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Perinatal exposure to valproic acid is commonly used for autism spectrum disorder (ASD) animal model development. The inhibition of histone deacetylases by VPA has been proposed to induce epigenetic changes during neurodevelopment, but the specific alterations in genetic expression underlying ASD-like behavioral changes remain unclear. We used qPCR-based gene expression and epigenetics tools and Western blotting in the hippocampi of neonatal valproic acid-exposed animals at 4 weeks of age and conducted the social interaction test to detect behavioral changes. Significant alterations in gene expression were observed in males, particularly concerning mRNA expression of Foxo3, which was significantly associated with behavioral changes. Moreover, notable differences were observed in H3K27ac chromatin immunoprecipitation, quantitative PCR (ChIP-qPCR), and methylation-sensitive restriction enzyme-based qPCR targeting the Foxo3 gene promoter region. These findings provide evidence that epigenetically regulated hippocampal Foxo3 expression may influence social interaction-related behavioral changes. Furthermore, identifying sex-specific gene expression and epigenetic changes in this model may elucidate the sex disparity observed in autism spectrum disorder prevalence. [ABSTRACT FROM AUTHOR]

Valproic acid (VPA) is a known drug for treating epilepsy and mood disorders; however, it is not recommended for pregnant women because of its possible teratogenicity. VPA affects neurotransmission and gene expression through epigenetic mechanisms by acting as a histone deacetylase inhibitor and has been used to establish animal models of autism spectrum disorder (ASD). However, studies on the long-term effects of early exposure to VPA on glucocorticoid and neurosteroid synthesis in the brain are lacking. Therefore, this study aimed to investigate the long-term changes in metabolic alterations and gene expression regulation according to sex, using metabolic steroid profiling data from cerebral cortex samples of rats four weeks after VPA exposure (400 mg/kg). In neonatal VPA-exposed models, estradiol levels decreased, and cytochrome P450 19A1 gene (Cyp19a1) expression was reduced in the prepubertal male cortex. Progesterone and allopregnanolone levels decreased, and 3β-hydroxysteroid dehydrogenase 1 gene (Hsd3b1) expression was also downregulated in the prepubertal female cortex. Furthermore, cortisol levels increased, and mRNA expression of the nuclear receptor subfamily 3 group C member 1 gene (Nr3c1) was downregulated in the cortices of both sexes. Unlike the neonatal VPA-exposed models, although a decrease in progestin and estradiol levels was observed in females and males, respectively, no differences were observed in cortisol levels in the cortex tissues of 8-week-old adult rats administered VPA for four weeks. These results indicate that early environmental chemical exposure induces long-term neurosteroid metabolic effects in the brain, with differences according to sex. [ABSTRACT FROM AUTHOR]

We tested the feasibility of automated discrimination of patients with panic disorder (PD) from healthy controls (HCs) based on multimodal physiological responses using machine learning. Electrocardiogram (ECG), electrodermal activity (EDA), respiration (RESP), and peripheral temperature (PT) of the participants were measured during three experimental phases: rest, stress, and recovery. Eleven physiological features were extracted from each phase and used as input data. Logistic regression (LoR), k‐nearest neighbor (KNN), support vector machine (SVM), random forest (RF), and multilayer perceptron (MLP) algorithms were implemented with nested cross‐validation. Linear regression analysis showed that ECG and PT features obtained in the stress and recovery phases were significant predictors of PD. We achieved the highest accuracy (75.61%) with MLP using all 33 features. With the exception of MLP, applying the significant predictors led to a higher accuracy than using 24 ECG features. These results suggest that combining multimodal physiological signals measured during various states of autonomic arousal has the potential to differentiate patients with PD from HCs. [ABSTRACT FROM AUTHOR]

