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1.
J Sch Nurs ; : 10598405241228448, 2024 Feb 19.
Article in English | MEDLINE | ID: mdl-38374640

ABSTRACT

COVID-19 brought significant changes to the role of school nurses, necessitating the development of remote health education programs. However, there is a lack of evidence and pedagogical lessons for digitally transforming education for socially vulnerable children. This qualitative study analyzes the health educational needs and barriers faced by children and service providers in a childcare-based obesity prevention program during the pandemic in South Korea. Through a thematic content analysis, four core themes emerged: (a) heightened concerns about obesity and the pandemic's impact on facilities, (b) unexpected positive outcomes of the program, (c) digital readiness gaps, and (d) insufficient program satisfaction (better than nothing). When designing a digital-based health education program for vulnerable children, assessing individual readiness and facility suitability is crucial. Additionally, school nurses should incorporate hybrid pedagogy, integrating technology-mediated activities. By leveraging technology effectively and considering individual and environmental factors, educators can provide comprehensive and accessible health education.

2.
Int J Mol Sci ; 24(22)2023 Nov 13.
Article in English | MEDLINE | ID: mdl-38003458

ABSTRACT

Although it has been suggested that toll-like receptor (TLR) 3 and TLR4 activation alters mesenchymal stromal cells (MSCs)' immunoregulatory function as anti- or pro-inflammatory phenotypes, we have previously confirmed that TLR4-primed hUCB-MSCs alleviate lung inflammation and tissue injury in an E. coli-induced acute lung injury (ALI) mouse model. Therefore, we hypothesized that strong stimulation of TLR3 or TLR4 prompts hUCB-MSCs to exhibit an anti-inflammatory phenotype mediated by extracellular vesicles (EVs). In this study, we compared the anti-inflammatory effect of TLR3-primed and TLR4-primed hUCB-MSCs against an LPS-induced ALI in vitro model by treating MSCs, MSC-derived conditioned medium (CM), and MSC-derived extracellular vesicles (EVs). LPS-induced rat primary alveolar macrophage and RAW 264.7 cells were treated with naïve, TLR3-, and TLR4-primed MSCs and their derived CM and EVs. Flow cytometry and ELISA were used to evaluate M1-M2 polarization of macrophages and pro-inflammatory cytokine levels, respectively. LPS-stimulated macrophages showed significantly increased pro-inflammatory cytokines compared to those of the normal control, and the percentage of M2 macrophage phenotype was predominantly low. In reducing the inflammatory cytokines and enhancing M2 polarization, TLR3- and TLR4-primed MSCs were significantly more effective than the naïve MSCs, and this finding was also observed with the treatment of MSC-derived CMs and EVs. No significant difference between the efficacy of TLR3- and TLR-primed MSCs was observed. Strong stimulation of TLR3- and TLR4-stimulated hUCB-MSCs significantly reduced pro-inflammatory cytokine secretion from LPS-induced macrophages and significantly enhanced the M2 polarization of macrophages. We further confirmed that TLR-primed MSC-derived EVs can exert anti-inflammatory and immunosuppressive effects alone comparable to MSC treatment. We hereby suggest that in the LPS-induced macrophage in vitro model, EVs derived from both TLR3 and TLR4-primed MSCs can be a therapeutic candidate by promoting the M2 phenotype.


Subject(s)
Acute Lung Injury , Extracellular Vesicles , Mesenchymal Stem Cells , Mice , Rats , Animals , Toll-Like Receptor 3 , Lipopolysaccharides/toxicity , Toll-Like Receptor 4 , Escherichia coli , Macrophages , Cytokines , Acute Lung Injury/chemically induced , Acute Lung Injury/therapy , Anti-Inflammatory Agents/pharmacology , Extracellular Vesicles/physiology
3.
Nutrients ; 15(8)2023 Apr 18.
Article in English | MEDLINE | ID: mdl-37111159

ABSTRACT

Diet-related disparities that have often been observed in vulnerable families may play a negative role in children's health and health-related quality of life. In South Korea, an afterschool care policy, called Community Childcare Center (CCC), was established in the 1960s to protect and educate vulnerable children; this role has expanded to provide meal services in recent times. Therefore, the CCCs' food environment has become a pivotal platform for observing children's nutrition and health-related disparities. Using a mixed-methods approach including a survey with self-reported questionnaires, field observation, and participant interviews, the food environment of CCC was explored alongside children's eating behaviors. Eating behaviors were not as healthy as expected. Although service providers and cooks reported in the survey responses that the centers' food environment was healthy, participant observations and interviews revealed a significant gap. Establishing a standardized food environment and improving the nutrition literacy of workers as a significant human resource at a CCC can promote healthy eating for vulnerable children. The findings suggest that in the absence of steps to improve the food environment of CCC, diet-related disparities may affect children's health in the future.


