Background: Dementia is a critical late-life health issue that occurs among members of aging societies. This study examined the relationships between eating out, dietary diversity, and mild cognitive impairment (MCI) among community-dwelling older adults. Methods: We analyzed data from 597 older adults (median age 73.0 years, interquartile range 69.0–78.0 years; 62.6% females). We applied the food frequency score to evaluate diet variety and the weekly consumption frequencies of ten food items were determined. The National Center for Geriatrics and Gerontology Functional Assessment Tool (NCGG-FAT) was used to evaluate MCI. Finally, we asked the participants how often they ate out each month; those who replied "none" were categorized into the "non-eating out" group. Results: The overall prevalence of MCI was 122 (20.4%), with a higher prevalence in the low dietary diversity group than in the high dietary diversity group (28.6% vs. 18.6%). After adjusting for covariates, the participants who self-described as not eating out were independently associated with low dietary diversity (odds ratio [OR]=1.97, 95% confidence interval [CI] 1.20–3.20), while low dietary diversity was associated with MCI (OR=1.72; 95% CI 1.02–2.87). Structural equation models revealed that not eating out had no direct effect on MCI but was associated with MCI via low dietary diversity (root mean square error of approximation=0.030, goodness-of-fit index=0.999, and adjusted goodness-of-fit index=0.984). Conclusions Although non-eating out may not have a direct effect on MCI, an indirect relationship may exist between eating-out habits and MCI via dietary diversity status.

Background: Dementia is a critical late-life health issue that occurs among members of aging societies. This study examined the relationships between eating out, dietary diversity, and mild cognitive impairment (MCI) among community-dwelling older adults. Methods: We analyzed data from 597 older adults (median age 73.0 years, interquartile range 69.0–78.0 years; 62.6% females). We applied the food frequency score to evaluate diet variety and the weekly consumption frequencies of ten food items were determined. The National Center for Geriatrics and Gerontology Functional Assessment Tool (NCGG-FAT) was used to evaluate MCI. Finally, we asked the participants how often they ate out each month; those who replied "none" were categorized into the "non-eating out" group. Results: The overall prevalence of MCI was 122 (20.4%), with a higher prevalence in the low dietary diversity group than in the high dietary diversity group (28.6% vs. 18.6%). After adjusting for covariates, the participants who self-described as not eating out were independently associated with low dietary diversity (odds ratio [OR]=1.97, 95% confidence interval [CI] 1.20–3.20), while low dietary diversity was associated with MCI (OR=1.72; 95% CI 1.02–2.87). Structural equation models revealed that not eating out had no direct effect on MCI but was associated with MCI via low dietary diversity (root mean square error of approximation=0.030, goodness-of-fit index=0.999, and adjusted goodness-of-fit index=0.984). Conclusions Although non-eating out may not have a direct effect on MCI, an indirect relationship may exist between eating-out habits and MCI via dietary diversity status.

Background: Dementia is a critical late-life health issue that occurs among members of aging societies. This study examined the relationships between eating out, dietary diversity, and mild cognitive impairment (MCI) among community-dwelling older adults. Methods: We analyzed data from 597 older adults (median age 73.0 years, interquartile range 69.0–78.0 years; 62.6% females). We applied the food frequency score to evaluate diet variety and the weekly consumption frequencies of ten food items were determined. The National Center for Geriatrics and Gerontology Functional Assessment Tool (NCGG-FAT) was used to evaluate MCI. Finally, we asked the participants how often they ate out each month; those who replied "none" were categorized into the "non-eating out" group. Results: The overall prevalence of MCI was 122 (20.4%), with a higher prevalence in the low dietary diversity group than in the high dietary diversity group (28.6% vs. 18.6%). After adjusting for covariates, the participants who self-described as not eating out were independently associated with low dietary diversity (odds ratio [OR]=1.97, 95% confidence interval [CI] 1.20–3.20), while low dietary diversity was associated with MCI (OR=1.72; 95% CI 1.02–2.87). Structural equation models revealed that not eating out had no direct effect on MCI but was associated with MCI via low dietary diversity (root mean square error of approximation=0.030, goodness-of-fit index=0.999, and adjusted goodness-of-fit index=0.984). Conclusions Although non-eating out may not have a direct effect on MCI, an indirect relationship may exist between eating-out habits and MCI via dietary diversity status.

