Pain accompanied by depressive symptoms is a common reason for seeking medical assistance, and many chronic pain patients experience comorbid depression. The brain-derived neurotrophic factor (BDNF) is a well-known neurotrophin expressed throughout the nervous system, playing a crucial role in neuronal growth and neuroplasticity. This study aimed to examine the effects of exercise on BDNF expression in the nervous system and reserpine (RSP)-induced pain-depression dyad. RSP (1 mg/kg) was subcutaneously administered once daily for three days in mice.The exercise was performed using a rota-rod tester for seven consecutive days following RSP administration. Pain responses were evaluated using von Frey filaments, and depression-like behaviors were assessed through forced swimming and open field tests. Immunofluorescence staining was performed to examine the changes in BDNF expression in the dorsal root ganglion (DRG), spinal cord, and hippocampus. Administration of RSP reduced mechanical paw withdrawal threshold, increased immobility time in the forced swimming test, and decreased movement in the open field test. The immunoreactivity of BDNF was increased in the DRG and spinal dorsal regions, and decreased in the hippocampus after RSP administration. Physical exercise significantly reduced the RSP-induced mechanical hypersensitivity and depression-like behaviors. In addition, exercise suppressed not only the increased expression of BDNF in the DRG and spinal dorsal regions but also the decreased expression of BDNF in the hippocampus induced by RSP administration. These findings suggest that repetitive exercise could serve as an effective and non-invasive treatment option for individuals experiencing both pain and depression by modulating BDNF expression.

Background: To overcome the limitations of relying on data from a single institution, many researchers have studied data linkage methodologies. Data linkage includes errors owing to legal issues surrounding personal information and technical issues related to data processing. Linkage errors affect selection bias, and external and internal validity. Therefore, quality verification for each connection method with adherence to personal information protection is an important issue. This study evaluated the linkage quality of linked data and analyzed the potential bias resulting from linkage errors. Methods: This study analyzed claims data submitted to the Health Insurance Review and Assessment Service (HIRA DATA). The linkage errors of the two deterministic linkage methods were evaluated based on the use of the match key. The first deterministic linkage uses a unique identification number, and the second deterministic linkage uses the name, gender, and date of birth as a set of partial identifiers. The linkage error included in this deterministic linkage method was compared with the absolute standardized difference (ASD) of Cohen’s according to the baseline characteristics, and the linkage quality was evaluated through the following indicators: linked rate, false match rate, missed match rate, positive predictive value, sensitivity, specificity, and F1-score. Results: For the deterministic linkage method that used the name, gender, and date of birth as a set of partial identifiers, the true match rate was 83.5 and the missed match rate was 16.5.Although there was bias in some characteristics of the data, most of the ASD values were less than 0.1, with no case greater than 0.5. Therefore, it is difficult to determine whether linked data constructed with deterministic linkages have substantial differences. Conclusion This study confirms the possibility of building health and medical data at the national level as the first data linkage quality verification study using big data from the HIRA. Analyzing the quality of linkages is crucial for comprehending linkage errors and generating reliable analytical outcomes. Linkers should increase the reliability of linked data by providing linkage error-related information to researchers. The results of this study will serve as reference data to increase the reliability of multicenter data linkage studies.

BACKGROUND/OBJECTIVES: Quercetin (QT) is a plant flavonoid that offers health benefits owing to its various bioactive properties; however, as a hydrophobic substance, it has considerably low bioavailability. We previously demonstrated that QT nanoemulsion (QT+NE) formulated via oil-in-water nanoemulsification exhibited more effective cholesterollowering activity than ordinary QT in high cholesterol-fed rats. In this study, we investigated the effects of QT+NE on the regulation of skeletal muscle mitochondrial function in high-fat diet (HD)-fed mice.MATERIALS/METHODS: C57BL/6J mice were fed a normal chow diet (ND), HD (45% of calories from fat), or HD with 0.05% QT+NE or QT for 11 weeks. We analyzed sirtuin 1 (SIRT1) activation, mitochondrial changes, and the expression of genes involved in mitochondrial biogenesis in skeletal muscle. RESULTS: Body weight and body weight gain decreased in the QT+NE group compared with that in the HD group (P < 0.05), but not in the QT group. Epididymal adipose tissue weight decreased in both the QT and QT+NE groups (P < 0.05). Plasma lipid levels also improved in both the QT and QT+NE groups (P < 0.05). QT+NE intake upregulated the messenger RNA levels of SIRT1, peroxisome proliferator-activated receptor-γ coactivator 1-α, nuclear respiratory factor 1, and mitochondrial transcription factor A in skeletal muscle compared with HD intake alone (P < 0.05), whereas QT did not. In particular, SIRT1 activity was significantly increased in the QT+NE group compared with that in the QT group (P < 0.05).HD intake reduced mitochondrial DNA content compared with ND intake; nevertheless, QT+NE intake retained it (P < 0.05). CONCLUSION Collectively, our findings suggest that QT+NE may be beneficial in enhancing mitochondrial biogenesis in skeletal muscle of HD-fed mice, which may be associated with SIRT1 activation.

