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BackgroundsFreezing of gait (FoG) is a common and debilitating symptom of Parkinson's disease (PD) that can lead to falls and reduced quality of life. Wearable sensors have been used to detect FoG, but current methods have limitations in accuracy and practicality. In this paper, we aimed to develop a deep learning model using pressure sensor data from wearable insoles to accurately detect FoG in PD patients.MethodsWe recruited 14 PD patients and collected data from multiple trials of a standardized walking test using the Pedar insole system. We proposed temporal convolutional neural network (TCNN) and applied rigorous data filtering and selective participant inclusion criteria to ensure the integrity of the dataset. We mapped the sensor data to a structured matrix and normalized it for input into our TCNN. We used a train-test split to evaluate the performance of the model.ResultsWe found that TCNN model achieved the highest accuracy, precision, sensitivity, specificity, and F1 score for FoG detection compared to other models. The TCNN model also showed good performance in detecting FoG episodes, even in various types of sensor noise situations.ConclusionsWe demonstrated the potential of using wearable pressure sensors and machine learning models for FoG detection in PD patients. The TCNN model showed promising results and could be used in future studies to develop a real-time FoG detection system to improve PD patients' safety and quality of life. Additionally, our noise impact analysis identifies critical sensor locations, suggesting potential for reducing sensor numbers.

The complex process of bone regeneration is influenced by factors such as inflammatory responses, tissue interactions, and progenitor cells. Currently, multiple traumas can interfere with fracture healing, causing the prolonging or failure of healing. In these cases, bone grafting is the most effective treatment. However, there are several drawbacks, such as morbidity at the donor site and availability of suitable materials. Advantages have been provided in this field by a variety of stem cell types. Adipose-derived stem cells (ASCs) show promise. In the radiological examination of this study, it was confirmed that the C/S group showed faster regeneration than the other groups, and Micro-CT also showed that the degree of bone formation in the defect area was highest in the C/S group. Compared to the control group, the change in cortical bone area in the defect area decreased in the sham group (0.874), while it slightly increased in the C/S group (1.027). An increase in relative vascularity indicates a decrease in overall bone density, but a weak depression filled with fibrous tissue was observed outside the compact bone. It was confirmed that newly formed cortical bone showed a slight difference in bone density compared to surrounding normal bone tissue due to increased distribution of cortical bone. In this study, we investigated the effect of bone regeneration by ADMSCs measured by radiation and pathological effects. These data can ultimately be applied to humans with important clinical applications in various bone diseases, regenerative, and early stages of formative differentiation.

Abstract Background Chronic kidney disease(CKD) is a major public health issue and is highly prevalent in the general population. Leptin is an adipose tissue-derived endocrine factor that has been associated with several metabolic factors involved in cardiovascular diseases. Several studies have investigated the association between leptin and renal diseases so far. But the results are conflicting between the studies. The objective of our study was to verify the direct association of serum leptin level with CKD development. Methods This prospective cohort study included 2646 adult aged 40–70 without CKD in the Korean Genome and Epidemiology Study(KoGES) across South Korea from November 2005 to February 2012. The primary outcome was the development of CKD as defined by National Kidney Foundation Kidney Disease Outcomes Quality Initiative (KDOQI). Multivariate stepwise logistic regression analysis was done to assess the independent associations, for with the incident of CKD as the dependent variable, in tertiles of leptin values. Results Among 1100 men and 1546 women with 2.8 mean years of follow-up, incidence of CKD was 18(1.63%) for men and 50(3.23%) for women. In the multivariate logistic regression models, individuals in the highest serum leptin tertile showed significant associations with risk of CKD after adjustment compared to the lowest tertiles in the population. The crude odds ratio for trend was 2.95(p = 0.004) for men. After adjusting for age, baseline eGFR variables showed correlation with statistical significance (OR for trend = 2.25, p = 0.037) for men. The same trends were also seen observed in all population and women also, but no statistical significance was found. Conclusions Higher plasma leptin levels are associated with the incidence of CKD, independent of traditional factors such as age, baseline eGFR. Our results suggest that leptin may partly explain part of the reported association between obesity and kidney disease.

