BACKGROUND/OBJECTIVES: The high consumption of purine-rich meat is associated with hyperuricemia. However, there is limited evidence linking the consumption of red and processed meat to the genetic risk of hyperuricemia. We investigated the relationship between various combinations of red and processed meat consumption and the polygenic risk scores (PRSs) and the incidence of hyperuricemia in middle-aged Koreans. SUBJECTS/METHODS: We analyzed the data from 44,053 participants aged ≥40 years sourced from the Health Examinees (HEXA) cohort of the Korean Genome and Epidemiology Study (KoGES). Information regarding red and processed meat intake was obtained using a semiquantitative food frequency questionnaire (SQ-FFQ). We identified 69 independent single-nucleotide polymorphisms (SNPs) at uric acid-related loci using genome-wide association studies (GWASs) and clumping analyses. The individual PRS, which is the weighted sum of the effect size of each allele at the SNP, was calculated. We used multivariable Cox proportional hazards models adjusted for covariates to determine the relationship between red and processed meat intake and the PRS in the incidence of hyperuricemia. RESULTS: During an average follow-up period of 5 years, 2,556 patients with hyperuricemia were identified. For both men and women, the group with the highest red and processed meat intake and the highest PRS was positively associated with the development of hyperuricemia when compared with the group with the lowest red and processed meat intake and the lowest PRS (hazard ratio [HR], 2.72; 95% confidence interval [CI], 2.10–3.53; P < 0.0001; HR, 3.28; 95% CI, 2.45–4.40; P < 0.0001). CONCLUSION Individuals at a high genetic risk for uric acid levels should moderate their consumption of red and processed meat to prevent hyperuricemia.

Purpose: Metabolic diseases share common risk factors, requiring the development of therapeutic agents with multi-target effects. Although the ameliorating effects of Porphyra tenera ethanol extract (PTE) have been reported on some individual metabolic disorders, studies addressing various other metabolic diseases are still limited. This study investigated the ameliorating effects of PTE supplementation for 12 weeks on obesity, dyslipidemia, and hepatic lipid metabolism in high-fat diet (HFD)-induced obese mice and its molecular mechanisms. Methods: Male C57BL/6 mice (n = 12/in each group) were divided into six groups for 12 weeks: control, HFD, chow diet + 1% porphyran, chow diet + 4% porphyran, HFD + 1% porphyran (HPYP-L), and HFD + 4% porphyran (HPYP-H). To confirm the attenuation of metabolic disease in vivo, mice in the HFD, HPYP-L and HPYP-H groups were fed 60% HFD to induce obesity. PTE was prepared using ethanol and dissolved in drinking water to concentrations of 1% and 4% porphyran. After 12 weeks of free PTE intake, body weight measurement, serum analysis, histopathological analysis, real-time quantitative polymerase chain reaction, and Western blot analysis of liver tissues were performed for comparative evaluation. Results: After 12 weeks, the HPYP-L and HPYP-H groups showed a decreased body weight, improved blood lipids, and reduced hepatic lipid droplet accumulation vs. the HFD group.Liver acetyl-CoA carboxylase, was suppressed in the HPYP-L group vs. the HFD group.The B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 protein and messenger RNA (mRNA) level ratio in the liver decreased after PTE intake, indicating inhibition of apoptosis.Interleukin-1 beta mRNA expression in the liver was reduced in the HPYP-L group vs. the HFD group. In the liver, lower protein carbonylation levels in the HPYP-H group indicated reduced oxidative stress, while the increased mitochondrial DNAuclear DNA ratio indicated improved mitochondrial function. Conclusion PTE protects against diet-induced metabolic disorders and could be a potential agent for the prevention and treatment of metabolic diseases.

