‫ͅۼ‬อછĵĹশ‫ۼ‬ոඤͅ൚֭ͅව̱̹֭łŎŊ͈ķĺķછ႕ͬచય̱̹͂ȃࠬൠ౵͉ව֭শͅ௶೰̱Ȃ

特別講演࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineĳııŮŨİťŭոષͬ‫ࠬࣞܢ଻ݢ‬ൠȂŉţłĲŤĩŏňŔőĪġ ķįĶĦոષͬྕ଻ࣞࠬൠ͂೰̱̹݅ȃȺࠫ‫ض‬Ȼķıĸ႕ĩĹĸĦĪ́űųŪŮŢųźġ
ൠ͈ခྫ͉́ခփओͬ෇̥̹͛̈́̽ĩĴįĴ ŷŴį ĴįĸɓȄűľıįĸĺĪȃ‫ࠬࣞܢ଻ݢ‬ൠ͈̜ͥછ႕͉́Ȃྕ଻ࣞࠬൠ͈̜͈ͥ́͜
֭ඤঘཌ͉ခփͅ೩ၚ̜̹́̽ĩĶįĶ ŷŴ ĲĹįĺɓȄűľıįıĲĪȃఉ་ၾٜଢ଼͉́Ȃ‫ࠬܢ଻ݢ‬ൠ౵͉֭ඤঘཌၚ͈ඊၛ̱̹ထ௶
֦ঊ̜̹̦́̽ȂŉţłĲŤ͉ခփ֦̈́ঊ͉̥̹́̈́̽ȃȺࠫაȻőńŊশయ͈łŎŊ͈‫͉ͅܢ଻ݢ‬ȂŉţłĲŤ͉̩́̈́Ȃ‫ࣞܢ଻ݢ‬ࠬൠ͉ౣ‫ܢ‬ထࢃ͂ྟ୪ͅ‫̤̱ͤ̀߸۾‬Ȃྕ଻എ̈́ࣞࠬൠͤ͢͜‫ࠬ̈́ࠣݢ‬ൠષઌ̦ਹါ̜̭̦́ͥ͂াऐ̯̹ͦȃ

会長招待講演 シンポジウムőńŊ̦࣐̹ͩͦȃ֭ඤঘཌၚ͉Ȃ‫ࠬࣞܢ଻ݢ‬ൠ͈̜ͥછ႕́ခփࣞͅၚ̜̹̦́̽ĩĺįĹ ŷŴį ĲįķɓȄűɃıįııĲĪȂྕ଻ࣞࠬ

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪈㪋㪐 䋭ĺ࠮ĳķ඾Ȫ࿐ȫġĲĲĻĵıȡĲĳĻĲıġġεΑΗȜٛાεΑΗȜġႉ઄ őńĲȶ૤৖ۛȷőńĲĮķłœŊłġųŦŨŶŭŢŵŦŴġŵũŦġŤŢųťŪŰŮźŰŤźŵŦġťŦŢŵũġŪůġťŰŹŰųŶţŪŤŪůĮŪůťŶŤŦťġŤŢųťŪŰŮźŰűŢŵũźġţźġ
ŮŰťŶŭŢŵŪůŨġŵũŦġőŊĴŌİłŬŵİŃŢťġűŢŵũŸŢźġ
ɛ౻നġࢤඵȂཤఆġဢ໹Ȃઐ๶ġୄ଼Ȃ‫ئ‬നġ݅ࢴȂఱ࿤ġგ௱Ȃฒ५ġ໌ং‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬We recently identified a novel gene, termed ARIA that is highly expressed in endothelial cells, and controls
angiogenesis through a modification of endothelial PTEN/PI3K pathway. Here we report a significant role of ARIA in
the regulation of cardiomyocyte death and cardiac function both in vitro and in vivo. We found a relatively highexpression of ARIA in mouse heart as well as in rat isolated cardiomyocytes. Overexpression of ARIA enhanced
cardiomyocyte death in vitro in association with the reduced Akt activity. To investigate the ARIA function in theheart in vivo, we generated ARIA-KO and cardiomyocyte-specific ϷMHC-ARIA-Tg mice. These mice were viable
and fertile, and no abnormality of the heart was observed. When cardiomyopathy was induced by doxorubicin, left
ventricular fractional shortening was significantly decreased in WT mice. Of note, fractional shortening was greater in
ARIA-KO mice, while it was worsened in ϷMHC-ARIA-Tg mice comparing with WT mice after the doxorubicintreatment. Cardiomyocyte apoptosis and cardiac fibrosis were significantly attenuated in ARIA-KO mice heart,
whereas they were deteriorated in ϷMHC-ARIA-Tg mice heart. The Akt/Bad pathway plays a crucial role in the
doxorubicin-induced cardiomyocyte death, and we found that phosphorylation of Akt and Bad was substantiallyenhanced in ARIA-KO mice heart, while they were reduced in ϷMHC-ARIA-Tg mice heart comparing with WT mice
after the doxorubicin-treatment. These revealed a previously undescribed function of ARIA in the cardiomyocyte
death, and shed light on ARIA as an attractive new pharmacotherapeutic target for the doxorubicin-induced
cardiomyopathy.

őńĲĮĸœŪŨũŵġŵŰġōŦŧŵġŗŦůŵųŪŤŶŭŢųġŊůŵŦųŭŦŢťġņŭŦŤŵųŪŤŢŭġŅŦŭŢźġťŶųŪůŨġœŪŨũŵġŗŦůŵųŪŤŶŭŢųġőŢŤŪůŨġ
őųŦťŪŤŵġŇŢŷŰųŢţŭŦġœŦŴűŰůŴŦġŪůġőŢŵŪŦůŵŴġŸŪŵũġńŢųťŪŢŤġœŦŴźůŤũųŰůŪŻŢŵŪŰůġŕũŦųŢűź
ɛಎോġ֗ఊ჊Ȃ࿤നġଢȂ୞‫ޘ‬ġࣈ໹Ȃ‫ུݠ‬ġࢫඵȂ५നġ࿹ঊȂ‫ؖ‬ఆġ‫ם‬ຳȂၖࡉġგࢼȂ௖ೳġ໌ংȂ‫ہ‬ாġঃ჊Ȃ௜࿤ġࡄࢁ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬໐࿝Introduction: Anatomical and electrical separation of left ventricular (LV) and right ventricular (RV) electrodes issignificant for successful cardiac resynchronization therapy (CRT). During bi-ventricular pacing, the electrical activation
was composed by RV and LV pacing wavefronts. So the region with latest activation during intrinsic rhythm might notcorrespond to the optimal pacing site during CRT. We assess the hypothesis that interlead electrical delay measurements
during RV and LV pacing besides intrinsic rhythm could predict favorable response to CRT.
Methods and Results: We evaluated 51 heart failure patients (age 64Ⱦ13 years, LVEF 28Ⱦ12%) who had successfully
implanted CRT. The LV-RV interlead electrical delay (IED) during intrinsic rhythm, RV pacing (RV pacing-LV
sensing: RVp-LVs) and LV pacing (LV pacing-RV sensing: LVp-RVs) were measured intraoperatively by utilizing
intracardiac electrograms. After CRT implantation, 33 (65%) patients responded to CRT. The responders showed asignificantly higher value of RVp-LVs compared with non-responders (166Ⱦ42 vs. 141Ⱦ36ms, respectively, p=0.04)
and the absolute value of the difference between RVp-LVs and LVp-RVs was lower in responders than in nonresponders (16Ⱦ19 vs. 28Ⱦ22ms, respectively, p=0.04). The IED during intrinsic rhythm (71Ⱦ53 vs. 40Ⱦ44ms,
p=0.07) and LVp-RVs (170Ⱦ47 vs. 146Ⱦ35, p=0.06) showed higher tendency in responders, however they couldn't
predict responders. Moreover, among narrow QRS patients (n=21; median QRS duration 118ms, 95 to 140ms), RVpLVs was significantly higher in responders than in non-responders (159Ⱦ32 vs. 121Ⱦ32ms, p=0.01). Same as the entire
cohort, the IED during intrinsic rhythm couldn't predict responders (59Ⱦ24 vs. 35Ⱦ36ms, p=0.11). At multivariate
analysis, RVp-LVs was the only independent predictor of reverse remodeling in narrow QRS subgroup (p=0.03).
Conclusion: Interlead electrical delay during intrinsic rhythm couldn't predict LV reverse remodeling after CRT.
However high value of RVp-LVs measured intraoperatively was associated with favorable response irrespective of QRS
width, which implies an optimal LV lead position during CRT implantation.
䋭 㪈㪌㪇 䋭őńĲĮĹ

ŊŮűųŰŷŦŮŦůŵġŰŧġńŢųťŪŢŤġŇŶůŤŵŪŰůġţźġŊůŤųŦŢŴŪůŨġŔŵŪŮŶŭŶŴġŔŵųŦůŨŵũġťŶųŪůŨġōŦŧŵġ
ŗŦůŵųŪŤŶŭŢųġőŢŤŪůŨġŪůġńŢųťŪŢŤġœŦŴźůŤũųŰůŪŻŢŵŪŰůġŕũŦųŢűź

Ĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜȂĳ გ‫ظ‬५ࡇၛ֓‫ش‬ఱ‫ڠ‬łųŦġŵũŦźġųŦŢŭŭźġůŰŵġŨŶŪŭŵźġŸũŰġűųŦŴŦůŵġŢŤŶŵŦġŤũŦŴŵġűŢŪůĭġůŰġŰţŴŵųŶŤŵŪŷŦġŤŰųŰůŢųźġ
ŢųŵŦųźġťŪŴŦŢŴŦġţźġńŕġŢůŨŪŰŨųŢűũźŀġ

口頭発表

őńĲĮĺ

会長招待講演 シンポジウム

Background Cardiac resynchronization therapy (CRT) is an established therapy in patients with severe heart failure
due to left ventricular (LV) dyssynchrony. Increasing stimulus strength (SS) of LV pacing could capture an enlarged
myocardial area and provide rapid electrical conduction. The aim of the present study was to investigate whether
increasing SS of LV pacing improves LV mechanical dyssynchrony and cardiac function in patients treated with CRT.
Methods and Results We enrolled 26 patients with CRT and changed SS of LV pacing into 3 conditions: 0V (CRToff), 2.5V (standard SS) and 5V (high SS). Electrocardiography and echocardiography were performed to assess QRS
duration, LV mechanical dyssynchrony, and cardiac function under each condition. QRS duration (CRT-off vs.
standard SS vs. high SS: 158.4 Ⱦ 42.7 ms vs. 138.6 Ⱦ 21.4 ms vs. 126.8 Ⱦ 23.1 ms, p <0.001), septal-posterior wallmotion delay (196.2 Ⱦ 100.4 ms vs. 126.5 Ⱦ 42.7 ms vs. 111.4 Ⱦ 55.3 ms, p =0.012), standard deviation of timefrom QRS (102.9 Ⱦ 51.1 ms vs. 69.6 Ⱦ 21.8 ms vs. 55.6 Ⱦ 19.4 ms, p <0.001) and LV stroke volume (42.3 Ⱦ 14.7
ml vs. 50.7 Ⱦ 15.5 ml vs. 63.8 Ⱦ 18.3 ml, p <0.001) improved significantly with increasing SS of LV pacing in CRT.
Conclusions Increasing SS of LV pacing in CRT improves LV mechanical dyssynchrony and cardiac function. The
capture of enlarged myocardial area by increasing SS of LV pacing might offer an acute hemodynamic benefit to thepatients treated with CRT.

特別講演ɛ୞‫ޘ‬ġࣈ໹ ĲȂ‫ݛ‬༗ġၦঃ ĳȂಎോġ֗ఊ჊ ĲȂ‫ུݠ‬ġࢫඵ ĲȂ५നġ࿹ঊ ĲȂ‫ؖ‬ఆġ‫ם‬ຳ ĲȂ࿤നġଢ ĲȂၖࡉġგࢼ ĲȂ௖ೳġ໌ং ĲȂ௜࿤ġࡄࢁ ĲȂ୤िġၦঃ ĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛ൥ࡔġႚঊȂ࿤࢛ġᔐຳȂ࿤ș࿐ġࢤȂࢃ൥ġဩ֚Ȃ୞ࡔġୃহȂ઀୼ġ‫ݛ‬ဎȂհനġ௛䋭 㪈㪌㪈 䋭著者索引

Background: Computed tomography angiography (CTA) has a potential accuracy for obstructive coronary arterydisease (CAD) in patients with ischemic chest pain at emergency department (ED). However, it remains unclear if theearly discharge of patients with a no-obstructive CAD with CTA is associated with a low risk of cardiac events inJapanese patients.Objective: From 2010 to 2012, 482 consecutive ischemic-type acute chest pain patients (mean age,
63 years; 75% male) who presented to the ED with low-to intermediate risk score, negative initial cardiac troponin T,
and non-ischemic ECG change were prospectively enrolled. Of these, 386 patients (155 patients were categorized as
non-obstructive CAD and 231 patients as non-CAD) were enrolled in this prospective study. The median follow-up
period was 2.0 years.Results: Eighty-nine (23%) of 386 patients had re-admitted to the ED due to recurrent chest painand diagnosed as vasospastic angina pectoris (VSA) with trans-catheter Ergometrine provocation test within 6 months.
Especially, 68 (77%) patients of these underwent this provocation test within initial 3 months. During follow-up, onepatient had syncope leading to the head trauma, and one patient had cardiopulmonary arrest due to vasospasm-induced
ischemic attack within 3 months. No patients had acute coronary syndrome due to atherosclerotic plaque rupture
during follow up. Conclusion: Our result indicates the potential existence of VSA behind the patients without
obstructive CAD by the CTA. Early discharge of acute chest pain patients with a negative CTA is associated with arisk of cardiac events due to VSAP within 6 months.

ポスター発表 ＹＩＡ選考発表࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬őńĲĮĲı ŐŷŦųġĳıĮźŦŢųġŕųŦůťġŰŧġŊůĮŉŰŴűŪŵŢŭġŎŰųŵŢŭŪŵźġŪůġńŢųťŪŰŨŦůŪŤġŔũŰŤŬġőŢŵŪŦůŵŴġŖŴŪůŨġ
őŦųŤŶŵŢůŦŰŶŴġńŢųťŪŰűŶŭŮŰůŢųźġŔŶűűŰųŵļġńŰŮűŢųŪŴŰůġţŦŵŸŦŦůġłńŔġŢůťġŏŰůĮłńŔġňųŰŶűŴ
ɛઐུġ‫ڠ‬Ȃհനġ௛Ȃ५आġଢঃȂ௷ၛġఊ֚Ȃ‫ݠ‬ઽġ࿷ၻȂ‫֔ז‬ġ၌ࢨȂ൥࿤ġٗঃȂஃ٬ġణ‫ו‬Ȃ઀౓ġਜ਼֚ȂाུġဉਏȂ࿤࢛ġܵຳȂࢃ൥ġဩ֚Ȃհ୔ġੇ‫ݛ‬Ȃ୞ࡔġୃহȂ઀୼ġ‫ݛ‬ဎ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ

Background:Percutaneous cardiopulmonary support (PCPS) has been utilized for patients complicating cardiogenic
shock due to acute coronary syndrome (ACS), myocarditis or cardiomyopathy. However, it remains unknown whether
there may be a trend of changing mortality and procedural complication over 20 years in critically ill patients withhemodynamic volume support by PCPS.Methods:We studied 101 consecutive patients (M/F, 67/34; age, 57Ⱦ18 years)
who received PCPS between 1991 and 2012.Cardiogenic shock was caused by ACS in 55 patients including left main
trunk diseases (LMT; n=25).Patients were divided into 3 groups by years; 1991-1997 (1st, n=17), 1998-2004 (2nd, n=30)
and 2005-2012 (3rd; n=54).Results:The overall rate of in-hospital mortality, bleeding complication and lower limb
ischemia was 65%, 81% and 24%, respectively.Over 20-years, in-hospital mortality remained high in both ACS (1st,87%;
2nd,91%; 3rd;79%; overall 85%) and non-ACS groups (1st,50%; 2nd,37%; 3rd,48%; overall 41%).Importantly,it wasmuch higher in ACS and non-ACS group (p<0.05).In ACS group, patients survived were characterized by lower
prevalence of cardiopulmonary arrest (survived,0% vs. died,28%) and Killip IV classification (survived,43% vs.
died,81%) on admission in comparison with patients died (P<0.05).Conclusions:Despite the over 20 year- development of
medical and mechanical therapy including PCPS, the rate of in-hospital mortality of cardiogenic shock still remains high,especially in patients with ACS.

őńĲĮĲĲ ņŭŦŷŢŵŪŰůġŰŧġŔŦųŶŮġŇŪţųŰţŭŢŴŵġňųŰŸŵũġŇŢŤŵŰųġĳĴġŪůġőŢŵŪŦůŵŴġŸŪŵũġŉŦŢųŵġŇŢŪŭŶųŦĻġłġ
őŰŵŦůŵŪŢŭġńŭŪůŪŤŢŭġŔŪŨůŪŧŪŤŢůŤŦ
ɛࣽೋġ๼ਏ ĲȂࣞᚰġฎࢨ ĲȂஃઔġฎং ĳȂਢനġࢴ ĲȂଫ࿤ġࢫຳ ĲȂఱࡔġܲဉ ĲȂಿ౓୼ġఽ࿟ ĲȂಱாġୃ‫ ܮ‬ĲȂ૰ॄġਜྶ ĲȂհ୔ġੇ‫ ݛ‬ĲȂཤ໓ġଽঃ Ĳ
Ĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜȂĳ ‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬Purpose: Fibroblast growth factor 23 (FGF23), one of phosphate-regulating hormones, is known to be linked to renal
function and predictive factor of the mortality in patients with chronic kidney disease, however the clinical role of
FGF23 in patients with heart failure (HF) is not been clarified. We aimed to determine the relation between serum
FGF23 levels and hemodynamic state, cardiac function in patients with HF and relatively preserved renal function.
Methods: We studied 726 participants from a community population, and prospectively enrolled 141 consecutive
hospitalized HF patients with more than 40 ml/min/1.73 m2 of estimated glomerular filtration rate (eGFR). We further
prospectively studied 117 patients with RHC. The clinical outcome was defined as the occurrence of either
cardiovascular death or re-hospitalization for HF, during 180 days after the entry to this study.
Results: The median FGF23 level of the patients with HF was significantly higher than that of healthy population who
were matched with gender and eGFR of HF population (39.1 [interquartile range: 31.3-51.9] vs. 28.3 [22.7-37.4]
pg/ml, respectively, p<0.001). RHC revealed that serum FGF23 levels have the inverse correlation with cardiac index(r=-0.31, p<0.001), mixed venous oxygen saturation (r=-0.41, p<0.001) and the positive tendency with right atrial
pressure (r=0.25, p=0.006). Importantly, the frequency of cardiac event was significantly higher in High FGF23 groupthan Low FGF23 group (p=0.03).
Conclusions: The serum FGF23 level was elevated in patients with heart failure and no overt renal diseases, with asignificant correlation with both hemodynamic state and clinical outcome. FGF23 could suggest to be accompaniedwith important pathophysiological roles in the process of deteriorating heart failure.
䋭 㪈㪌㪉 䋭ĺ࠮ĳķ඾Ȫ࿐ȫġĲĲĻĲıȡĲĳĻĲıġġεΑΗȜٛાεΑΗȜġ‫ܖ‬ய őŃĲȶྤ‫଼ࠁۯ‬Ȇࠬ‫ۯ‬૧୆ˍȷőŃĲĮĲŗŢŴŰũŪţŪůĮĳ ͈ဲଷ̦ક‫ু̫̤ͥͅۯا‬டอછਆនͅ‫̥̳͖ݞͬޣג‬ȉɛཤࡔġਜহ ĲȂႝ࿐ġࢫࢬ ĳȂ૩ോġୃࠃ ĲȂ‫֔݌‬ġྶ඾ࣝ ĲȂઐ‫ݳ‬ġद ĲȂऎ൥ġ࿭ঃ ĳȂࢺॄġఊ֚ Ĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

Ĳ ൐‫ނ‬੫ঊ֓‫ش‬ఱ‫ڠ֓ڠ‬໐ٜཎ‫ڠ‬Ȇอ୆୆໤‫࣒ڠ‬जȂĳ ൐ཤఱ‫حڠ‬Ⴂ֓‫ݪࡄڠ‬ਫ਼ਆន੏۪ࡄ‫ݪ‬໦࿤ȪŏŰųŮŢŭŪŻŢŵŪŰůȫ̞̹͂̽হၷ༹͈ࡄ‫̦̞ͥ́ͭૺ̦ݪ‬Ȃ໗ैဥ͈࿚ఴ̜ͤ͜Ȃ̯ͣ̈́ͥਆនࠬ‫͈ۯ‬ٜଢ଼͂૧̹̈́‫܈‬হၷ༹͈‫ٳ‬อ̦བͦͥ͘ȃ̷ུ̭́ࡄ‫͉́ݪ‬Ȃࠬ‫ۯ‬૧୆ͬଷࢄ̳ͥ૧֦ܰঊŗŢŴŰũŪţŪůĮĲ͈γκυΈ̜́ͥŗŢŴŰũŪţŪůĮĳȪŗłŔŉĳȫͬଷࢄ̳̭ͥ͂́Ȃুடอછਆន͈՛଻‫ͬا‬ଷࢄ̧̞̥́̈́࠿બ̳ͥমͬ࿒എ̱̹͂ȃ
Ȯऺၳ

特別講演

Ȯ࿒എȯ߃ාȂਆនࠬ‫ͬۯ‬ΗȜΊΛΠ̱̹ͅ໦ঊດഎহၷ࿪͈‫ٳ‬อ͞Ȃਆនࠬ‫̫ͥ̿߃ͅۯࠬુୃͬۯ‬ਆនࠬ‫اુୃۯ‬༹༷͂ȯఱಸ‫֦֒ࡔ͈܈‬ഥঊ͈̜֚̾́ͥAPC֒ഥঊͬ་։̵̯̹ApcMin/+ζ;Α͂ȂVASH2֒ഥঊͬΦΛ·ͺ;Π
ΠζΠτ·Ιϋͬ୓ಕ̱̀ࠬ‫ۯ‬ඤ࿂ͬດে̱Ȃᚇၠࡥ೰ࢃͅਆនͬഊ੄̱̀ൄࠫ୨༌ͬैୋ̱̹ȃ̯ͣͅȂ‫ڎ‬ਅζȜ΃Ȝͥࠖ͢ͅ࢕྾‫ע‬அ૗ͬਹ͇̀Ȃ‫ވ‬ઙതτȜΎȜࡐ๷‫́ޢ‬۷ख़̱̹ȃ̹͘Ȃഩঊࡐ๷‫಼ͥ͢ͅޢ‬๷ࠁఠ‫ڠ‬എ۷ख़ĭġ œŕĮőńœ͈̈́̓໦ঊ୆໤‫ڠ‬എٜଢ଼̤̭̹̈́̽͜ȃȮࠫ‫ࣉ͂ض‬ख़ȯ΋ϋΠυȜσ̜́ͥApcMin/+ζ;Α͈઀ಸષ๧͉ĭġ ՛଻‫ا‬̱̞̩̀౲‫́ٴ‬ȂŗłŔŉĳ͈อ࡛̦ਆនࠬ‫ۯ‬ਔսͅඅ։എͅࡉ̹ͣͦȃVash2-/-ζ;ᾼ൳ࠏ͈ਆនͬ๧‫֊ئ‬૒̱̹̭͂ͧȂŘŪŭťġ ŵźűŦͤ͢ਆនอ֗ဲଷ̦͙ͣͦȂࠬ‫̹ͦͣࡉ̦ا੃଼͈ۯ‬ȃ̭͈ࠫ‫ͤ͢ض‬ȂŗłŔŉĳͬဲଷ̳̭ͥ͂́ਆន
̦ଷࢄ̧́ͥ͂ࣉ̢̹̹ͣͦ͛Ȃ࢐෻ͤ͢ͅΘήσηνȜΗϋΠζ;Αͬै଼̱Ȃਆនอ֗͞ਆនࠬ‫͈ۯ‬་‫ͬا‬ٜଢ଼̱̹̭͂ͧȂ઀ಸ̤̫ͥͅਆន͈ࡘઁ͞ĭġ ࠬ‫͈̓̈́اુୃ͈ۯ‬་‫̹ͦͣࡉ̦ا‬ȃ̭͈̠͢ͅȂਆន͈ၻ଻Ȇ՛଻Ȃ̤͍͢ഢ֊ͬऒֲ̳ͥ΅Ȝέ͹·ΗȜ͈͉͂̈́ͥ‫̥ͬة‬Ȃਆនޫਫ਼͈๷઀੏۪ࠏ͈ণത̥ͣͺίυȜΙ̳ͥম̽̀͢ͅȂඅͅક‫ࠏܕا‬ਆនͬࢲၞ̳̹͈ͥ͛ঝ࢛̈́ͥͅ‫خ‬ෝ଻̦ఱ̧̞ȃ̹͘ĭġ ਆនࠬ‫̩͉̫̺̳̈́́ͥاુୃͬۯ‬Ȃਆនඤͅୃુࠬ‫ͬۯ‬ठࢹಃ̵̯ͥအ̈́ྤ‫ۯ‬Ȫࠬ‫ۯ‬ȂςϋΩ‫ۯ‬ȫၷ༹͈‫ٳ‬อ̈́̓ĭġ ࣽࢃ͈ႉ઄؊ဥ͜ͅఱ̞ͅ‫ܢ‬ఞ̦̀ͥ͂͜ࣉ̢
̹ͣͦȃζ;Αอ୆‫ܢ‬ఱෞ๧ৗ͈ࠬ‫ۯ‬࿌ࠁ଼ɛୌఆġ‫ ࢴد‬ĲĭĳȂ֞ߧġဉ ĳȂջ෯ġୃষ ĴȂ໚໐ġ࢕হ ĵȂ‫ז‬നġࢼ֚ ĳȂକ౓ġ࠲֚ ĲĭĶ

口頭発表

őŃĲĮĳ

会長招待講演 シンポジウム̱̹ζ;ΑȪVash2-/-ȫͬဥ̞̀ĭġ ŗłŔŉĳͬဲଷ̳̭ͥ͂ͥ͢ͅਆនอછ͞ਆនࠬ‫͈ۯ‬་‫ͬا‬ٜଢ଼̱̹ȃࠐশഎࠖͅ࢕

Ĳ ൳঎২ఱ‫ڠ‬ෞ‫شݪࡄڠش‬Ȃĳ Ք౶ࡇ૤૸વ‫ٺ‬৪΋υΣȜอోવ‫ݪࡄٺ‬ਫ਼ȂĴ ಆ෨ఱ‫֓ڠ֓ڠ‬ၷࠏȂሶ඿႒͈ఱෞ๧ৗ͉́૰ࠐழ૕͈ࠁ଼͕͖͂൳শ‫ۯࠬͅܢ‬࿌̦ࠁ଼̯̭̥ͦͥ͂ͣȂၰ৪͈‫͉ͅۼ‬ఱෞ๧ৗࠁ଼
ً͈೾̤̞̀ͅ‫͈̥ͣة‬ջం‫̦̭̜̦͂ͥ߸۾‬ထே̯ͦͥȃఱෞ๧ৗ͈૰ࠐழ૕ࠁ଼͈‫͉ࢹܥ‬৘ࡑ਀ܿ͞۷ख़ࠏ͈
อోًͤ͢ͅ‫ݲ‬਱ତා́๲࿬എͅࡄ‫̦̺ͭૺ̦ݪ‬Ȃ༷֚́ࠬ‫ۯ‬࿌ࠁ଼̞͉̾̀ͅȂอ୆͈͈̓শ‫ͅܢ‬Ȃ͈̠̱̓͢ͅ
̀੄ြ̩͈̥̞̹̀ͥ͂̽‫ུܖ‬എ̈́ࠁ଼ً೾̞͕̾̀͂ͭ̓͜ͅྶ̥̯̞̞ͣͦ̀̈́ͅȃ̷ِ̭́ș͉Ȃौා́͘ͅ
ࠬ‫ۯ‬τεȜΗȜζ;ΑȪŇŭŵĲĮŵťŴœŦť̤͍͢ ŇŭŬĲĮňŇőġ Ńłń ΠρϋΑΐͿΣΛ·ζ;Αȫͬဥ̞̀อ୆শ‫ྀ͈ܢ‬ఱෞ๧ৗࠬ‫ۯ‬࿌͈အঊͬ۷ख़̱̀Ȃ̷͈ࠫ‫ڠུͬض‬ٛ́อນ̱̹ȃུා͉Ȃංْ̹ͣͦ௨ͬ೰ၾٜଢ଼̳̭ͥ͂ͤ͢ͅȂఱෞ๧ৗ͈ࠬ‫ۯ‬࿌ࠁ଼͉֚ͅ೰͈ܰ௱଻̦̜̭ͥ͂ͬࡉ੄̱̹͈́Ȃ̷͈ࠫ‫ͬض‬༭̱̹̞࣬ȃ೰ၾٜଢ଼͉Ȃ૰ࠐழ૕̱͂
͈̀ෞ͈ႀྀ֖̤̫ͥࠬͅ‫ྟ͈ۯ‬ഽȂ̤͍ࠬ͢‫͈଻༷͈࢜ۯ‬ඵ͈̾۷ത́อ୆͈শ‫ྀ̹࣐̽ͅܢ‬ȃ̷͈ࠫ‫ض‬Ȃఱෞ๧ৗ͈ࠬ‫ۯ‬࿌͉ෞ͈ႀ֖͞อ୆͈শ‫ྟྀͅܢ‬ഽ̦։̭̦̈́ͥ͂া̯̹ͦȃ̹͘Ȃ̷̸ͦͦෞ͈ႀ֖ͤࠬ͢ͅ‫଻༷͈࢜ۯ‬͜։̭̦̈́ͥ͂া̯̹ͦȃ̭͈ͦͣࠫ‫͉ض‬Ȃఱෞ๧ৗ͈ࠁ଼ً೾̤̞̀ࠬͅ‫ۯ‬࿌ࠁ଼̦૰ࠐழ૕͈ࠁ଼͂‫͈̥ͣة‬ջం‫ͬ߸۾‬঵̞̭̽̀ͥ͂ͬাऐ̱̞̀ͥ͂ࣉ̢ͣͦͥȃ

ポスター発表 ＹＩＡ選考発表ĵ ྴࡣ‫ؚ‬ঌၛఱ‫ڠ‬࿪‫شݪࡄڠ‬ȂĶŋŔŕȂ̧̯̦̫

著者索引

䋭 㪈㪌㪊 䋭őŃĲĮĴ

଼੃ডཛळ༾͈౎໦‫ۯࠬ͂ا‬ਔ๧ळ༾͈͒໦‫̞̀̾ͅا‬ɛซாġ֚ฎ ĲȂളᰧġఽঃ ĳȂઐུġఊ჊ Ĳ
Ĳ ඾ུఱ‫ڠ֓ڠ‬໐‫ܥ‬ෝࠁఠ‫ࠏڠ‬ळ༾ठ୆Ȇ֊૒֓‫ڠ‬໦࿤Ȃĳ ඾ུఱ‫ڠ֓ڠ‬໐઀঱‫઀ࠏڠش‬঱‫ڠش‬໦࿤ĩ࿒എĪġ ŗŢŴŤŶŭŢųġ ŴűųŰŶŵŪůŨ̥ͣই̹̽ࠬ͘‫ۯ‬૧୆͉ĭġ ༃ळ༾͞໹‫޼ڲ‬ळ༾͈̈́̓ਔ๧ळ༾͈ၔ఑̻ͤࠬ͢ͅ‫଼͈ۯ‬੃‫̳࣐ͥ֊͂͒ا‬įġ ̭͈ਔ๧ळ༾͈ဇြ̞͉̾̀ࠬͅ‫ۯ‬ਔս͈‫ۼ‬ဩࠏۚळ༾̦ࣉ̢̞̦ͣͦ̀ͥĭġ ̺͘਱໦ٜྶ͉̯
̞̞ͦ̀̈́įġ ِș଼͉੃ডཛळ༾ဇြ͈ఉෝ଻ۚळ༾ ŅŦťŪŧŧŦųŦůŵŪŢŵŦťġ ŧŢŵġ ŤŦŭŭȪŅŇłŕȫ
ͬ໦ၗ̱ĭġ ̷͈ͦͣळ༾͉
‫ࠬݹ‬໐պ́ࠬ‫ۯ‬૧୆֦ঊͬ໦๥̱ĭġ ૧୆ࠬ‫ັͅۯ‬಍̱̀ਔ๧ळ༾ζȜ΃Ȝ͈łŔŎłͬอ࡛̳̭ͥ͂ͬ‫̹̱෇ږ‬įġ ̷̭́ࣽٝĭġ ডཛळ༾͈౎໦‫̦ا‬௯ૺً̳ͥ೾͂౎໦‫ا‬ডཛळ༾͈ࠬ‫ۯ‬ਔ๧ळ༾͈͒໦‫̹͓͛ͥͅ಺̞̀̾ͅا‬৘ࡑ࣐̹ͬ̽įġ ĩ༹༷Īġ Ĳĭġ ŅŇłŕͬࠬ‫ۯ‬ඤ๧ळ༾͂‫ވ‬෽ူ̱ĭġ ࠖ࢕அ૗͂Ųőńœ́ਔ๧ळ༾ζȜ΃Ȝ͈อ࡛ͬ‫̳ͥ෇ږ‬įġ ĳĭġŕňŇĮţŦŵŢ́ঁ̱ࠣņŎŕ̭̱̹ͬܳŏŎŶŎňळ༾଼͂੃ডཛळ༾ͬ‫ވ‬෽ူ̱ŅŇłŕ͈೰ၾ࣐̠ͬįġ ĩࠫ‫ض‬Īġ ࠬ‫ۯ‬ඤ๧ळ༾͈͂‫ވ‬෽ူ́ŅŇłŕ͉ŏňĳ͂łŔŎłͬอ࡛̱̹įġ ņŎŕळ༾͂‫ވ‬෽ူ̱̹ডཛळ༾͉౎໦‫̦ا‬௯ૺ̱̹įġ ĩࠫაĪġņŎŕळ༾̥͈ͣঁࠣ̽̀͢ͅডཛळ༾͉౎໦‫̦ا‬௯ૺ̯ͦĭġ౎໦‫ا‬ডཛळ༾͉ࠬ‫ۯ‬ඤ๧ळ༾̥͈ͣঁࠣͤ͢ͅĭġࠬ‫ۯ‬ਔ๧ळ༾͒͂໦‫̹̱ا‬įőŃĲĮĵ೩ॸளȆ೩‫ͤ͢ͅူו‬ည൵̯ͦͥ œŐŔ ̦‫̳͖ݞ‬ਆនࠬ‫ۯ‬ඤ๧͈͒‫ޣג‬ɛཤᕢġࠉ෗ ĲȂ‫ۼ‬୞ġජ࡮ ĲȂਝ५ġᎢ༟ ĲȂఱٖġ௱ࢣ ĲĭĶȂ߃൥ġ๼࿥ঊ ĲȂ‫౓ڙ‬ġ൹ ĲȂૺ൥ġୃ૞ ĳȂ๳നġణࢼ ĴȂ൥ᚧġੇྶ ĵȂ๳നġ‫ނ‬ঊ Ĳ
Ĳ ཤ٬ൽఱ‫ڠ‬ఱ‫֭ڠ‬ভ‫ۯࠬشݪࡄڠ‬୆໤‫ڠ‬Ȃĳ ཤ٬ൽఱ‫ڠ‬ভ‫࢛࣌شݪࡄڠ‬ພၑພఠ‫ڠ‬ȂĴ ཤ٬ൽఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬Ȇࡤ‫ڠشٸܕݟ‬Ȃĵ ཤ٬ൽఱ‫ڠ‬ఱ‫֭ڠ‬ভ‫شݪࡄڠ‬ভ‫ཻش‬ଜ‫ڠ‬ȂĶ ཤ٬ൽఱ‫ڠ‬ভ‫૷࢛࣌شݪࡄڠ‬౯ඤ‫ڠش‬ਆនࠬ‫͂ۯࠬુୃ͉ۯ‬๤‫ࢹ̈́੃ྚ̱̀ڛ‬௮̞̭̦ͬ͂̽̀ͥ͂౶̞ͣͦ̀ͥȃ႕̢͊Ȃࠬ‫ۯ‬ඤ๧ळ༾൳আ͈ࣣ͉ࠫ
ம̜́ͤȂࠬ‫͈ۯ‬൫ً଻ᄤૺͤ͢ͅழ૕‫ۼ‬գ̦̩̤ࣞ̈́̽̀ͤȂࠬ‫͈ۯ‬௢࣐̦၄ॠ̞̈́̽̀ͥͅȃ̷͈̹͛ਆនඤ́
͉ခ࢘̈́ࠬ‫ס‬੏۪̦ං̞̞ͣͦ̀̈́໐պ̦ంह̱Ȃਆន๷઀۪‫̫̤ͥͅޏ‬೩ॸளȆ೩‫̞͈֦̀̽̈́͂̾͂͌ࡔ͈ူו‬ͥȃ̭͈̠۪̈́͢‫ॸ଻ڰ͉̞̤̀ͅޏ‬ளਅġ ĩœŐŔĪġ ̦ಇୟ̱Ȃळ༾ঘ͈ည൵͞ळ༾͈௩૓Ȇဋ௢ͅ‫۾‬ဓ̳ͥΏΈ΢σഥోࠐႹ͈‫̠̠̞͂͢ͅا଻ڰ‬Ȃ̷͈ಇୟၾͅ؊̲̀ळ༾ͅచ̱̀։̈́ͥ‫̦̭̳͖͂ݞͬޣג‬౶̞ͣͦ̀ͥȃœŐŔ͈ಇୟ͉ਆនळ༾ͅŗņňŇ͈อ࡛ͬᄤૺ̵̯Ȃࠬ‫ۯ‬૧୆ͬ௯ૺ̱̞̭̦̀ͥ͂౶̞ͣͦ̀ͥȃ͉̭ͩͦͩͦͦ́͘Ȃਆនࠬ‫ۯ‬ඤ๧ळ༾ġ ĩŕŶŮŰųġ ŦůťŰŵũŦŭŪŢŭġ ŤŦŭŭ Ļġ ŕņńĪġ ͂ୃુࠬ‫ۯ‬ඤ๧ळ༾ġ ĩŏŰųŮŢŭġ ŦůťŰŵũŦŭŪŢŭġ ŤŦŭŭ Ļġ ŏņńĪġ ͬ໦ၗ෽ူ̱Ȃŕņń̦ŏņńͅ๤͓ŗņňŇ̈́̓အș̈́֒ഥঊอ࡛̦ᄤૺ̱̞̭̀ͥ͂Ȃ୆ంෝ̦̞̭ࣞ͂̈́̓ͬ༭̧̱̹࣬̀ȃ̱̥̱Ȃŕņń̤̫ͥͅœŐŔ͈ಇୟ̷͈͂࿨‫̺ྚ͉̞̀̾ͅڬ‬༭̦̞࣬̈́ȃུࡄ‫͉́ݪ‬Ȃ೩ॸளȆ೩‫̀̽͢ͅူו‬ည൵̯ͦͥ
œŐŔ͈ಇୟ̦‫̳͖ݞ‬ŕņń͈͒‫ͬޣג‬Ūů ŷŪŵųŰ͈ࠏٜ́ଢ଼̱̹ȃ̴͘Ȃζ;Α๧‫֊ئ‬૒ਆន̤̫ͥͅœŐŔ͈ޫहͬŅŪũźťųŰŦŵũŪťŪŶŮஅ૗ͤ͢ͅ‫خ‬ণ‫̭̹̱ͧ͂ا‬Ȃਆនࠬ‫̷͈̞̤֚̀͜ͅۯ‬໐́œŐŔ͈ಇୟ̦۷ख़̯̹ͦȃষͅȂਆន̥ͣŕņńͬ໦ၗ෽ူ̱Ȃ೩ॸளġ ĩĲĦŐĳĪȂ̜̞͉ͥ೩‫ူו‬ġ ĩıįĶĦࠬୄ‫܄‬ခ෽౷Īġ ‫́ئ‬෽ူ̱̹̭͂ͧȂœŐŔ̦ಇୟ̱
̹ȃ̹͘൳শͅŗņňŇ͈อ࡛̦ᄤૺ̱̞̹̀ȪœŦŢŭĮŵŪŮŦġ őńœ༹ȫȃ̷̭́œŐŔ͈ಇୟ͈ŗņňŇอ࡛ᄤૺ̤̫ͥͅ‫۾‬ဓٜͬଢ଼̳̹ͥ͛ͅȂŕņńͬœŐŔġ ŪůťŶŤŦųȂġ őźŰŤźŢůŪůͤ͢ͅੜၑ̱̹ȃőźŰŤźŢůŪůͤ͢ͅŕņń̤̫ͥͅŗņňŇ͈อ࡛ᄤૺ̦͙̹ͣͦȃոષͤ͢Ȃਆនඤ͈೩ॸளȆ೩‫͉́ޏ۪ူו‬Ȅŕņń͉œŐŔ͈ಇୟͤ͢ͅŗņňŇͬॲ୆̱Ȃ̷͈̞ࣞ୆
ంෝͬ‫ڕ‬ං̱̞̭̦̀ͥ͂াऐ̯̹ͦȃ䋭 㪈㪌㪋 䋭őŃĲĮĶ

ਆនࠬ‫ۯ‬ඤ๧̤̫ͥͅ ńřńœĸ ͈‫ܥ‬ෝٜଢ଼ɛ५നġ࠲ং ĲĭĳȂ‫ۼ‬୞ġජ࡮ ĲȂఱٖġ௱ࢣ ĲȂਝ५ġᎢ༟ ĲȂ๳നġణࢼ ĴȂ୼ུġణ༟ ĲȂłŭŢŮġŎŰũŢŮŮŢťġŕŰŸŧŪŬĲȂࣞ‫ޘ‬ġങ຃ ĳȂ૰५ġੇढ ĳȂ໌ຶġત૞ ĳȂ๳നġ‫ނ‬ঊ ĳĴ ཤ٬ൽఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬ક‫ شٸܕا‬Ĳ

ِș͉̭ͦ́͘ਆនࠬ‫ۯ‬ඤ๧ळ༾ġ ĩŕŶŮŰųġ ŦůťŰŵũŦŭŪŢŭġ ŤŦŭŭ Ļġ ŕņńĪġ ͬ໦ၗ෽ူ̱Ȅ̷̦ͦͣୃુࠬ‫ۯ‬ඤ๧ळ༾ġĩŏŰųŮŢŭġŦůťŰŵũŦŭŪŢŭġŤŦŭŭ ĻġŏņńĪġ͂๤‫ۯ̱ࠬ̀ڛ‬૧୆ෝ̦̞̭ࣞ͂Ȅအș̈́֒ഥঊ͈อ࡛̦ᄤૺ̱̞̭̀ͥ͂̈́̓ͬ

特別講演

Ĳ ཤ٬ൽఱ‫ڠ‬ভ‫ڠ‬໐ࠬ‫ۯ‬୆໤‫ޗڠ‬৒Ȃĳ ཤ٬ൽఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬Ȇࡤ‫شٸܕݟ‬Ȃ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine༭̧̱̹࣬̀ȅِș͉߃ාȄŕņń̤̞̀ͅอ࡛̦ᄤૺ̱̞̀ͥ֒ഥঊ̱͂̀ȄΉκ΃ͼϋτΓίΗȜ̜́ͥńřńœĸͬ‫͉́ݪ‬ŕņń̤̫ͥͅńřńœĸ͈‫ܥ‬ෝ̞ٜ̾̀ͅଢ଼̱̹ȅࠖ࢕ඵਹ྾‫ע‬அ૗ͤ͢ͅȄζ;Α๧‫֊ئ‬૒ਆនġ ĩ՛଻ࣱ૗ਆĪġ͍̈́ͣͅΪΠਆនġ ĩ۴‫܈‬Ȅ෹‫܈‬Ȅఱಸ‫܈‬Īġ ͈ࠬ‫̞̤̀ͅۯ‬ńřńœĸ͈อ࡛̦ୃુࠬ‫ࣞͤ͜͢ۯ‬ອഽͅ෇̹͛ͣͦȅζ;Α๧‫֊ئ‬૒ਆន̥ͣŕņńͬȄ΋ϋΠυȜσ̱͂̀ୃુζ;Α͈๧ໂ̥ͣŏņńͬ໦ၗ෽ူ̱Ȅńřńœĸ͈อ࡛ͬ๤‫̹̱ڛ‬̭͂ͧŕņń̤̞̀ͅอ࡛̦ᄤૺ̱̞̹̀ȅŴŪœŏłġ ͬဥ̞̀ŕņń̤̫ͥͅńřńœĸ͈‫ܥ‬ෝٜͬଢ଼̱̹ȅńřńœĸΦΛ·Θ;ϋͤ͢ͅȄဋ௢ෝȄ‫଼ࠁ࣌ۯ‬ෝȄ೩ࠬୄ೷ࢯ଻̦೩‫̹̱ئ‬ȅষͅȄńřńœĸ͈ς΄ϋΡȄńřńōĲĳ͉ŕņń͈́ņœŌΏΈ΢σͬ‫̱ا଻ڰ‬Ȅဋ௢ĭ ‫଼ͬࠁ࣌ۯ‬ည൵̱̞̭̦̀ͥ͂া̯̹ͦȅ̹͘ȄņōŊŔł༹ͤ͢ͅȄळ༾෽ူષୄಎ͈
ńřńōĲĳτασͬ๤‫̳͂ͥڛ‬ŕņń͉́ŏņń̥̹ͤࣞ̽͢ȅոષͤ͢Ȅŕņń͉ńřńōĲĳ İ ńřńœĸ΂ȜΠ·ρͼϋ‫ࢹܥ‬̞ͤࣞࠬ͢ͅ‫ۯ‬૧୆ෝͬ֋঵̱̞̭̦̀ͥ͂াऐ̯̹ͦȅ̯ͣͅȄŕņń̤̫ͥͅńřńœĸอ࡛ᄤૺ͈‫ܥ‬੬ͬౝ̹ͥ͛ȄŏņńͬŗņňŇ́ঁ̱̹̭ࠣ͂ͧȄńřńœĸ Ůœŏłอ࡛̦ᄤૺ̱̹ȅոષ͈ࠫ‫ͤ͢ض‬Ȅਆន๷઀۪‫̞̤̀ͅޏ‬ŕņń͉ńřńœĸ͈อ࡛̱ͬٚ̀ࠬ‫ۯ‬૧୆ͅ૬̩‫۾‬ဓ̱̞̀ͥ‫خ‬ෝ଻̦া̯̹ͦȅłűŰűŵŰŴŪŴġŰŧġŦůťŰŵũŦŭŪŢŭġŤŦŭŭŴġťŶųŪůŨġŵũŦġŧŰųŮŢŵŪŰůġŰŧġŵŰųŵŶŰŶŴġţŭŰŰťġŷŦŴŴŦŭŴġŪůġŵũŦġ
ŮŦŵŢŮŰųűũŪŤġXenopus laevisġŵŢŪŭ

口頭発表

őŃĲĮķ

会長招待講演 シンポジウムࡉ੄̱̹ȅńřńœĸ͉အș̈́‫܈‬ਆ͈ਆនࠬ‫̫̤ͥͅۯ‬อ࡛̦༭̯̞̦࣬ͦ̀ͥȄŕņń̤̫ͥͅ‫ܥ‬ෝ͉ະྶ̜́ͥȅུࡄɛ൥ࡔġୃგ ĲȂ‫ؖ‬ġකঊ ĳȂňũŢŻŪŻŢťŦũġŎŰũŢŮŮŢť Ĳ

䋭 㪈㪌㪌 䋭著者索引

The formation of tortuous blood vessels is associated with aging, ischemia, hypertension, and diabetes. Although this
vascular phenotype is suggested to play important roles in pathological changes, it remains unknown how the normal
vasculature deforms into the tortuous spiral twisting phenotype. In previous studies using a Xenopus laevis tail model,
we indicated preceding cell death in the areas of fins and tails just before the formation of tortuous vasculatures.
However, it is still uncertain which cell types undergo apoptosis in these areas, especially as for the endothelial cells,
the key player in the blood vessel formation. To understand the fate of the endothelial cells, we here used biotinylatedtomato lectin and active caspase-3 antibody and identified endothelial cells and apoptotic cell death, respectively,
during amphibian metamorphosis. Double immunohistochemical detection of the blood vessels and active caspase-3
revealed no endothelial cells positive for the active caspase-3 in premetamorphic tail at stage 54. However, the positive
cells were detected in the fins at metamorphic climax (stage 59). These cells were scattered in all regions of the tails at
late metamorphic climax (stage 64). Since tortuous blood vessels were not found in any region at stage 54 but formedat the edge of fins at stage 59 and spread throughout the tail at stage 64, endothelial cell death spatiotemporally
coincides with tortuous vascular phenotype. The total number of apoptotic cells detected in the tails was similar instage 59 and 64 tadpoles, although their number was small. Adjustment by the area of biotin-labeled blood vessels also
showed similar number of apoptotic cells in stage 59 and 64 tadpoles, suggesting a steady and gradual change in the
tortuous blood vessel formation. Taken together, tortuous vascular structure may be shaped by the steady and gradualapoptotic cell death of the endothelial cells in the regressing tails.

ポスター発表 ＹＩＡ選考発表

Ĳ ඾ུ֓‫ش‬ఱ‫ڠ‬Ⴧ૽ພࡄ‫ݪ‬ਫ਼ພၑ໐࿝Ȃĳ ඾ུ֓‫ش‬ఱ‫ڠ‬୆໤‫ޗڠ‬৒őŃĲĮĸ

ņŧŧŦŤŵŴġŰŧġńŌĳġŪůũŪţŪŵŰųġŰůġŢŤŤŶŮŶŭŢŵŪŰůġŰŧġŊŬŃġŢůťġűŦųŮŦŢţŪŭŪŵźġŪůġŷŢŴŤŶŭŢųġ
ŦůťŰŵũŦŭŪŢŭġŤŦŭŭŴġ
ɛՠ࿤ġဢ๼ ĲĭĳȂ઀࿤ġີ౳ ĳ
Ĳ ୷ဩఱ‫ڠ‬ఱ‫֭֒ݪࡄڠ֭֓ڠ‬ഥঊ୆‫ڠا‬Ȃĳġĩ ࢖़ Ī ൐‫ނ‬സ֓‫ڠ‬௙ࣣࡄ‫ݪ‬ਫ਼Ȇ֒ഥঊ٨་

Angiogenesis inhibitors have been searched as agents having a potential therapeutic value in various angiogenic
diseases and solid tumors. NF-kB activated through degradation of its endogenous inhibitor, IkB, has been implicatedin tumor malignancy. In canonical pathway of NF-kB activation, IkB is phosphorylated by IkB kinase (IKK) anddegraded by ubiquitin-proteasome. Also it has been shown that calpain degrades IkB phosphorylated by protein kinase
CK (casein kinase) 2, which is dysregulated in cancer. We found the suppressive effect of both IKK inhibitors andcalpain inhibitors on angiogenesis in chicken embryo chorioallantoic membrane (CAM). Recently, it is known that
IKK inhibitors are not significantly effective in suppression of growth of solid tumors. Therefore, we focused on the
involvement of CK2-dependent pathway in angiogenesis and found the reduction of VEGF and bFGF inducedangiogenesis in mouse dorsal pocket and the suppression of tube formation in vascular endothelial cells cultured on
matrigel by CK2 inhibitors. In this study, we examined on whether CK2 inhibitors reduce the permeability of vascularendothelial cells, as angiogenic-active vasculature shows high permeability. The effective concentration of CK2
inhibitor in the accumulation of IkB and NF-kB in the cytosol of endothelial cells decreased the permeability. CK2
inhibitors suppressed the degradation of IkB and the permeability, which is an indicator of active-angiogenesis, inendothelial cells. These results suggest that the suppression of NF-kB activation by CK2 inhibitor may lead to antiangiogenic conditions.

