Toshihiro Takeda

ORCID: 0000-0003-3073-7823
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Cardiac electrophysiology and arrhythmias
  • Biomedical Text Mining and Ontologies
  • Mitochondrial Function and Pathology
  • Signaling Pathways in Disease
  • Cardiovascular Function and Risk Factors
  • Electronic Health Records Systems
  • Cardiac Fibrosis and Remodeling
  • Topic Modeling
  • Atrial Fibrillation Management and Outcomes
  • Cardiac Ischemia and Reperfusion
  • Cardiac Arrhythmias and Treatments
  • Redox biology and oxidative stress
  • Heart Failure Treatment and Management
  • Pharmacy and Medical Practices
  • Autophagy in Disease and Therapy
  • Natural Language Processing Techniques
  • Cardiac Imaging and Diagnostics
  • Clinical practice guidelines implementation
  • Radiomics and Machine Learning in Medical Imaging
  • Lung Cancer Treatments and Mutations
  • Lipoproteins and Cardiovascular Health
  • Pharmacovigilance and Adverse Drug Reactions
  • Anesthesia and Sedative Agents
  • Ion channel regulation and function
  • Anesthesia and Pain Management

Osaka University
2016-2025

Translational Research Informatics Center (Japan)
2016-2024

University of Fukui
2020-2024

Osaka University Hospital
2023

Fukui Red Cross Hospital
2021-2023

Kagawa University
2013-2020

Kagawa University Hospital
2019

University of Regensburg
2018

Japan Hospital Association
2016

Kyoto University
2005-2011

Abstract Damaged mitochondria are removed by mitophagy. Although Atg32 is essential for mitophagy in yeast, no homologue has been identified mammalian cells. Here, we show that Bcl-2-like protein 13 (Bcl2-L-13) induces mitochondrial fragmentation and First, hypothesized unidentified receptors would share molecular features of Atg32. By screening the public database homologues, identify Bcl2-L-13. Bcl2-L-13 binds to LC3 through WXXI motif HEK293 In Bcl2-L-13, BH domains important...

10.1038/ncomms8527 article EN cc-by Nature Communications 2015-07-06

AbstractConstitutive autophagy is important for control of the quality proteins and organelles to maintain cell function. Damaged accumulate in aged organs. We have previously reported that cardiac-specific Atg5 (autophagy-related gene 5)-deficient mice, which was floxed out early embryogenesis, were born normally, showed normal cardiac function structure up 10 weeks old. In present study, determine longer-term consequences Atg5-deficiency heart, we monitored Atg5-deficient mice further 12...

10.4161/auto.6.5.11947 article EN Autophagy 2010-06-24

The molecular mechanism for the transition from cardiac hypertrophy, an adaptive response to biomechanical stress, heart failure is poorly understood. mitogen-activated protein kinase p38alpha a key component of stress pathways in various types cells. In this study, we attempted explore vivo physiological functions hearts. First, generated mice with floxed alleles and crossbred them expressing Cre recombinase under control alpha-myosin heavy-chain promoter obtain cardiac-specific knockout...

10.1128/mcb.24.24.10611-10620.2004 article EN Molecular and Cellular Biology 2004-11-30

Left ventricular remodeling that occurs after myocardial infarction (MI) and pressure overload is generally accepted as a determinant of the clinical course heart failure. The molecular mechanism this process, however, remains to be elucidated. Apoptosis signal-regulating kinase 1 (ASK1) mitogen-activated protein plays an important role in stress-induced apoptosis. We used ASK1 knockout mice (ASK -/- ) test hypothesis involved development left remodeling. ASK hearts showed no morphological...

10.1073/pnas.2136717100 article EN Proceedings of the National Academy of Sciences 2003-12-09

The Raf/MEK/extracellular signal–regulated kinase (ERK) signaling pathway regulates diverse cellular processes such as proliferation, differentiation, and apoptosis is implicated an important contributor to the pathogenesis of cardiac hypertrophy heart failure. To examine in vivo role Raf-1 heart, we generated muscle–specific Raf-1–knockout (Raf CKO) mice with Cre-loxP–mediated recombination. demonstrated left ventricular systolic dysfunction dilatation without or lethality. Raf CKO showed a...

