• Sleep Medicine and Psychophysiology
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• 제26권1호
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• pp.44-48
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• 2019

Objectives: Insomnia is one of the most prevalent sleep disorders. Recent studies suggest that cognitive and physical arousal play an important role in the generation of primary insomnia. Studies have also shown that information processing disorders due to cortical hyperactivity might interfere with normal sleep onset and sleep continuity. Therefore, focusing on central nervous system arousal and normalizing the information process have become current topics of interest. It has been well known that neurofeedback can reduce the brain hyperarousal by modulating patients' brain waves during a sequence of behavior therapy. The purpose of this study was to investigate effects of neurofeedback therapy on electroencephalography (EEG) characteristics in patients with primary insomnia. Methods: Thirteen subjects who met the criteria for an insomnia diagnosis and 14 control subjects who were matched on sex and age were included. Neurofeedback and sham treatments were performed in a random order for 30 minutes, respectively. EEG spectral power analyses were performed to quantify effects of the neurofeedback therapy on brain wave forms. Results: In patients with primary insomnia, relative spectral theta and sigma power during a therapeutic neurofeedback session were significantly lower than during a sham session ($13.9{\pm}2.6$ vs. $12.2{\pm}3.8$ and $3.6{\pm}0.9$ vs. $3.2{\pm}1.0$ in %, respectively; p < 0.05). There were no statistically significant changes in other EEG spectral bands. Conclusion: For the first time in Korea, EEG spectral power in the theta band was found to increase when a neurofeedback session was applied to patients with insomnia. This outcome might provide some insight into new interventions for improving sleep onset. However, the treatment response of insomniacs was not precisely evaluated due to limitations of the current pilot study, which requires follow-up studies with larger samples in the future.

• Journal of Life Science
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• 제33권12호
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• pp.1062-1073
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• 2023

Although depression is a common psychiatric disorder that negatively affects individuals and societies, its exact pathogenesis is not well understood. Stress is a major risk factor for depression and is known to increase susceptibility by triggering inflammation. Indeed, many preclinical and clinical studies have suggested a strong link between depression and inflammation. Depression is associated with increased levels of pro-inflammatory cytokines, such as interleukin (IL-)1β, IL-6, IL-12, tumor necrosis factor-α, and interferon-γ, and decreased levels of the anti-inflammatory IL-4, IL-10, and transforming growth factor-β. Administering pro-inflammatory cytokines causes depression-like behaviors in rodents. Conversely, administering anti-inflammatory drugs appears to ameliorate depressive symptoms. Although the importance of inflammation as a mediator of depression has been demonstrated, the mechanisms by which inflammation is activated in depression remain unclear. To address this issue, recent studies have focused on the importance of stress-induced sterile inflammation. Sterile inflammation refers to the activation of inflammatory processes due to physical and/or psychological stress in the absence of pathogens. Stress promotes the release of endogenous factors known as damage-associated molecular patterns (DAMPs), thereby triggering sterile inflammation. In turn, DAMPs are recognized by pattern recognition receptors, leading to the production of pro-inflammatory cytokines. Here, we review the role of DAMPs in depression based on preclinical and clinical evidence on the dysregulation of sterile inflammation.

• Journal of Genetic Medicine
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• 제8권2호
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• pp.119-124
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• 2011

Purpose: Supernumerary marker chromosome (SMC) could be associated with various phenotypic abnormalities based on the chromosomal origin of SMCs. The present study aimed to determine the genomic contents of SMCs using chromosomal microarray and to analyze molecular cytogenetic characterizations and clinical phenotypes in patients with SMCs. Materials and Methods: Among patients with SMCs detected in routine chromosomal analysis, SMCs originating from chromosome 15 were excluded from the present study. CGH-based oligonucleotide chromosomal microarray was performed in 4 patients. Results: The chromosomal origins of SMCs were identified in 3 patients. Case 1 had a SMC of 16.1 Mb in 1q21.1-q23.3. Case 2 showed 21 Mb gain in 19p13.11-q13.12. Case 3 had a 4.5 Mb-sized SMC rearranged from 2 regions of 2.5 Mb in 22q11.1-q11.21 and 2.0 Mb in 22q11.22-q11.23. Conclusion: Case 1 presented a wide range of phenotypic abnormalities including the phenotype of 1q21.1 duplication syndrome. In case 2, Asperger-like symptoms are apparently related to 19p12-q13.11, hearing problems and strabismus to 19p13.11 and other features to 19q13.12. Compared with cat-eye syndrome type I and 22q11.2 microduplication syndrome, anal atresia in case 3 is likely related to 22q11.1-q11.21 while other features are related to 22q11.22-q11.23. Analyzing SMCs using high-resolution chromosomal microarray can help identify specific gene contents and to offer proper genetic counseling by determining genotype-phenotype correlations.