őŃĲĮĹŗņňŇ ஷ‫ٺ‬ੜ౾ಎগࢃͅ۷ख़̯ͦͥ࿌྄ࠬ‫͈ۯ‬։ુ଻ȇ૧୆ॾζ;ᾼ̤̫ͥ࠿൦
ɛ૩നġՙȂಎࡔġ഼Ȃ૩ġཻ๼ȂाུġࡊংȂ୞֔ġཆဎཤၖఱ‫ڠ‬࿪‫ڠ‬໐໦ঊ࿪ၑ‫ޗڠ‬৒Ⱥ෸ࠊȻġ ŗŢŴŤŶŭŢųġ ŦůťŰŵũŦŭŪŢŭġ ŨųŰŸŵũġ ŧŢŤŵŰųġ ĩŗņňŇĪġ ͉Ȃ‫ح‬Ⴂؕแ་଻̤͍͢ൠෂພ࿌྄છ́۷ख़̯ͦͥ࿌྄ࠬ‫ۯ‬͈൫ً଻ᄤૺ͂։ુ૧୆̤̞̀ͅਹါ̈́࿨‫̞̲ͥ̀׵ͬڬ‬ȃ̷͈̹͛Ȃၰ৖͈ۛহၷ༹̱͂̀ࢯ ŗņňŇ ၷ༹̦ಕ࿒̯
̞̦ͦ̀ͥȂহၷ࣐̹ͬ̽ࢃ͈࿌྄ࠬ‫ࢹ͈ۯ‬௮͞ࢹ଼ळ༾Ȫඤ๧ळ༾̤͍͢βς΍ͼΠȫ͈έͿΦΗͼί͈་‫ا‬Ȃ̹͘ठࠁ଼̯̹ͦࠬ‫ܥ͈ۯ‬ෝ̞͉̾̀ͅྶ̥̯̞̞ͣͦ̀̈́ͅȃུࡄ‫͉́ݪ‬Ȃࠬ‫ۯ‬૧୆͈৘ࡑκΟσ̱͂̀ไဥ̯̞ͦ̀
ͥ૧୆ॾ‫ܢ‬ζ;Α͈࿌྄̤̞̀ͅȂŗņňŇġஷ‫ٺ‬ੜ౾ಎগࢃ͈࿌྄ࠬ‫࠿଼̞̀̾ͅࠁۯ‬൦࣐̹ͬ̽ȃȺ༹༷Ȼġ૧୆ॾ‫ܢ‬Ȫı̹͉͘ĵ඾Ⴂȫ͈ζ;ᾼġŗņňŇġ਋ယఘΙυΏϋ΅΢ȜΔஷ‫ٺ‬࿪̜́ͥġŌœŏķĴĴȪĲı ŮŨİŬŨȫ
ͬġĳ඾‫ۼ‬๧‫ئ‬ൎဓ̱̹ȃ̷̱̀Ȃ̷͈ࢃͅࠁ଼̯ͦͥ࿌྄ࠬ‫̫̤ͥͅۯ‬ඤ๧ळ༾̤͍͢βς΍ͼΠ͈་‫ا‬Ȃࠬၠ͈ခྫ̤
͍͢ழ૕͈ॸளેఠ̞̾̀ͅȂඅ։എζȜ΃Ȝͬဥ̞̀ࠖ࢕྾‫ע‬அ૗࣐̠̭ͬ͂ͤ͢ͅ࠿൦̱̹ȃȺࠫ‫ض‬Ȇࣉख़Ȼġı̹͉͘ĵ඾Ⴂζ;ᾼĳ඾‫ ͈ۼ‬ŌœŏķĴĴੜ౾࣐̠ͬ͂Ȃ࿌྄ࠬ‫͈ۯ‬૧୆ဲଷ͂࿉ळࠬ‫͈ۯ‬పੀ̦۷ख़̯
̹ͦȃ̴̞͈ͦ඾Ⴂ͈ζ;ᾼੜ౾࣐̹ͬ̽ાࣣ͜ͅȂੜ౾ಎগࢃĴ඾࿒̥ͣࠬ‫଼̦ࠁ͈ۯ‬ইͤ͘Ȃ̷͈ࢃ͈ࠬ‫ۯ‬࿌̦࿌྄ນ௄໐ͬໞ̠௸ഽͅఱ̧֑̞͉̈́෇̥̹͛ͣͦ̈́̽ȃ̱̥̱Ȃࠁ଼̯̹ͦࠬ‫ۯ‬࿌͉ͅȂࠬ‫͈ࠂۯ‬։ુ͂βς΍ͼΠ͈ġŢŭűũŢĮŴŮŰŰŵũġŮŶŴŤŭŦġŢŤŵŪůġ͈อ࡛௩‫̹ͦͣ͛෇̦ح‬ȃ̹͘Ȃࠁ଼̯̹ͦࠬ‫ۯ‬࿌ࠬ͜ͅၠ̦̜̭̦ͥ͂া̯̹ͦ
̦Ȃ̷ͦͣͥ͢ͅ࿌྄ழ૕͈͒ॸள‫͉͂ુୃ͉ݯރ‬։̞̹̈́̽̀ȃ̭͈ͦͣࠫ‫͉ض‬ȂŗņňŇġ ஷ‫ٺ‬ੜ౾ࢃͅठࠁ଼̯ͦ
̹ඤ๧ळ༾͞βς΍ͼΠ̦ୃુ͉͂։̈́ͥέͿΦΗͼίͬা̱Ȃࠬ‫ܥ͈ۯ‬ෝ͜ୃુ͉͂։̞̭̈́̽̀ͥ͂ͬাऐ̱
̞̀ͥȃ
ਲ̽̀Ȃ
‫܉‬৖ۛͅࢯġŗņňŇġၷ༹࣐̠ͬष͉ͅȂহၷਞၭࢃ͈ಕփ૬̞ࠐً۷ख़̦ຈါ̜́ͥ͂ࣉ̢̹ͣͦȃ䋭 㪈㪌㪍 䋭ĺ࠮ĳķ඾Ȫ࿐ȫġĲĲĻĲıȡĲĳĻĲıġġεΑΗȜٛાεΑΗȜġ‫ܖ‬ய őŃĲȶ୆ၑ‫଻ڰ‬໤ৗȟ̷͈ఈȷőŃĲĮĺńŢųťŪŰŵŰűũŪůĮĲġŢŤŤŦŭŦųŢŵŦŴġŵũŦġťŦŷŦŭŰűŮŦůŵġŰŧġŢŵũŦųŰŴŤŭŦųŰŵŪŤġŭŦŴŪŰůŴ
ɛള໐ġీ࿟Ȃᆇ૾֔ġ‫ࠃـ‬Ȃ݊౷ġक࿦‫ج‬Ȃ‫ؗ‬५ġဩ࠮Ȃള໐ġႡජȂಿ౓୼ġએ‫ܮ‬Ȃ५ུġ߽ࢁȂऎ൥ġ࠲ࢁȂչ൐ġঃঊɛࡼ਱၆ġ‫ޕ‬ঊȂ॓֔ġࠉ෗Ȃ૰‫݌‬ġ઎ঊȂ૧൥ġ࿹‫ج‬Ȃ઀५ġࢴ‫ם‬Ȃဠġ᠇Ȃ૒ಅġၨ֚Ȃ५ඤġ߼ࢬȂು५ġ࿸֚ȂനಎġՔȂ‫਀ع‬ġ‫ࣝݛ‬Ȃ૧൥ġၦ࣐ͺΡτΦιΟνςϋȪłŎȫ͉Ȃ૤ࠬ‫̲͉͛ͬࠏۯ‬Ȃ஠૸͈ழ૕́ॲ୆̯ͦͥఉद̈́୆ၑ‫ͬ଻ڰ‬ခ̳ͥβίΙΡ̜́ͥȃłŎ͈਋ယఘ̜́ͥńōœ͉ͅȂ਋ယఘ‫಺଻ڰ‬୯ΗϋΩ·œłŎő̦ࣣ̱ࠫȂ਋ယఘ‫ܥ‬ෝͬଷࢄ̱̞̀ͥȃِș͉̭ͦ́͘ȂœłŎő͈ಎ́͜œłŎőĳ͈ΦΛ·ͺ;Πζ;Α͈͙̦ȂłŎΦΛ·ͺ;Πζ;Α͂൳အ͈ࠬ‫͈ۯ‬อోະ஠ͤ͢ͅథ୆
౿ঘ̭͂̈́ͥ͂ͬࡉ੄̱Ȃࠬ‫̫̤ͥͅۯ‬łŎĮœłŎőˎࠏ͈ਹါ଻ͬ༭̧̱̹࣬̀ȃ༷֚ȂłŎ̤͍͢œłŎőĳ͉ಎଥ૰ࠐࠏ́ࣞ͜อ࡛ͬ෇͛ͥȃ̭ͦ́͘ͅłŎΰΞυΦΛ·ͺ;Πζ;Α̦Ȃ‫଻ݢ‬ෞ‫ࠬݹ‬ੜၑࢃȂෞඤॸ‫ا‬ΑΠτΑ̦ᄤૺ̱̀ࢸण̦௩՛̳ͥমȃłŎ઼ًอ࡛ζ;Α̦Ȃྕ଻ෞ‫ࠬݹ‬ੜၑࢃȂࠬ‫ۯ‬૧୆̦ᄤૺ̱Ȃ෇౶‫ܥ‬ෝ̦٨஝̳̭̦ͥ͂༭
̯̞࣬ͦ̀ͥȃ༷֚Ȃෞࠬ‫ۯ‬વ‫̫̤ͥͅٺ‬œłŎőĳ͈փ͉݅ະྶ̜́ͥȃłŎ̤͍͢œłŎőĳγκΦΛ·ͺ;Πζ;Α͉థ୆౿ঘ͈̹͛Ȃུࡄ‫଼͉́ݪ‬ఘ͈ංͣͦͥłŎ̤͍͢œłŎőĳΰΞυΦΛ·ͺ;Πζ;Α
ȪłŎĬİȽĭġ œłŎőĳĬİȽȫͬဥ̞̀Ȃಎఱෞ൲ྤ໾णͥ͢ͅෞ‫ࠬݹ‬κΟσĩŎńłŐκΟσĪͬै଼̱Ȃඤ֦଻łŎĮœłŎőĳࠏ͈‫଻ࠬݹ‬ෞࠬ‫ۯ‬વ‫̤ͅٺ‬̫ͥພఠ୆ၑ‫ڠ‬എփ݅ͬ࠿൦̱̹ȃ

ポスター発表 ＹＩＡ選考発表૞ਗఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪ພఠ‫࣒ڠ‬ज

口頭発表őŃĲĮĲı ‫଻ࠬݹ‬ෞࠬ‫ۯ‬વ‫̫̤ͥͅٺ‬ͺΡτΦιΟνςϋȽ œłŎőĳ ࠏ͈փ݅会長招待講演 シンポジウム

Cardiotrophin-1 (CT-1), a cytokine belonging to the interleukin-6 superfamily, was recently shown to be expressed in
the intima of early atherosclerotic lesions in the human carotid artery. CT-1 stimulates pro-atherogenic molecule
expression in human vascular endothelial cells (EC) and monocyte migration. However, it has not been reported
whether CT-1 accelerates atherosclerosis. This study was performed to examine the stimulatory effects of CT-1 on
human macrophage foam cell formation, human EC proliferation, and the migration and proliferation of humanvascular smooth muscle cells (VSMCs) in vitro, and on the development of atherosclerotic lesions in apolipoprotein Edeficient (ApoE-/-) mice in vivo. CT-1 was expressed at high levels in ECs and macrophages in both humans and
ApoE-/- mice. CT-1 significantly enhanced oxidized low-density lipoprotein-induced foam cell formation associatedwith increased levels of CD36 and acyl-CoA:cholesterol acyltransferase-1 (ACAT-1) expression in human monocytederived macrophages. CT-1 also significantly stimulated the migration and proliferation of human aortic VSMCs, but
not EC proliferation. Four-week-infusion of CT-1 into ApoE-/- mice significantly accelerated the development of aortic
atherosclerotic lesions with increased monocyte/macrophage infiltration and VSMC content in the aortic wall.
Activation of inflammasome, such as apoptosis-associated speck-like protein containing a caspase recruitment domain,
nuclear factor-ЀB, and cyclooxygenase-2, was observed in exudate peritoneal macrophages from ApoE-/- mice
infused with CT-1. Infusion of anti-CT-1 neutralizing antibody alone into ApoE-/- mice significantly suppressedmonocyte/macrophage infiltration in atherosclerotic lesions. These results indicate that CT-1 accelerates thedevelopment of atherosclerotic lesions by stimulating the inflammasome and foam cell formation associated with
CD36 and ACAT-1 up-regulation in macrophages and VSMC migration and proliferation, contributing to theoccurrence of atherosclerotic vascular diseases. Blockade of cardiotrophin-1 is expected to emerge as a new line oftherapy against atherosclerosis.

特別講演൐‫ނ‬࿪‫ش‬ఱ‫ڠ‬୆ྵ‫ڠش‬໐૤ࠬ‫ݪࡄڠش֓ۯ‬৒

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineĹĮĲı਩Ⴂ͈΂Α࿤୆߿ζ;ΑȂ̤͍͢łŎĬİȽȂœłŎőĳĬİȽζ;ᾼచ̱̀ŎńłŐੜၑ࣐̞ͬȂĳশ‫ࠬͅࢃۼ‬ၠͬอ࡛ٜଢ଼࣐̹ͬ̽ȃłŎĬİȽ̤͍͢œłŎőĳĬİȽ͉́Ȃ࿤୆߿ͅ๤‫̱̀ڛ‬Ȃෞࠬၠ͈ٝ໘̦ಁ‫̱װ‬Ȃෞਹၾ͈௩‫ͬ࢜߹ح‬෇̹͛ȃłŎĬİȽ͉́Ȃĳĵশ‫͈ࢃۼ‬୆ంၚ͈೩‫̹͛෇ͬئ‬ȃœłŎőĳĬİȽ͉́࿤୆߿ζ;ᾼ๤‫̱̀ڛ‬Ȃࢸणஜࢃ͂͜ෞ
ඤ͈œłŎőĳอ࡛͈೩‫̹͛෇ͬئ‬ȃ̴̞͈ͦζ;Ὰ̤̞͜ͅȂࢸणࢃ͈łŎอ࡛͉ᄤૺ̱̹̦ȂœłŎőĳĬİȽ͉́ȂࢵͅłŎอ࡛͈ષઌͬ෇͛ȂŊōĮĲϸ͞ŕŏŇĮϷ͈̈́̓‫׶‬છ଻΍ͼΠ΃ͼϋ͈อ࡛ષઌ߹࢜ͬ෇̹͛ȃłŎĮœłŎőĳࠏ͉Ȃෞ‫̞̤̀ࠬͅݹ‬Ȃࠬၠ͈֋঵͞‫׶‬છ͈ଷࢄͅ൱̞̞̀ͥ‫خ‬ෝ଻̦াऐ̯ͦͥȃ䋭 㪈㪌㪎 䋭著者索引

ठ‫̵̯ٳ‬Ȃෞඤࠬၠ͈ٝ໘ͬτȜΎȜΡΛίρȜ௡౾̀ࠗͅ௶̱̹ȃĳĵশ‫ͅࢃۼ‬ෞͬഊ੄̱Ȃພၑٜଢ଼̤͍֒͢ഥঊ

őŃĲĮĲĲ ŔĲőĳ ਋ယఘ͉ ŦŏŐŔĮŏŐ ࠐႹͬဲଷ̳̭ͥ͂ͤ͢ͅͺ΢έͻρ΅ΏȜΏοΛ·ͅచ̱̀ဲଷഎͅ൱̩
ɛ‫ུؖ‬ġհဎ ĲȂ፥ġࢬ ĲȂ‫ؖ݌‬ġგࢴ ĲȂఉ‫ݛ‬გġങঊ ĲĭĳȂఉ‫ݛ‬გġု Ĳ
Ĳ ߄ాఱ‫֓ڠ‬࿪༗࠲ࡄ‫ۯࠬࠏڠ֖֓ݪ‬໦ঊ୆ၑ‫ڠ‬Ȃĳ ୞୼ࡇၛۭࢌఱ‫ڠࢌۭڠ‬໐࠲ࢫ‫࣒ڠش‬जΑέͻϋΌΏϋˍĮςϋॸȪŔĲőȫ͉ŔĲőĲ̱ͬٚ̀ࠬ‫ۯ‬ඤ๧ळ༾͈Ψςͺ‫ܥ‬ෝͬ‫ۯ̭̳ࠬͤ͂ͥ͢ͅاޑ‬൫ً଻ͬဲଷ̳̭̦ͥ͂౶̞ͣͦ̀ͥȃ̱̥̱̦̈́ͣȄŔĲőĳ͈ࠬ‫ۯ‬൫ً଻ଷࢄ‫̫̤ͥͅࢹܥ‬࿨‫̺ྚ͉ڬ‬ະྶ̜́ͥȃ‫ࠬݱ‬ୄͺσήηϋȪŃŔłȫۜैͥ͢ͅෝ൲଻஠૸଻ͺ΢έͻρ΅ΏȜκΟσ̤̞̀ͅȄŔĲőĳĮŌŐζ;Ά͉ࠬಎΪΑΗηϋෛഽ͈௩‫͉ح‬࿤୆߿ȪŘŕȫζ;Α͂๤‫̱̀ڛ‬ओ։̦̥̹̦̈́̽Ȅࠬ‫ۯ‬൫ً଻ᄤૺȄࠬգ೩‫ئ‬Ȅఘ‫أ‬೩‫͍̤͢ئ‬౿ঘၚ̴͈̞ͦ͜՛‫̹̱ا‬ȃ̹͘Ȅͺ΢έͻρ΅ΏȜ͈ιΟͻ΀ȜΗȜ̜́ͥࠬ઀โ‫֦ا଻ڰ‬ঊȪőłŇȫͬ୓ಕ̳ͥκΟσ̤̞̀͜ͅȄŔĲőĳĮŌŐζ;Ά͉ࠬ‫ۯ‬൫ً଻ᄤૺ̤͍͢౿ঘၚ̦՛‫̹̱ا‬ȃőłŇൎဓͤ͢ͅఱ൲ྤ‫͍ݞ‬෹̤̫ͥͅ
łŬŵ͂ŦŏŐŔ͈ςϋॸ‫̦ا‬௩‫̦̹̱ح‬Ḙ͈̏؊൞͉ŔĲőĳĮŌŐζ;ΆŘŕζ;ᾼ๤‫̱̀ڛ‬௩‫̹̞̱̀ޑ‬ȃ൳အͅȄఱ൲ྤ̤̫ͥͅőłŇൎဓͥ͢ͅŤňŎő‫܄‬ၾ͈௩‫͜ح‬ŔĲőĳĮŌŐζ;Ά௩‫̹̞̱̀ޑ‬ȃŔĲőĳĮŌŐζ;Ὰ̤̞ͅȄŏŐŔஷ‫ٺ‬࿪ōĮŏłŎņ͈ൎဓ̜̞͉ͥŦŏŐŔ֒ഥঊŌŐ͉Ȅࢯࡔൎဓͥ͢ͅͺ΢έͻρ΅ΏȜ̤̞̀ࠬͅ‫ۯ‬൫ً଻ᄤૺȄࠬգ೩‫ئ‬Ȅఘ‫أ‬೩‫͍̤͢ئ‬౿ঘၚͬ٨஝̱̹ȃŔĲőĳĮŌŐζ;Α̥ͣౙၗ̱̹෹๷઀ࠬ‫ۯ‬ඤ๧ळ༾ȪŌŐĮņńȫ͉́࿤୆߿
ඤ๧ळ༾ȪŘŕĮņńȫ͂๤‫̱̀ڛ‬ȄőłŇ‫͍ݞ‬ŔĲőͥ͢ͅłŬŵ͂ŦŏŐŔ͈ςϋॸ‫͍̤͢ا‬ŏŐॲ୆̦ᄤૺ̱̞̹̀ȃőłŇͥ͢ͅळ༾‫ۼ‬୪಍ࣣ͈ࠫ༲ٟ͉ŌŐĮņń̤̞̀ͅ௩‫̱ޑ‬ȄōĮŏłŎņͤٝ͢ͅ໘̱̹ȃŏŐ͉ϸĮ΃ΞΣϋ͈ S ĮΣΠυΏσ
‫̧̱̭̀ܳ֨ͬا‬ඤ๧̤̫ͥͅळ༾‫ۼ‬୪಍ࣣࠫͬஷ‫̳ͥٺ‬ȃŌŐĮņń͉́ȄőłŇ‫͍ݞ‬ŔĲőġঁࠣͥ͢ͅϸĮ΃ΞΣϋ͈ S ĮΣΠυΏσ‫͉ا‬ŘŕĮņńͅ๤‫̱̀ڛ‬ᄤૺ̱Ḙ͉̏ͦōĮŏłŎņੜၑ̽̀͢ͅ೩‫̹̱ئ‬ȃոષ͈ࠫ‫̥ͣض‬Ȅࠬ‫ۯ‬ඤ๧ळ༾ͅ
อ࡛̳ͥŔĲőĳ͉łŬŵĮŦŏŐŔࠐႹͬဲଷ̳̭ͥ͂ͤ͢ͅͺ΢έͻρ΅ΏȜͥࠬ͢ͅ‫ۯ‬൫ً଻ᄤૺͅచ̱̀ཡࢄഎͅ
ैဥ̳ͥ͂ࠫა̯ͦȄŔĲőĳ஖఼എͺΌΣΑΠ͉ͺ΢έͻρ΅ΏȜ͈̈́̓ࠬ‫ۯ‬൫ً଻વ‫͈ٺ‬হၷ͈ດഎ͂̈́ͥ‫خ‬ෝ଻̦‫ܢ‬ఞ̯ͦͥȃőŃĲĮĲĳ ņůťŰŵũŦŭŪŢŭġłŏőİňńĮłġŴźŴŵŦŮġŤŢůġţŦġŢġŵũŦųŢűŦŶŵŪŤġŵŢųŨŦŵġŧŰųġŮŦŵŢţŰŭŪŤġŴźůťųŰŮŦ
ɛඃၣġ࠲ ĲȂఱ౓ġ࠲ఊ჊ ĳȂ࿉ġ࡙ࠦ ĲȂབ࠮ġೄਏ ĴȂಎ๶ġ֚გ ĵȂ‫୼ێ‬ġࡋহ Ĳ
Ĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼୆‫ڠا‬໐Ȃĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼ठ୆֓ၷ໐ȂĴ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼ळ༾୆໤‫ڠ‬໐Ȃĵ ‫ނ‬സఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬ႉ઄ພఠ֓‫ڠش‬

Background: Atrial natriuretic peptide (ANP) has been used clinically for the treatment of heart failure patients inJapan, and also exhibits a variety of physiological effects through binding guanylyl cyclase-A (GC-A) receptor. We
and other groups has been reported that GC-A is abundantly expressed in endothelial cells. In the present study, we
explored the therapeutic potential of endothelial ANP/GC-A system for the treatment of metabolic syndrome.
Methods: We generated endothelial cell-specific GC-A transgenic mice using Tie2 promoter and enhancer (EC-GC-ATg), inducible endothelial cell-specific GC-A transgenic mice (Inducible EC-GC-A-Tg), and also endothelial cellspecific GC-A knockout mice (EC-GC-A-KO). In addition, we used eNOS transgenic mice (eNOS-Tg). Insulin
resistance was evaluated by intra-peritoneal glucose tolerance test (IPGTT) and intra-peritoneal insulin tolerance test
(IPITT). Results: The phenotypes of EC-GC-A-Tg were very unique. Systolic blood pressure in EC-GC-A-Tg was
significantly lower compared with wild-type mice (WT). In addition, heat weight/body weight ratio and arterial
elastance were smaller and lower in EC-GC-A-Tg compared with WT. Synchrotron radiation angiography showeddecrease of basal vascular tone in EC-GC-A-Tg and increase in EC-GC-A-KO compared with in each control mice.
Basal body weight of WT and EC-GC-A-Tg, flox mice and EC-GC-A-KO were comparable. However, after taking 8
weeks of high-fat diet, increase of body weight of EC-GC-A-Tg was significantly less than WT. On the other hand,
EC-GC-A-KO showed more than increase of body weight. IPGTT and IPITT showed improvement of insulin tolerance
in EC-GC-A-Tg, and worsen in EC-GC-A-KO compared with in each control mice. Interestingly, Inducible EC-GC-ATg showed less increase of body weight accompanied by aging. The body weight of eNOS-Tg was comparable with
WT before and after taking 8 weeks of high-fat diet.Conclusions:These data suggest that endothelial ANP/GC-A
system can be a therapeutic target for metabolic syndrome.
䋭 㪈㪌㪏 䋭őŃĲĮĲĴ śŶŤŬŦų ρΛΠෞࢸणκΟσ̤̫ͥͅ łŮŭŰťŪűŪůŦ ͂ łŵŰųŷŢŴŵŢŵŪů ໵ဥൎဓ͈ෞ༗ࢌ࢘‫ض‬ɛນġ༿ຳȂ‫ع‬௖ġဉ๼Ȃ੄࢛ġ࠲ఊ჊Ȃ५‫ئ‬ġഔȂఊനġࢫ෗Ȃாനġ౺ঊȂՒ໐ġࢫඵ

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లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine‫ؖ‬५ఱ‫ڠ‬ఱ‫֭֓ڠ‬ভ࿪‫ڠ‬௙ࣣࡄ‫شݪ‬ෞ૰ࠐඤ‫ڠش‬ུ৘ࡑ͉́ȂłŮŭŰťŪűŪůŦġ ĩłŎĪ͂łŵŰųŷŢŴŵŢŵŪůġ ĩłŕĪͬ๬ྖκΟσρΛΠͅౙඊ̹͉͘໵ဥൎဓ̱Ȃ̷͈࢘‫̞֑͈ض‬ͬॸ‫ا‬ΑΠτΑ͞ůŦŶųŰŷŢŴŤŶŭŢųġ ŶůŪŵ͈̈́̓௰࿂̥ͣ࠿൦̱̹ȃȺ༹༷ȻśŶŤŬŦųρΛΠĩĹ਩ႢဎĪͬဥ̞ȂŗŦũŪŤŭŦ߲ȂłŎġ ĩĴŮŨİŬŨİ඾Īൎဓ߲Ȃłŕ ĩĲıŮŨİŬŨİ඾Ī ൎဓ߲ȂłŎĬłŕ໵ဥൎဓ߲ͅచ̱̀Ĳĳ਩Ⴂশͅĺı໦‫ֲۼ‬ಎఱෞ൲ྤ

特別講演Ⱥ෸ࠊȻ࡛हȂෞࢸणͅచ̳ͥহၷ༹͉ࡠ̤ͣͦ̀ͤȂ૧̹̈́হၷ༹͈‫ٳ‬อ̦ႉ઄࡛ા́‫̞ͥ̀ͦͣ͛ݥ̩ޑ‬ȃ̷̭́໾णࢃȂठ‫ۺ‬ၠ࣐̞ͬĳĵশ‫ͅࢃۼ‬౯൮̱ழ૕‫ڠ‬എ࠿൦࣐̹ͬ̽ȃȺࠫ‫ض‬Ȼழ૕‫ڠ‬എ࠿൦ͤ͢ͅŗŦũŪŤŭŦ߲ͅ๤͓ȂłŎ͂͜‫׶‬છζȜ΃Ȝ̤̫ͥͅ࠿൦͉́łŎ̱̩͉͜łŕౙඊൎဓ߲́ု଻ळ༾ତ͈ࡘઁͬ෇͛Ȃ໵ဥൎဓ̷߲̞́ͤ̽͢
̠ࡘઁ̱̞̹̀ȃ̹͘ȂŎŎőĮĺ͈อ࡛͉ŗŦũŪŤŭŦ߲ͅ๤͓Ȃłŕ߲̤͍͢໵ဥൎဓ߲́ဲଷ̯̤ͦ̀ͤȂńŰŭŭŢŨŦůĵ͈อ࡛͉łŕ߲̤͍͢໵ဥൎဓ߲́༗̹̞̹ͦ̀ȃ̹͘ȂłůŨŪŰŵŦůŴŪůġ ĳġ ŵźűŦġ Ĳġ ųŦŤŦűŵŰų͈ု଻ळ༾ତ͉łŎ߲́ࡘઁ̱Ȃłŕ߲̤͍͢໵ဥ߲̯́ͣͅࡘઁ̱̹ȃȺࠫაȻśŶŤŬŦųρΛΠ̤̞̀ͅȂłŎ͂łŕ͉ౙඊൎဓ͂๤‫̱̀ڛ‬໵ဥൎဓ̤ͅ
̞̀ෞ༗ࢌ࢘‫̩̦ࣞͤ͢ض‬Ȃ̷͈ι΃ΣΒθ̱͂̀ॸ‫ا‬ΑΠτΑ͈ဲଷȂůŦŶųŰŷŢŴŤŶŭŢųġ ŶůŪŵ༗ࢌ࢘‫۾̦̓̈́ض‬ဓ̱̞̭̦̀ͥ͂াऐ̯̹ͦȃɛ५‫ئ‬ġഔ ĲȂ‫ॄݠ‬ġ֚ඃ ĲȂୃུġგ૽ ĳĭĴȂఊനġࢫ෗ ĲȂாനġ౺ঊ ĲȂ౻നġ‫ج‬୆ ĲȂ઀ษġၦ࣐ ĳȂଫ࿤ġ‫ ܆‬ĳȂՒ໐ġࢫඵ Ĳ

口頭発表őŃĲĮĲĵ łōŔ ୢଡஜ‫̫̤ͥͅڙ‬อછஜ͈ࠬၠȆయ৫ ŶůŤŰŶűŭŪůŨį

会長招待講演 シンポジウム̱̩͉łŕౙඊൎဓ߲́ࢸणఘୟ͈ੀ઀̦ࡉͣͦȂ̷͉ͦ໵ဥൎဓ߲̯́ͣͅࡐಠ̜̹́̽ȃॸ‫ا‬ΑΠτΑζȜ΃Ȝ

Ĳ ‫ؖ‬५ఱ‫ڠ‬ఱ‫֭֓ڠ‬ভ࿪‫ڠ‬௙ࣣࡄ‫شݪ‬ෞ૰ࠐඤ‫ڠش‬Ȃĳ ༶ৣ஌֓‫ڠ‬௙ࣣࡄ‫ݪ‬ਫ਼໦ঊͼιȜΐϋΈΓϋΗȜȂȺ෸ࠊȻ߃ාȂୢଡࠬ‫ࢹ͈ۯ‬௮എȂ‫ܥ‬ෝഎ։ુ̦޼֎ੀ଻௰॑ࣁ‫ا‬છȪłōŔȫພఠͅ‫۾‬ဓ̳̭̦ͥ͂াऐ̯̞ͦ̀ͥȃ̷̭́łōŔκΟσζ;Αͬဥ̞̀ Ūůġ ŷŪŷŰ ͼιȜΐϋΈ࣐̞ͬȂ‫׋‬൲‫ܥ‬ෝવ‫ฺ̠࣐ͅૺ͈ٺ‬๷઀੏۪͈་‫̹͓಺ͬا‬ȃ̹͘Ȃ΂ȜΠρΐ΂ΈρέͻȜ༹ͬဥ̞̀ୢଡ͈ࠬၠ‫͍ݞ‬Έσ΋ȜΑయ৫ၾ͈௶೰࣐̞ͬȂ੏۪͂య৫͈ ŤŰŶűŭŪůŨ ‫ܥ‬ෝ̞̾̀ͅ࠿൦̱̹ȃȺ༹༷Ȼ৘ࡑ͉ͅłōŔ͈κΟσ൲໤̜́ͥňĺĴłΠρϋΑΐͿΣΛ·ζ;Αͬဥ̞̹ȃĲĳ਩ͬ‫׋‬൲વ‫ٺ‬อછஜȂĲķ਩ͬอછ੝‫ܢ‬ȂĲĺ਩ͬอછྎ‫͈ܢ‬κΟσ̱͂Ȃ΋ϋΠυȜσ̱͂̀࿤୆߿ζ;Αͬဥ̞̹ȃ‫ࡢڎ‬ఘཻ̞̾̀ͅଜ‫́ئ‬ୢଡĩōĵĮĶĪ್͈‫ݡ‬୨ੰ࣐̞ͬȂࠖ࢕૗ளͬಕවࢃͅඵ࢕ঊ႗ܳࠖ࢕ࡐ๷‫ͬޢ‬ဥ̞̀મळͅ۷ख़࣐ͬ̽
̹ȃ̹͘Ȃ༶ৣ଻ͺͼΕΠȜί́ດে̱̹ŪŰťŰŢůŵŪűźųŪůŦȂĳĮťŦŰŹźĮŅĮŨŭŶŤŰŴŦͬဥ̞̹΂ȜΠρΐ΂ΈρέͻȜ࣐̞ͬȂୢଡ͈ޫਫ਼ࠬၠ‫͍ݞ‬Έσ΋ȜΑయ৫ၾ͈௶೰࣐̹ͬ̽ȃȺࠫ‫ض‬ȻłōŔκΟσζ;Α͈ୢଡ͉́‫׋‬൲વ‫ͥͦͣࡉ̦ٺ‬ոஜ̥ͣ๷઀ࠬ‫͈ࠂۯ‬ੀ઀ͬ෇͛Ȃ‫׋‬൲વ‫ฺ̞࣐ͅૺ͈ٺ‬๷઀ࠬ‫ࠂ͈ۯ‬Ȃྟഽ͉ૺ࣐଻ͅࡘઁ̱̞̹̀̽ȃ̹͘Ȃ୤ࠬ‫௸ݩ‬ഽ͜‫׋‬൲વ‫ٺ‬อછஜ̥ͣခփͅ೩‫̱ئ‬Ȃ̷͈ࢃ̯ͣ͜ͅ೩‫̹̞̱̽̀ئ‬ȃࠬၠၾͅ‫͉̱̀۾‬අͅୢଡஜ‫࣐ૺ́ڙ‬ポスター発表 ＹＩＡ選考発表Ĵ ഩ‫ܨ‬೒૞ఱ‫୶ڠ‬౤ႀ֖‫ݪࡄ֗ޗ‬ΓϋΗȜ଻͈ࡘઁ̦ࡉ̹ͣͦȃ༷֚ȂΈσ΋ȜΑయ৫ၾ͉อછஜ֚ͅশഎͅ௩‫̱ح‬Ȃ̷͈ࢃພ‫̧̞̱̀ઁࡘฺ࣐̀̽ͅૺ͈ܨ‬Ȃ‫ͅ଻࣐ૺ̥ͣܢ‬વ‫̯ͦٺ‬௖చഎ‫̤ͤ̀̽ۿࠬͅݹ‬Ȃ̭͈ŶůŤŰŶűŭŪůŨ͉łōŔ́વ‫̞ޑ̦ٺ‬໐պ͕̓ࡐಠ̜̹̭́̽͂
̥ͣȂࠬ‫͈ࠂۯ‬։ુ̦łōŔພఠͅ૬̩‫۾‬ဓ̱̞̭̦̀ͥ͂াऐ̯̹ͦȃ䋭 㪈㪌㪐 䋭著者索引

ࠬၠ͂య৫̦ŤŰŶűŭŪůŨ̱̞̞̭̦̀̈́͂‫̧̹́෇ږ‬ȃȺࣉख़ȻłōŔκΟσζ;Α͈ୢଡ͉́ࠬၠȂయ৫͈ŤŰŶűŭŪůŨ்̦őŃĲĮĲĶ ডཛழ૕̤̫ͥͅ ŃŅŏŇ ͈୆ၑഎփ͈݅࠿൦
ɛಎࣺġකআ ĲȂ‫؍‬५ġ૯ၦ ĲȂ‫ؖ‬നġ੿ ĲȂ઀ႅġ޷ຳ ĲȂධ࿤ġഔ ĳ
Ĳ ୷ဩఱ‫ڠ‬ఱ‫֭ݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ૧‫ګ‬ఱ‫ڠ‬ఱ‫֭֓ڠ‬ভ‫ڠ‬௙ࣣࡄ‫شݪ‬੏۪‫ڠܕ‬໦࿤Ⱥ࿒എȻŃųŢŪůĮŅŦųŪŷŦťġ ŏŦŶųŰŵųŰűũŪŤġ ŇŢŤŵŰųȪŃŅŏŇȫ͉৽ͅෞඤ́ॲ୆໦๥̯ͦͥ૰ࠐ‫֦ူו‬ঊ̜́ͥȃণ઄‫ئ‬໐̤̞͉̀ͅιρΦ΋σΙϋ਋ယఘ͈‫ئ‬ၠΏΈ΢σ̱͂̀Ȃ̷͈਋ယఘ̜́ͥŕųŰűŰŮźŰŴŪůĮųŦŭŢŵŦťġ ŬŪůŢŴŦġ ŃġĩŕųŬŃĪͅैဥ̳̭ͥ͂ͤ͢ͅ୫૙ͬဲଷȂྎઑ͈։‫ا‬฽؊ͬ௯ૺ̳ͥȃ̱̥̱̭ͦ́͘ŃŅŏŇ̦ྎઑழ૕̤̞̀ͅ
͈̠̓̈́͢࿨‫͉̥̞̱̹ͥ̀ضͬڬ‬਱໦ٜͅྶ̯̞̥̹ͦ̀̈́̽ȃِࣽٝș͉ŃŅŏŇȆŕųŬŃ̦ྎઑழ૕̤̞̀ͅ
͜อ࡛̱̞̭̀ͥ͂Ȃ૙‫଻׎‬๬ྖζ;Α͈ডཛழ૕͉́ŃŅŏŇȆŕųŬŃ͈อ࡛ͅ་‫̭ͬ͂ͥͦͣࡉ̦ا‬૧̹ͅࡉ੄
̱̹ȃ̷ུ̭́ࡄ‫͉́ݪ‬အș̈́֒ഥঊ٨་ζ;Αͬဥ̞ডཛழ૕̤̫ͥͅŃŅŏŇȆŕųŬŃ͈୆ၑഎփ݅ͬ࠿൦̱̹ȃȺ༹༷Ȇࠫ‫ض‬ȻŔźůŢűŴŪůĮńųŦͬဥ̞̹૰ࠐळ༾අ։എŃŅŏŇࠧ৐ζ;ΑĩŔŚŏġ ŃŅŏŇġ ńŌŐĪ͉́‫ܡ‬༭͂൳အًͅ૙Ȇ๬ྖȆً‫ڰ‬൲ͬ෇̹͛ȃ̯ͣͅŢőĳĮńųŦͬဥ̞̹ডཛඅ։എŃŅŏŇࠧ৐ζ;ΑĩŢőĳġ ŃŅŏŇġ ńŌŐĪȂŕųŬŃࠧ৐ζ;ΑĩŢőĳġ ŕųŬŃġ ńŌŐĪ͜‫ًͅވ‬૙Ȇ๬ྖͬ෇͛Ȃডཛழ૕͈ŃŅŏŇȆŕųŬŃ͂ಎଥ૰ࠐࠏ͈͂Ⴒ‫͈۾‬ంह̦াऐ̯̹ͦȃ̱̥̱̭͈ͦͣζ;Ά͜ŔŚŏġ ŃŅŏŇġ ńŌŐ͂൳အ͈࣐൲։ુͬ෇̹̹͛͛ȂŢőĳġ ŕųŬŃġ ńŌŐζ;Α͈ಎଥ૰ࠐ
ழ૕͈́ŕųŬŃอ࡛ͬ‫̹̱෇ږ‬ȃෞழ૕஠ఘ͉́อ࡛་‫̦̹̥͉̥̽̈́́ͣྶ͉ا‬Ȃণ઄‫ئ‬໐͈͙́ບ‫̭̹̱͂ث‬ͧŕųŬŃ͈อ࡛̦ࡘઁ̱̞̭̦̀ͥ͂ྶ̥ͣ͂̈́ͤȂ̷ً͈̹͛ͅ૙Ȇ๬ྖࠁৗͬ೮̱̞̀ͥ͂ࣉ̢̹ͣͦȃ̯ͣͅłťŪűŰŲĮńųŦͬဥ̞̹ডཛळ༾අ։എŃŅŏŇࠧ৐ζ;ΑȆŕųŬŃࠧ৐ζ;ΑͬैୋȂ̭͈ͦͣζ;Ά͉ডཛழ૕͈
͙́‫ڎ‬șŃŅŏŇȂŕųŬŃ̦ࠧ৐̱̞̭̀ͥ͂ͬ‫̦̹̱෇ږ‬Ȃً૙Ȇ๬ྖࠁৗ͉೮̯̥̹̈́̽ȃȺ ࣉख़Ȼডཛழ૕̤̫ͅ
ͥŃŅŏŇȆŕųŬŃ͈୆ၑഎփ͉̺݅͘ྶ̥͉̩ͣ́̈́Ȃ̯ͣ̈́ͥ࠿൦͈̹͛ডཛழ૕අ։എŃŅŏŇ઼ًอ࡛ζ;ΑȂŕųŬŃ઼ًอ࡛ζ;Αͬैୋ̱̞̀ͥȃ䋭 㪈㪍㪇 䋭ĺ࠮ĳķ඾Ȫ࿐ȫġĲĲĻĲıȡĲĳĻĲıġġεΑΗȜٛાεΑΗȜġ‫ܖ‬ய őŃĲȶࠬ‫ۯ‬ඤ๧ळ༾Ȇࠬ‫ݩ‬௖ࡽैဥȟ̷͈ఈȷőŃĲĮĲķ ŉŪŨũġŧŢŵġťŪŦŵĮŪůťŶŤŦťġŭŦŶŬŰŤźŵŦġųŦŤųŶŪŵŮŦůŵġŪŴġŴŪŨůŪŧŪŤŢůŵŭźġŤŰŮűųŰŮŪŴŦťġŪůġńńœĳġ
ťŦŧŪŤŪŦůŵġŮŰŶŴŦį

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛఱाġଠঊ ĲȂࢺ൮ġ࠲༟ ĳȂ‫݌‬നġٗࢨ Ĳ

ɛչ൥ġੇ༟ ĲĭĳȂᚰനġੳ຃ ĲȂখઐġ࣠୆ ĳȂչ൥ġ݅হ ĳȂఱाġଠঊ ĲȂ‫݌‬നġٗࢨ Ĳ
Ĳ ൐‫ش֓ނ‬ভ‫ش‬ఱ‫ڠ‬Ȇఱ‫֭֓ڠ‬ভ‫ڠ‬௙ࣣࡄ‫شݪ‬Ȇ୶ૺႃၑ֓‫ڠش‬Ȃĳ ‫ڼ‬৆ٛ২·τΧ

著者索引䋭 㪈㪍㪈 䋭ポスター発表 ＹＩＡ選考発表[Background] Indoxyl sulfate is one of the major components of uremic toxin and is correlated with cardiovasculardisease in patients with chronic kidney disease (CKD). The Aryl hydrocarbon receptor (AhR) is a ligand-inducible
transcription factor known to mediate the toxic effects of numerous environmental contaminants including indoxyl
sulfate. In the present study, we investigated a potential role of AhR in indoxyl sulfate-induced leukocyte-endothelialinteraction.
[Results] HUVEC were transfected with siRNA of AhR (siAhR) and then treated with indoxyl sulfate for 20 h,followed by stimulation with TNF-Ϸ for 4 h. siAhR significantly decreased indoxyl sulfate-enhanced leukocyte
adhesion. Western blotting analysis revealed that siAhR abrogated indoxyl sulfate-enhanced expression of adhesion
molecule such as E-selectin. To our surprise, though indoxyl sulfate enhanced activation of JNK and NF-ЀB, siAhR
did not suppress their induction. siAhR did not affect indoxyl sulfate-induced reactive oxygen species production. To
assess the functional role of AhR in the indoxyl sulfate stimulated E-selectin gene induction, we conducted luciferase
promoter assay. We found that the promoter region of E-selectin, corresponding to -153 to -146 bps, was essential forthe effect of indoxyl sulfate mediated by AhR. Because the indoxyl sulfate response region is similar to AP-1 response
element and cAMP response element (CRE), we investigated which transcription factors were involved with indoxyl
sulfate-AhR pathway. Mutation in the indoxyl sulfate response region to AP-1 response element did not affect indoxyl
sulfate-induced E-selectin promoter activity; however, mutation to CRE decreased it. We also found that indoxyl
sulfate induced AP-1 transcriptional activity but not that of CRE.
[Conclusion] Our data suggest an important role for AhR in indoxyl sulfate-enhanced leukocyte-endothelialinteraction and provides a novel mechanistic insight into the CKD-related vascular inflammation.

口頭発表őŃĲĮĲĸ łųźŭġŉźťųŰŤŢųţŰůġœŦŤŦűŵŰųġŎŦťŪŢŵŦŴġŖųŦŮŪŤġŕŰŹŪůĮŪůťŶŤŦťġŗŢŴŤŶŭŢųġŊůŧŭŢŮŮŢŵŪŰů

会長招待講演 シンポジウム[Objective] MCP-1 and its receptor contribute the development of atherosclerosis. Dietary intake of fat containing foodis closely linked to the onset of metabolic disorders and atherosclerosis. In this study, we examined whether CCR2
plays a role in high fat induced vascular inflammation using intravital microscopic analysis (IVM). [Methods andResults] CCR2-deficient mice (CCR2-/-) or its wild-type counterpart (wt) (male, 7weeks of age) were fed high fat diet
(HFD; containing 20%fat, 1.25%cholesterol) for 4weeks. The interaction of leukocytes in the femoral artery as early as
4weeks in wt (13.0+/-3.10/104Ђm2) when compared to those fed normal diet (NC). In contrast, leukocyte recruitment
was almost completely abolished in CCR2-/- for 4weeks. (0.38+/-0.38, p<0.005 vs wt). Flow cytometric analysis of
migrated leukocytes in femoral artery revealed increase of CD45+CD11b+CD11c+cells in wt fed HFD whencompared to those mice fed NC. In addtion, those migrated leukocytes in CCR2-/- mice fed HFD diminished.Serumlevel of MCP-1 was elevated in wt fed HFD (268.1+/-41.8pg/ml), which didn't change in CCR2-/- mice (204.7+/10.8pg/ml). Serum level of cholesterol was equally elevated in wt (143.4+/-17.6mg/ml) and in CCR2-/- mice (135.7+/79.5). [Conclusion] CCR2 deficiency abolished leukocyte recruitment and migration in vascular inflammation without
affecting serum cholesterol level. Curren data indicate a novel role for MCP-1-CCR2 axis in metabolic disorder related
vascular inflammation.

