Tokyo Metropolitan Geriatric Hospital

Tokyo, Japan

Tokyo Metropolitan Geriatric Hospital

Tokyo, Japan

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Sakata R.,Tokyo Metropolitan Geriatric Hospital | Numaga J.,University of Tokyo
Clinical Interventions in Aging | Year: 2014

Background: To compare intraocular pressure (IOP) readings using the Icare rebound tonometer (RBT) versus the Goldmann applanation tonometer (GAT) in late elderly (aged 75 years or older) subjects with or without glaucoma, and to evaluate the influence of central corneal thickness (CCT) on IOP readings. Methods: The IOP measurements were obtained using the RBT and GAT, and CCT was measured using a specular-type microscope. Bland-Altman analysis was used to assess the clinical agreement between the two instruments. The influence of CCT adjusted for age on IOP readings was analyzed by multiple linear regression analysis. Results: This study included 58 eyes of 29 normal subjects and 54 eyes of 28 glaucoma patients. The mean age was 80.7±4.3 years (normal subjects) and 83.1±5.1 years (glaucoma patients). The mean IOP readings were 13.6±3.5 mmHg and 13.2±2.8 mmHg (using the RBT and GAT, respectively) for normal subjects, and13.6±3.3 mmHg and 13.5±2.9 mmHg for glaucoma patients. The 95% confidence interval of the differences between the two instruments was -3.3 to 4.0 mmHg for normal subjects and -2.9 to 1.6 mmHg for glaucoma patients. The IOP readings by two instruments were significantly correlated with CCT in eyes with glaucoma (for the RBT, β=0.036 and P=0.002, and for the GAT, β=0.021 and P=0.033) but not in normal eyes. Conclusion: IOP readings measured using the RBT and GAT showed within the allowable range in the late elderly subjects with or without glaucoma. Eyes with glaucoma were correlated closely with CCT using each instrument. © 2014 Sakata and Numaga.

Iriyama A.,Tokyo Metropolitan Geriatric Hospital | Iriyama A.,University of Tokyo | Aihara Y.,University of Tokyo | Yanagi Y.,University of Tokyo
Retina | Year: 2013

PURPOSE: To investigate the prevalence and characteristics of outer retinal tubulation (ORT) seen in inherited retinal degenerative diseases. METHODS: A total of 354 eyes of 177 patients were examined with spectral domain optical coherence tomography. One hundred and twelve patients had retinitis pigmentosa, 58 patients had cone dystrophy, and 7 patients had the Bietti crystalline dystrophy. The images obtained by horizontal and vertical scans were analyzed to explore the possible presence of ORT, estimate their prevalence, morphologic character, and their location in the retinal layers. RESULTS: With spectral domain optical coherence tomography, ORT was identified in 0 of 112 patients with retinitis pigmentosa, unilaterally in 3 of 58 patients with cone dystrophy, and bilaterally in 5 of 7 patients with the Bietti crystalline dystrophy. Outer retinal tubulation was detected under the fovea, and in the outer nuclear layer, ORT was detected in the Bietti crystalline dystrophy with a significantly higher frequency than in cone dystrophy (P < 0.001). CONCLUSION: There was a higher rate of ORT in the Bietti crystalline dystrophy among inherited retinal degenerative diseases. Copyright © Ophthalmic Communications Society, Inc.

Endo T.,Tokyo Metropolitan Geriatric Hospital
Journal of Biochemistry | Year: 2015

Most proteins are modified by glycans, which can modulate the biological properties and functions of glycoproteins. The major glycans can be classified into N-glycans and O-glycans according to their glycan-peptide linkage. This review will provide an overview of the O-mannosyl glycans, one subtype of O-glycans. Originally, O-mannosyl glycan was only known to be present on a limited number of glycoproteins, especially α-dystroglycan (α-DG). However, once a clear relationship was established between O-mannosyl glycan and the pathological mechanisms of some congenital muscular dystrophies in humans, research on the biochemistry and pathology of O-mannosyl glycans has been expanding. Because α-DG glycosylation is defective in congenital muscular dystrophies, which also feature abnormal neuronal migration, these disorders are collectively called α-dystroglycanopathies. In this article, I will describe the structure, biosynthesis and pathology of O-mannosyl glycans. © 2014 The Authors 2014. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved.