10.1172/jci20317 article EN Journal of Clinical Investigation 2004-10-01

Pretraining large-scale neural language models on raw texts has made a significant contribution to improving transfer learning in natural processing. With the introduction of transformer-based models, such as bidirectional encoder representations from transformers (BERT), performance information extraction free text improved significantly both general and medical domains. However, it is difficult train specific BERT perform well domains for which few databases high quality large size are...

10.1016/j.artmed.2024.102889 article EN cc-by Artificial Intelligence in Medicine 2024-05-05

The Raf/MEK/extracellular signal–regulated kinase (ERK) signaling pathway regulates diverse cellular processes such as proliferation, differentiation, and apoptosis is implicated an important contributor to the pathogenesis of cardiac hypertrophy heart failure. To examine in vivo role Raf-1 heart, we generated muscle–specific Raf-1–knockout (Raf CKO) mice with Cre-loxP–mediated recombination. demonstrated left ventricular systolic dysfunction dilatation without or lethality. Raf CKO showed a...

10.1172/jci200420317 article EN Journal of Clinical Investigation 2004-10-01

Transforming growth factor-beta1 (TGF-beta1) alters myocardial gene expression, resulting in myocyte hypertrophy, through activation of TGF-beta-activated kinase (TAK1), a member the mitogen-activated protein (MAPKKK) family. We hypothesized that TGF-beta1-TAK1-p38 MAPK pathway might be activated during ventricular remodeling after infarction (MI). One, 3, 7, and 14 days ligation left anterior descending coronary artery, noninfarcted tissue samples were obtained. Protein levels as well mRNA...

10.1152/ajpheart.00186.2005 article EN AJP Heart and Circulatory Physiology 2005-09-24

Cardiac-type sarco(endo)plasmic reticulum Ca2-ATPase (SERCA2a) plays a major role in cardiac muscle contractility. Phospholamban (PLN) regulates the function of SERCA2a via its Ser16-phosphorylation. Since it has been proposed that Ser/Thr residues on cytoplasmic and nuclear proteins are modified by O-linked N-acetylglucosamine (O-GlcNAc), we examined effect O-GlcNAcylation PLN rat adult cardiomyocytes. Studies using enzymatic labeling co-immunoprecipitation wild type series mutants showed...

10.1093/glycob/cwq071 article EN Glycobiology 2010-05-18

Sarcolipin (SLN) inhibits the cardiac sarco(endo)plasmic reticulum Ca(2+) ATPase (SERCA2a) by direct binding and is superinhibitory if it binds through phospholamban (PLN). To determine whether overexpression of SLN in heart might impair function, transgenic (TG) mice were generated with cardiac-specific NF-SLN (SLN tagged at its N terminus FLAG epitope). The level expression (the NF-SLN/PLN ratio) was equivalent to that which induces profound superinhibition when coexpressed PLN SERCA2a...

10.1073/pnas.0402596101 article EN Proceedings of the National Academy of Sciences 2004-06-16

Introduction Neither the pathophysiology nor an effective treatment for heart failure with preserved ejection fraction (HFpEF) has been elucidated to date. The purpose of this ongoing study is elucidate and prognostic factors patients HFpEF admitted participating institutes. We also aim obtain insights into development new diagnostic methods by analysing patient background factors, clinical data follow-up information. Methods analysis This a prospective, multicentre, observational aged ≥20...

10.1136/bmjopen-2020-038294 article EN cc-by-nc BMJ Open 2020-10-01

Extracting clinical terms from free-text format radiology reports is a first important step toward their secondary use. However, there no general consensus on the kind of to be extracted. In this paper, we propose an information model comprising three types entities: observations, findings, and modifiers. Furthermore, determine its applicability for in-house reports, extracted with state-of-the-art deep learning models compared results. We trained evaluated using 540 chest computed...