特別講演

Ĳ ൐‫ش֓ނ‬ভ‫ش‬ఱ‫ڠ‬ఱ‫֭֓ڠ‬ভ‫ڠ‬௙ࣣࡄ‫ૺ୶شݪ‬ႃၑ֓‫ڠش‬Ȃĳ ߇ਗఱ‫ڠ֓ڠ‬໐૤௫ࠬ‫ۯ‬ພఠଷࢄ‫ڠ‬őŃĲĮĲĹ ࣞডཛȆࣞ΋τΑΞυȜσ૙ൎဓ̦ρΛΠಸ‫ۯ‬ςϋΩ‫ס‬ಎ͈́ ŅőőĮŊŗ ‫ͅ଻ڰ‬ဓ̢ͥ‫ޣג‬ɛཅॄġ๼ࣄ ĲĭĳȂఱाġଠঊ ĲȂ߃൥ġგဎ ĳȂ‫݌‬നġٗࢨ Ĳ
Ĳ ൐‫ش֓ނ‬ভ‫ش‬ఱ‫ૺ୶ڠ‬ႃၑ֓‫ڠش‬Ȃĳ ̤ಋ͈କ੫ঊఱ‫ڠ‬୆‫ݪࡄ֗ޗޏ۪ڰ‬ΓϋΗȜ࿒എȁ߃ාȂൠෂພ̤͍͢๬ྖછ͈อછͅŅŪűŦűŵŪťźŭġ űŦűŵŪťŢŴŦĮŊŗġ ĩŅőőĮŊŗĪ͈อ࡛௩‫۾̦ح‬ဓ̱̞̯̀ͥ͂ͦȂŅőőĮŊŗ͈‫಺଻ڰ‬୯̦ൠෂພহၷ͈૧̹̈́ΗȜΊΛΠ̱͂̀ಕ࿒ͬਬ̞͛̀ͥȃ৘षȂࣞডཛ૙͈୫৾̽̀͢ͅȂࠬ‫́̓̈́ס‬ŅőőĮŊŗ͈อ࡛̦௩‫̦̭̳͂ͥح‬༭̯̞̦࣬ͦ̀ͥȂમळ̈́ι΃ΣΒθ͉ྶ̥̞̞ͣ͂̈́̽̀̈́ȃ̷ِ̭́ș͉ȂࣞডཛȆࣞ΋τΑΞυȜσ૙ͬ঵௽໅‫̵̹̯ك‬ρΛΠͬဥ̞̀Ȃ૙মဇြ͈ডཛ͈‫ݟ‬ਓࠐႹ͂̈́ͥಸ‫ۯ‬ςϋΩ‫́ס‬ŅőőĮŊŗอ࡛͈࠿൦࣐̹ͬ̽ȃ༹༷͂ࠫ‫ض‬ȁŔŅࠏρΛΠĩဎȂķ਩ႢĪͅచ̱ȂࣞডཛȆࣞ΋τΑΞυȜσ૙ĩĳıġ Ħ‫ݱ‬ডȂĲįĳĶġ Ħ΋τΑΞυȜσĪͬĹ਩‫ۼ‬ൎဓ̱̹ȃ̷͈ࢃȂಸ‫ۯ‬ςϋΩ‫ͬסࠬ͂ס‬ٝਓ̱Ȃ‫خ‬ဣ଻ŅőőĮŊŗ͈‫௶ͬ଻ڰ‬೰̱̹ȃ̷͈ࠫ‫ض‬Ȃಸ‫ۯ‬ςϋΩ‫̞̤̀ͅס‬Ȃ೒ુ૙߲́
ͅచ̱ȂࣞডཛȆࣞ΋τΑΞυȜσ૙߲͉́ခփͅ௩‫̹̞̱̀ح‬ĩőġ ɃıįıĶĪȃ̹͘Ȃࠬ‫ס‬ಎ͈ŅőőĮŊŗ‫͜଻ڰ‬೒ુ૙߲ͅ
๤͓ȂࣞডཛȆࣞ΋τΑΞυȜσ૙߲́ခփ̈́ᄤૺͬ෇̹͛ĩőġ Ƀġ ıįıĶĪȃষͅȂ‫خ‬ဣ଻ŅőőĮŊŗ͈ॲ୆௫‫ͬܕ‬අ೰̳ͥևȂ઀ಸȂಸ‫ۯ‬ςϋΩ‫͍̤͢ס‬ಸ‫྄ۼ‬ςϋΩ୯̥ͣٝਓ̱̹ςϋΩ‫͈ݩ‬ŅőőĮŊŗġ Ůœŏłอ࡛ͬ࠿൦̱̹ȃ̷͈ࠫ‫ض‬Ȃ઀ಸ͈́ŅőőĮŊŗġ Ůœŏłอ࡛̦ࣞডཛȆࣞ΋τΑΞυȜσ૙߲́ခփͅ௩‫̹̱ح‬ġ ĩőɃıįıĶĪȃ̹͘ȂςϋΩ‫͈ݩ‬ŅőőĮŊŗġ
Ůœŏłอ࡛ၾ͉ȂࣞডཛȆ΋τΑΞυȜσ૙́ခփ̈́་‫̹̥̽̈́ͦͣ͛෇̦ا‬ȃࠫაȁུࡄ‫̥ͣض͈ࠫݪ‬ȂࣞডཛȆࣞ΋τΑΞυȜσ૙͈୫৾̽̀͢ͅȂࠬ‫̩̫̺̈́́ס‬ಸ‫ۯ‬ςϋΩ‫ס‬ಎ́͜ŅőőĮŊŗ‫̦଻ڰ‬௩‫̥ͤ̈́͂ͣྶ̦̭̞̱͂ͥ̀ح‬Ȃ઀ಸழ૕͈́ŅőőĮŊŗ͈ॲ୆ࢵ૧̦‫۾‬ဓ̱̞̀ͥ‫خ‬ෝ଻̦াऐ̯̹ͦȃ̭͈ͦͣࠫ‫̥ͣض‬Ȃࣞডཛ૙͈঵௽୫৾ͥࠬ͢ͅൠ಺୯෫౦͈૧̹̈́‫ܥ‬੬̱͂̀Ȃಸ‫ۯ‬ςϋΩ‫ס‬ಎ͈́ŅőőĮŊŗ‫̦଻ڰ‬ਹါ͂̈́ͥ‫خ‬ෝ଻̦া̯̹ͦȃőŃĲĮĲĺ ೩ॸள۪‫͈́ئޏ‬෹ࠬ‫ۯ‬ςκΟςϋΈ̤̫ͥͅζ·υέ͹Ȝΐ͈൱̧ɛ௖෯ġࠋ ĲȂ໌നġ࠻຃ ĲȂग‫ع‬ġࢣ࣐ ĳȂհ໐ġࡓ ĲȂ୵෨ġࢤડ ĲȂ઀५ġဎࢩ ĲȂ૯ණġ֚჊ ĲȂ‫֔ז‬ġၻ२ ĴȂ઀৒ġ଼֚ Ĳ
Ĳ ൐‫ނ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ൐‫ش֓ނ‬ভ‫ش‬ఱ‫ڠ‬ඳহ৖ۛࡄ‫ݪ‬ਫ਼ΊΦθພၑ‫ڠ‬໦࿤ġȂĴ ুহ֓‫ش‬ఱ‫ڠ‬෹ࣞࠬգછ͉෹ࠬ‫ۯ‬ඤ๧ळ༾Ȃ໹‫޼ڲ‬ळ༾͈̈́̓։ુ̈́௩૓ͤ͢ͅ෹൲ྤ༃͈๬࢚Ȃඤ͈࣌‫ޛ‬ॏͬြ̹̱Ȃ෹൲ྤգ͈ಠ̱̞ષઌ̷ฺֲ̠͂ͦͅ૤ະ஠͒͂ঢͥထࢃະၻ͈৖̜ۛ́ͥȃ̷͈হၷ͈ࡎ͉ςκΟςϋΈͤ͢ͅ‫ޛ‬ॏȂ໾ण̱̹ࠬ‫ ͈ۯ‬ųŦŷŦųŴŦġ ųŦŮŰťŦŭŪůŨ ̜̦́ͥȂྚ̺ͅ෹ࠬ‫ۯ‬ςκΟςϋΈ͈ι΃ΣΒθ͉ྶ̥̞ͣ́̈́ȃ༷֚Ȃ௫‫ܕ‬વ‫͈ࢃٺ‬ழ૕ςκΟςϋΈ̤̞͉̀ͅζ·υέ͹Ȝΐĩඅͅ‫׶‬છဲଷ߿͈Ŏĳζ·υέ͹ȜΐĪ̦ਹါ̈́࿨‫̭̳̹ضͬڬ‬̦͂౶̞ͣͦ̀ͥȃ‫׶‬છ฽؊͉෹ࣞࠬգછ͈ພఠ͜ͅఱ̧̩‫۾‬Ⴒ̱̤̀ͤőŭŦŹŪŧŰųŮġ ŭŦŴŪŰů͈ਔս͉ͅζ·υέ͹Ȝΐ̷͈͞ఈ͈ࠬ‫ࠏݩ‬ळ༾̦ఉ̩෇͛ͣͦȂ̭͈ͦͣळ༾̦෹ࠬ‫ۯ‬ςκΟςϋΈ͜ͅਹါ̈́࿨‫ࣉ̞̱̹͂ͥ̀ضͬڬ‬̢ͣͦͥȃِș͉೩ॸள۪‫́ئޏ‬ζ;ΑͬĳĲ඾‫ۼ‬ব̳̭֗ͥ͂́ಎ൝ഽ͈෹ࣞࠬգκΟσζ;Αͬै଼̱Ȃࠐশഎͅ෹͈ࠬ‫ࠏݩ‬ळ༾͈ޭ଻་‫ͬا‬έυȜ΍ͼΠιΠςȜٜ́ଢ଼̱̹ȃ෹͈ζ·υέ͹Ȝΐ͉৽ͅńŅĲĲŤု଻͈෹༾ζ·υέ͹Ȝΐ͂ńŅĲĲŤ֮଻ŇĵİĹıု଻ōźķńု଻͈෹‫ۼ‬ৗ‫׶‬છৼܳ߿ĩŎĲĪζ·υέ͹ȜΐȂńŅĲĲŤ֮଻ŇĵİĹıု଻ōźķń֮଻͈෹‫ۼ‬ৗ‫׶‬છဲଷ߿ĩŎĳĪζ·υέ͹Ȝΐͅ໦႒̧̹́ȃ೩ॸளঁࠣࢃ‫͉ͅܢ଻ݢ‬෹‫ۼ‬ৗ‫׶‬છဲଷ߿ζ·υέ͹Ȝΐ̦௩‫̱ح‬Ȃ෹༾ζ·υέ͹Ȝΐ̦ࡘઁ̱̹ȃ̹͘Ȃζ·υέ͹Ȝΐޭ଻̦་‫̳ͥا‬ΗͼηϋΈ́෹ࠬ‫ۯ‬໹‫ڲ‬޼௄͈๬࢚̦୆̲̞̹̀ȃոષͤ͢೩ॸள‫ۯ͈ࠬ́ئ‬ςκΟςϋΈͅζ·υέ͹Ȝΐ̦ਹါ̈́࿨‫̞̱̹ͥ̀ضͬڬ‬‫خ‬ෝ଻̦াऐ̯̹ͦȃ೩ॸளঁࠣ‫́ئ‬෹ࣞࠬգછ͈ζ;ΑκΟσ͈อછι΃ΣΒθȂࠬ‫ۯ‬ςκΟςϋΈࠬͅ‫ࠏݩ‬ळ༾̦‫̳̹ض‬࿨‫ࣉ̞̀̾ͅڬ‬ख़̳ͥȃ䋭 㪈㪍㪉 䋭őŃĲĮĳı ෹ࣞࠬգછκΟσρΛΠ̤̫ͥͅഘଷࡠ͈࢘‫ض‬ɛळ୼ġՔ৘ ĲȂඤ൥ġဇႿ ĲȂֵ๶ġဉ෗ ĳȂᚧനġ࿾ ĲȂᎢ౓ġ૞֚ ĲȂ‫܊‬෫ġੇฎ ĲȂ؈ࡔġટܲ ĲȂ૩ᚧġఱဈ ĲȂࢺ࢛ġྶଲ ĲȂ௩५ġၑ Ĳ

Ŝ࿒എŞġ ෹ࣞࠬգછŜőŶŭŮŰůŢųźġ ŢųŵŦųŪŢŭġ ũźűŦųŵŦůŴŪŰůġ ĩőłŉĪŞ͉ਅș͈࿪सͤ͢ͅহၷ༹̦อജ̧̱̹̀ȃ̱̥̱Ȃ̷͈໦ঊι΃ΣΒθ͉ྚ̺ະྶ̜́ͥȃड߃Ȃőłŉۛ৪̤̫ͥࠬͅಎഘෛഽ೩‫̦ئ‬༭̯̦࣬ͦͥȂ̭ͦ́͘ͅőłŉພఠͬഘ͈۷ത̥ͣ࠿൦̱̹༭͉̞࣬̈́ȃུࡄ‫͉́ݪ‬Ȃőłŉພఠࠁ଼̤̫ͥͅഘ͈‫۾‬ဓȂ‫͍ݞ‬ഘଷࡠ͈࢘‫࠿̞̀̾ͅض‬特別講演

Ĳ ໶ࡩ֓‫ش‬ఱ‫ڠ‬ඤ‫ڠش‬੏۪‫ܕ‬ඤ‫ش‬Ȃĳ ໶ࡩ֓‫ش‬ఱ‫ڠ‬ພ֭ພၑ໐

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine൦̳ͥȃŜ༹༷ŞġĲı਩Ⴂဎ଻ ŔűųŢŨŶŦĮŅŢŸŭŦź ρΛΠͅκΦ·υΗςϋ ĩŎńŕĪ ͬķıŮŨİŬŨౙٝ๧‫ئ‬ಕৣ̱ȂőłŉκΟ߲Ş̱͂ȂρϋΘθ߲ͅ໦̫̱̹ȃ୆ၑ૙‫؂‬କͬൎဓ̱̹߲ͬ΋ϋΠυȜσ߲̱͂Ȃ̭ͦͣĴ߲‫́ۼ‬๤‫࠿ڛ‬൦࣐̹ͬ̽ȃŜࠫ‫ض‬Şġ őłŉĬŊœ߲́ࠬୄഘෛഽ೩‫̦̹͛෇ͬئ‬Ȃຫ͉ࠬĴ߲‫̹̥̽̈́͛෇̞̤̀ͅۼ‬ȃőłŉ߲͉́෹൲ྤࠬ‫ۯ‬໹‫޼ڲ‬๬࢚͞Ȃֲ৒գ͈ષઌͬ෇̹̦͛ȂőłŉȼŊœ߲͉́Ȃ̷ͦͣਫ਼ࡉ̦ဲଷ̯̹ͦȃ̹͘Ȃőłŉ߲͉́Ȃֲ৒ඤ͈࣌‫ڐ‬ఱ͞૤޼๬ఱֲ̈́̓૤ະ஠ਫ਼ࡉͬ෇̹̦͛ȂőłŉĬŊœ̷߲͉́ͦͣਫ਼ࡉ͜ဲଷ̯̹ͦȃ̹͘Ȃőłŉै଼Ĺ਩ࢃ͈୆ంၚ͉
őłŉ߲́Ķıɓ̜̹̦́̽ȂőłŉĬŊœ߲͉́Ĺıɓ͂٨஝̱̹ȃষͅȂ෹൲ྤȂ‫ֲ͍ݞ‬૤৒̤̫ͥͅळ༾ඤഘࣺ͙৾ͤ਋
ယఘŵųŢůŴŧŦųųŪůġ ųŦŤŦűŵŰųĲ ĩŕŧœĲĪอ࡛ͬ࠿൦̱̹̭͂ͧȂ΋ϋΠυȜσ߲ͅ๤̱őłŉ߲ȂőłŉĬŊœ̷߲͈͂͜ͅอ
࡛̦ᄤૺ̱̞̹̀ȃ̯ͣͅȂ୆ఘඤഘ಺୯֦ঊ̜́ͥΰίΏΐϋ֒ഥঊอ࡛ͬ࠿൦̱̹̭͂ͧȂ෹൲ྤ͉́Ĵ߲‫̤ͅۼ‬̞̀ओͬ෇̥̹̦͛̈́̽Ȃֲ૤৒̤̫ͥͅΰίΏΐϋอ࡛͉Ȃ΋ϋΠυȜσ߲ͅ๤̱őłŉ߲́ᄤૺ̱ȂőłŉĬŊœ߲͉́ࡘઁ̱̞̹̀ȃŜࠫაŞġ κΦ·υΗςϋညอőłŉκΟσρΛΠ̤̞̀ͅȂഘଷࡠͥ͢ͅőłŉພఠࠁ଼ဲଷ࢘‫̦ض‬া̯̹ͦȃŕŧœĲ͉ळ༾ඤഘະ௷শ̷͈ͅอ࡛̦ᄤૺ̱Ȃळ༾ඤ͈͒ഘࣺ͙̦৾ͤ௯ૺ̯ͦͥȃőłŉ߲͉́෹൲ྤȂ‫͍ݞ‬ֲ૤৒̤̞̀ͅŕŧœĲอ࡛̦ᄤૺ̱̞̹̭̀͂ͤ͢ȂőłŉȆֲ૤ະ஠ພఠࠁ଼̤̫ͥͅഘࣺ͙͈৾ͤ‫۾‬ဓ̦াऐ̯ͦ

会長招待講演 シンポジウムσͬै଼̱̹ȃŎńŕൎဓࢃံ඾ͤ͢೒ુ૙ͬဓ̢̹߲ͬőłŉ߲Ȃഘଷࡠ૙ͬဓ̢̹߲ͬŜőłŉĬ ŪųŰůġųŦŴŵųŪŤŵŪŰůġĩŊœĪ

̹ȃɛၖġೄ࣐ ĲĭĳȂᖱ࿐ġࢤ৘ ĳȂ૩‫ئ‬ġၧ֚ Ĳ
Ĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬ႉ઄֒ഥঊহၷ‫࣒ڠ‬जȂĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬ჇාȆଅ௫ඤ‫࣒ڠش‬ज͉਱໦ٜͅྶ̯̞̞ͦ̀̈́ȃ‫ݛ‬५಴ࡄ‫ͤ͢ͅݪ‬ȂͼϋΑςϋ೷ࢯ଻̦Ⴧ૽แ͈ࠁ଼ͬৼ̳̭̦ܳͥ͂া̯̞ͦ̀ͥȃ༷֚́łŅཎ࠿ෞ̤̞͉̀ͅൠෂພ͈ခྫͤ͢ͅłŅພၑ͉་‫̭̞̱͂̈́͜ا‬াऐ̯̞ͦ̀ͥȃ̭͈֚ࡉྭ੖̱̞̀
̠ͥ͢ͅࡉ̢ͥࠫ‫̥ͣض‬ൠෂພ̦łŅ͈อછ‫֦ࡏܓ‬ঊ̜́ͥ‫ܥ‬੬ͬჇ૽แ͈ࠁ଼ஜࢃ͈ĳ౲‫ͅٴ‬໦̫ٜ̀ྶ̧͈́ͥ
͉̞̥́̈́͂ैު‫ب‬୰ͬၛ̹̀ȃȪ༹༷ȫჇ૽แࠁ଼ஜͅ‫͉̱̀۾‬Ȃ࿤୆߿ζ;ᾼచ̱̀ࣞডཛ૙໅‫̹࣐̽ͬك‬ȃჇ૽แࠁ଼ࢃͅ‫͉̱̀۾‬Ȃ̳́ͅłŅ̈́ͥͅ‫̜ͥͅྵ׋‬łőő ŕŨ͂ൠෂພζ;Α̵̥̫ࣣ̹ͬൠෂພࣣ໵łŅζ;ΑłőőĬŰţİŰţġĩŕŢŬŦťŢĭġŔŢŵŰġŦŵġŢŭįġőŏłŔĭġĳıĲıĪġ͈ĲĹ̥࠮ෞ̤̫ͥͅΗ;͈ςϋॸ‫࠿ͬ̓̈́ا‬൦̱̹ȃȪࠫ‫ض‬ȫჇ૽แࠁ଼ஜͅ‫̱̀۾‬Ȃ࿤୆߿ζ;ᾼచ̱̀ࣞডཛ૙໅‫͉ك‬ෞඤϸͺηυͼΡĵıͬ௩‫̵̹̯ح‬ȃჇ૽แࠁ଼ࢃͅ‫͉̱̀۾‬ȂࣞႢ͈ൠෂພࣣ໵łŅζ;ΑłőőĬŰţİŰţ ̤̞̀ͅΗ;͈ςϋॸ‫̦ا‬ᄤૺ̱̹ȃ̹ࣞ͘ডཛ૙ͬ໅‫̹̱ك‬łőőİőŔζ;Ά͉ࠬಎϸͺηυͼΡ̦௩‫̹̱ح‬ȃȪࠫაȫłőŐņϻĵ͉Ⴧ૽แ͈ࠁ଼ͬ௯ૺ̳̭̦ͥ͂౶̞̦ͣͦ̀ͥȂͼϋΑςϋ೷ࢯ଻̷͉ͦͬ௯ૺ̳ͥ‫خ‬ෝ଻ͬခ̳ͥȃϸͺηυͼΡ͈ಇୟ͈͙͉́Η;͈ςϋॸ‫ا‬ᄤૺ͞૰ࠐ་଻͒͂ૺ
̞̦̈́͘Ȃ‫ح‬Ⴂ͂ൠෂພ̷ً̦͈೾͒͂௯ૺ̵̯ͥȃ̳̻̈́ͩ‫ح‬Ⴂ͂ൠෂພ͉łŅ̤̫ͥͅࢭુ଻֋঵‫ͬࢹܥ‬෫౦̯ř̦ຈါ̜́ͤȂ̭͈֦ঊ͈ٜྶ͉łŅْ͈‫ܢ‬എ̈́হၷ༹͈‫ٳ‬อ͍̩ࠫ̾͂ͅࣉ̢̹ͣͦȃ䋭 㪈㪍㪊 䋭著者索引

̵̭̦ͥ͂াऐ̯̹ͦȃłŅอછͅຈଌ͈Η;͈ςϋॸ‫ا‬ᄤૺ͉ͅϸͺηυͼΡ͈ಇୟͅ‫ྚ̢ح‬౶͈֦ঊŇłńŕŐœġ

ポスター発表 ＹＩＡ選考発表Ȫ࿒എȫൠෂພ̦ͺσΜΧͼζȜພĩłŅĪ͈ࢃഛഎ‫֦ࡏܓ‬ঊ̜̭̦́ͥ͂΋ϋΓϋ΍Αͬං̜̾̾ͥȃ̱̥̱Ȃ̷͈‫ܥ‬੬

口頭発表őŃĲĮĳĲ ͺσΜΧͼζȜພͅచ̳ͥࢭુ଻֋঵‫͈ࢹܥ‬ൠෂພͥ͢ͅ෫౦

őŃĲĮĳĳ ࠬ‫ۯ‬ඤ๧‫׶‬છ̽̀͢ͅॲ୆̯ͦͥ ņŎő ͈‫ܥ‬ෝٜଢ଼ɛ५ུġ୍আ ĲȂ൐ġ‫ם‬ၐ࠮ ĲĭĳȂఆઐġઍ ĴȂᚰോġસ ĲȂ୞֔ġုঊ ĲȂ૧๑നġੇ໹ ĴȂॕࡔġୃୄ Ĳ
Ĳ ີ५ఱ‫ڠ֓ڠ‬࿪‫ݪࡄڠ‬໐ພఠȆພၑ‫࣒ڠ‬जȂĳ ͺΑΞρΑୋ࿪ ĩ ‫ ڼ‬Ī Ψͼ΂ςȜΡίυΐͿ·ΠȂĴ ඊၛ࣐ଽ༹૽࣭ၛಿ਍֓ၷࡄ‫ݪ‬ΓϋΗȜΨͼ΂Ψϋ·΂ηΛ·ΑξΣΛΠ

Ⱥ͉̲͛ͅȻ
ņůťŰŵũŦŭŪŢŭġ ŮŪŤųŰűŢųŵŪŤŭŦŴġ ĩņŎőĪ̦෴ࠬછ͞ιΗδςΛ·ΏϋΡυȜθ͈̈́̓‫଻ݢ‬Ȇྕ଻‫׶‬છ଻৖ۛͅ
ฺ̞ࠬಎͅ௩‫̦̭̳͂ͥح‬༭̯̞࣬ͦ̀ͥȃ̱̥̱̦̈́ͣȂņŎő͈ॲ୆໐պ͞ι΃ΣΒθ̈́̓ྚٜྶ̈́໐໦̦ఉ̞ȃِș͉ȂŪůġ ŷŪŵųŰȂŪůġ ŷŪŷŰ͈́ņŎő͈࢘ၚഎ̈́ॲ୆ࠏٜ͂ଢ଼༹༷ͬ‫ږ‬ၛ̱ȂţŪŰŢŤŵŪŷŦġ ŤŢųųŪŦų̱͈͂̀‫خ‬ෝ଻ͬ࠿൦̱
̹ȃȺ༹༷Ȼࠬ‫ۯ‬ඤ๧ळ༾ͅచ̱‫׶‬છৼܳ໤ৗͬैဥ̵̯ȂņŎőͬŇłńŔٜ̽̀͢ͅଢ଼̱̹ȃळ༾͈‫׶‬છેఠ͉Ȃ‫ڎ‬ਅ‫׶‬છζȜ΃Ȝͬঐດ̱̀ͅບ‫̹̱ث‬ȃ̹͘ Ūů ŷŪŷŰ ͈࠿൦͉́Ȃ‫଻ݢ‬Ȇྕ଻‫׶‬છζ;ΑκΟσͬဥ̞ࠬಎņŎőͬŇłńŔٜ̽̀͢ͅଢ଼̱̹ȃ̯ͣͅņŎő͈ ţŪŰŢŤŵŪŷŦġ ŤŢųųŪŦųུ͈ৗͅท̹ͥ͛ȂņŎőͬβς΍ͼΠͅैဥ̵̯ळ༾‫ܥ‬ෝ͈ٜଢ଼ͬ
࣐̠͂͂͜ͅȂņŎőͅ༫‫̯ͥͦ܄‬ŮŪœŏł͈࿌္എٜଢ଼࣐̹ͬ̽ȃȺࠫ‫ض‬ȻŊů ŷŪŵųŰ ͈ٜଢ଼ࠏ̤̞̀ͅȂ‫׶‬છৼܳ໤ৗͬ
ैဥ̵̯̹ࠬ‫ۯ‬ඤ๧ळ༾͉‫׶̞ޑ‬છેఠͅ‫͂͂ͥ͜ͅۿ‬Ȃ‫׶‬છ͈ഽࣣ̞ͅ௖‫̱̀۾‬ņŎő͈ॲ୆ၾ̦௩‫̭̳ͬ͂ͥح‬೰ၾഎٜͅଢ଼଼̳̭̱̹ͥ͂ࢗͅȃ̹͘ȂŪůġ ŷŪŷŰ͉́Ȃ෴ࠬછκΟσζ;ΑȂιΗδςΛ·ΏϋΡυȜθζ;ᾼ̴͈̞̤̞ͦ̀͜చચ߲͂๤‫̱ࠬ̀ڛ‬ಎņŎőၾ͈௩‫̦ح‬۷ख़̯̹ͦȃ̹͘ȂņŎőْ໦ͤ͢ŮŪœŏłͬಒ੄̱ȂŮŪœŏłġ
ŢųųŢź࣐̹ͬ̽ࠫ‫ض‬Ȃ‫׶‬છ̽̀͢ͅņŎőಎ͈ŮŪœŏłழ଼̦ࠣႧͅ་‫̹̞̱̀ا‬ȃŊůġ ŴŪŭŪŤŰ ٜଢ଼͈ࠫ‫ض‬Ȃࠬ‫ۯ‬໹‫޼ڲ‬ळ༾İβς΍ͼΠ̦ņŎő͈ΗȜΊΛΠ̜́ͥ͂ࣉ̢̹ͣͦȃȺࣉख़Ȼޭ͛̀࢘ၚഎ̈́ņŎő͈ Ūů ŷŪŵųŰ ॲ୆ࠏ͈‫ږ‬ၛ଼̳ࢗͥ͂͂͜ͅͅȂŪů ŷŪŷŰ ͈௶೰ࠏ͜‫ږ‬ၛ̱̹ȃ̹͘ȂņŎőಎ͈ŮŪœŏłழ଼̦‫׶‬છ̽̀ࠣ͢ͅႧͅ་‫෇ږ̭̳ͬ͂ͥا‬̱̹ȃఱ་‫ྙޟ‬૬̞̭͂ͅȂņŎő͈ΗȜΊΛΠ̦ࠬ‫ۯ‬໹‫޼ڲ‬ळ༾İβς΍ͼΠ̜̭̦́ͥ͂াऐ̯̹ͦȃոષ͈ࠫ‫ض‬ȂņŎő͈ţŪŰŢŤŵŪŷŦġŤŢųųŪŦų̱͈͂̀‫خ‬ෝ଻̦ࣉ̢ͣͦͥ͂͂͜ͅȂ̷ུ͈ৗ͉ŮŪœŏł̜́ͥ‫خ‬ෝ଻̦‫̩ޑ‬াऐ̯̹ͦȃ䋭 㪈㪍㪋 䋭őŃĲĮĳĴ ςϋΩ‫ۯ‬ठ୆̫̹࢜ͅ‫ܖ‬யഎ࠿൦ɛଌ൥ġ෕ၖঊ ĲĭĳȂུఉġஂ ĲĭĳȂ‫ݛ‬༗നġੇ჊ ĲȂ૩നġ֗౳ ĳプログラム

ĺ࠮ĳķ඾Ȫ࿐ȫġĲĲĻĲıȡĲĳĻĲıġġεΑΗȜٛાεΑΗȜġ‫ܖ‬ய őŃĲȶࠬ‫ۯ‬ठ୆Ȇহၷȟ̷͈ఈȷ

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

Ĳ ൐‫ش֓ނ‬ভ‫ش‬ఱ‫ڠ‬୆૓‫ܥ‬ෝ‫ڠ۾ފ‬Ȃĳ ൐‫ش֓ނ‬ভ‫ش‬ఱ‫ڠ‬໦ঊळ༾‫ܥ‬ෝ‫ڠ‬༹̦ంह̵̴Ȃྚ̺হ࿴̦ࣾඳ̈́ພఠ̜́ͥȃِș͉̭֣ͦ́͘ͅक़ܿ੅ͬဥ̞̹୆ఘ‫ٳͬ੅଼ܿैۯ͈ࠬ́ٸ‬อ̱
̧̹̦̀Ȃ
ࣽٝȂ
ΪΠ๧ໂςϋΩ‫ۯ‬ဇြςϋΩ‫ۯ‬ඤ๧ळ༾
Ȫōņńȫ
ͬဥ̞̀Ȃ
ςϋΩ຾ਆ͈૧ܰহၷ༹༷͈‫ٳ‬อͬ࿒എͅȂ୆ఘ‫͈́ٸ‬࿉ळςϋΩ‫଼̹࣐̽ͬै͈ۯ‬ȃȺ༹༷ȻōņńȂࠬ‫ۯ‬ඤ๧ஜߐळ༾ȪŐņńȫȂōņń͂Őņńͬईࣣ̱̹͈ͬ͜Ȃ̷ͦ

特別講演Ⱥ࿒എȻ੅ࢃςϋΩ຾ਆ͉඿‫́܈‬Ĵ‫ڬ‬Ȃঊ‫́܈ݠ‬ĵ‫͈ۛڬ‬৪̦ᑋ̳ۛͥ͂ଔ೰̯ͦȂŒŐōͬ೩‫̵̦̯ͥئ‬Ȃْ‫ܢ‬എ̈́হၷ̸ͦρͼϋΩΗȜϋ‫ܖ‬โͅ෥ਅ̱Ȃ෽ူ࣐̹ͬ̽ȃ‫ܖ‬โͅळ༾̦ັ಍̱̹ࢃͅȂळ༾‫ٸ‬ζΠς·ᾼഢৢ࣐̹ͬ̽ȃै͈̞ࣞ໐պͅ୪಍̱̹ȃ୪಍শ‫ۯ͉ࠬۼ‬ඤ๧ळ༾̦ĳĵশ‫ۼ‬ոඤͅ୪಍̳͈ͥͅచ̱̀ȂĳĵȡĵĹশ‫ۼ‬ոඤ͂ັ಍͢ͅ
ͤಿ̞শ‫ͬۼ‬ါ̱̹ȃষͅ‫ܖ‬โͅ୪಍̱̹ςϋΩ‫ۯ‬ඤ๧ळ༾ͬळ༾‫ٸ‬ζΠς·ᾼഢৢ̱̹̭͂ͧȂࠬ‫ۯ‬ඤ๧ळ༾͂
൳အͅςϋΩ‫ۯ‬ඤ๧ळ༾́͜‫̹͛෇଼ͬࠁ͈࣌ۯ‬ȃ‫଼͈ࠁ࣌ۯ‬শ‫ۯ͉ࠬۼ‬ඤ๧͂๤‫̱ͤ̀͢ڛ‬ಿ̞শ‫ͬۼ‬ါ̱ĳĵȡĵĹশ‫ͬۼ‬ါ̱̹ȃ‫ވ‬ઙതτȜΎȜࡐ๷‫͉́ޢ‬ōņńͥ͢ͅ‫̹̯ͦ෇ږ଼̦ࠁ࣌ۯ‬ȃōņń͂Őņńͬईࣣ̱̹͈͉́͜Ȃ‫ۯ‬͈࣌ࠁ଼ͬ෇̥̹͛̈́̽ȃȺࠫაȻ֒ഥঊௌै͈̈́̓਀༹ͬঀဥ̳̭̩ͥ͂̈́Ȃ୆ఘ‫́ٸ‬࿉ळςϋΩ‫ͬۯ‬ଇ௸ͅै଼̳
଼̭̱̹ͥ͂ࢗͅȃ̹͘Őņń͂ōņńͬईࣣ෽ူ̱̹षͅ‫଼̥̭̹̥̯ͣ͂̽̈́ͦࠁ̦࣌ۯ‬ȂŐņń̦ōņńͅ໦‫̭̳ͥا‬͉̩͂̈́ȂŐņń͈֊૒ͤ͢ͅςϋΩ‫خ଼̳ͥࠁͬۯ‬ෝ଻̦೩̞̭̦͂াऐ̯̹ͦȃै଼̱̹ςϋΩ‫ܥ͈ۯ‬ෝ̞̾̀ͅ
͉ࣽࢃٜଢ଼ထ೰̜́ͥȃɛ୞ॄġణਏ ĲȂőŶŦůŵŦŴġŔŢůťųŢ ĳȂா౶ġୃ ĲȂড়ॄġ࣓঎ ĲȂ଼ଳġٗ֏ ĲȂࢡུġဉ໹ ĳȂ२ኈġٗ຃ ĴȂࣽ֔ġ‫ ྶם‬ĵ
Ĳ ߲෯ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬໦ঊळ༾୆໤‫ڠ‬Ȃĳ ߲෯ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬ෞ૰ࠐ‫ڠشٸ‬ȂĴ ߲෯ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬૰ࠐୈ૰֓‫ڠ‬Ȃĵ ൐‫ނ‬ఱ‫ڠ֓ڠ‬໐້௺ພ֭ෞ૰ࠐ‫شٸ‬

口頭発表őŃĲĮĳĵ ෞ๷઀ࠬ‫ۯ‬ඤ๧ळ༾֊૒ͥ͢ͅฒৗࢸणহၷ͈দ͙

会長招待講演 シンポジウム଼̱̹‫࣌ۯ‬ழ૕͉‫ވ‬ઙതτȜΎȜࡐ๷‫́ޢ‬۷ख़࣐̹ͬ̽ȃȺࠫ‫ض‬Ȼōņń͉Őņń͂൳အͅȂρͼϋΩΗȜϋ‫ܖ‬โ͈୪಍଻

Ⱥ࿒എȻ

Ⱥ༹༷Ȼ
଼ఘŔŅρΛΠඤ༫ͅ೰պഎͅ΀ϋΡΓςϋĮĲȪņŕĮĲȫͬಕৣ̱Ȃࢸणͬည൵̱Ȃĸ඾ࢃ଼ͅఘņĮňŇőĮŔŅρΛΠఱෞ̥ͣ಺ୋ̱̹ෞ๷઀ࠬ‫ۯ‬ඤ๧ळ༾ȪŎŗņńŴȫͬ೰պഎͅࢸण໐պͅ֊૒̱̹ȃచચ଼̱͉͂̀ఘņĮňŇőĮŔŅρΛΠఱෞ̥ͣ಺ୋ̱̹ଡ྄ळ༾ȪŎńŴȫ‫͍ݞ‬ıįĳĦŃŔłͬ‫͚܄‬ŉŃŔŔȪŃŔłȫͬဥ̞̹ȃळ༾֊૒Ĳĵ඾ࢃ࣐ͅ൲ٜଢ଼࣐̹ͬ̽ࢃȂఱෞͬഊ੄̱̀ழ૕‫ڠ‬എٜଢ଼࣐̹ͬ̽ȃȺࠫ‫ض‬Ȼ
ŎŗņńŴ֊૒߲͉́చચ߲ȪŎńŴ֊૒߲‫͍ݞ‬ŃŔłಕৣ߲ȫͅ๤͓̀ȂέΛΠίςϋΠদࡑ̤̞̀ͅࢃঠٝഢ‫͈ڙ‬٨஝̦෇͛ͣͦȂழ૕‫ڠ‬എٜଢ଼͉́ࢸण௏̤̫ͥͅठଡશ‫͈ا‬௯ૺ‫͍ݞ‬ඤ༫͈ఘୟ͈ٝ໘̦෇̹͛ͣͦȃ֊૒̯̹ͦ
ŎŗņńŴ͈֚໐͉ࠬ‫ࢹۯ‬௮ࣺ̞̹̦৾ͤͦ̀͘ͅȂထேͅ฽̱̀ఱ໐໦͉֊૒໐պͅၣ̹̽͘ȃ̹͘ඤ༫߃ཌྷ͈ࠬ‫ۯ‬ତͬତ̢̹̭͂ͧŎŗņńŴ֊૒߲͂చચ߲͈‫́ۼ‬ခփ̈́ओ͉෇̥̹͛ͣͦ̈́̽ȃ༷֚ŎŗņńŴ֊૒߲͉́చચ߲͂๤

ポスター発表 ＹＩＡ選考発表‫ͥࠬ͢ͅݹ‬ฒৗࢸण͉အș̈́૰ࠐછેȆୈ૰છે̹̳ͬͣ͂͜ࣉ̢̞̦ͣͦ̀ͥȂ̷͈࢘‫ض‬എহၷ༹͉ྚ̺ྫ̞ȃུࡄ‫ۯ͉ࠬ́ݪ‬૧୆௯ૺͬ‫ܢ‬ఞ̱̀ฒৗࢸण௏ͅෞ๷઀ࠬ‫ۯ‬ඤ๧ळ༾ͬ೰պഎͅ֊૒̱Ȃ̷͈࢘‫࠿ͬض‬൦̱̹ȃ͓̀ņŅĮĲု଻͈‫ا଻ڰ‬η·υΈςͺ͈ତ̦ઁ̥̹̈́̽ȃŎŗņńŴ߲́έΛΠίςϋΠদࡑ̤̫ͥͅ٨஝Ȃࢸण௏͈ठଡશ‫͈ا‬௯ૺ‫͍ݞ‬ඤ༫͈ఘୟ͈ٝ໘̦෇̹̦͛ͣͦȂ̭͉ͦ֊૒̯̹ͦŎŗņńŴ̦ࠬ‫ۯ‬૧୆ͬ௯ૺ̱̀ࠬၠͬ௩‫̢̞̩ͅࣉ̵͉͈̭̹̯͂ͥ͂͜͢ͅح‬ȃŎŗņńŴဇြ͈֦ঊ̦΂ςΌΟϋΡυ΍ͼΠ̷̞̱͈̈́ஜߐळ༾ͅ൱̧̥̫̀Ȃ৊͈॑ठଡશ‫ͬا‬௯ૺ̱̞̀ͥ‫خ‬ෝ଻̦ࣉ̢̦ͣͦͥȂ֊૒ඤ๧ळ༾ͥ͢ͅ‫׶‬છဲଷ࢘‫ͬض‬̱̹͈̜ٚ́ͥ͜‫خ‬ෝ଻͜๛೰̧̞́̈́ȃ̴̵̞ͦ͢ͅŎŗņńŴ֊૒ͥ͢ͅฒৗ
ࢸण٨஝͈໦ঊ‫̥͊ͦ̈́ͣͅྶ̦ࢹܥ‬Ȃฒৗࢸणͅచ̳ͥ࢘‫ض‬എহၷ༹͈‫ٳ‬อ̦௯ૺ̯̭̦ͦͥ͂‫ܢ‬ఞ̯ͦͥȃ䋭 㪈㪍㪌 䋭

著者索引

Ⱥࣉख़Ȼ

őŃĲĮĳĶ ࠬ‫ۯ‬૧୆ळ༾হၷဥΕȜΑ̱͈͂̀౎໦‫ا‬ডཛळ༾ɛઐུġఊ჊ ĲȂ໓‫ۼ‬ġ౺຃ ĲȂซாġ֚ฎ ĲȂളᰧġఽঃ ĴȂ‫ح‬࿤ġࢼ֚჊ ĳ
Ĳ ඾ུఱ‫ڠ֓ڠ‬໐‫ܥ‬ෝࠁఠ‫ࠏڠ‬ळ༾ठ୆Ȇ֊૒֓‫ڠ‬Ȃĳ ඾ུఱ‫ڠ‬୆໤঩࡙‫ڠش‬໐؊ဥ୆໤‫شڠش‬ȂĴ ඾ུఱ‫ڠ֓ڠ‬໐઀঱‫ڠش‬Ⱥ࿒എȻ଼੃ডཛळ༾ͬഛ֔෽ူ̳̭ͥ͂̽̀͢ͅංͣͦͥ౎໦‫ا‬ডཛळ༾ĩŅŦťŪŧŧŦųŦůŵŪŢŵŦťġ ŧŢŵġ ŤŦŭŭ Ļġ ŅŇłŕĪ͉Ȃ‫ۼ‬ဩࠏۚळ༾ĩŎŔńĪ͕͖֚ͅ౿̱̹ࠁৗ͂ఉෝ଻ͬা̳ȃࣽٝȂŅŇłŕ͈ࠬ‫଼ࢹۯ‬ळ༾͈͒໦‫ا‬ෝࠬ͞‫ۯ‬૧୆ෝͬ࠿൦
̱Ȃࠬ‫ۯ‬ठ୆֓ၷဥ͈ळ༾࡙̱͈͂̀ခဥ଻̞̾̀ͅ࠿൦̱̹ȃȺ༹༷ȻňŇőρασ̱̹ŅŇłŕͬဥ̞̀ࠬ‫ۯ‬ඤ๧ळ༾͈͂‫ވ‬෽ူ৘ࡑȂζ;Α๧‫͈͒ئ‬ζΠςΊσ༫ོ֊૒৘ࡑȂ;΍Ά‫ئ‬ঠ‫ࠬݹ‬໐պ͈͒֊૒৘ࡑ࣐̞ͬȂňŇőĬळ༾͈ࠁৗٜଢ଼࣐̹ͬ̽ȃ෽ူŅŇłŕ͈ŤŰůťŪŵŪŰůŦťġŮŦťŪŶŮ ĩńŎĪͬन̱৾Ȃᦡఝ୓ྤඤ๧ळ༾ĩŉŖŗņńĪ‫଼ͅࠁ࣌ۯ‬చ̳ͥ࢘‫͞ض‬Ȃ‫܄‬ခ̳ͥ΍ͼΠ΃ͼϋͬ࿌္എͅ೰ၾບ‫̱ث‬Ȃডཛழ૕ဇြۚळ༾ĩłŔńĪȂࣸଡŎŔń͂๤‫̹̱ڛ‬ȃ;΍Ά‫ئ‬ঠ‫ݹ‬ࠬκΟσͅచ̳ͥু‫ز‬ŅŇłŕ֊૒৘ࡑ࣐̞ͬȂ‫޼ࠬݹ‬ழ૕͈ࠬၠၾࠬ͞‫ྟۯ‬ഽͬࠐশഎͅ௶೰̱Ȃহၷ࢘‫͞ض‬հ஠଻ͬບ‫̹̱ث‬ȃȺࠫ‫ض‬ȻŅŇłŕ͉ࠬ‫ۯ‬ඤ๧ळ༾͈͂‫ވ‬෽ူͤ͢ͅȂϷŔŎłĬŏňĳĬβς΍ͼΠ͒໦‫̹̱ا‬ȃ̹͘ζ;Α๧‫ئ‬ͅŅŇłŕ༫ོζΠςΊσͬ֊૒̳ͥ͂Ȃ࢘ၚഎͅΊσඤ́ϷŔŎłĬࠬ‫ۯ‬໹‫޼ڲ‬ळ༾ͅ໦‫̹̱ا‬ȃ̹͘;΍Ά‫޼ࠬݹ‬ழ૕ͅŅŇłŕͬ֊૒̳ͥ͂ࣞອഽࠬͅ‫ۯ‬ඤ๧ळ༾ͅ໦‫̳ͥا‬ਫ਼ࡉ̦෇̹͛ͣͦȃ΍ͼΠ΃ͼϋͺτͼ͈ࠫ‫ض‬ȂŅŇłŕĮ
ńŎ͉ȂࣸଡŎŔńĮńŎ͞łŔńĮńŎ͕͖֚ͅ౿̱̹΍ͼΠ΃ͼϋอ࡛ίυέ͹ͼσͬা̱Ȃ೩ॸளૄ࠯‫́ئ‬෽ူ̳ͥ͂
őŭňŇĭġ ŗņňŇ͈̈́̓อ࡛௩‫ͬح‬া̱̹ȃ;΍Ά‫ئ‬ঠ‫ࠬݹ‬κΟσͅచ̳ͥ֊૒৘ࡑ͉́ȂŅŇłŕ֊૒߲͉Ȃ୆ၑ૙‫؂‬କൎဓ߲͞ྎઑࠬౙ‫֊ݩړ‬૒߲ͅ๤͓Ȃခփࠬͅၠ٨஝ͬা̱Ȃ‫޼ࠬݹ‬ழ૕͈ϷŔŎłĬࠬ‫ྟۯ‬ഽ̦ခփͅ௩‫̹̞̱̀ح‬ȃু‫ز‬ŅŇłŕ֊૒ฺ̞ͅ௮ਆន଻͞։ਫ਼଻໦‫ͬا‬া̳ਫ਼ࡉ͉෇̥̹͛ͣͦ̈́̽ȃȺࠫაȻŅŇłŕ͉ࠬ‫଼ࢹۯ‬ळ༾͈͒໦‫ا‬ෝͬা̳͂‫ͅވ‬ȂΩρ·ρͼϋ࢘‫ۯ̞ࠬࣞͥ͢ͅض‬૧୆௯ૺैဥͬা̱̹ȃ‫ئ‬ঠ‫ࠬݹ‬κΟσͅచ̳ͥু‫ز‬ŅŇłŕ֊૒͉́Ȃ̞ࣞࠬၠ٨஝࢘‫֊͂ض‬૒հ஠଻̦া̯̹ͦȃŅŇłŕ͉ඳহ଻ྎઑ൲ྤ৖ۛ̈́̓ͅచ̳ͥ૧̹̈́হၷဥळ༾̱͂
̀‫ܢ‬ఞ̧́ͥȃőŃĲĮĳķ ডཛழ૕͈ࠬ‫ͬۯ‬ດഎ̳͂ͥ΢Φ֓ၷͥ͢ͅࢯ๬ྖ୽ၞ
ɛ‫ུک‬ġგ઎ȂŉŰŴŴŦůġŎťįġŏŢŻŪųȂਝനġ‫ྔם‬Ȃ໶൥ġ৿Ȃࡔോġਜ‫݌‬ཤ٬ൽఱ‫ڠ‬ఱ‫֭ڠ‬࿪‫֭ݪࡄڠ‬߃ාȂ๬ྖฺ̠ͅডཛ૧୆ࠬͅ‫ۯ‬૧୆̦ຈଌ̜̭̦́ͥ͂ྶ̥ͣ͂̈́ͤȂ๬ྖহၷ͈̹͈͛૧̹̈́ດഎ̱͂̀ডཛ
ழ૕͈ࠬ‫ۯ‬ඤ๧ळ༾̦ಕ࿒̯̞ͦ̀ͥȃِș͉Ȃ஠૸ͅ໦ື̳ͥࠬ‫̻̠͈ۯ‬Ȃডཛळ༾ͅ‫ॸ͂ူו‬ளͬ‫ۯ̳ࠬͥݯރ‬͈‫ܥ‬ෝͬ஖఼എͅ೩‫̵̧̦̭̯͊ͦ́͂ͥئ‬հ஠̥̾࢘‫ض‬എ̈́๬ྖহၷ̦‫خ‬ෝ̈́ͥ͂ͅࣉ̢Ȃডཛழ૕͈ࠬ‫ͅۯ‬చ̱̀஖఼എ֓ͅ࿪໦ঊͬ௣ో̳̹͈ͥ͛ςεΕȜθ߿΢Φ௣ోΏΑΞθȪ΢ΦŅŅŔȫ͈‫ٳ‬อͅ಍਀̱̹ȃດഎ‫ا‬ς΄ϋΡ̱͂̀Ȃ
ডཛழ૕͈ࠬ‫ۯ‬ඤ๧ळ༾͈ळ༾ນ࿂ͅඅ։എͅอ࡛̳ͥίυΪΙϋͅచ̳ͥࣞ૶გ଻βίΙΡȪŌňňœłŌŅȫ
ͬဥ̞Ȃ୆ఘഐࣣ଻ডৗ̜́ͥ၅ؕγΑέ͹Ιΐσ΋ςϋ̤͍͢΋τΑΞυȜσ̥ͣ̈́ͥၥঊࠂ࿩ĲııůŮ͈΢ΦŅŅŔນ࿂ͅες΀ΙτϋΈς΋ȜσȪőņňȫ̱ͬٚ̀ਘૐ̱̹ȃζ;Α͈ডཛழ૕̥ͣ໦ၗ̱̹ࠬ‫ۯ‬ඤ๧͈੝య෽ူ
ळͬဥ̞̹Ūůġ ŷŪŵųŰ͈́࠿൦͈ࠫ‫ض‬Ȃς΄ϋΡਘૐ΢ΦŅŅŔ̦ডཛழ૕͈ࠬ‫ۯ‬ඤ๧ळ༾ͅޭ͛̀஖఼എͅඤ໑໤ͬ༗
঵̱̹ેఠࣺ̭̦́৾ͤͦͥ͂͘ྶ̥̹ͣ͂̈́̽ȃ̯ͣͅȂŪůġ ŷŪŷŰ ̤̫ͥͅ࠿൦́Ȃ஖఼എ̈́௣ో͉ͅౙͅς΄ϋΡͬ൏श̳̺̫̩ͥ́̈́Ȃ΢ΦŅŅŔ͈ၛఘഎհ೰଻̭̦ͬࣞ͛ͥ͂ޭ͛̀ਹါ̜̭́ͥ͂ͬࡉ੄̱ȂŪůġ ŷŪŷŰ ؊ဥ‫خ‬ෝ̈́őųŰũŪţŪŵŪůĮŵŢųŨŦŵŦťġ ůŢůŰűŢųŵŪŤŭŦŴȪőŕŏőȫ͈ࢹಃ଼̱̹ࢗͅȃষͅȂ๬ྖহၷ͈͒؊ဥ‫خ‬ෝ଻ͬບ‫̹̳͛ͥث‬ȂőŕŏőͅͺεΠȜΏΑည൵βίΙΡͬඤ༫̱̀૙‫଻׎‬๬ྖζ;ᾼ๶୓ྤͤ͢Ĵ඾ͅĲ͈ٝ‫́ڞۼ‬ൎဓ̱̹ࠫ‫ض‬ȂĴı඾ࢃ͉ͅࡐಠ̈́ఘਹ͈ࡘઁ̦෇͛ͣͦȂডཛழ૕͜ခփͅੀ઀̳̭̦ͥ͂฻ྶ̱̹ȃ༷֚Ȃ൳̲ດഎ‫ا‬ς΄ϋΡ͂ͺεΠȜΏΑည൵βίΙΡͬႲ̱̹ࠫဏࣣβίΙΡͬൎဓ̱̹ાࣣ͉ͅĳ෼ոષ͈ൎဓၾ̤̞̀͜ͅခփ̈́ఘਹ͈ࡘ
ઁ͉෇̥̹̭̥͛ͣͦ̈́̽͂ͣȂőŕŏő͉ Ūůġ ŷŪŷŰ ̤̫ͥͅෝ൲എ࿪໤௣ో̤̞̀ͅȂဏࣣβίΙΡ͉́৘࡛ະ‫خ‬ෝ̈́࿹պ଻ͬခ̳ͥ͂ࣉ̢̹ͣͦȃ䋭 㪈㪍㪍 䋭őŃĲĮĳĸ ŅőőĵġŪůũŪţŪŵŪŰůġŢŮŦŭŪŰųŢŵŦŴġűųŦŴŴŶųŦĮŰŷŦųŭŰŢťĮŪůťŶŤŦťġũŦŢųŵġŧŢŪŭŶųŦġţźġųŦŷŦųŴŢŭġŰŧġ
ŮŪŵŰŤũŰůťųŪŢŭġťŢŮŢŨŦį

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛ୒५ġେ຃Ȃा൐ġణঊȂ໲লġ઎ဎȂ୼ଳġহढȂ৒ࡔġཅྶɛ୷ဩġद෕ ĲȂ໛֔ġ֚ ĲȂ঳֔ġ࠲ఊ ĳȂ໛ࡔġ࿆༸ ĲȂབ࠮ġೄਏ Ĳ

口頭発表őŃĲĮĳĹ ૤௫ठ୆ͬ࿒ঐ̱̹૤޼ळ༾໦Ⴈည൵֦ঊ͈ౝ॑

会長招待講演 シンポジウム[INTRODUCTION] Maladapitive cardiac hypertrophy is associated with diseased mitochondrial remodeling. We havereported that the activation of incretine-receptor by exendin-4 (Ex4) could reverse such a mitochondrial remodeling indiabetic myocardium; however, its impact on the pathological cardiac remodeling induced by pressure overload (TAC)
remains unclear. [METHODS] Mice were allocated into 6 groups; sham and TAC with and without (CON), alogliptin
treatment (ALO; 10mg/kg/day, for 4 weeks), and Ex4-treatment (24nmole/kg/day, for 4 weeks) (sham-CON, TACCON, sham-ALO, TAC-ALO, sham-Ex4, and TAC-Ex4) and analyzed at the age of 18 week-old. [RESULTS]
Increase in heart weight and left-ventricular (LV) hypertrophy were observed in TAC-CON, which were reversed by
ALO and Ex4 treatment. Echocardiography revealed that TAC promoted reduced systolic and diastolic LV function,
which was ameliorated by ALO and Ex4. Circulating DPP4 activity in TAC-CON was elevated (1.37+/-0.05-foldincrease versus sham-CON, n=8) with concomitant reduction of circulating GLP-1 level (0.76+/-0.05-fold decline
versus sham-control, n=8). Cardiac cyclic AMP (cAMP) concentration and protein kinase A (PKA) activity weredecreased in TAC-CON. Both treatment with ALO and Ex4 enhanced cardiac cyclic AMP levels as well as PKA
activity. Expression ratio of cardiac mitofusin (Mfn)1 and Mfn2 was elevated in TAC heart, which was reduced byboth ALO and Ex4 treatment. Mitophagic indicator molecules PARKIN and PINK1 levels were suppressed by ALO
and Ex4, suggesting reduction of damaged mitochondria, which was confirmed by transmission electron microscopy.
[CONCLUSIONS] DPP4 inhibition ameliorates pressure-overload-induced heart failure by reversal of mitochondrial
damage through the GLP-1/cAMP/PKA axis.

