Objectives: This study investigated the association between exacerbated economic hardship during the coronavirus disease 2019 (COVID-19) pandemic and changes in the health behaviors of Korean adolescents. Methods: We analyzed data from the 2021 Korea Youth Risk Behavior Survey and included 44 908 students (22 823 boys and 22 085 girls) as study subjects. The dependent variables included changes in health behaviors (breakfast habits, physical activity, and alcohol use) that occurred during the COVID-19 pandemic. The aggravation of economic hardship by COVID-19 and the subjective economic status of the family were used as exposure variables. Multiple logistic regression analysis was utilized to calculate the prevalence odds ratios (PORs). Results: Severe exacerbation of a family’s economic hardship due to COVID-19 was negatively associated with the health behaviors of adolescents, including increased breakfast skipping (POR, 1.85; 95% confidence interval [CI], 1.55 to 2.21 for boys and POR, 1.56; 95% CI, 1.27 to 1.92 for girls) and decreased physical activity (POR, 1.37; 95% CI, 1.19 to 1.57 for boys and POR, 1.38; 95% CI, 1.19 to 1.60 for girls). These negative changes in health behaviors were further amplified when combined with a low subjective family economic status. Conclusions The experience of worsening household hardship can lead to negative changes in health behavior among adolescents. It is crucial to implement measures that address the economic challenges that arise from stressful events such as COVID-19 and to strive to improve the lifestyles of adolescents under such circumstances.

PURPOSE: Caffeine is the most widely consumed psychostimulant of the methylxanthine class. Among adolescents, high-dose of caffeine consumption has increased rapidly over the last few decades due to the introduction of energy drinks. However, little is known about the time-dependent effect of high doses of caffeine consumption in adolescents. The present study aims to examine the short- and long-term influence of high-dose caffeine on behavior of adolescence. METHODS: The animals were divided into three groups: a “vehicle” group, which was injected with 1 ml of phosphate-buffered saline for 14 days; a “Day 1” group, which was injected with caffeine (30 mg/kg), 2 h before the behavioral tests; and a “Day 14” group, which was infused with caffeine for 14 days. An open-field test, a Y-maze test, and a passive avoidance test were conducted to assess the rats'activity levels, anxiety, and cognitive function. RESULTS: High-dose caffeine had similar effects in short-and long-term treatment groups. It increased the level of locomotor activity and anxiety-like behavior, as evidenced by the increase in the number of movements and incidences of rearing and grooming in the caffeine-treated groups. No significant differences were observed between the groups in the Y-maze test. However, in the passive avoidance test, the escape latency in the caffeine-treated group was decreased significantly, indicating impaired memory acquisition. CONCLUSION: These results indicate that high-dose caffeine in adolescents may increase locomotor activity and anxiety-like behavior and impair learning and memory, irrespective of the duration of administration. The findings will be valuable for both evidence-based education and clinical practice.
Adolescent ; Animals ; Anxiety ; Behavior Rating Scale ; Caffeine ; Cognition ; Education ; Energy Drinks ; Grooming ; Humans ; Incidence ; Learning ; Locomotion ; Memory ; Models, Animal ; Motor Activity ; United Nations

Phosphorylation levels of glycogen synthase kinase 3β (GSK3β) negatively correlated with psychomotor stimulant-induced locomotor activity. Locomotor sensitization induced by psychomotor stimulants was previously shown to selectively accompany the decrease of GSK3β phosphorylation in the nucleus accumbens (NAcc) core, suggesting that intact GSK3β activity in this region is necessary for psychomotor stimulants to produce locomotor sensitization. Similarly, GSK3β in the NAcc was also implicated in mediating the conditioned effects formed by the associations of psychomotor stimulants. However, it remains undetermined whether GSK3β plays a differential role in the two sub-regions (core and shell) of the NAcc in the expression of drug-conditioned behaviors. In the present study, we found that GSK3β phosphorylation was significantly lower in the NAcc shell obtained from rats expressing amphetamine (AMPH)-induced conditioned locomotor activity. Further, we demonstrated that these effects were normalized by treatment with lithium chloride, a GSK3β inhibitor. These results suggest that the behavior produced by AMPH itself and a conditioned behavior formed by associations with AMPH are differentially mediated by the two sub-regions of the NAcc.

