Selection of Catechin Biosynthesis-Related Genes and Functional Analysis from Chromosome-Level Genome Assembly in C. sinensis L. Variety 'Sangmok'.

Camellia is an important plant genus that includes well-known species such as C. sinensis, C. oleifera, and C. japonica. The C. sinensis cultivar 'Sangmok', one of Korea's standard types of tea landraces, is a small evergreen tree or shrub. Genome annotation has shown that Korean tea plants have special and unique benefits and superior components, such as catechin. The genome of Camellia sinensis cultivar 'Sangmok' was assembled on the chromosome level, with a length of 2678.62 Mbp and GC content of 38.16%. Further, 15 chromosome-scale scaffolds comprising 82.43% of the assembly (BUSCO completeness, 94.3%) were identified. Analysis of 68,151 protein-coding genes showed an average of 5.003 exons per gene. Among 82,481 coding sequences, the majority (99.06%) were annotated by Uniprot/Swiss-Prot. Further analysis revealed that 'Sangmok' is closely related to C. sinensis, with a divergence time of 60 million years ago. A total of 3336 exclusive gene families in 'Sangmok' were revealed by gene ontology analysis to play roles in auxin transport and cellular response mechanisms. By comparing these exclusive genes with 551 similar catechin genes, 17 'Sangmok'-specific catechin genes were identified by qRT-PCR, including those involved in phytoalexin biosynthesis and related to cytochrome P450. The 'Sangmok' genome exhibited distinctive genes compared to those of related species. This comprehensive genomic investigation enhances our understanding of the genetic architecture of 'Sangmok' and its specialized functions. The findings contribute valuable insights into the evolutionary and functional aspects of this plant species.

Depletion of hepatic forkhead box O1 does not affect cholelithiasis in male and female mice.

Cholelithiasis is one of the most prevalent gastroenterological diseases and is characterized by the formation of gallstones in the gallbladder. Both clinical and preclinical data indicate that obesity, along with comorbidity insulin resistance, is a predisposing factor for cholelithiasis. Forkhead box O1 (FoxO1) is a key transcription factor that integrates insulin signaling with hepatic metabolism and becomes deregulated in the insulin-resistant liver, contributing to dyslipidemia in obesity. To gain mechanistic insights into how insulin resistance is linked to cholelithiasis, here we determined FoxO1's role in bile acid homeostasis and its contribution to cholelithiasis. We hypothesized that hepatic FoxO1 deregulation links insulin resistance to impaired bile acid metabolism and cholelithiasis. To address this hypothesis, we used the FoxO1LoxP/LoxP-Albumin-Cre system to generate liver-specific FoxO1-knockout mice. FoxO1-knockout mice and age- and sex-matched WT littermates were fed a lithogenic diet, and bile acid metabolism and gallstone formation were assessed in these animals. We showed that FoxO1 affected bile acid homeostasis by regulating hepatic expression of key enzymes in bile acid synthesis and in biliary cholesterol and phospholipid secretion. Furthermore, FoxO1 inhibited hepatic expression of the bile acid receptor farnesoid X receptor and thereby counteracted hepatic farnesoid X receptor signaling. Nonetheless, hepatic FoxO1 depletion neither affected the onset of gallstone disease nor impacted the disease progression, as FoxO1-knockout and control mice of both sexes had similar gallstone weights and incidence rates. These results argue against the notion that FoxO1 is a link between insulin resistance and cholelithiasis.

A Noncanonical Role for Plasminogen Activator Inhibitor Type 1 in Obesity-Induced Diabetes.

