Clothing Pressure Measurement and Subjective Wear Test of Commercial Bra Tops for The Development of Active Senior’s Yoga Wear

Recently, women in 50~60s are constantly investing time in their workouts because they are interested in the quality of their lives. Among various indoor activities, they enjoy yoga because these are easy to access and good to make beautiful body shape (Yu & Choi, 2013). According to the market survey, sports wear companies lack awareness of the need for yoga clothing by elderly women, and women in their 50s and 60s have had difficulty buying yoga suits that fit their bodies. In this paper, basic information for the development of yoga wear was studied focused on bra top that is the most important part affecting the fit of yoga wear

Gene 33/Mig6 Inhibits Hexavalent Chromium-Induced DNA Damage and Cell Transformation in Human Lung Epithelial Cells

Hexavalent Chromium [Cr(VI)] compounds are human lung carcinogens and environmental/occupational hazards. The molecular mechanisms of Cr(VI) carcinogenesis appear to be complex and are poorly defined. In this study, we investigated the potential role of Gene 33 (ERRFI1, Mig6), a multifunctional adaptor protein, in Cr(VI)-mediated lung carcinogenesis. We show that the level of Gene 33 protein is suppressed by both acute and chronic Cr(VI) treatments in a dose- and time-dependent fashion in BEAS-2B lung epithelial cells. The inhibition also occurs in A549 lung bronchial carcinoma cells. Cr(VI) suppresses Gene 33 expression mainly through post-transcriptional mechanisms, although the mRNA level of gene 33 also tends to be lower upon Cr(VI) treatments. Cr(VI)-induced DNA damage appears primarily in the S phases of the cell cycle despite the high basal DNA damage signals at the G2M phase. Knockdown of Gene 33 with siRNA significantly elevates Cr(VI)-induced DNA damage in both BEAS-2B and A549 cells. Depletion of Gene 33 also promotes Cr(VI)-induced micronucleus (MN) formation and cell transformation in BEAS-2B cells. Our results reveal a novel function of Gene 33 in Cr(VI)-induced DNA damage and lung epithelial cell transformation. We propose that in addition to its role in the canonical EGFR signaling pathway and other signaling pathways, Gene 33 may also inhibit Cr(VI)-induced lung carcinogenesis by reducing DNA damage triggered by Cr(VI)

Gene 33/Mig6 Regulates Apoptosis and the DNA Damage Response through Independent Mechanisms

Gene 33 (Mig6, ERRFI1) is an inducible adaptor/scaffold protein whose expression can be induced by both stress and mitogenic signals. It contains multiple domains for protein-protein interaction and is involved in a broad spectrum of cellular functions. Gene 33 promotes apoptosis in a cell type-dependent manner. A recent study has linked Gene 33 to the DNA damage response (DDR) induced by hexavalent chromium [Cr(VI)]. Here we show that Gene 33 induces apoptosis via both c-Abl/p73 and EGFR/AKT-dependent pathways in lung epithelial and lung carcinoma cells. Ectopic expression of Gene 33 also triggers DDR in an ATM-dependent fashion and through pathways with or without association with apoptosis. We observed significant presence of Gene 33 in the nucleus and chromatin. We show that the nuclear localization of Gene 33 is dependent on its 14-3-3 binding domain. We find that the chromatin localization of Gene 33 is, at least in part, dependent on its EBD motif. Our data also show that Gene 33 may regulate chromatin targeting of c-Abl and EGFR. Moreover, we observed strong association of Gene 33 with histone H2AX and that Gene 33 promotes interaction between ATM and histone H2AX without triggering DNA damage. Our study reveals novel nuclear functions of Gene 33, which mediate DDR and apoptosis through independent mechanisms. Given our previous finding that Gene 33 depletion promotes Cr(VI)-induced DNA damage, our data suggest that Gene 33 may foster DNA repair by activating DDR

Culturally inclusive learning for Indigenous students in a Learning Management System (LMS)