Alteration in stress response seems to affect the development of psychiatric disorders. In this study, we aimed to investigate whether baseline peripheral biomarkers could predict the reduction of stress response among patients with major depressive disorder (MDD) and panic disorder (PD). Patients with MDD (n = 41) and PD (n = 52) and healthy controls (HC, n = 59) were selected and regularly followed up with five visits for 12 weeks. The severity of stress at every visit was assessed using the Stress Response Inventory (SRI), and peripheral biomarkers were measured by blood tests at baseline and 2, 4, 8, and 12 weeks. Interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, C-reactive protein (CRP), adiponectin, and leptin levels were analyzed using enzyme-linked immunosorbent assays. Reduction of stress response was defined as the difference in SRI score between baseline and 12 weeks divided by the baseline score. SRI scores were significantly (p < 0.0001) higher in patients with MDD and PD than in HC at every visit after adjusting for variables. In multivariable linear regression, adiponectin levels at baseline were significantly associated with reduction of stress response in patients with PD. When adiponectin increased 1 mg/l, stress response decreased 0.781 points (β = −0.781, S.E. = 0.220, p = 0.001). Among the subscales of SRI, somatization had a moderate negative correlation with adiponectin levels (r = −0.469). There was no significant association between baseline peripheral biomarkers and reduction of stress response in patients with MDD. Our study showed an inverse association between baseline adiponectin levels and stress response changes in patients with PD, but not in patients with MDD. Thus, differentiated approaches for assessing and treating stress responses of patients with PD and MDD might be helpful. Larger and longitudinal studies are necessary to establish the role and mechanism of action of adiponectin in regulating stress responses in PD. [ABSTRACT FROM AUTHOR]

• Mitochondrial dysfunction was observed in the PPA-treated SH-SY5Y cells. • Mitochondrial biogenesis-related protein expression was increased by PPA treatment. • PPA treatment induce ASCL1 and LFNG gene expression change. Studies in animal models have shown that the short-chain fatty acid, propionic acid (PPA), interferes with mitochondrial metabolism leading to mitochondrial dysfunction and behavioral abnormalities. The aim of this study was to investigate the effects of PPA on mitochondrial function and gene expression in neuronal cells. SH-SY5Y cells and normal human neural progenitor (NHNP) cells were exposed to 1, 5 mM PPA for 4 or 24 h and we found that the mitochondrial potential measured in SH-SY5Y cells decreased in a dose-dependent manner after PPA treatment. Electron microscopy analysis revealed that the size of the mitochondria was significantly reduced following PPA treatment. A dose-dependent increase in the mitochondrial DNA copy number was observed in the PPA-treated cells. The expression of the mitochondrial biogenesis-related proteins PGC-1α, TFAM, SIRT3, and COX4 was significantly increased after PPA treatment. Transcriptome analysis revealed that mRNA expression in the notch signaling-related genes ASCL1 and LFNG changed after PPA treatment and the positive correlated protein expression changes were also observed. These results revealed that PPA treatment may affect neurodevelopment by altering mitochondrial function and notch signaling-related gene expression. [ABSTRACT FROM AUTHOR]

Background: The current method to evaluate major depressive disorder (MDD) relies on subjective clinical interviews and self-questionnaires.Objective: Autonomic imbalance in MDD patients is characterized using entropy measures of heart rate variability (HRV). A machine learning approach for screening depression based on the entropy is demonstrated.Methods: The participants experience five experimental phases: baseline (BASE), stress task (MAT), stress task recovery (REC1), relaxation task (RLX), and relaxation task recovery (REC2). The four entropy indices, approximate entropy, sample entropy, fuzzy entropy, and Shannon entropy, are extracted for each phase, and a total of 20 features are used. A support vector machine classifier and recursive feature elimination are employed for classification.Results: The entropy features are lower in the MDD group; however, the disease does not have a significant effect. Experimental tasks significantly affect the features. The entropy did not recover during REC1. The differences in the entropy features between the two groups increased after MAT and showed the largest gap in REC2. We achieved 70% accuracy, 64% sensitivity, and 76% specificity with three optimal features during RLX and REC2.Conclusion: Monitoring of HRV complexity changes when a subject experiences autonomic arousal and recovery can potentially facilitate objective depression recognition. [ABSTRACT FROM AUTHOR]