Sawabe M.,Tokyo Metropolitan Geriatric Hospital
Geriatrics and Gerontology International | Year: 2010

The large and medium-sized arteries in elderly people show varying degrees of intimal and medial change. The medial change is known as age-related medial degeneration and sclerosis (ARMDS). The ARMDS results in systolic hypertension and left ventricular hypertrophy of the heart as a result of loss of arterial elasticity. It also causes aortic dilatation, or even aortic aneurysm. The ARMDS and atherosclerosis are distinct entities, but are often overlapped and confused with each other. The present review mainly focuses on ARMDS and briefly addresses atherosclerosis, and aging of arterioles, capillaries and veins. The smooth muscle cells in the inner half of the aortic media of elderly people degenerate and undergo apoptosis. This causes degradation of elastin fibers and the accumulation of collagen fibers in the media, but the inflammatory infiltrates are scarce. Biochemical studies showed an age-related decrease of elastin and its crosslinks, and an increase of collagen and its crosslink. Because the turnover of elastin is very long, it likely suffers from glycation (Maillard reaction) and glyco-oxidative reaction. The advanced glycation end-products accumulate in the aortic media with increasing age. Alcian-blue positive mucin accumulates in aortic media in elderly people. The major component of the increase of aortic mucin is chondroitin-6-sulfate. Microcalcification is frequent in the inner acellular portion of the aortic media in elderly people. Calcium contents increase with age. In conclusion, the ARMDS is a distinct pathological entity with clinical significance. The pathogenesis of ARMDS is unclear; the mechanical stress of elastin, endothelial dysfunction, and glycation of elastin are proposed. © 2010 Japan Geriatrics Society.

Sugihara T.,Tokyo Metropolitan Geriatric Hospital | Harigai M.,Tokyo Medical University
Drugs and Aging | Year: 2016

Elderly rheumatoid arthritis (RA) is classified into two clinical subsets, elderly-onset RA (EORA) and younger-onset elderly RA. With the improvement of life expectancy in the general population and advent of the super-aging society, the number of patients with EORA is anticipated to increase. Both large and small joints are affected initially at onset, and individuals with early EORA have higher scores of disease activity and levels of acute-phase reactants than those with early younger-onset RA. EORA is a progressive disease similar to younger-onset RA. Tumor necrosis factor (TNF) inhibitors are equally or slightly less effective in elderly patients than in younger patients with RA, and disease duration may have a greater impact on disease outcomes than age. Evidence of non-TNF biological disease-modifying antirheumatic drug use in EORA is limited. TNF inhibitors may not increase the risk for infection in elderly patients any more than methotrexate; however, increasing age is an independent and strong risk factor for serious infections in patients with RA. Treatment choice in patients with EORA is strongly influenced by comorbidities, especially cardiovascular disease, chronic lung disease, and frailty. To prevent progression to irreversible geriatric syndromes, non-frail patients with EORA, who are aging successfully should undergo intensive treatment using the treat-to-target strategy, and pre-frail and frail patients with EORA should be treated with the aim of returning to a non-frail or pre-frail stage, respectively. An appropriate treatment strategy for EORA and younger-onset elderly RA should be developed in the next decade using a multi-disciplinary approach. © 2016, The Author(s).

The purpose of this study was to examine the association between objective measures of sleep quality and obesity in older community-dwelling people. This cross-sectional study included 189 community-dwelling adults aged ≥ 80 yr (83.4 ± 2.5 yr [age range, 80-95 yr]). Participants wore an accelerometer (ActiGraph GT3X+) on their non-dominant wrist 24 hr per day for 7 consecutive nights. Sleep parameters measured included total sleep time, sleep efficiency, and wake after sleep onset (WASO) during the night. Associations between sleep parameters and obesity were investigated by using multivariate logistic regression analysis. In multivariate models, those with sleep efficiency lower than 85% had a 2.85-fold increased odds of obesity, compared with those with sleep efficiency of 85% or higher. Similarly, those with WASO of ≥ 60 min (compared with < 60 min) had a 3.13-fold increased odds of obesity. However, there were no significant associations between total sleep time or self-reported napping duration and obesity. We found that poor sleep quality was an independent risk factor for obesity in community-dwelling Japanese adults aged ≥ 80 yr, even after controlling for potential confounding factors, including daily physical activity. © 2015 The Korean Academy of Medical Sciences.

Araki A.,Tokyo Metropolitan Geriatric Hospital
Nippon rinsho. Japanese journal of clinical medicine | Year: 2010

Insulin resistance in peripheral tissues has been suggested to have a crucial role for the pathogenesis of type 2 diabetes. Diabetic people had a 1.5 to 4 fold risk for Alzheimer disease as well as vascular dementia. The insulin resistance (i.e., hyperinsulinemia) in people with impaired glucose tolerance has been one of risk factors for cognitive decline as well as atherosclerotic disease. In contrast, impaired insulin signaling and insulin resistance in brain has been found to be important role for the pathogenesis of Alzheimer disease. Peripheral hyperinsulinemia may link to cerebral insulin resistance, leading to the inhibition of removal of amyloid beta protein and the increase of tau hyperphosphorylation. Several studies have shown that insulin sensitizers (pioglitazone and rosiglitazone) improve cognition and memory in patients with mild Alzheimer disease as well as animal model of Alzheimer disease. Therefore, insulin sensitizers may have one of the effective measures of the prevention of both types of dementia in people with diabetes mellitus.