特別講演ྴࡣ‫ؚ‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬

Ĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼ळ༾୆໤‫ڠ‬໐Ȃĳ ൐‫ނ‬ఱ‫ڠ‬໦ঊ୆໤‫ݪࡄڠ‬ਫ਼໦ঊ‫ܥ‬ෝࠁఠࡄ‫ݪ‬໦࿤‫ܥ‬ෝͬٝ໘̳̺̫͈ͥ૤޼ळ༾͈ठ୆͉ະ‫خ‬ෝ̜́ͥ͂ࣉ̢̞ͣͦ̀ͥȃఘ଻ۚळ༾̥ͣ໦‫̹̱ا‬૤޼̦ठ୆‫خ‬ෝ૤޼͈̈́ͥ͂ͅ༭̦̜࣬ͥȃ༷֚́Ȃळ༾ਔ‫಺ܢ‬୯֦ঊġ ĩ΍ͼ·ςϋȂ΍ͼ·ςϋջం଻΅΢ȜΔĪġ ͬ૤޼ळ༾ͅอ࡛
̱̀໦Ⴈͬည൵̱Ȃ‫ܥ‬ෝະ஠ͅ‫̹̽ۿ‬૤௫͈ठ୆ͬদ͙̹ࡄ‫͉́ݪ‬Ȃ೩‫̹̱ئ‬૤‫ܥ‬ෝͬ٨஝̳͈ͥ́࢘͘‫̥͉̽̈́ض‬̹ȃሶ඿႒͉͂։̈́ͤȂ‫ݿ‬႒͞ၰ୆႒͈૤௫͉૤޼ळ༾͈໦Ⴈ̽̀͢ͅठ୆‫خ‬ෝ̜́ͥȃ̷͈̹͛Ȃ઀߿‫ݿ‬႒ͬκΟσͅ૤޼໦Ⴈ͈‫ࡔུܖ‬ၑͬၑٜ̳̭ͥ͂́૤޼໦Ⴈည൵ͥ͢ͅሶ඿႒͈૤௫ठ୆͈ΪϋΠͬංͣͦͥ͂ࣉ̢̹ȃজ଼̹̻͉੃૤޼́͜໦Ⴈͥ͢ͅठ୆̦‫خ‬ෝ̈́ΔήρέͻΛΏν͈૤௫อ୆ͅ಍࿒̱Ȃශ‫֦ͥ̈́ة‬ঊ̦ळ༾ਔ‫಺ͬܢ‬୯̱̞̥̀ͥͬ௴̢̭̱̹ͥ͂ͅȃ̭͈̹͛Ȃȶ໦Ⴈ̱̞̀ͥ૤޼ȷ͂ȶ໦Ⴈ͈೪গ̱̞̀ͥ૤޼ȷͬߊ༆̳͓̩ͥȂ૤޼අ։എͅŇŶŤŤŪġ ĩŧŭŶŰųŦŴŤŦůŵġ ŶţŪŲŶŪŵŪůŢŵŪŰůĮţŢŴŦťġ ŤŦŭŭġ ŤźŤŭŦġ ŪůťŪŤŢŵŰųĪġ ͬอ࡛̳ͥΠρϋΑΐͿΣΛ·ĩŕŨĪࡢఘġĩńŮŭŤĳĻŇŶŤŤŪĪġ ͬैୋ̱ȂńŮŭŤĳġ ĩńŢųťŪŢŤġ ŮźŰŴŪůĮŭŪŨũŵġ ŤũŢŪůġ ĳĪġ ίυκȜΗȜջం଻ͅŮŗŦůŶŴġ ĩŔİňĳİŎ‫ܢ‬Īġ ͂ŮńũŦųųźġĩňıİňĲ‫ܢ‬Īġͬอ̵࡛̯̹ȃŇŶŤŤŪ̦ࡢఘ૤௫́͜ळ༾ਔ‫ͬܢ‬฽‫̹̳͛ͥͅ෇ږ̥̳ͥד‬Ȃࡢఘ̥ͣං̹ŇŶŤŤŪ
อ࡛૤޼ळ༾͈ࠖ࢕͂Ȃΰ΅ΑΠஅ૗͈া̱̹ळ༾ਔ‫̦֚͂ܢ‬౿̳̭ͥ͂ͬŇłńŔġ ĩŇŭŶŰųŦŴŤŦůŤŦĮŢŤŵŪŷŢŵŦťġ ŤŦŭŭġ
Έٜଢ଼̳̭ͥ͂ͤ͢ͅŮŗŦůŶŴု଻ळ༾͈‫̞̦ࣣࣞڬ‬Ȃ̳̻̈́ͩ໦Ⴈ௩૓̦େͭ̈́อ୆শ‫࠿ͬܢ‬൦̱̹ȃ໦Ⴈ௩૓͈
େ̜ͭ́ͥĴ඾࿒᥷̥ͣŮŗŦůŶŴု଻ळ༾͂ŮńũŦųųźု଻ळ༾̷̸ͬͦͦŇłńŔ́໦̱৾œŏłΏȜ·΀ϋᾺ֒ͅഥঊอ࡛ٜଢ଼࣐̹ͬ̽ȃळ༾ਔ‫۾ܢ‬Ⴒ֒ഥঊո‫͈ٸ‬໦๥֦ঊͅ಍࿒̱̹ࠫ‫ض‬Ȃ૤޼ळ༾͈໦Ⴈည൵֦ঊ͈࢓༞̱͂̀
ȶ໦๥֦ঊŎȷͬࡉ੄̱̹ȃ૤޼ळ༾͈͒໦Ⴈ௯ૺ࢘‫̭̹͓ͧ͂಺ͬض‬ȂŎ͉ΔήρέͻΛΏν̀ͅ૤޼ळ༾ତͬ௩‫ح‬̵̯̭̦ͥ͂‫خ‬ෝ̈́໦ঊ̜́ͥ͂໦̥̹̽ȃ䋭 㪈㪍㪎 䋭著者索引

ŴŰųŵŪůŨĪġ ٜଢ଼́‫̹̱෇ږ‬ȃ௽̞̀ȂŕŨġ ĩńŮŭŤĳĻŇŶŤŤŪĪġ ᥷ͬ୆ࢃ̥ͣĲ̥࠮̹ͩͤࠖͅ࢕͈อ࡛ΩΗȜϋͬͼιȜΐϋ

ポスター発表 ＹＩＡ選考発表ሶ඿႒͈૤޼ळ༾͈ఱ฼͉୆ࢃ̩̈́͘͜໦Ⴈͬ೪গ̳ͥȃ଼੃ࢃ͜૤޼ळ༾͈໦Ⴈ̦̭ܳͥ͂༭̯̹̦࣬ͦȂ૤௫őŃĲĮĳĺ ਆនࠬ‫ۯ‬ඤ๧ळ༾͈͒ ŪůġŷŪŷŰġŴŪœŏł ൵ව༹͈‫ږ‬ၛɛᗣ֔ġဋ ĲȂษ५ġࢼ૽ ĲȂऎ൥ġ࿾ٚ ĲȂ໶൥ġ৿ ĲȂਝനġ‫ ྔם‬ĲȂఱٖġ௱ࢣ ĳĭĴȂ๳നġ‫ނ‬ঊ ĳȂࡔോġਜ‫ ݌‬Ĳ
Ĳ ཤ٬ൽఱ‫ڠ‬ఱ‫ڠ‬࿪‫֭ݪࡄڠ‬Ȃĳ ཤ٬ൽఱ‫ڠ‬ఱ‫֭ڠ‬ভ‫࢛࣌شݪࡄڠ‬ພఠ‫࣒ڠ‬जࠬ‫ۯ‬୆໤‫ޗڠ‬৒ȂĴ ཤ٬ൽఱ‫ڠ‬ఱ‫֭ڠ‬ভ‫૷࢛࣌شݪࡄڠ‬౯ඤ‫ڠش‬ਆនࠬ‫ۯ‬ඤ๧ळ༾ġ ĩŕņńŴĪġ ͉Ȃਆន଼͈ಿͅ૬̩‫۾‬Ⴒ̳̭̦ͥ͂༭̯̤࣬ͦ̀ͤȂఉ̩͈ΈσȜί̦ࡄ‫͛ૺͬݪ‬̞̀ͥȃŕņńŴ͈̜ͥ֒ഥঊ͈࿨‫̹͓͛ͥͅ಺ͬڬ‬Ȃࢯఘൎဓͥ͢ͅஷ‫͞ٺ‬΋ϋΟͻΏο΢σΦΛ·ͺ;Πζ;Α
͈ैୋ̦࡛̈́̓हဥ̞̞ͣͦ̀ͥȃ̱̥̱̦̈́ͣȂ༹̭͈༷͉ͦͣ́ैୋͅশ‫͂ۼ‬๯ဥ̦ଣ͚ևȂచય͈֒ഥঊ̦ໝ
ତంह̳ͥાࣣ͉ͅ৘ࡑ͈ΟΎͼϋ̦๱ુࣾͅඳ̜́ͥȃ̭͈̭̦͂ŕņńŴ଼͈̦ͭಿ͈͒‫ܙ‬ဓ͈ၑٜͬཐ̬̤̀
ͤȂͤ͢۰༒ͅŕņńŴ͈֒ഥঊͬௌै̳ͥܿ੅͈‫ږ‬ၛ̦‫̞ͥ̀ͦͣ̀͛ݥ‬ȃِș͉Ȃζ;Αࡢఘτασ̤̞̀ͅඅ೰
͈௫‫ͅܕ‬ŴŪœŏłͬ௣ో‫خ‬ෝ̈́ఉ‫ܥ‬ෝ଻΀ϋαυȜί߿΢Φࢹ௮ఘġĩŎņŏŅĪġ͈‫ٳ‬อͬૺ̧̹͛̀ȃ̭ͦ́͘ͅȂਆនळ༾͞۴௫ͅŴŪœŏłͬ൵ව̱Ȃඅ೰͈֒ഥঊ͈อ࡛ͬဲଷ‫خ‬ෝ̜̹̭́̽͂ͬ༭̱̞࣬̀ͥȃࣽٝȂུΏΑΞθͬ؊ဥ̱ŕņńŴඅ։എ̈́ŴŪœŏł௣ోΏΑΞθ͈ࢹಃͬদ͙̹ȃŕņńŴ͈͒ດഎঐ࢜଻ͬŎņŏŅͅັဓ̳ͥ࿒എ́ȂŤźŤŭŪŤġĩœňŅŧŌĪġĩŤœňŅĪġ́ŎņŏŅͬਘૐ̱̹ġĩœňŅĮŎņŏŅĪȃŤœňŅ͉ਆន͈ࠬ‫ۯ‬ඤ๧ळ༾ͅ஖఼എࣞͅอ࡛̱̀
̞ͥϷŗϸĴͼϋΞΈςϋ͈‫ܡ‬౶͈ς΄ϋΡ̜́ͥȃκΟσ̱͉͂̀Ȃࠬ‫͈ۯ‬ཅີ̈́ΪΠଅळ༾̦ͭŐŔĮœńĮĳळ༾ͬ๧‫֊ئ‬૒̳̭ͥ͂́ैୋ̱̹౜‫܈‬ζ;Αͬဥ̞̹ȃ̭͈ζ;ᾼచ̱̀Ȃඤ๧ळ༾ζȜ΃ȜCd31ͅచ̳ͥŴŪœŏłͬ໑ව̱̹œňŅĮŎņŏŅͬ୓ྤඤൎဓ̱ȂŎņŏŅ͈ਆនඤޫह͂ŴŪœŏłͥ͢ͅΦΛ·Θ;ϋͬບ‫̹̱ث‬ȃൎဓࢃ͈୨༌ͬ‫ވ‬ઙതτȜΎȜ௢औ߿ࡐ๷‫̀̽͢ͅޢ‬۷ख़̱̹̭͂ͧȂŴŪœŏłဇြ͈ࠖ࢕̦ ŪŴŰŭŦŤŵŪů ု଻͈ඤ๧ळ༾͂‫ޫވ‬ह̱̞̀ͥအঊ̦෇̹͛ͣͦȃ̹͘Ȃ೰ၾഎőńœ༹̽̀͢ͅCd31 Ůœŏłၾ̦ࡘઁ̱̞̭̦̀ͥ͂ྶ̥̹ͣ͂̈́̽ȃडࢃͅȂœňŅĮŎņŏŅͥ͢ͅহၷ࢘‫ͬض‬ບ‫̹̱ث‬ȃহၷဥ֒ഥঊ̱͉͂̀ȂVEGFR2ͬ஖఼̱̹ȃVegfr2ͅచ̳ͥŴŪœŏłͬĵįıġŮŨİŬṸ֚඾̧̤ͅĴٝൎဓ̱̹̭͂ͧȂࠬ‫ۯ‬࿂ୟ͈ࡘઁ͂ਆន଼ಿ͈ಁ‫̹ͦͣࡉ̦װ‬ȃոષ͈̭͂ͤ͢ȂœňŅĮ
ŎņŏŅ͉ŕņńŴ͈‫ܥ‬ෝٜଢ଼ͅခဥ̜̭̦́ͥ͂াऐ̯̹ͦȃ䋭 㪈㪍㪏 䋭őńĳĮĲĳ ྕ଻֋঵൫ଢ଼̦‫ܢڞ׿‬ΑΞϋΠඤठ‫ޛ‬ॏอ୆ͅဓ̢ͥ‫࠿͈̞̀̾ͅޣג‬൦ɛࡼ਱ദġࢬඵ ĲȂઐ๶ģ̜̭̇ ĲȂ‫ع‬ఆġࢼ໹ ĲȂ౓‫ڈ‬ġഔ ĲȂೞུġࠃ௱ ĲȂा౓ġ౶຃ ĲȂ࿐ఆġ૨२ ĲȂ֔ષġ߼ং ĲȂ൥നġฎ ĲȂୌఆġ៍૽ ĳȺ࿒എȻ൫ଢ଼ۛ৪ͅచ̳ͥ࿪सဣ੄଻ΑΞϋΠȪŅņŔȫ͈ခ࢘଻̦ྚ̺‫ږ‬ၛ̱̞̞̀̈́ಎȂ൫ଢ଼ۛ৪͈͒ŅņŔ͈ಿ‫࢘ܢ‬‫͉ض‬ະྶ̜́ͥȃུࡄ‫͈ݪ‬࿒എ͉ȂŅņŔͬၣ౾̱̹൫ଢ଼ۛ৪͈‫ܢڞ׿‬ठ‫ޛ‬ॏȪŭŢŵŦġ ŤŢŵŤũġ Ŷűȫ̞̾̀ͅȂ๱൫ଢ଼ۛ৪͂
๤‫࠿̱̀ڛ‬൦̳̭ͥ͂ȃ
Ⱥ༹༷Ȼ
చય͉Ȃ
ĳııĵාĹ࠮̥ͣĳıĲıාķ࠮́͘ͅ൚֭́ŅņŔၣ౾଼̱̹ࢗͅછ႕́Ȃ੝ٝέ΁

特別講演

Ĳ ‫ނ‬സలඵ୤਱লພ֭Ȃĳ ൑૾ٛພ֭

プログラム

ĺ࠮ĳĸ඾Ȫ߄ȫġĲĳĻĶıȡĲĴĻĲĶġġεΑΗȜٛાεΑΗȜġႉ઄ őńĳȶ‫ۯࠬ଻ࠬݹ‬৖ۛȟఱ൲ྤ৖ۛȷ

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineυȜͺΛί௮‫́ג‬ठ‫ޛ‬ॏ̦̩̈́‫ͅܢڞ׿‬ठ‫ޛ‬ॏ̧̹̱̹ͬછ႕ȃྕ଻֋঵൫ଢ଼͈ခྫ́ႉ઄෸ࠊȂພ་෸ࠊȂ೰ၾഎ႕̜̹́̽ȃ‫ܢڞ׿‬ठ‫ޛ‬ॏછ႕͉ĵı႕́Ȃ൫ଢ଼ۛ৪͉ĺ႕Ȫດഎພ་ठ࣐ࠬठ࠺੅
Ȫŕōœȫ
ķ႕ȫ
Ȃ
๱൫ଢ଼ۛ৪͉ĴĲ႕Ȫŕōœĳĸ
႕ȫ̜̹́̽ȃ‫ܢڞ׿‬ठ‫ޛ‬ॏ͈́͘‫͉ۼܢ‬Ȃ൫ଢ଼ۛ৪́๱൫ଢ଼ۛ৪ͅ๤͓̀ခփͅౣੀ̱̞̹̀Ȫĸĳĵįĺ඾ġ ŷŴġ ĲĲĶĴįĹ඾ĭġ űɁıįııĶȫ
ȃۛ৪෸ࠊ͉́൫ଢ଼ۛ৪ͅ๤͓̀๱൫ଢ଼ۛ৪͉ࣞႢ̜̹́̽
Ȫķĳįĳपġ ŷŴġ ķĺįĲपĭġ űľıįıĵȫ
̷̦͈ఈ͈ႉ
઄෸ࠊ͉ͅၰ߲ͅओ̦̥̹̈́̽ȃພ་෸ࠊ͉́Ȃພ་ಿ͉൫ଢ଼ۛ৪́ౣ̞߹࢜ȪĲĴįĹŮŮġ ŷŴġ ĲĺįķŮŮĭġ űɁıįıķȫ̜́ͤȂड઀ࠬ‫ࠂۯ‬ȪŎōŅȫ͉൫ଢ଼ۛ৪́ఱ̧̞߹࢜
ȪĲįıĳŮŮġ ŷŴġ ıįķĴŮŮĭġ űľıįıĸȫ
̜̹́̽ȃ̹͘๱൫ଢ଼ۛ৪ͅ๤̱Ȃ൫ଢ଼ۛ৪́୞‫ا٭‬ພ་̦ࣞၚ̜̹́̽
ȪķķįĸĦġŷŴġĲķįĲĦĭġűɁıįııĳȫ
ȃΑΞϋΠࠂ
ȪĴįıŮŮġŷŴġĳįĺŮŮĭġűɁıįĶĲȫ
ȂΑΞϋΠၣ౾শडఱΨσȜϋգȪĲĹįĺŢŵŮġ ŷŴġ ĲĹįĶŢŵŮĭġ űɁıįĸĹȫ͉ͅओ̦̥̹̦̈́̽Ȃ൫ଢ଼߲́௙ΑΞϋΠಿ̦ౣ̥̹̽
ȪĲĺįıŮŮġ ŷŴġ ĳĺįĹŮŮĭűɁıįıĶȫ
ȺࠫࢊȻȃ൫ଢ଼ۛ৪͉́๱൫ଢ଼ۛ৪ͅ๤̱̀ȂŅņŔၣ౾ࢃ͈‫ܢڞ׿‬ΑΞϋΠठ‫ޛ‬ॏ்̦ͤ͢‫ͅܢ‬อછ̳̭̦ͥ͂া̯ͦȂಕփͬါ̳ͥ͂ࣉ̢̹ͣͦȃɛઐུġ‫ ڠ‬ĲȂհനġ௛ ĲȂ‫ॄݠ‬ġੇ֚ ĴȂ༌‫ؖ‬ġခ ĲȂळനġဢং ĳȂ‫౓ז‬ġ࠻प ĳȂ࿤࢛ġܵຳ ĲȂ૩֔ġࢗ ĲȂ઀୼ġ‫ݛ‬ဎ ĲȂ‫୼ێ‬ġࡋহ ĳ

䋭 㪈㪍㪐 䋭著者索引

Background: Ghrelin is a novel growth hormone (GH)-releasing peptide originally isolated from the stomach.
Experimental studies have demonstrated that ghrelin possesses a variety of cardioprotective effectsȁincluding
improvement of energy balance and regulation of autonomic nervous system activity. However, the role of ghrelinȁ
remains unknown in patients with acute myocardial infarction (AMI). Methods: Forty-seven consecutive patients weredivided into the following 4 groups: 16 patients with AMI, 12 patients with unstable angina pectoris (UAP), 13 patientswith stable angina pectoris (SAP), and 6 control patients without coronary artery disease. Serum ghrelin levels were
measured and compared. In the AMI group, serial changes in ghrelin levels and its relationship with clinical variables
was investigated.Results: Compared to the control (72Ⱦ26 fmol/mL), SAP (69Ⱦ47 fmol/mL), and UAP (72Ⱦ31
fmol/mL) groups, serum ghrelin levels on admission were significantly lower in the AMI group (27Ⱦ12 fmol/mL, PɃ
0.01). However, serum ghrelin levels increased linearly (day2, 30Ⱦ15fmol/mL; day 7, 39Ⱦ18fmol/mL; day 14, 49Ⱦ
28fmol/mL; PɃ0.01). In patients with AMI, the ratio of day 14 to admission serum ghrelin levels, an index of AMIrelated acute changes in ghrelin, correlated positively with peak creatine phosphokinase levels (R=0.72, PɃ0.01) andinversely with left ventricular ejection fraction (R=-0.53, PɃ0.05). Conclusions:ȁGhrelin secretion is significantly
suppressed in association with myocardial infarct size and cardiac function. Taking the various cardioprotectiveȁ
effects of ghrelin into account, the present findings support future study of ghrelin administration as a therapeutic
option for AMI patients.

ポスター発表 ＹＩＡ選考発表

Ĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬Ȃĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼ȂĴ ߃‫ܪ‬ఱ‫ڠ֓ڠ‬໐੏۪‫ܕ‬ඤ‫ش‬

口頭発表őńĳĮĲĴ őŭŢŴŮŢġňũųŦŭŪůġōŦŷŦŭŴġŪůġőŢŵŪŦůŵŴġŸŪŵũġłŤŶŵŦġŎźŰŤŢųťŪŢŭġŊůŧŢųŤŵŪŰů

会長招待講演 シンポジウム‫ۍ‬൲ྤٜଢ଼༹ȪŒńłȫ̞̾̀ͅ࠿൦̱̹ȃȺࠫ‫ض‬Ȼ۷ख़‫ۼܢ‬ಎͅŅņŔၣ౾࣐̹ͬ̽છ႕͉ĲĺĹĵ႕Ȃ̠̻൫ଢ଼ۛ৪͉ĲĹĵőńĳĮĲĵ łŤŶŵŦġűũŢŴŦġŨŭŶŤŰŴŦġŧŭŶŤŵŶŢŵŪŰůġŸŢŴġůŦŨŢŵŪŷŦŭźġŤŰųųŦŭŢŵŦťġŸŪŵũġŮźŰŤŢųťŪŢŭġŴŢŭŷŢŨŦġ
ŢŧŵŦųġŢŤŶŵŦġŮźŰŤŢųťŪŢŭġŪůŧŢųŤŵŪŰůġĮŊůŷŰŭŷŦŮŦůŵġŰŧġŮŰůŰŤźŵŦġŴŶţŴŦŵŴĮ
ɛ঳࢛ġ֘ঊȂࣽୌġຮဎȂୌ࢛ġ‫ܧ‬Ȃ๶ॄġဎ֚Ȃ౓ུġܲ঎Ȃ୬‫ݳ‬ġ୍ȂൌఆġཆࢤȂ‫؂‬࿤ġణતȂ५࿤ġܲংȂಞ࿤ġ࿭Ȃ५࢛ġ౺ဇȂ໹നġ‫ݛ‬๼ঊȂ‫ݛ‬༗ġၦঃȂ୤िġၦঃგ‫ظ‬५ࡇၛ֓‫ش‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬

AbstractBackground: It remains unclear whether glycemic fluctuation immediately after acute myocardial infarction(AMI) can affect myocardial damage. We investigated the impact of glucose fluctuation on myocardial salvage
following successful recanalization of primary AMI.Methods and Results: We studied 30 consecutive patients with
AMI. Glycemic variability, indicated as the mean amplitude of glycemic excursion (MAGE), was determined by acontinuous glucose monitoring system. Three subsets (CD14+CD16-, CD14++CD16+ and CD14+-CD16+) were
measured by flow cytometry 1, 2, 3, 4 and 5days after AMI onset. A 2-h oral glucose test was performed in 18 patients
who had no previous diagnosis of diabetes and/or glycated hemoglobin (HbA1c) of less than 6.5%, after the onset of
AMI at 2 weeks. Plasma levels of active glucagon-like peptide (GLP)-1 were measured in each sample. The extent of
myocardial salvage 7 days after AMI was evaluated by cardiovascular magnetic resonance imaging. MAGE and thepeak levels of CD14+CD16- monocytes were significantly negatively correlated with myocardial salvage index (MSI).
MAGE was significantly correlated with the peak levels of CD14+CD16- monocytes. Of interest, plasma GLP-1 levels
were significantly positively correlated with MSI and significantly negatively correlated with MAGE.Conclusions:Glucose fluctuations during the acute phase of AMI affect the MSI, indicating that manipulation of glucose variability
from peak to nadir might be a potential therapeutic target for salvaging ischemic damage.

őńĳĮĲĶ ŉźŢŭŶųŰůŪŤġŢŤŪťġŪŴġŪůŷŰŭŷŦťġŪůġŢţťŰŮŪůŢŭġŢŰųŵŪŤġŢůŦŶųźŴŮġŪůġŮŪŤŦġŵũųŰŶŨũġńŅĵĵ
ɛ२ࢡġ‫ ހ‬ĲȂༀᚧġ༸ঊ ĳȂඵ‫ݠ‬ġ஝໲ ĳȂչ൥ġࢼ Ĳ
Ĳ ‫ؖ‬५ఱ‫ڠ‬ఱ‫֭֓ڠ‬ভ࿪‫ڠ‬௙ࣣࡄ‫شݪ‬੏۪‫ܕ‬ඤ‫ش‬Ȃĳ ‫ؖ‬५ఱ‫ڠ‬ఱ‫֭֓ڠ‬ভ࿪‫ڠ‬௙ࣣࡄ‫شݪ‬໦ঊ֓‫ڠا‬

Background: Abdominal aortic aneurysm(AAA) is characterized by the destruction of tissue architecture due tochronic inflammation of unknown etiology. Hyaluronic acid(HA) is one of major ECM components in aortic vessel.
Recently, small fragmented HA by degradation has been shown to play an important role in inflammation throughCD44, a principal receptor of HA. We investigated a role of HA and CD44 on the development of AAA in mice.
Methods: CaCl2-induced AAA was used in to CD44-/- and wild type(WT) mice. In addition, ApoE-/-/CD44+/+ miceand ApoE-/-/CD44-/-mice were infused with AngII (1000 ng/kg /minute).
Results: Six week after application of CaCl2, the diameter of aorta in CD44-/-mice (12%Ⱦ13%, n=10) was
significantly smaller than that in WT mice (53%+12%, n=10). The elevated expression of matrix metalloproteinase(MMP)-2, -9 and MCP-1 in WT aorta at one week after CaCl2 treatment were significantly ameliorated in CD44-/mice. The recruitment of macrophages to AAA lesion in WT mice was significantly greater than that in CD44-/- mice.
Furthermore, we assessed HA metabolism in AAA lesion. One week after CaCl2 treatment, the increased expression of
hyaluronidase 1 and the decreased expression of HA synthase 2 were observed in WT mice. Oral administration of Lascorbic acid 6-hexadecanoate (Vcpal), a hyaluronidase inhibitor reduced CaCl2-induced AAA formation in WT mice.
In contrast, AngII-induced AAA did differ between ApoE-/-/CD44+/+ mice and ApoE-/-/CD44-/-mice. Finally wedemonstrated that low-molecular-weight proinflammatory forms of HA, but not high-molecular-weight HA, stimulated
MMP-9 production in peritoneal macrophages, considerably more than those from CD44-/-mice.
Conclusion: HA degradation is involved in CaCl2-induced AAA through CD44. Control of HA degradation or CD44
may be promising therapeutic target of AAA.

䋭 㪈㪎㪇 䋭őńĳĮĲķ ષუ൲ྤ̤̫ͥࠬͅ‫ۯ‬ಎඤ྄ໝࣣఘ࢚͂ඤ๧ջం଻ࠬ‫ڐۯ‬ಫ฽؊͈൳শ௶೰͈ခ
ဥ଻ͅ‫࠿̳ͥ۾‬൦

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛ࢛֔ġ༸გȂಅུġ‫ޕ‬຃Ȃઐུġ࠲঄Ȃോനġ࠲‫ז‬Ȃᨑ५ġྣ

Ⱥ෸ࠊȻ
ġ ߃ාȂ
ષუ൲ྤ̤̫ͥࠬͅ‫ۯ‬ඤ࣌ࠂࠗ௶Ȃ̷ͦͅ‫̩̿ܖ‬ඤ๧ջం଻ࠬ‫ڐۯ‬ಫ฽؊ȪŧŭŰŸġ ŮŦťŪŢŵŦťġ ťŪŭŢŵŢŵŪŰůĻġ
ŇŎŅȫບ‫ث‬Ȃ̯͉ͣͅಎඤ྄ໝࣣఘ࢚ȪŪůŵŪŮŢġ ŮŦťŪŢġ ŵũŪŤŬůŦŴŴĻġ ŊŎŕȫ͈൳শࠗ௶ͬ฼ু൲എ࣐̠̭̦͂ͅ‫خ‬ෝ͂
̹̈́̽ȃ
̱̥̱Ȃ
ષუ൲ྤŊŎŕ͂ŇŎŅȂ‫ۍ‬൲ྤ৖ۛςΑ·͈‫۾‬Ⴒ଻̞͈̾̀ͅ࠿൦͉ਰ໦࣐̞̞ͩͦ̀̈́ͅȃ

特別講演ఱिঌၛఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ⱥ༹༷Ȼġ൲ྤࣁ‫֦ࡏܓا‬ঊͬခ̱‫ۍ‬൲ྤ৖͈ۛ‫ܡ‬؉̦̞̈́Ⴒ௽છ႕ĳıı႕ĩ౳଻Ĳĵĳ૽ȂĶĺȾĲĴपĪͬచય̱͂̀ષუ൲
‫۾‬Ⴒ଻̧̾ͅ࠿൦̱̹ȃષუ൲ྤŊŎŕ͂ŇŎŅ͉ŖŏņřņŇͬဥ̞̀൳শ௶೰࣐̹ͬ̽ȃȺࠫ‫ض‬Ȼġ ఉ་ၾٜଢ଼͈ࠫ‫ض‬ȂŇŎŅ͂ષუ൲ྤŊŎŕ͉ාႢȂհ୓শࠬ‫͈ࠂۯ‬ఈȂࡽ̞ͅခփ̈́௖‫ͬ߸۾۾‬া̱̹ȃ̹͘Ȃၰ৪͉ŇœŔ̷̸͂ͦͦ͜ඊၛ̱̹௖‫̹͙͛͂ͬ߸۾۾‬ȃ̯ͣͅȂచયͬœŦŤŦŪŷŦųġ ŐűŦųŢŵŪůŨġ ńũŢųŢŤŵŦųŪŴŵŪŤެ஌̥ͣං
̹ͣͦŇŎŅġ ĩĶįĶĦĪĭġષუ൲ྤŊŎŕġ ĩıįĴ ŮŮĪ͈ঢഐ΃ΛΠ΂έ౵ͤ͢ͅː͈̾ΈσȜίͅ໦‫̱ڬ‬ŇœŔ̥ͣං̹ͣͦΈσȜί‫͈ۼ‬Ĳıා‫ۍ‬൲ྤςΑ·ͬ๤‫̳͂ͥڛ‬ȂŇŎŅ೩౵ȪɃĶįĶĦȫ̥̾ષუ൲ྤŊŎŕ๬࢚ȪɄıįĴ ŮŮȫͬခ̳ͥΈσȜί͉́ఈ͈ΈσȜί͂๤‫̱ڛ‬Ĳıා‫ۍ‬൲ྤςΑ·̦ಠྶͅષઌ̱̞̹̀ġĩĲĺįıȾĲĲįĴĦĪȃ
ȺࠫაȻġ ષუ൲ྤŊŎŕ͂ŇŎŅ͈‫͉ͅۼ‬Ȃခփ̈́௖‫̹͛෇ͬ߸۾۾‬ȃષუ൲ྤŊŎŕ͂ŇŎŅ͈൳শບ‫ۍ͉ث‬൲ྤ৖ۛςΑ·ͬခ̳ͥછ႕͈ςΑ·௄༆‫ͅا‬ခဥ̜́ͥ‫خ‬ෝ଻̦̜ͥȃ

会長招待講演 シンポジウムྤŊŎŕ͂ŇŎŅĭġႉ઄෸ࠊĭġ୆‫ڠا‬ΩριȜΗȜĭġ‫ۍ‬൲ྤ৖͈ۛထ௶֦ঊ̱͈͂̀ŇųŢŮŪůŨũŢŮġœŪŴŬġŔŤŰųŦġĩŇœŔĪ͈͂

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪈㪎㪈 䋭ĺ࠮ĳĸ඾Ȫ߄ȫġĲĴĻĳıȡĲĴĻĶıġġεΑΗȜٛાεΑΗȜġႉ઄ őńĳȶྎઑࠬ‫ۯ‬৖ۛȷőńĳĮĲĸ ńŰůŵŦŮűŰųŢųźġņůťŰŷŢŴŤŶŭŢųġŕũŦųŢűźġŧŰųġŃŶŦųŨŦųĨŴġŅŪŴŦŢŴŦ
ɛ‫ࡔع‬നġਘ૸Ȃाུġ૝ࢁȂࡔനġ࢕֚჊Ȃ୞ࡔġୃহȂհനġ௛Ȃ઀୼ġ‫ݛ‬ဎ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜ૤௫ࠬ‫ۯ‬ඤ‫ش‬Little has progressed in the treatment of thromboangitis obliterans called Buerger's disease since Dr. Winiwarter firstdescribed a case of strange form of endarteritis and endophlebitis with foot gangrene in 1879. This unique vasculardisease named after Dr. Buerger in 1908 has yet benefited from contemporary endovascular therapy. There has been
rapid growth in endovascular therapy on the atherosclerotic population basis worldwide. With the tremendous
advancement of endovascular technology and the exponential expertise of endovascular technique, Buerger's disease
has entered the domain of catheter-based revascularization. We have experienced with successful recanalization casesof occlusive native vessels and failed bypass graft in Buerger's disease patients. Here, we will present the significant
role of contemporary endovascular therapy for Buerger's disease.

őńĳĮĲĹ ൚̤̫֭ͥͅঅঠ‫଻ݢ‬൲ྤ໾णછ႕̤̫ͥͅ࠿൦͍̈́ͣͅࢯࠬ஀ၷ༹͈ਹါ଻
ɛ५ུġ߼ఊȂ஠ġۖȂչ൥ġ෗ࢫȂऎ໦၌ġ୍Ȃୌġ૯ࢤȂུ५ġ૨֚჊ȂგനġೄຮȂ५࢛ġ૯֚჊Ȃષႅġఱ༟Ȃၛ୼ġࢬࢣȂṈġࠏ߃ࢺสฦঌၛ௙ࣣ֓ၷΓϋΗȜঅঠ‫଻ݢ‬൲ྤ໾णછ͉Ĵı඾ոඤ͈ঘཌၚĺĮĲĶĦ́অঠ୨౯ၚĲĶĮĳĶĦ͂ထࢃະၻ̈́৖̜ۛ́ͤȂ૷౯̤͍͢হၷͅ
ඳਸ਼̳̭̦ͥ͂ఉ̞ȃ̷͈ࡔ֦̱͈͂̀ण஀છ̦ĵ‫̜ͤ́ڬ‬Ȃ̷͈ఉ̩͉૤པळ൲͈͂‫۾‬Ⴒ଻̦াऐ̯̞ͦ̀ͥȃ̷̭́Ȃ൚̤̫֭ͥͅঅঠ‫଻ݢ‬൲ྤ໾णછ႕͈হၷ଼ୡͬ࠿൦̱̹ȃచયછ႕͉ĳııķාĲĲ࠮̥ͣĳıĲĳාĲĲ࠮͈́͘ķා‫ۯࠬͅۼ‬ඤহၷ࣐̹ͬ̽ĴĶછ႕Ĵĸۛঠ̜́ͥȃۛ৪෸ࠊ͉ĸĸįĺȾĹįĹपȪ౳଻ĲĺȆ੫଻ĲķȫĭġŦňŇœĻġĸĶįĲȾĴĸįĺĭġૢ̧̹ͤۛ৪̦ĲĶછ႕ĩĵĲĦȫ̜̹́̽ȃอછࢃķশ‫ۼ‬ոඤ͈છ႕͉ĲĲછ႕Ȃอછࢃĳĵশ‫ۼ‬ոષ͈છ႕͉Ĳķછ႕̜̹́̽ȃࣣ໵છ̜́ͥ૤པळ൲͉ĳĳછ႕ĩķĴĦĪ̜ͤȂࢯާࡥၷ༹̦࣐̞̹͈͉ͩͦ̀Ĳĳછ႕̜̹́̽ȃ̯ͣͅȂŘŢųŧŢųŪůঀဥ႕
͉ĲĲ႕̜̹̦́̽ȂőŕĮŊŏœɄĲįķ̜̹́̽છ႕͉Ĳ႕͈͙̜̹́̽ȃࠫ‫͉ض‬ఱ୨౯ķİĴĸ႕ĩĲķįĳĦĪȆ઀୨౯ĳİĴĸ႕ĩĶįĵĦĪ̜́ͤȂ֭ඤঘཌĲĵįĳĦȆĲා୆ంၚķĸįĸĦȆ‫ݣ‬ঠၚĹĴįĹĦ̜̹́̽ȃ൚̤̞֭̀ࣞͅႢ‫̧̹ۛͤૢͥ͢ͅا‬৪ତ͈௩‫ͤ͢ͅح‬Ȃ૤པळ൲ࣣ໵̱̹‫଻ݢ‬໾णછ႕̦௩‫̞̱ͥ̀ح‬ȃ̷͈อછ̥ͣ਋૷́͘ͅশ‫̥̥̦ͤۼ‬Ȃ̷͈হၷ͜
ඳਸ਼̳ͥȃ̷̭́Ȃࠬ஀ထཡ̦ਹါ̜̦́ͥŘŢųŧŢųŪů͈ঢഐহၷ֖͈֋঵̦ࣾඳ̜̭̥́ͥ͂ͣ૧ܰࠐ࢛ࢯާࡥ࿪́
͈ࠬ஀ထཡ̦‫ܢ‬ఞ̯ͦͥȃ䋭 㪈㪎㪉 䋭őńĳĮĲĺ ୃુଅ‫ܥ‬ෝ߲̤̫ͥࠬͅୄͼϋΡ΅Ώσၤॸෛഽ͂ᴢ൲ྤࣁ‫ا‬ഽ͈͂‫߸۾‬ɛႝ࿐ġૺȂ୞֔ġਜਏȂড়നġု໹ȂૈġုဈȂఱ଩ġೄࢬȂఊനġ౺෗Ȃനಎġഓ૽Ȃ؈ఆġ௛Ȃ֔ષġုٚȂ৒ࡔġཅྶȺ෸ࠊȻෂඉ଻ඉள̜́ͥͼϋΡ΅ΏσၤॸĩŪůťŰŹźŭġ ŴŶŭŧŢŵŦĻġ ŊŔĪ͉Ȃྕ଻ଅ௫ພĩńŌŅĪ͈ૺ࣐௯ૺैဥ͞૤ࠬ‫ۯ‬৖͈ۛૺ࣐͜ͅ‫۾‬ဓ̱̞̭̦̀ͥ͂߃ා༭̯̞࣬ͦ̀ͥȃ̱̥̱Ȃୃુଅ‫ܥ‬ෝۛ৪߲̤̫ͥͅŊŔ౵͂൲ྤࣁ‫̾ͅ߸۾͈ا‬̞͈̀ႉ઄എ̈́༭͉࣬ઁ̞̈́ȃِࣽٝș͉Ȃଅ‫ܥ‬ෝୃુ߲̤̫ͥͅȂŊŔ౵͂ᴢ൲ྤίρȜ·͈͂‫۾‬Ⴒ̞̾̀ͅ࠿൦̱̹ȃ

特別講演ྴࡣ‫ؚ‬ఱ‫ڠ֓ڠ‬໐້௺ພ֭੏۪‫ܕ‬ඤ‫ڠش‬プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineȺ༹༷Ȼࠐ๧എ‫ۍ‬൲ྤࠁ଼੅ͬထ೰̱̞̀ͥ‫଻ࠬݹ‬૤৖ۛۛ৪͈̠̻Ȃ‫ۍ଻ݢ‬છ࢓߲Ȃྕ଻ଅ௫ພۛ৪ĩńŌŅġ ŴŵŢŨŦĴ ո߲ȇĲįĳȾıįĶĶЂŨİŮŭĪȃ஠છ႕ͅᴢ൲ྤ΀΋Ȝ࠿औͬ੅ஜͅঔ࣐̱̹ȃȺࠫ‫ض‬Ȼࡄ‫ݪ‬చય৪͈̠̻ĳĹྴĩĳĶįĳĦĪͅ௩‫ح‬ᴢ൲ྤίρȜ·ĩĸĶŵũġ űŦųŤŦůŵŪŭŦĻġ ŮŦŢůġ ŤŢųŰŵŪťġ ŊŎŕɄĲįĸŮŮĪͬ෇͛ȂࠬୄŊŔ౵͈Ĵ໦պ౵༆ͅ௩‫ح‬ᴢ൲ྤίρȜ·͈ခພၚͬ࠿൦̱̹̭͂ͧȂ̷̸ͦͦȂĲķįĳĦȂ
ĲĶįĹĦȂ
ĵĵįĵĦ͂ŊŔࣞ౵߲̦೩౵߲Ȃಎ൝౵߲ͅ๤͓ခփͅခພၚ̦̥ࣞ̽
̹ĩőľıįıĲĲĪȃఉ་ၾυΐΑΞͻΛ·ٜଢ଼́ȂාႢȂ‫׸ݎ‬ȂఘਹঐତĩŃŎŊĪȂࣞࠬգȂডৗ։ુછȂൠෂພȂŦňŇœ̞̾̀ͅ༞
ୃ̱̹ࢃ͜Ȃ
ࣞŊŔ౵ĩŐœĵįķĺĭġ ĺĶĦńŊĻĲįĴĵĮĲķįĵġ ĭőɃıįıĲĶĪ͉Ȃᴢ൲ྤࣁ‫ا‬ഽ͈ඊၛ̱̹ܰ೰֦ঊ̞̹͂̈́̽̀ȃȺࠫࢊȻࠬୄŊŔෛഽ͉Ȃୃુଅ‫ܥ‬ෝ߲̤̞̀ͅᴢ൲ྤίρȜ·͈௩‫͂ح‬ခփͅ‫۾‬Ⴒ̱̞̹̀ȃࠬୄŊŔෛഽ்͉‫͈ܢ‬൲ྤࣁ‫ૺا‬࣐͈ζȜ΃Ȝ̠͂̈́ͤͥȃɛऎ൥ġࢭఊȂಎ࿤ġဇ๼ঊȂນġ༿ຳȂࣞ‫ݠ‬ġ঩ܽȂ૩ུġജාȂாനġ౺ঊȂ੄࢛ġ࠲ఊ჊Ȃ५‫ئ‬ġഔȂՒ໐ġࢫඵȺછ႕ȻĴĸप੫଻Ⱥ৽ஶȻऒ‫͈܉‬ণႁ೩‫ئ‬Ȃֲ‫ئ‬ঠ͈౎ႁȺ࡛ພႤȻřĮĸාĴ࠮ͤ͢࿩Ĳٝİ࠮͈ອഽ́ऒ‫ֲ͙̳̥͈͞܉‬ષ‫ئ‬ঠ͈౎ႁ̦ତশ‫̥ͣۼ‬฼඾ً̹֚ͩͤͅ଻ͅ੄࡛̳ͥ΀άΕȜΡͬ߫ͤ༐̱Ȃฏ൲଻൮೑ฺ̠̭̜̹ͬ͂̽͜ȃřĮķාĵ࠮ୈऔ͈̹͛൚֭ͅව̱̹֭षͅऒஜ൮ဩͅྫછ࢓଻͈ೊ‫଻ݰ‬ෞࢸणͬ෇̹͛ȃࠐ૙ൽ૤΀΋Ȝ࠿औ́ఱ൲ྤ
༕ͅρϋήσ᝻ᮊͬ෇̹̹͛͛૤ࡔ଻ෞण஀͈‫خ‬ෝ଻ͬࣉ̢χȜέ͹ςϋ൵ව̱̹ȃ̷͈ࢃ൮೑อैͅచ̱̀‫ॸ؂‬υιςΐϋ̦೏‫ࢃ̹̽̈́ͅح‬Ȃ࿩Ĵා‫͉ۼ‬൳အ͈อै͉෇̩̹͛ͣͦ̈́̈́̽ȃ̱̥̱řĮĴාĶ࠮ࣼͤ͢อै͈ठอͬ෇
͛ȂřාĲ࠮̥͉ͣĴȽĵٝİ࠮͈ອഽ́อैͬ߫ͤ༐̱̹ȃอै͉࠮ࠐஜͅఉ̩੄࡛̳ͥ߹̦̜̹࢜̽ȃ൳ාĶ࠮ĳĶ඾ऒ‫͈܉‬ণႁ೩‫ئ‬Ȃֲ‫ئ‬ঠ౎ႁ̦੄࡛̱Ȃłພ֭̀ͅ൮໐ŎœłȂෞࠬ‫ۯ‬௮‫࠿ג‬औঔ࣐̱̹̭͂ͧȂऒ͈ᴢ໐ඤࠛ൲ྤͅ‫ޛ‬ॏਫ਼ࡉͬ෇͛ķ࠮Ĳ඾൚֭ͅഢ֭͂̈́ͥȃഢ֭শ͉ͅ‫ͅܡ‬Ŏœł͈́‫ޛ‬ॏພ་͉ક৐̱̞̹̀ȃ̱̥̱ව֭ࢃȂ࠮ࠐ‫ֲͅܢ‬‫ئ‬ঠ͈౎ႁછેခͤȂ൮໐Ŏœł́ऒඤࠛ൲ྤ͈‫ޛ‬ॏພ་ͬ෇̹͛ȃ̹͘൳শ‫ۯࠬͅܢ‬ඤ๧‫ܥ‬ෝ͈೩‫΀ͬئ‬ϋΡΩΛΡ
ٜଢ଼́෇̹͛ȃ༞‫͂ס‬հ୓‫ح‬ၷ́ࠐً͙̹̭ͬ͂ͧȂံ඾͉ͅ൳‫ޛ‬ॏਫ਼ࡉ͉٨஝̱̹ȃȺࣉख़Ȼུછ႕͉‫̥̾଻ݙخ‬฽໘଻ͅऒ൮‫ٸڀ‬ඤࠛ൲ྤ͈ࠬ‫ۯ‬ᓕੀਫ਼ࡉͬ෇̹͛ȃ̭ͦ́͘͜൳အ͈છ႕͉ઁତ႕༭̯̞̦࣬ͦ̀ͥȂ൮‫ڀ‬ඤ൲ྤ̷͈͈ࡔ֦̱͂̀థ঱‫͈̥ͣܢ‬ඤࠛ൲ྤ͈อ୆֦̳ܳͥͅࢹ௮എ̈́ါ֦͂Ȃུછ႕̤̞͉̀ͅ࠮ࠐਔ‫ۯ̦ࠬܢ‬ඤ๧‫ܥ‬ෝͬ་‫̵̯ا‬Ȃඤࠛ൲ྤ͈ᓕੀͅ‫خ̞̱͖ͥ̀ݞͬޣג‬ෝ଻̦ଔ೰̯̹ͦȃ䋭 㪈㪎㪊 䋭著者索引

‫͈଻ݙخ‬ᓕੀͬ߫ͤ༐̳œŦŷŦųŴŪţŭŦġ ńŦųŦţųŢŭġ ŗŢŴŰŤŰůŴŵųŪŤŵŪŰůġ ŔźůťųŰŮŦ
ȪœńŗŔȫ
͉͂։̈́ͥພఠ͂ࣉ̢ͣͦͥȃ

ポスター発表 ＹＩＡ選考発表‫ؖ‬५ఱ‫ڠ֓ڠ‬໐૰ࠐඤ‫ش‬

口頭発表őńĳĮĳı œŦŤŶųųŦůŵġŷŢŴŰŴűŢŴŮġŰŧġŵũŦġŤŦųŷŪŤŢŭġŊńł ͈ Ĳ ႕

会長招待講演 シンポジウムષĪͬੰ‫̹̱ࠗٸ‬ĲĲĲ႕ͬࠬୄŊŔෛഽͤ͢ͅĴ໦պͅߊ໦ĩ೩ŊŔ߲ȇıįĳķȾĲįĲЂŨİŮŭȂಎŊŔ߲ȇıįķĴȾıįĲıЂŨİŮŭȂࣞŊŔőńĳĮĳĲ ૧ܰ‫ٳ‬อ͈ࠬၠ‫଼ࠁ஀ࠬئ‬ෝٜଢ଼ΏΑΞθȪŕĮŕłŔȫͥࠬ͢ͅ஀છထ౶͈দ͙
ɛչ൥ġၦঃ ĲȂ‫ז‬ၖġ༸ࣝ ĲĭĳȂळ୼ġგ࿟ ĲĭĳȂ‫࢛ޘ‬ġચ૽ ĴȂ‫܃‬५ġ଺჊ Ĳ
Ĳ ৅঱ോఱ‫ڠ‬ఱ‫֭֓ڠ‬ভ‫ڠ‬௙ࣣࡄ‫شݪ‬ΏΑΞθࠬ஀ଷࢄ‫ڠ‬ȪιΟͻεςΑႲࠈ֓‫ڠ‬ȫȂĳ ൥૩ࢥު‫ڼ‬৆ٛ২ȂĴ ৅঱ോఱ‫ڠ‬ఱ‫֭֓ڠ‬ভ‫ڠ‬௙ࣣࡄ‫ۯࠬشݪ‬య৫ພఠٜଢ଼‫ڠ‬Ⱥ෸ࠊȻࣞࠬգ͞ডৗ։ુછ͈̈́̓୆‫ڰ‬ਠ‫۝‬ພ͉Ȃ૤޼ࢸण͞ෞࢸण͈̈́̓ࠬ஀છ͈‫֦ࡏܓ‬ঊ̱͂̀౶̞ͣͦ̀ͥȃ̭͈ͦͣ‫֦ࡏܓ‬ঊ͉Ȃࠬ‫׶଻ྕͅۯ‬છ̧̭̱ͬ֨ܳȂ൲ྤࣁ‫̵̭̯́͂ͥ௸حͬا‬Ȃࠬ஀છ͈ςΑ·̞ͬࣞ͛̀ͥ͂ࣉ
̢̞ͣͦ̀ͥȃ̱̥̱̦̈́ͣȂ̭͈ͦͣ‫֦ࡏܓ‬ঊ̦Ȃࠬ‫଼ࠁ஀͈ࠬס‬ෝͅ‫͉̞̀̾ͅޣג̳͖ݞ‬Ȃ̜ͤ͘౶̞ͣͦ̀̈́
̞ȃ̭͉ͦȂਲြ͈ࠬ஀গࠬႀ֖͈࠿औ̦Ȃ੄ࠬ߹͈࢜૷౯ͬ࿒എ̱̞͂̀̀Ȃࠬ஀߹͈ٜ࢜ଢ଼͉ͅະ̧̜̹̹࢜́̽
͛͂ࣉ̢ͣͦͥȃ߃ාِș͉Ȃࠬ஀߹ٜ࢜ͬଢ଼̱̠ͥ࠿औΏΑΞθ̱͂̀Ȃࠬၠ‫଼ࠁ஀ࠬئ‬ෝٜଢ଼ΏΑΞθȪŕĮŕłŔȫ
ͬ‫ٳ‬อ̱̹͈́Ȃ̭ͦͬဥ̞̀‫֦ࡏܓۍ‬ঊ̦ࠬ‫଼ࠁ஀͈ࠬס‬ෝͅ‫࠿ͬޣג̳͖ݞ‬൦̱̹ȃġȺ༹༷ȻၠႹඤͅழ૕֦ঊ͂΋ρȜΊϋͬࡥ௖‫̱ا‬ȂΪΠ͈ίρȜ·෫Ⴈ໐պͬ࿅༩ठ࡛̱̹ζͼ·υΙΛίͬै଼̱Ȃळ൲ྤ͈́Βς௸ഽͅ௖൚̳ͥ௸ഽ́஠ࠬͬၠ̱Ȃࠬ஀ࠁ଼ً೾ْͬ௨ບ‫̳͂͂ͥ͜ͅث‬ȂၠႹඤգ͈ષઌͬ೰ၾບ
‫̹̱ث‬ȃٜଢ଼చય̱͉͂̀Ȃ൲ྤࣁ‫ا‬ညอဥࣞডཛ૙୫৾ζ;ΑȂ೒ુ૙୫৾ζ;ΑȂࣞࠬգুடอછρΛΠȂୃુࠬգచચρΛΠ͈ࠬ‫ͬס‬ဥ̞̹ȃ̹͘Ȃࢯࠬ઀โ࿪͈࿪࢘ບ‫ͬث‬࿒എ̱͂̀ȂͺΑάςϋඤ໚ۛ৪ȂͺΑάςῧ·υάΡΈτσ໵ဥۛ৪Ȃ͍̈́ͣͅ࠲ુ૽͈ࠬ‫͜ס‬ٜଢ଼̱̹ȃȺࠫ‫ض‬Ȼࣞডཛ૙ͬ୫̵̯̹৾ζ;Α͈ࠬ‫ͬס‬ٜଢ଼̱̹̭͂ͧȂ೒ુ૙ͬ୫̵̯̹৾ζ;Α͈ࠬ‫͂ס‬๤͓̀ࠬ஀ࠁ଼
ෝ̦ᄤૺ̱̞̀̀ȂၠႹ͈໾णͅঢ͈ͥ́͘শ‫̦ۼ‬ခփͅౣੀ̱̞̹̀ȃ̹͘ȂࣞࠬգুடอછρΛΠ͈ࠬ‫͜ס‬ȂୃુࠬգρΛΠ͈ࠬ‫ͅס‬๤͓̀ࠬ஀ࠁ଼ෝ̦ᄤૺ̱̞̹̀ȃͺΑάςϋඤ໚ۛ৪͈ࠬ‫͉́ס‬Ȃࠬ઀โ͈ු಍ෝ͉࠲ુ૽͂
͕͖൳൝̺̹̦̽Ȃ̷͈ࢃ͈ࠬ஀͈հ೰‫ဲ̦ا‬ଷ̯ͦȂၠႹ͈໾णͅঢ̥̹ͣ̈́̽ȃ̱̥̱̦̈́ͣȂͺΑάςϋۛ৪͈࿩ĳĶĦ͉Ȃ
࠲ુ૽͂൳အ͈գ෨ࠁ́ၠႹ͈໾णͅঢͤȂͺΑάςϋ೷ࢯ଻͂ࣉ̢̹ͣͦȃȺࠫაȻκΟσ൲໤ͬဥ̞̹࠿൦ͤ͢ͅȂࣞࠬգ͞ডৗ։ુછ͈̈́̓୆‫ڰ‬ਠ‫۝‬ພ͉Ȃࠬ‫଼ࠁ஀͈ࠬס‬ෝͬᄤૺ̵̯ͥ‫خ‬ෝ଻̦া̯̹ͦȃ̹͘Ȃࠬ‫଼ࠁ஀͈ࠬס‬ෝ͈ٜଢ଼ͅȂŕĮŕłŔ̦ခဥ̜́ͥ‫خ‬ෝ଻̦া̯̹ͦȃ䋭 㪈㪎㪋 䋭ĺ࠮ĳĸ඾Ȫ߄ȫġĲĳĻĶıȡĲĴĻĶıġġεΑΗȜٛાεΑΗȜġ‫ܖ‬ய őŃĳȶྤ‫଼ࠁۯ‬Ȇࠬ‫ۯ‬૧୆ ĳȷőŃĳĮĴı ࠬ‫̦ا੃଼ۯ‬ඤ๧ळ༾͈ ōŊŇœ อ࡛ͬည൵̳ͥ
ɛ५୼ġఱঃȂ࿐࡫‫ؚ‬ġࢼࢫȂŋŪŢġŘŦŪŻũŦůȂśũŢůŨġōŪȂ‫ݐ‬നġྚြȂչ๤֔ġଢ࢜Ȃࣞாġ૝ࢨ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineఱिఱ‫ڠ‬๷୆໤ພࡄ‫ݪ‬ਫ਼ૂ༭ഥో໦࿤

͉Ȃඤ๧ळ༾͈ਔսͅంह̳ͥōŦŶŬŦŮŪŢġ ŊůũŪţŪŵŰųźġ ŇŢŤŵŰųġ œŦŤŦűŵŰųġ ĩōŊŇœĪͬอ࡛̳ͥͺΑΠυ΍ͼΠͅैဥ̳ͥȃ̭ͦͤ͢ͅȂͺΑΠυ΍ͼΠ̥͈ͣŗņňŇॲ୆̦ဲଷ̯ͦȂࠬ‫͈ۯ‬૝ಿ̦ଷࢄ̯ͦͥȃً̭͈೾̦༲ٟ̳ͥ͂Ȃࠬ‫ۯ‬ࢹ௮઼ً͈ࠁ଼̦̾̈́ͥͅȃ̭͈ࠬ‫ۯ‬૧୆ً೾͈ࠬ‫ۯ‬ඤ๧ळ༾͉͕͂ͭ̓ͅōŊŇœ̦อ࡛̱̞̞̀̈́ȃ༷֚́Ȃ଼ఘ;

特別講演૧୆ॾ‫͈ܢ‬ζ;Α࿌྄͈ࠬ‫ۯ‬૧୆ً೾̤̞̀ͅȂࠬ‫ۯ‬ඤ๧ळ༾̥ͣ໦๥̯ͦͥōŦŶŬŦŮŪŢġŊůũŪţŪŵŰųźġŇŢŤŵŰųġĩōŊŇĪ

Ώ̥ͣ໦ၗ̱̹ࠬ‫ۯ‬ඤ๧ळ༾ͬဥ̞̹ٜଢ଼͉́ȂōŊŇ͈ഞ‫̦ح‬ŗņňŇ͞ţŇňŇঁࠣͥࠬ͢ͅ‫ۯ‬૧୆ͬဲଷ̧̭́ͥ͂
ࠬ‫͈ۯ‬հ೰‫͂ا‬ōŊŇœ͈อ࡛ͅ௖‫ب̜̦͂ͥ߸۾۾‬୰ͬၛ̀Ȃζ;Αథ঱‫଼͂ܢ‬ఘ‫͈ܢ‬ඤ๧ळ༾͈ōŊŇœġ อ࡛ၾ͈་
‫͈ا‬ٜଢ଼͂ōŊŇœอ࡛ͬည൵̳ͥࠬ‫֦ا੃଼ۯ‬ঊ͈ౝ࣐̹॑ͬ̽ȃ̹͘Ȃࠬ‫ͬۯฺࠬ̀̽ͅا੃଼ۯ‬ၔ఑̻̳ͥ༃ळ༾
̦ඤ๧ळ༾͈ōŊŇœอ࡛ͬଷࢄ̳̥ͥͬ࠿൦̱̹ȃɛ౻‫ؖ‬ġཆణ ĲȂಎ‫ؖ‬ġၻგ ĲȂப࿤໐ġଢ ĳȂ๳࢛ġࣝ૕ ĲȂခനġု ĲȂ༌‫ؖ‬ġଢࢬ ĲȂհ‫ݳ‬ġీ ĲȂୃ࿐ġࣧ ĲȂషࡔġ߽ঊ ĲȂฒ֔ġۚࢫ ĳȂ઀৒ġ଼֚ Ĳ

口頭発表őŃĳĮĴĲ łůŨŪŰűŰŪŦŵŪůĮĲġŅŦųŪŷŦťġŧųŰŮġŗŢŴŤŶŭŢųġŔŮŰŰŵũġŎŶŴŤŭŦġńŦŭŭŴġŊŴġņŴŴŦůŵŪŢŭġŧŰųġ
łųŵŦųŪŰŨŦůŦŴŪŴġŢŧŵŦųġŉŪůťŭŪŮţġŊŴŤũŦŮŪŢ

会長招待講演 シンポジウム̦༭̯̤࣬ͦ̀ͤȂࠬ‫ۯ‬ඤ๧ळ༾̤̫ͥͅōŊŇœ͈อ࡛͂ࠬ‫ۯ‬૧୆ဲଷैဥ̞͉̾̀ͅȂ̺͘ະྶ̈́ത̦ఉ̞ȃِș͉Ȃ

Ĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼૤௫୆ၑ‫ܥ‬ෝ໐

著者索引

䋭 㪈㪎㪌 䋭ポスター発表 ＹＩＡ選考発表

Background and Aim: Angiopoietin-1 (Ang1) has been reported to be essential for vascular homeostasis via promoting
vascular maturation and integrity. Ang1 conventional knockout (KO) mouse is reported as embryonically lethal due tothe defects of vascular maturation and heart trabeculation. Vascular smooth muscle cells 0(VSMCs) constantly secretAng1 to stabilize vascular endothelial cells through Tie2, a specific receptor for Ang1. However, the role of Ang1
derived from VSMCs in ischemic condition remains unclear to date. The present study aims to reveal the role of Ang1
derived from VSMCs in angiogenesis and arteriogenesis after ischemia in adulthood. Methods and Results: We createdtamoxifen-induced smooth muscle cell specific Ang1 KO (Ang1SMCKO) mice through crossing floxed Ang1
(Ang1flox/flox) mice with SM-MHC-Cre(ER)T2 mice. We subjected control and Ang1SMCKO mice to a hindlimb
ischemia (HLI). Ang1SMCKO mice showed significantly impaired blood flow recovery and treadmill-running
capacity compared with control on and after 10 days in response to HLI. Whereas the capillary angiogenesis evaluatedby anti-CD31-immunostaining was almost comparable between control and Ang1SMCKO mice, arteriogenesis andcollateral formation evaluated by both anti-alpha-SMA immunostaining and X-ray microangiography was significantly
impaired in Ang1CKO mice compared with those in control. Consistently, Ang1SMCKO mice displayed enhanced
vascular permeability after HLI compared with control. Furthermore, infiltration of M2-like macrophages expressing
both F4/80 and MRC1, which has been reported to have pro-arteriogenic characters, was reduced in the ischemic limb
muscles of Ang1SMCKO mice compared with those in control. Conclusion: Collectively, Ang1 derived from VSMCs
is essential for arteriogenesis and collateral formation after HLI presumably via macrophage skewing into the M2-likephenotype.

