A5088439484- Parkinson's Disease Mechanisms and Treatments
- Amyotrophic Lateral Sclerosis Research
- Neurological disorders and treatments
- Genetic Neurodegenerative Diseases
- Neuroscience and Neuropharmacology Research
- Alzheimer's disease research and treatments
- Neurological diseases and metabolism
- Autophagy in Disease and Therapy
- Nuclear Receptors and Signaling
- Mitochondrial Function and Pathology
- Nerve injury and regeneration
- Botulinum Toxin and Related Neurological Disorders
- Cardiac Arrhythmias and Treatments
- Ubiquitin and proteasome pathways
- Lysosomal Storage Disorders Research
- Neurogenetic and Muscular Disorders Research
- Atrial Fibrillation Management and Outcomes
- Coronary Interventions and Diagnostics
- Cellular transport and secretion
- interferon and immune responses
- Endoplasmic Reticulum Stress and Disease
- RNA regulation and disease
- Cardiac electrophysiology and arrhythmias
- Neuroinflammation and Neurodegeneration Mechanisms
- Cardiac Imaging and Diagnostics
Hirosaki University
2016-2025
National Hospital Organization
2016-2025
Mitsui Memorial Hospital
2025
Yokohama City University Medical Center
2024
Yokohama City University
2024
Kanagawa Cardiovascular and Respiratory Center
2020
Tokyo Women's Medical University
2007-2017
Azienda Ospedaliero-Universitaria Careggi
2017
Kanazawa Medical Center
2016
Nagoya City University
2010-2015
Degeneration of the cardiac sympathetic nerve occurs in both Parkinson's disease (PD) and dementia with Lewy bodies begins early progression PD, accounting for reduced uptake meta-iodobenzylguanidine even stages body (LBD). We previously demonstrated that degeneration distal axons precedes loss their mother neurons paravertebral ganglia, suggesting dominant PD. Because α-synuclein is one key molecules pathogenesis this disease, we further investigated how aggregates are involved...
Decreased cardiac uptake of meta ‐iodobenzylguanidine (MIBG) on [ 123 I] MIBG myocardial scintigraphy has been reported in the early stages Parkinson’s disease (PD), which suggests involvement sympathetic nerve process PD. For confirmation, we immunohistochemically examined tissue, ganglia and medulla oblongata 20 patients with incidental Lewy body (ILBD), is thought to be a presymptomatic stage PD, 10 control subjects, using antibodies against tyrosine hydroxylase (TH) neurofilament (NF)....
Many neurodegenerative diseases share a common pathological feature: the deposition of amyloid-like fibrils composed misfolded proteins. Emerging evidence suggests that these proteins may spread from cell-to-cell and encourage propagation neurodegeneration in prion-like manner. Here, we demonstrated α-synuclein (αSYN), principal culprit for Lewy pathology Parkinson's disease (PD), was present endosomal compartments detectably secreted into extracellular milieu. Unlike prion protein, αSYN...
There are regional differences in the patient characteristics, management, and outcomes of hospitalized patients with heart failure (HF). The aim this study was to evaluate clinical characteristics Japanese who HF on basis left ventricular ejection fraction (LVEF) stratum.We retrospectively conducted a multicentre cohort 1245 decompensated between 2013 2014. Of these patients, 36% had an LVEF < 40% [HF reduced (HFrEF), median age 72 years, 71% male], 21% 40-49% mid-range EF (HFmrEF), 77 56%...
Abstract Galectin-9 is a member of the galectin family and has been identified as an eosinophil chemoattractant produced by activated T lymphocytes. Vascular endothelial cells play important role in initial step recruitment activation immune inflammatory responses. We have addressed stimulation galectin-9 expression cells. was detected membrane cytosolic fractions human umbilical vein stimulated with interferon-γ (IFN-γ). IFN-γ also enhanced adhesion eosinophilic leukemia-1 to monolayers, it...
α-Synuclein is a major protein component deposited in Lewy bodies and neurites that extensively phosphorylated at Ser129, although its role neuronal degeneration still elusive. In this study, several apoptotic pathways were examined α-synuclein-overexpressing SH-SY5Y cells. Following the treatment with rotenone, mitochondrial complex I inhibitor, wild type cells demonstrated intracellular aggregations, which shared number of features bodies, overexpressing S129A mutant, phosphorylation...
Staphylococcal enterotoxins (SEs) produced by Staphylococcus aureus are the most recognizable bacterial superantigenic toxins causing food poisoning in humans throughout world. However, it remains unclear how SEs induce emesis and its emetic signal pathway. We investigated a mechanism of SEA-induced using small animal model, house musk shrew. animals was inhibited 5-hydroxytryptamine (5-HT) synthesis inhibitor 5-HT(3) receptor antagonist. SEA could increase 5-HT release intestine....
The histopathological hallmark of multiple system atrophy is the appearance intracellular inclusion bodies, named glial cytoplasmic inclusions, which are mainly composed alpha-synuclein fibrils. In vivo visualization deposition should be used for diagnosis and assessment therapy severity pathological progression in atrophy. Because 2-[2-(2-dimethylaminothiazol-5-yl)ethenyl]-6-[2-(fluoro)ethoxy] benzoxazole could stain alpha-synuclein-containing inclusions post-mortem brains, we compared...