A Learning Management System (LMS) such as Blackboard, Moodle and Web City has been utilised for enhancing the quality of learning and teaching in Australian universities. Yet there are no specific university policies and guidelines addressing the digital divide in the use of an LMS. In particular, Indigenous cultural values are rarely considered in LMS based learning design. As a result, the equity gap in terms of the quality of learning opportunities for Indigenous students remains unidentified. In this context, the project was aimed at identifying cultural needs of Indigenous students in the online learning environment and articulating culturally inclusive learning for Indigenous students in an LMS. Based on the literature review in the fields of culturally inclusive learning, online and blended learning, and Aboriginal pedagogies, we created a conceptual framework for culturally inclusive learning with four dimensions: communication, collaboration, community, and interculturality that was used in the following three stages: policy and guideline review, quantitative data analysis, and qualitative data analysis

Dietary patterns and metabolic syndrome risk factors among adolescents

PurposeUnbalanced diets and decreased physical activity have contributed to increased prevalence of obesity and metabolic syndrome in adolescents. We have performed a systematic review and data analysis to examine the association between dietary pattern and metabolic syndrome risk factors in adolescents.MethodsWe searched the PubMed and BioMedLib databases for appropriate articles published during the past 10 years and selected 6 articles. The studies reviewed applied factor analysis or cluster analysis to extract dietary patterns. For data analysis, we examined the association between dietary patterns and the prevalence of metabolic syndrome risk factors using data of 3,168 adolescents (13 to 18 years) obtained from 4 consecutive Korean Nutrition Health and Nutrition Examination Surveys (1998, 2001, 2005, and 2007 to 2009).ResultsOur systematic review confirmed that western dietary patterns are positively associated with metabolic syndrome risk factors such as obesity and elevated triglycerides, while traditional dietary patterns were negatively associated. Data analysis found that the number of adolescents aged 16 to 18 years who had "Rice & Kimchi" dietary pattern decreased, while the number having western dietary patterns increased during the 1998 to 2009 time frame. There were no changes in the dietary patterns in adolescents aged 13 to 15 years. The risk of elevated serum triglycerides and reduced serum high density lipoprotein cholesterol was high in the "Rice & Kimchi" dietary pattern compared to the other dietary pattern groups.ConclusionBecause adolescents' dietary patterns are changing continuously and have long-term effects, further studies on the dietary patterns of adolescents and their health effects into adulthood are necessary

Association between exposure to traffic-related air pollution and pediatric allergic diseases based on modeled air pollution concentrations and traffic measures in Seoul, Korea: a comparative analysis

Background Pediatric allergic diseases are a major public health concern, and previous studies have suggested that exposure to traffic-related air pollution (TRAP) exposure is a risk factor. These studies have typically assessed TRAP exposure using traffic measures, such as distance to major roads, or by modeling air pollutant concentrations; however inconsistent associations with pediatric allergic diseases have often been found. Using road proximity and density, we previously found an association between TRAP and atopic eczema among approximately 15,000 children living in Seoul, Korea, heavily populated and highly polluted city in which traffic is a major emission source. We aimed to conduct a parallel analysis using modeled air pollution concentrations and thus examine the consistency of the association. Specifically, we examined the associations of individual-level annual-average concentrations of NO2, PM10, and PM2.5 with symptoms and diagnoses of three pediatric allergic diseases including asthma, allergic rhinitis, and atopic eczema. Methods The study population included 14,614 children from the Seoul Atopy Friendly School Project Survey in Seoul, Korea, in 2010. To assess individual exposures to TRAP among these children, we predicted annual-average concentrations of NO2, PM10, and PM2.5 at the childrens home addresses in 2010 using universal kriging and land use regression models along with regulatory air quality monitoring data and geographic characteristics. Then, we estimated odds ratios (ORs) of the three allergic diseases for interquartile increases in air pollution concentrations after adjusting for individual risk factors in mixed effects logistic regression. Results Symptoms and diagnoses of atopic eczema symptoms showed an association with NO2 (OR = 1.07, 95% confidence interval = 1.02–1.13; 1.08, 1.03–1.14) and PM10 (1.06, 1.01–1.12; 1.07, 1.01–1.13). ORs of PM2.5 were positive but not statistically significant (1.01, 0.95–1.07; 1.04, 0.98–1.10). No association was found between asthma and allergic rhinitis, although PM2.5 showed a marginal association with allergic rhinitis. Conclusions Our consistent findings regarding the association between TRAP and the prevalence of atopic eczema using traffic measures and surrogate air pollutants suggested the effect of TRAP on childrens health. Follow-up studies should elucidate the causal link, to support subsequent policy considerations and minimize adverse health effects in children.This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2013R1A6A3A04059017, 2018R1A2B6004608) and the National Cancer Center of Korea (NCC-1810220-01). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Severe protein C deficiency in a newborn caused by a homozygous pathogenic variant in the PROC gene: a case report

