A5101939729- Amyloidosis: Diagnosis, Treatment, Outcomes
- Alzheimer's disease research and treatments
- Prion Diseases and Protein Misfolding
- Genetics, Aging, and Longevity in Model Organisms
- Trace Elements in Health
- Drug Transport and Resistance Mechanisms
- Peroxisome Proliferator-Activated Receptors
- Dermatological and Skeletal Disorders
- Nuclear Structure and Function
- Adipose Tissue and Metabolism
- Birth, Development, and Health
- Circadian rhythm and melatonin
- Telomeres, Telomerase, and Senescence
- Cholesterol and Lipid Metabolism
- RNA Research and Splicing
- Mitochondrial Function and Pathology
- Coenzyme Q10 studies and effects
- Neuroinflammation and Neurodegeneration Mechanisms
- Eosinophilic Disorders and Syndromes
- Neuroendocrine regulation and behavior
- Liver Disease Diagnosis and Treatment
- Endoplasmic Reticulum Stress and Disease
- Skin and Cellular Biology Research
- Genetic Associations and Epidemiology
- Diabetes and associated disorders
Shinshu University
2015-2024
Meio University
2024
Nagano University
2022-2023
Nagano University of Health and Medicine
2021-2023
Toyota Transportation Research Institute
2013-2015
Ōtani University
1998-2014
Bengbu Medical College
2011
Azabu University
2008-2011
Institute on Aging
2004-2011
Ehime University
2010
The present study was conducted to define the relationship between anti-aging effect of ubiquinol-10 supplementation and mitochondrial activation in senescence-accelerated mouse prone 1 (SAMP1) mice.Here, we report that dietary with prevents age-related decreases expression sirtuin gene family members, which results peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a major factor controls biogenesis respiration, as well superoxide dismutase 2 (SOD2) isocitrate...
Our recent studies revealed that supplementation with the reduced form of coenzyme Q10 (CoQ10H2) inhibits oxidative stress and slows process aging in senescence-accelerated mice. CoQ10H2 adipocyte differentiation regulates lipid metabolism. In present study, we show dietary significantly white adipose tissue content improved function brown by regulating expression metabolism-related factors KKAy mice, a model obesity type 2 diabetes. liver, cytoplasmic Ca2+ levels consequently inhibited...
AA amyloidosis is one of the principal causes morbidity and mortality in captive cheetahs (Acinonyx jubatus), which are danger extinction, but little known about underlying mechanisms. Given transmissible characteristics amyloidosis, transmission between may be a possible mechanism involved high incidence amyloidosis. In this study animals with we found that cheetah feces contained amyloid fibrils were different from those liver regard to molecular weight shape had greater transmissibility....
Oxidative damage in endothelial cells is proposed to play an important role dysfunction and atherogenesis. We previously reported that the reduced form of coenzyme Q10 (CoQ10H2) effectively inhibits oxidative stress decelerates senescence senescence-accelerated mice. Here, we treated human umbilical vein (HUVECs) with H2O2 investigated protective effect CoQ10H2 against senescence, damage, reduction cellular functions. found markedly number senescence-associated β-galactosidase-positive...
Two putative serum precursors which cross-react with antiserum against murine senile amyloid protein (ASSAM) were isolated from the high density lipoprotein (HDL) of normal mouse serum.Apolipoproteins designated "aPOSASsA~-I" and POSAS SASS AM-^" have same molecular weight as tissue fibril protein.ApoSASSAM-1 apoSASsAM.2migrate to an intermediate position between apoA-I apoC on alkalineurea polyacrylamide gel electrophoresis are present mainly in HDL apoproteins a slight extent very low when...
We segregated a QTL for peak BMD on Chr 13 by generating congenic sublines of the senescence-accelerated mouse SAMP6. Sfrp 4 within this locus was responsible lower SAMP6.Our genome-wide linkage study using SAMP6 and SAMP2 showed significant quantitative trait (QTL) chromosome (Chr) 13. To verify gene that regulates BMD, we generated strain, P6.P2-Pbd2(b), which carried 15-cM interval an osteoporotic background, Pbd2 increased in SAMP6.To narrow down interval, new subline P6.P2-13. studied...
Three types of apolipoprotein A-II (apoA-II) proteins (A, B and C) were predicted from the nucleotide sequence apoA-II cDNA. Substitution amino acid residues was noted at four positions (type A: Pro-5, Asp-20, Met-26, Ala-38; B: Glu-20, Val-26, Val-38; C: Gln-5, Ala-38). Each type identifiable by digestion amplified DNA PCR, using restriction-fragment-length polymorphism gene for restriction enzymes Cfr13I MspI. The molecular determined among 23 strains mice including nine senescence...
Heparan sulfate proteoglycans (HSPGs) are ubiquitous components of pathologic amyloid deposits in the organs patients with disorders such as Alzheimer's disease or systemic light chain (AL) reactive (AA) amyloidosis. Molecular imaging methods for early detection limited and generally unavailable outside United Kingdom. Therefore, there is an urgent need to develop novel, specific amyloidophilic radiotracers assist diagnosis, prognostication, monitoring response therapy. Amyloid-associated...
Apolipoprotein B (apoB) mRNA is modified by a post-transcriptional editing reaction (C to U) changing glutamine (CAA) translational stop codon (UAA) and producing apoB-48 in mammalian liver intestine.Developmental age-related changes apoB were studied using two mouse strains with different aging processes (SAM-R/1 normal process SAM-P/l an accelerated process).During growth of both strains, the proportion unedited (apoB-100) decreased from 80% fetal at 17th day gestation 30% mature...