掲載種別：研究論文（学術雑誌）   出版者・発行元：MDPI AG  

Necroptosis, a form of necrosis, and alterations in mitochondrial dynamics, a coordinated process of mitochondrial fission and fusion, have been implicated in the pathogenesis of cardiovascular diseases. This study aimed to determine the role of mitochondrial morphology in canonical necroptosis induced by a combination of TNFα and zVAD (TNF/zVAD) in H9c2 cells, rat cardiomyoblasts. Time-course analyses of mitochondrial morphology showed that mitochondria were initially shortened after the addition of TNF/zVAD and then their length was restored, and the proportion of cells with elongated mitochondria at 12 h was larger in TNF/zVAD-treated cells than in non-treated cells (16.3 ± 0.9% vs. 8.0 ± 1.2%). The knockdown of dynamin-related protein 1 (Drp1) and fission 1, fission promoters, and treatment with Mdivi-1, a Drp-1 inhibitor, had no effect on TNF/zVAD-induced necroptosis. In contrast, TNF/zVAD-induced necroptosis was attenuated by the knockdown of mitofusin 1/2 (Mfn1/2) and optic atrophy-1 (Opa1), proteins that are indispensable for mitochondrial fusion, and the attenuation of necroptosis was not canceled by treatment with Mdivi-1. The expression of TGFβ-activated kinase (TAK1), a negative regulator of RIP1 activity, was upregulated and the TNF/zVAD-induced RIP1-Ser166 phosphorylation, an index of RIP1 activity, was mitigated by the knockdown of Mfn1/2 or Opa1. Pharmacological TAK1 inhibition attenuated the protection afforded by Mfn1/2 and Opa1 knockdown. In conclusion, the inhibition of mitochondrial fusion increases TAK1 expression, leading to the attenuation of canonical necroptosis through the suppression of RIP1 activity.

DOI： 10.3390/ijms25052905

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記述言語：英語   出版者・発行元：(一社)日本循環器学会  

医中誌

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掲載種別：研究論文（学術雑誌）   出版者・発行元：Springer Science and Business Media LLC  

その他リンク： https://link.springer.com/article/10.1007/s11010-024-04951-z/fulltext.html

DOI： 10.1007/s11010-024-04951-z

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

It has been reported that autophagic activity is disturbed in the skeletal muscles of dystrophin-deficient mdx mice and patients with Duchenne muscular dystrophy (DMD). Transcriptional regulations of autophagy by FoxO transcription factors (FoxOs) and transcription factor EB (TFEB) play critical roles in adaptation to cellular stress conditions. Here, we investigated whether autophagic activity is dysregulated at the transcription level in dystrophin-deficient muscles. Expression levels of autophagy-related genes were globally decreased in tibialis anterior and soleus muscles of mdx mice compared with those of wild-type mice. DNA microarray data from the NCBI database also showed that genes related to autophagy were globally downregulated in muscles from patients with DMD. These downregulated genes are known as targets of FoxOs and TFEB. Immunostaining showed that nuclear localization of FoxO1 and FoxO3a was decreased in mdx mice. Western blot analyses demonstrated increases in phosphorylation levels of FoxO1 and FoxO3a in mdx mice. Nuclear localization of TFEB was also reduced in mdx mice, which was associated with elevated phosphorylation levels of TFEB. Collectively, the results suggest that autophagy is disturbed in dystrophin-deficient muscles via transcriptional downregulation due to phosphorylation-mediated suppression of FoxOs and TFEB.

DOI： 10.1038/s41598-024-51746-9

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

All eukaryotic cells require a minimal iron threshold to sustain anabolic metabolism. However, the mechanisms by which cells sense iron to regulate anabolic processes are unclear. Here we report a previously undescribed eukaryotic pathway for iron sensing in which molecular iron is required to sustain active histone demethylation and maintain the expression of critical components of the pro-anabolic mTORC1 pathway. Specifically, we identify the iron-binding histone-demethylase KDM3B as an intrinsic iron sensor that regulates mTORC1 activity by demethylating H3K9me2 at enhancers of a high-affinity leucine transporter, LAT3, and RPTOR. By directly suppressing leucine availability and RAPTOR levels, iron deficiency supersedes other nutrient inputs into mTORC1. This process occurs in vivo and is not an indirect effect by canonical iron-utilizing pathways. Because ancestral eukaryotes share homologues of KDMs and mTORC1 core components, this pathway probably pre-dated the emergence of the other kingdom-specific nutrient sensors for mTORC1.