Background: Dementia is a critical late-life health issue that occurs among members of aging societies. This study examined the relationships between eating out, dietary diversity, and mild cognitive impairment (MCI) among community-dwelling older adults. Methods: We analyzed data from 597 older adults (median age 73.0 years, interquartile range 69.0–78.0 years; 62.6% females). We applied the food frequency score to evaluate diet variety and the weekly consumption frequencies of ten food items were determined. The National Center for Geriatrics and Gerontology Functional Assessment Tool (NCGG-FAT) was used to evaluate MCI. Finally, we asked the participants how often they ate out each month; those who replied "none" were categorized into the "non-eating out" group. Results: The overall prevalence of MCI was 122 (20.4%), with a higher prevalence in the low dietary diversity group than in the high dietary diversity group (28.6% vs. 18.6%). After adjusting for covariates, the participants who self-described as not eating out were independently associated with low dietary diversity (odds ratio [OR]=1.97, 95% confidence interval [CI] 1.20–3.20), while low dietary diversity was associated with MCI (OR=1.72; 95% CI 1.02–2.87). Structural equation models revealed that not eating out had no direct effect on MCI but was associated with MCI via low dietary diversity (root mean square error of approximation=0.030, goodness-of-fit index=0.999, and adjusted goodness-of-fit index=0.984). Conclusions Although non-eating out may not have a direct effect on MCI, an indirect relationship may exist between eating-out habits and MCI via dietary diversity status.

Introduction: Long-term cardiac hypertrophy causes heart failure. One of the mechanisms of this transition from hypertrophy to heart failure is collapse of hypoxic response and angiogenesis. Heat shock protein 27 (HSP27) was found to act as an anti-apoptotic protein and its phosphorylation is responsible for the protection of cells against heat stress. HSP27 has been reported to regulate p53 expression, which contributes to down-regulate angiogenic factors through hypoxia inducible factor-1α(HIF-1α). We have reported that thermal therapy, namely Waon therapy, improves cardiac and vascular function in patients with chronic heart failure. However, the effect of this therapy on cardiac hypertrophy due to pressure overload is unknown. The purpose of this study is to investigate the effects and mechanisms of thermal therapy (Waon therapy) on the transition from cardiac hypertrophy to heart failure after pressure overload. Methods: Cardiac hypertrophy was induced by transverse aortic constriction (TAC) in C57BL/6 mice. At 2 weeks after TAC, all mice were examined by echocardiography and showed left ventricular hypertrophy. Then, mice were randomly divided into thermal therapy or untreated group. Thermal therapy group received thermal therapy using an experimental far infrared ray dry sauna, which elevates the core temperature by 1 degree Celsius for 30 minutes, daily for 4 weeks. Sham operated mice were used as control. At 6 weeks after TAC, we measured body weight, heart rate and blood pressure before sacrifice, and eviscerated heart and leg muscle. Western blot analysis of p53, phosphorylated HSP27, HIF-1α and vascular endothelial growth factor (VEGF) was performed using extracted protein form heart. Results: At 6 weeks after TAC, body weight, heart rate and blood pressure did not differ in three groups. Echocardiography showed that left ventricular fractional shortening of thermal therapy group was significantly larger than that of untreated group (Sham vs. Untreated vs. Thermal; 50.0±1.7 vs. 36.7±1.3 vs. 46.2±0.5, P<0.01, n=6 each). Heart weight/tibia length ratio of thermal therapy group was significantly smaller than that of untreated group (6.7±0.1 vs. 9.7±0.5 vs. 7.9±0.2, P<0.01, n=9 each). Western blot showed that thermal therapy increased phosphorylation of HSP27 and reduced p53. Thermal therapy also increased HIF-1α and VEGF at 6 weeks after TAC. Capillary/myofiber ratio was larger in thermal therapy group than that in untreated group (1.71±0.05 vs. 2.04±0.04 vs. 2.41±0.10, P<0.01, n=4 each). Conclusion: Thermal therapy, namely Waon therapy, prevented the transition from cardiac hypertrophy to heart failure induced by pressure overload in mice. As the mechanism, thermal therapy amplified the phosphorylation of HSP27 and inhibited p53, increased HIF-1α and VEGF, and then increased angiogenesis.