Objective: Previous research on autism spectrum disorder (ASD) in Koreans has primarily focused on genetic diversity because of its high heritability. However, the emerging recognition of transgenerational epigenetic changes has recently shifted research attention towards epigenetic perspectives. Methods: This study investigated the DNA methylation patterns of the promoter regions of candidate genes such asNR3C1, ASCL1, and FOXO3 in blood samples from ASD probands and their unaffected siblings. The analysis included 54 families (ASD proband group: 54; unaffected biological sibling group: 63). The diagnostic process involved screening the probands and their siblings for ASD based on the Diagnostic and Statistical Manual of Mental Disorders 5th edition.Intelligence, social ability, and medical history were thoroughly assessed using various scales and questionnaires.Genomic DNA from blood samples was analyzed using a methylation-sensitive quantitative polymerase chain reaction to examine the DNA methylation status of candidate genes. Results: Methylation levels in candidate gene promoter regions differed significantly between the proband and sibling groups for all candidate genes. Correlation analysis between the proband and sibling groups revealed strong and significant correlations in NR3C1 and ASCL1 methylation. Additionally, in the analysis of the relationship between DNA and ASD phenotypes, FOXO3 methylation correlated with social quotient in probands, and ASCL1 methylation was associated with nonverbal communication, and daily living skills as measured by the Korean Vineland Adaptive Behavior Scale. Notably, ASCL1 methylation was significantly associated with parental age at pregnancy. Conclusion This study proposes DNA methylation of NR3C1, ASCL1, and FOXO3 in peripheral blood samples is a potential epigenetic biomarker of ASD.

Objective: Previous research on autism spectrum disorder (ASD) in Koreans has primarily focused on genetic diversity because of its high heritability. However, the emerging recognition of transgenerational epigenetic changes has recently shifted research attention towards epigenetic perspectives. Methods: This study investigated the DNA methylation patterns of the promoter regions of candidate genes such asNR3C1, ASCL1, and FOXO3 in blood samples from ASD probands and their unaffected siblings. The analysis included 54 families (ASD proband group: 54; unaffected biological sibling group: 63). The diagnostic process involved screening the probands and their siblings for ASD based on the Diagnostic and Statistical Manual of Mental Disorders 5th edition.Intelligence, social ability, and medical history were thoroughly assessed using various scales and questionnaires.Genomic DNA from blood samples was analyzed using a methylation-sensitive quantitative polymerase chain reaction to examine the DNA methylation status of candidate genes. Results: Methylation levels in candidate gene promoter regions differed significantly between the proband and sibling groups for all candidate genes. Correlation analysis between the proband and sibling groups revealed strong and significant correlations in NR3C1 and ASCL1 methylation. Additionally, in the analysis of the relationship between DNA and ASD phenotypes, FOXO3 methylation correlated with social quotient in probands, and ASCL1 methylation was associated with nonverbal communication, and daily living skills as measured by the Korean Vineland Adaptive Behavior Scale. Notably, ASCL1 methylation was significantly associated with parental age at pregnancy. Conclusion This study proposes DNA methylation of NR3C1, ASCL1, and FOXO3 in peripheral blood samples is a potential epigenetic biomarker of ASD.