10.1016/j.jbi.2021.103729 article EN cc-by-nc-nd Journal of Biomedical Informatics 2021-03-10

Background An association between uric acid (UA) and cardiovascular diseases, including heart failure (HF), has been reported. However, whether UA is a causal risk factor for HF controversial. In particular, the prognostic value of lowering in patients with preserved ejection fraction (HFpEF) unclear. Methods Results We enrolled HFpEF from PURSUIT‐HFpEF (Prospective Multicenter Observational Study Patients With Heart Failure Preserved Ejection Fraction) registry. investigated was correlated...

10.1161/jaha.122.026301 article EN cc-by-nc-nd Journal of the American Heart Association 2022-09-21

Background— Mitochondria play pivotal roles in cell death; the loss of mitochondrial membrane potential (ΔΨ m ) is earliest event that commits to death. Here, we report novel real-time imaging ΔΨ individual cardiomyocytes within perfused rat hearts using 2-photon laser-scanning microscopy, which has unique advantages over conventional confocal microscopy: greater tissue penetration and lower toxicity. Methods Results— The Langendorff-perfused heart was loaded with a fluorescent indicator ,...

10.1161/circulationaha.106.628834 article EN Circulation 2006-09-26

The free radical scavenger 3-methyl-1-phenyl-2-pyrazolin-5-one (edaravone) is used to treat patients with ischemic brain damage. We and others reported previously that in vitro vivo reactive oxygen species (ROS) act as second messengers develop cardiac hypertrophy. In this study, we an murine model of pressure overload-induced hypertrophy examine the effects edaravone on left ventricular animals were subjected transverse thoracic aorta constriction, (10 mg/kg) was infused intraperitoneally...

10.1161/01.hyp.0000163461.71943.e9 article EN Hypertension 2005-04-12

Cardiomyocyte death plays an important role in the pathogenesis of heart failure. The nuclear factor (NF)-κB signaling pathway regulates cell death, however, effect NF-κB on can vary different cells or stimuli. purpose present study was to clarify vivo response pressure overload. First, we subjected C57Bl6/J mice overload by means transverse aortic constriction (TAC) and examined activity IκB kinase (IKK) were activated after TAC. Then, investigated activation using cardiac-specific...

10.1161/circresaha.108.193318 article EN Circulation Research 2009-05-29

Calpains make up a family of Ca(2+)-dependent intracellular cysteine proteases that include ubiquitously expressed μ- and m-calpains. Both are heterodimers consisting distinct large catalytic subunit (calpain 1 for μ-calpain calpain 2 m-calpain) common regulatory 4). The physiological roles remain unclear in the organs, including heart, but it has been suggested is activated by Ca(2+) overload diseased hearts, resulting cardiac dysfunction. In this study, cardiac-specific 4-deficient mice...

10.1074/jbc.m111.248088 article EN cc-by Journal of Biological Chemistry 2011-07-28

Cardiomyocytes proliferate during fetal life but lose their ability to soon after birth and further increases in cardiac mass are achieved through an increase cell size or hypertrophy. Mammalian target of rapamycin complex 1 (mTORC1) is critical for growth proliferation. Rheb (Ras homologue enriched brain) one the most important upstream regulators mTORC1. Here, we attempted clarify role heart using cardiac-specific Rheb-deficient mice (Rheb(-/-)). Rheb(-/-) died from postnatal day 8 10. The...

10.1074/jbc.m112.423640 article EN cc-by Journal of Biological Chemistry 2013-02-21

Background Stent thrombosis (ST) remains a significant medical issue. In particular, longer-term mortality and clinical predictors after ST occurrence have yet to be elucidated. Methods Results This was multicenter, retrospective, observational study. A total of 187 definite cases from January 2008 December 2017 were enrolled, the long-term outcomes investigated. The primary outcome measure cumulative occurrence. addition, independent assessed. Among stent types causing ST, bare-metal stent,...

10.1161/jaha.121.023276 article EN cc-by-nc-nd Journal of the American Heart Association 2022-04-04
Coming Soon ...