Depressive symptoms are related to abnormalities in the autonomic nervous system (ANS), and physiological signals that can be used to measure and evaluate such abnormalities have previously been used as indicators for diagnosing mental disorder, such as major depressive disorder (MDD). In this study, we investigate the feasibility of developing an objective measure of depressive symptoms that is based on examining physiological abnormalities in individuals when they are experiencing mental stress. To perform this, we recruited 30 patients with MDD and 31 healthy controls. Then, skin conductance (SC) was measured during five 5-min experimental phases, comprising baseline, mental stress, recovery from the stress, relaxation, and recovery from the relaxation, respectively. For each phase, the mean amplitude of the skin conductance level (MSCL), standard deviations of the SCL (SDSCL), slope of the SCL (SSCL), mean amplitude of the non-specific skin conductance responses (MSCR), number of non-specific skin conductance responses (NSCR), and power spectral density (PSD) were evaluated from the SC signals, producing 30 parameters overall (six features for each phase). These features were used as input data for a support vector machine (SVM) algorithm designed to distinguish MDD patients from healthy controls based on their physiological responses. Statistical tests showed that the main effect of task was significant in all SC features, and the main effect of group was significant in MSCL, SDSCL, SSCL, and PSD. In addition, the proposed algorithm achieved 70% accuracy, 70% sensitivity, 71% specificity, 70% positive predictive value, 71% negative predictive value in classifying MDD patients and healthy controls. These results demonstrated that it is possible to extract meaningful features that reflect changes in ANS responses to various stimuli. Using these features, detection of MDD was feasible, suggesting that SC analysis has great potential for future diagnostics and prediction of depression based on objective interpretation of depressive states. [ABSTRACT FROM AUTHOR]

Background: Heart Rate Variability (HRV) parameters have been used to evaluate the autonomic nervous system. We hypothesized that patients with major depressive disorder (MDD) and panic disorder (PD) showed different HRV profiles compared to healthy controls. We also hypothesized that we could predict the responder groups in the MDD and PD patients, using differences in HRV indices between the stress and rest phases.Methods: 28 MDD patients and 29 PD patients were followed for 12 weeks, and we also followed 39 healthy control subjects. We measured HRV parameters at the rest, stress, and recovery phases.Results: Patients with MDD and PD demonstrated lower pNN50 than controls during the stress (F = 7.49, p = 0.001), and recovery phases (F = 9.43, p = 0.0001). Patients with MDD and PD also showed higher LF/HF ratio than controls during the stress phase (F = 6.15, p = 0.002). Responders in the PD group presented a lower level of LF/HF ratio during the stress phase compared to non-responders (F = 10.14, p = 0.002), while responders in the MDD group showed a lower level of heart rate during all three phases, compared to non-responders. Additionally, we could predict treatment response in patients with MDD using ΔLF/HF ratio (OR: 1.33, 95% CI = 1.07-1.65, p = 0.011) and ΔpNN50 (OR: 1.49, 95% CI 1.09-1.77, p = 0.014).Conclusion: The changes of HRV parameters of pNN50 and LF/HF ratio between the stress and recovery phase may be clinical markers of predictors of treatment responsiveness in MDD and PD patients. [ABSTRACT FROM AUTHOR]

• FOXO3 induction by acute valproate exposure was confirmed at in vivo model in juvenile male hippocampus only. • Proneural gene expression, ASCL1 and NGN2, were upregulated by FOXO3 down expression in FOXO3 siRNA treated PC12 cells. • Mitochondria biogenesis related gene expressions were regulated by FOXO3 expression in FOXO3 siRNA treated PC12 cells. Valproic acid (VPA), an anticonvulsant and mood stabilizer, may affect Notch signaling and mitochondrial function. In a previous study, acute VPA exposure induced increased expression of FOXO3, a transcription factor that shares common targets with pro-neuronal ASCL1. In this study, intraperitoneal acute VPA (400 mg/kg) administration in 4-week-old mice increased and decreased FOXO3 and ASCL1 expression, respectively, in the hippocampus, associated with sex-based differences. Treatment of Foxo3 siRNA increased the mRNA expression levels of Ascl1, Ngn2, Hes6, and Notch1 in PC12 cells. Furthermore, VPA exposure induced significant expression changes of mitochondria-related genes, including COX4 and SIRT1 , in hippocampal tissues, associated with sex-based differences. This study suggests that acute VPA exposure differently affects proneural gene expression via FOXO3 induction in the hippocampus based on sex. [ABSTRACT FROM AUTHOR]