The recent discovery of water ice in the lunar polar shadowed regions (PSRs) has driven interest in robotic exploration, due to its potential utilization to generate water, oxygen, and hydrogen that would enable sustainable human exploration in the future. However, the absence of direct sunlight in the PSRs poses a significant challenge for the robotic operation to obtain clear images, consequently impacting crucial tasks such as obstacle avoidance, pathfinding, and scientific investigation. In this regard, this study proposes a visual simultaneous localization and mapping (SLAM)-based robotic mapping approach that combines dense mapping and low-light image enhancement (LLIE) methods. The proposed approach was experimentally examined and validated in an environment that simulated the lighting conditions of the PSRs. The mapping results show that the LLIE method leverages scattered low light to enhance the quality and clarity of terrain images, resulting in an overall improvement of the rover’s perception and mapping capabilities in low-light environments.

Abstract Background Hypertension (HTN), diabetes mellitus (DM), and dyslipidemia (DL) are well-known risk factors of cardiovascular disease (CVD), but not all patients develop CVDs. Studies have been limited investigating genetic risk of CVDs specific to individuals with metabolic diseases. This study aimed to identify disease-specific and/or common genetic loci associated with CVD susceptibility in chronic metabolic disease patients. Methods We conducted a genome-wide association study (GWAS) of a multiple case–control design with data from the City Cohort within Health EXAminees subcohort of the Korean Genome and Epidemiology Study (KoGES_HEXA). KoGES_HEXA is a population-based prospective cohort of 173,357 urban Korean adults that had health examinations at medical centers. 42,393 participants (16,309 HTN; 5,314 DM; 20,770 DL) were analyzed, and each metabolic disease group was divided into three CVD case-controls: coronary artery disease (CAD), ischemic stroke (IS), and cardio-cerebrovascular disease (CCD). GWASs were conducted for each case–control group with 7,975,321 imputed single nucleotide polymorphisms using the Phase 3 Asian panel from 1000 Genomes Project, by logistic regression and controlled for confounding variables. Genome-wide significant levels were implemented to identify important susceptibility loci. Results Totaling 42,393 individuals, this study included 16,309 HTN (mean age [SD], 57.28 [7.45]; 816 CAD, 398 IS, and 1,185 CCD cases), 5,314 DM (57.79 [7.39]; 361 CAD, 153 IS, and 497 CCD cases), and 20,770 DL patients (55.34 [7.63]; 768 CAD, 295 IS, and 1,039 CCD cases). Six genome-wide significant CVD risk loci were identified, with relatively large effect sizes: 1 locus in HTN (HTN-CAD: 17q25.3/CBX8-CBX4 [OR, 2.607; P = 6.37 × 10−9]), 2 in DM (DM-IS: 4q32.3/MARCH1-LINC01207 [OR, 5.587; P = 1.34 × 10−8], and DM-CCD: 17q25.3/RPTOR [OR, 3.511; P = 1.99 × 10−8]), and 3 in DL (DL-CAD: 9q22.2/UNQ6494-LOC101927847 [OR, 2.282; P = 7.78 × 10−9], DL-IS: 3p22.1/ULK4 [OR, 2.162; P = 2.97 × 10−8], and DL-CCD: 2p22.2/CYP1B1-CYP1B1-AS1 [OR, 2.027; P = 4.24 × 10−8]). Conclusions This study identified 6 susceptibility loci and positional candidate genes for CVDs in HTN, DM, and DL patients using an unprecedented study design. 1 locus (17q25.3) was commonly associated with CAD. These associations warrant validation in additional studies for potential therapeutic applications.

Abstract Among the three isoforms encoded by Rtn4, Nogo-A has been intensely investigated as a central nervous system inhibitor. Although Nogo-A expression is increased in muscles of patients with amyotrophic lateral sclerosis, its role in muscle homeostasis and regeneration is not well elucidated. In this study, we discovered a significant increase in Nogo-A expression in various muscle-related pathological conditions. Nogo−/− mice displayed dystrophic muscle structure, dysregulated muscle regeneration following injury, and altered gene expression involving lipid storage and muscle cell differentiation. We hypothesized that increased Nogo-A levels might regulate muscle regeneration. Differentiating myoblasts exhibited Nogo-A upregulation and silencing Nogo-A abrogated myoblast differentiation. Nogo-A interacted with filamin-C, suggesting a role for Nogo-A in cytoskeletal arrangement during myogenesis. In conclusion, Nogo-A maintains muscle homeostasis and integrity, and pathologically altered Nogo-A expression mediates muscle regeneration, suggesting Nogo-A as a novel target for the treatment of myopathies in clinical settings.