Obesity is a major risk factor for type 2 diabetes because of chronic hepatic inflammation and resultant insulin resistance. Hepatocyte growth factor (HGF) is responsible for resetting hepatic homeostasis after injury following activation by urokinase-type plasminogen activator (u-PA; encoded by the PLAU gene). Plasminogen activator inhibitor type-1 (PAI-1; encoded by the SERPINE1 gene), a u-PA inhibitor and antifibrinolytic agent, is often elevated in obesity and is linked to cardiovascular events. We hypothesized that, in addition to its role in preventing fibrinolysis, elevated PAI-1 inhibits HGF's activation by u-PA and the resultant anti-inflammatory and hepatoprotective properties. Wild-type and PAI-1 knockout (KO) mice on a high-fat diet both became significantly heavier than lean controls; however, the obese KO mice demonstrated improved glucose metabolism compared with wild-type mice. Obese KO mice also exhibited an increase in conversion of latent single-chain HGF to active two-chain HGF, coinciding with an increase in the phosphorylation of the HGF receptor (HGFR or MET, encoded by the MET gene), as well as dampened inflammation. These results strongly suggest that, in addition to its other functions, PAI-mediated inhibition of HGF activation prohibits the resolution of inflammation in the context of obesity-induced type 2 diabetes.

Psychological Development during Medical School Clerkship: Relationship to Resilience.

OBJECTIVE: The authors investigated changes in medical students' defenses during clerkship and examined the effects of these changes on students' resilience. METHODS: Between 2012 and 2014, all year-2 preclinical students (N = 249) at Gyeongsang National University Medical School were asked to participate. Those who agreed to participate (N = 237) completed the Korean version of the Defense Style Questionnaire (K-DSQ) and the Connor-Davidson resilience scale-10 (CD-RISC-10). After clerkship, students who proceeded to year 4 in 2 years (n = 187 (93 females), aged 24-38 years (mean, 28.9 ± 2.8 years)) completed the K-DSQ, CD-RISC-10, and the Korean version of the Hospital Anxiety and Depression Scale (K-HADS) in September 2014, 2015, and 2016. RESULTS: The use of adaptive (W = 11,603.5, p < 0.001, r = 0.39) and self-inhibiting (W = 10,901.5, p < 0.001, r = 0.32) styles increased significantly after clerkship. A multiple linear regression analysis showed that changes in adaptive defense styles (B = 1.336, SE = 0.386, ß = 0.218, p = 0.001) during clerkship were significantly related to resilience after adjusting for age, sex, depression, and anxiety. CONCLUSIONS: Both positive personality development and maladaptive changes in defenses were evident. An increase in the adaptive defense style score was related to resilience.

APOC3 Protein Is Not a Predisposing Factor for Fat-induced Nonalcoholic Fatty Liver Disease in Mice.

Nonalcoholic fatty liver disease (NAFLD), characterized by excessive fat accumulation in liver, is prevalent in obesity. Genetic factors that link obesity to NAFLD remain obscure. Apolipoprotein C3 (APOC3) is a lipid-binding protein with a pivotal role in triglyceride metabolism. Humans with APOC3 gain-of-function mutations and mice with APOC3 overproduction are associated with hypertriglyceridemia. Nonetheless, it remains controversial whether APOC3 is culpable for diet-induced NAFLD. To address this fundamental issue, we fed APOC3-transgenic and wild-type littermates a high fructose diet or high fat diet, followed by determination of the effect of APOC3 on hepatic lipid metabolism and inflammation and the progression of NAFLD. To gain mechanistic insight into NAFLD, we determined the impact of APOC3 on hepatic triglyceride synthesis and secretion versus fatty acid oxidation. APOC3-transgenic mice were hypertriglyceridemic, culminating in marked elevation of triglycerides, cholesterols, and non-esterified fatty acids in plasma. Despite the prevailing hypertriglyceridemia, APOC3-transgenic mice, relative to wild-type littermates, had similar weight gain and hepatic lipid content without alterations in hepatic expression of key genes involved in triglyceride synthesis and secretion and fatty acid oxidation. APOC3-transgenic and wild-type mice had similar Kupffer cell content without alterations in hepatic expression of pro- and anti-inflammatory cytokines. APOC3 neither exacerbated diet-induced adiposity nor aggravated the degree of steatosis in high fructose or high fat-fed APOC3-transgenic mice. These effects ensued independently of weight gain even after 10-month high fat feeding. We concluded that APOC3, whose dysregulation is liable for hypertriglyceridemia, is not a predisposing factor for linking overnutrition to NAFLD in obesity.

