記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Frontiers in Aging Neuroscience  

Introduction: Cerebral white matter hyperintensities (WMHs) are commonly found in the aging brain and have been implicated in the initiation and severity of many central nervous system diseases. Furthermore, an increased WMH volume indicates reduced brain health in older adults. This study investigated the association between WMH volume and physical activity in older adults with depressive symptoms (DS) and mild memory impairment (MMI). Factors associated with the WMH volume were also investigated. Methods: A total of 57 individuals aged over 65 years with DS and MMI were included in this study. The participants underwent magnetic resonance imaging to quantify WMH volumes. After WMH volume was accumulated, normalized to the total intracranial volume (TIV), the percentage of WMH volume was calculated. In addition, all participants wore a triaxial accelerometer for 2 weeks, and the average daily physical activity and number of steps were measured. The levels of blood biomarkers including cortisol, interleukin-6 (IL-6), brain-derived insulin-like growth factor-1, and brain-derived neurotrophic factor were measured. Motor and cognitive functions were also assessed. Results: Faster maximum walking speed and longer time spent engaged in moderate physical activity were associated with a smaller percent of WMH volume, whereas higher serum IL-6 levels were associated with a larger percent of WMH volume. The number of steps per day, time spent engaged in low levels of physical activity, cognitive function, and all other measured biomarkers were not significantly associated with percent of WMH volume. Discussion: Higher blood inflammatory cytokine levels, shorter duration of moderate physical activity, and lower maximum walking speed were associated with a higher percent of WMH volume. Our results provide useful information for maintaining brain health in older adults at a high risk of developing dementia and may contribute to the development of preventive medicine for brain health.

DOI： 10.3389/fnagi.2024.1337397

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記述言語：日本語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Scientific Reports  

Remote ischemic perconditioning (RIPerC) is a novel neuroprotective method against cerebral infarction that has shown efficacy in animal studies but has not been consistently neuroprotective in clinical trials. We focused on the temporal regulation of ischemia–reperfusion by RIPerC to establish an optimal method for RIPerC. Rats were assigned to four groups: 10 min ischemia, 5 min reperfusion; 10 min ischemia, 10 min reperfusion; 5 min ischemia, 10 min reperfusion; and no RIPerC. RIPerC interventions were performed during ischemic stroke, which was induced by a 60-min left middle cerebral artery occlusion. Infarct volume, sensorimotor function, neurological deficits, and cellular expressions of brain-derived neurotrophic factor (BDNF), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and caspase 3 were evaluated 48 h after the induction of ischemia. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) was also performed. RIPerC of 10 min ischemia/10 min reperfusion, and 5 min ischemia/10 min reperfusion decreased infarct volume, improved sensorimotor function, decreased Bax, caspase 3, and TUNEL-positive cells, and increased BDNF and Bcl-2 expressions. Our findings suggest RIPerC with a reperfusion time of approximately 10 min exerts its neuroprotective effects via an anti-apoptotic mechanism. This study provides important preliminary data to establish more effective RIPerC interventions.

DOI： 10.1038/s41598-023-29475-2

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Aging  

5’-Adenosine monophosphate-activated protein kinase (AMPK) is a metabolic sensor that serves as a cellular housekeeper; it also controls energy homeostasis and stress resistance. Thus, correct regulation of this factor can enhance health and survival. AMPK signaling may have a critical role in aging-associated brain diseases. Some in vitro studies have shown that 1,5-anhydro-D-fructose (1,5-AF) induces AMPK activation. In the present study, we experimentally evaluated the effects of 1,5-AF on aging-associated brain diseases in vivo using an animal model of acute ischemic stroke (AIS), stroke-prone spontaneously hypertensive rats (SHRSPs), and the spontaneous senescence-accelerated mouse-prone 8 (SAMP8) model. In the AIS model, intraperitoneal injection of 1,5-AF reduced cerebral infarct volume, neurological deficits, and mortality. In SHRSPs, oral administration of 1,5-AF reduced blood pressure and prolonged survival. In the SAMP8 model, oral administration of 1,5-AF alleviated aging-related decline in motor cognitive function. Although aging reduced the expression levels of peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α) and brain-derived neurotrophic factor (BDNF), we found that 1,5-AF activated AMPK, which led to upregulation of the PGC-1α/BDNF pathway. Our results suggest that 1,5-AF can induce endogenous neurovascular protection, potentially preventing aging-associated brain diseases. Clinical studies are needed to determine whether 1,5-AF can prevent aging-associated brain diseases.

DOI： 10.18632/aging.205228

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記述言語：日本語   出版者・発行元：(一社)日本基礎理学療法学会  

その他リンク： https://search.jamas.or.jp/default/link?pub_year=2023&ichushi_jid=J07591&link_issn=&doc_id=20231108350001&doc_link_id=%2Fch1ufund%2F2023%2F002601%2F001%2F0001-0010%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fch1ufund%2F2023%2F002601%2F001%2F0001-0010%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Arthritis Research and Therapy  