Abstract Understanding the mechanisms underlying the metabolically unhealthy normal weight (MUHNW) and metabolically healthy obese (MHO) phenotypes is important for developing strategies to prevent cardiometabolic diseases. Here, we conducted genome-wide association studies (GWASs) to identify the MUHNW and MHO genetic indices. The study dataset comprised genome-wide single-nucleotide polymorphism genotypes and epidemiological data from 49,915 subjects categorised into four phenotypes—metabolically healthy normal weight (MHNW), MUHNW, MHO, and metabolically unhealthy obese (MUHO). We conducted two GWASs using logistic regression analyses and adjustments for confounding variables (model 1: MHNW versus MUHNW and model 2: MHO versus MUHO). GCKR, ABCB11, CDKAL1, LPL, CDKN2B, NT5C2, APOA5, CETP, and APOC1 were associated with metabolically unhealthy phenotypes among normal weight individuals (model 1). LPL, APOA5, and CETP were associated with metabolically unhealthy phenotypes among obese individuals (model 2). The genes common to both models are related to lipid metabolism (LPL, APOA5, and CETP), and those associated with model 1 are related to insulin or glucose metabolism (GCKR, CDKAL1, and CDKN2B). This study reveals the genetic architecture of the MUHNW and MHO phenotypes in a Korean population-based cohort. These findings could help identify individuals at a high metabolic risk in normal weight and obese populations and provide potential novel targets for the management of metabolically unhealthy phenotypes.

Increasing evidence suggests a pivotal role of receptor-interacting protein kinase 1 (RIPK1), an initiator of necroptosis, in neuroinflammation. However, the precise role of RIPK1 in microglial activation remains unclear. In the present study, we explored the role of RIPK1 in lipopolysaccharide (LPS)-induced neuroinflammation and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model mice by using RIPK1-specific inhibitors necrostatin-1 (Nec-1) and necrostatin-1 stable (Nec-1s). Nec-1/Nec-1s or RIPK1 siRNA inhibited the production of proinflammatory molecules and the phosphorylation of RIPK1-RIPK3-MLKL and cell death in LPS-induced inflammatory or LPS/QVD/BV6-induced necroptotic conditions of BV2 microglial cells. Detailed mechanistic studies showed that Nec-1/Nec-1s exerted anti-inflammatory effects by modulating AMPK, PI3K/Akt, MAPKs, and NF-κB signaling pathways in LPS-stimulated BV2 cells. Subsequent in vivo studies showed that Nec-1/Nec-1s inhibited microglial activation and proinflammatory gene expression by inhibiting the RIPK1 phosphorylation in the brains of LPS-injected mice. Furthermore, Nec-1/Nec-1s exert neuroprotective and anti-inflammatory effects in MPTP-induced PD mice. We found that p-RIPK1 is mainly expressed in microglia, and thus RIPK1 may contribute to neuroinflammation and subsequent cell death of dopaminergic neurons in MPTP-induced PD model mice. These data suggest that RIPK1 is a key regulator of microglial activation in LPS-induced neuroinflammation and MPTP-induced PD mice.

Abstract Background In the age of aging, Korea’s current medical delivery system threatens to increase the number of medical and caring refugees. This study attempts to develop an integrated senior citizen-oriented healthcare service system in which daily care, professional care, and rehabilitation are organically organized between medical institutions and local communities, thereby meeting the daily life needs of the elderly and inducing well-being, wellness, and well-dying. Methods To develop the integrated healthcare system, data collection and analyses were conducted through a systematic review, literature review, benchmarking, focus group interviews, and expert consultation. Results The senior-specific, citizen-oriented healthcare service system developed in this study is designed to screen patients aged 65 or older within 24 h of being admitted, using the Geriatric Screening for Care-10. If there is reason for concern as a result of the screening, further evaluation is performed through assessment. Doctors and nurses create a care plan and a discharge plan based on the results from the screening and assessment. The nurse further uses the screening to monitor the patient’s condition before discharge. Based on the screening results at the time of discharge, a transitional care plan is prepared and provided to elderly patients and/or their families. This process enables a systematic link between medical institutions and community resources, aiming for the continuous management of health issues. It also establishes a multidisciplinary treatment plan that considers patients and their families so that diseases common to the elderly are diagnosed and treated promptly. Conclusions The most important issue for the elderly is to be able to live healthily and independently for the rest of their lives through well-being, wellness, and well-dying. The senior-specific, citizen-oriented healthcare service proposed in this study is an integrated medical treatment system for elderly users the implementation of which requires the daily care, professional care, and rehabilitation of elderly members of society to be organically organized according to the role of the patients, their families, and the caregiver.