Effect of Hypertriglyceridemia on Beta Cell Mass and Function in ApoC3 Transgenic Mice.

Hypertriglyceridemia results from increased production and decreased clearance of triglyceride-rich very low-density lipoproteins, a pathological condition that accounts for heightened risk of ischemic vascular diseases in obesity and type 2 diabetes. Despite its intimate association with insulin resistance, whether hypertriglyceridemia constitutes an independent risk for beta cell dysfunction in diabetes is unknown. Answering this fundamental question is stymied by the fact that hypertriglyceridemia is intertwined with hyperglycemia and insulin resistance in obese and diabetic subjects. To circumvent this limitation, we took advantage of apolipoprotein C3 (ApoC3)-transgenic mice, a model with genetic predisposition to hypertriglyceridemia. We showed that ApoC3-transgenic mice, as opposed to age/sex-matched wild-type littermates, develop hypertriglyceridemia with concomitant elevations in plasma cholesterol and non-esterified fatty acid levels. Anti-insulin and anti-glucagon dual immunohistochemistry in combination with morphometric analysis revealed that ApoC3-transgenic and wild-type littermates had similar beta cell and alpha cell masses as well as islet size and architecture. These effects correlated with similar amplitudes of glucose-stimulated insulin secretion and similar degrees of postprandial glucose excursion in ApoC3-transgenic versus wild-type littermates. Oil Red O histology did not visualize lipid infiltration into islets, correlating with the lack of ectopic triglyceride and cholesterol depositions in the pancreata of ApoC3-transgenic versus wild-type littermates. ApoC3-transgenic mice, despite persistent hypertriglyceridemia, maintained euglycemia under both fed and fasting conditions without manifestation of insulin resistance and fasting hyperinsulinemia. Thus, hypertriglyceridemia per se is not an independent risk factor for beta cell dysfunction in ApoC3 transgenic mice.

Construction of 3D multicellular microfluidic chip for an in vitro skin model.

Current in vitro skin models do not recapitulate the complex architecture and functions of the skin tissue. In particular, on-chip construction of an in vitro model comprising the epidermis and dermis layer with vascular structure for mass transport has not been reported yet. In this study, we aim to develop a microfluidic, three-dimensional (3D) skin chip with fluidic channels using PDMS and hydrogels. Mass transport within the collagen hydrogel matrix was verified with fluorescent model molecules, and a transport-reaction model of oxygen and glucose inside the skin chip was developed to aid the design of the microfluidic skin chip. Comparison of viabilities of dermal fibroblasts and HaCaT cultured in the chip with various culture conditions revealed that the presence of flow plays a crucial role in maintaining the viability, and both cells were viable after 10 days of air exposure culture. Our 3D skin chip with vascular structures can be a valuable in vitro model for reproducing the interaction between different components of the skin tissue, and thus work as a more physiologically realistic platform for testing skin reaction to cosmetic products and drugs.

Forkhead Box O6 (FoxO6) Depletion Attenuates Hepatic Gluconeogenesis and Protects against Fat-induced Glucose Disorder in Mice.