Background: Osteoarthritis (OA) is a degenerative joint disease associated with aging, which often leads to joint stiffness and disability. Exercise is one of the most important non-pharmacological treatments and is prescribed as an indispensable treatment for OA. However, whether physical exercise is beneficial for preventing the progression of OA symptoms with age is poorly understood. We investigated the effects of exercise on spontaneously developed knee OA using male senescence-accelerated mouse prone 8 (SAMP8). Methods: To examine age-related changes in the knee joints of SAMP8, knee articular cartilage changes, synovitis, knee joint flexion and extension angles, swelling, walking ability, and quadriceps muscle atrophy were analyzed at 3, 5, 7, and 9 months. SAMP8 were required to run at a speed of 10 m/min for 15 min/day from 7 to 9 months of age. The knee joint pathologies and symptoms of exercising and non-exercising mice were compared by histological, immunohistochemical, and morphometrical analyses. Results: The mice presented with various histological changes, including cartilage destruction, osteocyte formation, synovitis, declined joint angles, and swelling. Notably, medial and posterior cartilage destruction was more severe than that of the lateral and anterior cartilage. Knee joint angles were significantly correlated with the histological scores (modified Mankin and OARSI, osteophyte formation and synovial lining cell layer). Exercise did not attenuate cartilage degeneration in the medial and posterior tibial plateau, although the articular cartilage of the anterior and lateral tibial plateau and its histological scores was remained and significantly improved, respectively, by exercise. Exercise suppressed the age-related decline of collagen type II-positive areas in the remaining articular cartilage and improved the OA symptoms. Exercise reduced the expression of monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-α positive macrophages in the synovium. Conclusion: This study revealed that SAMP8 developed spontaneous knee OA with age, which resembled the disease symptoms in humans. Low-intensity exercise temporarily alleviated degeneration of the remaining cartilage, synovitis, and age-related decreases in knee flexion angle, stride length, and muscle atrophy in SAMP8. However, exercise during OA progression with age may cause mechanical stress that could be both beneficial and detrimental to joint health.

DOI： 10.1186/s13075-023-03162-z

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Neuroscience Letters  

Physical exercise is beneficial for preventing Alzheimer's disease (AD) and cognitive decline through several mechanisms, including suppression of neuroinflammation and neuronal loss in the hippocampus. Despite these exercise-induced benefits in AD pathology, less attention has been paid to the importance of maintaining exercise and the consequences of detraining. This study aimed to investigate the effects of early exercise intervention and detraining on age-related cognitive decline and its protective mechanisms using senescence-accelerated mouse prone 8 (SAMP8). These mice were divided to four groups: no-exercise (No-Ex, n = 9), 4 months (4 M)-detraining (n = 11), 2 months (2 M)-detraining (n = 11), and long-term exercise (LT-Ex, n = 13). Age-related cognitive decline was prevented in the LT-Ex group compared with the No-Ex group through the suppression of neuronal loss, enhanced brain-derived neurotrophic factor (BDNF), and inhibition of neuroinflammation corresponding to reduced M1 and increased M2 microglia in the hippocampus. No significant differences were observed in cognitive function between the detraining and No-Ex groups. However, the 2 M−detraining group showed increased BDNF positive area in the CA1 region and the enhancement of anti-inflammatory M2 phenotype microglia. In contrast, no statistically beneficial exercise-induced changes in the hippocampus were observed in the 4 M−detrainig group. These results showed that early exercise intervention prevented age-related cognitive deficits in AD progression by suppressing neuronal loss and neuroinflammation in the hippocampus. Exercise-induced benefits, including the anti-inflammation in the hippocampus, may be retained after exercise cessation, even if exercise-induced beneficial effects decline in a time-dependent manner.

DOI： 10.1016/j.neulet.2023.137297

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Journal of Ethnopharmacology  

Ethnopharmacological relevance: Ninjin'yoeito (NYT), a traditional Japanese Kampo medicine consisting of 12 herbs, has been reported to improve cognitive dysfunction, depression, and neurological recovery in patients with neurovascular diseases such as Alzheimer's disease and stroke. Several studies have reported that the NYT components exert neurotrophic, neurogenic, and neuroprotective effects. In addition, exercise enhances neuroprotection and functional recovery after stroke. Rehabilitative exercises and pharmacological agents induce neurophysiological plasticity, leading to functional recovery in stroke patients. These reports indicate that NYT treatment and exercise may promote functional recovery following stroke through their beneficial effects. However, no study has determined the effects of NYT and the possible mechanisms of neurorepair and functional recovery after stroke. Aim of the study: This study aimed to investigate the combined effects of NYT and exercise on neuroprotection and functional recovery and the underlying mechanisms in a rat ischemic stroke model. Materials and methods: Stroke was induced with 60-min middle cerebral artery occlusion (MCAO) followed by reperfusion in adult male Sprague-Dawley rats. After stroke, the rats were assigned to four groups: ischemia reperfusion (IR), NYT, exercise (Ex), and NYT + Ex. NYT-treated rats were fed a diet containing 1% NYT one day after stroke. Exercise was performed using a motorized treadmill for 5 days a week (8–15 m/min, 20 min/day), starting 3 days after stroke. The NYT treatment and exercise were continued for 4 weeks after the stroke. Infarct volume, neurological deficits, sensorimotor functions, expression of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase A (TrkA) and B (TrkB), caspase-3 activity, and the p-Akt/Akt ratio were examined by immunohistochemistry and western blotting. Results: Compared to the IR group, all treated groups indicated reduced infarct volumes. The NYT + Ex group showed significantly improved waking time and beam walking score compared with the IR group. The expression of NGF/TrkA/p-TrkA and BDNF/TrkB was significantly increased in the NYT + Ex group compared with those in the IR group, whereas the number of caspase-3 positive cells around the lesion was significantly lower in the NYT + Ex group than in the IR group. In addition, the ratio of p-Akt/Akt was significantly higher in the NYT + Ex group than in the IR group. Conclusions: This study suggests that NYT in combination with exercise provides neuroprotective effects and improves sensorimotor function by stimulating NGF/TrkA and BDNF/TrkB, and by activating the Akt pathway in ischemic stroke of rats. NYT may be an effective adjunctive agent in post-stroke rehabilitation.

