Development of a campus-based intervention program to strengthen food literacy among university students: A qualitative formative study

Objectives: This study aimed to develop a campus-based intervention program to enhance food literacy (FL) among university students. Methods: In the initial phase, we conducted a literature review of FL intervention studies and held in-depth interviews with university students to identify facilitators and barriers to improving and practicing FL. Expert counseling sessions were conducted with nutrition education, marketing, and service design professionals. The results of this phase led to the creation of an initial curriculum draft. In the second phase, a follow-up survey was conducted with young adults to assess the acceptability of the developed curriculum. After the follow-up survey, additional meetings were conducted with the aforementioned experts, and the curriculum was further refined based on their input. Results: An 11-week FL intervention program was devised using constructs from the Social Cognitive Theory. The weekly curriculum consisted of 90-min theory-based and 90-min hands-on experience sessions. Three primary aspects of FL were covered: nutrition and food safety, cultural and relational dimensions, and socio-ecological aspects. Program highlights included cooking sessions for crafting traditional Korean desserts, lectures on animal welfare, insights into zero-waste practices, and communal eating experiences. Based on the study team’s previous research, the program also addressed mindful eating, helping participants understand the relationship with their eating habits, and providing strategies to manage negative emotions without resorting to food. Yoga sessions and local farm visits were incorporated into the curriculum to promote holistic well-being. Conclusions: This study elucidated the comprehensive process of creating a campus-based curriculum to enhance FL among university students, a group particularly susceptible to problematic eating behaviors and low FL levels. The developed program can serve as a blueprint for adaptation to other campuses seeking to bolster students’ FL

Information Security Modeling for the Operation of a Novel Highly Trusted Network in a Virtualization Environment

A novel network architecture to be deployed in Korea is so called HTN (highly trusted network). The aim of HTN is the seamless communication of information in a secure manner, anytime and anywhere, in the national administration network infrastructure. In this paper, we present the results of information security modeling for the HTN. Through the use of security modeling procedure, we derive the requirements and corresponding technology for security control of the system by analyzing threat elements and attack possibility. First we analyze threat of each component for the HTN by STRIDE modeling and later construct an attack tree by analyzing attack examples for every threat. Finally we propose the security requirements and technology to respond against them, based on the analyzed threats and attack examples

Minor Ginsenoside Rg2 and Rh1 Attenuates LPS-Induced Acute Liver and Kidney Damages via Downregulating Activation of TLR4-STAT1 and Inflammatory Cytokine Production in Macrophages

Ginsenosides have been reported to have various biological effects, such as immune regulation and anticancer activity. In this study, we investigated the anti-inflammatory role of a combination of Rg2 and Rh1, which are minor ginsenosides, in lipopolysaccharide (LPS)-stimulated inflammation. In vitro experiments were performed using the RAW264.7 cell line, and an in vivo model of inflammation was established using LPS-treated ICR mice. We employed Griess assay, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, quantitative reverse transcriptase-polymerase chain reaction, western blotting, immunofluorescence staining, and hematoxylin and eosin staining to evaluate the effect of Rg2 and Rh1. We found that Rg2 and Rh1 significantly decreased LPS-induced major inflammatory mediator production, inducible-nitric oxide synthase expression, and nitric oxide production in macrophages. Moreover, Rg2 and Rh1 combination treatment inhibited the binding of LPS to toll-like receptor 4 (TLR4) on peritoneal macrophages. Therefore, the combination of ginsenoside Rg2 and Rh1 suppressed inflammation by abolishing the binding of LPS to TLR4, thereby inhibiting the TLR4-mediated signaling pathway. The combined ginsenoside synergistically blocked LPS-mediated PKCδ translocation to the plasma membrane, resulting in p38-STAT1 activation and NF-κB translocation. In addition, mRNA levels of pro-inflammatory cytokines, including TNF-α, IL-1β, and IFN-β, were significantly decreased by combined ginsenoside treatment. Notably, the 20 mg/kg ginsenoside treatment significantly reduced LPS-induced acute tissue inflammation levels in vivo, as indicated by the tissue histological damage scores and the levels of biochemical markers for liver and kidney function from mouse serum. These results suggest that the minor ginsenosides Rg2 and Rh1 may play a key role in prevention of LPS-induced acute inflammation and tissue damage

Minor Ginsenoside Rg2 and Rh1 Attenuates LPS-Induced Acute Liver and Kidney Damages via Downregulating Activation of TLR4-STAT1 and Inflammatory Cytokine Production in Macrophages

Ginsenosides have been reported to have various biological effects, such as immune regulation and anticancer activity. In this study, we investigated the anti-inflammatory role of a combination of Rg2 and Rh1, which are minor ginsenosides, in lipopolysaccharide (LPS)-stimulated inflammation. In vitro experiments were performed using the RAW264.7 cell line, and an in vivo model of inflammation was established using LPS-treated ICR mice. We employed Griess assay, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, quantitative reverse transcriptase-polymerase chain reaction, western blotting, immunofluorescence staining, and hematoxylin and eosin staining to evaluate the effect of Rg2 and Rh1. We found that Rg2 and Rh1 significantly decreased LPS-induced major inflammatory mediator production, inducible-nitric oxide synthase expression, and nitric oxide production in macrophages. Moreover, Rg2 and Rh1 combination treatment inhibited the binding of LPS to toll-like receptor 4 (TLR4) on peritoneal macrophages. Therefore, the combination of ginsenoside Rg2 and Rh1 suppressed inflammation by abolishing the binding of LPS to TLR4, thereby inhibiting the TLR4-mediated signaling pathway. The combined ginsenoside synergistically blocked LPS-mediated PKCδ translocation to the plasma membrane, resulting in p38-STAT1 activation and NF-κB translocation. In addition, mRNA levels of pro-inflammatory cytokines, including TNF-α, IL-1β, and IFN-β, were significantly decreased by combined ginsenoside treatment. Notably, the 20 mg/kg ginsenoside treatment significantly reduced LPS-induced acute tissue inflammation levels in vivo, as indicated by the tissue histological damage scores and the levels of biochemical markers for liver and kidney function from mouse serum. These results suggest that the minor ginsenosides Rg2 and Rh1 may play a key role in prevention of LPS-induced acute inflammation and tissue damage.</jats:p