DOI： 10.1038/s41556-023-01225-6

PubMed

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

Sirtuins (SIRT) exhibit deacetylation or ADP-ribosyltransferase activity and regulate a wide range of cellular processes in the nucleus, mitochondria and cytoplasm. The role of the only sirtuin that resides in the cytoplasm, SIRT2, in the development of ischemic injury and cardiac hypertrophy is not known. In this paper, we show that the hearts of mice with deletion of Sirt2 (Sirt2-/-) display improved cardiac function after ischemia-reperfusion (I/R) and pressure overload (PO), suggesting that SIRT2 exerts maladaptive effects in the heart in response to stress. Similar results were obtained in mice with cardiomyocyte-specific Sirt2 deletion. Mechanistic studies suggest that SIRT2 modulates cellular levels and activity of nuclear factor (erythroid-derived 2)-like 2 (NRF2), which results in reduced expression of antioxidant proteins. Deletion of Nrf2 in the hearts of Sirt2-/- mice reversed protection after PO. Finally, treatment of mouse hearts with a specific SIRT2 inhibitor reduced cardiac size and attenuates cardiac hypertrophy in response to PO. These data indicate that SIRT2 has detrimental effects in the heart and plays a role in cardiac response to injury and the progression of cardiac hypertrophy, which makes this protein a unique member of the SIRT family. Additionally, our studies provide a novel approach for treatment of cardiac hypertrophy and injury by targeting SIRT2 pharmacologically, providing a novel avenue for the treatment of these disorders.

DOI： 10.7554/eLife.85571

PubMed

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Proper nuclear organization is critical for cardiomyocyte function, because global structural remodeling of nuclear morphology and chromatin structure underpins the development and progression of cardiovascular disease. Previous reports have implicated a role for DNA damage in cardiac hypertrophy; however, the mechanism for this process is not well delineated. AMPK (AMP-activated protein kinase) family of proteins regulates metabolism and DNA damage response (DDR). Here, we examine whether a member of this family, SNRK (SNF1-related kinase), which plays a role in cardiac metabolism, is also involved in hypertrophic remodeling through changes in DDR and structural properties of the nucleus. METHODS: We subjected cardiac-specific Snrk-/- mice to transaortic banding to assess the effect on cardiac function and DDR. In parallel, we modulated SNRK in vitro and assessed its effects on DDR and nuclear parameters. We also used phosphoproteomics to identify novel proteins that are phosphorylated by SNRK. Last, coimmunoprecipitation was used to verify Destrin (DSTN) as the binding partner of SNRK that modulates its effects on the nucleus and DDR. RESULTS: Cardiac-specific Snrk-/- mice display worse cardiac function and cardiac hypertrophy in response to transaortic banding, and an increase in DDR marker pH2AX (phospho-histone 2AX) in their hearts. In addition, in vitro Snrk knockdown results in increased DNA damage and chromatin compaction, along with alterations in nuclear flatness and 3-dimensional volume. Phosphoproteomic studies identified a novel SNRK target, DSTN, a member of F-actin depolymerizing factor proteins that directly bind to and depolymerize F-actin. SNRK binds to DSTN, and DSTN downregulation reverses excess DNA damage and changes in nuclear parameters, in addition to cellular hypertrophy, with SNRK knockdown. We also demonstrate that SNRK knockdown promotes excessive actin depolymerization, measured by the increased ratio of G-actin to F-actin. Last, jasplakinolide, a pharmacological stabilizer of F-actin, rescues the increased DNA damage and aberrant nuclear morphology in SNRK-downregulated cells. CONCLUSIONS: These results indicate that SNRK is a key player in cardiac hypertrophy and DNA damage through its interaction with DSTN. This interaction fine-tunes actin polymerization to reduce DDR and maintain proper cardiomyocyte nuclear shape and morphology.