DOI： 10.1016/j.jep.2022.115927

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記述言語：日本語   出版者・発行元：一般社団法人 日本基礎理学療法学会  

DOI： 10.24780/jjptf.p-01-20

CiNii Research

記述言語：日本語   出版者・発行元：一般社団法人 日本基礎理学療法学会  

<p>　本研究は自然発症型変形性膝関節症（以下，膝OA）を呈する老化促進マウス（SAMP8）を用いて，トレッドミル運動と水泳がOA病態，関節可動域，横径，歩容に及ぼす影響を調べ，運動効果の違いを明らかにすることを目的とした。マウスを非運動群，トレッドミル運動群，水泳群（各6匹）に無作為に分類した。トレッドミル運動は速度10～12 m/min，水泳は水温37～38℃で，15分/ 日，週5日，6週間実施した。非運動群と比較して，両運動群は膝関節可動域や歩幅の改善を示した。さらにII 型コラーゲン陽性軟骨細胞の増加，MMP-13陽性軟骨細胞の減少，滑膜のTNF-<i>α</i>陽性細胞の減少を認めた。特に水泳群の歩幅は有意な改善を認め，軟骨恒常性維持に重要なタンパク質であるII型コラーゲン陽性軟骨細胞は有意に増加していた。本研究は，運動が加齢による軟骨変性を緩和し，関節可動域や歩容を改善させることを示した。また，水泳が膝OA軟骨の恒常性維持や歩容改善に有益であることを示唆した。</p>

DOI： 10.24780/jjptf.jjptf_2023-01

CiNii Research

記述言語：日本語   掲載種別：研究論文（学術雑誌）   出版者・発行元：International Journal of Molecular Sciences  

Physical frailty is an aging-related clinical syndrome involving decreases in body weight, mobility, activity, and walking speed that occurs in individuals with sarcopenia and is accelerated by increased oxidative stress. Ninjin’yoeito, a traditional Japanese Kampo medicine, is used for treating conditions, including anemia and physical weakness. Here, we investigated whether ninjin’yoeito could improve physical frailty by controlling oxidative stress in the senescence-accelerated mouse prone 8 (SAMP8) model. First, SAMP8 mice were divided into two groups, ninjin’yoeito treated and untreated, with the former consuming a diet containing 3% ninjin’yoeito from 3 months of age. At 7 months of age, body weight, motor function, locomotor activity, and mean walking speed were measured. Subsequently, mice were euthanized and measured for muscle weight, 8-hydroxy-2′-deoxyguanosine levels in muscle and brain, and cleaved caspase-3 expression in brain. The results showed reductions in weight, locomotor function, locomotion, and average walking speed in the untreated group, which were significantly improved by ninjin’yoeito. Furthermore, 8-hydroxy-2′-deoxyguanosine levels were reduced in muscle and brain from ninjin’yoeito-treated mice, compared with the levels in untreated mice; cleaved caspase-3 expression was similarly reduced in brain from the treated mice, indicating reduced apoptosis. Our findings suggest that ninjin’yoeito inhibits sarcopenia-based physical frailty through its antioxidant effects.

DOI： 10.3390/ijms231911183

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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：International Journal of Molecular Sciences  

Knee arthrofibrosis is a common complication of knee surgery, caused by excessive scar tissue, which results in functional disability. However, no curative treatment has been established. E8002 is an anti-adhesion material that contains L-ascorbic acid, an antioxidant. We aimed to evaluate the efficacy of E8002 for the prevention of knee arthrofibrosis in a rat model, comprising injury to the surface of the femur and quadriceps muscle 1 cm proximal to the patella. Sixteen male, 8week-old Sprague Dawley rats were studied: in the Adhesion group, haemorrhagic injury was induced to the quadriceps and bone, and in the E8002 group, an adhesion-preventing film was implanted between the quadriceps and femur after injury. Six weeks following injury, the restriction of knee flexion owing to fibrotic scarring had not worsened in the E8002 group but had worsened in the Adhesion group. The area of fibrotic scarring was smaller in the E8002 group than in the Adhesion group (p < 0.05). In addition, the numbers of fibroblasts (p < 0.05) and myofibroblasts (p < 0.01) in the fibrotic scar were lower in the E8002 group. Thus, E8002 reduces myofibroblast proliferation and fibrotic scar formation and improves the range of motion of the joint in a model of knee injury.

DOI： 10.3390/ijms23031239

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記述言語：日本語   出版者・発行元：一般社団法人 日本基礎理学療法学会  

DOI： 10.24780/jjptf.o-1-6-2

CiNii Research

記述言語：日本語   出版者・発行元：一般社団法人 日本基礎理学療法学会  

DOI： 10.24780/jjptf.p-2-1-7

CiNii Research

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Scientific Reports  

The gut microbiota has tremendous potential to affect the host’s health, in part by synthesizing vitamins and generating nutrients from food that is otherwise indigestible by the host. 1,5-Anhydro-d-fructose (1,5-AF) is a monosaccharide with a wide range of bioactive potentials, including anti-oxidant, anti-inflammatory, and anti-microbial effects. Based on its potential benefits and minimal toxicity, it is anticipated that 1,5-AF will be used as a dietary supplement to support general health. However, the effects of 1,5-AF on the gut microbiota are yet to be clarified. Here, using an unbiased metagenomic approach, we profiled the bacterial taxa and functional genes in the caecal microbiota of mice fed a diet containing either 2% 1,5-AF or a reference sweetener. Supplementation with 1,5-AF altered the composition of the gut microbiota, enriching the proportion of Faecalibacterium prausnitzii. 1,5-AF also altered the metabolomic profile of the gut microbiota, enriching genes associated with nicotinamide adenine dinucleotide biosynthesis. These findings support the potential benefits of 1,5-AF, but further studies are required to clarify the impact of 1,5-AF on health and disease.