Objective: Few cases of Takotsubo cardiomyopathy with apical hypertrophic cardiomyopathy (APH)-like morphological changes during the recovery process have been reported.Patient: A 56-year-old woman diagnosed with Takotsubo cardiomyopathy showed a morphology similar to that of APH during recovery. We examined this patient using 2D speckle-tracking echocardiography based on the method used for hypertrophic cardiomyopathy, which suggested that the circumferential strain (CS) of the middle wall indicated myocardial function of the left ventricle, and the CS of the inner wall was associated with left ventricular chamber function.Results: We measured the CS of the endocardial, middle, and epicardial layers and found that the apical inner layer CS (CSinner), middle layer CS, and outer layer CS were all decreased at the onset. CSinner showed a strong tendency to recover on echocardiography performed when APH-like morphology was observed.Conclusion: The morphology of the apex in our case likely contributed to the maintenance of chamber function.

INTRODUCTION: The pathophysiology and mechanism of in-stent restenosis (ISR) after implantation of second-generation drug-eluting stents (DESs) are not fully clear. We compared the morphological characteristics of ISR between first- and second-generation DESs using frequency domain optical coherence tomography (OCT). METHODS: Patients who underwent follow-up coronary angiography (CAG) after first-generation (CYPHER™ and TAXUS™) and second-generation (Nobori®, PROMUS Element™, Resolute Integrity and XIENCE) DES implantations were examined. ISR was defined as lesions of over 50% diameter stenosis at follow-up CAG. Frequency domain OCT was performed at the time of revascularisation of ISR. Tissue morphology was assessed at minimum lumen area. OCT images of DESs at both early (≤ 1 year) and late (> 1 year) phase follow-up were compared. RESULTS: On qualitative OCT assessment, the ratios of homogeneous, layered, heterogeneous without-attenuation and heterogeneous with-attenuation morphologies were 57.1%, 17.1%, 20.0% and 5.7%, respectively, for second-generation DES ISR (n = 35), and 16.7%, 25.0%, 25.0% and 33.3%, respectively, for first-generation DES ISR (n = 36). At late phase follow-up, homogeneous morphology was significantly more common for second-generation DES ISR compared to first-generation DES ISR (first-generation: 8.0% vs. second-generation: 50.0%; p < 0.01) while heterogeneous with-attenuation morphology was significantly more common for first-generation DES ISR (first-generation: 44.0% vs. second-generation: 5.6%; p < 0.01). CONCLUSION Homogeneous tissue morphology was more frequently found for second-generation than first-generation DES ISR, especially in the late phase. This suggested that neointimal hyperplasia was the main mechanism in second-generation DES ISR, and that the neointima was stabilised, much like in bare metal stent implantation.
Aged ; Constriction, Pathologic ; pathology ; Coronary Angiography ; Coronary Restenosis ; diagnostic imaging ; pathology ; Coronary Vessels ; diagnostic imaging ; pathology ; surgery ; Drug-Eluting Stents ; adverse effects ; Female ; Humans ; Incidence ; Male ; Metals ; Middle Aged ; Neointima ; Retrospective Studies ; Tomography, Optical Coherence