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JeongSil Choi,Heakyung Moon,Mijeong Park 한국여성건강간호학회 2023 여성건강간호학회지 Vol.29 No.3
Purpose: The aim of this study was to explore the continuous usage intention of head-mounted display-based virtual reality (HMD-based VR) content among college students. The study also sought to understand how this intention is influenced by factors related to personal cognition, social aspects, VR content, and HMD-related elements.Methods: This descriptive correlational study used a self-report questionnaire to survey 217 students from two universities in Korea who had prior experience with HMD-based VR content.Results: The mean score for continuous usage intention of HMD-based VR content was 2.59±0.57 points (range, 1–5 points). Regarding the average frequency of HMD-based VR content usage, 64.5% of participants reported using it 1 to 2 times, while 91.7% indicated a total HMD-based VR usage period of less than 6 months. Factors such as personal cognition, VR content, social aspects, and HMD-related elements had explanatory power of 35.1%, 10.7%, 4.4%, and 2.5%, respectively, for the continuous usage intention of HMD-based VR content. Additionally, engagement (β=.45, p<.001), influential others (β=.37, p<.001), environmental support (β=–.18, p=.030), and cyber sickness (β=–.21, p=.001) were identified as having a significant influence.Conclusion: When developing HMD-based VR content, strategies to improve users’ personal cognition should be included. Additionally, it is necessary to develop strategies that enhance enjoyment and interest in the content, while also facilitating ongoing social support. Furthermore, coping strategies should be devised that take into account cyber sickness, a potential side effect of these devices.
Jin, Li Hua,Choi, Jung Kyoon,Kim, Byungil,Cho, Hwan Sung,Kim, Jihyun,Kim-Ha, Jeongsil,Kim, Young-Joon American Society for Microbiology 2009 Molecular and cellular biology Vol.29 No.6
<B>ABSTRACT</B><P><I>Drosophila</I> producing a mutant form of the putative transcription coregulator, Split ends (Spen), originally identified in the analysis of neuronal development, display diverse immune defects. In order to understand the role of Spen in the innate immune response, we analyzed the transcriptional defects associated with <I>spen</I> mutant hemocytes and their relationship to the Notch signaling pathways. Spen is regulated by the Notch pathway in the lymph glands and is required for Notch-dependent activation of a large number of genes involved in energy metabolism and differentiation. Analysis of the epigenetic marks associated with Spen-dependent genes indicates that Spen performs its function as a coactivator by regulating chromatin modification. Intriguingly, expression of the Spen-dependent genes was transiently downregulated in a Notch-dependent manner by the Dif activated upon recognition of pathogen-associated molecules, demonstrating the existence of cross talk between hematopoietic regulation and the innate immune response. Our observations reveal a novel connection between the Notch and Toll/IMD signaling pathways and demonstrate a coactivating role for Spen in activating Notch-dependent genes in differentiating cells.</P>
Jihyun Kim,Nuri Choi,Jeongsil Kim-Ha 생화학분자생물학회 2023 BMB Reports Vol.56 No.4
Glial cells play important roles during neurogenesis and inmaintaining complex functions of the nervous system. Here,we report the characterization of a gene, Sdr, which contains aputative insulin-like growth factor receptor domain and is requiredto maintain critical nervous system functions in Drosophila. Sdr is expressed in glial cells during embryonic and larval stagesof development, but its role in adult flies is poorly understood. As insulin signaling is important throughout the lifespan inhuman, we investigated the Sdr’s role in adult flies. Our resultsdemonstrate that Sdr is expressed on surface glial cells thatsurround the nervous system. Mutation of Sdr did not affect developmentbut caused defects in locomotion and lifespan. Sdrmutants also showed increasingly severe defects in the bloodbrain-and blood-retina-barriers as they aged. Therefore, wesuggest a novel role of Sdr in maintaining the integrity of theblood-brain- and blood-retina-barriers in adult flies.