Although many genome-wide association studies (GWASs) have evaluated the association with metabolic disorders, the current study is the first attempt to analyze the genetic risk factors for various metabolic disorders according to sex and age groups of the life course in Korean adults. A total population of 50,808 people were included in this GWAS. The genetic traits for eight metabolic phenotypes were investigated in peri-, and postmenopausal women compared to a younger group or men of corresponding age groups. The metabolic phenotypes include general obesity, abdominal obesity, hypertension, type 2 diabetes, hypercholesterolemia, hypertriglyceridemia, hypo-high-density lipoprotein cholesterolemia, and metabolic syndrome. In the total participants, GWAS results for eight metabolic phenotypes found 101 significant loci. Of these, 15 loci were the first reported to be associated with the risk of metabolic disorder. Interestingly, some of the significant loci presented the association with the various phenotypes, which presented when there was a correlation between phenotypes. In addition, we analyzed divided by gender and age (young adult, peri-menopausal group, older adult), and specifically identified specific loci in peri-menopausal women. Meanwhile, several genetic factors associated with metabolic disorders were newly reported in our study. In particular, several genes were significantly associated with one of the metabolic phenotypes in only a single specific group. These findings suggest that menopausal transition rather than aging itself potentiates the influence of genetic risks on metabolic disorders. In addition, some genetic loci with low frequencies may play a role in the metabolic disturbances in a specific sex and age group. The genetic traits derived from our study may contribute to understanding the genetic risk factors for metabolic disorders in the Korean population.

Few studies have investigated the effects of calcium supplementation on cardiovascular outcomes in individuals with low calcium intake in real-world settings. This study examined the association between calcium supplementation and cardiovascular outcomes in the Korean population in a real-world setting. This large retrospective cohort study included patients aged ≥45 years first prescribed calcium supplements in 2010. Age- and sex-matched controls were recruited among those who had no prescription for calcium supplements. Longitudinal data were collected on 31 December 2018. Kaplan–Meier estimation and Cox proportional hazard regression analysis were performed. The cumulative incidence of acute myocardial infarction, ischemic stroke, and death was significantly higher in the calcium supplementation group than in the control group (p < 0.05 by log-rank test). The calcium supplementation group had a significantly higher risk of myocardial infarction, ischemic stroke, and death than the control group. Compared to the control group, the hazard ratios (95% confidence intervals) of the incidence of myocardial infarction, stroke, and death in the supplementation group were 1.14 (1.03–1.27), 1.12 (1.05–1.20), and 1.40 (1.32–1.50), respectively, after adjusting for confounding variables. Considering the associated cardiovascular risk, calcium supplementation for osteoporosis treatment should be administered cautiously.

Objective Epidemiological studies on the association of serum oestradiol levels and inflammatory markers have reported inconsistent and conflicting results. Therefore, we investigated the association between serum oestradiol and high-sensitivity C-reactive protein (CRP) levels in women on the basis of their menopausal status. Methods This cross-sectional study examined the association between serum oestradiol and CRP levels on the basis of menopausal status in 151 premenopausal women aged 42.7 ± 6.7 years and 394 postmenopausal women aged 58.1 ± 6.7 years who participated in a health examination program. Multiple linear regression analysis was conducted using CRP levels as the dependent variable. Results Multiple linear regression analysis showed that serum oestradiol levels were inversely associated with CRP levels in premenopausal women (β coefficient = −0.298) after adjusting for age, body mass index, smoking, mean arterial pressure, and levels of fasting plasma glucose, triglycerides, high-density lipoprotein cholesterol, aspartate aminotransferase, and alanine aminotransferase. However, this association was not found in postmenopausal women after adjusting for the same confounding factors. Conclusions Serum oestradiol levels are inversely associated with CRP levels in premenopausal women, but not in postmenopausal women. Lower oestrogenic activity may at least partly contribute to the pathogenesis of chronic inflammation, particularly in premenopausal women.