Background/Aims: A limited number of studies addressed MRI-based neurodegenerative changes in subjective memory impairment (SMI). We investigated changes in white matter (WM) microstructures as well as gray matter (GM) macrostructures in subjects with SMI of high and low risk for progression. Methods: A modeling scale (score range, 0-6) developed for prediction of SMI progression was used to divide SMI subjects (n = 46) into two groups: a high risk of progression (score ⩾ 3; n = 19) and a low risk of progression (score ⩽ 2; n = 27). Cross-sectional comparisons were performed using a region-of-interest-based diffusion tensor imaging (DTI) analysis, cortical thickness analysis, and hippocampal volumetry. Results: The high-risk group had more microstructural disruption shown by lower fractional anisotropy in the hippocampus, parahippocampal gyrus, supramarginal gyrus, and parts of frontotemporal lobes. On the other hand, GM macrostructural changes did not differ between the groups and were not associated with modeling scale scores. Conclusion: SMI subjects with a high risk of progression had more WM microstructural disruption than those with a low risk, and the changes were not explained by GM atrophy. Our findings suggest that the degree of microstructural alterations in SMI may be distinctive according to the risk factors and may precede GM atrophy. [ABSTRACT FROM AUTHOR]

We report an enhancement in light emission efficiency form Si nanocrystal (NC) light-emitting diodes (LEDs) via surface plasmons (SPs) by employing Au nanoparticles (NPs). Photoluminescence intensity of Si NCs with Au NPs was enhanced by 2 factors of magnitude due to the strong coupling of Si NCs and SP resonance modes of Au NPs. The electrical characteristics of Si NC LED were significantly improved, which was attributed to an increase in an electron injection into the Si NCs due to the formation of inhomogeneous Schottky barrier at the SiC-indium tin oxide interface. Moreover, light output power from the Si NC LED was enhanced by 50% due to both SP coupling and improved electrical properties. The results presented here can provide a very promising way to significantly enhance the performance of Si NC LED. [ABSTRACT FROM AUTHOR]

Valproic acid (VPA) is an antiepileptic drug found to induce mitochondrial dysfunction and autophagy in cancer cell lines. We treated the SH-SY5Y cell line with various concentrations of VPA (1, 5, and 10 mM). The treatment decreased cell viability, ATP production, and mitochondrial membrane potential and increased reactive oxygen species production. In addition, the mitochondrial DNA copy number increased after VPA treatment in a dose-dependent manner. Western blotting showed that the levels of mitochondrial biogenesis-related proteins (PGC-1α, TFAM, and COX4) increased, though estrogen-related receptor expression decreased after VPA treatment. Further, VPA treatment increased the total and acetylated FOXO3a protein levels. Although SIRT1 expression was decreased, SIRT3 expression was increased, which regulated FOXO3 acetylation in the mitochondria. Furthermore, VPA treatment induced autophagy via increased LC3-II levels and decreased p62 expression and mTOR phosphorylation. We suggest that VPA treatment induces mitochondrial biogenesis and autophagy via changes in FOXO3a expression and posttranslational modification in the SH-SY5Y cell line. [ABSTRACT FROM AUTHOR]

Trimethyltin (TMT) is an irreversible neurotoxicant. Because prenatal TMT exposure has been reported to induce behavioral changes, this study was conducted to observe gender differences and epigenetic changes using a mouse model. In behavioral testing of offspring at 5 weeks of age, the total times spent in the center, corner, or border zones in the male prenatal TMT-exposed mice were less than those of control unexposed mice in the open-field test. Female TMT-exposed mice scored lower on total numbers of arm entries and percentages of alternations than controls in the Y-maze test with lower body weight. We found that only TMT-exposed males had fewer copies of mtDNA in the hippocampus and prefrontal cortex region than controls. Additional epigenetic changes, including increased 5-methyl cytosine/5-hydroxymethyl cytosine levels in the male TMT hippocampus, were observed. After methylation binding domain (MBD) sequencing, multiple signaling pathways related to metabolism and neurodevelopment, including FoxO signaling, were identified by pathway analysis for differentially methylated regions (DMRs). Increased FOXO3 and decreased ASCL1 expression were also observed in male TMT hippocampi. This study suggests that sex differences and epigenetics should be more carefully considered in prenatal toxicology studies. [ABSTRACT FROM AUTHOR]