őŃĳĮĴĳ ‫ܡ‬ంࠬ‫ۯ̫̤ࠬͥͅۯ‬ඤ๧ۚळ༾ΏΑΞθ͈௫‫ܕ‬ठ୆̤̫ͥͅ࿨‫ڬ‬ɛ৹ႅġసȂඤ൥ġંൽȂࣞၻġგࢤȂఆઐġঃၦȂ࿐࡫‫ؚ‬ġࢼࢫȂࣞாġ૝ࢨఱिఱ‫ڠ‬๷୆໤ພࡄ‫ݪ‬ਫ਼ૂ༭ഥో໦࿤

Ⱥ࿒എȻਅș͈୆ఘழ૕͉́ȂΪ΀ρσ΅Ȝͬခ̳ͥఘ଻ۚळ༾ΏΑΞθ̦ంह̱Ȃழ૕͈֋঵̤͍͢ठ୆࣓ͅࡃ̳ͥȃ߃ාȂِș଼͉ఘζ;Α͈৽ͅ‫ئ‬ঠ޼ර͈ࠬ‫̞̤̀ͅۯ‬Ȃࠬ‫ۯ‬૧୆ͅಎ૤എ̈́࿨‫ۯ̳̹ࠬضͬڬ‬ඤ๧ۚळ༾̦ంह̳
ͥ‫خ‬ෝ଻ͬ༭̱̹࣬ȃࣽٝȂ۴௫͈‫ܡ‬ంࠬ‫ۯ଼̳ࠬͥࢹͬۯ‬ඤ๧ळ༾߲ͅΪ΀ρσ΅Ȝͬခ̳ͥࠬ‫ۯ‬ඤ๧ۚळ༾ΏΑΞθ̦ంह̧̳̥ͥ̾ͅ૧̹ͅ࠿൦࣐̹ͬ̽ȃȺ༹༷ȻĹ਩Ⴂ͈ńĶĸŃōİķġ ζ;Αͤ͢۴௫ͬ৾ͤ੄̱Ȃࣖளੜၑ̽̀͢ͅĲ̾Ĳ͈̾ळ༾ౙպͅ໦ၗ̱̹ȃŇłńŔ̀ͅńŅĴĲု଻ńŅĵĶ֮଻͈ࠬ‫ۯ‬ඤ๧ळ༾໦ْಎ͈ŔŪťŦġ űŰűŶŭŢŵŪŰůȪŔőȫ
ळ༾ͬ൳೰̱Ȃ̷͈୆໤‫ڠ‬എඅ଻̤͍͢۴ठ୆̤̫ͥͅ࿨‫࠿̞̀̾ͅڬ‬൦࣐̹ͬ̽ȃȺࠫ‫ض‬Ȼ۴௫͈‫ܡ‬ంࠬ‫଼̳ࠬͥࢹͬۯ‬‫ۯ‬ඤ๧ळ༾͈ĲįĵɓͅŔőळ༾̦ంह̱̹ȃࠬ‫ۯ‬ඤ๧Ŕőळ༾͉Ȃࠬ‫ۯ‬ඤ๧͈ఱ໐໦ͬ୸͛ͥŎŢŪůġ űŰűŶŭŢŵŪŰůġ ĩŎőĪळ༾ͅ๤͓ŗŪŵųŰષ͈́ࠬ‫ۯ‬ඤ๧΋υΣȜࠁ଼ෝ̦ခփ̥̹ࣞ̽ͅȃࠬ‫ۯ‬ඤ๧Ŕőळ༾͈อ୆౲‫̫̤ͥͅٴ‬อ࡛အ৆ٜͬଢ଼
̱̹̭͂ͧȂ
థ঱‫̞̤̀ͅܢ‬Ŕőळ༾͉ంह̴̱̤̀ͣȂ੄୆்‫͈ܢ‬୆ఘ۪‫́ئޏ‬੭șͅ੄࡛̱Ȃ੄୆ࢃĴ਩࿒ͅίρΠȜͅో̳̭̦̥̹ͥ͂ͩ̽ȃ̹͘ȂŔőळ༾͉୆ఘඤ́ুࡨໝୋෝͬခ̳ͥۚळ༾‫ͬ଻ڰ‬ခ̱ȂĲ͈̾Ŕőळ༾̥ͣŔőळ༾̤͍͢Ŏőळ༾ၰ৪̥ͣࢹ଼̯ͦͥࠬ‫ࢹۯ‬௮ͬࢹಃ̳̭̦̥̹ͥ͂ͩ̽ȃ༷֚ȂŎőळ༾͉ুࡨໝୋෝ̤͍ࠬ͢‫ࢹۯ‬ಃෝͬခ̴̯ȂŔőळ༾̦Ŏőळ༾ͤ͢͜ષպͅպ౾̱̀ࠬ‫ۯ‬ඤ๧ळ༾͈Ϊ΀ρσ΅Ȝͬࢹಃ̱̞̀ͥ‫خ‬ෝ଻̦ࣉ̢ͣͦ
̹ȃĸıĦ۴௫໐໦୨ੰ࣐̠ͬ͂Ȃ۴ठ୆ً͈೾́۴௫ࠬ‫ۯ‬ඤ๧ळ༾͈Ŕő໦ْ̦௩‫̱ح‬Ȃ૧̹̈́ࠬ‫ࢹۯ‬ಃ࣓ͅࡃ̳ͥ͂
͂͜ͅ۴ळ༾௩૓֦ঊ̜́ͥŘůŵĳ̤͍͢ŉňŇͬॲ୆̱̀۴ठ୆࣓ͅࡃ̳ͥ‫خ‬ෝ଻̦ࣉ̢̹ͣͦȃȺࠫაȻ‫ܡ‬ంࠬ‫ͅۯ‬̤̞̀੄୆ࢃࠬͅ‫ۯ‬ඤ๧ۚळ༾ΏΑΞθ̦ࢹಃ̯ͦȂ௫‫ܕ‬ठ୆࣓ͅࡃ̳ͥ‫خ‬ෝ଻̦ࣉ̢ͣͦͥȃུΏΑΞθ͈̯ٜͣ̈́ͥྶ̦ࠬ‫͍̤͢ۯ‬௫‫ܕ‬ठ୆͈૧̹̈́ଷࢄ༹‫ٳ‬อ̦̭̦̾̈́ͥ͂ͅ‫ܢ‬ఞ̯ͦͥȃőŃĳĮĴĴ ŔŦŮŢűũŰųŪůĴņİőŭŦŹŪůŅĲ ࠐႹͥ͢ͅྤ၁྄૧୆ࠬ‫ဲ଼͈ࠁۯ‬ଷ࢘‫ض‬ɛଌനġࡊঃ ĲȂ‫ڜ‬ġᄨယ ĲȂఱ୞ġྶ୆ ĲȂ౻നġ૯࿟ ĲȂ૒ఆġྶ‫ د‬ĳȂ‫݌‬ఆġಿ‫ ݛ‬Ĳ
Ĳ ‫ނ‬സఱ‫ڠ‬ఱ‫ڠش܉شݪࡄڠ֭֓ڠ‬Ȃĳ ૰࡫ఱ‫ڠ‬ఱ‫ۯ֭ࠬڠ‬୆໤‫ڠ‬Ⱥ࿒എȻྤ၁྄૧୆ࠬ‫ۯ‬Ȫńŏŗȫ͈ૺً࣐೾ͅŔŦŮŢűũŰųŪůĴņİőŭŦŹŪůŅĲ͈ࠐႹ̦‫۾‬ဓ̱̞̭̀ͥ͂‫ࠐ͈̭͍ݞ‬Ⴙͬঁ̳̭̦ࠣͥ͂ńŏŗဲଷ࢘‫ͬض‬঵̭̾͂ͬা̳ȃȺచય༹༷͂Ȼ৘ࡑ͉ͅńĶĸİŃōķζ;Α͈‫܉‬ೲͅτȜΎȜͬચৣ̱ńŏŗͬࠁ̵଼̯ͥκΟσͬဥ̞̹ȃτȜΎȜચৣࢃĲȂĴȂĶȂĸ඾࿒ͅ࿌྄૗ளષ๧İྤ၁྄ໝࣣఘͬन৾ȂŮœŏł
ͬಒ੄̱ȂœŕĮőńœ༹̀ͅŔŦŮŢűũŰųŪůĴņȂőŭŦŹŪůŅĲ͈ࠐশഎ་‫̹̱௶ࠗͬا‬ȃ̹͘τȜΎȜೄࢃͅŔŦŮŢűũŰųŪůĴņġ
ıįĲЂŨ̹͉͘ŃŔłġ ıįĲЂŨͬઝঊఘಎͅൎဓ̱Ȃĸ඾ࢃͅέρΛΠζ;ϋΠ༹ͬဥ̞̀ńŏŗ΍ͼΒͬĳ߲‫́ۼ‬๤‫̱ڛ‬̹ȃōŰŴŴġ Űŧġ ŧŶůŤŵŪŰůͬ࠿൦̳̹ͥ͛ȂőŭŦŹŪůŅĲ΋ϋΟͻΏο΢σΦΛ·ͺ;Πζ;ᾼచ̱̀ŔŦŮŢűũŰųŪůĴņġ
ıįĲЂŨઝঊఘඤಕৣ࣐̞ͬȂΦΛ·ͺ;ΠγκΗͼί͂ΦΛ·ͺ;ΠΰΞυΗͼί͈ඵ߲‫́ۼ‬ńŏŗ΍ͼΒͬ๤‫̱ڛ‬̹ȃȺࠫ‫ض‬ȻőŭŦŹŪůŅĲ͈อ࡛͉τȜΎȜચৣࢃĶ඾࿒̥ͣĲįĸĳ෼͂ခփͅષઌ̱̞̹̀ȃ༷֚ŔŦŮŢűũŰųŪůĴņ͈อ࡛ၾ͉τȜΎȜચৣࢃĶ඾࿒ͅıįĴĹ෼͂ခփͅࡘઁ̱̞̹̀ȃέρΛΠζ;ϋΠ͈́ńŏŗ͈࿂ୟ͉ŃŔłൎဓ߲͉́
ĲķĴĳıįĺȾĹĴĲķįıЂŮĳȂŔŦŮŢűũŰųŪůġĴņൎဓ߲͉́ĺĵĹĸįĵȾĵĵĳĵįĲЂŮĳ͂ńŏŗࠁ଼͉ŔŦŮŢűũŰųŪůĴņ̽̀͢ͅခ
փͅဲଷ̯̹ͦȪůľķĮĺ‫܉‬ȂűɃıįıĲȫȃőŭŦŹŪůŅĲ΋ϋΟͻΏο΢σΦΛ·ͺ;Πζ;ᾼ̤̫ͥńŏŗ࿂ୟ͉ȂΦΛ·ͺ;ΠγκΗͼί͉́ĳĵĺĳıįĹȾĳĵķĹĵįĹЂŮ ĳ ȂΦΛ·ͺ;ΠΰΞυΗͼί͉́ĲĴĲĶĳįķȾĸĺĸĴįıЂŮ ĳ ͂ŔŦŮŢűũŰųŪůĴņ͈ńŏŗဲଷ࢘‫͉ض‬őŭŦŹŪůŅĲͬΦΛ·ͺ;Π̳̭ͥ͂́ક৐̱̹ȪůľĸĮĹ‫܉‬ȂűľıįıĲĵȫȃ
ȺࠫაȻζ;ΑńŏŗκΟσ̤̞̀ͅȂŔŦŮŢűũŰųŪůĴņ̷͈͂਋ယఘ͈őŭŦŹŪůŅĲ̦ńŏŗ͈ૺജً೾ͅ‫۾‬ဓ̱Ȃńŏŗࠁ଼ͬဲଷ̧́
ͥ‫خ‬ෝ଻̦াऐ̯̹ͦȃ䋭 㪈㪎㪍 䋭őŃĳĮĴĵ ŮŪŤųŰœŏłĮĲĳĶţġųŦŨŶŭŢŵŦŴġţŭŰŰťġŷŦŴŴŦŭġŧŰųŮŢŵŪŰůġŷŪŢġŵųŢůŴŭŢŵŪŰůŢŭġŴŶűűųŦŴŴŪŰůġŰŧġŗņĮ
ŤŢťũŦųŪů

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineɛఆઐġঃၦȂ࿐࡫‫ؚ‬ġࢼࢫȂඤ൥ġંൽȂࣞாġ૝ࢨ

Ĳ ŎŪŤųŰĮŴŪŨůŢŭŪůŨġœŦŨŶŭŢŵŪŰůġŕŦŤũůŰŭŰŨźġŖůŪŵĭġńŦůŵŦųġŧŰųġōŪŧŦġŔŤŪŦůŤŦġŕŦŤũůŰŭŰŨŪŦŴĭġœŊŌņŏġłťŷŢůŤŦťġŔŤŪŦůŤŦġŊůŴŵŪŵŶŵŦġ
ĳ ŊůŴŵŪŵŶŵŦġŰŧġŃŪŰŮŢŵŦųŪŢŭŴġŢůťġŃŪŰŦůŨŪůŦŦųŪůŨĭġŕŰŬźŰġŎŦťŪŤŢŭġŢůťġŅŦůŵŢŭġŖůŪŷŦųŴŪŵźĴ ŅŦűŢųŵŮŦůŵġŰŧġŗŢŴŤŶŭŢųġŃŪŰŭŰŨźĭġŊůŴŵŪŵŶŵŦġŰŧġŅŦŷŦŭŰűŮŦůŵĭġłŨŪůŨġŢůťġńŢůŤŦųĭġŕŰũŰŬŶġŖůŪŷŦųŴŪŵźĵ ŕũŦġŗŪŤŵŰųġńũŢůŨġńŢųťŪŢŤġœŦŴŦŢųŤũġŊůŴŵŪŵŶŵŦĭġŎŰŭŦŤŶŭŢųġńŢųťŪŰŭŰŨźġŢůťġŃŪŰűũźŴŪŤŴġŅŪŷŪŴŪŰůĶ ŕũŦġŔŤũŰŰŭġŰŧġōŪŧŦġŢůťġŉŦŢŭŵũġŔŤŪŦůŤŦŴĭġłŴŵŰůġŖůŪŷŦųŴŪŵź䋭 㪈㪎㪎 䋭著者索引

Transglutaminase 2 (TG2) is a calcium dependent enzyme that catalyzes the cross-linking of proteins or incorporation ofpolyamines into substrates through formation of isopeptide bond. It has been implicated in formation of new blood vessels(angiogenesis) during wound healing process. In the previous meeting, we had focused on a role of TG2 in tumor growth andtumor associated angiogenesis, compared it as assessed by the dorsal air sac animal models and tumor transplantation
models. Tumor growth in TG2-/- mice was slower than that in TG2 +/+ mice, and tumor associated angiogenesis was seen in
B6 TG2 +/+ mice, but not in TG2 -/- mice. Similar defects in angiogenesis were also observed in both matrigel plugs andaorta ring assays. Primary endothelial cells (ECs) isolated from TG2 -/- mice lost their capability of forming capillary
networks on the matrigel, but did not differ in attachment and proliferation compared with ECs from TG2 +/+ mice.
However, TG2 -/- mice displayed any obvious abnormalities in blood vessel formation during developmental process. Here,
we analyzed underlying molecular mechanism in mice lung ECs. Affymetrix microarray system was used to compare theexpression pattern of every transcript gene between VEGF treated-lung ECs isolated from TG2+/+ mice and those from
TG2-/- mice. TG2-/- ECs expressed almost 10 fold increased levels of an anti-angiogenic factor, VASH1 than TG2+/+ ECs.
Further western blotting and real time PCR analyses revealed that TG2 regulates VASH1 protein and gene expression levels
at upstream of the RB-E2Fs-EZH2 axis. These data confirmed an essential role of TG2 in lung cancer for pathologicalangiogenesis via suppressing VASH1. Regulation of tumor angiogenesis by TG2 without affecting developmental
angiogenesis will provide a clue to selective regulation of tumor-angiogenesis.

ポスター発表 ＹＩＡ選考発表ɛ ōņņġņŶůĮŔŦŰĲĭĳȂŔŖśŖŌŊġŚŢŴŶũŪųŰ ĴȂŊŊŔŎłłġŔŪŪųŪġņ ĵȂňœłŉłŎġœŰţŦųŵġŎįġĵȂňœŊŇŇŊŏġŎŢųŵŪů ĶȂŌłňņńŉŊŌłġŉŪųŰźŶŬŪ ĳȂŔłŕŐġŚŢŴŶŧŶŮŪ ĴȂŌŐŋŊŎłġŔŰŪŤũŪ Ĳĭĳ

口頭発表őŃĳĮĴĶ ŕųŢůŴŨŭŶŵŢŮŪůŢŴŦġĳġœŦŨŶŭŢŵŦŴġņśŉĳĮŗłŔŉĲġőŢŵũŸŢźġŪůġłůŨŪŰŨŦůŦŴŪŴĭġņŴűŦŤŪŢŭŭźġ
ŕŶŮŰųĮŪůťŶŤŦťġłůŨŪŰŨŦůŦŴŪŴ

会長招待講演 シンポジウム

MicroRNAs (miRNAs) are single-stranded, short non-coding RNAs that regulate gene expression through base-pairing withcomplementary sequences within mRNA 3'-UTR region, resulting in translational repression or target mRNA degradation.
Crucial roles of miRNAs have been reported for many aspects of development, homeostasis and diseases, therefore, we
searched for miRNAs involving angiogenesis. We first evaluated the expression of miRNAs in primary endothelial cells(ECs) from hindlimb muscle ischemia model mouse by quantitative real-time PCR analysis. In vitro study, miR-125b, among
upregulated miRNAs in primary ECs under hypoxia, overexpressing human umbilical vein endothelial cells (HUVECs)
exhibited reduced tube formation capacity. Mir-125b was transiently upregulated on stimulation with pro-angiogenic factors,
vascular endothelial growth factor (VEGF) or basic fibroblast growth factor (bFGF). Overexpressing miR-125b on HUVECs
reduced vascular endothelial cadherin (VE-cadherin) expression. To assess miR-125b downregulates VE-cadherin synthesis
by direct binding to VE-cadherin mRNA 3'-UTR region, we constructed luciferase reporter vectors encoding the complete
wild type 3'-UTR of VE-cadherin mRNA as well as parallel control vectors containing mismatches in the predicted miR125b binding site. Co-transfection of miR-125b with the wild-type luciferase reporter gene resulted in a significant decreasein luciferase activity. In contrast, co0transfection with mismatched-type luciferase reporter gene did not change luciferase
activity. When miR-125b was transfected into HUVECs, VE-cadherin mRNA level was never changed. Thus, we concluded
that miR-125b regulated VE-cadherin expression on ECs through translational suppression. Injecting miR-125b into thetumor showed suppressed VE-cadherin expression and non-functional blood vessels were formed, resulting in inhibition oftumor growth. It has been suggested that pro-angiogenic signals in ECs also upregulate anti-angiogenic molecules
simultaneously via negative feedback. Although miR-125b induction in ECs is transient after pro-angiogenic stimulation,
prolonged overexpression of miR-125b could result in blood vessel regression. Thus, miR-125b may be usuful in cancer
therapy by inhibiting tumor angiogenesis.

特別講演ఱिఱ‫ڠ‬๷୆໤ພࡄ‫ݪ‬ਫ਼ૂ༭ഥో໦࿤

őŃĳĮĴķ ઀൲໤ͅచ̳ͥ‫ۍ‬൲ྤ௮‫ٳ༹͈਀ג‬อɛခ෯ġ࿺֚჊ ĲȂ௉ུġ୍হ ĲȂஂ‫ز‬ġࢫࢤ ĲȂୌ५ġ֚ࢗ ĳȂߪࡔġဉ‫ ܖ‬ĳȂ٬ཤġࢨ֚ ĲȂ઀୼ġ‫ݛ‬ဎ Ĳ
Ĳ ߧུఱ‫ڠ֓ڠ‬໐້௺ພ֭੏۪‫ܕ‬ඤ‫ش‬Ȃĳ ൐‫ނ‬ఱ‫ڠ‬య৫୆ၑ‫ޗڠا‬৒‫ۍ‬൲ྤ͉‫ޛ‬ॏȆ໾णͤ͢ͅ‫ޛ‬૤છ͞૤޼ࢸण̈́̓ͬ୆̲ͥႉ઄ષ๱ુͅਹါ̈́ࠬ‫̜ͥ́ۯ‬ȃ૽‫͈ۼ‬ાࣣȂ‫ۍ‬൲ྤ͈ບ‫ۍ͉ث‬൲ྤ௮‫ג‬Ȃ૤௫˟˰Ȃ૤޼ΏϋΙΈρέͻȜ͈̈́̓ໝତ͈κΘςΞͻȜͤ͢ͅບ‫خث‬ෝ̜̦́ͥȂζ;Α͈̈́̓઀൲໤̷̤̞͉͈̀ͅບ‫͉ث‬শ̱͂̀ࣾඳ̜́ͥȃ̷͉͈̠ͩͦͩͦ̈́͢࿚ఴٜͬࠨ̱Ȃ‫ۍ‬൲ྤࡄ‫ͤͬ͢ݪ‬۰༒࣐̠̭͂ͬͅ࿒എ̱͂̀Ȃ઀൲໤̤̫ͥͅ‫ۍ‬൲ྤ௮‫ג‬Ȇບ‫ٳ༹͈਀ث‬อͬদ͙̹ȃȁ̴͉̲͛͘ͅȂຊ৪൝̦ոஜอນ
̱̹ͼϋ·ͬဥ̞̹‫ۍ‬൲ྤ௮‫༹̞̻̀ͬ͜਀ג‬Ȃζ;Αո‫઀͈ٸ‬൲໤̤̫ͥͅ‫ۍ‬൲ྤ௮‫̹࣐̽ͬג‬ȃ̞̾̿̀Ȃζ;ᾼ̤̫ͥ‫ۍ‬൲ྤບ‫ͤͬ͢ث‬೰ၾഎ࣐̠̭͂ͬͅ࿒എ̱͂̀Ȃζͼ·υέͻσ͈൝գൎဓ࣐̹ͬ̽ȃ̯ͣͅȂ๷ळࢹ௮͈‫خ‬ণ‫̹̠࣐͛ͬͅا‬Ȃ୆ఘࠖͅ࢕ດেτ·Ιϋͬࠐ୓ྤഎͅൎဓ̱̀Ȃ৘ఘࡐ๷‫ͅئޢ‬۷ख़̤̭̹ͬ̈́̽ȃ̴༹̞͈༷̤̞ͦ̀͜ͅȂ‫ۍ‬൲ྤ͈‫خ‬ণ‫خ̦ا‬ෝ̜̹́̽ȃུอນ̤̞͉̀ͅߓఘ႕ͬ೹া̱̀ત̳ٚͥȃ䋭 㪈㪎㪏 䋭ĺ࠮ĳĸ඾Ȫ߄ȫġĲĳĻĶıȡĲĴĻĶıġġεΑΗȜٛાεΑΗȜġ‫ܖ‬ய őŃĳȶྤ‫଼ࠁۯ‬Ȇࠬ‫ۯ‬૧୆ Ĵ ȟ໦‫ا‬௩૓ȷőŃĳĮĴĸ ‫ۼ‬ဩࠏ̤͍͢૰ࠐࠏळ༾໦‫ا‬ෝͬခ̳ͥ࿉ळࠬ‫ۯ‬ਔळ༾ȪńŢűŪŭŭŢųźġŴŵŦŮġŤŦŭŭŴȫ
‫͈ڼ‬ਏၛ̷͈͂අ଻ٜଢ଼

Ĳ ՞୼֓‫ش‬ఱ‫ڠ‬੏۪Ȇࡤ‫ݟ‬Ȇ૰ࠐພఠඤ‫ش‬Ȃĳ ՞୼֓‫ش‬ఱ‫ڠ‬૤ࠬ‫ۯ‬ठ୆୶౤֓ၷ‫ٳ‬อ࣒जȺ෸ࠊȻழ૕‫ۼ‬ဩࠏۚळ༾ȪŎŔńȫ͉အș̈́ழ૕ͅంह̱Ȃழ૕ςκΟςϋΈȆਘ໘ठ୆ͅ‫ܙ‬ဓ̱̞̯̞̀ͥ͂ͦ̀ͥȃ଼ఘழ૕ŎŔń͉ͅ૰ࠐळ༾໦‫ا‬ෝ̭̦ͬ̾͂͜༭̯̞̦࣬ͦ̀ͥȂŎŔńͅŏŦŶųŢŭġ ŴŵŦŮġ ŤŦŭŭŴ̱͈͂̀ෝႁ̦̜͈ͥ

特別講演ɛ৅ࡔġ૯ਏ ĲȂ୼༏ġ੓֚ ĲĭĳȂઐ࿐ġࢣਏ ĲȂ५ඤġකং ĲȂ୒ઔġో࿟ ĲȂஃ࿤࿒ġࢴ ĲȂಅࡔġခঃ ĲĭĳȂಿ౓໐ġೄࢨ Ĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine̥Ȃໝତ͈ۚळ༾̦ईह̱̞͈̥̀ͥະྶ̜́ͥȃ࿉ळࠬ‫ۯ‬ਔळ༾Ȫőńȫ͉๷઀ࠬ‫͈ۯ‬հ೰଻̈́̓ͅ‫ܙ‬ဓ̱̞̦̀ͥȂ̴̤ͣȂ൳ळ༾͈අ଻͞࿨‫͉̞̀̾ͅڬ‬ະྶ̈́ത̦ఉ̞ȃِș͉ۚळ༾အőń͈අ଻ͬྶ̥̳̹ͣͥ͛ͅͅȂྎઑழ૕࿉ळࠬ‫̥ͣۯ‬൳ळ༾‫ͬڼ‬ਏၛ̱̹ȃȺ༹༷͂ࠫ‫ض‬Ȼ‫أ‬ഽۜ਋଻ŔŗĵıŕࢯࡔŕŨζ;Α͈વ‫ٺ‬ఱద൲ྤਔսͅอో̳ͥ࿉
ळࠬ‫ۯ‬ழ૕̥ͣȂŎłńŔΏΑΞθͤ͢ͅŏňĳȆńŅĲĵķု଻ळ༾ͬ໦ၗ̱Ȃະঘ‫ا‬ळ༾ͬਏၛ̱̹ȃౙ֚ळ༾̥ͣ·υȜϋ‫̹̱ا‬ळ༾‫͉ڼ‬Ȃőṉ͈́͂̀අಭഎ̈́ࠁఠȂ‫ܥ‬ෝȂ֒ഥঊอ࡛ͬা̱̞̹̀ȃőńळ༾‫͈ڼ‬ಎ́Ȃডཛࣸٔ͞Ȃ඲ࣸळ༾໦‫̓̈́ا‬ŎŔńအ͈ఉ໦‫ا‬ෝͬ̾͜ळ༾‫ͬڼ‬஖೰̱̹ȃ൳ळ༾͉Έςͺࠏळ༾͞૰ࠐळ༾͈̞͒ࣞ໦‫ا‬ෝͬခ̱̀
̞̹ȃŎŔń̤͍͢ŏŦŶųŢŭġŴŵŦŮġŤŦŭŭŴအ͈අ଻ͬ̾͜ਔळ༾ȪńŢűŪŭŭŢųźġŴŵŦŮġŤŦŭŭŴļġńŢűŔńȫ͉Ȃ̷ͦুఘ́ࣞၚഎͅ࿉
ळࠬ‫͜ۯ‬ठࢹಃ̧̳̭̦ͥ͂́Ȃ୆ఘ̤̞̞̀ࣞࣸͅ‫޼ڒ‬ழ૕ठ୆ෝͬခ̱̞̹̀ȃఉ໦‫ا‬ෝ͈೾ഽ͈։̈́ͥńŢűŔń
ۚळ༾ρͼήρςȜͬࢹಃ̱Ȃ̭͈ͦͣळ༾߲́ζͼ·υͺτͼٜଢ଼࣐̹ͬ̽ȃȺࠫაȻྎઑழ૕͈࿉ळࠬ‫̥ͣۯ‬Ȃ‫ۼ‬ဩࠏ̴͈͙̈́ͣ‫᥷ٸ‬ဩဇြ૰ࠐळ༾͈͒໦‫ا‬ෝͬခ̳ͥਔळ༾ńŢűŔńळ༾‫ͬڼ‬൳೰̱̹ȃȁِș͈ਏၛ̱̹ńŢűŔń
ۚळ༾ρͼήρςȜ͉Ȃழ૕ඤńŢűŔń͈අ଻ٜྶ͚̫̹ͅȂ൳ळ༾͈ఉ໦‫ا‬ෝ֋঵̈́̓‫ܥ‬ෝٜଢ଼͈̹͛ͅခဥ̈́ΜȜσ̜́ͥȃɛ੄࢛ġ࿻௱ ĲȂ୼ॄġၦঃ ĲȂ‫ݡ‬ાġੇ༟ ĲȂ֙‫ٵ‬ġ੗ຳ ĳȂ࿤ಎġ࿆‫ ܮ‬ĴȂ઀ႅȪ‫׆ک‬ȫġࢼঊ Ĵ
Ĳ ඊၛ࣐ଽ༹૽ॲުܿ੅௙ࣣࡄ‫ݪ‬ਫ਼࠲ࢫࢥ‫ݪࡄڠ‬໐࿝Ȃĳ ‫ش֓਀܊‬ఱ‫ڠ֓ڠ‬໐Ȃ

口頭発表őŃĳĮĴĹ ŎŦťŢŬŢġŪŴġŢġůŦŸġŢůŪŮŢŭġŮŰťŦŭġŵŰġŴŵŶťźġŭźŮűũŢŵŪŤġťŦŷŦŭŰűŮŦůŵġŢůťġųŦŨŦůŦųŢŵŪŰů

会長招待講演 シンポジウム߃ාȂŎŔńအ͈ఉ໦‫ا‬ෝ̭̦ͬ̾͂͜ྶ̥̞ͣ͂̈́̽̀ͥȃ̱̥̱Ȃۚळ༾‫ܥ‬ෝͬ̾͜őń͈஖఼എ൳೰༹͉‫ږ‬ၛ̱̀Ĵ ‫ܖ‬ய୆໤‫ݪࡄڠ‬ਫ਼শߗ‫ۼ‬ଷࢄࡄ‫ݪ‬৒

著者索引

䋭 㪈㪎㪐 䋭ポスター発表 ＹＩＡ選考発表

The lymphatic system plays an essential role in the maintenance of fluid homeostasis, fat absorption, and immune
responses, and is also involved in the pathogenesis of several human diseases, such as solid tumor metastasis,
lymphedema, and inflammation. Although the lymphatic vasculature is a very important organ, its development has
been poorly understood for a long time, because the lack of specific markers has complicated the identification oflymphatic vessels, and small animal model that can be genetically manipulated to discover the function of novel
lymphagiogenic candidates.
Small fish are a useful model animal to study developmental biology. From the nineteenth century, some observations
on the lymphatic system of fish were published by anatomists. However, Vogel and Claviez (1981) reported aconnection between the lymphatic system and the vascular system, through inter-arterial-anastomoses in fish. Thesefindings led to the theory that fish do not possess a lymphatic system but have two circulation systems, the primary andsecondary circulation systems. The theory has led to the recent view that zebrafish lacks a well-established lymphatic
vasculature and is unsuited for the animal model to study lymphangiogenesis (Ny et al. 2005). However, Yaniv et al.
(2006) show that zebrafish possess the lymphatic vessels that shares many of the morphological, molecular andfunctional characteristics of the lymphatic vessels found in other vertebrates, by using the transgenic line expressing
GFP in vascular endothelium under the control of zebrafish fli1 promoter. In addition, recently, we generated atransgenic medaka fish in which the lymphatic vessels are visible in vivo by transferring the promoter of medaka flt4
driving the expression of GFP, using a see-through medaka line (Deguchi et al. 2012). This model will be a useful tool
for analyzing lymphatic development and regeneration.

őŃĳĮĴĺ łŴűűĲġűŭŢźŴġŢġŤųŶŤŪŢŭġųŰŭŦġŪůġŭźŮűũŢŵŪŤġŷŢŴŤŶŭŢųġŧŶŴŪŰůġŢůťġŭźŮűũĮŷŦůŰŶŴġŤŰůůŦŤŵŪŰůġ
ťŶųŪůŨġŮŰŶŴŦġŦŮţųźŰŨŦůŦŴŪŴ
ɛ໹ോġୃ௱Ȃ࢜ġ࠲ఊȂōŪŶġřŪůźŪȂ૩ზġ֚੿Ȃ౻നġఱਏ૰࡫ఱ‫ڠ‬ఱ‫ۯࠬشݪࡄڠ֭֓ڠ‬୆໤‫ڠ‬໦࿤

During an initial phase of lymphatic vascular development, endothelial cells in the jugular vein differentiate into
lymphatic endothelial cells. These cells lose their polarity, start migrating dorsolaterally, and form a vascular structureof the primary lymph sacs from which lymphatic vessels develop further by vascular sprouting. It is hypothesized thatcell-cell adhesion and motility should tightly be regulated during these processes. However, molecular mechanism
underlying them remains unclear. We previously identified apoptosis stimulating protein of p53 (Aspp1) as anendothelial-specific gene functioning in mouse embryogenesis. Much attention has been given to the Aspp family
proteins as tumor suppressors, but in vivo role of Aspp1 remained to be elucidated. Our study showed that Aspp1 is aregulator for lymphatic tubulogenesis since Aspp1 knockout (Aspp1-/-) embryos showed subcutaneous edema anddisorganized lymphatic vasculature. Confocal microscopy of whole-mount embryos revealed a defect in fusion
between lymphatic islands to form tubular vasculature. In C57BL/6 genetic background, we also found a defective
development of lymph-venous connection site in venous angle which leads to a strong edema in a portion of Aspp1-/embryos. Based on these in vivo findings, we investigate how Aspp1 regulates lymphatic vascular development using a
differentiation culture system from embryonic stem cells into endothelial cells. Compared to wild-type endothelial
cells, Aspp1-/- endothelial cells fail to show a morphological change from a sheet-like cluster into a network ofendothelial cells. Here we would like to discuss the role of Aspp1 in lymphatic tubular formation at a cellular level.

őŃĳĮĵı ŕũŦġŔĲőĲĮœġųŦŤŦűŵŰųġŴŶţŵźűŦġŧŰųġŴűũŪůŨŰŴŪůŦġĲĮűũŰŴűũŢŵŦġŮŦťŪŢŵŦŴġŢůŨŪŰŨŦůŪŤġ
ųŦŴűŰůŴŦŴġŦŭŪŤŪŵŦťġţźġŢġůŰŷŦŭġůŶŤŭŦŪŤġŢŤŪťġŢůŢŭŰŨŶŦġńŐłĮńŭ
ɛࡼ਱၆ġ੓ٚ ĲȂߦനġణຳ ĳȂ઀Ⴙġგయ ĳȂुࡔġ‫ܮ‬გ ĴȂ‫܃‬५ġඃࡉ ĴȂࣞനġཻ‫ ܮ‬ĵȂ઀ाġฎ઎ ĲȂ઀ୌġၻআ ĵȂ೓ུġ֘ঊ ĵ
Ĳ ࣝ୼ఱ‫ڠ֓ڠ‬໐֓‫ܥၙুشڠ‬ෝ୆ၑ‫ڠ‬Ȃĳ ࣝ୼ఱ‫ڠ֓ڠ‬໐֓‫شڠ‬๧ໂ‫ڠش‬ȂĴ ඃോ໲ၑఱ‫୼ࣝڠ‬࿪‫ڠ‬໐Ȃĵ ࣝ୼ఱ‫ڠ֓ڠ‬໐֓‫شڠ‬࿪໤୆ఘૂ༭‫ڠ‬We have recently developed a novel nucleic acid analogue termed COA-Cl that elicits strong angiogenic activities comparable
to those by VEGF. Although angiogenic responses induced by COA-Cl took place via the classic MAP kinase cascade Raf-1MEK-ERK1/2, molecular target of COA-Cl that transmits extracellular stimulation to intracellular signaling remained
unknown. The Sphingosine 1-phosphate receptor S1P1-R subtype is a G-protein coupled receptor that is indispensable during
normal blood vessel development in utero. Because both COA-Cl and S1P are strongly angiogenic and are small molecule
agents, we developed a hypothesis that COA-Cl utilizes S1P1-R for its signaling. Western blot analyses (WB) in cultured
human umbilical vein endothelial cells (HUVEC) revealed that phosphorylation/activation of MAP kinase ERK1/2 elicited by
COA-Cl was almost completely abrogated by W146, a specific antagonist for S1P1, and by VPC23019, a dual antagonist for
S1P1/S1P3. WB revealed that HUVEC express much more abundant S1P1 receptor protein than S1P2 or S1P3. More
importantly, when endothelial tube forming activity was assessed by means of a co-culture assay of HUVEC with normal
human fibroblasts followed by CD31 staining, COA-Cl-induced promotion of tube formation responses were dramaticallyreduced by W146 and by VPC23019. We further characterized signaling responses of HUVEC to COA-Cl in comparison withthose induced by S1P1. ERK1/2 activation by COA-Cl was sensitive to: pertussis toxin, an inhibitor of G-protein Ϸ i/osubunits; U73122, an inhibitor of phospholipase-C (PLC); and BAPTA-AM, an intracellular calcium chelator. An
immunoprecipitation assay revealed that COA-Cl induced significant tyrosine phosphorylation of p130CAS, a known substrateof Src-family tyrosine kinases (SFK). Conversely, PP2, an inhibitor of SFK, abrogates COA-Cl-induced responses at bothlevels of ERK1/2 phosphorylation and tube formation. Collectively, our results point out the S1P1 receptor subtype as a targetof COA-Cl, at which this small nucleic acid analogue mediates angiogenic responses in human vascular endothelial cells.

䋭 㪈㪏㪇 䋭őŃĳĮĵĲ ෹൲ྤ଻෹ࣞࠬգછ͈ૺജ̤̫ͥͅΙυΏϋ΅΢ȜΔ őŚŌĳ ͈࿨‫ڬ‬ɛ૬֔ġཆ࣠ ĲȂಎఆġྶࢤ ĲĭĳȂඤ‫ޘ‬ġ‫ܖ‬ਏ ĲȂ‫ࡓٴ‬ġ௛ ĲȂခ‫݌‬ġ૯ ĲȂఱ୼ġ஝໲ ĲȂି࿤ġ‫ أ‬ĲȂ༌ఆġ૯‫ ܮ‬ĲĭĴȂ߄֔ġࠃၑ ĲȂഎાġ୉ྶ Ĳ
Ĵ ২ٛ༗ࡏ‫ނ‬സພ֭෹ࠬ‫ࠬࣞ଻ۯ‬գછ͉ࡔ֦ະྶ͈ထࢃະၻ̈́৖̱ۛ͂̀౶̞̦ͣͦ̀ͥȂࠬ‫ڐۯ‬ಫ࿪͈൵වͤ͢ͅఱ̧̩ထࢃ̦٨
஝̯̹ͦȃ̱̥̱̦̈́ͣड߃͈ༀ࣭τΐΑΠςȜĩųŦŷŦŢŭġ ŴŵŶťźĪ͉́Ķා́ĴıĦ৻͈છ႕̦ঘཌ̱̞̞̠࡛̀ͥ͂ે

特別講演

Ĳ ‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬ఱ‫઀֭ڠ‬঱੏۪‫ܕ‬ඤ‫ش‬Ȃ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine̦̜ͤȂ෹ࣞࠬգ૷ၷ͉̺̺͘͘٨஝͈ဒ౷ͬॼ̱̞̀ͥȃոஜ͉෹ळ൲ྤਓੀࠬ͞஀ࠁ଼̦ਹါ̧̯̹̦͂ͦ̀Ȃ࢘‫͞ض‬հ஠଻ͅచ̱̀͜ະ൫ྶ̈́ത̦ఉ̞͈̦࡛ે̜́ͥȃոஜِͤ͢ș͉૤ࠬ‫ۯ‬ΑΠτᾼͤ͢๱਋ယఘ߿ΙυΏϋ΅΢ȜΔőŚŌĳ̦‫̯ͦا଻ڰ‬ĭࠬ‫ۯ‬ςκΟςϋΈͬᄤૺ̵̯̭ͥ͂ͬ༭̧̱̹࣬̀ĩńŪųŤŶŭŢŵŪŰůġ ĳııĸĪȃ̹͘෹ழ૕͉ͅőŚŌĳ౩ฒ̦ఉ̩ంह̱ࠬ‫ۯ‬ඤ๧ࠬ͞‫ۯ‬໹‫޼ڲ‬஠๊ͅ໦ື̱̞̀ͥȃِࣽٝș͉őŚŌĳ໦ঊ͂෹ࣞࠬգ଻ςκΟςϋΈ̞̾̀ͅࡄ‫̹࣐̽ͬݪ‬ȃ෹ࣞࠬգછκΟσ๊̱͉֚͂̀എ̩͢ͅঀဥ̯̞ͦ̀ͥ೩ॸள໅‫ك‬ညอ଻෹ࣞࠬ
գછκΟσͬनဥ̱ζ;ΑĩńĶĸŃōİķĮŋĪͬॸளĲıĦ‫͈ئ‬೩ॸள໅‫ͬك‬ķ਩‫̹࣐̽ۼ‬ȃ̴͘෹ழ૕̤̞̀͜ͅ೩ॸளͅ
ͤ͢őŚŌĳ͉‫̹̱෇ږ̭̞̯ͬ͂ͥ̀ͦا଻ڰ‬ȃষֲͅ৒գ௶೰࣐̹̭ͬ̽͂ͧŘŕζ;Ά͉ĳĵŮŮŉŨɨĶĵŮŮŉŨ͈͒ષઌͬ෇̹̦͛őŚŌĳŌŐζ;Ά͉ခփֲͅ৒գષઌ̦ဲଷ̯̞̹ͦ̀ȃழ૕ບ‫̞̤̀͜ͅث‬őŚŌĳŌŐζ;Άಎ྄௄͈๬࢚̦ဲଷ̯ͦȂ௩૓ळ༾͜ࡘઁ̱̞̹̀ȃոஜ͈༭̥࣬ͣőŚŌĳĩŇłŌĪ͉űĶĴ͂ŎŅŎĳ͈ࣣࠫͬ௷ા౩ฒ̱͂̀΍εȜΠ̱űĶĴ͈໦ٜͅ‫ܙ‬ဓ̳̞̹ͥ͂̽༭̦̜࣬ͥĩŎŰŭġ ńŦŭŭįĳııĹĭŋġ ŃŪŰŭġ ńũŦŮįĳıĲıĪȃ
৘ष೩ॸளͤ͢ͅőŚŌĳŌŐζ;Ά͉űĳĲ઼ً̦อ࡛̱̤̀ͤळ༾௩૓ဲଷͅ‫۾‬ဓ̱̞͈̀ͥ͂͜ࣉ̢̹ͣͦȃ͘

会長招待講演 シンポジウム࡛हȂ෹ळ൲ྤඤ྄௄Ȃಎ྄௄͈௩૓͞໦‫ا‬ည൵Ȃ‫׶‬છȂळ༾൲֥̦̈́̓૧̹̈́হၷΗȜΊΛΠ̱͂̀ಕ࿒̯̞ͦ̀ͥȃ̳́ͅ૧̹̈́࿪स̱͂̀ΙυΏϋ΅΢ȜΔஷ‫ٺ‬࿪͞྾‫ဲע‬ଷस͞ႉ઄؊ဥ̯̞̦ͦ̀ͥȂ෹ࣞࠬգછͅచ̳ͥহၷ

̹űĶĴ͂őŚŌĳ͈ࣣࠫ͜೩ॸளঁࠣͤ͢ͅఱ̧̩་‫̳ͥا‬ȃŉŊŇĲϷ͈‫ړ‬ඤ֊࣐͜Řŕͅ๤͓őŚŌĳŌŐζ;ΆဲଷΈ΢σͅఉ࿂എͅैဥ̱̞̀ͥ‫خ‬ෝ଻̦̜ͤȂহၷΗȜΊΛΠ̱͂̀͜ࣉ̢̠ͥ໦ঊ͂ࣉ̢ͥȃőŃĳĮĵĳ ࠬ‫ۯ‬໹‫޼ڲ‬ळ༾ͅచ̳ͥΣ΋Ιϋ͈໦‫ا‬Ȇ౎໦‫ैا‬ဥͅ‫̳ͥ۾‬ٜଢ଼

口頭発表̯̤ͦ̀ͤȂഢৢτασ́͜ŉŊŇĲϷ‫۾‬Ⴒ໦ঊ͈ષઌ̦ဲଷ̯̞̹ͦ̀ȃȁőŚŌĳ໦ঊ͉෹൲ྤςκΟςϋΈࠁ଼͈Ώɛ‫݌‬५ġ૝ং ĲȂೊġૼ֚ ĲȂୌ५ġୃ຃ ĲȂგஂġࢣ঎ ĳȂಎఆġઆ౳ Ĳ