Research on the association of serum folate levels with metabolic syndrome (MetS) in premenopausal women is lacking. This study was aimed to investigate this association in 1730 premenopausal women using the 2016 to 2018 Korean National Health and Nutrition Examination Survey data. Participants’ mean age and BMI were 35.9 years and 22.7 kg/m2, respectively. Participants were divided into three groups according to serum folate tertiles. Odds ratios (OR) and 95% confidence intervals (CIs) for abdominal obesity, elevated blood pressure (BP), high fasting plasma glucose (FPG), high triglycerides (TG), low high-density lipoprotein cholesterol (HDL-C), and MetS were calculated in multiple logistic regression models adjusted for possible confounders, by serum folate level tertiles. Prevalence of MetS (14.9, 11.0, and 8.6%); abdominal obesity (17.8, 16.0, and 11.4%); high TG (17.5, 14.0, and 11.1%); and low HDL-C (50.3, 44.6, and 42.5%) decreased with increasing folate level tertile. Prevalence of elevated BP (14.3, 12.0, and 11.7%) and high FPG (11.9, 15.8, and 13.0%) showed no significant differences according to serum folate level tertiles. The multivariate-adjusted ORs (95% CIs) for MetS, abdominal obesity, elevated BP, high TG, and low HDL-C in the highest folate level tertile were 2.17 (1.46–3.22), 1.80 (1.25–2.60), 1.77 (1.16–2.70), 1.90 (1.35–2.67), and 1.49 (1.14–1.94), respectively. The ORs for high FPG did not show significant differences according to serum folate level tertiles. In conclusion, serum folate levels were inversely associated with an increased risk of MetS in Korean premenopausal women. These results suggest that MetS can be prevented and managed by improving the serum folate levels in premenopausal women.

With the recent discovery of water-ice and lava tubes on the Moon and Mars along with the development of in-situ resource utilization (ISRU) technology, the recent planetary exploration has focused on rover (or lander)-based surface missions toward the base construction for long-term human exploration and habitation. However, a 3D terrain map, mostly based on orbiters’ terrain images, has insufficient resolutions for construction purposes. In this regard, this paper introduces the visual simultaneous localization and mapping (SLAM)-based robotic mapping method employing a stereo camera system on a rover. In the method, S-PTAM is utilized as a base framework, with which the disparity map from the self-supervised deep learning is combined to enhance the mapping capabilities under homogeneous and unstructured environments of planetary terrains. The overall performance of the proposed method was evaluated in the emulated planetary terrain and validated with potential results.

Androgen signaling via the androgen receptor (AR) is involved in normal prostate development and prostate cancer progression. In addition to androgen binding, a variety of protein kinases, including cyclic AMP-dependent protein kinase A (PKA), can activate the AR. Although hormone deprivation, especially that of androgen, continues to be an important strategy for treating prostate cancer patients, the disease ultimately progresses to castration-resistant prostate cancer (CRPC), despite a continuous hormone-deprived environment. To date, it remains unclear which pathways in this progression are active and targetable. Here, we performed a proteomic analysis of VCaP cells stimulated with androgen or forskolin to identify proteins specific for androgen-induced and androgen-bypassing signaling, respectively. Patterns of differentially expressed proteins were quantified, and eight proteins showing significant changes in expression were identified. Functional information, including a Gene Ontology analysis, revealed that most of these proteins are involved in metabolic processes and are associated with cancer. The mRNA and protein expression of selected proteins was validated, and functional correlations of identified proteins with signaling in VCaP cells were assessed by measuring metabolites related to each enzyme. These analyses offered new clues regarding effector molecules involved in prostate cancer development, insights that are supported by the demonstration of increased expression levels of the eight identified proteins in prostate cancer patients and assessments of the progression-free interval. Taken together, our findings show that aberrant levels of eight proteins reflect molecular changes that are significantly regulated by androgen and/or PKA signaling pathways, suggesting possible molecular mechanisms of CRPC.