DOI： 10.1038/s41598-021-99052-y

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：International Journal of Molecular Sciences  

Mitochondrial functional abnormalities or quantitative decreases are considered to be one of the most plausible pathogenic mechanisms of Parkinson’s disease (PD). Thus, mitochondrial complex inhibitors are often used for the development of experimental PD. In this study, we used rotenone to create in vitro cell models of PD, then used these models to investigate the effects of 1,5-anhydro-D-fructose (1,5-AF), a monosaccharide with protective effects against a range of cytotoxic substances. Subsequently, we investigated the possible mechanisms of these protective effects in PC12 cells. The protection of 1,5-AF against rotenone-induced cytotoxicity was confirmed by increased cell viability and longer dendritic lengths in PC12 and primary neuronal cells. Furthermore, in rotenone-treated PC12 cells, 1,5-AF upregulated peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) expression and enhanced its deacetylation, while increasing AMP-activated protein kinase (AMPK) phosphorylation. 1,5-AF treatment also increased mitochondrial activity in these cells. Moreover, PGC-1α silencing inhibited the cytoprotective and mitochondrial biogenic effects of 1,5-AF in PC12 cells. Therefore, 1,5-AF may activate PGC-1α through AMPK activation, thus leading to mitochondrial biogenic and cytoprotective effects. Together, our results suggest that 1,5-AF has therapeutic potential for development as a treatment for PD.

DOI： 10.3390/ijms22189941

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Brain Structure and Function  

Preconditioning exercise prior to stroke exerts neuroprotection, which is an endogenous strategy that leads the brain cells to express several intrinsic factors and inhibits their apoptosis. However, it is unclear how long these benefits last after exercise cessation. The aim of this study was to investigate the effects of detraining on preconditioning exercise-induced neuroprotective potential after stroke. Rats were trained using a treadmill for aerobic exercise 5 days each week for 3 weeks, and their neuroprotective effects were examined until 3 weeks after exercise cessation. Stroke was induced by 60 min of left middle cerebral artery occlusion at 3 days, 1, 2, and 3 weeks after exercise cessation. Infarct volume, neurological deficits, sensorimotor function, expression levels of brain-derived neurotrophic factor (BDNF), hypoxia-induced factor-1α (HIF-1α), glial fibrillary acidic protein (GFAP), and P2X7 receptors, and apoptosis activity were examined using immunohistochemical and western blot analyses. Preconditioning exercise significantly reduced infarct volume and ameliorated sensorimotor function after stroke, and its beneficial effects were observed until 2 weeks after exercise cessation. The expression level of BDNF in the ischemic brain was significantly upregulated at 3 days after exercise cessation; however, the expression levels of HIF-1α, GFAP, and P2X7 receptor were significantly increased until 2 weeks after exercise cessation; thereby, significant anti-apoptotic effects were lost at 3 weeks of detraining. Our findings suggest that preconditioning exercise-induced neuroprotective potential may be lost shortly after exercise cessation. Neuroprotection through intrinsic protective factors, such as BDNF and HIF-1α, may provide different neuroprotective mechanisms in a time-dependent manner during detraining.

DOI： 10.1007/s00429-021-02317-5

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Molecular Neurobiology  

Subarachnoid hemorrhage (SAH) is a catastrophic form of stroke responsible for significant morbidity and mortality. Oxidative stress, inflammation, and neuronal apoptosis are important in the pathogenesis of early brain injury (EBI) following SAH. Preconditioning exercise confers neuroprotective effects, mitigating EBI; however, the basis for such protection is unknown. We investigated the effects of preconditioning exercise on brain damage and sensorimotor function after SAH. Male rats were assigned to either a sham-operated (Sham) group, exercise (Ex) group, or no-exercise (No-Ex) group. After a 3-week exercise program, they underwent SAH by endovascular perforation. Consciousness level, neurological score, and sensorimotor function were studied. The expression of nuclear factor erythroid 2 p45-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), 4-hydroxynonenal (4HNE), nitrotyrosine (NT), ionized calcium-binding adaptor molecule 1 (Iba1), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), interleukin 1β (IL-1β), 14–3-3γ, p-β-catenin Ser37, Bax, and caspase-3 were evaluated by immunohistochemistry or western blotting. The terminal deoxynucleotidyl transferase-mediated biotinylated dUTP nick end labeling (TUNEL) assay was also performed. After SAH, the Ex group had significantly reduced neurological deficits, sensorimotor dysfunction, and consciousness disorder compared with the No-Ex group. Nrf2, HO-1, and 14–3-3γ were significantly higher in the Ex group, while 4HNE, NT, Iba1, TNF-α, IL-6, IL-1β, Bax, caspase-3, and TUNEL-positive cells were significantly lower. Our findings suggest that preconditioning exercise ameliorates EBI after SAH. The expression of 4HNE and NT was reduced by Nrf2/HO-1 pathway activation; additionally, both oxidative stress and inflammation were reduced. Furthermore, preconditioning exercise reduced apoptosis, likely via the 14–3-3γ/p-β-catenin Ser37/Bax/caspase-3 pathway.