Abstract: Background: The genetic factors that determine the heterogeneity of cognitive impairment in Alzheimer's disease (AD) patients have been rarely reported. We aimed to investigate the association between top hits of genome-wide association studies (GWAS) and specific cognitive domains in AD patients. Methods: We investigated 86 single nucleotide polymorphisms (SNPs) selected from 12 genes (ABCA7, APOE, BIN1, CD2AP, CD33, CLU, CR1, EPHA1, LRAT, MS4A6A, PCDH11X, and PICALM) based on results of the recent GWAS and genotyped in 211 AD cases. We also analyzed results of comprehensive neuropsychological evaluations in all cases. We performed multiple regression analyses. Results: There were four significant associations between genotypes and phenotypes of AD patients: CR1 SNP rs11803956 correlated with Mini-Mental State Examination (MMSE) score (β=1.718, Pcorrected =0.002); ABCA7 SNP rs3752232 correlated with Rey Complex Figure Test (RCFT) copy score (β=−6.861, Pcorrected =0.013); APOE SNP rs2075650 correlated with the percentile of RCFT copy score (β=14.005, Pcorrected =0.021) and the percentile of total score in phonemic fluency (β=11.052, Pcorrected =0.035). Conclusion: Our results suggest that CR1, ABCA7, and APOE correlate with specific aspects of cognitive impairments in AD patients. [Copyright &y& Elsevier]

Highlights: [•] We investigated brain MD changes in Parkinson's disease patients. [•] MD changes in corticofugal tract, cingulum and other white matter tracts in PD. [•] MD changes in left putamen, caudate, pallidum and thalamus in PD [Copyright &y& Elsevier]

Background: Previous physiology-driven pain studies focused on examining the presence or intensity of physical pain. However, people experience various types of pain, including social pain, which induces negative mood; emotional distress; and neural activities associated with physical pain. In particular, comparison of autonomic nervous system (ANS) responses between social and physical pain in healthy adults has not been well demonstrated., Methods: We explored the ANS responses induced by two types of pain-social pain, associated with a loss of social ties; and physical pain, caused by a pressure cuff-based on multimodal physiological signals. Seventy-three healthy individuals (46 women; mean age = 20.67 ± 3.27 years) participated. Behavioral responses were assessed to determine their sensitivity to pain stimuli. Electrocardiogram, electrodermal activity, photoplethysmogram, respiration, and finger temperature (FT) were measured, and 12 features were extracted from these signals., Results: Social pain induced increased heart rate (HR) and skin conductance (SC) and decreased blood volume pulse (BVP), pulse transit time (PTT), respiration rate (RR), and FT, suggesting a heterogeneous pattern of sympathetic-parasympathetic coactivation. Moreover, physical pain induced increased heart rate variability (HRV) and SC, decreased BVP and PTT, and resulted in no change in FT, indicating sympathetic-adrenal-medullary activation and peripheral vasoconstriction., Conclusion: These results suggest that changes in HR, HRV indices, RR, and FT can serve as markers for differentiating physiological responses to social and physical pain stimuli., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Jang, Eum, Yoon, Sohn and Byun.)

