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This study aims to analyze the effects of COVID-19 stress on healing behavior in residential spaces. Based on the results, the study further examines the residential space as a healing environment according to space use behavior in the post-COVID era. A survey including 2101 Korean people was conducted. The COVID Stress Scale for Korean People (CSSK) was used to identify COVID-19 stress. In addition, using a literature review on healing environment factors and behavioral changes after the pandemic, survey questions were developed to assess changes in healing behavior. A frequency analysis was conducted for sociodemographic factors, and the relationship between COVID stress factors and healing behavior factors in residential spaces was examined using factor and correlation analyses. Multiple regression analysis was conducted to verify the effects of COVID stress factors on changes in healing behavior. The results revealed that COVID stress affected healing behavior in residential spaces; however, there were differences in healing behavior depending on the COVID stress factors. Fear of being infected positively affected infection prevention behavior in homes. Anger towards others negatively affected the establishment of elements that support various activities in the residential spaces and furniture arrangement. Stress from social distancing difficulties affected healing behavior in residential spaces but was not related to infection prevention behavior. Residential spaces can serve as healing spaces when people are provided with various spatial factors that support diverse types of behavior during a pandemic crisis.

The aim of this study was 1) to investigate the prevalence and pattern of dental anomalies (DAs), 2) to compare DAs according to the type of malocclusion, and 3) to investigate the correlation between tooth impaction and other DAs in the Korean orthodontic population.A total of 3,240 orthodontic patients were classified as Class I, Class II, or Class III malocclusion groups. The presence and location of common DAs, including impaction, microdontia, agenesis, supernumerary tooth, transposition, and fusion, were identified by examining diagnostic records. Furthermore, samples were classified as Group 1 without impaction or Group 2 with impaction. The prevalence of other DAs concurrent with impaction was investigated and compared to Group 1.Impaction was the most prevalent DA, followed by microdontia, agenesis, and supernumerary. Class I and Class III groups showed the same order of prevalence, but agenesis was more frequent than microdontia in the Class II group. The prevalence of the four DAs was lowest in the Class III group. Overall, 8.6% of patients were classified into Group 2. The incidence of DAs other than impaction and the prevalence of multiple concurrent DAs were significantly higher in Group 2. Impaction showed a significant relationship with supernumerary tooth, transposition, and fusion.The prevalence and pattern of DAs varied depending on the type of malocclusion. As there was a higher risk of other DAs in patients with impacted teeth, early detection of the impacted tooth and a detailed diagnosis of other possible DAs may be essential.

The Iris Music Project is a non-profit dedicated to reimagining residential and healthcare communities as spaces of creative exchange. By February 2020, our chamber music group, the Iris Piano Trio, had developed a model for music programming at Charles E. Smith Life Communities (CESLC) in Rockville, Maryland (United States), that emphasized collaborative relationships between professional musicians and community members. The COVID-19 pandemic severely disrupted the Trio’s work and tested its model. In this article, we describe how the Trio remained connected and relevant to CESLC residents by experimenting with virtual programmes that adapted our model to a digital setting. We argue that our prior relationships with residents and staff enabled us to impact their lives throughout the pandemic despite the isolation created by COVID-19 closures. The pandemic strained, but did not fundamentally change, the Trio’s ensemble-in-residence model, suggesting its potential as a generalized model in the field of music and health.

Microglial phagocytosis and clearance are important for the removal of amyloid-β (Aβ) plaques in Alzheimer’s disease (AD). Chronic exposure of microglia to Aβ plaques leads to microglial metabolic dysfunction, and dysregulation of microglia can accelerate the deposition of Aβ plaques and cause learning and memory impairment. Thus, regulating microglial Aβ clearance is crucial for the development of therapeutics for AD-related dementia. Here, Down syndrome critical region 1 (DSCR1) deficiency ameliorated Aβ plaque deposition in the 5xFAD mouse model of AD by altering microglial activity; however, the Aβ synthesis pathway was not affected. DSCR1 deficiency improved spatial learning and memory impairment in 5xFAD mice. Furthermore, DSCR1-deficient microglia exhibited accelerated lysosomal degradation of Aβ after phagocytosis, and BV2 cells with stable knockdown of DSCR1 demonstrated enhanced lysosomal activity. RNA-sequencing analysis showed that the transcriptional signatures associated with responses to IFN-γ were significantly up-regulated in DSCR1-knockdown BV2 cells treated with Aβ. Our data strongly suggest that DSCR1 is a critical mediator of microglial degradation of amyloid plaques and a new potential microglial therapeutic target in AD.