DOI： 10.1007/s12035-021-02506-7

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記述言語：日本語   出版者・発行元：コ・メディカル形態機能学会  

記述言語：日本語   出版者・発行元：IEEE Transactions on Applied Superconductivity  

As a high-temperature superconducting (HTS) conductor with a large current capacity applicable to a nuclear fusion experimental device, REBCO (REBa2CuOy) tapes and high-purity aluminum sheets are alternately laminated, placed in a groove of an aluminum alloy jacket having a circular cross section, and the lid is friction-stir welded. To make the current distribution and mechanical characteristics uniform, the conductor is twisted at the end of the manufacturing process. In the early prototype conductor, when the Ic was measured in liquid nitrogen under self-magnetic field conditions, Ic degradations were observed from the beginning, and the characteristic difference between the two prototype samples under the same manufacturing conditions were large. Furthermore, Ic degradation was progressed by repeating the thermal cycle from room temperature to liquid nitrogen temperature. This Ic degradation did not occur uniformly in the longitudinal direction of the conductor but was caused by local Ic degradation occurring at multiple locations. If the conductor was not manufactured uniformly in the longitudinal direction, the difference in thermal shrinkage between the REBCO tape and the aluminum alloy jacket caused local stress concentration in the REBCO tape and buckling occurred. Element experiments to explain this mechanism were conducted to clarify the conditions under which Ic degradation due to buckling occurs. Then prototype conductors were tested with improved manufacturing methods, and as a result, Ic degradation could be suppressed to 20% or less. We have achieved the prospect of producing a conductor with uniform characteristics in the longitudinal direction.

DOI： 10.1109/TASC.2021.3069923

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Experimental Neurology  

It is well known that physical exercise reduces the risk of Alzheimer's disease (AD) and age-related cognitive decline. However, its mechanisms are still not fully understood. This study aimed to investigate the effect of aging and rotarod exercise (Ex) on cognitive function and AD pathogenesis in the hippocampus using senescence-accelerated mice prone 8 (SAMP8). Cognitive functions clearly declined at 9-months of age. Amyloid-beta (Aβ) deposition, neuronal loss, and glia activation-induced neuroinflammation increased with aging. The rotarod Ex prevented the decline of cognitive functions corresponding to the suppression of Aβ deposition, neuroinflammation, neuronal loss, inducible nitric oxide synthase (NOS) activities, and neuronal NOS activities. In addition, the rotarod Ex suppressed proinflammatory M1 phenotype microglia and A1 phenotype astrocytes. Our findings suggest that low-intensity motor balance and coordination exercise prevented age-related cognitive decline in the early stage of AD progression, possibly through the suppression of hippocampal Aβ deposition, neuronal loss, oxidative stress, and neuroinflammation, including reduced M1 and A1 phenotypes microglia and astrocytes.

DOI： 10.1016/j.expneurol.2020.113590

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記述言語：英語   掲載種別：学位論文（博士）   出版者・発行元：Journal of Neuroinflammation  

DOI： 10.1186/s12974-020-1709-8

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出版者・発行元：International Journal of Environmental Research and Public Health  

DOI： 10.3390/ijerph17155337

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出版者・発行元：International Journal of Molecular Sciences  