Purpose: Metabolic diseases share common risk factors, requiring the development of therapeutic agents with multi-target effects. Although the ameliorating effects of Porphyra tenera ethanol extract (PTE) have been reported on some individual metabolic disorders, studies addressing various other metabolic diseases are still limited. This study investigated the ameliorating effects of PTE supplementation for 12 weeks on obesity, dyslipidemia, and hepatic lipid metabolism in high-fat diet (HFD)-induced obese mice and its molecular mechanisms. Methods: Male C57BL/6 mice (n = 12/in each group) were divided into six groups for 12 weeks: control, HFD, chow diet + 1% porphyran, chow diet + 4% porphyran, HFD + 1% porphyran (HPYP-L), and HFD + 4% porphyran (HPYP-H). To confirm the attenuation of metabolic disease in vivo, mice in the HFD, HPYP-L and HPYP-H groups were fed 60% HFD to induce obesity. PTE was prepared using ethanol and dissolved in drinking water to concentrations of 1% and 4% porphyran. After 12 weeks of free PTE intake, body weight measurement, serum analysis, histopathological analysis, real-time quantitative polymerase chain reaction, and Western blot analysis of liver tissues were performed for comparative evaluation. Results: After 12 weeks, the HPYP-L and HPYP-H groups showed a decreased body weight, improved blood lipids, and reduced hepatic lipid droplet accumulation vs. the HFD group.Liver acetyl-CoA carboxylase, was suppressed in the HPYP-L group vs. the HFD group.The B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 protein and messenger RNA (mRNA) level ratio in the liver decreased after PTE intake, indicating inhibition of apoptosis.Interleukin-1 beta mRNA expression in the liver was reduced in the HPYP-L group vs. the HFD group. In the liver, lower protein carbonylation levels in the HPYP-H group indicated reduced oxidative stress, while the increased mitochondrial DNAuclear DNA ratio indicated improved mitochondrial function. Conclusion PTE protects against diet-induced metabolic disorders and could be a potential agent for the prevention and treatment of metabolic diseases.

Purpose: Metabolic diseases share common risk factors, requiring the development of therapeutic agents with multi-target effects. Although the ameliorating effects of Porphyra tenera ethanol extract (PTE) have been reported on some individual metabolic disorders, studies addressing various other metabolic diseases are still limited. This study investigated the ameliorating effects of PTE supplementation for 12 weeks on obesity, dyslipidemia, and hepatic lipid metabolism in high-fat diet (HFD)-induced obese mice and its molecular mechanisms. Methods: Male C57BL/6 mice (n = 12/in each group) were divided into six groups for 12 weeks: control, HFD, chow diet + 1% porphyran, chow diet + 4% porphyran, HFD + 1% porphyran (HPYP-L), and HFD + 4% porphyran (HPYP-H). To confirm the attenuation of metabolic disease in vivo, mice in the HFD, HPYP-L and HPYP-H groups were fed 60% HFD to induce obesity. PTE was prepared using ethanol and dissolved in drinking water to concentrations of 1% and 4% porphyran. After 12 weeks of free PTE intake, body weight measurement, serum analysis, histopathological analysis, real-time quantitative polymerase chain reaction, and Western blot analysis of liver tissues were performed for comparative evaluation. Results: After 12 weeks, the HPYP-L and HPYP-H groups showed a decreased body weight, improved blood lipids, and reduced hepatic lipid droplet accumulation vs. the HFD group.Liver acetyl-CoA carboxylase, was suppressed in the HPYP-L group vs. the HFD group.The B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 protein and messenger RNA (mRNA) level ratio in the liver decreased after PTE intake, indicating inhibition of apoptosis.Interleukin-1 beta mRNA expression in the liver was reduced in the HPYP-L group vs. the HFD group. In the liver, lower protein carbonylation levels in the HPYP-H group indicated reduced oxidative stress, while the increased mitochondrial DNAuclear DNA ratio indicated improved mitochondrial function. Conclusion PTE protects against diet-induced metabolic disorders and could be a potential agent for the prevention and treatment of metabolic diseases.