Excessive endogenous glucose production contributes to fasting hyperglycemia in diabetes. FoxO6 is a distinct member of the FoxO subfamily. To elucidate the role of FoxO6 in hepatic gluconeogenesis and assess its contribution to the pathogenesis of fasting hyperglycemia in diabetes, we generated FoxO6 knock-out (FoxO6-KO) mice followed by determining the effect of FoxO6 loss-of-function on hepatic gluconeogenesis under physiological and pathological conditions. FoxO6 depletion attenuated hepatic gluconeogenesis and lowered fasting glycemia in FoxO6-KO mice. FoxO6-deficient primary hepatocytes were associated with reduced capacities to produce glucose in response to glucagon. When fed a high fat diet, FoxO6-KO mice exhibited significantly enhanced glucose tolerance and reduced blood glucose levels accompanied by improved insulin sensitivity. These effects correlated with attenuated hepatic gluconeogenesis in FoxO6-KO mice. In contrast, wild-type littermates developed fat-induced glucose intolerance with a concomitant induction of fasting hyperinsulinemia and hyperglycemia. Furthermore, FoxO6-KO mice displayed significantly diminished macrophage infiltration into liver and adipose tissues, correlating with the reduction of macrophage expression of C-C chemokine receptor 2 (CCR2), a factor that is critical for regulating macrophage recruitment in peripheral tissues. Our data indicate that FoxO6 depletion protected against diet-induced glucose intolerance and insulin resistance by attenuating hepatic gluconeogenesis and curbing macrophage infiltration in liver and adipose tissues in mice.

Allergic diseases, excessive Internet use and suicidal ideation in Korean adolescents.

OBJECTIVE: The aim of this study is to evaluate the relation between suicidal ideation, allergic diseases, and excessive Internet use in Korean youth using a national representative dataset. METHODS: Data from the Korean Youth Risk Behavior Web-Based Survey (KYRBWS), conducted by the Korean Centers for Disease Control and Prevention, were used in this study. Complex sample logistic regression and structural equation modeling were performed to define the relation between suicidal ideation, allergic disease and excessive Internet use. RESULTS: A total of 73,238 students participated in this survey. In Korea, 19.3% of adolescents had suicidal ideation in the previous year. Asthma (OR=1.23, 95% CI=1.15-1.32, p<0.01) and allergic rhinitis (OR=1.17, 95% CI=1.11-1.22, p<0.01) were identified as risk factors for suicidal ideation after adjusting for school and family factors. Structural equation modeling showed that excessive Internet use interacted with the association between allergic diseases and suicidal ideation. CONCLUSION: Allergy problems could positively affect suicidal ideation in Korean adolescents. Excessive Internet use could be a mediating factor between allergic disease and suicidal ideation.

Activation of protein kinase C-mitogen-activated protein kinase signaling in response to inositol starvation triggers Sir2p-dependent telomeric silencing in yeast.

Depriving wild type yeast of inositol, a soluble precursor for phospholipid, phosphoinositide, and complex sphingolipid synthesis, activates the protein kinase C (PKC)-MAPK signaling pathway, which plays a key role in the activation of NAD(+)-dependent telomeric silencing. We now report that triggering PKC-MAPK signaling by inositol deprivation or by blocking inositol-containing sphingolipid synthesis with aureobasidin A results in increased telomeric silencing regulated by the MAPK, Slt2p, and the NAD(+)-dependent deacetylase, Sir2p. Consistent with the dependence on NAD(+) in Sir2p-regulated silencing, we found that inositol depletion induces the expression of BNA2, which is required for the de novo synthesis of NAD(+). Moreover, telomeric silencing is greatly reduced in bna2Δ and npt1Δ mutants, which are defective in de novo and salvage pathways for NAD(+) synthesis, respectively. Surprisingly, however, omitting nicotinic acid from the growth medium, which reduces cellular NAD(+) levels, leads to increased telomeric silencing in the absence of inositol and/or at high temperature. This increase in telomeric silencing in response to inositol starvation is correlated to chronological life span extension but is Sir2p-independent. We conclude that activation of the PKC-MAPK signaling by interruption of inositol sphingolipid synthesis leads to increased Sir2p-dependent silencing and is dependent upon the de novo and salvage pathways for NAD(+) synthesis but is not correlated with cellular NAD(+) levels.

ATF4 protein deficiency protects against high fructose-induced hypertriglyceridemia in mice.