DOI： 10.3390/ijms21113972

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PubMed

出版者・発行元：Neurological Research  

DOI： 10.1080/01616412.2019.1580458

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PubMed

出版者・発行元：Brain Structure and Function  

DOI： 10.1007/s00429-018-1815-x

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PubMed

出版者・発行元：Brain Structure and Function  

DOI： 10.1007/s00429-018-1800-4

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PubMed

出版者・発行元：公益社団法人 日本理学療法士協会  

<p>【はじめに、目的】</p><p>腰椎変性すべり症は，加齢による退行変性の代表的な疾患である。また、椎間関節水腫(facet effusion:FE)は腰椎変性すべりの生じている椎間関節裂隙部にT2強調画像で高輝度の変化を示す。本研究の目的はすべり症患者のFEの存在率やすべり椎間以外のFEの有無を調査し、さらに、FEと椎体周囲筋の断面積測定を行う。そして、腰部疾患を有さない高齢者との比較やすべりの程度での比較、すべりの程度、FE、筋断面積の関連性の検討を行うことである。</p><p>【方法】</p><p>腰椎変性すべり症と診断されたL4/5変性すべり症患者36名（すべり症群：男性7名、女性29名、66.3±8.8歳）を対象とした。また、腰椎疾患を有さない高齢者10名（男性4名、女性6名、63.8±11.3歳）を対照群とした。側方X線画像、MRI画像正中矢状断面像を用いて、Meyerding分類によるL4/5すべりの程度とTaillard法によるL4/5椎体すべり率を計測した。さらに、L4/5椎体の不安定性の評価としてX線（立位）とMRI（臥位）におけるすべり率の差を算出し、3%を基準に椎体不安定性を評価した。L3/4、L4/5、L5/S1におけるFEの有無や面積を測定した。さらに、L4下部レベルの大腰筋と脊柱起立筋の筋断面積を測定した。また、脂肪を含めた非収縮性組織（筋内の高輝度に表出されている部分）を測定し、筋断面積から非収縮性組織の差として除脂肪面積を算出した。さらに、脂肪面積と除脂肪面積から脂肪率を算出した。FEや筋断面積の計測にはMRIのT2強調画像を用いた。臨床症状としてL4/5すべり症患者の25名の痛みの程度（VAS）をカルテより収集した。統計処理は各群の正規性検定を行い、その後の統計学的検定を選択し検討した。有意水準は5%とし、統計処理ソフトは、SPSS(Version20, IBM, USA)を使用した。</p><p>【結果】</p><p>FEはすべり症群の100%、対照群の90%に観察された。対照群のFE面積はすべり症群と比較してL4/5椎体間で有意に小さかった（p<0.01）。Meyerding分類1°群や椎体不安定性3%以上群のFE面積は対照群と比較して有意に大きかった。すべり症群のすべり率や痛みの程度が大腰筋面積と有意な負の相関関係を認めた(r=-0.40、r=-0.41、p<0.05）。また、すべり率と脊柱起立筋の脂肪率に有意な正の相関を認めた(r=0.42、p<0.01)</p><p>【結論（考察も含む）】</p><p>L4/5すべり症群だけでなく対照群においてもFEが観察され、FEは椎間不安定性だけでなく椎体や椎間関節の加齢変化により生じる可能性が示唆された。L4/5すべり症患者では近接する椎体関節にもFEが観察され、椎間不安定性はFEの大きさに影響することが示唆された。椎体のすべり率や疼痛は大腰筋と関係があり、姿勢変化との関係が示唆された。すべり率と脊柱起立筋の脂肪率に正の相関があり、脊柱起立筋内の質的変化とすべりの程度に関係があることが示唆された。</p><p>【倫理的配慮，説明と同意】</p><p>本研究は霧島整形外科倫理審査委員会の承認（承認番号：00006）を得て行った。</p>

DOI： 10.14900/cjpt.46S1.H2-7_2

CiNii Research

出版者・発行元：コ・メディカル形態機能学会  

<p>腹部深層筋の収縮は胸腰筋膜を介した腰椎の剛性の増加や腹腔内圧の増加に関与し、姿勢保持や腰椎の安定性に重要な役割を持っている。本研究は超音波診断（エコー）装置を用いて、側腹筋の加齢変化と腰椎術後患者の安静、Draw-in、頭部挙上における側腹筋筋厚変化を調べることを目的とした。手術目的で当院に入院した中高年期の男性腰椎変性疾患患者13名（腰椎患者群、平均年齢：67歳）を対象とした。また、加齢による体幹筋変化を調べるために健常若年男性10名（若年者群、平均年齢22歳）を対照とした。エコー装置を用いて腹横筋、内・外腹斜筋の筋厚を計測した。腰椎患者群は術前、術後2日、術後7日に計測を行った。加齢による変化では、腹横筋筋厚に大きな変化は認められなかったが、安静時外腹斜筋は腰椎患者群で約51％有意に低下していた（p＝0.0001）。中高年期の腰椎患者群は若年者と比較して脂肪組織や非収縮性組織が増加しており、その傾向は深層筋より表層筋に著明であった。術前術後の変化では、安静時腹横筋筋厚は術前と比較して術後7日で約17％有意に低下していた（p＝0.012）。術後のDraw-in、頭部挙上により腹横筋、内腹斜筋の筋厚は増加した。本研究は、側腹筋の加齢変化が深層筋より表層筋に顕著であり、Draw-inや頭部挙上は表層筋より深層筋を活性化させることを示した。また、腰椎術後患者は手術侵襲や安静による活動量の低下により術後早期に腹横筋の萎縮を生じる可能性があることを示唆した。</p>

DOI： 10.11172/keitaikinou.18.2

CiNii Research

出版者・発行元：公益社団法人 日本理学療法士協会  

<p>【はじめに、目的】細胞内には内在性保護因子が存在し、それらは脳虚血などの病態から細胞を保護するために活性化される。また、運動は、脳梗塞後に神経保護効果をもたらすことが報告され、そのメカニズムには内因性保護因子の活性化が関与している。本研究では、そのような内因性保護因子の中から転写因子の一つであるHIF-1α、内因性保護タンパクである14-3-3γに着目し、定期的な運動介入による脳虚血耐性の獲得と脳梗塞後の神経保護メカニズムについて調べた。</p><p>【方法】7週齢の雄性SDラット26匹を用い、3週間のトレッドミル運動群 (Ex-only群、n=6)、運動後に脳梗塞を作製する群(Ex群、n=7)、運動介入せず脳梗塞を作製する群(No-Ex群、n=7)、正常対照群(Control群、n=6)、の4群に分類した。トレッドミル運動は25m/minで30分/日、週5回行った。No-Ex群とControl群はゲージ内で3週間自由飼育した。運動終了後に60分間の虚血と再灌流障害により脳梗塞を作製し、脳梗塞作製48時間後に神経学的所見や運動機能評価を行い、脳を採取した。脳梗塞巣の体積、HIF-1α、14-3-3γ、活性化アストロサイトのマーカーであるGFAP、神経細胞のマーカーであるNeuN、アポトーシスに関与するBax、Caspase 3の発現を免疫組織化学染色及びWestern blotting法を用いて調べた。</p><p>【結果】定期的な運動介入による脳内変化に関して、Ex-only群のHIF-1αと14-3-3γの発現が有意に増加し(ｐ<0.05)、神経細胞やアストロサイト上で発現が観察された。脳梗塞作成後には、Ex群の脳梗塞巣の体積がNo-Ex群と比べて有意に小さく(p<0.05)、運動機能は有意に改善していた(p<0.05)。脳梗塞発症後には、No-Ex群に比べ、Ex群で14-3-3γの発現量が有意に増加し(p<0.05)、Bax、Caspase 3の発現は有意に減少していた(p<0.05)。</p><p>【考察】3週間の運動介入を行うことで内因性保護因子であるHIF-1α、14-3-3γの発現を誘導することが明らかとなり、虚血応答に対するこれらの因子が増加することは、運動によって脳虚血耐性が獲得出来たことを示唆している。我々の先行研究では予防的な運度介入は脳梗塞後の血管新生促進、グリア細胞の増殖促進、神経栄養因子の発現増加が生じることを報告しており、今回の運動群における脳梗塞後の神経保護メカニズムにはHIF-1αの発現に伴う14-3-3γ発現増加、血管新生促進、神経栄養因子の発現増加、14-3-3γのBax制御によるポトーシス抑制が関与していることが示唆された。</p><p>【結論】我々の研究は、予防理学療法の視点から運動による脳虚血耐性の獲得と脳梗塞後の神経保護効果とそのメカニズムを明らかにした。</p><p>【倫理的配慮，説明と同意】本研究は鹿児島大学動物実験委員会の承認を得て実施した。</p>