Although typically associated with onset in young adults, multiple sclerosis (MS) also attacks the elderly, which is termed late-onset MS. The disease can be recapitulated and studied in a mouse model, experimental autoimmune encephalomyelitis (EAE). The onset of induced EAE is delayed in aged mice, but disease severity is increased relative to young EAE mice. Given that CD4

With increasing time spent indoors during the coronavirus disease pandemic, occupants are increasingly affected by indoor space environmental factors. Environmental color stimulates human vision and affects stress levels. This study investigated how changing environmental color chroma affected heart rate variability (HRV) and stress. The HRV of nine males and fifteen females was measured during exposure to 12 color stimuli with changes in chroma under green/blue hues and high/low-value conditions, and a stress assessment was performed. The effect of chroma on the HRV of males and females was verified, but the interaction effect between chroma and gender was not. ln(LF) and RMSSD were valid parameters. ln(LF) of males and females decreased as chroma increased under the green hue and low-value conditions; RMSSD was reduced as chroma increased in the blue hue and low-value conditions. ln(LF) decreased as chroma increased under blue hue and high-value conditions in males. Color–stress evaluation revealed that the higher chroma under high-value conditions, the more positive the stress emotion, and the lower the chroma under low-value conditions, the more negative the stress emotion. As chroma increased under low-value conditions, color is a stress factor; for men, this effect was more evident in the blue hue.

Pump it up Carbon nanotube yarns can be used as electrochemical actuators because infiltration with ions causes a contraction in length and an expansion in diameter. Either positive or negative ions can cause this effect. Chu et al. constructed an all-solid-state muscle that eliminated the need for an electrolyte bath, which may expand the potential for its use in applications. By infiltrating the yarns with charged polymers, the fibers start partially swollen, so the length can increase through the loss of ions. It is thus possible to increase the overall stroke of the muscle. Further, these composite materials show a surprising increase in stroke with scan rate. Science , this issue p. 494

Dysregulation of extracellular matrix proteins in obese adipose tissue (AT) induces systemic insulin resistance. The metabolic roles of type VI collagen and its cleavage peptide endotrophin in obese AT are well established. However, the mechanisms regulating endotrophin generation remain elusive. Herein, we identified that several endotrophin-containing peptides (pre-endotrophins) were generated from the COL6A3 chain in a stepwise manner for the efficient production of mature endotrophin, partly through the action of hypoxia-induced matrix metalloproteinases (MMPs), including MMP2, MMP9, and MMP16. Hypoxia is an upstream regulator of COL6A3 expression and the proteolytic processing that regulates endotrophin generation. Hypoxia-inducible factor 1α (HIF1α) and the hypoxia-associated suppression of microRNA (miR)-29 cooperatively control the levels of COL6A3 and MMPs, which are responsible for endotrophin generation in hypoxic ATs. Adipocyte-specific Hif1a knock-out (APN-HIF1αKO) mice fed a chronic high-fat diet exhibited the significant amelioration of both local fibro-inflammation in AT and systemic insulin resistance compared to the control littermates, partly through the inhibition of endotrophin generation. Strikingly, adenovirus-mediated miR-29 overexpression in the ATs of APN-HIF1αKO mice in obesity significantly decreased endotrophin levels, suggesting that miR-29, combined with HIF1α inhibition in AT, could be a promising therapeutic strategy for treating obesity and related metabolic diseases.

Geoscientific Model Development, 15 (13), ISSN:1991-9603, ISSN:1991-959X

Although typically associated with onset in young adults, multiple sclerosis (MS) also attacks aged people, which is termed late-onset MS. The disease can be recapitulated and studied in the aged mouse model of experimental autoimmune encephalomyelitis (EAE). The onset of induced EAE is delayed in aged mice, but the disease severity is increased relative to standard EAE in young mice. Given that CD4+FoxP3+ regulatory T (Treg) cells play an ameliorative role in MS/EAE severity and the aged immune system accumulates Treg cells, failure of these cells to prevent or ameliorate EAE disease is enigmatic. When analyzing the distribution of Treg cells in EAE mice, the aged mice exhibited a higher proportion of polyclonal(pan) Treg cells and a lower proportion of antigen-specific-Treg cells in their periphery, but lower proportions of pan- and antigen-specific-Treg cells in the central nervous system (CNS). Furthermore, in the aged CNS, Treg cells exhibited a higher plasticity and T effector (Teff) cells exhibited a greater clonal expansion, which disrupted the Treg/Teff balance. Transiently inhibiting FoxP3 expression in peripheral Treg cells partially ameliorated the disease and corrected Treg distribution in the aged mice. These results provide evidence that accumulated aged Treg cells play a detrimental role in neuronal inflammation of aged MS.HighlightsQuestionCD4+ regulatory T (Treg) cells typically play an ameliorative role in multiple sclerosis (MS) onset and severity. However, why aged immune system has accumulated peripheral Treg cells, but the elderly has more severe MS symptoms?FindingsAged Treg cells cannot easily distribute to the CNS of aged EAE mice, and those aged Treg cells that did enter the CNS exhibited increased plastic features. However, transient inhibition of peripherally accumulated Treg cells corrected Treg distribution and partially ameliorated the disease in the aged mice.Conclusion and mechanistic insightsAccumulated aged Treg cells within an “inflammaging” condition do not play an ameliorative role but are potentially detrimental for inflamed CNS repair processes in aged EAE mice due to impeding the trafficking of immune cells into the inflamed CNS.