Ⱥ࿒എȻΗΨ΋‫׸‬ಎͅ‫̈́৽ͥͦ͘܄‬୆ၑ‫଻ڰ‬໤ৗ͈̜֚̾́ͥΣ΋Ιϋ͉ࠬ‫ۯ‬໹‫޼ڲ‬ळ༾ĩŗŔŎńĪ͈ဋ௢ͬ௯ૺ̱Ȃ൲ྤࣁ‫ا‬છۛ৪̤̞͉̀ͅίρȜ·ࠁ଼ͅ‫۾‬ဓ̱̞̀ͥ͂ࣉ̢̞ͣͦ̀ͥȃ̱̥̱ȂΣ΋Ιϋ̦͈̓အ̈́ι΃ΣΒθ́ळ༾ဋ௢ෝͬ௯ૺ̱̞͈̥͉̀ͥྚ̺ྶ̥̯̞̞ͣͦ̀̈́ͅȃِș͉Σ΋Ιϋͥ͢ͅळ༾ဋ௢͈௯ૺ͉ŗŔŎń͈ນ࡛߿̦௩૓߿ͅ߃̞̹̿ࠫ‫̢ࣉ̥̞͉͂̈́́ض‬ȂΣ΋ΙϋͅཕႺ̱̹ŗŔŎń͈֒ഥঊอ࡛ȂΗϋΩ·ৗอ࡛͈ίυέ͹ͼσ͂Ŏłőࠏ΅΢ȜΔ͈‫଻ڰ‬τασٜͬଢ଼̱̹ȃȺ༹༷Ȼ஠֒ഥঊอ࡛ٜଢ଼͉ͅζ;Αఱ൲ྤ໹‫޼ڲ‬ဇြ͈łńıĲळ༾͂ΪΠୃુఱ൲ྤ෽ူळ༾ĩŉŶłŰŔŎळ༾Īͬဥ̞̹ȃ஠֒ഥঊٜଢ଼͉Σ΋ΙϋͬĵĹশ‫ۼ‬ཕႺ̵̯̹ळ༾߲͂Ȃ΋ϋΠυȜσळ༾߲̥ͣ஠œŏłͬಒ੄̱Ȃ൐τ͈ĴŅĮŨŦůġ ŐŭŪŨŰġ ŤũŪűġ ŤŅŏłͬဥ̞̹ȃςͺσΗͼθőńœٜଢ଼͉́Σ΋Ιϋͬıĭġ ĳĵĭġ ĵĹশ‫ۼ‬ཕႺ̵̯̹ŉŔŎńळ༾̥ͣ஠
œŏłͬಒ੄̱̹ȃ̷̱̀Ȃ̷͈஠œŏł̥ͣŤŅŏłͬΞϋίτȜΠ଼̱ࣣ̱͂̀Ȃ‫ڎ‬໹‫޼ڲ‬ζȜ΃Ȝ֒ഥঊ͈ίρͼζȜͬဥ̞ٜ̀ଢ଼̱̹ȃΗϋΩ·อ࡛ၾ͈་‫͍̤͢ا‬ȂŎłőࠏ΅΢ȜΔ͈‫΀;͉ا଻ڰ‬ΑΗϋήυΛΞͻϋΈٜͤ͢ͅଢ଼
̱̹ȃĩůńũœĪ΍ήξΣΛΠ̦อ࡛̱Ȃ̹͘Σ΋ΙϋཕႺͤ͢ͅอ࡛τασ̦་‫̹̞̱̀ا‬ȃςͺσΗͼθőńœ͈ࠫ‫ض‬Ȃη΂ΏϋŊŊĲı͂΃σεΣϋ͉௩‫̱ح‬ȂϷͺ·Ιϋ͉ࡘઁ̱̹ȃη΂ΏϋŊŊĲĲȂϸͺ·ΙϋȂŔŎĳĳ͉௩‫̹̜̽́࢜߹ح‬ȃŎłőࠏ΅΢ȜΔ͈‫ا଻ڰ‬τασ͉űĴĹŎłőŌ͉ͅ་‫̦̹̥̽̈́ͦͣࡉ̦ا‬ȂņœŌĲİĳ͂ŋŏŌ͉ͅ‫̹ͦͣࡉ̦࢜߹͈ا଻ڰ‬ȃȺࠫაȻŗŔŎń͉ͅոஜ̥ͣ༭̯̞࣬ͦ̀ͥů ńũœϷ˓ո‫͈ٸ‬΍ήξΣΛΠ͈อ࡛͜‫̯ͦ෇ږ‬ȂΣ΋Ιϋͥ͢ͅอ࡛಺
୯ͬ਋̫̞̀ͥ͂ࣉ̢ͣͦͥȃ̷̱̀Ȃ໹‫޼ڲ‬ζȜ΃Ȝ֒ഥঊ͈ٜଢ଼ࠫ‫͂ض‬ŎłőࠏΏΈ΢σ͈ᄤૺ̥ͣȂΣ΋Ιϋ͉ŗŔŎń͈ࠁৗͬ໐໦എͅ௩૓߿ͅ൵̩‫خ‬ෝ଻̦̜̭̦ͥ͂াऐ̯̹ͦȃ䋭 㪈㪏㪈 䋭著者索引Ⱥࠫ‫ض‬Ȼ஠֒ഥঊอ࡛ٜଢ଼͈ࠫ‫̥ͣض‬ȂłńıĲळ༾ȂŉŶłŰŔŎळ༾‫ͅވ‬ତਅ႒͈Σ΋Ιϋ଻ͺΓΙσ΋ςϋ਋ယఘ

ポスター発表 ＹＩＡ選考発表

Ĳ ߲෯ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬ພఠਆន࿪ၑ‫ڠ‬Ȃĳ ߲෯ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬୆‫ڠا‬ĺ࠮ĳĸ඾Ȫ߄ȫġĲĳĻĶıȡĲĴĻĶıġġεΑΗȜٛાεΑΗȜġ‫ܖ‬ய őŃĳȶૂ༭ഥోȟι΃Σ΃σΑΠτΑȟ̷͈ఈȷőŃĳĮĵĴ ŇŌĶıķġŪůťŶŤŦŴġŦůťŰŵũŦŭŪŢŭġťźŴŧŶůŤŵŪŰůġŵũųŰŶŨũġŢŵŵŦůŶŢŵŪŰůġŰŧġłŬŵġŢůťġņœŌĲİĳġ
ŪůťŦűŦůťŦůŵŭźġŰŧġŤŢŭŤŪůŦŶųŪůġŪůũŪţŪŵŪŰůġŢůťġŵũŦġŤŢŴűŢŴŦġűŢŵũŸŢź
ɛࢺ࢛ġၻඵ ĲĭĳĭĴȂ൥େġࢡ߼ ĳĭĴȂ‫ݛ‬༗ġਜং ĵȂ઀୼ġ߼‫ ޕ‬ĳĭĴȂ৹ႅġ֚჊ Ĳ
Ĳ ໶ࡩ֓‫ش‬ఱ‫ޏ۪ڠ‬ထཡ֓‫࣒ڠ‬जȂĳ ໶ࡩ֓‫ش‬ఱ‫ڠ‬ඤ‫࣒ڠش‬जࠬ‫ס‬ඤ‫ش‬ȂĴ ໶ࡩ֓‫ش‬ఱ‫୶ڠ‬౤֓‫ݪࡄڠ‬ਫ਼ळ༾֊૒໐࿝Ȃĵ ໶ࡩ֓‫ش‬ఱ‫֒ڠ‬ഥ‫࣒ڠ‬ज

Calcineurin inhibitors such as cyclosporin A (CsA) and FK506 have been used in solid organ and haematopoietic stem
cell transplantations to suppress immune function. However, these immunosuppresants are associated with severe
endothelial dysfunction. We investigated whether CsA and FK506 induce endothelial dysfunction using a threedimensional culture blood vessel model, in which human umbilical vein endothelial cells form and maintain capillarylike tube and lumen structures. We found that FK506, but not CsA, induced breakdown of the tube structures and cell
death. FK506 inhibited calcineurin activity, but FK506-induced tube breakdown and cell death was not suppressed by
RNA interference targeting calcineurin AϷ. FK506 also induced caspase activation, but caspase inhibition byzVAD(OMe)-fmk failed to suppress FK506-induced tube breakdown and cell death. FK506 induced attenuation of Aktand extracellular-regulated kinase 1/2 (ERK1/2). Furthermore, Akt inhibition by LY294002 or ERK1/2 inhibition by
PD98059 induced tube breakdown and cell death. Present results suggest that FK506 induces endothelial dysfunction
through attenuation of Akt and ERK1/2 independently of calcineurin inhibition and the caspase pathway. (Cellular
Signalling, in press)őŃĳĮĵĵ ࠬ‫ۯ‬ඤ๧ळ༾̤̫ͥͅ œŢŴňœőĳ ͈ςϋॸ‫͈ا‬ٜଢ଼ɛష࿤ġ੗֚Ȃಿ႘ġ࠻ఊ჊Ȃཱġၦ࢕ࢩോ࣭षఱ‫ڠ‬࿪‫ڠ‬໐࿪‫شڠ‬œŢŴġ ŨŶŢůźŭġ ůŶŤŭŦŰŵŪťŦĮųŦŭŦŢŴŪůŨġ űųŰŵŦŪůġ ĳȪœŢŴňœőĳȫ͉ȂΈͺΣϋΤ·τ΂ΙΡ࢐֦۟ঊ͈Ĳ̜̾́ͤȂŴŮŢŭŭġ
ň౩ฒৗ͈œŢűĲͬ‫̵̯ͥا଻ڰ‬ȃِș͉ड߃ȂΪΠœŢŴňœőĳ͈ͺές΃Μι΄΀σ௖൳֒ഥঊ̦อ୆੝‫ͅۯ͈ࠬܢ‬අ։എͅอ࡛̱̞̭̀ͥ͂Ȃ̤͍ࠬ͢‫଼ͅࠁۯ‬ਹါ̈́࿨‫̦̞̱̥ͥ̀ͣͅྶ̭̞̱̹ͬ͂ͥ̀ضͬڬ‬Ȃ̷͈મळ̾ͅ
̞͉̀ၻ̩໦̥̞̞̽̀̈́ȃौාུ͈‫ڠ‬̤̞ٛ̀ͅȂœŢűĲ͈‫ͬا଻ڰ‬œŢŭňŅŔĮœŃŅͬဥ̞̹űŶŭŭġ ťŰŸů༹́࠿੄̱ȂņńŗųŢŴŨųűĳ̦œŢűĲ͈‫ͬ଻ڰ‬ᄤૺ̱̞̭̀ͥ͂Ȃ̤͍͢Ȃ̭͈œŢŴňœőĳͥ͢ͅœŢűĲ͈‫͉ا଻ڰ‬ŃłőŕłĮłŎੜၑ̽̀͢ͅဲଷ̯̭ͦͥ͂ͬྶ̥̱ͣͅȂœŢŴňœőĳ͉ńŢĳĬΏΈ΢σ̽̀͢ͅœŢűĲ‫಺ͬ଻ڰ‬୯̳̭ͥ͂ͬ༭̱̹࣬ȃِࣽٝș͉ȂœŢŴňœőĳ͈‫ܥ‬ෝٜଢ̷଼࣐̠̜̹͈ͬ̽̀ͅςϋॸ‫̞̀̾ͅا‬಍࿒̱̹ȃœŢŴňœőέ͹ηςȜ͉ςϋॸ‫̯ͦا‬̭̦ͥ͂౶̤ͣͦ̀ͤȂඅͅœŢŴňœőĲ͞œŢŴňœőĴ͉Ȃςϋॸ‫̦଻ڰ̷͈̀̽͢ͅا‬ଷࢄ̯̭̦ͦͥ͂༭̯̞࣬ͦ̀
ͥȃ̱̥̱̦̈́ͣȂœŢŴňœőĳ͈ςϋॸ‫̺ྚ͉ا‬༭̴̯̤࣬ͦ̀ͣȂ̷͈‫ܥ‬ෝ͜ྚ౶͈̜́ͥ͘͘ȃུࡄ‫͉́ݪ‬ȂœŢŴňœőĳ͈ςϋॸ‫઼ً̞̀̾ͅޣג̷͈͂ا‬อ࡛‫ैͬڼ‬ୋ̳̭ͥ͂̽̀͢ͅ࠿൦̱̹ȃࠬ‫ۯ‬ඤ๧အळ༾‫ڼ‬ņńŗĴıĵ
ͅŮŰŤŬȂųŢŴŨųűĳ̤͍͢‫ڎ‬ͺηΦॸ౾۟ųŢŴŨųűĳα·ΗȜͬΠρϋΑέͿ·Ώοϋ̱հ೰എ઼ًอ࡛‫ڼ‬ņńŗųŢŴŨųűĳȂ‫ڎ‬ͺηΦॸ౾۟‫͍̤͢ڼ‬΋ϋΠυȜσ‫̜ͥ́ڼ‬ņńŗŮŰŤŬͬౙၗ̱̹ȃষͅȂœŢŴňœőĳ͈ςϋॸ‫̞̀̾ͅا‬ȂőũŰŴĮ
ŵŢŨġŔŅŔĮőłňņͬဥ̞̀࠿൦࣐̹ͬ̽ȃ̭͈ࠫ‫ض‬ȂœŢŴňœőĳ̦೰ુેఠ̤̞̀ͅςϋॸ‫̥̈́͂ͣྶ̦̭̞̱͂ͥ̀ا‬ͤȂ̭͈ςϋॸ‫͉ا‬őũŰųţŰŭġ ĲĳĮŮźųŪŴŵŢŵŦġ ĲĴĮŢŤŦŵŢŵŦġ ĩőŎłĪঁࠣ̽̀͢ͅᄤૺ̳̭̦ͥ͂໦̥̹̽ȃ̯ͣͅȂ̷͈ςϋॸ‫̯ͥͦا‬ͺηΦॸ͈͉֚̾ͅȂΙυΏϋ̦‫̭̞͂ͥ̀ͦ͘܄‬Ȃ̤͍͢Ȃ௩૓֦ঊ൝͈ঁࠣ̽̀͢ͅΙυΏϋ̦ςϋॸ‫̹̱̥ͣͅྶ̭̯ͬ͂ͥͦا‬ȃœŢŴňœőĳ͈ςϋॸ‫͈ا‬ΏΈ΢σഥోࠐႹ൝̞͉̾̀ͅȂࣽࢃ࠿൦̧̱࣐̹̞̀ȃ䋭 㪈㪏㪉 䋭őŃĳĮĵĶ ೩ॸளညอ଻෹ࣞࠬգκΟσ́ ŊōĮķİŕũĲĸ ळ༾ΏΈ΢σ͉෹ࠬ‫ۯ‬ςκΟςϋΈͅຈଌ̜́ͥ

Ĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼૤௫୆ၑ‫ܥ‬ෝ໐ȂĴ ఱिఱ‫ڠ‬ఱ‫ܕݟࡤشݪࡄࠏڠ֭֓ڠ‬Ȇ྾‫ע‬ͺτσΆȜඤ‫ش‬࿒എȇ෹ࣞࠬգછ͉߃ා͈΀ϋΡΓςϋ਋ယఘᒅࢯ࿪͞őŅņĶஷ‫ٺ‬࿪̈́̓ͥ͢ͅহၷ͈ຽ‫ͤ͢ͅݞ‬Ȃ̷͈ထࢃ͈٨஝

特別講演ɛ༌‫ؖ‬ġଢࢬ ĲȂಎ‫ؖ‬ġၻგ ĲȂப࿤໐ġଢ ĳȂ༗୵ġೄ‫ ܧ‬ĴȂ֞‫ڈ‬ġ߰࣪ ĳȂ๳࢛ġࣝ૕ ĲȂခനġု ĲȂհ‫ݳ‬ġీ ĲȂ౻‫ؖ‬ġཆణ ĲȂୃ࿐ġࣧ ĲȂషࡔġ߽ঊ ĲȂฒ֔ġۚࢫ ĳȂ઀৒ġ଼֚ Ĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine͉࿒‫̜̦͈̞̱ͥ͘͜ژ‬ȃ̱̥̱̦̈́ͣȂࢵͅ෹ࣞࠬգછ͈ထࢃͬ٨஝̳͉ͥͅ૧͈ܰহၷ༹‫ٳ‬อ̦ຈါ̜́ͥȃ̭̯̞ͦ̀ͥȃ̹͘Ȃ෹༾ષ๧අ։എŊōĮķ઼ًอ࡛ζ;Α͉Ȃুடࠐً́෹൲ྤςκΟςϋΈ̭̱ͬܳȂ෹ࣞࠬգͬอછ
̳̭̦ͥ͂౶̞ͣͦ̀ͥȃ̷ِ̭́ș͉೩ॸளညอ଻෹ࣞࠬգζ;ΑκΟσ͈́ࢯŊōĮķ਋ယఘρΛΠκΦ·υȜ΢σࢯఘĩŎœĲķĮĲĪͥ͢ͅŊōĮķΏΈ΢σ৭౯͈࢘‫࠿ͬض‬൦̱̹ȃ༹༷͂ࠫ‫ض‬ȇ೩ॸள໅‫̹̱ͬك‬ńĶĸŃōķζ;Α͈෹ழ૕́
͉ŊōĮķŮœŏł͈อ࡛̦ခփͅ௩‫̹̞̱̀ح‬ȃ̷̭́ńĶĸŃōķζ;ΆŎœĲķĮĲൎဓͤ͢ͅ೩ॸளညอ଻෹ࣞࠬգอછ
̦ဲଷ̧̥́ͥͬ࠿൦̱̹ȃĹ਩Ⴂ͈ζ;ᾼచ̱̀ŎœĲķĮĲĩŎœĲķĮĲൎဓ߲Ī̱̩͉͜ρΛΠŊŨňĩ΋ϋΠυȜσ߲ĪͬĳŮŨ୓ಕ̱̀Ȃ̷͈ೄࢃ̥ͣॸளෛഽĲıĦ͈́೩ॸள໅‫ٳͬك‬ই̱̹ȃ֚਩‫͈߲ڎྀͅۼ‬ζ;ᾼచ̱̀ŎœĲķĮĲ̱̩͉͜ρΛΠŊŨňͬıįĶŮŨໜ࣌ඤൎဓ̱̀Ȃĵ਩‫ۼ‬೩ॸள໅‫́ࢃ̹̱ك‬Ȃֲ૤΃ΞȜΞσ࠿औֲͥ͢ͅ৒ਓੀ‫ܢ‬գĩœŗŔőĪͬ௶೰̱Ȃֲ৒ऒ৒ਹၾ๤͂෹൲ྤ͈ಎ྄༃࢚ͬ௶೰̳̭ͥ͂́෹ࣞࠬգͬບ‫̹̱ث‬ȃ΋ϋΠυȜσ߲͂๤‫ڛ‬̱̀ŎœĲķĮĲൎဓ߲͉́ȂœŗŔőષઌȆֲ৒๬ఱȆ෹൲ྤςκΟςϋΈ͈஠̦̀ခփͅဲଷ̯̞̹ͦ̀ȃ̹͘Ȃ೩ॸள໅‫ك‬ζ;Α෹͉ͅ‫׶‬છ଻ΰσΩȜŕळ༾͈֚Տ߿̜́ͥŕũĲĸळ༾̦൲֥̯̤ͦ̀ͤȂࢵͅȂŊōĮĲĸ̷͈͞‫ئ‬ၠ͈ࢡಎ‫ݩ‬௢‫֦଻ا‬ঊ͈อ࡛̦ᄤૺ̱̞̹̀ȃŎœĲķĮĲൎဓ߲͉́Ȃ̷͈ͦͣอ࡛ᄤૺ̦ဲଷ̯̤ͦ̀ͤȂ෹ࠬ‫ۯ‬ςκΟςϋΈ͈

会長招待講演 シンポジウムͦ́͘ͅ‫׶‬છ଻΍ͼΠ΃ͼϋŪůŵŦųŭŦŶŬŪůĮķĩŊōĮķĪ͉෹൲ྤ଻෹ࣞࠬգۛ৪͈ࠬୄ͞෹̷͈́อ࡛̦ᄤૺ̳ͥ͂༭࣬

֦͉֚ͅŕũĲĸळ༾͈෹͈͒൲֥̦‫̞͂ͥ̀̽ͩ۾‬ଔख़̯̹ͦȃࠫაȇŎœĲķĮĲͥ͢ͅŊōĮķΏΈ΢σ৭౯͉ζ;Α͈೩াऐ̯̹ͦȃ

őŃĳĮĵķ ŕŶŮŰųĮťŦųŪŷŦťġŮŪœŏłġŪŴġŵųŢůŴűŰųŵŦťġŵŰġŦůťŰŵũŦŭŪŢŭġŤŦŭŭŴġţźġŮŪŤųŰŷŦŴŪŤŭŦŴ

Ĳ ཤ٬ൽఱ‫ڠ‬ভ‫ۯࠬشݪࡄڠ‬୆໤‫ޗڠ‬৒Ȃĳ ཤ٬ൽఱ‫ڠ‬ভ‫૷࢛࣌شݪࡄڠ‬౯ඤ‫ޗڠش‬৒ȂĴ ཤ٬ൽఱ‫ڠ‬ভ‫࢛࣌شݪࡄڠ‬ພၑພఠ‫ޗڠ‬৒Ȃĵ ཤ٬ൽఱ‫شݪࡄڠ֓ڠ‬੏۪‫ޗڠشٸܕݟࡤܕ‬৒ȂĶ ࣭ၛ̦ͭࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼໦ঊळ༾হၷࡄ‫ݪ‬໦࿤䋭 㪈㪏㪊 䋭著者索引

Increasing evidence indicates that tumor blood vessels differ from their normal counter parts. We previously reported
that tumor endothelial cells (TECs) differ from normal endothelial cells (NECs). For examples, TECs areproangiogenic with upregulation the specific gene expressions.In addition, TECs were resistant to anticancer drugs.
Our recent study showed that tumor conditioned medium induced drug resistance in NECs (Am. J. Pathol., 2012) andTECs were heterogeneous according to the malignancy status of the tumor (Am. J. Pathol., 2012). These results
suggest that tumor-derived factor might be affecting TEC abnormality. One of the tumor-derived factors is tumor
microvesicles (TMV). TMV are 50 nm -a few Ђm diameter particles, which are secreted from tumor cells. TMV
contain many kinds of miRNAs and proteins. Recently, we reported that TMV were uptaken through endocytosis andthey promote angiogenic properties in NECs (PLoS ONE 2012). Some reports suggest that the molecules might workthrough taken up by the donor cells. In this study, we focused on miRNA as the bioactive molecules, which could betransported into NECs from tumor cells. We performed miRNA microarray with miRNA isolated from TMV and
identified specific miRNA (miR-X) in high-metastatic TMV. Furthermore, miR-X expression was upregulated inNECs by TMV treatment. These results suggest that TMV-miR-X could be transferred into NECs. The further studies
are currently ongoing to address how tumor-derived miR-X affects on endothelial cells.

ポスター発表 ＹＩＡ選考発表ɛ୼ུġణ༟ ĲȂਝ५ġᎢ༟ ĲȂఱٖġ௱ࢣ ĲĭĳȂ‫ۼ‬୞ġජ࡮ ĲȂૺ൥ġୃ૞ ĴȂ๳നġణࢼ ĵȂ઀ाġജࠄ ĶȂ၂౓ġࢣࢩ ĶȂ๳നġ‫ނ‬ঊ Ĳ

口頭発表ॸளညอ଻෹ࣞࠬգ͈อછͬဲଷ̱̹̭̥͂ͣȂŊōĮķΏΈ΢σ৭౯̦෹൲ྤ଻෹ࣞࠬգ͈হၷͅခဥ̜́ͥ‫خ‬ෝ଻̦őŃĳĮĵĸ ŗŢŴŰũŪţŪůĮĲ ̦ည൵̳ͥ๷઀‫ཱུۯ‬࿫ࢃਘૐ͂ ŗņňŇ ΏΈ΢σഥో͈͂‫߸۾‬ɛ઀ႅġ๼༠Ȃႝ࿐ġࢫࢬȂऎ൥ġ࿭ঃ൐ཤఱ‫حڠ‬Ⴂ֓‫ݪࡄڠ‬ਫ਼ਆន੏۪ࡄ‫ݪ‬໦࿤ພഎ̈́ࠬ‫ۯ‬૧୆͉Ȃ̷ͦͣ৖ພ͈՛‫͞ا‬ఈ͈໵อພ̧̭̳ͬ֨ܳఱ̧̈́ါ֦̜́ͤȂඅͅ‫͉́܈‬ਆនࠬ‫ۯ‬૧୆͈ဲଷ̦হၷ͈ΗȜΊΛΠ̱͂̀ಕ࿒̯̞ͦ̀ͥȃ̱̥̱̦࡛̈́ͣहȂ৽࣐̞ͩͦ̀ͥͅŗņňŇġ ͈ಎგࢯఘͥ͢ͅহၷౙ
ඊ͉́ࢯਆន࢘‫̩৻̦ض‬Ȃ‫̢̀ح‬ਆនࠬ‫ۯ‬૧୆̦ŇňŇĮĳ൝͈ఈ͈ࠬ‫ۯ‬૧୆֦ঊ͒ջం֊࣐̳̭ͥ͂ͤ͢ͅࢯŗņňŇၷ༹̦̥̩̞̠࢘̈́̈́ͥ͂࿚ఴത̦̜ͥȃِș̦൳೰̱̹໦๥ΗϋΩ·ৗŗŢŴŰũŪţŪůĮĲȪŗłŔŉĲȫ͉Ȃࠬ‫ۯ‬ඤ๧ळ༾̤ͅ
̞̀ŗņňŇ͞ŇňŇĮĳͤ͢ͅอ࡛͂໦๥̦ည൵̯ͦͥࠬ‫ۯ‬૧୆͈Υ΄ΞͻήέͻȜΡΨΛ·֦ঊ̜̦́ͥȂŗłŔŉĲ̦
͈̠̓͢ͅࢯࠬ‫ۯ‬૧୆࢘‫͉̥̳̹ͣͬ͜ض‬ະྶ̜̹́̽ȃࣽٝȂِș͉ŗłŔŉĲ̦ࠬ‫ۯ‬ඤ๧ळ༾̤̞̀ͅ๷઀‫ཱུ͈ۯ‬࿫ࢃਘૐ͈̜֚̾́ͥϷĮΙνȜήςϋ͈౎ΙυΏϋ‫ͬا‬ည൵̳̭ͥ͂ͤ͢ͅŗņňŇΏΈ΢σഥోͬဲଷ̱ȂŗņňŇ
ͥࠬ͢ͅ‫ۯ‬ඤ๧ळ༾͈ဋ௢௯ૺैဥͬஷ‫̹̱̥ͣͅྶ̭̳ͬ͂ͥٺ‬ȃࠬ‫ۯ‬ඤ๧ळ༾ͅŗłŔŉĲͬैဥ̵̯ͥ͂ϷĮΙνȜήςϋ͈౎ΙυΏϋ‫̦ا‬௯ૺ̱ȂŗņňŇঁࠣ̽̀͢ͅည൵̯ͦͥőŌńϷ̤͍͢łŬŵ͈ςϋॸ‫ا‬τασ͈ષઌ̦ဲଷ̯
ͦ̀ဋ௢௯ૺैဥ͜ஷ‫̹̯ͦٺ‬ȃ༷֚ȂठΙυΏϋ‫ࣖا‬ள̜́ͥŕŕōȪΙνȜήςϋΙυΏϋς΄ȜΔȫͬŗłŔŉĲ͂
‫ۯࠬͅވ‬ඤ๧ळ༾ͅैဥ̵̯ͥ͂ȂŗłŔŉĲͥ͢ͅϷĮΙνȜήςϋ͈౎ΙυΏϋ‫ا‬τασ̦΋ϋΠυȜσ͂൳೾ഽ͘
́೩‫̱ئ‬ȂŗņňŇঁࠣͅည൵̯ͦͥőŌńϷ̤͍͢łŬŵ͈ςϋॸ‫ا‬௯ૺ̤͍͢ळ༾ဋ௢͈௯ૺैဥٝ͜໘̱̹ȃ̭͈ͦͣࠫ‫̥ͣض‬ȂŗłŔŉĲͥ͢ͅࢯࠬ‫ۯ‬૧୆࢘‫͉ض‬Ȃࠬ‫ۯ‬ඤ๧ळ༾̤̫ͥͅ౎ΙυΏϋ‫ا‬ϷĮΙνȜήςϋ͈௩‫ฺ̠ͅح‬ŗņňŇΏΈ΢σഥో͈ဲଷ̤͍͢ळ༾ဋ௢͈ဲଷ֦̳ܳͥ͂ͅࣉ̢ͣͦȂŗłŔŉĲ̦ࠬ‫ۯ‬૧୆হၷ͈૧̹̈́ΗȜΊΛΠ͂̈́ͤං̭̦ͥ͂াऐ̯̹ͦȃőŃĳĮĵĹ ŅŪŧŧŦųŦůŤŦŴġŪůġœŦŮŰťŦŭŪůŨġőųŰŤŦŴŴġŢŧŵŦųġŗŢŴŤŶŭŢųġŊůūŶųźġţŦŵŸŦŦůġŊůŵųŢŤųŢůŪŢŭġŢůťġ
ņŹŵųŢŤųŢůŪŢŭġłųŵŦųŪŦŴĻġłůŢŭźŴŪŴġŖŴŪůŨġŢġŏŰŷŦŭġŎŰťŦŭġŪůġŎŪŤŦ
ɛോఆġਕં ĲȂಎ૰ġ߼ඃ ĲȂऎനġଽၦ ĴȂߴ५ġࢬ ĲȂߪ෨ġ૾๼ ĲȂ૩‫ئ‬ġၧ֚ ĳ
Ĳ ఱिఱ‫ࢫ࠲ڠ‬อో֓‫࣒ڠ‬जȂĳ ఱिఱ‫ڠ‬ႉ઄֒ഥঊহၷ‫࣒ڠ‬जȂĴ ඃോఱ‫ڠ‬੏۪‫ܕ‬ඤ‫࣒ڠش‬ज

Background & Purpose: The effectiveness of angioplasty and stenting in intracranial atherosclerotic diseases iscontroversial due to high rates of delayed restenosis and hemorrhage compared to extracranial arteries. However, themechanisms underlying these differences are still unclear because of lack of pathophysiological studies. In the present
study, we established vascular injury model in the intracranial artery in mice and compared the process of remodelingto that in femoral arteries.
Methods: The coated suture was inserted into the origin of middle cerebral artery in male FVB mice. The artery was
scratched for 10 times. The femoral artery was injured with a straight spring wire.
Results: The injured arteries were dilated twice as large as the normal arteries and the endothelial cells and smoothmuscle cells (SMCs) were completely lost on day 1 both in the intracranial and femoral arteries. Compared to theremodeling process in the femoral arteries, the following points are unique in intracranial arteries: 1) delayed
continuous formation of neointima, 2) continuous loss of SMCs in media, 3) accumulation of macrophages in the
media on day 14, 4) continuous growing of adventitia with macrophages. Although the process of remodeling wasdifferent, the systemic administration of rapamycin prevented the neointimal formation with complete reendothelialization in intracranial arteries on day 56.
Conclusions: These findings suggest that intracranial arteries might be more fragile after injury caused by PTA andstenting, and that the protection of endothelium and SMCs might be important to inhibit cerebral hemorrhage. Also,
longer-lasting drug releases might be needed to prevent neointimal formation in intracranial arteries since theneointimal formation gradually grew until day 56.
䋭 㪈㪏㪋 䋭őŃĳĮĵĺ ŊůŧŭŶŦůŤŦġŰŧġŦůťŰŵũŦŭŪŢŭġŤŦŭŭġťŦůŴŪŵźġŰůġŤźŵŰŬŪůŦĮŪůťŶŤŦťġŦůťŰŵũŦŭŪŢŭġŢŤŵŪŷŢŵŪŰů
ɛᚰനġੳ຃ȂఱाġଠঊȂ‫݌‬നġٗࢨ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine൐‫ش֓ނ‬ভ‫ش‬ఱ‫ૺ୶ڠ‬ႃၑ֓‫ڠش‬

会長招待講演 シンポジウム

Western blotting, and cell surface expression of E-selectin, analyzed by FACS, were significantly higher at high celldensity than at low cell density (3.48Ⱦ0.99 fold ; P<0.01, 1.68Ⱦ0.4 fold ; P<0.05, respectively). Western blotting
analysis showed that p65 phosphorylation and nuclear translocation by TNFϷ were similar irrespective of cell density.
The JNK phosphorylation level, but not p38, in TNFϷ-activated HUVEC was lower in the high cell density culture
than in the low cell density culture (P<0.05).
[Conclusion] Our data suggest that cell density dramatically affect endothelial expression of E-selectin via
mechanisms independent from NFЀB or MAPK pathway. Elucidation of cell density-dependent susceptibility to
inflammation may shed a novel light on the mechanisms of endothelial activation and further understanding of vascularinflammation.

特別講演[Objective] To elucidate the factors affecting endothelial susceptibility to inflammation, we studied the effects of celldensity on endothelial cell activation induced by TNFϷ.
[Methods and Results] HUVEC were seeded at low cell density (0.725ȿ104/cm2) or at high cell density (2.9ȿ
104/cm2) and then cultured 36 hours followed by stimulation with TNFϷ. Total E-selectin protein levels, analyzed by

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪈㪏㪌 䋭ĺ࠮ĳĸ඾Ȫ߄ȫġĲĳĻĶıȡĲĴĻĶıġġεΑΗȜٛાεΑΗȜġ‫ܖ‬ய őŃĳȶ൲ྤࣁ‫ا‬ȷőŃĳĮĶı łœŊłġŮŰťŪŧŪŦŴġŵũŦġűŭŢŲŶŦġŷŶŭůŦųŢţŪŭŪŵźġŵũųŰŶŨũġŵũŦġŤŰůŵųŰŭġŰŧġŮŢŤųŰűũŢŨŦġŧŰŢŮġŤŦŭŭġ
ŧŰųŮŢŵŪŰů
ɛઐ๶ġୄ଼Ȃ౻നġࢤඵȂཤఆġဢ໹Ȃ‫ئ‬നġ݅ྶȂఱ࿤ġგ௱Ȃ௖෯ġဇ‫ج‬Ȃฒ५ġ໌ং‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬Atherosclerosis is the primary cause for the cardiovascular disease, and macrophages play essential roles in all phasesof atherosclerosis from development of fatty streak to processes of plaque rupture. Here we show that ARIA, a genethat we recently identified, plays a unique role in the progression of atherosclerosis through a modification ofmacrophage functions. We have reported that ARIA is highly expressed in endothelial cells and regulates theendothelial PI3K/Akt signaling. Currently, we found a significant expression of ARIA in macrophages, and identified
that loss of ARIA enhanced macrophage Akt activity. Recently, it has been reported that macrophage Akt modifies
foam-cell formation by negatively regulating the expression of ACAT-1, an enzyme that esterifies cholesterol andpromotes its storage into the lipid droplets. In consistent with the enhanced Akt activity, ARIA-deletion reduced
ACAT-1 expression in macrophages. When challenged with acetylated-LDL, macrophages isolated from ARIA-KO
mice showed significantly reduced foam-cell formation, whereas expression of scavenger receptors and uptake ofacetylated-LDL were not different from those in WT macrophages. Of note, inhibition of PI3K/Akt signaling abolishedthe reduction of farm-cell formation in macrophages isolated from ARIA-KO mice. To investigate a role of ARIA in
the pathogenesis of atherosclerosis in vivo, we generated mice with targeted deletion of both ARIA and ApoE
(ARIA/ApoE-DKO). When fed a high-cholesterol diet, ARIA/ApoE-DKO mice showed modestly but significantly
reduced atherosclerotic lesion formation relative to ApoE-KO mice. Moreover, we found that oil red-O-positive lipid
area was significantly reduced, while the collagen fiber content was increased in atherosclerotic plaques of
ARIA/ApoE-DKO mice. Also, high-cholesterol diet-induced foam-cell formation was significantly ameliorated inresident peritoneal macrophages isolated from ARIA/ApoE-DKO mice. Together, silencing of ARIA reduced theplaque vulnerability through a control of macrophage foam-cell formation, and thus ARIA offers a unique therapeuticpotential in the treatment of atherosclerotic diseases.

őŃĳĮĶĲ őŦųŪŢŰųŵŪŤġŢťŪűŰŴŦġŵŪŴŴŶŦĮŴűŦŤŪŧŪŤġŢŤŵŪŷŢŵŪŰůġŰŧġŵũŦġųŦůŪůġŢůŨŪŰŵŦůŴŪůġŴźŴŵŦŮġ
ŤŰůŵųŪţŶŵŦŴġŵŰġŢŵũŦųŰŴŤŭŦųŰŴŪŴġťŦŷŦŭŰűŮŦůŵġŪůġŶůŪůŦűũųŦŤŵŰŮŪŻŦťġŢűŰņĮİĮġŮŪŤŦ
ɛ୼૽ġࢼ෗ ĲȂවࢺġఱٚ ĲȂ‫ح‬൥ġఽ ĲȂ୤༃ġ‫ج‬ਏ ĲȂ‫܅‬നġ௛ ĲȂࣞനġฎܵ ĲȂ৹ऴġ‫ܮ‬෗ ĲȂ૩ġణୄ ĳȂฒ५ġ໌ং ĲȂ५നġࢼ෗ Ĳ
Ĳ ‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬ଅ௫ඤ‫ڠش‬

Chronic kidney disease (CKD) is an independent risk factor for the development of cardiovascular disease. The
perivascular adipose tissue is closely implicated in the development of atherosclerosis; however, the contribution to
CKD-associated atherogenesis remains undefined. Eight-week-old apoE-deficient mice were uninephrectomized andfed a high-cholesterol diet starting at 12 weeks of age. The atherosclerotic lesion area in the thoracic aorta wascomparable in 16-week-old uninephrectomized (UNX) mice and sham control mice; however, the lesion area wasmarkedly exaggerated in 20-week-old UNX mice compared with the control (54%, P < 0.05). While the accumulationof monocytes/macrophages and the mRNA expression levels of inflammatory cytokines/chemokines in the thoracic
periaortic adipose tissue (PAT) did not differ between the 2 groups, angiotensinogen (AGT) mRNA expression and theangiotensin II (Ang II) concentration in the PAT were significantly higher in 16-week-old UNX mice than in thecontrol (1.9- and 1.5-fold increases vs. control, respectively; P < 0.05). Ang II concentrations in both the plasma andepididymal white adipose tissue (WAT) were comparable between the 2 groups, suggesting that PAT-specificactivation of the renin angiotensin system (RAS) is primarily involved in CKD-associated atherogenesis. The HOMAIR index and plasma insulin level after glucose loading were significantly elevated in 16-week-old UNX mice. In vitro
stimulation of preadipocytes with insulin exaggerated the AGT mRNA expression along with increased mRNA
expression of PPARϹ. These findings suggest that PAT-specific RAS activation probably primarily contributes inaccelerating atherosclerotic development in UNX mice and could thus represent a therapeutic target for preventing
CKD-associated atherogenesis.
䋭 㪈㪏㪍 䋭őŃĳĮĶĳ ŃŰůŦġŮŢųųŰŸġŢůŨŪŰŵŦůŴŪůġłŕĳġųŦŤŦűŵŰųġťŦŧŪŤŪŦůŤźġŢŨŨųŢŷŢŵŦŴġŢŵũŦųŰŴŤŭŦųŰŴŪŴġţźġ
ŦŭŪŮŪůŢŵŪůŨġŮŢŤųŰűũŢŨŦġŭŪŷŦųġřġųŦŤŦűŵŰųĮŮŦťŪŢŵŦťġŢůŵŪĮŢŵũŦųŰŨŦůŪŤġŢŤŵŪŰůŴĲ ‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ Քຎఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬໦ঊ૤ࠬ‫ۯ‬୆໤Ȇ࿪ၑ‫ڠ‬

Ĳ ൐‫ش֓ނ‬ভ‫ش‬ఱ‫ڠ‬ఱ‫֭֓ڠ‬ভ‫ڠ‬௙ࣣࡄ‫ૺ୶شݪ‬ႃၑ֓‫ڠش‬Ȃĳ ΃σάΑ ĩ ‫ ڼ‬Ī ࡄ‫ݪ‬ਫ਼䋭 㪈㪏㪎 䋭著者索引

Background: Chronic inflammation of adipose tissue plays a crucial role in the pathology of metabolic syndrome aswell as even atherosclerosis. In the present study, we investigated whether a milk protein derived tripeptide, valineproline-proline (VPP), has an anti-inflammatory effect on adipose tissue of high fat diet (HFD) fed mice.
Methods: Male C57BL/6J mice (7 weeks of age) were fed with a normal chow (NC group), a high fat diet (HFD) andplain tap water (control group) or water containing 0.3 mg / mL VPP (VPP-treated group) ad libitum for 10 weeks.
Results: We observed the expression levels of integrins in peripheral monocytes after HFD with or without VPP. VPP
treatment significantly decreased the expression of integrin CD18 on monocyte in the peripheral blood. However,monocyte chemoattractant protein-1 (MCP-1) in the peripheral blood was not decreased in the VPP-treated groupcompared to those in the control group. We observed accumulations of activated monocytes and pro-inflammatory
macrophages by flow cytometry in the stromal vascular fraction of adipose tissues induced with HFD-feeding.
Treatment with VPP reduced macrophage infiltration in the adipose tissues of HFD-fed mice as compared with thecontrol group. The quantitative RT-PCR analysis revealed that the expressions of the MCP-1 and pro-inflammatory
cytokine IL-6 in the adipose tissue was decreased in the VPP treated group compared to the control group.
Conclusion: These observations indicate that oral administration of VPP exerts anti-inflammatory property at least on
adipose tissue in the HFD-fed mice, which may eventually lead to a solution to help the primary prevention of chronic
inflammation-related diseases.

ポスター発表 ＹＩＡ選考発表ɛ௖ࡔġࢼఊ჊ ĲĭĳȂఱाġଠঊ ĲȂ‫݌‬നġٗࢨ Ĳ

口頭発表őŃĳĮĶĴ łġŮŪŭŬġűųŰŵŦŪůġťŦųŪŷŦťġŵųŪűŦűŵŪťŦĭġŗŢŭĮőųŰĮőųŰġĩŗőőĪĭġųŦťŶŤŦŴġũŪŨũġŧŢŵġťŪŦŵĮŪůťŶŤŦťġ
ŢťŪűŰŴŦġŵŪŴŴŶŦġŪůŧŭŢŮŮŢŵŪŰůġŪůġŮŪŤŦ

会長招待講演 シンポジウム[BACKGROUND] The angiotensin II (Ang II) type 2 (AT2) receptor is crucially involved in atherogenesis; however,bone marrow (BM) AT2-mediated anti-atherogenic action remains undefined. [METHOD AND RESULT] We
generated BM chimera apoE-deficient (apoE-/-) mice whose BM cells were repopulated with AT2-deficient (Agtr2-/-)or wild type (Agtr2+/+) cells. Eight weeks after BM transplantation, all mice were fed a western diet for two months.
Atherosclerotic lesion area was significantly increased in apoE-/-/BM-Agtr2-/- mice compared with apoE-/-/BM-Agtr2+/+
mice (51%, P<0.05), accompanied by the enhanced accumulation of MOMA-2 positive cells (P<0.01). Hemodynamic
data and lipid profile did not differ between the two groups. We first examined the expression levels of macrophage
liver X receptors (LXRϷ and ϸ), which have been reported to exert anti-atherogenic actions by reducing proinflammatory response and promoting cholesterol efflux and macrophage emigration. The mRNA expression of LXR
ϸ but not LXRϷ, was significantly decreased in Agtr2-/- thioglycollate-induced peritoneal macrophages (TGPM)
compared with Agtr2+/+ TGPM (P<0.01). Inversely, LXRϸ mRNA expression was markedly increased by cotreatment of angiotensin II (100nM) with AT1 receptor blocker, Olmesartan (P<0.05). Treatment with LXR agonist(GW3965) significantly attenuated LPS-induced mRNA expressions of TNF-Ϸ, IL-1ϸ, and IL-6 in Agtr2+/+ TGPM
(P<0.05), however, anti-inflammatory effect of LXR agonist was markedly reduced in Agtr2-/- TGPM. Furthermore,
the mRNA expression level of ATP-binding cassette transporter ABCA1 and cholesterol efflux were much lower in
Agtr2-/- TGPM than Agtr2+/+ TGPM (P<0.05). The expression level of CCR7, essentially implicated in macrophageemigration, was significantly attenuated in Agtr2-/- TGPM (P<0.05). [CONCLUSION] Our findings demonstrate that
BM-AT2 deficiency aggravates atherosclerosis, at least in part, by eliminating anti-atherogenic properties elicited bymacrophage LXR activation, suggesting that AT2-mediated regulation of macrophage LXR activity could be a novel
therapeutic target for the prevention of atherosclerosis.

特別講演ɛ‫ح‬൥ġఽ ĲȂࣞനġฎܵ ĲȂ୼૽ġࢼ෗ ĲȂ‫܅‬നġ௛ ĲȂවࢺġఱٚ ĲȂ৹ऴġ‫ܮ‬෗ ĲȂ౻നġࢤඵ ĲȂ࿆࿐ġୃਏ ĳȂཱඤġୃ঄ ĳȂฒ५ġ໌ং ĲȂ५നġࢼ෗ Ĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & MedicineőŃĳĮĶĵ ࠬ‫ۯ‬౮଻஌֋̤̫ͥͅίυΑΗΈρϋΟͻϋ ņ ਋ယఘ ņőĵ ͈࿨‫࠿͈ڬ‬൦ɛঌ୼ġణࢩ ĲȂ‫؍‬५ġথঊ ĲȂධాġ‫ ށ‬ĳȂ୞୼ġ݅ࢬ Ĳ
Ĳ ‫؍‬ຩঌၛఱ‫ڠ֓ڠ‬໐੏۪ଷࢄ֓‫ڠ‬Ȃĳ ൐‫ނ‬঴ࠃ֓ఱळ༾୆ၑ‫ڠ‬෸ࠊ͂࿒എȇఱ൲ྤរ͞൲ྤࣁ‫͉́ا‬ίυΑΗΈρϋΟͻϋņ͈ॲ୆̦ᄤૺ̱̞̭̦̀ͥ͂౶̤ͣͦ̀ͤȂِș͉̭͈ͦͣࠬ‫ۯ‬໹‫́޼ڲ‬ίυΑΗΈρϋΟͻϋņ਋ယఘņőĵ͈อ࡛̦ષઌ̱̞̭̀ͥ͂ͬྶ̧̥̱̹ͣ̀ͅȃ౮଻஌֋͉
ࠬ‫͈ۯ‬ႁ‫ڠ‬എඅ଻ͬܰ೰̱Ȃ̷͈ࠁ଼೩‫͉ئ‬৖͈ۛૺ࣐ͅ‫۾‬ဓ̳̭̥ͥ͂ͣȂུࡄ‫͉́ݪ‬ņőĵΏΈ΢σ̦౮଻஌֋ͅ
‫̭̳̥ͬ͂ͥͣͅྶͬޣג̳͖ݞ‬࿒എ̱̹͂ȃ༹༷ȇũŶŮŢůņőĵĩŭŰŹİȽĪġ ζ;Α͂ ŔŎĳĳġ ńųŦζ;Α͈͂࢐෻́ैୋ
̱̹ࠬ‫ۯ‬໹‫޼ڲ‬අ։എͅņőĵ֒ഥঊ઼ًͬอ̵࡛̯̹ζ;ΑȪņőĵŕňȫͬै଼̱̹ȃఱ൲ྤ̥ͣŮœŏłͬಒ੄̱Ȃ೰ၾഎœŕĮőńœ͂ζͼ·υͺτͼ࣐̹ͬ̽ȃ΀ρΑΙ΃அ૗́ఱ൲ྤ౮଻஌֋͈ࠁఠͬ۷ख़̱Ȃ྾‫ע‬ழ૕அ૗́ఱ൲ྤ
̤̫ͥͅņőĵ͈อ࡛ͬ࠿൦̱̹ȃͺϋΆ΂ΞϋΏϋŊŊĩłŕŊŊĪĩĳįĳЂŨİŬŨİŮŪůĪͬˎ਩‫ۼ‬ൎဓ̱̹ζ;Α͈ఱ൲ྤͬഊ੄
̱Ȃఱ൲ྤࠂ͂ఱ൲ྤඤգͬ൳শࠗ௶̳̭ͥ͂́ࠬ‫ۯ‬౮଻ͬ௶೰̱̹ȃࠫ‫ض‬ȇඤ֦଻͈ζ;ΑņőĵŮœŏł͈อ࡛͉ͅ
ओ̦̥̹̦̈́̽Ȃņőĵŕň͈͙́ũŶŮŢůņőĵŮœŏł઼ً͈อ࡛̦‫̧̹́෇ږ‬ȪůľĹȫȃ྾‫ע‬ழ૕அ૗ͤ͢ͅȂņőĵŕň͈ఱ൲ྤ໹‫͈́޼ڲ‬ņőĵ౩ฒ઼ً͈อ࡛̦‫̧̹́෇ږ‬ȃழ૕‫ڠ‬എ͉ͅņőĵŕň͂΋ϋΠυȜσζ;Ά౮଻஌֋ࠁ଼͈
ྶ̥ͣ̈́ओ͉෇̴͛ͣͦȂࠬ‫ۯࠬ͞ࠂۯ‬౮଻͜ͅओ̦෇̥̹͛ͣͦ̈́̽ȃ̱̥̱̦̈́ͣȂłŕŊŊൎဓͤ͢ͅȂņőĵŕň͉́΋ϋΠυȜσζ;ᾼ๤͓̀ࠬ‫ڐ͈ࠂۯ‬ఱ̦෇͛ͣͦȪĲįıķȾıįıĶŮŮġ ŷŴįġ ıįĺĹȾıįıĶŮŮĭġ ůľĴĮĵȫȂࠬ‫ۯ‬౮଻̦ņőĵŕň́೩‫̹̞̱̀ئ‬ȪůľĴĮĵȫȃζͼ·υͺτͼ͈ࠫ‫̥ͣض‬Ȃ౮଻஌֋͈ࢹ଼ါள̜́ͥņŭŢŴŵŪůȂōźŴźŭġ ŰŹŪťŢŴŦȂ
ŇŪţųŪŭŭŪůĮĲȂŇŪţųŪŭŭŪůĮĳ͉ņőĵŕň́΋ϋΠυȜσζ;ᾼ๤͓̀ओ͉̥̹̦̈́̽Ȃ౮଻ͬ໦ٜ̳ͥࣖள̜́ͥŎŎőĮĺĩĲįĸ෼ĭġ ůľĵĭġ űɃıįıĶĪ͉ષઌ̱̞̹̀ȃ̷͈ఈࠬ‫ۯ‬໦‫۾ͅا‬ဓ̳ͥ֒ഥঊȂŉŰŹŢĲĲ͈อ࡛ષઌ̦෇̹͛ͣͦĩĳįĳĲ෼ĭġůľĵĭġ űɃıįıĶĪȃ
ࠫაḙ͈̑ͦͣࠫ‫ۯࠬͤ͢ض‬໹‫͈޼ڲ‬ņőĵΏΈ΢σ͉łŕŊŊంह‫́ئ‬౮଻஌֋͈໦ٜ̦ᄤૺ̳̭ͥ͂́
ࠬ‫ۯ‬౮଻ͬ೩‫̵̦̭̯͂ͥئ‬াऐ̯̹ͦȃőŃĳĮĶĶ ŕųŢůŴűŭŢůŵŢŵŪŰůġŰŧġũŪŨũĮŤũŰŭŦŴŵŦųŰŭġťŪŦŵĮŪůťŶŤŦťġŪůŧŭŢŮŮŢŵŰųźġűŦųŪŢŰųŵŪŤġŢťŪűŰŴŦġŵŪŴŴŶŦġ
ŦŹŢŨŨŦųŢŵŦŴġŢŵũŦųŰŴŤŭŦųŰŴŪŴġťŦŷŦŭŰűŮŦůŵġŪůġųŦŤŪűŪŦůŵġŢűŰņġťŦŧŪŤŪŦůŵġŮŪŤŦ
ɛවࢺġఱٚȂܸ‫ٮ‬ġ֚ٗȂ৹ऴġ‫ܮ‬෗Ȃ‫ح‬൥ġఽȂ‫܅‬നġ௛Ȃ୼૽ġࢼ෗Ȃ५നġࢼ෗‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬ఱ‫شݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬[BACKGROUND] Perivascular adipose tissue has been reported to contribute to vascular function and remodelingthrough various kinds of adipose-derived factors; however, the causal relation between perivascular adipose tissue andatherosclerosis remains undefined.
[METHOD AND RESULT] We first examined the phenotypic changes of periaortic adipose tissue (PAT)surrounding the thoracic aorta in apoE deficient (apoE-/-) mice after 4 weeks of high-cholesterol diet. The expression
levels of adipocyte differentiation-related genes (SREBP1c, PPARϹ, FABP4), inflammatory cytokines (TNFϷ, IL-6,
MCP-1), and macrophage marker (CD68, CD11c) were dramatically increased compared with those in apoE-/- mice
fed a chow diet (P<0.05). These findings were not observed in epididymal white adipose tissue, suggesting that depotspecific inflammatory response was elicited by feeding a high-cholesterol diet. Moreover, this inflammatory response
was completely inhibited by treatment with Olmesartan (1mg/kg/day). To examine whether PAT-specificinflammatory response promotes atherosclerosis development, we developed PAT transplantation model, in whichisolated PAT from 16-weeks-old donor apoE-/- mice fed a 8 weeks of high-cholesterol diet (PAT-HCD) or chow diet
(PAT-CD) was transplanted into 20-weeks-old recipient apoE-/- mice alongside the abdominal aorta. Oil-red-O staining
4 weeks later showed a 2.1 fold-increase in atherosclerotic lesion area of distal abdominal aorta in PAT-HCD micecompared with those in sham control mice (P<0.05), whereas no significant increase was observed in PAT-CD mice,suggesting that PAT-specific inflammatory response primarily contributes to the progression of atherosclerosis in aparacrine manner. In contrast, atherosclerosis development in the recipient mice whose transplanted PAT was isolated
from ARB treated donor mice was completely diminished to the similar level as sham control mice.
[CONCLUSION] Our findings demonstrated for the first time that high-cholesterol diet-induced PAT-specificinflammatory response promotes the development of atherosclerosis, and phenotypic modulation of PAT could be
potential therapeutic strategy for preventing atherosclerotic disease.
䋭 㪈㪏㪏 䋭őŃĳĮĶķ ŎŢŵŦųůŢŭġũŪŨũĮŧŢŵġťŪŦŵġŦŹŢŨŨŦųŢŵŦŴġŢŵũŦųŰŴŤŭŦųŰŴŪŴġťŦŷŦŭŰűŮŦůŵġŪůġŢťŶŭŵġŰŧŧŴűųŪůŨġţźġ
ŢŶŨŮŦůŵŪůŨġŮŢŤųŰűũŢŨŦġűųŰŪůŧŭŢŮŮŢŵŰųźġųŦŴűŰůŴŦġŪůġűŦųŪŢŰųŵŪŤġŢťŪűŰŴŦġŵŪŴŴŶŦ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛ৹ऴġ‫ܮ‬෗ȂවࢺġఱٚȂܸ‫ٮ‬ġ֚ٗȂ‫ح‬൥ġఽȂ୼૽ġࢼ෗Ȃ‫܅‬നġ௛Ȃ໛‫ݳ‬ġࡐٚȂ५നġࢼ෗

口頭発表őŃĳĮĶĸ łġŏŰŷŦŭġœŢţţŪŵġŎŰťŦŭġŰŧġőŭŢŲŶŦġņųŰŴŪŰůġŸŪŵũġŔűŰůŵŢůŦŰŶŴġłŵũŦųŰŵũųŰŮţŰŵŪŤġ
ŐŤŤŭŶŴŪŰůġ

会長招待講演 シンポジウム[BACKGROUND] Maternal obesity has been shown to promote the development of metabolic disorders such as
obesity and insulin resistance in adult offspring; however, its effect on atherogenesis remains undefined.
[METHOD AND RESULT] Male and female apoE-/- mice were mated and fed a high-fat diet (HFD) or chow diet(CD) at eight weeks of age. Female apoE-/- mice received either HFD or CD during gestation and lactation. Offspringof both groups were fed a CD between 5 and 8 weeks of age, and then fed a high-cholesterol diet until 20 weeks of age.
Male offspring obtained from dams fed a HFD (OH mice) showed an increased atherosclerotic lesion development inentire aorta by 205 % (P<0.01) compared with those from dams fed a CD (OC mice). Body weight and blood pressure
before and after high-cholesterol feeding did not differ between OH and OC mice. We first examined the inflammatory
response in epididymal white adipose tissue; however, proinflammatory gene expression levels such as TNFϷ, IL-6,
and MCP-1 did not differ between the 2 groups. Consistent with this finding, serum levels of TNFϷ, IL-6, and MCP-1
were equivalent between the 2 groups. We next examined the inflammatory response in periaortic adipose tissue (PAT)and found that mRNA expression levels of MCP-1 and monocytes/macrophages markers such as CD68 and F4/80
were markedly increased in OH mice compared with OC mice. Immunohistochemical analysis also showed theincreased number of MAC2-positive cells in OH mice compared with OC mice (234.8Ⱦ13.6 cells/mm2 vs. 149.3Ⱦ
13.3 cells/mm2, P<0.05).
[CONCLUSION] Our findings demonstrate that maternal high-fat diet exaggerates atherosclerosis development in
adult offspring by, at least in part, augmenting macrophage inflammatory response in periaortic adipose tissue. PATspecific inflammatory response in adult offspring provides a new insight into the mechanisms of developmental
programming of atherosclerotic diseases.