Objective: This study aimed to examine the efficacy and safety of nepafenac ophthalmic suspension compared to placebo in the management of postoperative inflammation and ocular pain in Japanese patients undergoing cataract surgery. Methods: This was a multicenter, randomized, double-masked, placebo-controlled clinical study. Patients received nepafenac or placebo TID beginning 1 day before cataract surgery and continuing on the day of surgery for 14 days. One additional drop was administered on the day of surgery. The primary efficacy variables were the percentage of patients cured at postoperative day 14 visit (cure defined as aqueous cells score + aqueous flare score = 0) and the percentage of patients who were pain free at all postoperative visits. Results: The cure rate on day 14 after surgery was 71.4% (75/105) in the nepafenac group and 28.6% (30/105) in the placebo group, showing a significant difference in cure rate between groups. The nepafenac group demonstrated higher cure rates than those in the placebo group, with a significant difference in cure rate on days 7 and 14 postoperatively. The ocular pain-free rate was 96.2% (102/106) in the nepafenac group and 67.6% (71/105) in the placebo group, showing a significant difference between groups. Concerning adverse events (AEs), 26 AEs were reported in 21 subjects (19.6%) in the nepafenac group and 31 AEs were reported in 24 subjects (22.4%) in the placebo group. Conclusion: Nepafenac ophthalmic suspension is a nonsteroidal anti-inflammatory drug effective in the prevention of postoperative inflammation and ocular pain associated with cataract surgery. © 2011 The Author(s).

Tanei R.,Tokyo Metropolitan Geriatric Hospital | Hasegawa Y.,Tokyo Metropolitan Geriatric Hospital | Sawabe M.,Tokyo Metropolitan Geriatric Hospital
Journal of the European Academy of Dermatology and Venereology | Year: 2013

Background/Objectives: Atopic dermatitis (AD) in the elderly is gradually increasing in industrialized countries in association with the aging of society. We report herein four cases of elderly AD {three extrinsic [immunoglobulin (Ig)E-mediated allergy]; one intrinsic (non-IgE-allergy)} in which we investigated the presence of IgE+ cells in lesional skin. Methods/Results Single immunohistochemical and double immunofluorescence stainings were performed for skin biopsy specimens from AD patients and non-atopic control subjects with chronic eczema. In the lesional lichenified skin of patients with extrinsic elderly AD, numerous IgE+ cells were found among inflammatory cells infiltrates in the upper dermis. Comparative analysis of single immunohistochemistry results using serial paraffin and/or frozen sections found that many IgE+ cells showed identical distributions to tryptase+ mast cells. IgE+ cells coincident with CD1a+ Langerhans cells in the epidermis were found in small numbers only in frozen sections. Double immunofluorescence staining for IgE and CD11c revealed cells coexpressing IgE and CD11c with a dendritic morphology in the papillary and upper dermis. These IgE+ mast cells and IgE+ CD11c+ cells were also found in cured normal-looking skin from a patient with extrinsic elderly AD after successful treatment. Although only a few weakly positive IgE+ cells were detected, no IgE+CD11c+ cells were found in specimens from patients with intrinsic elderly AD or non-atopic chronic eczema. Conclusion: IgE-mediated allergic inflammation may play an important role in the pathobiology of elderly AD, similar to other age groups of AD. © 2012 European Academy of Dermatology and Venereology.

Kanemaru K.,Tokyo Metropolitan Geriatric Hospital
Brain and Nerve | Year: 2013

Aberrant protein aggregation is closely linked to the molecular pathogeneses of most neurodegenerative diseases. The major components of pathological aggregates have been characterized in various neurodegenerative diseases; for example, amyloid β-protein and phosphorylated tau in Alzheimer's disease, α-synuclein in Parkinson's disease, SOD1 or TDP-43 in amyotrophic lateral sclerosis, and huntingtin in Huntington's disease. These misfolded protein aggregates play a vital role in disease initiation and progression, and they have recently been shown to have prion-like spreading or seeded aggregation properties. Immunotherapy with specific monoclonal antibodies is a promising approach to clear misfolded protein aggregates and treat various neurodegenerative diseases; it is planned for use in clinical trials in the near future.

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