Background: Automatic diagnosis of depression based on speech can complement mental health treatment methods in the future. Previous studies have reported that acoustic properties can be used to identify depression. However, few studies have attempted a large-scale differential diagnosis of patients with depressive disorders using acoustic characteristics of non-English speakers., Objective: This study proposes a framework for automatic depression detection using large-scale acoustic characteristics based on the Korean language., Methods: We recruited 153 patients who met the criteria for major depressive disorder and 165 healthy controls without current or past mental illness. Participants' voices were recorded on a smartphone while performing the task of reading predefined text-based sentences. Three approaches were evaluated and compared to detect depression using data sets with text-dependent read speech tasks: conventional machine learning models based on acoustic features, a proposed model that trains and classifies log-Mel spectrograms by applying a deep convolutional neural network (CNN) with a relatively small number of parameters, and models that train and classify log-Mel spectrograms by applying well-known pretrained networks., Results: The acoustic characteristics of the predefined text-based sentence reading automatically detected depression using the proposed CNN model. The highest accuracy achieved with the proposed CNN on the speech data was 78.14%. Our results show that the deep-learned acoustic characteristics lead to better performance than those obtained using the conventional approach and pretrained models., Conclusions: Checking the mood of patients with major depressive disorder and detecting the consistency of objective descriptions are very important research topics. This study suggests that the analysis of speech data recorded while reading text-dependent sentences could help predict depression status automatically by capturing the characteristics of depression. Our method is smartphone based, is easily accessible, and can contribute to the automatic identification of depressive states., (©Ah Young Kim, Eun Hye Jang, Seung-Hwan Lee, Kwang-Yeon Choi, Jeon Gue Park, Hyun-Chool Shin. Originally published in the Journal of Medical Internet Research (https://www.jmir.org), 25.01.2023.)

Objective: In this study, we investigated sex- and region-specific effects of acute trimethyltin (TMT) exposure on mitochondrial biogenesis., Methods: We treated TMT to primary neuronal cultures and 4-week-old male and female mice. We measured the mitochondrial DNA copy numbers using the quantitative polymerase chain reaction method. We also measured mitochondrial biogenesis related genes (sirtuin-1, estrogen-related receptor alpha, cytochrome C oxidase subunit IV) by western blotting., Results: The mitochondrial DNA copy number increased in the primary hippocampal neuron; however, it decreased in the primary cortical neuron. The mitochondrial copy number increased in the hippocampus and decreased in the cortex in the TMT treated female mice, though the mitochondrial copy number increased in both cortex and hippocampus in the TMT treated male mice. TMT treatment increased sirtuin-1 expression in the male hippocampus but did not in the female brain. In the female brain, estrogen-related receptor alpha expression decreased in the cortex though there is no significant change in the male brain. The protein level of mitochondrial protein, cytochrome C oxidase subunit IV, increased in both cortex and hippocampus after TMT injection in male mice brain, but not in female mice brain., Conclusion: Our data suggest that acute TMT exposure induces distinct sex-specific metabolic characteristics in the brain before significant sexual maturation.

Background/aim: In this study, we investigated sex-specific effects of acute exposure to trimethyltin, a known neurotoxicant on metabolic steroids., Materials and Methods: We administered intraperitoneally 2.3 mg/kg trimethyltin to 4-week-old male mice and measured the levels of metabolic steroids 24 h after treatment. We also measured mRNA and protein levels of cytochrome P450 1B1 using real-time polymerase chain reaction and western blotting., Results: Cortisol levels in the cortex increased in both sexes following acute trimethyltin exposure. The estradiol levels decreased, and the 4-hydroxyestradiol levels increased only in females. We also observed increased cytochrome P450 1B1 mRNA and protein levels only in the female cortex., Conclusion: Acute trimethyltin exposure induces distinct sex-specific metabolic changes in the brain before significant sexual maturation., (Copyright© 2021, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Emotions are experienced differently by individuals, and thus, it is important to account for individuals' experienced emotions to understand their physiological responses to emotional stimuli. The present study investigated the physiological responses to a fear-inducing stimulus and examined whether these responses can predict experienced fear. A total of 230 participants were presented with neutral and fear-inducing film clips, after which they self-rated their experienced emotions. Physiological measures (skin conductance level and response: SCL, SCR, heart rate: HR, pulse transit time: PTT, fingertip temperature: FT, and respiratory rate: RR) were recorded during the stimuli presentation. We examined the correlations between the physiological measures and the participants' experienced emotional intensity, and performed a multiple linear regression to predict fear intensity based on the physiological responses. Of the participants, 92.5% experienced the fear emotion, and the average intensity was 5.95 on a 7-point Likert scale. Compared to the neutral condition, the SCL, SCR, HR, and RR increased significantly during the fear-inducing stimulus presentation whereas FT and PTT decreased significantly. Fear intensity correlated positively with SCR and HR and negatively with SCL, FT, PTT, and RR. The multiple linear regression demonstrated that fear intensity was predicted by a combination of SCL, SCR, HR, FT, and RR. Our findings indicate that the physiological responses to experiencing fear are associated with cholinergic, sympathetic, and α-adrenergic vascular activation as well as myocardial β-sympathetic excitation, and support the use of multimodal physiological signals for quantifying emotions., (Copyright: © 2020 University of Economics and Human Sciences in Warsaw.)

