OBJECTIVES: The present study investigated current practices of insomnia treatment among Korean doctors in clinical settings. METHODS: A total of 100 doctors participated in the present study and filled out a series of survey questions regarding their treatment of insomnia patients. RESULTS: The results revealed that the primary type of insomnia treatment was pharmacological and that the most popular medication was zolpidem. The majority of doctors reported that they also utilized non-pharmacological treatments such as sleep hygiene education and cognitive-behavioral therapy. However, these treatments tended to result in low satisfaction. In addition, the doctors perceived that patients largely preferred pharmacological treatments to non-pharmacological ones and did not have sufficient knowledge of non-pharmacological treatments. CONCLUSION: Many doctors believed that non-pharmacological treatments for insomnia were important, but reported that they were difficult to implement in practice. The results of this study suggest that improved medical conditions for non-pharmacological treatments and education of physicians are necessary to appropriately treat insomnia.
Education ; Humans ; Hygiene ; Sleep Initiation and Maintenance Disorders*

Autism spectrum disorders (ASDs) are neurodevelopmental disorders that share behavioral features, the results of numerous studies have suggested that the underlying causes of ASDs are multifactorial. Behavioral and/or neurobiological analyses of ASDs have been performed extensively using a valid model of prenatal exposure to valproic acid (VPA). Abnormal synapse formation resulting from altered neurite outgrowth in neural progenitor cells (NPCs) during embryonic brain development has been observed in both the VPA model and ASD subjects. Although several mechanisms have been suggested, the actual mechanism underlying enhanced neurite outgrowth remains unclear. In this study, we found that VPA enhanced the expression of brain-derived neurotrophic factor (BDNF), particularly mature BDNF (mBDNF), through dual mechanisms. VPA increased the mRNA and protein expression of BDNF by suppressing the nuclear expression of methyl-CpG-binding protein 2 (MeCP2), which is a transcriptional repressor of BDNF. In addition, VPA promoted the expression and activity of the tissue plasminogen activator (tPA), which induces BDNF maturation through proteolytic cleavage. Trichostatin A and sodium butyrate also enhanced tPA activity, but tPA activity was not induced by valpromide, which is a VPA analog that does not induce histone acetylation, indicating that histone acetylation activity was required for tPA regulation. VPA-mediated regulation of BDNF, MeCP2, and tPA was not observed in astrocytes or neurons. Therefore, these results suggested that VPA-induced mBDNF upregulation was associated with the dysregulation of MeCP2 and tPA in developing cortical NPCs.
Acetylation ; Astrocytes ; Autism Spectrum Disorder ; Brain ; Brain-Derived Neurotrophic Factor* ; Butyric Acid ; Histones ; Methyl-CpG-Binding Protein 2 ; Neurites ; Neurodevelopmental Disorders ; Neurons ; RNA, Messenger ; Stem Cells* ; Synapses ; Tissue Plasminogen Activator ; Up-Regulation ; Valproic Acid*

The authors note that on page 685, the acknowledgement of “This study was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. 2017R1D1A1B03031920),” should instead appear as “This study was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. 2017R1D1A1B03031920) and Chung-Ang University Research Grants in 2017.”