Objective: Previous research on autism spectrum disorder (ASD) in Koreans has primarily focused on genetic diversity because of its high heritability. However, the emerging recognition of transgenerational epigenetic changes has recently shifted research attention towards epigenetic perspectives. Methods: This study investigated the DNA methylation patterns of the promoter regions of candidate genes such asNR3C1, ASCL1, and FOXO3 in blood samples from ASD probands and their unaffected siblings. The analysis included 54 families (ASD proband group: 54; unaffected biological sibling group: 63). The diagnostic process involved screening the probands and their siblings for ASD based on the Diagnostic and Statistical Manual of Mental Disorders 5th edition.Intelligence, social ability, and medical history were thoroughly assessed using various scales and questionnaires.Genomic DNA from blood samples was analyzed using a methylation-sensitive quantitative polymerase chain reaction to examine the DNA methylation status of candidate genes. Results: Methylation levels in candidate gene promoter regions differed significantly between the proband and sibling groups for all candidate genes. Correlation analysis between the proband and sibling groups revealed strong and significant correlations in NR3C1 and ASCL1 methylation. Additionally, in the analysis of the relationship between DNA and ASD phenotypes, FOXO3 methylation correlated with social quotient in probands, and ASCL1 methylation was associated with nonverbal communication, and daily living skills as measured by the Korean Vineland Adaptive Behavior Scale. Notably, ASCL1 methylation was significantly associated with parental age at pregnancy. Conclusion This study proposes DNA methylation of NR3C1, ASCL1, and FOXO3 in peripheral blood samples is a potential epigenetic biomarker of ASD.

BACKGROUND/OBJECTIVES: Quercetin (QT) is a plant flavonoid that offers health benefits owing to its various bioactive properties; however, as a hydrophobic substance, it has considerably low bioavailability. We previously demonstrated that QT nanoemulsion (QT+NE) formulated via oil-in-water nanoemulsification exhibited more effective cholesterollowering activity than ordinary QT in high cholesterol-fed rats. In this study, we investigated the effects of QT+NE on the regulation of skeletal muscle mitochondrial function in high-fat diet (HD)-fed mice.MATERIALS/METHODS: C57BL/6J mice were fed a normal chow diet (ND), HD (45% of calories from fat), or HD with 0.05% QT+NE or QT for 11 weeks. We analyzed sirtuin 1 (SIRT1) activation, mitochondrial changes, and the expression of genes involved in mitochondrial biogenesis in skeletal muscle. RESULTS: Body weight and body weight gain decreased in the QT+NE group compared with that in the HD group (P < 0.05), but not in the QT group. Epididymal adipose tissue weight decreased in both the QT and QT+NE groups (P < 0.05). Plasma lipid levels also improved in both the QT and QT+NE groups (P < 0.05). QT+NE intake upregulated the messenger RNA levels of SIRT1, peroxisome proliferator-activated receptor-γ coactivator 1-α, nuclear respiratory factor 1, and mitochondrial transcription factor A in skeletal muscle compared with HD intake alone (P < 0.05), whereas QT did not. In particular, SIRT1 activity was significantly increased in the QT+NE group compared with that in the QT group (P < 0.05).HD intake reduced mitochondrial DNA content compared with ND intake; nevertheless, QT+NE intake retained it (P < 0.05). CONCLUSION Collectively, our findings suggest that QT+NE may be beneficial in enhancing mitochondrial biogenesis in skeletal muscle of HD-fed mice, which may be associated with SIRT1 activation.

BACKGROUND/OBJECTIVES: Quercetin (QT) is a plant flavonoid that offers health benefits owing to its various bioactive properties; however, as a hydrophobic substance, it has considerably low bioavailability. We previously demonstrated that QT nanoemulsion (QT+NE) formulated via oil-in-water nanoemulsification exhibited more effective cholesterollowering activity than ordinary QT in high cholesterol-fed rats. In this study, we investigated the effects of QT+NE on the regulation of skeletal muscle mitochondrial function in high-fat diet (HD)-fed mice.MATERIALS/METHODS: C57BL/6J mice were fed a normal chow diet (ND), HD (45% of calories from fat), or HD with 0.05% QT+NE or QT for 11 weeks. We analyzed sirtuin 1 (SIRT1) activation, mitochondrial changes, and the expression of genes involved in mitochondrial biogenesis in skeletal muscle. RESULTS: Body weight and body weight gain decreased in the QT+NE group compared with that in the HD group (P < 0.05), but not in the QT group. Epididymal adipose tissue weight decreased in both the QT and QT+NE groups (P < 0.05). Plasma lipid levels also improved in both the QT and QT+NE groups (P < 0.05). QT+NE intake upregulated the messenger RNA levels of SIRT1, peroxisome proliferator-activated receptor-γ coactivator 1-α, nuclear respiratory factor 1, and mitochondrial transcription factor A in skeletal muscle compared with HD intake alone (P < 0.05), whereas QT did not. In particular, SIRT1 activity was significantly increased in the QT+NE group compared with that in the QT group (P < 0.05).HD intake reduced mitochondrial DNA content compared with ND intake; nevertheless, QT+NE intake retained it (P < 0.05). CONCLUSION Collectively, our findings suggest that QT+NE may be beneficial in enhancing mitochondrial biogenesis in skeletal muscle of HD-fed mice, which may be associated with SIRT1 activation.