Objectives: This study investigated the association between the frequency and pattern of eating alone and the mental health status according to region in Korean adults. Methods: The data of 10,040 Korean adults aged ≥ 19 years from the Korea National Health and Nutrition Examination Survey (KNHANES) 2017 and 2019 were used.Participants were divided into 4 groups based on their frequency of eating alone: none (all meals together), 1, 2, and 3 meals/day alone. The regions were divided into urban and rural areas. Mental health status was assessed by stress recognition, depressive symptoms, and suicidal ideation. Multivariable logistic regressions were conducted to estimate the adjusted odds ratios (AORs) with 95% confidence intervals (CIs) on the association of the frequency and pattern of eating alone with poor mental health after controlling for covariates. Results: Among Korean adults, 74.1% ate more than one meal a day alone. Individuals having 3 meals a day alone tended to be less educated, single, single person households, or living in urban areas (all P < 0.05). In rural areas, those having 3 meals/ day alone had higher odds of stress recognition (AOR: 1.55, 95% CI: 1.02-2.35) than those having all meals together. In urban areas, individuals eating alone 3 times/day had higher odds of stress recognition (AOR: 1.60, 95% CI: 1.31-1.96), depressive symptoms (AOR: 1.61, 95% CI: 1.23-2.12), and suicidal ideation (AOR: 2.14, 95% CI: 1.42-3.22) compared to those having all meals together. Urban residents having dinner alone had higher odds of depressive symptoms (AOR: 1.29, 95% CI: 1.05-1.58) and suicidal ideation (AOR: 1.66, 95% CI: 1.19-2.33) than those having dinner with others. Conclusions Our findings showed that the frequency and patterns of eating alone were differentially associated with increased odds of poor mental health according to region of residence. Nutrition education is needed for those frequently eating alone, particularly those living in urban areas, to highlight the advantages of eating together and to ensure that they have balanced and healthy meals even if they eat alone.

An organoid is a self-organized three-dimensional structure derived from stem cells that mimics the structure, cell composition, and functional characteristics of specific organs and tissues and is used for evaluating the safety and effectiveness of drugs and the toxicity of industrial chemicals. Organoid technology is a new methodology that could replace testing on animals testing and accelerate development of precision and regenerative medicine. However, large variations in production can occur between laboratories with low reproducibility of the production process and no internationally agreed standards for quality evaluation factors at endpoints. To overcome these barriers that hinder the regulatory acceptance and commercialization of organoids, Korea established the Organoid Standards Initiative in September 2023 with various stakeholders, including industry, academia, regulatory agencies, and standard development experts, through public and private partnerships. This developed general guidelines for organoid manufacturing and quality evaluation and for quality evaluation guidelines for organoid-specific manufacturing for the liver, intestines, and heart through extensive evidence analysis and consensus among experts. This report is based on the common standard guideline v1.0, which is a general organoid manufacturing and quality evaluation to promote the practical use of organoids. This guideline does not focus on specific organoids or specific contexts of use but provides guidance to organoid makers and users on materials, procedures, and essential quality assessment methods at end points that are essential for organoid production applicable at the current technology level.

Purpose: Claudins are a type of tight junction proteins in human endothelia and epithelia. Ozone brings about oxidative stress and lung inflammation in humans and experimental models. However, the impact of ozone on claudins in subjects with asthma remains poorly understood. The aim of this study was to find variations in the tight junction proteins claudin-4 and claudin-5 in subjects with asthma in relation to ambient ozone concentration. Methods: We previously recruited 50 patients with stable/exacerbated asthmatics and 25 controls. Furthermore, to examine the influence of ozone concentration, we reanalyzed 18 patients with stable or exacerbated asthma and 3 controls. The plasma claudin-4 and claudin-5 levels in response to high concentrations of ozone were compared to stable/exacerbated asthma, and controls. Results: The lung functions were significantly lower in subjects with asthma than those in controls. Blood eosinophil proportions were significantly higher in exacerbated asthmatics than in subjects with stable asthma. In high concentration period of ozone, plasma claudin-4 levels were significantly higher in subjects with exacerbated asthma (0.44 ± 0.30 ng/mL, P = 0.005) or stable asthma (0.38± 0.31 ng/mL, P= 0.009) compared to those in control subjects (0.16± 0.1 ng/mL). Plasma claudin-5 levels were lower in subjects with stable asthma (2.97 ± 1.38 ng/mL, P = 0.011) than in control subjects (6.92 ± 3.9 ng/mL), and higher in subjects with exacerbated asthma (7.49 ± 4.23 ng/mL, P < 0.001) than those with stable asthma. Conclusion These results reveal that claudins be changed in patients with asthma following ozone exposure in subjects with asthma.