Cancer metabolism is considered as one of major cancer hallmarks. It is important to understand cancer-specific metabolic changes and its impact on cancer biology to identify therapeutic potentials. Among cancer-specific metabolic changes, a role of serine metabolism has been discovered in various cancer types. Upregulation of serine synthesis pathway (SSP) supports cell proliferation and metastasis. The change of serine metabolism is, in part, mediated by epigenetic modifiers, such as Euchromatic histone-lysine N-methyltransferase 2 and Lysine Demethylase 4C. On the other hand, SSP also influences epigenetic landscape such as methylation status of nucleic acids and histone proteins via affecting S-adenosyl methionine production. In the review, we highlight recent evidences on interactions between SSP and epigenetic regulation in cancer. It may provide an insight on roles and regulation of SSP in cancer metabolism and the potential of serine metabolism for cancer therapy.
Biology ; Cell Proliferation ; Epigenomics* ; Hand ; Histone-Lysine N-Methyltransferase ; Histones ; Lysine ; Metabolism* ; Methionine ; Methylation ; Neoplasm Metastasis ; Nucleic Acids ; Serine* ; Up-Regulation

AMP-activated protein kinase (AMPK) activators have garnered significant attention for their potential to prevent the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) into liver fibrosis and to fundamentally improve liver function. The broad spectrum of pathways regulated by AMPK activators makes them promising alternatives to conventional liver replacement therapies and the limited pharmacological treatments currently available. In this study, we aim to illustrate the newly detailed multiple mechanisms of MASLD progression based on the multiple-hit hypothesis. This model posits that impaired lipid metabolism, combined with insulin resistance and metabolic imbalance, initiates inflammatory cascades, gut dysbiosis, and the accumulation of toxic metabolites, ultimately promoting fibrosis and accelerating MASLD progression to irreversible hepatocellular carcinoma (HCC). AMPK plays a multifaceted protective role against these pathological conditions by regulating several key downstream signaling pathways. It regulates biological effectors critical to metabolic and inflammatory responses, such as SIRT1, Nrf2, mTOR, and TGF-β, through complex and interrelated mechanisms. Due to these intricate connections, AMPK’s role is pivotal in managing metabolic and inflammatory disorders. In this review, we demonstrate the specific roles of AMPK and its related pathways. Several agents directly activate AMPK by binding as agonists, while some others indirectly activate AMPK by modulating upstream molecules, including adiponectin, LKB1, and the AMP: ATP ratio. As AMPK activators can target each stage of MASLD progression, the development of AMPK activators offers immense potential to expand therapeutic strategies for liver diseases such as MASH, MASLD, and liver fibrosis.

AMP-activated protein kinase (AMPK) activators have garnered significant attention for their potential to prevent the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) into liver fibrosis and to fundamentally improve liver function. The broad spectrum of pathways regulated by AMPK activators makes them promising alternatives to conventional liver replacement therapies and the limited pharmacological treatments currently available. In this study, we aim to illustrate the newly detailed multiple mechanisms of MASLD progression based on the multiple-hit hypothesis. This model posits that impaired lipid metabolism, combined with insulin resistance and metabolic imbalance, initiates inflammatory cascades, gut dysbiosis, and the accumulation of toxic metabolites, ultimately promoting fibrosis and accelerating MASLD progression to irreversible hepatocellular carcinoma (HCC). AMPK plays a multifaceted protective role against these pathological conditions by regulating several key downstream signaling pathways. It regulates biological effectors critical to metabolic and inflammatory responses, such as SIRT1, Nrf2, mTOR, and TGF-β, through complex and interrelated mechanisms. Due to these intricate connections, AMPK’s role is pivotal in managing metabolic and inflammatory disorders. In this review, we demonstrate the specific roles of AMPK and its related pathways. Several agents directly activate AMPK by binding as agonists, while some others indirectly activate AMPK by modulating upstream molecules, including adiponectin, LKB1, and the AMP: ATP ratio. As AMPK activators can target each stage of MASLD progression, the development of AMPK activators offers immense potential to expand therapeutic strategies for liver diseases such as MASH, MASLD, and liver fibrosis.

AMP-activated protein kinase (AMPK) activators have garnered significant attention for their potential to prevent the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) into liver fibrosis and to fundamentally improve liver function. The broad spectrum of pathways regulated by AMPK activators makes them promising alternatives to conventional liver replacement therapies and the limited pharmacological treatments currently available. In this study, we aim to illustrate the newly detailed multiple mechanisms of MASLD progression based on the multiple-hit hypothesis. This model posits that impaired lipid metabolism, combined with insulin resistance and metabolic imbalance, initiates inflammatory cascades, gut dysbiosis, and the accumulation of toxic metabolites, ultimately promoting fibrosis and accelerating MASLD progression to irreversible hepatocellular carcinoma (HCC). AMPK plays a multifaceted protective role against these pathological conditions by regulating several key downstream signaling pathways. It regulates biological effectors critical to metabolic and inflammatory responses, such as SIRT1, Nrf2, mTOR, and TGF-β, through complex and interrelated mechanisms. Due to these intricate connections, AMPK’s role is pivotal in managing metabolic and inflammatory disorders. In this review, we demonstrate the specific roles of AMPK and its related pathways. Several agents directly activate AMPK by binding as agonists, while some others indirectly activate AMPK by modulating upstream molecules, including adiponectin, LKB1, and the AMP: ATP ratio. As AMPK activators can target each stage of MASLD progression, the development of AMPK activators offers immense potential to expand therapeutic strategies for liver diseases such as MASH, MASLD, and liver fibrosis.