DNA methylation is a crucial epigenetic modification in the establishment of cell-type-specific characteristics. However, how DNA methylation is selectively reprogrammed at adipocyte-specific loci during adipogenesis remains unclear. Here, we show that the transcription factor, C/EBPδ, and the DNA methylation eraser, TET3, cooperatively control adipocyte differentiation. We perform whole-genome bisulfite sequencing to explore the dynamics and regulatory mechanisms of DNA methylation in adipocyte differentiation. During adipogenesis, DNA methylation selectively decreases at adipocyte-specific loci carrying the C/EBP binding motif, which correlates with the activity of adipogenic promoters and enhancers. Mechanistically, we find that C/EBPδ recruits a DNA methylation eraser, TET3, to catalyse DNA demethylation at the C/EBP binding motif and stimulate the expression of key adipogenic genes. Ectopic expression of TET3 potentiates in vitro and in vivo adipocyte differentiation and recovers downregulated adipogenic potential, which is observed in aged mice and humans. Taken together, our study highlights how targeted reprogramming of DNA methylation through cooperative action of the transcription factor C/EBPδ, and the DNA methylation eraser TET3, controls adipocyte differentiation.

Color is the most potent stimulating factor affecting human vision, and the environmental color of an indoor space is a spatial component that affects the environmental stress level. As one of the methods of assessing the physiological response of the autonomic nervous system that influences stress, heart rate variability (HRV) has been utilized as a tool for measuring the user’s stress response in color environments. This study aims to identify the effects of the changes of hue, brightness, and saturation in environmental colors on the HRV of two groups with different stress levels—the stress potential group (n = 15) and the healthy group (n = 12)—based on their stress level indicated by the Psychosocial Well-being Index (PWI). The ln(LF), ln(HF), and RMSSD values collected during the subjects’ exposure to 12 environments colors of red and yellow with adjusted saturation and brightness, were statistically analyzed using t-test and two-way ANOVA. The results show that the HRV values in the two groups did not significantly vary in response to the changes in hue, brightness and saturation. The two groups’ stress factors distinguished according to the stress levels by the PWI scale affected the In(LF) parameter, which demonstrates that the PWI index can be utilized as a reliable scale for measuring stress levels. The ultra-short HRV measurement record and the use of a sole In(LF) parameter for stress assessment are regarded as the limitations of this study.

The purpose of this research was to explore the experiences of Korean-Vietnamese multicultural families when visiting their maternal homeland, Vietnam, and to investigate the educational program of supporting their visits. The research participants were 42 Korean-Vietnamese multicultural families who participated in the program. Researchers collected data through group discussion and pre- and follow-up interviews with participants. The results of this research were as follows. As for the children, first, they became closer to the culture of their mother’s country. Second, they confirmed family affection when they received love and a hearty welcome from their maternal family members. Third, their interest in the Vietnamese language, food, clothing, and shelter increased through personally experiencing and understanding Vietnamese culture. Fourth, visiting their maternal home helped them understand and form a positive view of their own multicultural identity. As for the mothers, their confidence was restored while they shared the joy of the family reunion. Second, the mothers were able to please their parents by showing their happy married life. Third, the mothers were able to expand exchanges among marriage-immigrant women and find hope for the future by interacting with other multicultural families. As for the fathers, first, through the visit to their wife’s parents’ home, they understood the difficulties that their wife underwent in Korea and their attitude changed in that they made efforts to be more considerate towards their wife. Second, they felt a more intimate connection with their wife’s family as a result of receiving a hearty welcome and having a good time. Third, they discovered the multicultural potential of their children and thought about their children’s future in a positive way. It is expected that the educational program of supporting visits to their maternal home will be developed into one that supports the holistic development and growth of multicultural family children with the goal of helping those children to develop multicultural capabilities and grow to be global leaders.