This study compared the clinical outcomes and safety of meropenem–colistin versus meropenem–tigecycline in the treatment of adult patients with carbapenem-resistant Acinetobacter baumannii (CRAB) pneumonia. A retrospective observational study of patients with CRAB pneumonia was performed at a 1048-bed university-affiliated hospital in the Republic of Korea between June 2013 and January 2020. All adult patients initially treated with meropenem–colistin were compared with those treated with meropenem–tigecycline to evaluate in-hospital mortality and adverse events. Altogether, 66 patients prescribed meropenem–colistin and 24 patients prescribed meropenem–tigecycline were included. All patients had nosocomial pneumonia, and 31.1% had ventilator-associated pneumonia. The minimum inhibitory concentrations of meropenem ≤ 8 μg/mL and tigecycline ≤ 2 μg/mL were 20.0% and 81.1%, respectively. The in-hospital and 28-day mortality rates were 40% and 32%, respectively. In the Cox proportional hazard regression analysis, predictors associated with in-hospital mortality included procalcitonin ≥ 1 ng/mL (adjusted hazard ratio (aHR), 3.39; 95% confidence interval (CI) 1.40–8.19; p = 0.007) and meropenem–colistin combination therapy (aHR, 2.58; 95% CI, 1.07–6.23; p = 0.036). Episodes of nephrotoxicity were significantly more common in the meropenem–colistin group than in the meropenem–tigecycline group (51.5% vs. 12.5%, p = 0.001). Meropenem–tigecycline combination therapy might be a valuable treatment option for patients with CRAB pneumonia.

This study aimed to investigate the effects of semi-immersive virtual reality-based cognitive training (VRCT) combined with locomotor activity on cognitive function, balance, and gait ability in older adults. Eighteen community-dwelling older adults participated in this study. Subjects who met the selection criteria were assigned to an experimental group (n = 9) and a control group (n = 9). The experimental group received VRCT combined with locomotor activity for 30 min a day, three times a week, for 6 weeks. The control group received tabletop activity-based cognitive training for the same amount of time. Before and after the training, the Korean Mini-Mental State Examination (K-MMSE), Trail Making Test (TMT; A and B), and Digit Span Test (DST; forward and backward) were used to evaluate cognitive function; and the Timed Up and Go (TUG) test and 10-m Walking Test (10MWT) were used to evaluate the improvement in the balance and gait ability parameters. After the intervention, the experimental group showed a significantly greater improvement in the TMT-A (p = 0.045) and DST-backward (p = 0.012) scores compared with the control group. Regarding the gait ability variable, the experimental group showed a significant improvement in the 10MWT test (p = 0.001). This study confirmed that semi-immersive VRCT combined with locomotor activity is useful for improving cognitive function and gait ability in older adults. Therefore, VRCT combined with locomotor activity can be used as a simultaneous intervention for cognitive rehabilitation and functional capacity improvement in older adults.

Abstract Background Aging is an inevitable part of life. One can maintain well-being and wellness even after discharge and/or transition if his or her functional decline is minimized, sudden decline is prevented, and functioning is promoted during hospitalization. Caring appropriately for elderly patients requires the systematic application of Senior-Friendly Hospital principles to all operating systems, including medical centres’ organization and environment, as well as patient treatment processes. The Senior-Friendly Hospital framework is valid and important for patient safety and quality improvement. This study aimed to make recommendations regarding the development of the Korean Framework for Senior-Friendly Hospitals for older patients’ care management, patient safety interventions, and health promotion, via a Delphi survey. Methods Two rounds of Delphi surveying were conducted with 15 participants who had at least 3 years’ experience in accreditation surveying and medical accreditation standards, survey methods, and accreditation investigator education. In each round, we calculated statistics describing each standard’s validity and feasibility. Results The Korean Framework for Senior-Friendly Hospitals included 4 Chapters, 11 categories, and 67 standards through consensus of the Senior-Friendly Hospitals task force and experts’ peer review. After the two rounds of Delphi surveying, validity evaluation led to no changes in standards of the Senior-Friendly Hospitals; however, the number of standards showing adequate validity decreased from 67 to 58. Regarding feasibility, no changes were necessary in the standards; however, the number of categories showing adequate feasibility decreased from 11 to 8 and from 67 to 30, respectively. The excluded categories were 3.2, 4.2, and 4.3 (service, transportation, and signage and identification). The highest feasibility values were given to standards 2.1.1, 4.1.4, and 4.1.6. The highest feasibility score was given to standard 2.4.2. Conclusions The Korean Framework for Senior-Friendly Hospitals needs to include 4 Chapters, 8 categories, and 30 standards. The Accreditation Program for Healthcare Organizations should include Senior-Friendly Hospitals -relevant standards considering Korea’s medical environment.