This report presents guidelines for the systematic management of packaging, storage, transportation, and traceability of source cells used for organoid research. Given the important role of source cells in organoid studies, it is important to ensure the preservation of their quality and integrity throughout transportation and distribution processes. The proposed guidelines, therefore, call for a cohesive strategy through these stages to minimize the risks of contamination, deterioration, and loss–threats that significantly compromise the safety, efficacy, and efficiency of source cells. Central to these guidelines is the quality control measures that include roles and responsibilities across the entire supply chain, with recommendations specific to packaging materials, transportation facilities, and storage management. Furthermore, the need for an integrated management system is emphasized, spanning from source cell collection to the final application. This system is crucial for maintaining the traceability and accountability of source cells, facilitating the sharing, distribution, and utilization on a global scale, and supporting to advance organoid research and development.

Purpose: Junctional adhesion molecule (JAM)-A is an immunoglobulin-like molecule that colocalizes with tight junctions (TJs) in the endothelium and epithelium. It is also found in blood leukocytes and platelets. The biological significance of JAM-A in asthma, as well as its clinical potential as a therapeutic target, are not well understood. The aim of this study was to elucidate the role of JAM-A in a mouse model of asthma, and to determine blood levels of JAM-A in asthmatic patients. Materials and Methods: Mice sensitized and challenged with ovalbumin (OVA) or saline were used to investigate the role of JAM-A in the pathogenesis of bronchial asthma. In addition, JAM-A levels were measured in the plasma of asthmatic patients and healthy controls. The relationships between JAM-A and clinical variables in patients with asthma were also examined. Results: Plasma JAM-A levels were higher in asthma patients (n=19) than in healthy controls (n=12). In asthma patients, the JAM-A levels correlated with forced expiratory volume in 1 second (FEV1%), FEV1/forced vital capacity (FVC), and the blood lymphocyte proportion. JAM-A, phospho-JNK, and phospho-ERK protein expressions in lung tissue were significantly higher in OVA/OVA mice than in control mice. In human bronchial epithelial cells treated with house dust mite extracts for 4 h, 8 h, and 24 h, the JAMA, phospho-JNK, and phospho-ERK expressions were increased, as shown by Western blotting, while the transepithelial electrical resistance was reduced. Conclusion These results suggest that JAM-A is involved in the pathogenesis of asthma, and may be a marker for asthma.

Background: The latent reservoir of Human Immunodificiency Virus-1 (HIV-1) has been a major barrier to the complete eradication of HIV-1 and the development of HIV therapy. Longterm non-progressors (LTNPs) are a rare group of patients with HIV-1 who can spontaneously control HIV-1 replication without antiretroviral therapy. Transcriptome analysis is necessary to predict the pathways involved in the natural control of HIV-1, elucidate the mechanisms involved in LTNPs, and find biomarkers for HIV-1 reservoir therapy. Materials and Methods: In this study, we obtained peripheral blood mononuclear cells from two LTNP subjects at multiple time points and performed RNA-sequencing analyses. Results: We found that LTNPs and normal subjects had different transcriptome profiles. Functional annotation analysis identified that differentially expressed genes in LTNPs were enriched in several biological pathways such as cell cycle-related pathways and the transforming growth factor-beta signaling pathway. However, genes that were downregulated in LTNPs were associated with immune responses such as the interferon response and IL2-STAT5 signaling. Protein-protein interaction network analysis showed that CD8A, KLRD1, ASGR1, and MLKL, whose gene expression was upregulated in LTNPs, directly interacted with HIV-1 proteins. The network analysis also found that viral proteins potentially regulated host genes that were associated with immune system processes, metabolic processes, and gene expression regulation. Conclusion Our longitudinal transcriptome analysis of the LTNPs identified multiple previously undescribed pathways and genes that may be useful in the discovery of novel therapeutic targets and biomarkers.