Hypertriglyceridemia is the most common lipid disorder in obesity and type 2 diabetes. It results from increased production and/or decreased clearance of triglyceride-rich lipoproteins. To better understand the pathophysiology of hypertriglyceridemia, we studied hepatic regulation of triglyceride metabolism by the activating transcription factor 4 (ATF4), a member of the basic leucine zipper-containing protein subfamily. We determined the effect of ATF4 on hepatic lipid metabolism in Atf4(-/-) mice fed regular chow or provided with free access to fructose drinking water. ATF4 depletion preferentially attenuated hepatic lipogenesis without affecting hepatic triglyceride production and fatty acid oxidation. This effect prevented excessive fat accumulation in the liver of Atf4(-/-) mice, when compared with wild-type littermates. To gain insight into the underlying mechanism, we showed that ATF4 depletion resulted in a significant reduction in hepatic expression of peroxisome proliferator-activated receptor-γ, a nuclear receptor that acts to promote lipogenesis in the liver. This effect was accompanied by a significant reduction in hepatic expression of sterol regulatory element-binding protein 1c (SREBP-1c), acetyl-CoA carboxylase, and fatty-acid synthase, three key functions in the lipogenic pathway in Atf4(-/-) mice. Of particular significance, we found that Atf4(-/-) mice, as opposed to wild-type littermates, were protected against the development of steatosis and hypertriglyceridemia in response to high fructose feeding. These data demonstrate that ATF4 plays a critical role in regulating hepatic lipid metabolism in response to nutritional cues.

Nasopharyngeal metatranscriptomics reveals host-pathogen signatures of pediatric sinusitis.

Acute sinusitis (AS) is the fifth leading cause of antibiotic prescriptions in children. Distinguishing bacterial AS from common viral upper respiratory infections in children is crucial to prevent unnecessary antibiotic use but is challenging with current diagnostic methods. Despite its speed and cost, untargeted RNA sequencing of clinical samples from children with suspected AS has the potential to overcome several limitations of other methods. However, the utility of sequencing-based approaches in analysis of AS has not been fully explored. Here, we performed RNA-seq of nasopharyngeal samples from 221 children with clinically diagnosed AS to characterize their pathogen and host-response profiles. Results from RNA-seq were compared with those obtained using culture for three common bacterial pathogens and qRT-PCR for 12 respiratory viruses. Metatranscriptomic pathogen detection showed high concordance with culture or qRT-PCR, showing 87%/81% sensitivity (sens) / specificity (spec) for detecting bacteria, and 86%/92% (sens/spec) for viruses, respectively. We also detected an additional 22 pathogens not tested for in the clinical panel, and identified plausible pathogens in 11/19 (58%) of cases where no organism was detected by culture or qRT-PCR. We assembled genomes of 205 viruses across the samples including novel strains of coronaviruses, respiratory syncytial virus (RSV), and enterovirus D68. By analyzing host gene expression, we identified host-response signatures that distinguished bacterial and viral infections and correlated with pathogen abundance. Ultimately, our study demonstrates the potential of untargeted metatranscriptomics for in depth analysis of the etiology of AS, comprehensive host-response profiling, and using these together to work towards optimized patient care.

Usefulness of the combined application of the Mood Disorder Questionnaire and Bipolar Spectrum Diagnostic Scale in screening for bipolar disorder.