DOI： 10.14900/cjpt.46S1.I-56_1

CiNii Research

出版者・発行元：公益社団法人 日本理学療法士協会 九州ブロック会  

<p>【目的】</p><p>加齢に伴う腰椎変性疾患患者の腹部体幹筋の量的・質的変化に関する報告は少ない。本研究は超音波診断（エコー）装置を用いて、脊椎変性疾患を伴った中高齢者の安静、Draw-in、頭部挙上による側腹筋の筋厚や筋輝度を若年者と比較し、加齢による影響を調べた。さらに、腰椎手術前、術後早期の側腹筋の筋厚変化と術後早期のDraw-in、頭部挙上による腹部深層筋の筋厚を測定し、手術侵襲が腹部体幹筋に及ぼす影響を調べた。</p><p>【方法】</p><p>中高齢期の男性腰椎変性疾患患者13名（腰椎患者：平均年齢：67歳）と健常若年男性10名（若年者：平均年齢22歳）を対象とした。エコー装置（東芝社製、NEMIO SSA-550A）を用いて安静時、Draw-in、頭部挙上時にそれぞれ腹横筋、内・外腹斜筋の筋厚を計測した。腰椎患者は手術前日（術前）、術後2日、術後7</p><p>日に計測を行った。測定姿位は仰臥位とし、プローブの位置は左前腋窩線と臍部水平線の交点になるようにした。また、計測前に健常成人4名を対象として、検者内信頼性を検討し高い信頼性が得られた。統計学的検定にはWilcoxonの符号順位検定、フリードマン検定を行い、有意水準は5％とした。</p><p>【結果】</p><p>腰椎患者と若年者の腹横筋筋厚に大きな変化は認められなかったが、安静時外腹斜筋は腰椎患者で約51％有意に低下していた（p＝0.0001）。中高齢期の腰椎患者は若年者と比較して脂肪組織や非収縮性組織が増加しており、その傾向は深層筋より表層筋に著明であった。術前・術後の変化では、安静時腹横筋の筋厚は術前と比較して術後7日で約17％有意に低下していた（p＝0.012）。術後のDraw-in、頭部挙上により腹横筋、内腹斜筋の筋厚は増加したが、術前と比較して各運動課題による腹横筋筋厚の増加量は減少していた。</p><p>【考察】</p><p>加齢による変化と類似して中高齢期の腰椎患者は腹部表層筋になるほど筋厚減少や筋輝度変化が著明であった。Belavý（2017）らは若年者を対象とした安静臥床実験において、腹横筋の筋厚減少が早期から生じることを報告している。腹部深層筋は安静の影響を受けやすく、今回、腰椎患者は背部筋への手術侵襲や術後早期の活動低下が原因となり腹横筋の筋厚減少を生じたと考えられた。腰椎術後早期において、Draw-in や頭部挙上は表層筋より深層筋を活性化させた。これは起居動作獲得に向けた準備運動として、術後早期から深層筋を賦活化する運動が実行可能であることを示唆している。今後症例数を増やし腰椎疾患の特徴を明かにしていきたい。</p><p>【まとめ】</p><p>本研究は、側腹筋の加齢変化が深層筋より表層筋に顕著であり、Draw-in や頭部挙上は表層筋より深層筋を活性化させることを示した。また、腰椎術後患者は手術侵襲や安静による活動量の低下により術後早期に腹横筋の萎縮を生じる可能性があることを示唆した。</p><p>【倫理的配慮，説明と同意】</p><p>本研究は所属施設の倫理審査委員会の承認を得て実施した。実施に際し、被験者に対して口頭にて研究趣旨を十分説明し同意を得た上で実施した。開示すべき利益相反はない。</p>