特別講演‫ނ‬സຸၛ֓‫ش‬ఱ‫ڠ‬੏۪‫ܕ‬ඤ‫ش‬ɛհඃġ‫ܔ‬໲ ĲȂഎાġഓढ ĲȂဇືġրဎ ĲȂಎ࿤ġ‫ ژ‬ĳȂग୼ġࡋඵ ĲȂࢺ൮ġ࠲༟ Ĳĭĳ䋭 㪈㪏㪐 䋭著者索引

Background: Plaque erosion is known to be a major cause of coronary atherothrombosis that leads to acute coronary
syndrome. However, the mechanism of atherothrombosis on plaque erosion remains poorly understood, because of thelack of appropriate animal models. Here we report a first animal model of plaque erosion with spontaneous
atherothrombotic occlusion.
Methods and Results: The occurrence of atherothrombosis was examined in femoral arteries of Japanese white rabbits
fed a high cholesterol diet by high-resolution ultrasonography. Balloon injury of femoral arteries caused neointima
formation, but did not result in atherothrombosis. Importantly, the addition of angiotensin II infusion caused
spontaneous atherothrombotic occlusion of the injured arteries at median 5.5 weeks (6/6 animals). After the occurrenceof acute thrombotic occlusion, the presence of thrombosis was confirmed by angiographic and histopathologic
examination. Histochemical analysis in the atherothrombotic sites revealed; 1) no severe stenosis (% stenosis: 49Ⱦ7),2) no plaque rupture or lipid core, and, 3) no PECAM1-positive endothelial layer. Interestingly, there were smoothmuscle-like cells (ϷSMA+/SM1, SM2, SMemb and calponin-) with tissue factor expression at the neointimathrombus interface (NTI), and some of these cells were positive for RAM-11. Oral treatment with dabigatran (10mg/kg/day) or rivaroxaban (3 mg/kg/day) combined with aspirin (20 mg/kg/day) prevented atherothrombotic occlusionin this model.
Conclusion: We established for the first time an appropriate and valid animal model of spontaneous atherothromobotic
occlusion due to plaque erosion in rabbits, which mimicked the pathological features of plaque erosion seen in humancoronary arteries. This model may provide a clue to a mechanistic understanding of plaque erosion and to thedevelopment of drugs that prevent or delay plaque erosion and subsequent atherothrombosis.

ポスター発表 ＹＩＡ選考発表

Ĳ ߇ਗఱ‫ڠ‬ఱ‫֭ݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ش‬Ȃĳ ߇ਗఱ‫ڠ‬ఱ‫֭ݪࡄڠ֭֓ڠ‬੏۪‫ܕ‬ພ୶౤֓ၷࡄ‫ٳݪ‬อ‫࣒ڠ‬ज䋭 㪈㪏㪐 䋭

プログラムలĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

特別講演
会長招待講演 シンポジウム

ＹＩＡ選考発表

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引䋭 㪇㪇㪇 䋭ŚŊł ஖ࣉอນ
Ȫ‫ܖ‬யࠏȫĺ࠮ĳĹ඾ȪാȫġĲĲĻ ııȡĲĳĻ ııġġలˍٛાŚŊłĮĲœŰŭŦŴġŰŧġŵũŦġŉųŵġŧŢŮŪŭźġŰŧġŏŰŵŤũġťŰŸůŴŵųŦŢŮġŵųŢůŴŤųŪűŵŪŰůġŧŢŤŵŰųŴġŪůġŦůťŰŵũŦŭŪŶŮġ
ťŶųŪůŨġŤŢųťŪŰŷŢŴŤŶŭŢųġŮŰųűũŰŨŦůŦŴŪŴ

Ĳ ජၻࡇၛ֓‫ش‬ఱ‫ڠ‬੏۪‫ܕ‬ΏΑΞθ֓‫ڠش‬Ȃĳ ජၻࡇၛ֓‫ش‬ఱ‫ڠ‬లඵඤ‫ش‬ȂĴ ŅŦűŢųŵŮŦůŵġŰŧġőŢŵũŰŭŰŨźĭġŕũŦġŖůŪŷŦųŴŪŵźġŰŧġŊŭŭŪůŰŪŴ Ȃĵ ŅŦűŢųŵŮŦůŵġŰŧġŎŰŭŦŤŶŭŢųġŃŪŰŭŰŨźĭġŕũŦġŖůŪŷŦųŴŪŵźġŰŧġŕŦŹŢŴĭġŔŰŶŵũŸŦŴŵŦųůġŎŦťŪŤŢŭġńŦůŵŦų

łűŦŭŪůġţŭŰŤŬŴġťŪŦŵĮŪůťŶŤŦťġŰţŦŴŪŵźġţźġűųŰŮŰŵŪůŨġŷŢŴŤŶŭŢųġŪůŵŦŨųŪŵź

口頭発表

ŚŊłĮĳ

会長招待講演 シンポジウム

Formation of the cardiovascular system is a key event during early embryogenesis, and is essential for further
embryonic development and growth. During vascular development, various growth and differentiation factors, such as
Notch, TGFϸ superfamily and VEGF, functionally interact with each other and act on endothelial cells (EC) andsmooth muscle cells (SMC) to form vascular specific structures. Previously, we and others reported that the Hrt familyof transcriptional repressors, also called Hey/Hesr/CHF/Herp, plays critical roles for cardiovascular development
downstream of Notch signaling. Mice null for either Hrt1 or Hrt2 did not show early vascular phenotypes, but their
combined loss resulted in embryonic lethality with impairment of angiogenesis. While Hrt1 and Hrt2 are expressed inendothelial cells (EC) as well as smooth muscle cells of embryonic vasculature, it remained unclear which vascular cell
type requires Hrt1/Hrt2 functions. In the present study, we showed that EC-specific deletion of Hrt2 in global Hrt1
null mice (EC-DKO) resulted in abnormal vascular morphogenesis virtually identical to the global Hrt1/Hrt2 double
KO (DKO) phenotype. In addition to vascular development, EC-DKO embryos showed apparent abnormalities in
cardiac morphogenesis, especially in endothelial-mesenchymal transformation that is essential for the formation of
endocardial cushion tissues, primordia of cardiac valves and septum. These observations indicate that Hrt functions in
EC are indispensable for normal cardiovascular morphogenesis. In the scratch assay using cultured EC, siRNAmediated knockdown of HRT1 and HRT2 markedly suppressed VEGF-induced cell migration. Among VEGFdependent signaling events, phosphorylation of Src family kinases, which are implicated in EC migration during
vascular formation, almost diminished in EC with the HRT1/HRT2 knockdown. Phosphorylation of Src family kinases
also decreased in EC-DKO embryos, suggesting that Hrt1 and Hrt2 have an important role for regulation of VEGFdependent endothelial migration during vascular development and morphogenesis.

特別講演ɛा໐ġୃ‫ ם‬ĲȂ૩‫ؖ‬ġଢ ĳȂ࢛֔ġ༸ঊ ĲȂ֔‫ؖ‬ġ༸ঊ ĲȂକനġࡋ ĲȂส฽‫܃‬ġ๼გ ĲȂऎ൥ġ࡚‫ ܖ‬ĲȂչ൥ġਕဢ ĲȂႅġ਍ြ ĲȂŎŢůŶŦŭġŖŵŴŦŵ ĴȂņųŪŤġŐŭŴŰů ĵȂ࿐ఆġࢬ ĳȂಎ୼ġਘ Ĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicineɛᚧआġ๼‫ ح‬ĲĭĳȂ‫ح‬হ‫ؚ‬ġ࠲ఊႿ ĳȂ࿐࡫‫ؚ‬ġࢼࢫ ĲȂࣞ࿐ġٗढ ĳȂఆઐġঃၦ ĲȂࣞாġ૝ࢨ Ĳ

䋭 㪈㪐㪊 䋭著者索引

The function of blood and lymphatic vessels is closely associated with the expansion of adipose tissue, leading toobesity, which is a risk factor for type 2 diabetes and hypertension. Remarkable report demonstrated that surviving
Prox1 heterozygous mice showed abnormal lymphatic patterning and adult-onset obesity, suggesting that accumulationof adipose tissue could be tightly linked with lymphatic function. However, little is known about how lymphatic andblood vascular integrity influences adipocyte dynamics. Here we showed that apelin inhibited diet-induced obesity bypromoting vessel integrity.
Apelin is an endogenous ligand for G protein-coupled receptor, APJ. Apelin transgenic mice develop enlarged, but notleaky, blood vessels, in ischemia, leading to functional recovery (Kidoya et al., Blood, 2010). Our previous report
showed that apelin attenuates UVB-induced edema formation and inflammation by stabilizing lymphatic structure(Sawane et al., AJP, 2011). Therefore, we investigated whether apelin had a potential to block the accumulation of
adipose tissue by promoting vessel integrity. Surprisingly, genetic deletion of apelin markedly enhanced diet-induced
obesity associated with the abnormal leakage and enlargement of lymphatic vasculature. Co-culture of 3T3-L1
preadipocytes with lymphatic endothelial cells revealed that oleic acid increased in plasma from high-fat-diet enhanced
endothelial hyperpermeability and adipocyte differentiation. Interestingly, apelin inhibited the hyperpermeability ofendothelial cells exposed to oleic acid via normalization of VE-cadherin expression. These data indicates that oleic
acid in high-fat-diet enhances the leakiness of vasculatures via disruption of VE-cadherin, and that dietary fatty acids
from the vessels mediate adipocyte hypertrophy. Finally, overexpression of apelin in skin inhibited abnormal
lymphatic and blood vascular enlargement induced by high-fat-diet, resulting in decreased subcutaneous fat tissue.
These results indicate that apelin inhibits diet-induced obesity by enhancing vessel integrity. Apelin might be a new
therapeutic target in the treatment of obesity and its related diseases (Sawane et al., Diabetes, 2013).

ポスター発表 ＹＩＡ選考発表

Ĳ ఱिఱ‫ڠ‬๷୆໤ພࡄ‫ݪ‬ਫ਼ૂ༭ഥో໦࿤Ȃĳ ‫ڼ‬৆ٛ২঩୆൴ς΍ȜΙΓϋΗȜ૧ႀ֖ࡄ‫ٳݪ‬อΓϋΗȜŚŊłĮĴ

ŃŎőĮĺİłōŌĮĲġŴŪŨůŢŭŴġůŦŨŢŵŪŷŦŭźġųŦŨŶŭŢŵŦġŵũŦġŭźŮűũŢŵŪŤġŷŦŴŴŦŭġŧŰųŮŢŵŪŰůġŪůġ
ťŦŷŦŭŰűŮŦůŵġŢůťġŤŢůŤŦųġţźġťŰŸůųŦŨŶŭŢŵŪůŨġőųŰŹĲ
ɛ‫݌‬ઐġࢫဉ ĲȂōŦŦġŚŶŭŪŢġňįĳȂ୤ೋġဉ֚ ĲȂന࢛ġႎජ ĲȂႝ࿐ġဢ ĲȂńŶůũŢġŔŢųŢġŊįġĴȂႝ࿐ġတ‫ ج‬ĲȂ५ॄġ౺ঊ ĲȂࠋġઆࢤ ĲȂ૩‫ئ‬ġ༗ࢨ ĲȂŐũġŔįġőŢŶŭġĵȂśŪŮŮŦųŴġŕŦųŦŴŢġłįġĶȂōŦŦġŔŦĮŋŪůġķȂ
őŪŦŵųŢŴġŌųŪŴŵŪŢůġĴĭĸȂŌŰũġňŰŶġŚŰŶůŨġĳȂള໐ġഔ჊ ĲĭĹȂ‫׬ݠ‬ġࢼ໹ Ĳ
Ĳ ൐‫ނ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬໦ঊພၑ‫࣒ڠ‬जȂĳ ōŢţŰųŢŵŰųźġŧŰųġŗŢŴŤŶŭŢųġŃŪŰŭŰŨźġŢůťġŔŵŦŮġńŦŭŭĭġŌŰųŦŢġłťŷŢůŤŦťġŊůŴŵŪŵŶŵŦġŰŧġŔŤŪŦůŤŦġŢůťġŕŦŤũůŰŭŰŨźġĩŌłŊŔŕĪĭġŅŢŦūŦŰůĭġ

ŌŰųŦŢȂĴ ŅŦűŢųŵŮŦůŵġŰŧġŎŦťŪŤŢŭġŃŪŰŤũŦŮŪŴŵųźġŢůťġŃŪŰűũźŴŪŤŴĭġŅŪŷŪŴŪŰůġŰŧġŗŢŴŤŶŭŢųġŃŪŰŭŰŨźĭġŌŢųŰŭŪůŴŬŢġŊůŴŵŪŵŶŵŦŵĭġŔŵŰŤŬũŰŭŮĭġ
ŔŸŦťŦůȂĵ ŅŦűŢųŵŮŦůŵġŰŧġőũźŴŪŰŭŰŨźġŢůťġŇŶůŤŵŪŰůŢŭġňŦůŰŮŪŤŴĭġńŰŭŭŦŨŦġŰŧġŎŦťŪŤŪůŦĭġŖůŪŷŦųŴŪŵźġŰŧġŇŭŰųŪťŢĭġňŢŪůŦŴŷŪŭŭŦĭġŇōĭġ
ŖįŔįłįȂĶ ŅŦűŢųŵŮŦůŵġŰŧġńŢůŤŦųġŃŪŰŭŰŨźġŢůťġŔŶųŨŦųźĭġŌŪŮŮŦŭġńŢůŤŦųġńŦůŵŦųĭġŕũŰŮŢŴġŋŦŧŧŦųŴŰůġŖůŪŷŦųŴŪŵźĭġőũŪŭŢťŦŭűũŪŢĭġőłĭġ
ŖįŔįłįȂķ ŅŦűŢųŵŮŦůŵġŰŧġŎŰŭŦŤŶŭŢųġŃŪŰŭŰŨźġŢůťġňŦůŦŵŪŤŴĭġŋŰũůŴġŉŰűŬŪůŴġŖůŪŷŦųŴŪŵźġŔŤũŰŰŭġŰŧġŎŦťŪŤŪůŦĭġŃŢŭŵŪŮŰųŦĭġŎŅĭġ
ŖįŔįłįȂĸ ŅŦűŢųŵŮŦůŵġŰŧġōŢţŰųŢŵŰųźġŎŦťŪŤŪůŦġŎŢŭŮŰĭġōŶůťġŖůŪŷŦųŴŪŵźĭġōŶůťĭġŔŸŦťŦůȂĹ ̧̯̦̫ġŋŔŕ

Lymphatic vessels play critical roles in the maintenance of fluid homeostasis and in pathological conditions including
inflammation and cancer metastasis. While mutations in ALK1, a member of the TGF-ϸ/BMP receptor family, havebeen linked to hereditary hemorrhagic telangiectasia, a human vascular disease, the roles of ALK-1 signals in
lymphatic vessel formation largely remain to be elucidated. We show that ALK-1 signals inhibit lymphatic vessel
formation. Lymphatic vessels were enlarged in multiple organs in Alk1-depleted mice. These inhibitory effects of
ALK-1 signaling were mediated by BMP-9, a specific ligand for ALK-1, which decreased the number of cultured
lymphatic endothelial cells (LECs). Bmp9-deficient mouse embryos consistently exhibited enlarged dermal lymphatic
vessels by increasing the number of Prox1-positive LECs. BMP-9 also inhibited lymphatic vessel formation during
chronic inflammation in immuno-competent mice and in multiple types of Bmp9-transduced tumors grafted toimmuno-compromised mice. BMP-9 downregulated the expression of the transcription factor Prox1, which isnecessary to maintain LEC identity. Furthermore, silencing Prox1 expression inhibited LEC proliferation by
downregulating multiple cyclin family members. Our findings reveal a novel molecular basis for the physiological andpathological roles of BMP-9/ALK-1 signals in lymphatic vessel formation.

ŚŊłĮĵńťŤĵĳ ͉ ŧŮůŭĴ ̱ͬٚ̀ඤ๧ळ༾͈ঝે‫଼ͬࠁ௷ب‬ည൵̱ࠬ‫ۯ‬૧୆ͬ௯ૺ̳ͥ
ɛ৹५ġ࿺‫ ܮ‬ĲȂ໛ࡔġ࿆༸ ĲȂհ൥ġࢫঃ ĲĭĳȂઐനġൽ࣐ ĴȂབ࠮ġೄਏ Ĳ
Ĳ ࣭ၛ੏۪‫ܕ‬ພࡄ‫ݪ‬ΓϋΗȜࡄ‫ݪ‬ਫ਼ळ༾୆໤‫ڠ‬໐Ȃĳ ൐ཤఱ‫֭ڠ‬࿪‫شݪࡄڠ‬ळ༾ૂ༭࿪‫ڠ‬໦࿤ȂĴ ‫ނ‬സఱ‫ڠ‬ఱ‫֭ڠ‬୆ྵ‫شݪࡄڠش‬୆ఘଷࢄ‫ڠ‬ࠬ‫ۯ‬૧୆͉Ȃ‫ܡ‬ం͈ࠬ‫̥ͣۯ‬ඤ๧ळ༾̦੄ٔȆ໦খ̱Ȃ૧̹̈́ࠬ‫ۯ‬࿌ͬࢹಃ̳ͥίυΓΆ̜ͥȃࠬ‫ۯ‬૧୆ً೾͈ඤ
๧ळ༾͉Ȃ‫ڰ‬อͅळ༾ࠁఠȂ‫׋‬൲ෝͬ་‫̵̯ا‬Ȃ૧̹̈́ࠬ‫ۯ‬࿌ͬࢹಃ̳̦ͥȂ̷͈ଷࢄι΃ΣΒθ͉ྶ̥̯̞ͣͦ̀ͅ
̞̈́ȃळ༾͈ࠁఠȆ‫׋‬൲ෝ͉ȂœũŰłȂœŢŤĲĭġ ńťŤĵĳͬయນ̱̹͂œũŰέ͹ηςȜň౩ฒৗͥ͢ͅͺ·Ιϋळ༾ࣸ‫͈ڒ‬ठ༎଼̽̀͢ͅଷࢄ̯̞ͦ̀ͥȃུࡄ‫͈ݪ‬࿒എ͉Ȃࠬ‫ۯ‬૧୆ً೾͈ඤ๧ळ༾͈ࠁఠȆ‫׋‬൲ෝଷࢄͅ‫ͥͩ۾‬ΏΈ΢σഥోࠏٜͬྶ̳̹ͥ͛Ȃࠖ࢕୆ఘͼιȜΐϋΈܿ੅ͬߐঀ̱̀œũŰέ͹ηςȜň౩ฒৗͥ͢ͅͺ·Ιϋळ༾ࣸ‫͈ڒ‬ठ༎଼̦ࠬ‫ۯ‬૧୆̞̥ͬͅଷࢄ̱̞͈̥̀ͥྶ̥̳̭̜ͣͥ͂́ͥͅȃ᥷̦൫ྶ́୆̧̹ࠬ͘͘‫ͬۯ‬۷ख़̧́ͥΔήρέͻΛΏνͬκΟσ൲໤̱͂̀ဥ̞ȂĲĪͺ·Ιϋळ༾ࣸ‫خͬڒ‬ণ‫̳ا‬ͥࠖ࢕ίυȜή̤͍͢ĳĪńťŤĵĳ‫خͬ଻ڰ‬ণ‫̳ͥا‬Ňœņŕĩࠖ࢕‫΀ྺވ‬ΥσΆȜഢ֊ĪΨͼ΂Γϋ΍Ȝͬඤ๧ळ༾́อ࡛
̳ͥΠρϋΑΐͿΣΛ·ΔήρέͻΛΏνͬਏၛ̱Ȃ୯‫͍̤͢ۯࠬۼ‬๶௰୓ྤ͈ࠬ‫ۯ‬૧୆ً೾ͬ۷ख़̱̹ȃ‫ܡ‬ం͈ࠬ‫̹̱ٔ੄̥ͣۯ‬ඤ๧ळ༾͈୶൵౤͉́Ȃͺ·Ιϋ஍֋́ྖ̹̯̹ͦঝે‫଼̯ͦࠁ̦௷ب‬Ȃ̷͈ঝે‫́௷ب‬ńťŤĵĳ̦‫ڰ‬଻‫̦̭̞̱͂ͥ̀ا‬া̯̹ͦȃńťŤĵĳඅ։എஷ‫ٺ‬౩ฒৗ̜́ͥłńŌĵĳͬඤ๧ळ༾́අ։എͅอ̵࡛̯ͥ͂ඤ๧ळ༾
͈ঝે‫̦௷ب‬ક৐̱Ȃࠬ‫ۯ‬૧୆̦ஷ‫̥̭̹̯ͣ͂ͦٺ‬ńťŤĵĳ̦อ̳ٔͥඤ๧ळ༾͈୶൵౤́ঝે‫଼ͬࠁ௷ب‬ည൵̱Ȃࠬ‫ۯ‬૧୆ͬ௯̱̞̭̦̀ͥ͂ྶ̥̹ͣ̈́̽ͅȃ̹͘Ȃࠬ‫ۯ‬૧୆ً೾͈ඤ๧ळ༾̤̞̀ͅȂΈͺΣϋΤ·τ΂ΙΡ࢐֦۟ঊłųũŨŦŧĺţ̦ńťŤĵĳ͈‫ͅا଻ڰ‬ਹါ̜́ͥ‫خ‬ෝ଻ͬাऐ̱̹ȃ̯ͣͅȂńťŤĵĳ͈‫ئ‬ၠ́ঝે‫଼ͬࠁ௷ب‬ଷࢄ̳ͥͺ·Ιϋଷࢄ֦ঊ̱͂̀Ȃέ΁σηϋέ͹ηςȜͅ௺̳ͥŇŰųŮŪůĮŭŪŬŦĴĩŇŮůŭĴĪͬ൳೰̱̹ȃȁոષ͈ࠫ‫̥ͣض‬ȂłųũŨŦŧĺţ̽̀͢ͅ‫̹̯ͦا଻ڰ‬ńťŤĵĳ̦ȂŇŮůŭĴ̱ͬٚ̀ඤ๧ळ༾͈ঝે‫଼ͬࠁ௷ب‬ည൵̱Ȃࠬ‫ۯ‬૧୆ͬ௯ૺ̳̭̦ͥ͂াऐ̯̹ͦȃ䋭 㪈㪐㪋 䋭ŚŊł ஖ࣉอນȪႉ઄ࠏȫĺ࠮ĳĹ඾ȪാȫġĲĲĻ ııȡĲĲĻ ĵĶġġలˎٛાŚŊłĮĶőųŰŵŦŤŵŪŷŦġųŰŭŦġŰŧġŵũŦġŧŢŵĮťŦųŪŷŦťġŴŦŤųŦŵŦťġŧŢŤŵŰųġŰŮŦůŵŪůġŪůġűŢŵũŰŭŰŨŪŤŢŭġŷŢŴŤŶŭŢųġ
ųŦŮŰťŦŭŪůŨ

Ĳ ྴࡣ‫ؚ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬੏۪‫ܕ‬ඤ‫ڠش‬Ȃĳ ྴࡣ‫ؚ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬໦ঊ੏۪‫ܕ‬ພ‫ڠ‬ΩȜ΅ϋΕϋພ‫۾‬Ⴒ໦ঊϷΏΤ·τͼϋ͈૧ܰ‫ܥ‬ෝȽ‫ح‬Ⴂ଻৖̱͈ۛ͂̀ιΗδςΛ·છ࢓߲‫̷͈͍ݞ‬૤ࠬ‫ࣣۯ‬໵છ͈ພఠ͈́࿨‫ڬ‬Ƚɛవࡉġဢ֚ ĲȂಎ૰ġ߼ඃ ĳȂ૰੄ġࠗ ĴȂ५ུġࢼ֚ ĲȂ૩‫ئ‬ġၧ֚ ĴȂ߄നġհঃ ĵȂᖱ࿐ġࢤ৘ Ĳ

口頭発表

ŚŊłĮķ

会長招待講演 シンポジウム

Background: Obesity is associated with the development of vascular disorders including atherosclerosis and vascularrestenosis after angioplasty. Omentin is an adipose-derived cytokine, which is downregulated by obese conditions.
Recently, we have reported that plasma omentin levels are decreased in patients with coronary artery disease. Here, weinvestigate whether omentin can modulate neointimal hyperplasia and vascular smooth muscle cell (VSMC) behavior
in vivo and in vitro.
Methods and Results: An adenoviral vector expressing human omentin (Ad-OMT) or ϸ-galactosidase as a control was
injected into wild-type (WT) mice at 3 days before mechanical vascular injury. Ad-OMT-treated WT mice had theincreased levels of plasma human omentin (1353.9Ⱦ169.6 ng/ml) on the 5th day after injection, whereas humanomentin was undetectable in plasma of control-treated WT mice. Systemic delivery of Ad-OMT significantly
attenuated neointimal thickening at 21 days after vascular injury, compared with control (p<0.01, n=8). Ad-OMT also
decreased the number of bromodeoxyuridine (BrdU) positive proliferating cells in the neointima at day 10 after
vascular injury (p<0.01, n=5). In cultured VSMCs, treatment with recombinant omentin protein attenuated VSMC
proliferation and chemotactic activity induced by various growth factors. Omentin suppressed growth factor-induced
phosphorylation of ERK in VSMCs. Treatment of VSMCs with omentin stimulated AMPK phosphorylation in a timedependent manner. Furthermore, blockade of AMPK prevented the inhibitory effect of omentin on growth factorstimulated VSMC proliferation and ERK phosphorylation. Finally, we generated fat-specific transgenic miceexpressing the human omentin gene under the control of the aP2 promoter, and these mice exhibited a marked
reduction in neointimal formation after vascular injury compared to littermate control mice.
Conclusion: Omentin functions as a fat-derived secreted factor that protects against the progression of pathologicalvascular remodeling through its ability to activate AMPK within VSMCs.

特別講演ɛ૒ఆġဈٚ ĲȂড়നġႚ ĲȂఱ‫ޘ‬ġࢼඵ ĳȂ‫ུש‬ġࠉ ĲȂ༌‫ؖ‬ġ݅෗ ĲȂ‫ݠ‬໐ġՔ ĲȂ૰ࡔġܲࢩ ĲȂઐ๶ġ֚ࢤ ĲȂൖஃġఱဈ ĲȂ்୼ġ౺ঊ ĲȂչ൥ġଠ༠ ĲȂ৒ࡔġཅྶ ĲȂఱඤġ઺ခ ĳ

プログラム

లĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

Ĳ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬ჇාȆଅ௫ඤ‫ڠش‬Ȃĳ ఱिఱ‫ڠ‬ఱ‫ࢫ࠲֭ڠ‬อో֓‫ڠ‬ȂĶ ఱिఱ‫ڠ‬ఱ‫֒شݪࡄࠏڠ֭֓ڠ‬ഥঊহၷ‫ڠ‬Ŝ෸ࠊ‫͍ݞ‬࿒എŞِș͉ΩȜ΅ϋΕϋພ͈ࡔ֦֒ഥঊ͈̜֚̾́ͥ͜౎ξΫ΅Ιϋ‫ࣖا‬ளŖńŉōĲ̦ࠬ‫ͅۯ‬ඤह̳̭ͥ
͂ͬࡉ੄̱Ȃࠬ‫ۯ‬ςκΟςϋΈ͈ଷࢄ໦ঊ̜̭́ͥ͂ͬ͜༭̱̹࣬ȃࢵͅȂ̷͈ດഎ౩ฒ͈̜֚̾́ͥϷΏΤ·τͼϋĩŔŏńłĪࠬ͜‫ۯ‬ඤ๧ͅอ࡛Ȃ໦๥̯̞̭ͦ̀ͥ͂ͬอࡉ̱Ȃࠬಎ͜ͅŔŏńł̦‫֦଻ס‬ঊ̱͂̀ంह̳̭̦ͥ͂‫੄෇ږ‬ြ̹ȃ̷̭́Ȃ๊֚ਬ౬Ĳĳıı૽͈ႉ઄࠿ఘͬဥ̞̹‫؍‬౯ࡄ‫̭̹࣐ͧ͂̽ͬݪ‬ȂࠬಎŔŏńł͉ιΗδςΛ·છ࢓߲ĩŎŦŵŔĪͅచ̱༗ࢌഎͅैဥ̳̦ͥȂ‫ح‬Ⴂ͂͂͜ͅ೩‫̠̞̳͂ͥئ‬૧͈࡛ܰયͬอࡉ̱Ȃඅ̷͈ͅ೩‫͉ࠬئ‬գ͈ષઌ͞
ͼϋΑςϋ೷ࢯ଻͈՛‫̩ޑͅا‬௖‫ͬ۾‬া̳̭͂ͬࡉ੄̱̹ȃ̹͘Ȃζ;Ά͜‫ح‬Ⴂฺ͂ࠬͅಎŔŏńł͉೩‫̱ئ‬ȂŔŏńł
ΦΛ·ͺ;Πζ;ΑĩŌŐĪ͉ŎŦŵŔ͈ນ࡛߿ͬ೮̱̹ȃոષͤ͢Ȃུࡄ‫͉́ݪ‬Ⴧ‫۾ا‬Ⴒ໦ঊ̱͈͂̀Ŕŏńł̞̾̀ͅȂൠయ৫‫ۯ͍ࠬݞ‬ඤ๧‫ܥ‬ෝ̷͈͞ࢭુ଻͈෫౦ͤ͢ͅৼ̯ܳͦͥൠෂພࣞࠬ͞գȂ൲ྤࣁ‫۾͈͂ا‬Ⴒͅઙതͬ൚̀Ȃ̷͈ͦͣພఠ̤̫ͥͅ໦ঊ‫ܥ‬ෝٜͬྶ̳̭ͥ͂ͬ࿒എ̳͂ͥȃŜ༹༷͂ࠫ‫ض‬Şġ ൠయ৫Ļġ ς΋ϋΫ΢ϋΠŔŏńłഞ‫ͤ͢ͅح‬ডཛळ༾ࣸ͞‫޼ڒ‬ळ༾̤̞̀ͅͼϋΑςϋτΓίΗȜ͉͂ඊၛ̱̀ňŢţĲĮőŊĴŌĮłŬŵࠐႹ̱̹ͬٚňōŖŕĮĵͥ͢ͅΈσin vivó͜Ȃζ;ᾼς΋ϋΫ΢ϋΠŔŏńłͬൎဓ̳̭ͥ͂ͤ͢ͅȂൠయ৫‫ܥ‬ෝ͈٨஝ͬ෇̹͛ȃࠬ‫ۯ‬ඤ๧‫ܥ‬ෝĻġ ࠬ‫ۯ‬ඤ๧͉́ς΋ϋΫ΢ϋΠŔŏńłഞ‫ͤ͢ͅح‬ňŢţĲĮőŊĴŌĮłŬŵࠐႹ̳ͬٚͥŦŏŐŔ͈‫ैا଻ڰ‬ဥ̦୆̲ȂŏŐॲ୆͈௩‫ح‬‫ވ͍ݞ‬෽ူ̱̹ࠬ‫ۯ‬໹‫͈́޼ڲ‬ŤňŎőॲ୆̦௩‫̹̱ح‬ȃŔŏńłġ ŌŐ̥͈ͣഊ੄ఱ൲ྤ͉́ͺΓΙσ΋ςϋͥ͢ͅ౸۱
฽؊͈ࡘ৻ͬ෇͛Ȃࠬ‫ۯ‬ඤ๧͈́ŏŐॲ୆೩‫ฺ̠͂ͅئ‬ଔख़̯ͦͥࠬ‫ۯ‬ඤ๧‫ܥ‬ෝ೩‫̹͛෇ͬئ‬ȃŔŏńł͂łűŰņ͈ΘήσΦΛ·ͺ;Πζ;Αͬैୋ̱Ȃ൲ྤࣁ‫࠿̞̀̾ͅا‬൦̱̹̭͂ͧȂ΋ϋΠυȜσͅ๤̷̱͈՛‫̹͛෇ͬا‬ȃŜࠫაŞŔŏńł
͉Ⴧ‫۾ͅا‬Ⴒ̱Ȃ‫ح‬Ⴂ଻৖̱͈ۛ͂̀ŎŦŵŔȂඅࣞࠬͅգ͞ൠయ৫։ુ͂‫۾‬Ⴒ̱̞̀ͥ‫خ‬ෝ଻̦াऐ̯ͦȂड͜ਹါ̈́
ထࢃܰ೰֦ঊ̜́ͥ૤ࠬ‫ࣣۯ‬໵છͅ‫۾‬Ⴒ̱̞̀ͥ‫خ‬ෝ଻̦ࣉ̢̹ͣͦȃ䋭 㪈㪐㪌 䋭著者索引΋Ȝᾼ͈ࣺ͙৾ͤ‫۾‬ဓ̱̹ȃࢵ̷͈ͅષၠ͈τΓίΗȜ̱͂̀ň౩ฒ‫ވ‬࿨਋ယఘ͈̜֚̾́ͥōőłœĳͬ൳೰̱̹ȃ

ポスター発表 ＹＩＡ選考発表Ĵ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬௙ࣣΰσΑίυκȜΏοϋ‫ڠش‬Ȃĵ ఱिఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬ႉ઄֒ഥঊহၷ‫ڠ‬ȂŚŊłĮĸ

ńŢŭűŢŪůĮķ ͥ͢ͅ൲ྤࣁ‫ا‬ພ་̤͍͢ζ·υέ͹Ȝΐ űŪůŰŤźŵŰŴŪŴ ͈ଷࢄɛ‫ॄݠ‬ġఽ჊ ĲȂ៴෨ġ֚ຳ ĳȂ૱ġੳ঎ ĴȂဿġ઀༰ ĲȂ߄५ġਁၖ ĲȂ฽಴ġဢ෗ ĴȂߪࡔġဉ‫ ܖ‬ĵȂ‫ॄݠ‬ġડ Ĳ
Ĳ ઎გఱ‫ڠ֓ڠ‬໐୆‫࣒ڠا‬जȂĳ ࠄ؊݅ੂఱ‫ڠ֓ڠ‬໐ٜཎ‫ޗڠ‬৒ȂĴ ൐‫ނ‬സ֓‫ڠ‬௙ࣣࡄ‫ݪ‬ਫ਼΃σΩͼϋίυΐͿ·ΠȂĵ ൐‫ނ‬ఱ‫ڠ‬ఱ‫شݪࡄࠏڠ֭֓ڠ‬໦ঊळ༾୆໤‫ࢲ୺ڠ‬య৫୆ၑ‫ڠا‬໦࿤ňŰŭťŴŵŦŪůɕŃųŰŸů͈ͣ་଻ōŅō‫ب‬୰̦൲ྤࣁ‫͈ا‬ພఠ୆ၑ‫ͬڠ‬୘‫̞̱ݛ̱̀ے‬ȃ̱̥̱Ȃ෽ူζ·υέ͹Ȝΐ̤̫ͥͅ་଻ōŅō͈ࣺ͙͉৾ͤ๤‫ڛ‬എ೩ෛഽ́཈გ̳̹ͥ͛Ȃ൳‫ب‬୰͈͙͉́৘षࠬͅ‫ۯ‬༃̭́ܳͥζ·υέ͹Ȝΐ༺ྏ‫ͬا‬਱໦୰ྶ̧̞́̈́ȃ߃ා೹੹̯̞ͦ̀ͥ֩ैဥȪűŪůŰŤźŵŰŴŪŴȫκΟσ͉Ȃζ·υέ͹Ȝΐ̤̫ͥͅōŅō͈ࣺ͙̦৾ͤ཈გ̱̞̭̥̈́͂̈́̓ͣȂ་଻ōŅō‫ب‬୰ͬ༞̧̱ۖ́ͥ͂̀ಕ࿒ͬਬ̞̦͛̀ͥȂ̷͈ଷࢄ‫͈ࢹܥ‬৘ఠ͉ྶ̥̞̞ͣ̈́̽̀̈́ͅȃུࡄ‫͉́ݪ‬Ȃळ༾ඤńŢ ĳĬ ۜ਋଻ίυΞͺȜΔȨ΃σΩͼϋȪńłőŏȫȩέ͹ηςȜͅ௺̳ͥńłőŏķ̦๷઀‫ۯ‬ଷࢄ̱ͬٚ̀ζ·υέ͹Ȝΐ͈űŪůŰŤźŵŰŴŪŴ͍̈́ͣͅ൲ྤࣁ‫ا‬ພ་͈ࠁ଼ͅ‫ܙ‬ဓ̳̭ͥ͂ͬ੝͛̀
ྶ̥̱̹͈ͣ͂́Ȃ̭̭ͅ༭̱̹̞࣬ȃCapn6͂ōŅō਋ယఘȪldlrȫ͈ඵਹࠧఅζ;ΑȪCapn6 -/y/ldlr -/-ȫͅĲĳ਩‫ࣞۼ‬ডཛ૙ͬ໅‫̭̹̱ͧ͂ك‬ȂCapn6࿤୆߿ȪCapn6 +/y/ldlr -/-ȫζ;Α͂๤‫̱̀ڛ‬ఱ൲ྤ͈൲ྤࣁ‫ا‬ພ་ࠁ଼̦ࡐಠͅဲଷ̯ͦ
̹ȃńłőŏķ͉൲ྤࣁ‫ا‬ພ་͈༺ྏ‫ا‬ζ·υέ͹Ȝΐͅޫह̱ȂCapn6͈ࠧఅ͉ພ་͈͒ζ·υέ͹Ȝΐ൲֥͈ࡘઁȂ൳ळ༾͈๷઀‫ࢹۯ‬௮͈։ુ̤͍͢΋τΑΞυȜσ‫܄‬ၾ͈೩‫̧̹̱̭ܳ֨ͬئ‬ȃ̹͘Ȃńłőŏķ͉ࣸଡဇြζ·υέ͹Ȝΐ͈໦‫ً͈ا‬೾́ŕŏŇĮϷঁࠣͤ͢ͅอ࡛ည൵̯ͦȂ൳ळ༾͈๷઀‫ࢹۯ‬௮ࢹಃ͍̈́ͣͅ๷઀‫ۯ‬ջంഎ̈́ůŢŵŪŷŦġōŅō͈ࣺ͙৾ͤȪűŪůŰŤźŵŰŴŪŴȫͅ૬̩‫۾‬ဓ̳̦ͥȂॸ‫ا‬ōŅō͈ࣺ͙৾ͤ͞ŎĲζ·υέ͹Ȝΐ‫۾‬Ⴒ໦ঊ͈อ࡛་൲͉ͅ‫̱ޣג‬̞̭̭̭̦̈́͂͂͂ྶ̥̹ͣ͂̈́̽ȃ༷֚Ȃŋĸĵĵġ įĲζ·υέ͹Ȝΐ͈͒ Capn6 ͈൵ව͉ŎńőĮĲͥ͢ͅΉκΗ΅ΏΑ͈೩‫ͬئ‬ြ̱̹ȃ̱̹̦̽̀Ȃńłőŏķ͉൲ྤࣁ‫ا‬ພ་ඤ͈ζ·υέ͹Ȝΐ́‫׶‬છ଻ঁࠣͤ͢ͅอ࡛ည൵̯ͦȂ൳ळ༾͈๷઀‫ࢹۯ‬௮ࢹಃ͍̈́ͣͅűŪůŰŤźŵŰŴŪŴ‫ڕ଻ڰ‬ංͅ‫ܙ‬ဓ̳༷֚ͥ́Ȃ൲ྤࣁ‫ا‬ພ་̥͈ͣ΀ηΈτȜΏοϋͬ೩‫̯ئ‬̵̭ͥ͂́ພ་͈͒ζ·υέ͹Ȝΐ͈ಇୟͬ௯ૺ̵̯ͥ͂ࣉ̢ͣͦͥȃ䋭 㪈㪐㪍 䋭プログラムలĳĲٝ඾ུࠬ‫ۯ‬୆໤֓‫ڠ‬ٛ‫੅ڠ‬ਬٛ
Beyond the Cutting Edge of the Vascular Biology & Medicine

特別講演
会長招待講演 シンポジウム

著者索引

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引

第21回日本血管生物医学会学術集会
Beyond the Cutting Edge of the Vascular Biology & Medicine（抄録掲載ページ）英
ADAMS, Ralf H.
ALAM, Mohammad T.

い飯田 修 (Iida Osamu)
飯田 卓馬 (Iida Takuma)
井岡 朋子 (Ioka Tomoko)
井垣 達吏 (Igaki Tatsushi)
五十嵐 恭子 (Igarashi Kyoko)
五十嵐 淳介 (Igarashi Junsuke)
生田 新一郎 (Ikuta Shinichro)井口 朋和 (Iguchi Tomokazu)
井口 朋子 (Iguchi Tomoko)
幾野 毅 (Ikuno Takeshi)
池岡 邦泰 (Ikeoka Kuniyasu)
池田 宏二 (Ikeda Koji)
池田 聡司 (Ikeda Satoshi)
池田 真也 (Ikeda Shinya)
池田 大樹 (Ikeda Daiki)
池田 智之 (Ikeda Tomoyuki)
池田 佳生 (Ikeda Yoshio)
池田 義 (Ikeda Tadashi)
砂河 孝行 (Isagawa Takayuki)
石井 邦雄 (Ishii Kunio)
石井 規夫 (Ishii Norio)
石井 秀樹 (Ishii Hideki)
石井 陽子 (Ishii Yoko)
石川 桂二郎 (Ishikawa Keijiro)
石川 義弘 (Ishikawa Yoshihiro)
石崎 泰樹 (Ishizaki Yasuki)
石橋 耕平 (Ishibashi Kouhei)
石橋 達朗 (Ishibashi Tatsuro)
石原 隆行 (Ishihara Takayuki)− 199 −

OC2-14 (123)OC2-14 (123)
YIA-1 (193)
基礎S-4-2* (68)
OB1-8 (132), PB1-10* (157)
PB2-40* (180)OC2-17 (125)
PC2-16* (171)YIA-1 (193)
OB3-24* (140)
OC2-18 (125), OB2-16 (136),
PB2-31* (175), PB2-45 (183)
臨床S-7-5* (113), PC1-6* (150),
PB2-50 (186), PB2-52 (187)OC1-8 (120)
PB2-33 (176)
PB2-39 (180)OC2-17 (125)
PB1-14 (159)
OB3-24 (140)
PB1-19 (162)
PB1-8 (156)
PC1-4 (148)
PC2-19 (173)
PB1-22 (164)
OC1-11 (122)
PB2-54 (188)
PB1-24* (165)
PC1-7 (150), PC1-8* (151)
OC1-11 (122)OC2-14 (123)

著者索引

朝倉 正紀 (Asakura Masanori)
浅沼 博司 (Asanuma Hiroshi)
浅野目 晃 (Asanome Akira)浅原 孝之 (Asahara Takayuki)
芦名 功平 (Ashina Kohei)
芦野 洋美 (Ashino Hiromi)
東 英梨月 (Azuma Erika)

安藤 康史 (Ando Koji)
安徳 喜文 (Antoku Yoshibumi)

ポスター発表 ＹＩＡ選考発表

浅海 泰栄 (Asaumi Yasuhide)

有馬 勇一郎 (Arima Yuichiro)
有吉 真 (Ariyoshi Makoto)
粟田 政樹 (Awata Masaki)
安斉 俊久 (Anzai Toshihisa)

口頭発表赤澤 宏 (Akazawa Hiroshi)
赤津 裕一 (Akatsu Yuichi)
安藝 翔 (Aki Sho)
秋田 英万 (Akita Hidetaka)
秋山 廣輔 (Akiyama Kousuke)OC1-2* (117)
OC2-15 (124)PC1-7 (150), PC1-8 (151)
PB2-53* (187)
PB2-37 (179)
PB1-27* (167)
PB2-51 (186)
臨床S-1-3 (78), PC1-8 (151),
PC2-14 (170)
臨床S-5-4* (102)OB1-9* (133), YIA-3 (194)OB3-19* (138)
PB1-26 (166), PB1-29 (168)OB1-10 (133), OB1-11 (134),
PB1-4 (154), PB1-5 (155),
PB2-46 (183)
OC1-3 (118), OC1-4 (118),
OC1-6 (119), PC1-10 (152)
OC2-22 (127), PC1-11 (152)
PC1-11 (152)
PB2-37 (179)
臨床S-7-2* (110)OB3-21* (139)
PB1-7* (156)
PB1-22 (164)

阿部 七郎 (Abe Shichiro)
安部 元 (Abe Hajime)
安部 まゆみ (Abe Mayumi)
荒川 鉄雄 (Arakawa Tetsuo)
荒木 栄一 (Araki Eiichi)
有田 茂子 (Arita Shigeko)
有田 陽 (Arita Yoh)

OC1-12 (122)PC1-10 (152)
PB1-13 (159), PB1-14 (159),
PC2-20 (173)
臨床S-1-5* (80)
PB1-19 (162)
OB2-17* (137)
OC1-3 (118), OC1-4 (118)
PC1-4 (148)
臨床S-3-5 (91)
基礎S-1-5 (55), OC2-18 (125),
OB2-16* (136), PB2-31 (175),
PB2-45 (183)
PB2-36* (178)
PB2-41 (181)OC2-14* (123)
臨床S-3-2* (88), OC1-6 (119),PC1-5 (149), PC1-10 (152),
PC1-11 (152)
OB1-5* (131), YIA-4 (194)
PB2-57* (189)

会長招待講演 シンポジウムあ相川 幸生 (Aikawa Yukio)
相澤 義房 (Aizawa Yoshifusa)
相庭 武司 (Aiba Takeshi)
相原 浩太郎 (Aihara Kotaro)
青沼 達也 (Aonuma Tatsuya)
青山 盛彦 (Aoyama Morihiko)
赤壁 佳樹 (Akakabe Yoshiki)
赤阪 隆史 (Akasaka Takashi)

東 純哉 (Azuma Jyunya)
足立 太一 (Adachi Taichi)
阿部 康二 (Abe Koji)

特別講演

CUNHA, Sara I.
ERIC, Olson
FRUTTIGER, Marcus
GHAZIZADEH, Mohammad
GRAHAM, Robert M.
GRIFFIN, Martin
GUILLERMO, Oliver
HAFEZI-MOGHADAM, Ali
HOSSEN, Md. NazirIISMAA, Siiri E
JIA, Weizhen
KOH, Gou YoungKURTZ, Theodore W.
LEE, Eun-Seo
LEE, Se-Jin
LEE, Yulia G.
LIAO, James
LIU, Xinyi
MANUEL, Utset
MCDONALD, Donald
OH, S. PaulPIETRAS, Kristian
PUENTES, Sandra
YAN, YiZANDI, Souska
ZHANG, LiZIMMERS, Teresa A.