DOI： 10.1161/CIRCULATIONAHA.123.066002

PubMed

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記述言語：英語   出版者・発行元：(一社)日本循環器学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Systemic branched-chain amino acid (BCAA) metabolism is dysregulated in cardiometabolic diseases. We previously demonstrated that upregulated AMP deaminase 3 (AMPD3) impairs cardiac energetics in a rat model of obese type 2 diabetes, Otsuka Long-Evans-Tokushima fatty (OLETF). Here, we hypothesized that the cardiac BCAA levels and the activity of branched-chain α-keto acid dehydrogenase (BCKDH), a rate-limiting enzyme in BCAA metabolism, are altered by type 2 diabetes (T2DM), and that upregulated AMPD3 expression is involved in the alteration. Performing proteomic analysis combined with immunoblotting, we discovered that BCKDH localizes not only to mitochondria but also to the endoplasmic reticulum (ER), where it interacts with AMPD3. Knocking down AMPD3 in neonatal rat cardiomyocytes (NRCMs) increased BCKDH activity, suggesting that AMPD3 negatively regulates BCKDH. Compared with control rats (Long-Evans Tokushima Otsuka [LETO] rats), OLETF rats exhibited 49% higher cardiac BCAA levels and 49% lower BCKDH activity. In the cardiac ER of the OLETF rats, BCKDH-E1α subunit expression was downregulated, while AMPD3 expression was upregulated, resulting in an 80% lower AMPD3-E1α interaction compared to LETO rats. Knocking down E1α expression in NRCMs upregulated AMPD3 expression and recapitulated the imbalanced AMPD3-BCKDH expressions observed in OLETF rat hearts. E1α knockdown in NRCMs inhibited glucose oxidation in response to insulin, palmitate oxidation, and lipid droplet biogenesis under oleate loading. Collectively, these data revealed previously unrecognized extramitochondrial localization of BCKDH in the heart and its reciprocal regulation with AMPD3 and imbalanced AMPD3-BCKDH interactions in OLETF. Downregulation of BCKDH in cardiomyocytes induced profound metabolic changes that are observed in OLETF hearts, providing insight into mechanisms contributing to the development of diabetic cardiomyopathy.

DOI： 10.14814/phy2.15608

PubMed

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：American Society for Clinical Investigation  

DOI： 10.1172/JCI154491

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担当区分：筆頭著者   掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier {BV}  

DOI： 10.1016/j.yjmcc.2018.05.003

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Diabetes mellitus is a major risk factor for acute kidney injury (AKI). Here, we hypothesized that suppression of autophagic response underlies aggravation of renal ischemia/reperfusion (I/R) injury by type 2 diabetes mellitus (T2DM). In OLETF, a rat model of T2DM, and its non-diabetic control, LETO, AKI was induced by unilateral nephrectomy and 30-min occlusion and 24-h reperfusion of the renal artery in the contralateral kidney. Levels of serum creatinine and blood urea nitrogen and tubular injury score after I/R were significantly higher in OLETF than in LETO. Administration of chloroquine, a widely used autophagy inhibitor, aggravated I/R-induced renal injury in LETO, but not in OLETF. In contrast to LETO, OLETF exhibited no increase in autophagosomes in the proximal tubules after I/R. Immunoblotting showed that I/R activated the AMPK/ULK1 pathway in LETO but not in OLETF, and mTORC1 activation after I/R was enhanced in OLETF. Treatment of OLETF with rapamycin, an mTORC1 inhibitor, partially restored autophagic activation in response to I/R and significantly attenuated I/R-induced renal injury. Collectively, these findings indicate that suppressed autophagic activation in proximal tubules by impaired AMPK/ULK1 signaling and upregulated mTORC1 activation underlies T2DM-induced worsening of renal I/R injury.

DOI： 10.1038/s41598-017-05667-5

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: The role of necroptosis in myocardial injury has not been fully characterized. Here we examined roles of mitochondrial permeability transition pore (mPTP) and autophagy in necroptosis of cardiomyocytes. METHODS AND RESULTS: In H9c2 cells, necroptosis was induced by treatment with TNF-α (TNF) and z-VAD-fmk (zVAD) for 24h, and necroptotic death was determined by LDH release (as % of total). TNF/zVAD increased LDH release from 16.6±4.3% to 60.6±2.7%, and the LDH release was suppressed by necrostatin-1 (29.4±4.0%), a RIP1 inhibitor, and by siRNA-mediated knockdown of RIP3 (27.7±2.0%), confirming RIP1-RIP3-dependent necroptosis. TNF/zVAD-induced necroptosis was not attenuated by mPTP inhibitors or GSK-3β inhibitors. TNF/zVAD increased LC3-II level, but the change was not further enhanced by bafilomycin A1. The increase of LC3-II by TNF/zVAD was associated with suppression of both autophagic flux and LC3-LAMP1 co-localization. TNF/zVAD did not modify phosphorylation of Akt, p70s6K, AMPK, ULK1 or VASP but significantly increased RIP1-p62 binding and conversely reduced p62-LC3 binding. Rapamycin inhibited RIP1-p62 and RIP1-RIP3 interactions induced by TNF/zVAD and partly restored autophagic flux and suppressed LDH release in TNF/zVAD-treated cells. The effect of rapamycin on LDH release was reduced by knockdown of Atg5 expression. Knockdown of p62 by siRNA augmented LDH release by TNF/zVAD. CONCLUSION: Suppression of autophagic flux contributes to RIP1-RIP3 interaction and necroptosis of cardiomyocytes, and sequestration of p62 from its interaction with LC3-II by p62-RIP1 interaction possibly underlies the suppressed autophagy. The mPTP is unlikely to play a major role in execution of necroptosis in cardiomyocytes.