Nogo-A (Rtn 4A), a member of the reticulon 4 (Rtn4) protein family, is a neurite outgrowth inhibitor protein that is primarily expressed in the central nervous system (CNS). However, previous studies revealed that Nogo-A was upregulated in skeletal muscles of Amyotrophic lateral sclerosis (ALS) patients. Additionally, experiments showed that endoplasmic reticulum (ER) stress marker, C/EBP homologous protein (CHOP), was upregulated in gastrocnemius muscle of a murine model of ALS. We therefore hypothesized that Nogo-A might relate to skeletal muscle diseases. According to our knocking down and overexpression results in muscle cell line (C2C12), we have found that upregulation of Nogo-A resulted in upregulation of CHOP, pro-inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α, while downregulation of Nogo-A led to downregulation of CHOP, IL-6 and TNF-α. Immunofluorescence results showed that Nogo-A and CHOP were expressed by myofibers as well as tissue macrophages. Since resident macrophages share similar functions as bone marrow-derived macrophages (BMDM), we therefore, isolated macrophages from bone marrow to study the role of Nogo-A in activation of these cells. Lipopolysaccharide (LPS)-stimulated BMDM in Nogo-KO mice showed low mRNA expression of CHOP, IL-6 and TNF-α compared to BMDM in wild type (WT) mice. Interestingly, Nogo knockout (KO) BMDM exhibited lower migratory activity and phagocytic ability compared with WT BMDM after LPS treatment. In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-α in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-α. Furthermore, upregulation of Nogo-A in dystrophin-deficient (mdx) murine model, myopathy and Duchenne muscle dystrophy (DMD) clinical biopsies was associated with upregulation of CHOP, IL-6 and TNF-α. To the best of our knowledge, this is the first study to demonstrate Nogo-A as a regulator of inflammation in diseased muscle and bone marrow macrophages and that deletion of Nogo-A alleviates muscle inflammation and it can be utilized as a therapeutic target for improving muscle diseases.

The aim of this study was to investigate the longitudinal change in muscle mass over 10 years according to serum calcium levels and calcium intake. A total of 1497 men and 1845 women aged 50 years and older were included. Significant muscle loss (SML) was defined as a 5% or greater loss from baseline, while time-dependent development of SML was assessed according to quartiles for corrected calcium level and daily calcium intake using Cox regression models. The incidence of SML was 6.7 and 7.7 per 100-person-years among men and women, respectively. Groups with the lowest corrected calcium levels had more prominent SML than those with higher calcium levels, regardless of sex. The relationship between SML and calcium intake was significant only among women. The hazard ratio for SML per 1 mmol/L increase in corrected calcium level was 0.236 and 0.237 for men and women, respectively. In conclusion, low serum calcium levels may predict SML among adults aged ≥ 50 years, while low calcium intake may be a predictor for muscle loss among women. Therefore, encouraging dietary calcium intake among middle-aged and older adults for preservation of muscle mass should be considered.

The role of sodium in hypertension remains unresolved. Although genetic factors have a significant impact on high blood pressure, studies comparing genetic susceptibility between people with low and high sodium diets are lacking. We aimed to investigate the genetic variations related to hypertension according to sodium intake habits in a large Korean population-based study. Data for a total of 57,363 participants in the Korean Genome and Epidemiology Study Health Examination were analyzed. Sodium intake was measured by a semi-quantitative food frequency questionnaire. We classified participants according to sodium intake being less than or greater than 2 g/day. We used logistic regression to test single-marker variants for genetic association with a diagnosis of hypertension, adjusting for age, sex, body mass index, exercise, alcohol, smoking, potassium intake, principal components 1, and principal components 2. Significant associations were defined as p < 5 × 10−8. In participants whose sodium intake was greater than 2 g/day, chromosome 6 open reading frame 10 (C6orf10)-human leukocyte antigen (HLA)-DQB1 rs6913309, ring finger protein (RNF)213 rs112735431, glycosylphosphatidylinositol anchored molecule-like (GML)- cytochrome P450 family 11 subfamily B member 1(CYP11B1) rs3819496, myosin light chain 2 (MYL2)-cut like homeobox 2 (CUX2) rs12229654, and jagged1 (JAG1) rs1887320 were significantly associated with hypertension. In participants whose intake was less than 2 g/day, echinoderm microtubule-associated protein-like 6(EML6) rs67617923 was significantly associated with hypertension. Genetic susceptibility associated with hypertension differed according to sodium intake. Identifying gene variants that contribute to the dependence of hypertension on sodium intake status could make possible more individualized nutritional recommendations for preventing cardiovascular diseases.