Background Severe protein C deficiency is a rare and inherited cause of thrombophilia in neonates. Protein C acts as an anticoagulant, and its deficiency results in vascular thrombosis. Herein, we report a case of protein C deficiency with a homozygous pathogenic variant in a term neonate, with good outcomes after proper treatment. Case presentation A four-day-old male newborn was transferred to the Seoul National University Hospital on account of dark red to black skin lesions. He was born full-term with an average birth weight without perinatal problems. There were no abnormal findings in the prenatal tests, including intrauterine sonography. The first skin lesion was observed on his right toes and rapidly progressed to proximal areas, such as the lower legs, left arm, and buttock. Under the impression of thromboembolism or vasculitis, we performed a coagulopathy workup, which revealed a high D-dimer level of 23.05 μg/ml. A skin biopsy showed fibrin clots in most capillaries, and his protein C activity level was below 10%, from which we diagnosed protein C deficiency. On postnatal day 6, he experienced an apnea event with desaturation and an abnormal right pupillary light reflex. Brain computed tomography showed multifocal patchy intracranial hemorrhage and intraventricular hemorrhage with an old ischemic lesion. Ophthalmic examination revealed bilateral retinal traction detachments with retinal folds. Protein C concentrate replacement therapy was added to previous treatments including steroids, prostaglandin E1, and anticoagulation. After replacement therapy, there were no new skin lesions, and the previous lesions recovered with scarring. Although there were no new brain hemorrhagic infarctions, there was ongoing ischemic tissue loss, which required further rehabilitation. Ophthalmic surgical interventions were performed to treat the bilateral retinal traction detachments with retinal folds. Molecular analysis revealed a homozygous pathogenic variant in the PROC gene. Conclusion Severe protein C deficiency can manifest as a fatal coagulopathy in any organ. Early diagnosis and proper treatment, including protein C concentrate replacement, may improve outcomes without serious sequelae

Caspase-4 is essential for saikosaponin a-induced apoptosis acting upstream of caspase-2 and γ-H2AX in colon cancer cells

Saikosaponin a (SSa), a bioactive phytochemical from Bupleurum, triggers sequential caspase-2 and caspase-8 activation, and thereby induces caspase-mediated apoptosis in human colon carcinoma (HCC) cells. However, the upstream mechanism of caspase-2 activation remains unknown. Therefore, we investigated the signaling mechanisms underlying SSa-induced caspase activation and apoptosis in HCC cells. SSa treatment triggered marked antitumor effects, especially in HCC cells, in a cell culture model and a mouse xenograft model. SSa also induced the activation of several endoplasmic reticulum (ER) stress signals. Specifically, caspase-4, a critical regulator of ER stress-induced apoptosis, was activated significantly after SSa treatment. Mechanistically, selective inhibition of caspase-4 suppressed SSa-induced apoptosis, colony inhibition, and the activation of caspase-3, -8, and -2, but not vice versa. Consistent with the important role of caspase-2 in the DNA damage response, SSa induced DNA damage, as evidenced by a cytokinesis-block micronucleus assay, single-cell gel electrophoresis, and an increase in the levels of γ-H2AX, a DNA damage marker. Moreover, inhibition of caspase-4 activation inhibited SSa-induced histone H2AX phosphorylation. Taken together, these results suggest that caspase-4 is an upstream regulator of SSa-induced DNA damage and caspase activation in HCC cells. Given that SSa-induced apoptosis appeared to be specific to certain cell types including HCC cells, SSa may be a promising cancer therapy agent in certain types of cancer