Objective: Previous research on autism spectrum disorder (ASD) in Koreans has primarily focused on genetic diversity because of its high heritability. However, the emerging recognition of transgenerational epigenetic changes has recently shifted research attention towards epigenetic perspectives. Methods: This study investigated the DNA methylation patterns of the promoter regions of candidate genes such asNR3C1, ASCL1, and FOXO3 in blood samples from ASD probands and their unaffected siblings. The analysis included 54 families (ASD proband group: 54; unaffected biological sibling group: 63). The diagnostic process involved screening the probands and their siblings for ASD based on the Diagnostic and Statistical Manual of Mental Disorders 5th edition.Intelligence, social ability, and medical history were thoroughly assessed using various scales and questionnaires.Genomic DNA from blood samples was analyzed using a methylation-sensitive quantitative polymerase chain reaction to examine the DNA methylation status of candidate genes. Results: Methylation levels in candidate gene promoter regions differed significantly between the proband and sibling groups for all candidate genes. Correlation analysis between the proband and sibling groups revealed strong and significant correlations in NR3C1 and ASCL1 methylation. Additionally, in the analysis of the relationship between DNA and ASD phenotypes, FOXO3 methylation correlated with social quotient in probands, and ASCL1 methylation was associated with nonverbal communication, and daily living skills as measured by the Korean Vineland Adaptive Behavior Scale. Notably, ASCL1 methylation was significantly associated with parental age at pregnancy. Conclusion This study proposes DNA methylation of NR3C1, ASCL1, and FOXO3 in peripheral blood samples is a potential epigenetic biomarker of ASD.

BACKGROUND/OBJECTIVES: Quercetin (QT) is a plant flavonoid that offers health benefits owing to its various bioactive properties; however, as a hydrophobic substance, it has considerably low bioavailability. We previously demonstrated that QT nanoemulsion (QT+NE) formulated via oil-in-water nanoemulsification exhibited more effective cholesterollowering activity than ordinary QT in high cholesterol-fed rats. In this study, we investigated the effects of QT+NE on the regulation of skeletal muscle mitochondrial function in high-fat diet (HD)-fed mice.MATERIALS/METHODS: C57BL/6J mice were fed a normal chow diet (ND), HD (45% of calories from fat), or HD with 0.05% QT+NE or QT for 11 weeks. We analyzed sirtuin 1 (SIRT1) activation, mitochondrial changes, and the expression of genes involved in mitochondrial biogenesis in skeletal muscle. RESULTS: Body weight and body weight gain decreased in the QT+NE group compared with that in the HD group (P < 0.05), but not in the QT group. Epididymal adipose tissue weight decreased in both the QT and QT+NE groups (P < 0.05). Plasma lipid levels also improved in both the QT and QT+NE groups (P < 0.05). QT+NE intake upregulated the messenger RNA levels of SIRT1, peroxisome proliferator-activated receptor-γ coactivator 1-α, nuclear respiratory factor 1, and mitochondrial transcription factor A in skeletal muscle compared with HD intake alone (P < 0.05), whereas QT did not. In particular, SIRT1 activity was significantly increased in the QT+NE group compared with that in the QT group (P < 0.05).HD intake reduced mitochondrial DNA content compared with ND intake; nevertheless, QT+NE intake retained it (P < 0.05). CONCLUSION Collectively, our findings suggest that QT+NE may be beneficial in enhancing mitochondrial biogenesis in skeletal muscle of HD-fed mice, which may be associated with SIRT1 activation.