OBJECTIVE: This study aimed to examine whether combined application of the Mood Disorder Questionnaire (MDQ) and Bipolar Spectrum Diagnostic Scale (BSDS) is more effective than exclusive application of either tool in screening for bipolar disorder (BD). METHOD: The MDQ and BSDS were completed by a total of 113 patients diagnosed with BD and major depressive disorder who were experiencing a current major depressive episode. The initial diagnosis of the subject was confirmed during a 1-year follow-up period. When each MDQ and BSDS optimal cutoff score was calculated, a modified scoring method for the MDQ that considered only one item was used to increase its performance in this population. The following three combinations of the cutoff scores for the two tools were used to screen for BD: (A) The score on either the MDQ or BSDS was greater than or equal to the cutoff score; (B) the scores on both the MDQ and BSDS were greater than or equal to the cutoff score; and (C) Reducing either cutoff score by 1 point resulted in the MDQ and BSDS scores being greater than or equal to the cutoff score. The sensitivity, specificity, positive predictive value, and negative predictive value of the three methods, the MDQ, and the BSDS were compared for screening BD. RESULTS: The sensitivity and specificity of the MDQ were 0.741 and 0.844, respectively, and those for the BSDS were 0.731 and 0.742, respectively. These indicators for the combined application of the MDQ and BSDS were as follows, respectively: method A 0.901 and 0.688, method B 0.580 and 0.875, and method C 0.691 and 0.844. Method A was superior to using one measure alone as well as to methods B and C with regard to sensitivity and negative predictive values. Method A also showed a higher sensitivity for BD subtypes than did the individual tools. Compared with the use of individual instruments, method A showed a similar positive predictive value. CONCLUSION: This study suggests that combined use of the MDQ and BSDS is more effective than the individual use of either of these measures in screening for BD. The data also showed that when both tools were used, the most effective interpretation of the results in terms of screening for BD was achieved when positive scores were defined as those that were equal to or greater than the cutoff for the MDQ or BSDS.

Support for the Use of a New Cutoff to Define a Positive Urine Culture in Young Children.

BACKGROUND: Conventional urine culture selects for a narrow range of organisms that grow well in aerobic conditions. In contrast, examination of bacterial gene sequences in the urine provides a relatively unbiased evaluation of the organisms present. Thus, by using 16S ribosomal ribonucleic acid (rRNA) gene amplicon sequencing as the reference standard, we now have the ability to assess the accuracy of urine culture in diagnosing urinary tract infection (UTI). METHODS: We enrolled febrile children 1 month to 3 years of age that underwent bladder catheterization for suspected UTI. Using 16S rRNA gene amplicon sequencing as the reference standard, we calculated the accuracy of urine culture at various cutoffs (10 000, 50 000, and 100 000 colony forming units per milliliter). Children with ≥80% relative abundance of any organism on 16S rRNA gene amplicon sequencing with elevated urinary markers of inflammation were defined as having a UTI. RESULTS: When using a cutoff of 10 000 CFU/mL, the sensitivity and specificity of urine culture were 98% (95% confidence interval [CI]: 93%-100%) and 99% (95% CI: 97%-100%), respectively. Using a cutoff of 50 000 colony forming units per mL decreased sensitivity to 80% (95% CI: 68%-93%) without changing the specificity. Using a cutoff of 100 000 further decreased sensitivity to 70% (95% CI: 55%-84%). CONCLUSIONS: Conventional culture remains an accurate method of diagnosing UTIs in young children; however, these data suggest that a cutoff of 10 000 colony forming units per mL provides the optimal balance between sensitivity and specificity for children undergoing bladder catheterization.

Biomarkers for febrile urinary tract infection in children.

Background: The current reference standard for pediatric urinary tract infection (UTI) screening, the leukocyte esterase (LE) dipstick test, has suboptimal accuracy. The objective of this study was to compare the accuracy of novel urinary biomarkers to that of the LE test. Methods: We prospectively enrolled febrile children who were evaluated for UTI based on their presenting symptoms. We compared the accuracy of urinary biomarkers to that of the test. Results: We included 374 children (50 with UTI, 324 without UTI, ages 1-35 months) and examined 35 urinary biomarkers. The urinary biomarkers that best discriminated between febrile children with and without UTI were urinary neutrophil gelatinase-associated lipocalin (NGAL), IL-1ß, CXCL1, and IL-8. Of all examined urinary biomarkers, the urinary NGAL had the highest accuracy with a sensitivity of 90% (CI: 82-98) and a specificity of 96% (CI: 93-98). Conclusion: Because the sensitivity of the urinary NGAL test is slightly higher than that of the LE test, it can potentially reduce missed UTI cases. Limitations of using urinary NGAL over LE include increased cost and complexity. Further investigation is warranted to determine the cost-effectiveness of urinary NGAL as a screening test for UTI.