DOI： 10.32298/kyushupt.2019.0_13

CiNii Research

出版者・発行元：Scientific Reports  

DOI： 10.1038/s41598-018-34220-1

Scopus

PubMed

出版者・発行元：International Journal of Molecular Sciences  

DOI： 10.3390/ijms19051513

Scopus

PubMed

出版者・発行元：Journal of Pain Research  

DOI： 10.2147/JPR.S156326

Scopus

PubMed

出版者・発行元：公益社団法人 日本理学療法士協会  

<p>【はじめに，目的】</p><p></p><p>神経因性疼痛に対する運動負荷は疼痛過敏を緩和することが報告されているが，その疼痛緩和メカニズムに関しては不明な点も多い。今回，絞扼性神経損傷（Chronic Constriction injury：CCI）モデルを用いて1週，3週，5週後の脊髄後角におけるグリア細胞やopioid受容体の変化，opioid受容体の拮抗薬投与による疼痛変化を調べた。</p><p></p><p>【方法】</p><p></p><p>7週齢の雄性SDラットを運動群，非運動群，正常対照群（n=3）に分けた。右坐骨神経の結紮によりCCIモデルを作製し，速度20m/min，30分間，5日/週，5週間運動を行った。術前，CCI後1週，2週，3週，4週，5週にVon Frey Testを実施し，50%疼痛閾値を算出した。CCI後1週（運動群n=3，非運動群n=4），3週（運動群n=4，非運動群n=6），5週（運動群n=6，非運動群n=5）に腰膨大部と中脳を採取して免疫組織学的観察を行った。腰膨大部を抗Iba1抗体，抗GFAP抗体，抗μ-opioid受容体抗体で染色した。中脳水道灰白質は抗β-endorphin/met-enkephalin抗体で染色した。染色切片より陽性細胞面積を定量化した。3週と5週後に生理食塩水に溶解したNaloxone（10mg/kg）を運動群のラットの腹腔内に投与し，投与前，投与後1，2，3，4時間後に疼痛域値の変化を調べた（n=6）。統計学的検定には，SPSSを使用し一元配置または二元配置分散分析後，多重比較検定を実施し，有意水準は5％とした。</p><p></p><p>【結果】</p><p></p><p>CCI後1週で両群とも疼痛が最大となった。4週，5週には運動群の疼痛閾値は非運動群と比較して有意に改善を認めた。CCI後1週において，損傷側腰髄後角のIba1陽性細胞は両群ともに非損傷側と比較して有意に増加していた。非運動群のGFAP陽性細胞は損傷側と非損傷側において大きな違いは見られなかったが，運動群のGFAP陽性細胞は損傷側で増加していた。μ-opioid受容体陽性細胞は脊髄後角の第I層に限局して観察されたが，損傷側と非損傷側で明らかな染色性の違いは観察されなかった。3週，5週後には運動群のIba1とGFAP陽性面積は非運動群と比較して減少していた。運動群の中脳水道灰白質におけるβ-endorphin/met-enkephalin陽性細胞面積は非運動群と比べて有意に増加していた。Naloxone投与により運動群の疼痛域値の低下を認め，4時間後には投与前の値に回復した。</p><p></p><p>【結論】</p><p></p><p>運動による疼痛緩和のメカニズムとして内因性オピオイドシステムの活性化が知られている。動物実験では十分な強度と期間の運動は中枢と末梢のβ-endorphinの放出を生じ，疼痛軽減に関与していることが報告されている。今回の結果は，疼痛の発現や維持には脊髄後角におけるミクログリアやアストロサイトの活性化が関与しており，運動による疼痛緩和には脊髄後角でのグリア細胞の活性化抑制が影響していることを示した。Naloxone投与により疼痛が再燃したことより，運動による中脳水道灰白質における内因性オピオイドの増加がopioid受容体を介して疼痛緩和に作用していることが示唆された。</p>

DOI： 10.14900/cjpt.2016.0630

CiNii Research

J-GLOBAL

記述言語：日本語   出版者・発行元：コ・メディカル形態機能学会  

記述言語：日本語   出版者・発行元：コ・メディカル形態機能学会  

J-GLOBAL

J-GLOBAL

J-GLOBAL

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：(公社)日本理学療法士協会  

出版者・発行元：(公社)日本理学療法士協会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

腹部深層筋の収縮は胸腰筋膜を介した腰椎の剛性の増加や腹腔内圧の増加に関与し、姿勢保持や腰椎の安定性に重要な役割を持っている。本研究は超音波診断(エコー)装置を用いて、側腹筋の加齢変化と腰椎術後患者の安静、Draw-in、頭部挙上における側腹筋筋厚変化を調べることを目的とした。手術目的で当院に入院した中高年期の男性腰椎変性疾患患者13名(腰椎患者群、平均年齢:67歳)を対象とした。また、加齢による体幹筋変化を調べるために健常若年男性10名(若年者群、平均年齢22歳)を対照とした。エコー装置を用いて腹横筋、内・外腹斜筋の筋厚を計測した。腰椎患者群は術前、術後2日、術後7日に計測を行った。加齢による変化では、腹横筋筋厚に大きな変化は認められなかったが、安静時外腹斜筋は腰椎患者群で約51%有意に低下していた(p=0.0001)。中高年期の腰椎患者群は若年者と比較して脂肪組織や非収縮性組織が増加しており、その傾向は深層筋より表層筋に著明であった。術前術後の変化では、安静時腹横筋筋厚は術前と比較して術後7日で約17%有意に低下していた(p=0.012)。術後のDraw-in、頭部挙上により腹横筋、内腹斜筋の筋厚は増加した。本研究は、側腹筋の加齢変化が深層筋より表層筋に顕著であり、Draw-inや頭部挙上は表層筋より深層筋を活性化させることを示した。また、腰椎術後患者は手術侵襲や安静による活動量の低下により術後早期に腹横筋の萎縮を生じる可能性があることを示唆した。(著者抄録)

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：コ・メディカル形態機能学会  

出版者・発行元：(公社)日本理学療法士協会