Purpose: The purpose of this study was to evaluate the effects of an education program for mothers of late-preterm infants on parenting confidence, breastfeeding rate, and infants' growth and readmission rate., Methods: The participants were 53 mothers of late-preterm infants (26 in the experimental group and 27 in the control group). The experimental group was administered the late-preterm care education program while the control group received standard care. The program consisted of two sessions during hospitalization after birth, one session at the time of discharge, and telephone and social networking service consultations at weekly intervals for the month following discharge. The collected data were analyzed using the t-test, χ 2 test, and repeated-measures analysis of variance., Results: Parenting confidence and the breastfeeding rate were significantly higher in the experimental group than in the control group. However, there was no significant difference in the late-preterm infants' growth and readmission rates between the experimental and control groups., Conclusion: A care education program for mothers of late-preterm infants can be a useful nursing intervention in clinical practice., Competing Interests: No existing or potential conflict of interest relevant to this article was reported., (Copyright © 2020 Korean Academy of Child Health Nursing. All rights reserved.)

This study proposes a simple method of fabricating flexible electronic devices using a metal template for passive alignment between chip components and an interconnect layer, which enabled efficient alignment with high accuracy. An electrocardiogram (ECG) sensor was fabricated using 20 µm thick polyimide (PI) film as a flexible substrate to demonstrate the feasibility of the proposed method. The interconnect layer was fabricated by a two-step photolithography process and evaporation. After applying solder paste, the metal template was placed on top of the interconnect layer. The metal template had rectangular holes at the same position as the chip components on the interconnect layer. Rectangular hole sizes were designed to account for alignment tolerance of the chips. Passive alignment was performed by simply inserting the components in the holes of the template, which resulted in accurate alignment with positional tolerance of less than 10 µm based on the structural design, suggesting that our method can efficiently perform chip mounting with precision. Furthermore, a fabricated flexible ECG sensor was easily attachable to the curved skin surface and able to measure ECG signals from a human subject. These results suggest that the proposed method can be used to fabricate epidermal sensors, which are mounted on the skin to measure various physiological signals.

CD38 is an enzyme that catalyzes the formation of cyclic ADP ribose and nicotinic acid adenine dinucleotide phosphate, both of which are involved in the mobilization of Ca(2+) from intracellular stores. Recently, CD38 has been shown to regulate oxytocin release from hypothalamic neurons. Importantly, CD38 mutations are associated with autism spectrum disorders (ASD) and CD38 knockout (CD38(-/-)) mice display ASD-like behavioral phenotypes including deficient parental behavior and poor social recognition memory. Although ASD and learning deficits commonly co-occur, the role of CD38 in learning and memory has not been investigated. We report that CD38(-/-) mice show deficits in various learning and memory tasks such as the Morris water maze, contextual fear conditioning, and the object recognition test. However, either long-term potentiation or long-term depression is not impaired in the hippocampus of CD38(-/-) mice. Our results provide convincing evidence that CD38(-/-) mice show deficits in various learning and memory tasks including spatial and non-spatial memory tasks. Our data demonstrate that CD38 is critical for regulating hippocampus-dependent learning and memory without modulating synaptic plasticity.