SL-2* (44)OB1-11 (134), PB1-5 (155),
OB1-10 (133)
YIA-3 (194)
YIA-1 (193)
OB1-7 (132)
PB1-6 (155)
PB2-35 (177)
PB2-35 (177)
OB1-7 (132)
OC1-11 (122)
PB1-26 (166)
PB2-35 (177)
PB2-30 (175)
YIA-3 (194)SL-1* (43)
PB2-35* (177)
YIA-3 (194)
YIA-3 (194)OB3-23 (140)
PB2-39 (180)
YIA-1 (193)
OB1-12 (134)
YIA-3 (194)
YIA-3 (194)
PB1-24 (165)
OB1-4* (130)
OC1-11 (122)
PB2-30 (175)
YIA-3 (194)プログラム* 筆頭著者

* 筆頭著者（抄録掲載ページ）

石原 正治 (Ishihara Masaharu)

石丸 侑希 (Ishimaru Yuki)
和泉 孝志 (Izumi Takashi)
泉家 康宏 (Izumiya Yasuhiro)
磯 達也 (Iso Tatsuya)
磯貝 純夫 (Isogai Sumio)
五十殿 弘二 (Isodono Koji)
市川 圭 (Ichikawa Kei)
市川 泰広 (Ichikawa Yasuhiro)
市堀 泰裕 (Ichibori Yasuhiro)
伊藤 俊輔 (Ito Shunsuke)
伊東 進 (Itoh Susumu)
伊藤 隆史 (Ito Takashi)
伊藤 之康 (Ito Nobuyasu)
伊藤 裕 (Itoh hiroshi)
伊藤 浩 (Ito Hiroshi)
伊東 史子 (Itoh Fumiko)
伊藤 瑞穂 (Ito Mizuho)
伊藤 宗洋 (Ito Munehiro)
伊藤 義治 (Itoh Yoshiharu)
稲垣 薫克 (Inagaki Tadakatsu)
稲熊 裕 (Inaguma Yutaka)
猪野 靖 (Ino Yasushi)
井上 啓司 (Inoue Keiji)
井上 剛 (Inoue Tsuyoshi)
井上 博文 (Inoue Hirofumi)
井上 陽介 (Inoue Yosuke)
伊比井 崇向 (Ibi Takahisa)
今井 英明 (Imai Hideaki)
今泉 勉 (Imaizumi Tsutomu)
今津 美樹 (Imazu Miki)
今西 敏雄 (Imanishi Toshio)
入江 大介 (Irie Daisuke)
岩破 俊博 (Iwasaku Toshihiro)
岩永 善隆 (Iwanaga Yoshitaka)
岩部 真人 (Iwabu Masato)
岩部 美紀 (Iwabu Miki)

臨床S-1-4 (79), OC1-2 (117),
OC1-3 (118), OC1-4 (118),
OC1-6 (119), PC1-5 (149),
PC1-9 (151), PC1-10 (152),
PC2-17 (172)
OB3-20 (138)
PB2-42 (181)
PB2-36 (178)
基礎S-3-2* (63)OB2-15 (136), PB2-38 (179)
OC2-16 (124), PC2-12* (169)
OB1-7 (132)
PB2-54* (188)
OC1-9* (121)
PB1-17* (161)
OB1-7 (132)
PC2-21* (174)PC1-3 (148), PC2-18 (172)
臨床S-3-6 (92)
PC2-15 (170)
OB1-7* (132), PC1-2 (147),
PB1-9 (157)
YIA-5 (195)
YIA-1 (193)
PB1-17 (161)
PB2-45 (183)
PB1-2 (153)
PC2-14 (170)
OC2-16 (124), PC2-12 (169)
PC1-1 (147)
OB1-2 (129)
PC2-19 (173)
PB2-30 (175)
PB1-24 (165)
臨床S-1-6 (81)PC1-11* (152)
臨床S-1-3* (78), PC2-14 (170)
PB2-51 (186), PB2-52 (187),
PB2-55* (188), PB2-56 (189)OC1-10 (121), PB1-20 (163)
OC2-17 (125)
臨床S-6-2 (106)
臨床S-6-2* (106)う
上田 友哉 (Ueda Tomoya)
臨床S-5-5 (103), OC2-19 (126)
植田 初江 (Ishibashi-Ueda Hatsue) OC2-13 (123)
上田 恭敬 (Ueda Yasunori)
臨床S-4-6* (98), OC1-5 (119)
植竹 龍一 (Uetake Ryuichi)
OB1-8 (132), PB1-10 (157)
上野 雅史 (Ueno Masafumi)
OC2-17 (125)
上松 正朗 (Uematsu Masaaki)
OC2-14 (123)
植村 明嘉 (Uemura Akiyoshi)
基礎S-1-4* (54), PB2-33 (176)
上村 史朗 (Uemura Shiro)
臨床S-5-5 (103), OC2-19 (126)
植村 祐介 (Uemura Yusuke)
YIA-5* (195)
上山 知己 (Ueyama Tomomi)
OB3-26 (141), OB3-27 (142)
内橋 基樹 (Uchihashi Motoki)
PB2-41 (181)え江頭 健輔 (Egashira Kensuke)
江口 明世 (Eguchi Akiyo)
江口 正倫 (Eguchi Masamichi)
江口 良二 (Eguchi Ryoji)
江崎 太一 (Ezaki Taichi)
枝松 剛生 (Edamatsu Takeo)
榎本 敬 (Enomoto Takashi)
依馬 正次 (Ema Masatsugu)

PB1-16 (161), PB2-57 (189)OC1-10 (121), PB1-20 (163)
OC1-8* (120)
PB2-43* (182)
PB1-1 (153)
PB1-17 (161)
YIA-5 (195)
基礎S-1-3* (53), OB2-13 (135),
PB1-2 (153)お
尾池 雄一 (Oike Yuichi)
扇田 久和 (Ogita Hisakazu)
大石 明生 (Oishi Akio)
大内 乗有 (Ouchi Noriyuki)
大賀 則孝 (Ohga Noritaka)

大川 善文 (Okawa Yoshifumi)
大木 浩司 (Ohki Kohji)
大郷 剛 (Ogo Takeshi)
大坂 瑞子 (Osaka Mizuko)

大澤 毅 (Osawa Tsuyoshi)
大杉 直弘 (Osugi Naohiro)
太田 智之 (Ota Tomoyuki)
太田 康之 (Ohta Yasuyuki)
大谷 健太郎 (Otani Kentaro)
大谷 朋仁 (Ohtani Tomohito)
大沼 俊名 (Oonuma Toshina)
大野 和則 (Ohno Kazunori)
大場 雄介 (Ohba Yusuke)
大橋 浩二 (Ohashi Koji)
大原 貴裕 (Ohara Takahiro)
大星 真貴子 (Oboshi Makiko)
大森 啓介 (Omori Keisuke)
岡 敦子 (Ishizuya-Oka Atsuko)
岡田 将 (Okada Sho)
岡田 保典 (Okada Yasunori)
小形 岳寛 (Ogata Takehiro)
岡村 英夫 (Okamura Hideo)
岡本 慎 (Okamoto Shin)
岡本 安雄 (Okamoto Yasuo)
小川 久雄 (Ogawa Hisao)

小川 啓恭 (Ogawa Hiroyasu)
沖山 葉月 (Okiyama Hazuki)
奥野 圭祐 (Okuno Keisuke)
奥野 祐次 (Okuno Yuji)
奥原 祥貴 (Okuhara Yoshitaka)
奥村 聡 (Okumura Satoshi)− 200 −

臨床S-3-3* (89)OB1-1 (129)
PB2-33 (176)
臨床S-5-6* (104), YIA-5 (195)
OB1-9 (133), OB1-10 (133),
OB1-11 (134), PB1-4 (154),
PB1-5 (155), PB1-29 (168),
PB2-46 (183)
PB2-41 (181)OC2-22 (127)OC1-7 (120)
PB1-16* (161), PB1-17 (161),
PB1-18 (162), PB2-49 (185),
PB2-53 (187)
PC1-1 (147), PC1-2 (147)
PC2-19 (173)
PC2-19 (173)
PB1-13 (159), PB1-14 (159)
PB1-12 (158)
OC1-9 (121)OB1-12* (134)
PC1-6 (150), PB2-50 (186)
OB1-11 (134)
臨床S-5-6 (104), YIA-5 (195)
PC1-11 (152)
OC1-10 (121)
OB3-21 (139)
PB1-6 (155)
PB1-15 (160)
臨床S-3-6 (92)
OB3-26 (141), OB3-27 (142)
PC1-7 (150), PC1-8 (151)
OC2-14 (123)基礎S-3-3 (64), OB3-19 (138),
PB1-11* (158)
臨床S-1-4 (79), OC1-2 (117),
OC1-3 (118), OC1-6 (119),PC1-5 (149), PC1-9 (151),
PC1-10 (152), PC2-13 (169),
PC2-17 (172), PB2-36 (178)
PB2-43 (182)
PB1-9 (157)
OC2-14 (123)OC2-21* (127)OC1-10 (121), PB1-20 (163)
PC2-19 (173)第21回日本血管生物医学会学術集会
Beyond the Cutting Edge of the Vascular Biology & Medicine（抄録掲載ページ）
OC2-20* (126)
OC1-7 (120)OB3-21 (139)
PC2-14 (170)
基礎S-2-2* (58)
OC2-15 (124)
基礎S-5-5* (75), PB2-46 (183)
PB1-7 (156)
PB1-14 (159)
PB1-13* (159), PC2-20 (173)
PC2-14 (170)

河原田 修身 (Kawarada Osami)
寒川 賢治 (Kangawa Kenji)
神吉 康晴 (Kanki Yasuharu)
神崎 秀明 (Kanzaki Hideaki)
神崎 万智子 (Kanzaki Machiko)
神田 貴史 (Kanda Takashi)
菅野 巌 (Kanno Iwao)
上林 大輔 (Kambayashi Daisuke)
神原 貴広 (Kambara Takahiro)

PC2-17* (172)
OC1-6 (119), PB1-12 (158),
PC2-13 (169)
PC1-2 (147)
PC1-11 (152)
OC2-20 (126)
OC2-14 (123)
PB1-14 (159)
PC1-3 (148), PC2-18 (172)YIA-5 (195)

海北 幸一 (Kaikita Koichi)
階元 聡 (Kaimoto Satoshi)
郭 从容 (Guo Congrong)
影近 弘之 (Kagechika Hiroyuki)
角谷 瞳 (Kakutani Hitomi)
笠井 淳司 (Kasai Atsushi)
風間 智彦 (Kazama Tomohiko)
梶本 和昭 (Kajimoto Kazuaki)
加治屋 健太朗 (Kajiya Kentaro)
柏田 建 (Kashiwada Takeru)
片岡 崇弘 (Kataoka Takahiro)

木下 博之 (Kinoshita Hiroyuki)
木船 智司 (Kifune Satoshi)
木村 英二 (Kimura Eiji)
木村 晋三 (Kimura Shinzo)
木村 弘 (Kimura Hiroshi)く草野 研吾 (Kusano Kengo)
久保 秀司 (Kubo Shuji)
久保 隆史 (Kubo Takashi)
久保田 俊郎 (Kubota Toshiro)
窪田 泰夫 (Kubota Yasuo)
久保田 義顕 (Kubota Yoshiaki)
熊谷 渉平 (Kumagai Shohei)
熊坂 礼音 (Kumasaka Reon)
熊田 全裕 (Kumada Masahiro)
倉田 智子 (Kurata Tomoko)
倉知 正 (Kurachi Masashi)
栗波 仁美 (Kurinami Hitomi)
栗原 智宏 (Kurihara Tomohiro)
栗原 裕基 (Kurihara Hiroki)PC1-5 (149), PC1-7 (150),
PC1-8 (151)
PB2-43 (182)
PC1-8 (151), PC2-14 (170)
PB1-23 (165)
PB2-40 (180)
基礎S-5-1* (71)
OB3-25* (141)
OC1-3 (118), OC1-4 (118)
OC1-9 (121)
PB1-13 (159), PB1-14 (159),
PC2-20 (173)
PB1-24 (165)
PB2-48 (184)
臨床S-3-6 (92)
基礎S-1-2 (52), PB2-36 (178),
YIA-7 (196)け
弦間 昭彦 (Gemma Akihiko)− 201 −

OB2-14 (135)

著者索引

川辺 淳一 (Kawabe Jun-ichi)
河村 浩平 (Kawamura Kohei)
川本 泰輔 (Kawamoto Taisuke)

北原 秀治 (Kitahara Syuji)
北村 洋平 (Kitamura Youhei)
橘田 未来 (Kitta Miku)
木戸屋 浩康 (Kidoya Hiroyasu)

ポスター発表 ＹＩＡ選考発表

門脇 孝 (Kadowaki Takashi)
金井 恵理 (Kanai Eri)
金谷 智明 (Kanaya Tomoaki)
金田 安史 (Kaneda Yasufumi)
金山 朱里 (Kaneyama Shuri)
加野 浩一郎 (Kano Koichiro)
鹿原 真樹 (Kabara Maki)
鎌倉 史郎 (Kamakura Shiro)
神出 計 (Kamide Kei)
神山 俊哉 (Kamiyama Toshiya)
神吉 昭子 (Kamiyoshi Akiko)
河相 裕美 (Kawai Hiromi)
川上 りか (Kawakami Rika)
川上 利香 (Kawakami Rika)
川崎 隆史 (Kawasaki Takashi)
川崎 友裕 (Kawasaki Tomohiro)
川瀬 治哉 (Kawase Haruya)
川田 啓之 (Kawata Hiroyuki)
河手 久香 (Kawate Hisaka)
河野 浩章 (Kawano Hiroaki)
川人 浩之 (Kawahito Hiroyuki)

岸本 忠三 (Kishimoto Tadamitsu)
北風 政史 (Kitakaze Masafumi)

OB1-4 (130)
PB2-55 (188), PB2-56 (189)
PB1-9 (157)
PB2-51 (186), PB2-52 (187),
PB2-55 (188), PB2-56 (189)OC2-18 (125)
OC1-6 (119), OC2-22 (127),
OB1-4 (130), PC1-11 (152)
PC1-1 (147), PB1-1* (153)
PC1-6 (150), PB2-50 (186)
PB2-30 (175)
基礎S-2-5 (61), OB2-16 (136),
PB2-30 (175), PB2-32 (176),
PB2-34 (177), YIA-2 (193)
PC1-4 (148)
臨床S-4-3 (95)
OB2-15* (136)
OC2-16 (124), PC2-12 (169)
YIA-1 (193)

口頭発表

片岡 有 (Kataoka Yu)
片岡 義之 (Kataoka Yoshiyuki)
片村 真紀 (Katamura Maki)
勝谷 友宏 (Katsuya Tomohiro)
桂 彰宏 (Katsura Akihiro)
加藤 拓 (Kato Taku)

PB2-36 (178)
PB2-41 (181)
PB2-33 (176)
PB2-35 (177)
PB1-4 (154)
OB3-20* (138)
PB1-25 (166)
PB1-26* (166)
YIA-2 (193)
OB2-14* (135)
OC2-18 (125), PB2-31 (175),
PB2-45* (183)
PC2-13 (169)
YIA-5 (195)
PB2-41 (181)OC2-24 (128)
OB1-9 (133), YIA-3 (194)
PB2-51 (186), PB2-52* (187),
PB2-55 (188), PB2-56 (189)
臨床S-6-2 (106)
PB2-41 (181)OC1-3 (118), OC1-4 (118)
YIA-6 (195)
臨床S-3-5* (91), YIA-7 (196)
PB1-25 (166)
PB2-37* (179)
PC1-7 (150)
YIA-6 (195)
PB1-5 (155)
OB1-8 (132), PB1-10 (157)
PB1-13 (159)
OC2-13* (123)OC2-19 (126)
PB2-38 (179)
臨床S-1-4 (79), 臨床S-4-3* (95)
OB3-22 (139), PB1-27 (167)
OC2-19 (126)
PB1-10 (157)
OC1-8 (120)
PB2-51* (186), PB2-52 (187),
PB2-55 (188), PB2-56 (189)
PB2-37 (179)
OC2-16 (124), PC2-12 (169)OB1-10 (133), OB1-11 (134),
PB1-5 (155), PB2-46* (183)

木岡 秀隆 (Kioka Hidetaka)
鬼界 雅一 (Kikai Masakazu)
菊地 沙矢佳 (Kikuchi Sayaka)
岸田 聡 (Kishida Sou)

会長招待講演 シンポジウム

き
か

特別講演

奥山 裕司 (Okuyama Yuji)
尾崎 公美 (Ozaki Kimi)
尾崎 博 (Ozaki Hiroshi)
尾崎 雄一 (Ozaki Yuichi)
長船 健二 (Osafune Kenji)
小澤 拓也 (Ozawa Takuya)
落谷 孝広 (Ochiya Takahiro)
小野 富男 (Ono Tomio)
小畠 隆行 (Obata Takayuki)
表 芳夫 (Omote Yoshio)
折居 誠 (Orii Makoto)プログラム* 筆頭著者

* 筆頭著者（抄録掲載ページ）こ
小泉 昭夫 (Koizumi Akio)
臨床S-6-4 (108)
小出 優史 (Koide Yuji)
OC1-8 (120)
河野 隆志 (Kohno Takashi)
臨床S-3-2 (88)郡山 弘 (Koriyama Hiroshi)
OC2-24* (128), PB2-48 (184)古賀 伸彦 (Koga Nobuhiko)
臨床S-4-3 (95)
小坂 展慶 (Kosaka Nobuyoshi)
PB2-46 (183)
小坂 博昭 (Kosaka Hiroaki)
PB2-40 (180)
小柴 和子 (Koshiba-Takeuchi Kazuko) OB1-6 (131)小嶋 聡一 (Kojima Soichi)
PB2-35 (177)
小島 淳 (Kojima Sunao)
臨床S-2-5* (86)
小島 瑞代 (Kojima Mizuyo)
OB1-6 (131)
小谷 順一 (Kotani Jun-ichi)
OC1-9 (121)
小谷 順一 (Kotani Jun-ichi)
PC1-10 (152)
児玉 和久 (Kodama Kazuhisa)
臨床S-4-2 (94)
児玉 紀洋 (Kodama Norihiro)
臨床S-1-6 (81)後藤 葉一 (Goto Yoichi)
OC1-3 (118), OC1-4 (118),
PC1-5 (149), PC1-9 (151),
PC1-10 (152)兒仁井 花恵 (Konii Hanae)
PB1-9 (157)
小西 良士 (Konishi Ryoji)
PB2-40 (180)小林 順二郎 (Kobayashi Jynjiro) OC1-1 (117)小林 果 (Kobayashi Hatasu)
臨床S-6-4 (108)小林 美穂 (Kobayashi Miho)
PB2-47* (184)小林 欣夫 (Kobayashi Yoshio)
PB1-15 (160)小林（梶浦）浩子PB2-38 (179)(Kajiura-Kobayashi Hiroko)
小夫家 和宏 (Kobuke Kazuhiro)
小松 誠 (Komatsu Sei)
小室 一成 (Komuro Issei)

小山 雄広 (Koyama Katsuhiro)
小山 晃英 (Koyama Teruhide)
近藤 和雄 (Kondo Kazuo)
近藤 美弥子 (Kondoh Miyako)

OC2-17 (125)
臨床S-4-2* (94)
基礎S-1-5 (55), 臨床S-5-4 (102),
OC1-9 (121), OC2-15 (124),
OC2-18 (125), OC2-20 (126),
OC2-23 (128), OB2-16 (136),
OB3-28 (142), OB3-29 (143),
PB1-19 (162), PB2-31 (175),
PB2-45 (183)
PB1-19 (162)
OB1-8 (132), PB1-10 (157)
PB1-18 (162)
PB1-4 (154)さ
崔 弘 (Cui Hong)齋藤 穎 (Saito Satoshi)
斎藤 能彦 (Saito Yoshihiko)
坂上 倫久 (Sakaue Tomohisa)
榊原 紀和 (Sakakibara Norikazu)
坂田 泰史 (Sakata Yasushi)
坂田 隆造 (Sakata Ryuzo)
坂谷 知彦 (Sakatani Tomohiko)
坂部 正英 (Sakabe Masahide)
坂元 顕久 (Sakamoto Akihisa)
坂本 謙司 (Sakamoto Kenji)
坂本 伸吾 (Sakamoto Shingo)
坂本 裕樹 (Sakamoto Hiroki)
佐久間 理吏 (Sakuma Masashi)
桜井 敬之 (Sakurai Takayuki)

PB1-11 (158)
臨床S-4-4 (96)
臨床S-5-5 (103), OC2-19 (126)
OB1-2* (129)
PB2-40 (180)OC1-9 (121), OC2-20 (126)
OB3-24 (140)
OC2-16 (124), PC2-12 (169)
YIA-1* (193)
基礎S-4-4 (70)
PB1-8 (156)
PC2-17 (172)
OC1-3 (118), OC1-4 (118),
PC1-5 (149), PC1-10 (152)
臨床S-1-2* (77)OB1-8 (132), PB1-10 (157)

櫻井 遊 (Sakurai Yu)
佐々木 文之 (Sasaki Fumiyuki)
笹原 正清 (Sasahara Masakiyo)
佐田 政隆 (Sata Masataka)
里 直行 (Sato Naoyuki)
佐藤 公雄 (Satoh Kimio)
佐藤 玄基 (Sato Genki)
佐藤 健吾 (Sato Kengo)
佐藤 恒太 (Sato Kota)
佐藤 大輔 (Sato Daisuke)
佐藤 琢真 (Sato Takuma)
佐藤 靖史 (Sato Yasufumi)

佐藤 悠介 (Sato Yusuke)
里見 和浩 (Satomi Kazuhiro)
眞田 文博 (Sanada Fumihiro)
佐野 元昭 (Sano Motoaki)
佐分利 誠 (Saburi Makoto)
澤 芳樹 (Sawa Yoshiki)
澤田 悠 (Sawada Hisashi)
澤根 美加 (Sawane Mika)
三田 祥寛 (Sanda Yoshihiro)

PB1-29* (168)OC1-11 (122)
PB1-22 (164)
OB3-29 (143), PB2-48 (184)
PB1-21* (163)
臨床S-3-1* (87)
YIA-1 (193)
PB1-9 (157)
PC2-20* (173)
OC1-8 (120)OC1-1 (117)
基礎S-5-3* (73), OB2-17 (137),
PB1-1 (153), PB2-35 (177),
PB2-47 (184)
PB1-29 (168)PC1-7 (150), PC1-8 (151)
OC1-12* (122)
基礎S-4-1* (67)
PC1-3 (148), PC2-18 (172)
OC1-9 (121)OC1-10* (121), PB1-20 (163)
YIA-2* (193)
OC1-7 (120)し塩野 泰紹 (Shiono Yasutsugu)
篠原 信雄 (Sinohara Nobuo)
柴崎 貢志 (Shibasaki Koji)
柴田 宗彦 (Shibata Munehiko)
柴田 陽平 (Shibata Yohei)
柴田 玲 (Shibata Rei)

PC2-14 (170)
OB1-10 (133)
PB1-24 (165)
OC2-23* (128)
PC2-19 (173)
基礎S-2-4* (60), 臨床S-5-6 (104),
臨床S-7-1 (109), YIA-5 (195)澁谷 正史 (Shibuya Masabumi)
OB2-17 (137)
島田 健永 (Shimada Kenei)
PC2-16 (171)
島野 仁 (Shimano Hitoshi)
臨床S-6-3* (107)
嶋村 邦宏 (Shimamura Kunihiro) PC2-14 (170)
島村 宗尚 (Shimamura Munehisa) OC2-24 (128), PB2-48* (184)清水 良子 (Shimizu-Hirota Ryoko) 臨床S-3-6* (92)清水 渉 (Shimizu Wataru)
臨床S-2-1* (82)
下川 宏明 (Shimokawa Hiroaki)
IL-1* (47), 臨床S-3-1 (87)
下田 将之 (Shimoda Masayuki)
臨床S-3-6 (92)
下田 義晃 (Shimoda Yoshiaki)
PC1-6 (150), PB2-50 (186)
小路 和代 (Shoji Kazuyo)
PB2-40 (180)白井 幹康 (Shirai Mikiyasu)
PB2-31 (175), PB2-45 (183)
白記 達也 (Shiraki Tatsuya)
OC2-14 (123)
白山 武司 (Shirayama Takeshi)
PC1-6 (150), PB2-50 (186),
PB2-51 (186), PB2-52 (187)
新藤 隆行 (Shindo Takayuki)
基礎S-3-1* (62), OB1-8 (132),
PB1-10 (157)
進藤 正信 (Shindoh Masanobu)
PB1-4 (154), PB2-46 (183)
新藤 優佳 (Shindo Yuka)
PB1-10 (157)す末弘 淳一 (Suehiro Jun-ichi)
菅 竜也 (Suga Tatsuya)
菅野 康夫 (Sugano Yasuo)
菅原 裕 (Sugawara Yu)− 202 −

PC1-2 (147)
OC2-17 (125)PC1-11 (152)
OC2-19 (126)第21回日本血管生物医学会学術集会
Beyond the Cutting Edge of the Vascular Biology & Medicine（抄録掲載ページ）

杉田 純一 (Sugita Junichi)
杉原 隆太 (Sugihara Ryuta)
鈴木 進 (Suzuki Susumu)
鈴木 洋 (Suzuki Hiroshi)
鈴木 康弘 (Suzuki Yasuhiro)

OB1-6 (131)
PB1-19 (162)
臨床S-5-5* (103), OC2-19 (126)
PB1-5 (155), OB1-10 (133)
PB2-37 (179)
PC2-16 (171)
PC2-19 (173)
OC1-9 (121)
PC1-3 (148), PC2-18 (172)
PC2-19 (173)
OC2-18 (125)
OB1-8* (132), PB1-10 (157)
基礎S-4-3* (69)

谷垣 徹 (Tanigaki Toru)
谷本 貴志 (Tanimoto Takashi)
谷山 義明 (Taniyama Yoshiaki)
田原 敦子 (Tahara Atsuko)
田原 宣広 (Tahara Nobuhiro)

OC2-16 (124), PC2-12 (169)
PC2-14 (170)
OC1-12 (122)
臨床S-1-6 (81)
臨床S-1-6* (81)ちそ相馬 桂 (Soma Katsura)
相馬 由佳 (Souma Yuka)
添田 恒有 (Soeda Tsunenari)
曽野部 崇 (Sonobe Takashi)
反町 洋之 (Sorimachi Hiroyuki)

千葉 彩乃 (Chiba Ayano)陳 震一 (Chen Zhenyi)

PB1-19* (162)
PB2-50 (186)
OC2-19 (126)
PB2-31 (175), PB2-45 (183)
YIA-7 (196)つて出口 健太郎 (Deguchi Kentaro)
出口 友則 (Deguchi Tomonori)
寺井 健太 (Kenta Terai)
寺口 郁子 (Teraguchi Ikuko)

PB1-13 (159), PC2-20 (173)
PB2-38* (179)OB2-14 (135), PB1-28 (167)
PC2-14* (170)と徳留 健 (Tokudome Takeshi)
戸倉 新樹 (Tokura Yoshiki)礪波 一夫 (Tonami Kazuo)
鳥羽 健 (Toba Ken)
豊崎 美紅 (Toyozaki Miku)
鳥山 佑一 (Toriyama Yuichi)

PB1-12* (158)
OB2-18 (137)
YIA-7 (196)
OC2-15 (124)
PB1-18* (162)
OB1-8 (132), PB1-10 (157)

内藤 尚道 (Naito Hisamichi)
内藤 由朗 (Naito Yoshiro)
永井 利幸 (Nagai Toshiyuki)
永井 良三 (Nagai Ryozo)
中尾 一和 (Nakao Kazuwa)− 203 −

基礎S-2-5* (61), PB2-32 (176),
PB2-34 (177)
OC1-10 (121), PB1-20 (163)
OC1-3 (118), OC1-4 (118),
PC1-10 (152)
OC2-23 (128), PB1-19 (162)
PB1-12 (158)

著者索引

な

ポスター発表 ＹＩＡ選考発表

OB1-3 (130)
OB1-7 (132)
YIA-2 (193)
基礎S-2-1* (57), 基礎S-2-5 (61),OB2-16 (136), PB2-30 (175),
PB2-32 (176), PB2-34 (177),
YIA-2 (193)
高島 成二 (Takashima Seiji)
IL-1* (48), 臨床S-6-1* (105),
OB1-4 (130)高田 博輝 (Takata Hiroki)
PB2-51 (186), PB2-52 (187)
高田 麻紀 (Takata Maki)
PB2-40 (180)
高野 雅充 (Takano Masamichi)
臨床S-4-5* (97)高橋 宣敦 (Takahashi Nobuatsu)
PC1-2* (147)
高橋 典彦 (Takahashi Norihiko)
PB1-5 (155)
高橋 将文 (Takahashi Masafumi) 臨床S-3-4* (90)
高濱 博幸 (Takahama Hiroyuki)
OC1-6 (119), PC1-11 (152)
鷹見 洋一 (Takami Yoichi)
YIA-6* (195)
高宮 資宜 (Takamiya Motonori)
PC2-20 (173)高山 忠輝 (Takayama Tadateru)
臨床S-4-4* (96)
高良 和宏 (Takara Kazuhiro)
PB2-32 (176)
瀧野 純一 (Takino Jun-ichi)
PB2-44* (182)
瀧原 圭子 (Yamauchi-Takihara Keiko) OC2-18 (125), PB2-31 (175),
PB2-45 (183)田口 瑠奈 (Taguchi Luna)
YIA-3 (194)
多久和 典子 (Takuwa Noriko)
基礎S-3-3 (64), OB3-19 (138),
PB1-11 (158)
多久和 陽 (Takuwa Yoh)
基礎S-3-3 (64), OB3-19 (138),
PB1-11 (158)

塚本 郁子 (Tsukamoto Ikuko)
PB2-40 (180)
塚本 蔵 (Tsukamoto Osamu)
OB1-4 (130)
辻 明宏 (Tsuji Akihiro)
OC1-7* (120)辻村 卓也 (Tsujimura Takuya)
OC2-14 (123)
椿本 恵則 (Tsubakimoto Yoshinori) OC2-16* (124), PC2-12 (169)壷阪 義記 (Tsubosaka Yoshiki)OB3-21 (139)

口頭発表た高井 義美 (Takai Yoshimi)
高木 尊大 (Takagi Takahiro)
高木 雅哉 (Takagi Masaya)
高倉 伸幸 (Takakura Nobuyuki)

PB1-28* (167)
PB2-42 (181)

会長招待講演 シンポジウム

せ清野 精彦 (Seino Yoshihiko)
臨床S-4-5 (97)
瀬口 理 (Seguchi Osamu)
OC1-1 (117)妹尾 絢子 (Seno Ayako)
臨床S-5-5 (103)
瀬ノ口 隆文 (Senokuchi Takafumi) PC1-4 (148)
全 完 (Zen Kan)
PC1-3 (148), PC2-18 (172)
仙波 宏章 (Senba Hiroaki)
PB1-19 (162)竹内 純 (Takeuchi Jun)
武田 憲彦 (Takeda Norihiko)
竹田 征治 (Takeda Yukiji)
武冨 紹信 (Taketomi Akinobu)
竹原 有史 (Takehara Naofumi)
竹本 恭彦 (Takemoto Yasuhiko)
畳 陽祐 (Tatami Tosuke)
橘 公一 (Tachibana Kouichi)
立川 弘孝 (Tatsukawa Hirotaka)
田中 哲人 (Tanaka Akihito)
田中 敏郎 (Tanaka Toshio)
田中 愛 (Tanaka Megumu)
田中（大石）由美子(Oishi-Tanaka Yumiko)

特別講演

OB3-28* (142)
OC1-5 (119)PC2-19* (173)
OB1-9 (133), YIA-3 (194)
PB1-1 (153), PB2-47 (184)
PB2-35 (177)鈴木 夕佳 (Suzuki Yuka)
YIA-3 (194)
須田 謙史 (Suda Kenji)
PB2-33* (176)
須藤 乃里子 (Oshima-Sudo Noriko) PB1-23* (165)
砂川 賢二 (Sunagawa Kenji)
PB2-57 (189)
角南 春樹 (Sunami Haruki)
OC1-1 (117)プログラム* 筆頭著者

* 筆頭著者（抄録掲載ページ）

中尾 新太郎 (Nakao Shintaro)
中尾 光善 (Nakao Mitsuyoshi)
永尾 宗子 (Nagao Hiroko)
中岡 良和 (Nakaoka Yoshikazu)

中神 啓徳 (Nakagami Hironori)
中川 修 (Nakagawa Osamu)
中込 敦士 (Nakagomi Atsushi)
永里 朋香 (Nagasato Tomoka)
中島 啓裕 (Nakashima Takahiro)
中島 育太郎 (Nakajima Ikutaro)
永田 浩一 (Nagata Koh-ichi)
中谷 大作 (Nakatani Daisaku)
中谷 武嗣 (Nakatani Takeshi)
中西 直彦 (Nakanishi Naohiko)
中西 宣文 (Nakanishi Norifumi)
中西 秀彦 (Nakanishi Hidehiko)
中西 道郎 (Nakanishi Michio)
中野 覚 (Nakano Kaku)
中野 由美子 (Nakano Yumiko)
中原 努 (Nakahara Tsutomu)
長嶺 憲太郎 (Nagamine Kentaro)
中村 彰男 (Nakamura Akio)
中村 明宏 (Nakamura Akihiro)
中村 哲平 (Nakamura Teppei)
永谷 憲歳 (Nagaya Noritoshi)
中山 博之 (Nakayama Hiroyuki)
成瀬 雅衣 (Naruse Masae)
南都 清範 (Nanto Kiyonori)
南都 伸介 (Nanto Shinsuke)OC1-11* (122)
基礎S-4-4* (70)OB1-10* (133)
基礎S-1-5* (55), OC2-18* (125),
OB2-16 (136), PB2-31 (175),
PB2-45 (183)
臨床S-5-2* (100), OC2-24 (128),
PB2-48 (184), YIA-6 (195)
基礎S-1-6* (56), YIA-1 (193)
PB1-15* (160)
PC2-21 (174)
OC1-3* (118)
PC1-7* (150), PC1-8 (151)
PB1-2 (153)
OC2-20 (126)
OC1-1 (117)
OB3-26* (141), OB3-27 (142)
OC1-7 (120)PC1-1* (147)
OC1-4 (118), PC1-5 (149)
PB2-57 (189)PC2-20 (173)
PB1-8 (156)
PB2-44 (182)
PB2-42 (181)
PB2-41 (181)OC2-22* (127)OC1-6 (119), PC2-13 (169)
OB3-25 (141)
PB1-24 (165)
OC2-14 (123)OC1-9 (121), OC2-14 (123),
OC2-20 (126)に新飯田 俊平 (Niida Shumpei)
PB1-22 (164)西 真宏 (Nishi Masahiro)PC1-3 (148), PC2-18 (172)
西江 友美 (Nishie Tomomi)
OB2-13 (135)
西口 毅 (Nishiguchi Tsuyoshi)
PC2-14 (170)
西村 智 (Nishimura Satoshi)
OB3-28 (142)西村 眞人 (Nishimura Masato)
PC2-12 (169)
西村 嘉晃 (Nishimura Yoshiaki V.) PB1-2* (153)
西本 裕二 (Nishimoto Yuji)
OC1-5 (119)
西山 功一 (Nishiyama Koichi)
基礎S-1-2* (52), PB2-36 (178)
西山 正彦 (Masahiko Nishiyama) PB2-42 (181)
新田 良和 (Nitta Yoshikazu)
臨床S-1-6 (81)
二宮 善文 (Ninomiya Yoshifumi) PC2-15 (170)の野口 暉夫 (Noguchi Teruo)

野田 崇 (Noda Takashi)
野出 孝一 (Node Koichi)
野中 茂紀 (Nonaka Shigenori)
野々木 宏 (Nonogi Hiroshi)
野間 玄督 (Noma Kensuke)
は羽尾 裕之 (Hao Hiroyuki)
萩倉 一博 (Hagikura Kazuhiro)
橋口 照人 (Hashiguchi Teruto)
橋本 崇弘 (Hashimoto Takahiro)
長谷川 晶紀 (Hasegawa Akinori)
長谷川 拓也 (Hasegawa Takuya)
長谷部 直幸 (Hasebe Naoyuki)
秦 勝志 (Hata Shoji)
秦 広樹 (Hata Hiroki)
畠山 浩人 (Hatakeyama Hiroto)
八反丸 美和 (Hattammaru Miwa)
服部 光治 (Hattori Mitsuharu)
濱岡 哲郎 (Hamaoka Tetsuro)
濱島 丈 (Hamashima Takeru)
濱田 勝彦 (Hamada Katsuhiko)
浜田 淳一 (Hamada Junichi)
早川 智子 (Hayakawa satoko)
早川 幹人 (Hayakawa Mikito)
林 寿来 (Hayashi Hisaki)
原島 秀吉 (Harashima Hideyoshi)
原田 光一郎 (Harada Koichiro)
坂東 泰子 (K. Bando Yasuko)

臨床S-4-1* (93), OC1-10 (121),
OC2-13 (123), PB1-20 (163)
PB1-3* (154), PB1-25 (166)
PC2-21 (174)OB2-16 (136)
PB1-9 (157)
PC1-11 (152)
PB2-37 (179)
YIA-7 (196)OC1-1 (117)
PB1-29 (168)YIA-1 (193)
PB1-2 (153)
OB3-26 (141), OB3-27 (142)
PB1-22 (164)
PB1-17 (161), PB2-49* (185)OB1-11 (134)
YIA-5 (195)
臨床S-2-3* (84)
YIA-1 (193)
PB1-26 (166), PB1-29 (168)PC2-17 (172)
OB3-22 (139), PB1-27 (167)ひ東 幸仁 (Higashi Yukihito)
東邦 康智 (Higashikuni Yasutomi)
東山 繁樹 (Higashiyama Shigeki)
樋口 香織 (Higuchi Kaori)
樋口 義治 (Higuchi Yoshiharu)
肥後 修一朗 (Higo Shuichiro)
彦惣 俊吾 (Hikoso Syungo)
樋田 京子 (Hida Kyoko)ね根本 貴祥 (Nemoto Takayoshi)

臨床S-1-4* (79), 臨床S-4-3 (95),
OC1-2 (117), OC1-3 (118),
OC1-4 (118), OC1-6 (119),PC1-5 (149), PC1-9 (151),
PC1-10 (152), PC2-13 (169)
PC1-7 (150), PC1-8 (151)
臨床S-1-2 (77), 臨床S-5-1* (99)
PB2-38 (179)
PC1-9 (151)
OB3-23* (140)

OC1-5* (119)
樋田 泰浩 (Hida Yasuhiro)

人見 次郎 (Hitomi Jiro)
人見 敏明 (Hitomi Toshiaki)
日野 信次朗 (Hino Shinjiro)
兵藤 守 (Hyodo Mamoru)− 204 −

OB3-23 (140)
OB3-29* (143)OB1-2 (129)
OC2-18 (125), PB2-31 (175),
PB2-45 (183)
臨床S-4-4 (96)OC2-15* (124)
OC2-20 (126)
基礎S-5-4* (74), OB1-9 (133),
OB1-11 (134), PB1-4 (154),
PB1-5 (155), PB1-29 (168),
PB2-46 (183)
OB1-10 (133), OB1-11 (134),
PB1-4 (154), PB1-5 (155),
PB2-46 (183)
OB2-15 (136)
臨床S-6-4* (108)
基礎S-4-4 (70)
PB1-26 (166), PB1-29 (168)第21回日本血管生物医学会学術集会
Beyond the Cutting Edge of the Vascular Biology & Medicine（抄録掲載ページ）
OB2-18* (137)
PB2-39* (180)
PC2-14 (170)
OB1-3 (130)
臨床S-2-2* (83)
臨床S-4-4 (96)
臨床S-4-4 (96)OB3-23 (140)
OC1-10 (121)OC2-22 (127)OC1-10 (121), PB1-20 (163)ほPB1-4* (154)
PB2-36 (178)
PB2-41 (181)
PB2-45 (183)
PC2-21 (174)
PB1-20* (163)
PC2-13 (169)
臨床S-3-6 (92)
PB2-44 (182)
OB3-21 (139)
PB2-52 (187)
臨床S-1-6 (81)
PB1-23 (165)ま間石 奈湖 (Maishi Nako)

OB1-10 (133), OB1-11* (134),
PB1-4 (154), PB1-5 (155),
PB2-46 (183)

宮崎 章 (Miyazaki Akira)宮崎 一徳 (Miyazaki Kazunori)
宮崎 俊一 (Miyazaki Shunichi)
宮崎 拓郎 (Miyazaki Takuro)
宮園 浩平 (Miyazono Kohei)
宮部 愛 (Miyabe Megumi)
宮本 康二 (Miyamoto Koji)− 205 −

OB3-24 (140)
PB1-24 (165)
OC2-14 (123)
YIA-1 (193)
PB1-2 (153)
臨床S-4-5 (97)
臨床S-1-6 (81)OC1-9 (121)
OB3-22 (139)
基礎S-5-2* (72), PC1-2 (147)
OC2-20 (126)
PB2-54 (188)
OC2-15 (124), OC2-20 (126)
基礎S-3-4* (65), PB1-15 (160)
OB3-26 (141), OB3-27* (142)
OC1-3 (118), OC1-4 (118),
PC1-10 (152)
臨床S-3-5 (91), YIA-7 (196)
PB1-14 (159)
OC2-17 (125), PC2-13 (169)
臨床S-3-5 (91), YIA-7* (196)OB1-9 (133), YIA-3 (194)
YIA-5 (195)
PC1-7 (150), PC1-8 (151)

著者索引

北條 敬之 (Hojo Takayuki)
掃本 誠治 (Hokimoto Seiji)
星野 温 (Hoshino Atsushi)
保仙 直毅 (Hosen Naoki)
細川 和也 (Hosokawa Kazuya)
細川 愛実 (Hosokawa Manami)
細田 洋司 (Hosoda Hiroshi)
堀 進悟 (Hori Shingo)
堀 隆光 (Hori Takamitsu)
堀 正敏 (Hori Masatoshi)
堀内 正嗣 (Horiuchi Masatsugu)
本多 亮博 (Honda Akihiro)
本多 泉 (Honda Izumi)み
南方 謙二 (Minakata Kenji)
三國 雅彦 (Mikuni Masahiko)
水上 雪香 (Mizukami Yukika)
水田 賢 (Mizuta Ken)
水谷 健一 (Mizutani Ken-ichi)
水野 杏一 (Mizuno Kyoichi)
溝口 ミノリ (Mizoguchi Minori)
溝手 勇 (Mizote Isamu)
三井 統子 (Mitsui Toko)
南 敬 (Minami Takashi)
南口 仁 (Minamiguchi Hitoshi)
南沢 享 (Minamisawa Susumu)
南野 哲男 (Minamino Tetsuo)
南野 徹 (Minamino Tohru)
宮川 浩太郎 (Miyagawa Kotaro)
宮城 唯良 (Miyagi Tadayoshi)

ポスター発表 ＹＩＡ選考発表

藤盛 好啓 (Fujimori Yoshihiro)
藤原 正和 (Fujiwara Masakazu)
藤原 玲子 (Fujiwara Reiko)
舟田 晃 (Funada Akira)松村 剛 (Matsumura Takeshi)
松本 健 (Matsumoto Ken)松本 健嗣 (Matsumoto Kenji)
松本 貴樹 (Matsumoto Takaki)
松本 太郎 (Matsumoto Taro)
松本 学 (Matsumoto Manabu)
的場 聖明 (Matoba Satoaki)
的場 哲哉 (Matoba Tetsuya)
真鍋 一郎 (Manabe Ichiro)
丸井 晃 (Marui Akira)丸山 征郎 (Maruyama Ikuro)
丸山 徳見 (Maruyama Tokumi)
丸山 尚樹 (Maruyama Naoki)

口頭発表

福本 義弘 (Fukumoto Yoshihiro)
藤尾 慈 (Fujio Yasushi)
藤澤 俊明 (Fujisawa Toshiaki)
藤田 晃輔 (Fujita Kosuke)
藤田 知之 (Fujita Tomoyuki)
藤田 博 (Fujita Hiroshi)
藤田 雅史 (Fujita Masashi)
藤野 雅史 (Fujino Masashi)

PB2-41* (181)
PB2-56 (189)OC1-7 (120)
PB1-28 (167)
OC1-9 (121)
PC1-4* (148)
OC1-7 (120)
基礎S-1-1* (51), OB1-5 (131),
OB2-14 (135), PB1-28 (167),
YIA-4 (194)
臨床S-1-6 (81)OB3-25 (141)
PB1-4 (154)
OC2-17* (125)OC1-1 (117)
OC2-16 (124), PC2-12 (169)
OC2-14 (123)OC1-3 (118), OC1-4 (118),
PC1-5* (149), PC1-10 (152)
PB2-43 (182)
PB1-6* (155)
PC1-9* (151)
PC1-11 (152)

OB3-20 (138)
OC1-8 (120)
PC1-3 (148), PC2-18 (172)
PB2-31 (175), PB2-45 (183)
PB1-14 (159)
OB1-1* (129)
臨床S-7-2 (110)OB3-24 (140)
OC1-10 (121), PB1-20 (163)
PB1-1 (153)
臨床S-5-5 (103)OC2-16 (124), PC2-12 (169)
YIA-5 (195)
PC1-6 (150), PB2-50* (186)
OC1-5 (119)
PB2-37 (179)
YIA-4 (194)
基礎S-1-5 (55), OB1-6* (131),
OB2-16 (136)
PC1-4 (148)
OB2-13* (135)
PC2-16 (171)
臨床S-5-5 (103)
PB1-3 (154), PB1-25* (166)
PC1-10* (152), PC2-13* (169)
PB2-41 (181)
PB2-57 (189)
OC2-23 (128), PB1-19 (162)
OB3-24 (140)
PC2-21 (174)
PB2-40 (180)
OB3-26 (141), OB3-27 (142)

会長招待講演 シンポジウムふ
深井 邦剛 (Fukai Kuniyoshi)
福居 顕介 (Fukui Kensuke)
福井 重文 (Fukui Shigefumi)
福井 一 (Fukui Hajime)
福嶌 教偉 (Fukushima Norihide)
福田 一起 (Fukuda Kazuki)
福田 哲也 (Fukuda Tetsuya)
福原 茂朋 (Fukuhara Shigetomo)

前田 定秋 (Maeda Sadaaki)
前村 浩二 (Maemura Koji)
槇 系 (Maki Kei)
正木 豪 (Masaki Takeshi)
正本 和人 (Masamoto Kazuto)
真島 崇 (Majima Takashi)
増田 治史 (Masuda Haruchika)
升本 英利 (Masumoto Hidetoshi)
増山 理 (Masuyama Tohru)
松居 彩 (Matsui aya)
松井 勝 (Matsui Masaru)
松尾 あきこ (Matsuo Akiko)
松尾 一宏 (Matsuo Kazuhiro)
松尾 清成 (Matsuo Kiyonari)
松尾 浩志 (Matsuo Koushi)
松木 孝樹 (Matsuki Motoki)
松田 道行 (Matsuda Michiyuki)
松永 太一 (Matsunaga Taichi)

特別講演

平川 聡史 (Hirakawa Satoshi)
平島 正則 (Hirashima Masanori)
平田 久美子 (Hirata Kumiko)
平田 健一 (Hirata Ken-ichi)
平野 照之 (Hirano Teruyuki)
平山 篤志 (Hirayama Atsushi)
廣 喬史 (Hiro Takafumi)
廣井 透雄 (Hiroi Yukio)
廣田 誠一 (Hirota Seichi)
弘田 辰彦 (Hirota Tatsuhiko)
廣谷 信一 (Hirotani Shinichi)

プログラム* 筆頭著者

* 筆頭著者（抄録掲載ページ）

宮本 裕治 (Miyamoto Yuji)
宮脇 昭光 (Miyawaki Akimitsu)
三好 亨 (Miyoshi Toru)

OC1-10 (121)
OB3-25 (141)
PC2-15* (170)む向 健太 (Mukai Kenta)
村田 幸久 (Murata Takahisa)
村田 欣洋 (Murata Yoshihiro)
村松 史隆 (Muramatsu Fumitaka)
村松 昌 (Muramatsu Masashi)
室原 豊明 (Murohara Toyoaki)

PB2-39 (180)
OB3-21 (139)
OC1-1 (117)
PB2-32 (176), PB2-34* (177),
YIA-2 (193)
PB1-22 (164)
基礎S-2-4 (60), 臨床S-5-6 (104),
臨床S-7-1* (109), OB3-22 (139),
PB1-27 (167), PC2-19 (173),
YIA-5 (195)も毛 源傑 (Mao Yuanjie)
毛利 友美 (Mohri Tomomi)
茂木 正樹 (Mogi Masaki)
望月 直樹 (Mochizuki Naoki)

PB1-12 (158)
OB3-25 (141)
PB2-52 (187)
基礎S-1-1 (51), OB1-5 (131),
OB2-14 (135), OB2-16 (136),
PB1-12 (158), PB1-28 (167),
YIA-4 (194)
本山 晋一郎 (Motoyama Shinichiro) PC1-3* (148), PC2-18 (172)
森 麻美 (Mori Asami)
PB1-8 (156)
森 泰清 (Mori Yasukiyo)
PB2-51 (186)
森井 功 (Morii Isao)
PC2-13 (169)
森岡 崇 (Morioka Takashi)
YIA-1 (193)
森澤 大祐 (Morisawa Daisuke)OC1-10 (121), PB1-20 (163)
森下 保幸 (Morishita Yasuyuki)
YIA-3 (194)
森下 竜一 (Morishita Ryuichi)
臨床S-5-2 (100),
臨床S-7-3* (111), OC1-12 (122),
OC2-24 (128), PB1-21 (163),
PB2-48 (184), YIA-6 (195)
森島 正恵 (Morishima Masae)
PB1-1 (153)
森田 茜 (Morita Akane)
PB1-8* (156)
森田 育男 (Morita Ikuo)
OB2-17 (137), PB1-23 (165)
森田 佳宏 (Morita Yoshihiro)
OC1-7 (120)
盛彦 青山 (Morihiko Aoyama)
OB3-22 (139)
森本 展年 (Morimoto Nobutoshi) PC2-20 (173)
守屋 孝洋 (Moriya Takahiro)
OB1-5 (131)
森山 典晃 (Moriyama Noriaki)
OC1-4* (118)
森脇 一将 (Moriwaki Kazamasa) PB2-39 (180)
文字 昭雄 (Monji Akio)
OB3-22* (139), PB1-27 (167)や
柳生 剛 (Yagyu Takeshi)
安居 琢 (Yasui Taku)
安田 聡 (Yasuda Satoshi)

安田 昌和 (Yasuda Masakazu)

OC1-6* (119)OC2-18 (125), PB2-31 (175),
PB2-45 (183)
臨床S-1-4 (79), OC1-2 (117),
OC1-3 (118), OC1-4 (118),
OC1-6 (119), PC1-5 (149),
PC1-9 (151), PC1-10 (152),
PC2-13 (169), PC2-17 (172)
OC2-17 (125)簗瀬 正伸 (Yanase Masanobu)
山内 啓弘 (Yamauchi Akihiro)
山内 敦司 (Yamauchi Atsushi)
山内 敏正 (Yamauchi Toshimasa)
山内 豊彦 (Yamauchi Toyohiko)
山川 大史 (Yamakawa Daishi)
山口 真一郎 (Yamaguchi Shinichiro)
山口 智由 (Yamaguchi Tomoyuki)
山崎 智子 (Yamazaki Tomoko)
山治 憲二 (Yamaji Kenji)
山下 潤 (Yamashita Jun K.)

山下 徹 (Yamashita Toru)
山田 健司 (Yamada Kenji)
山田 沙梨恵 (Yamada Sarie)
山田 典一 (Yamada Norikazu)
山田 浩之 (Yamada Hiroyuki)

山田 優子 (Yamada Yuko)
山名 祥太 (Yamana Shota)
山根 崇史 (Yamane Takafumi)
山野 貴司 (Yamano Takashi)
山水 康平 (Yamamizu Kohei)
山本 和幸 (Yamamoto Kazuyuki)
山本 圭吾 (Yamamoto Keigo)
山本 啓太 (Yamamoto Keita)
山本 浩一 (Yamamoto Koichi)
山本 誠士 (Yamamoto Seiji)
山本 崇之 (Yamamoto Takayuki)
山本 広之 (Yamamoto Hiroyuki)

OC1-1 (117)
OB1-8 (132), PB1-10 (157)
PB2-37 (179)
臨床S-6-2 (106)
OB2-18 (137)
PB2-30* (175)
PC1-3 (148), PC2-18 (172)
PC2-14 (170)
YIA-3 (194)OC2-17 (125)
基礎S-1-5 (55), 基礎S-2-3* (59),OB1-6 (131), OB2-16 (136),
OB3-24 (140)
PB1-13 (159), PB1-14* (159),
PC2-20 (173)
PB1-5* (155)
PC1-4 (148)
臨床S-2-4* (85)
臨床S-1-1* (76), PB2-51 (186),
PB2-52 (187), PB2-55 (188),
PB2-56 (189)PC1-7 (150), PC1-8 (151)
OB1-3* (130)
OC1-3 (118), OC1-4 (118),
PC1-10 (152)
PC2-14 (170)
OB1-6 (131)
OB1-11 (134)
PB1-9 (157)
PC1-3 (148), PC2-18* (172)
臨床S-5-3* (101), YIA-6 (195)
PB1-22* (164)
臨床S-7-1 (109)OC2-17 (125)ゆ湯浅 大祐 (Yuasa Daisuke)
弓場 俊輔 (Yuba Shyunsuke)
由布 威雄 (Yufu Takeo)

YIA-5 (195)
PB2-38 (179)
PB2-57 (189)よ楊 磊 (Yang Lei)
横溝 岳彦 (Yokomizo Takehiko)
横山 詩子 (Yokoyama Utako)
横山 真隆 (Yokoyama Masataka)
吉井 明日香 (Yoshii Asuka)
吉岡 和晃 (Yoshioka Kazuaki)
吉田 茂生 (Yoshida Shigeo)
吉田 雅幸 (Yoshida Masayuki)

吉松 康裕 (Yoshimatsu Yasuhiro)
吉村 長久 (Yoshimura Nagahisa)
好本 裕平 (Yoshimoto Yuhei)
吉山 伸司 (Yoshiyama Shinji)
葭山 稔 (Yoshiyama Minoru)− 206 −

OB1-8 (132), PB1-10 (157)
OC1-11 (122)
PB2-54 (188)
PB1-15 (160)
PC1-1 (147), PB1-1 (153)
基礎S-3-3* (64), OB3-19 (138),
PB1-11 (158)
OC1-11 (122)
PB1-16 (161), PB1-17 (161),
PB1-18 (162), PB2-49 (185),
PB2-53 (187)OB1-9 (133), YIA-3* (194)
PB2-33 (176)
PB1-24 (165)
PB2-42* (181)
PC2-16 (171)第21回日本血管生物医学会学術集会
Beyond the Cutting Edge of the Vascular Biology & Medicine（抄録掲載ページ）

米澤 朋子 (Yonezawa Tomoko)
PC2-15 (170)
米満 吉和 (Yonemitsu Yoshikazu) 臨床S-7-4* (112)プログラム* 筆頭著者らり
力武 良行 (Rikitake Yoshiyuki)

臨床S-3-5 (91), YIA-7 (196)
OC2-24 (128), PB1-21 (163),
YIA-6 (195)特別講演

雷 小峰 (Lei Xiao-Feng)樂木 宏実 (Rakugi Hiromi)

OB1-3 (130)

若林 一郎 (Wakabayashi Ichiro)
若林 卓 (Wakabayashi Taku)
若山 勇紀 (Wakayama Yuki)
和田 直敏 (Wada Naotoshi)
渡邉 真言 (Watanabe Makoto)渡邉 琢也 (Watanabe Takuya)
渡部 琢也 (Watanabe Takuya)
渡部 徹也 (Watanabe Tetsuya)
渡邉 拓史 (Watanabe Hirofumi)
渡部 麗奈 (Watanabe Rena)
渡部 徹郎 (Watabe Tetsuro)

PB2-51 (186), PB2-52 (187),
PB2-55 (188), PB2-56* (189)
PB2-43 (182)
基礎S-2-5 (61), PB2-32* (176)
YIA-4* (194)PC1-3 (148), PC2-18 (172)
OC2-19* (126)
OC1-1* (117)
OB1-7 (132), PB1-9* (157)
OC2-14 (123)
PB1-3 (154), PB1-25 (166)
PB1-9 (157)
基礎S-3-5* (66), OB1-9 (133),
YIA-3 (194)

会長招待講演 シンポジウム

わ
若菜 紀之 (Wakana Noriyuki)

口頭発表
ポスター発表 ＹＩＡ選考発表

著者索引− 207 −