Spatiotemporal Patterns of Suicide in Korea From 2009 to 2019 Using Geographic Information Systems.

Objective: When analyzing factors related to suicide, it is necessary to consider the regional characteristics of the areas where individuals live in addition to individual factors. This study aimed to investigate the spatiotemporal association between suicide rates and geographic features and the patterns of this association for all administrative areas in South Korea from 2009 to 2019. Methods: The data used in this study were obtained from the National Statistical Office of the Korean Statistical Information Service. For suicide rates, age-standardized mortality index data per 100 000 people were used. All administrative districts from 2009 to 2019 were divided into 229 regions. Emerging hotspot analysis was used for a 3-dimensional analysis to simultaneously evaluate temporal and spatial clusters. Results: In the 229 regions, there were 27 (11.8%) hotspots and 60 (26.2%) cold spots. Hotspot pattern analysis found 2 (0.9%) new spots, 1 (0.4%) persistent spot, 23 (10.0%) sporadic spots, and 1 (0.4%) oscillating spot. Conclusion: This study found geographic differences in the spatiotemporal patterns of suicide rates in South Korea. The utilization of national resources for suicide prevention should be selectively and intensively prioritized in 3 areas that exhibit unique spatiotemporal patterns.

Association Between Depressed Mood Changes and Physical Activity Among Adolescents Post COVID-19 Pandemic.

Objectives: Following the coronavirus disease 2019 (COVID-19) pandemic, adolescents have experienced decreased physical activity and a decline in mental health. This study analyzed the association between changes in depressed mood after the COVID-19 pandemic and physical activity among adolescents. Methods: The analysis was based on the results of the 17th Youth Health Behavior Online Survey conducted in 2021, which included 54848 middle and high school students in South Korea. Information on physical activity included low-intensity physical activity lasting >60 min/day, high-intensity physical activity, and strength training exercises. A logistic regression analysis was performed to evaluate the association between physical activity and changes in depression after the COVID-19 pandemic. Results: After adjusting for sociodemographic characteristics and previous depression, adolescents who performed strength training exercises more than once per week had a 0.95-fold lower risk (odds ratio [OR]=0.948, 95% confidence interval [CI]=0.905-0.994, p= 0.027) of increasing depression after the COVID-19 pandemic, while the risk of decreasing depression increased by 1.22-fold (OR=1.215, 95% CI=1.131-1.305, p<0.001). The results were not significant for low-intensity physical activity for >60 min/day and high-intensity physical activity. Conclusion: Strength-training exercises are significantly associated with the prevention of depression among adolescents following the COVID-19 pandemic.

Dietary Carotene Intake and Suicidal Ideation in Korean Females: Analysis of Data From the Korea National Health and Nutrition Examination Survey (2012, 2013, and 2015).

OBJECTIVE: The suicide rate in Korea was the highest among countries in the Organisation for Economic Co-operation and Development in 2019. In a previous study, higher intake of vegetables and fruits was associated with a lower risk of suicidal ideation, and carotene-rich fruits and vegetables lowered the risk of depression. This study aimed to examine the direct relationship between carotene intake and suicidal ideation, adjusting for the effect on depression. METHODS: This study used data from the Korea National Health and Nutrition Examination Survey (KNHANES) conducted in 2012, 2013, and 2015. Carotene intake was assessed through a food intake frequency survey with a 24-hour recall. Suicidal ideation and depression were assessed using the mental health section of the KNHANES. We applied logistic regression to assess the relationship between carotene intake and suicidal ideation, adjusting for potential confounders. RESULTS: A total of 5,480 females aged 19-64 years were included in this study. Carotene intake was significantly lower in the suicidal ideation group (3,034.5±1,756.4 µg/day) than in the nonsuicidal ideation group (3,225.4±1,795.1 µg/day) (p=0.015). We found a significant inverse association between carotene intake and the risk of suicidal ideation after adjusting for potential confounders (odds ratio=0.934, 95% confidence interval=0.873-0.999). CONCLUSION: These results suggest that carotene intake may be inversely associated with the risk of suicidal ideation. Our findings may inform the development of new nutritional interventions to prevent increases in the risk of suicide worldwide.