DOI： 10.1016/j.yjmcc.2017.06.008

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Sleep-disordered breathing (SDB) is highly prevalent in patients with diabetes mellitus (DM) and heart failure (HF) and contributes to poor cardiovascular outcomes. Enlarged glycemic variability (GV) is a risk factor of cardiac events independently of average blood glucose level, but the influence of SDB on GV is uncertain. In this study, we examined whether the impact of SDB on GV is modified by the presence of DM with or without HF. METHODS AND RESULTS: Two hundred three patients (67.5±14.1 [SD] years old, 132 males) who were admitted to our institute for examination or treatment of DM and/or HF underwent continuous glucose monitoring and polysomnography. Both HbA1c (8.0±2.0 vs. 5.7±0.4%) and mean amplitude of glycemic excursion (MAGE, median: 95.5 vs. 63.5 mg/dl) were significantly higher in a DM group (n = 100) than in a non-DM group (n = 103), but apnea-hypopnea index (AHI: 29.0±22.7 vs. 29.3±21.5) was similar in the two groups. AHI was correlated with log MAGE in the non-DM group but not in the DM group, and multivariate regression analysis revealed that AHI was an independent variable for log MAGE in the non-DM group but not in the DM group. We then divided the non-DM patients into two subgroups according to BNP level (100 pg/ml). AHI was positively correlated with log MAGE (r = 0.74, p<0.001) in the non-DM low-BNP subgroup, but such a correlation was not found in the non-DM high-BNP subgroup. Continuous positive airway pressure (CPAP) reduced MAGE from 75.3 to 53.0 mg/dl in the non-DM group but did not reduce MAGE in the DM group. CONCLUSION: Severity of SDB was associated with higher GV, but DM as well as HF diminished the contribution of SDB to GV. Treatment with CPAP was effective for reduction of GV only in patients without DM.

DOI： 10.1371/journal.pone.0188689

PubMed

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

A 65-year-old male developed acute myocardial infarction due to coronary artery dissection and tricuspid valve injury after blunt chest trauma. Acute myocardial infarction was treated by coronary artery intervention; however, refractory heart failure with pleural effusion remained. The first transthoracic echocardiography (TTE) on admission failed to clearly visualize the tricuspid valve and right ventricle due to poor image quality. A follow-up TTE with contrast ultrasonography revealed pericardial rupture in addition to tricuspid regurgitation. Ruptures of the tricuspid papillary muscle and pericardium were confirmed during surgery and were repaired successfully. Blunt chest trauma results in various cardiac injuries including cardiac rupture, intramural hematoma, valvular injury, coronary artery injury, and electrical disturbances, leading to critical conditions and high mortality. Of such blunt trauma-induced injuries, coronary artery dissection, tricuspid valve injury, and pericardial rupture caused by blunt chest trauma are rare, and simultaneous occurrence of the three types of injuries that were successfully repaired has not been reported. In addition, this case indicates the utility of contrast ultrasonography for diagnosis of pericardial rupture caused by blunt chest trauma.

DOI： 10.1007/s10396-015-0663-z

PubMed

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

Web of Science

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

Web of Science

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担当区分：筆頭著者   掲載種別：研究発表ペーパー・要旨（国際会議）  

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

DOI： 10.1161/res.131.suppl_1.P3014

Web of Science

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記述言語：英語  

医中誌

J-GLOBAL

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

Web of Science

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

DOI： 10.1161/res.127.suppl_1.263

Web of Science

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記述言語：英語   出版者・発行元：(一社)日本循環器学会  

医中誌

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記述言語：英語   出版者・発行元：(一社)日本循環器学会  

医中誌

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記述言語：日本語   掲載種別：記事・総説・解説・論説等（学術雑誌）   出版者・発行元：公益財団法人 日本心臓財団  