A master immunoregulator FoxP3-expressing CD4+ Treg cellsplay an ameliorative role in the severity of MS/EAE disease. However, it is contradictory that the aged T cell immune system possesses relatively enhanced thymic CD4+ Treg generation and accumulated peripheral CD4+ Treg cells, but coupled with severe MS/EAE symptoms and pathology. Using single-cell (sc)-RNA-Seq assay, we found that CNS-infiltrating CD4+ Treg cells in aged EAE mouse model had increased pathogenic properties, showing co-expression of infg and il17a with foxp3, and reduced suppressive effect, exhibiting increased clonal expansion of pathogenic CD4+ T cells. These indicate changed Treg quality in aged EAE mice. Transient inhibition of aged peripheral FoxP3+ Treg cells mitigated the disease severity in the aged mice. The ameliorative effect was more significant when partially inhibiting FoxP3+ Treg cells with a drug P300i than completely depleting FoxP3+ Treg cells in FoxP3DTR transgenic mice. The mitigation is probably attributed to the correction of Treg cell distribution outside and inside the CNS. By inhibiting accumulated FoxP3+ Treg cells adhering to the brain’s choroid plexus (outside the CNS), the IFN-g-producing cells can be restored, thereby, the impediment of immune cell trafficking into the inflamed CNS is released in aged EAE mice. As a result, the proportion of myelin-specific CD4+ Treg cells inside the CNS was increased for repairing neuroinflammatory damage. Together, the underlying mechanism of severe MS symptoms in elderly patients is associated with the accumulation of Treg cells outside the CNS, which prevents the reparative antigen-specific Treg cells from entering the CNS during the disease. Supported by NIH/NIAID R01AI121147

Extracellular matrix dysregulation is associated with chronic liver disease. CollagenVI-alpha3 chain (COL6A3) is a biomarker for hepatic fibrosis and poor prognosis of hepatocellular carcinoma (HCC), but its function in liver pathology remains unknown. High levels of COL6A3 and its cleaved product, endotrophin (ETP) in tumor-neighboring regions are strongly associated with poor prognosis in HCC patients. Here, we report that the high levels of ETP in injured hepatocytes induce JNK-dependent hepatocyte apoptosis and activate nonparenchymal cells to lead further activation of hepatic inflammation, fibrosis, and apoptosis. Nevertheless ETP per se showed limited phenotypic changes in normal liver tissues. Furthermore, inhibition of ETP activity by utilizing neutralizing antibodies efficiently suppressed the pathological consequences in chronic liver diseases. Our results implicate ETP mechanistically as a crucial mediator in reciprocal interactions among various hepatic cell populations in the pathogenesis of chronic liver disease, and it could be a promising therapeutic target particularly in individuals with high local levels of COL6A3. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Age‐related thymic atrophy results in reduced output of naïve conventional T (Tcon) cells. However, its impact on regulatory T (Treg) cells is insufficiently understood. Given evidence that thymic Treg (tTreg) cell generation is enhanced in the aged, atrophy thymus and that the aged periphery accumulates peripheral Treg (pTreg) cells, we asked why these Treg cells are unable to effectively attenuate increased autoreactivity‐induced chronic inflammation in the elderly. We designed a mock‐self‐antigen chimera mouse model, in which membrane‐bound ovalbumin (mOVA) transgenic mice, bearing a FoxN1‐floxed gene for induction of conditional thymic atrophy, received OVA‐specific (OT‐II) T‐cell receptor (TCR) transgenic progenitor cells. The chimeric mice with thymic atrophy exhibited a significant decrease in OVA‐specific tTreg and pTreg cells but not polyclonal (pan)‐Treg cells. These OVA‐specific pTreg cells were significantly less able to suppress OVA‐specific stimulation‐induced proliferation in vitro and exhibited lower FoxP3 expression. Additionally, we conducted preliminary TCR repertoire diversity sequencing for Treg cells among recent thymic emigrants (RTEs) from Rag(GFP)‐FoxP3(RFP) dual‐reporter mice and observed a trend for decreased diversity in mice with thymic atrophy compared to littermates with normal thymus. These data indicate that although the effects of age‐related thymic atrophy do not affect pan‐Treg generation, certain tissue‐specific Treg clones may experience abnormal agonist selection. This, combined with enhanced pan‐pTreg cells, may greatly contribute to age‐related chronic inflammation, even in the absence of acute autoimmune disease in the elderly.