( Wook-bin Lee ),( Won Young Choi ),( Dong-hyun Lee ),( Hyeran Shim ),( Jeongsil Kim-ha ),( Young-joon Kim ) 생화학분자생물학회(구 한국생화학분자생물학회) 2019 BMB Reports Vol.52 No.2
Upon viral infection, the 2’, 5’-oligoadenylate synthetase (OAS)-ribonuclease L (RNaseL) system works to cleave viral RNA, thereby blocking viral replication. However, it is unclear whether OAS proteins have a role in regulating gene expression. Here, we show that OAS1 and OAS3 act as negative regulators of the expression of chemokines and interferon-responsive genes in human macrophages. Clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-associated protein-9 nuclease (Cas9) technology was used to engineer human myeloid cell lines in which the OAS1 or OAS3 gene was deleted. Neither OAS1 nor OAS3 was exclusively responsible for the degradation of rRNA in macrophages stimulated with poly(I:C), a synthetic surrogate for viral double-stranded (ds)RNA. An mRNA sequencing analysis revealed that genes related to type I interferon signaling and chemokine activity were increased in OAS1<sup>-/-</sup> and OAS3<sup>-/-</sup> macrophages treated with intracellular poly(I:C). Indeed, retinoic-acid-inducible gene (RIG)-I- and interferon-induced helicase C domain-containing protein (IFIH1 or MDA5)-mediated induction of chemokines and interferon-stimulated genes was regulated by OAS3, but Toll-like receptor 3 (TLR3)- and TLR4-mediated induction of those genes was modulated by OAS1 in macrophages. However, stimulation of these cells with type I interferons had no effect on OAS1- or OAS3- mediated chemokine secretion. These data suggest that OAS1 and OAS3 negatively regulate the expression of chemokines and interferon-responsive genes in human macrophages. [BMB Reports 2019; 52(2): 133-138]
( Si-cho Kim ),( Jiwon Kim ),( Da-won Kim ),( Yanghee Choi ),( Kyunghyun Park ),( Eun Ju Cho ),( Su Jong Yu ),( Jeongsil Kim-ha ),( Young-joon Kim ) 생화학분자생물학회 2022 BMB Reports Vol.55 No.11
Hepatocellular carcinoma (HCC) is dangerous cancer that often evades early detection because it is asymptomatic and an effective detection method is lacking. For people with chronic liver inflammation who are at high risk of developing HCC, a sensitive detection method for HCC is needed. In a meta-analysis of The Cancer Genome Atlas pan-cancer methylation database, we identified a CpG island in the USP44 promoter that is methylated specifically in HCC. We developed methylation-sensitive high-resolution melting (MS-HRM) analysis to measure the methylation levels of the USP promoter in cell-free DNA isolated from patients. Our MS-HRM assay correctly identified 40% of patients with early-stage HCC, whereas theα-fetoprotein test, which is currently used to detect HCC, correctly identified only 25% of early-stage HCC patients. These results demonstrate that USP44 MS-HRM analysis is suitable for HCC surveillance. [BMB Reports 2022; 55(11): 553-558]
Intragenic CpG islands play important roles in bivalent chromatin assembly of developmental genes
Lee, Sun-Min,Lee, Jungwoo,Noh, Kyung-Min,Choi, Won-Young,Jeon, Sejin,Oh, Goo Taeg,Kim-Ha, Jeongsil,Jin, Yoonhee,Cho, Seung-Woo,Kim, Young-Joon National Academy of Sciences 2017 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.114 No.10
<P>CpG, 5'-C-phosphate-G-3', islands (CGIs) have long been known for their association with enhancers, silencers, and promoters, and for their epigenetic signatures. They are maintained in embryonic stem cells (ESCs) in a poised but inactive state via the formation of bivalent chromatin containing both active and repressive marks. CGIs also occur within coding sequences, where their functional role has remained obscure. Intragenic CGIs (iCGIs) are largely absent from housekeeping genes, but they are found in all genes associated with organ development and cell lineage control. In this paper, we investigated the epigenetic status of iCGIs and found that they too reside in bivalent chromatin in ESCs. Cell type-specific DNA methylation of iCGIs in differentiated cells was linked to the loss of both the H3K4me3 and H3K27me3 marks, and disruption of physical interaction with promoter regions, resulting in transcriptional activation of key regulators of differentiation such as PAXs, HOXs, and WNTs. The differential epigenetic modification of iCGIs appears to be mediated by cell type-specific transcription factors distinct from those bound by promoter, and these transcription factors may be involved in the hypermethylation of iCGIs upon cell differentiation. iCGIs thus play a key role in the cell type-specific regulation of transcription.</P>