Sleep/wake estimation using only anterior tibialis electromyography data.

BACKGROUND: In sleep efficiency monitoring system, actigraphy is the simplest and most commonly used device. However, low specificity to wakefulness of actigraphy was revealed in previous studies. In this study, we assumed that sleep/wake estimation using actigraphy and electromyography (EMG) signals would show different patterns. Furthermore, each EMG pattern in two states (sleep, wake during sleep) was analysed. Finally, we proposed two types of method for the estimation of sleep/wake patterns using only EMG signals from anterior tibialis muscles and the results were compared with PSG data. METHODS: Seven healthy subjects and five patients (2 obstructive sleep apnea, 3 periodic limb movement disorder) participated in this study. Night time polysomnography (PSG) recordings were conducted, and electrooculogram, EMG, electroencephalogram, electrocardiogram, and respiration data were collected. Time domain analysis and frequency domain analysis were applied to estimate the sleep/wake patterns. Each method was based on changes in amplitude or spectrum (total power) of anterior tibialis electromyography signals during the transition from the sleep state to the wake state. To obtain the results, leave-one-out-cross-validation technique was adopted. RESULTS: Total sleep time of the each group was about 8 hours. For healthy subjects, the mean epoch-by-epoch results between time domain analysis and PSG data were 99%, 71%, 80% and 0.64 (sensitivity, specificity, accuracy and kappa value), respectively. For frequency domain analysis, the corresponding values were 99%, 73%, 81% and 0.67, respectively. Absolute and relative differences between sleep efficiency index from PSG and our methods were 0.8 and 0.8% (for frequency domain analysis). In patients with sleep-related disorder, our proposed methods revealed the substantial agreement (kappa > 0.61) for OSA patients and moderate or fair agreement for PLMD patients. CONCLUSIONS: The results of our proposed methods were comparable to those of PSG. The time and frequency domain analyses showed the similar sleep/wake estimation performance.

Myeloid FoxO1 depletion attenuates hepatic inflammation and prevents nonalcoholic steatohepatitis.

Hepatic inflammation is culpable for the evolution of asymptomatic steatosis to nonalcoholic steatohepatitis (NASH). Hepatic inflammation results from abnormal macrophage activation. We found that FoxO1 links overnutrition to hepatic inflammation by regulating macrophage polarization and activation. FoxO1 was upregulated in hepatic macrophages, correlating with hepatic inflammation, steatosis, and fibrosis in mice and patients with NASH. Myeloid cell conditional FoxO1 knockout skewed macrophage polarization from proinflammatory M1 to the antiinflammatory M2 phenotype, accompanied by a reduction in macrophage infiltration in liver. These effects mitigated overnutrition-induced hepatic inflammation and insulin resistance, contributing to improved hepatic metabolism and increased energy expenditure in myeloid cell FoxO1-knockout mice on a high-fat diet. When fed a NASH-inducing diet, myeloid cell FoxO1-knockout mice were protected from developing NASH, culminating in a reduction in hepatic inflammation, steatosis, and fibrosis. Mechanistically, FoxO1 counteracts Stat6 to skew macrophage polarization from M2 toward the M1 signature to perpetuate hepatic inflammation in NASH. FoxO1 appears to be a pivotal mediator of macrophage activation in response to overnutrition and a therapeutic target for ameliorating hepatic inflammation to stem the disease progression from benign steatosis to NASH.