Subject(s)
Child Care , Child Health , Humans , Child , Quality of Life , Diet , Child Day Care Centers , Meals
4.
Healthcare (Basel) ; 10(12)2022 Nov 28.
Article in English | MEDLINE | ID: mdl-36553913

ABSTRACT

The COVID-19 pandemic has highlighted the importance of technology for communication and social interactions. Especially for children in low-income families-a vulnerable population suffering from health and digital disparities-the situation worsened during the pandemic. Earlier studies in times of COVID-19 suggested that the children in Korea who usually do homework and dine at community childcare centers (CCCCs, free after-school care places) need to learn more about how to eat healthily and how to interact with others using digital technology. Therefore, to reduce these children's health and digital inequalities, an interactive live and online cooking program was developed and provided to 313 children and 95 staff members at the 29 CCCCs located in the southern provinces in South Korea. The aim of the current study was to explore the experiences of children and staff with the program. After surveying their experiences, a high degree of satisfaction was found (children: 3.60 ± 0.10; staff: 3.63 ± 0.08 points out of 4.00). Aspects that needed improvement in the program were related to (in)experience in online technology, the frequency and timing of the cooking classes, and the communication between the centers and (online) chefs. In addition, in a word cloud analysis, terms such as 'fun', 'delicious', and 'want' were highlighted for children, and terms such as 'participating' and 'preparation' dominantly appeared for the staff. In the analysis of negative experiences, terms related to environmental factors such as 'sound', 'hear', and 'voice' were highlighted. This novel but preliminary approach for children from low-income families, by integrating cooking with digital technology, indicates that with enough digital support, the CCCCs are a promising platform to promote healthy eating and digital literacy. Optimizing and disseminating these strategies during this pandemic period, and future pandemics, could be beneficial to keep children in their communities healthy, and ultimately reduce socioeconomic health disparities.

5.
Int J Mol Sci ; 23(20)2022 Oct 14.
Article in English | MEDLINE | ID: mdl-36293106

ABSTRACT

Cumulative studies have indicated that high-dose vitamin C has antitumor effects against a variety of cancers. However, the molecular mechanisms underlying these inhibitory effects against tumorigenesis and metastasis, particularly in relation to pancreatic cancer, are unclear. Here, we report that vitamin C at high concentrations impairs the growth and survival of pancreatic ductal adenocarcinoma (PDAC) cells by inhibiting glucose metabolism. Vitamin C was also found to trigger apoptosis in a caspase-independent manner. We further demonstrate that it suppresses the invasion and metastasis of PDAC cells by inhibiting the Wnt/ß-catenin-mediated epithelial-mesenchymal transition (EMT). Taken together, our results suggest that vitamin C has therapeutic effects against pancreatic cancer.


Subject(s)
Carcinoma, Pancreatic Ductal , Pancreatic Neoplasms , Humans , Wnt Signaling Pathway , beta Catenin/metabolism , Ascorbic Acid/pharmacology , Cell Proliferation , Carcinoma, Pancreatic Ductal/pathology , Pancreatic Neoplasms/pathology , Epithelial-Mesenchymal Transition , Carcinogenesis , Caspases/metabolism , Glucose/pharmacology , Cell Line, Tumor , Cell Movement , Pancreatic Neoplasms
6.
Exp Mol Med ; 53(12): 1877-1887, 2021 12.
Article in English | MEDLINE | ID: mdl-34876693

ABSTRACT

BIX01294 (BIX), an inhibitor of the G9a histone methyltransferase, has been reported to have antitumor activity against a variety of cancers. However, the molecular mechanisms underlying its anticancer effects, particularly those against lung cancer, remain unclear. Here, we report that BIX induces apoptotic cell death in EGFR-mutant non-small cell lung cancer (NSCLC) cells but not in their wild-type counterparts. Treatment with BIX resulted in a significant reduction in the EGFR level and inhibition of EGFR signaling only in EGFR-mutant NSCLC cells, leading to apoptosis. BIX also inhibited mitochondrial metabolic function and decreased the cellular energy levels that are critical for maintaining the EGFR level. Furthermore, BIX transcriptionally downregulated the transcription of branched-chain α-keto acid dehydrogenase (BCKDHA), which is essential for fueling the tricarboxylic acid (TCA) cycle. Interestingly, this BCKDHA downregulation was due to inhibition of Jumanji-domain histone demethylases but not the G9a histone methyltransferase. We observed that KDM3A, a Jumonji histone demethylase, epigenetically regulates BCKDHA expression by binding to the BCKDHA gene promoter. BIX exposure also led to a significant decrease in the EGFR level, causing apoptosis in EGFR-TKI (tyrosine kinase inhibitor)-resistant cell lines, which are dependent on EGFR signaling for survival. Taken together, our current data suggest that BIX triggers apoptosis only in EGFR-mutant NSCLC cells via inhibition of BCKDHA-mediated mitochondrial metabolic function.


Subject(s)
3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)/metabolism , Adenocarcinoma of Lung/genetics , Adenocarcinoma of Lung/metabolism , Azepines/pharmacology , Quinazolines/pharmacology , Signal Transduction/drug effects , Adenocarcinoma of Lung/pathology , Apoptosis/genetics , Biomarkers , Cell Line, Tumor , Citric Acid Cycle , Disease Susceptibility , Drug Resistance, Neoplasm/genetics , Energy Metabolism , ErbB Receptors/genetics , ErbB Receptors/metabolism , Histone Demethylases , Humans , Immunohistochemistry , Mitochondria/metabolism , Models, Biological , Protein Kinase Inhibitors/pharmacology
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