背景および目的：成人期に達した川崎病既往者の冠動脈後遺症病変の長期的変化については，長い間議論が継続しているにもかかわらず，いまだに一定の見解に至っていない．冠動脈後遺症を伴う川崎病既往者はもちろんのこと，冠動脈後遺症を伴わない川崎病既往者においても成人期の急性冠症候群発症の報告が散見されるため，当院での成人期川崎病，特に冠動脈後遺症を伴わない症例に着目し，その追跡状況およびその予後を調査した．

方法：2017年12月時点で20歳以上の当科受診歴のある川崎病既往患者を抽出した．当院小児科より成人科移行として紹介された56例，または産科より川崎病既往のため心機能および冠動脈瘤評価目的で紹介された9例の計65例を検討した．

結果：当科最終通院時点での年齢は平均25.9歳，予後調査時点での平均年齢は33.9歳であった．川崎病診断後，急性期に静注用免疫グロブリン（IVIG）療法が確認できた症例は8例，アスピリン内服のみの症例が23例であった．IVIG施行を確認しえた8症例は1986年以降に発症の症例で，冠動脈瘤形成を1例に認めるが，急性期一過性冠動脈拡大，退縮は認めなかった．冠動脈後遺症を伴わない川崎病既往者57例中，予後調査時点で連絡可能であった全51例に心臓突然死，急性冠症候群の発症は認めなかった．

結論：現在までに当科受診の冠動脈後遺症を伴わない川崎病既往患者に心臓突然死および急性冠症候群の発症を認めてはいないが，近年これらの報告が散見されるため，そのリスクベネフィットを十分説明したうえでの追跡が重要であると思われた．

DOI： 10.11281/shinzo.50.1289

CiNii Research

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担当区分：筆頭著者   掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

Web of Science

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担当区分：筆頭著者   掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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担当区分：筆頭著者   記述言語：日本語   出版者・発行元：医歯薬出版(株)  

その他リンク:： https://search.jamas.or.jp/default/link?pub_year=2017&ichushi_jid=J00060&link_issn=&doc_id=20170719010009&doc_link_id=issn%3D0039-2359%26volume%3D262%26issue%3D3%26spage%3D243&url=http%3A%2F%2Fwww.pieronline.jp%2Fopenurl%3Fissn%3D0039-2359%26volume%3D262%26issue%3D3%26spage%3D243&type=PierOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00005_2.gif

医中誌

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記述言語：英語   出版者・発行元：(一社)日本循環器学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本内分泌学会  

医中誌

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

Web of Science

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

DOI： 10.1016/j.cardfail.2016.07.055

Web of Science

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

Web of Science

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

Web of Science

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

医中誌

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担当区分：筆頭著者   掲載種別：研究発表ペーパー・要旨（国際会議）  

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記述言語：英語  

医中誌

J-GLOBAL

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記述言語：日本語   出版者・発行元：科学評論社  

その他リンク:： https://search.jamas.or.jp/link/ui/2016075832

CiNii Research

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J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

医中誌

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担当区分：筆頭著者   掲載種別：研究発表ペーパー・要旨（国際会議）  

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担当区分：筆頭著者   記述言語：日本語   掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）   出版者・発行元：(公社)日本超音波医学会  

医中誌

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担当区分：筆頭著者   記述言語：日本語   掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）   出版者・発行元：(公社)日本超音波医学会  

医中誌

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開催年月日： 2022年9月 - 2022年10月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2022年7月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2020年11月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2020年7月

会議種別：ポスター発表  

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開催年月日： 2020年7月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2018年1月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2017年11月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2017年10月

記述言語：英語   会議種別：口頭発表（一般）  

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開催年月日： 2017年8月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2017年3月

記述言語：英語   会議種別：口頭発表（一般）  

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開催年月日： 2016年12月

記述言語：英語   会議種別：口頭発表（一般）  

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開催年月日： 2016年8月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2016年4月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2016年3月

記述言語：英語   会議種別：口頭発表（一般）  

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開催年月日： 2014年5月

記述言語：英語   会議種別：口頭発表（一般）  

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開催年月日： 2013年10月

記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：英語   会議種別：公開講演，セミナー，チュートリアル，講習，講義等  

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記述言語：英語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：シンポジウム・ワークショップ パネル（指名）  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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会議種別：公開講演，セミナー，チュートリアル，講習，講義等  

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記述言語：英語   会議種別：公開講演，セミナー，チュートリアル，講習，講義等  

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記述言語：英語   会議種別：ポスター発表  

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記述言語：英語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：公開講演，セミナー，チュートリアル，講習，講義等  

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会議種別：公開講演，セミナー，チュートリアル，講習，講義等  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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種別：大会・シンポジウム等 

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