Traditionally, Centella asiatica leaf extracts are used to treat neurodegenerative diseases in India. Centella asiatica is reportedly used to enhance memory and treat dementia, but its promoting effect on neural stem cell differentiation has not been studied yet. In the present study, we investigated whether or not Centella asiatica leaf extracts act on neuronal precursor cells and neuronal cell lines to induce neuronal differentiation, neurite outgrowth, and neuroprotection. The neurogenesis-promoting potential of Centella asiatica leaf extracts was determined by differentiation assay on neural stem cells isolated from mouse embryos and PC12 cell lines. To understand the contribution of specific neural cell types towards increase after Centella asiatica treatment, neural stem cells were differentiated into various neural subtypes and checked by Western blotting using neural cell lineage-specific antibody markers. Neuroprotective activity of Centella asiatica was analyzed in PC12 cells exposed to 100 microM of H2O2. Cell growth was analyzed by MTT assay while cell death was analyzed by Western blotting detection of apoptosis-related proteins. Cells treated with Centella asiatica had significantly longer primary and secondary neurites as well as a higher number of neurites per cell compared to control cells. Expression levels of TUBBIII, TH, NF, and BDNF increased upon Centella asiatica treatment, suggesting that Centella asiatica has a neurogenesis-promoting effect. Centella asiatica also inhibited oxidative stress-induced neural cell damage through regulation of apoptosis- and cell cycle-related proteins. Thus, leaf extracts of Centella asiatica might promote neurogenesis, neuroregeneration, and neuroprotection in the context of neurodegenerative diseases.
Animals ; Blotting, Western ; Brain-Derived Neurotrophic Factor ; Cell Death ; Cell Line ; Centella* ; Dementia ; Embryonic Structures ; India ; Memory ; Mice ; Neural Stem Cells ; Neurites ; Neurodegenerative Diseases ; Neurogenesis* ; Neurons* ; Neuroprotective Agents ; PC12 Cells

Although the corresponding author of article is Mi Ra Kim, the name and e-mail address of the first author, Hye-kyung Shim were incorrectly given instead.

BACKGROUND: Researchers have shown that eosinophil peroxidase (EPO) is a relatively accurate marker of eosinophilia and eosinophil activity. However, its use as a marker of eosinophilic inflammation in nasal secretions is limited because the diagnostic cutoff values of EPO for use as a one-time test for allergic diseases such as allergic rhinitis have not been established. PURPOSE: To identify the correlation between nasal eosinophil count and EPO in children and adolescents with rhinitis. METHODS: We recruited patients <18 years of age with rhinitis for more than 2 weeks or more than 2 episodes a year whose nasal eosinophil and EPO were measured at a single allergy clinic. The eosinophil percentage was calculated by dividing the eosinophil count by the number of total cells under light microscopy at ×1,000 magnification. EPO and protein were measured from nasal secretions. We retrospectively analyzed the correlation between nasal eosinophils and protein-corrected EPO (EPO/protein) value. RESULTS: Of the 67 patients enrolled, 41 were male (61.2%); the mean age was 8.2±4.0 years. The median nasal eosinophil count was 1 and percentage was 1%. The median protein-corrected EPO value was 12.5 ng/μg (range, 0–31 ng/μg). There was a statistically significant correlation between eosinophil count and percentage (P<0.001). However, the eosinophil percentage and EPO did not correlate. The eosinophil count and EPO had a statistically significant correlation (P =0.01). The EPO cutoff value examined for nasal eosinophil counts of 2, 5, 10, and 20 was 17.57 ng/μg regardless of the reference count. The largest area under the curve value was obtained when the receiver operating characteristic curve was drawn using the eosinophil count of 2. CONCLUSION: Nasal eosinophil count was significantly associated with protein-corrected EPO.
Adolescent ; Child ; Eosinophil Peroxidase ; Eosinophilia ; Eosinophils ; Humans ; Hypersensitivity ; Inflammation ; Male ; Microscopy ; Retrospective Studies ; Rhinitis ; Rhinitis, Allergic ; ROC Curve