BACKGROUND/OBJECTIVES: Obesity is a complex metabolic disorder characterized by excessive adipose tissue accumulation, dysregulated lipid metabolism, and insulin resistance, leading to an increased risk of metabolic disease. While Withania somnifera (AS) and Chrysanthemum zawadskii Herbich var. latilobum (Maxim.) Kitamura (C) have traditionally been used for their metabolic regulatory properties, their combined effects on adipogenesis, lipogenesis, lipolysis, and insulin signaling remain unexplored. Therefore, this study aimed to evaluate the anti-obesity effects of AS, C, and their optimal combination (ASC) in 3T3-L1 adipocytes by investigating their impact on lipid metabolism and glucose homeostasis.MATERIALS/METHODS: Following adipogenic differentiation, 3T3-L1 adipocytes were treated with AS, C, and ASC at different concentrations. RESULTS: AS, C, and ASC significantly inhibited adipogenesis by downregulating cyclic adenosine monophosphate (cAMP) response element-binding protein, peroxisome proliferator-activated receptor gamma, CCAAT/enhancer-binding proteins alpha and beta phosphorylation, thereby reducing lipid accumulation in adipocytes. They also suppressed lipogenesis by downregulating the expression of dephosphorylated acetyl-CoA carboxylase, fatty acid synthase, and lipoprotein lipase. In contrast, they markedly enhanced lipolysis, as evidenced by increased hormone-sensitive lipase and protein kinase A expression, along with elevated glycerol release and cAMP levels. Furthermore, AS, C, and ASC activated energy metabolism pathways, as indicated by the upregulation of AMP-activated protein kinase, uncoupling protein 1, and carnitine palmitoyltransferase 1A, suggesting a transition toward enhanced mitochondrial fatty acid oxidation. Notably, AS, C, and ASC significantly improved insulin signaling by restoring insulin receptor substrate 1, phosphoinositide 3-kinase, and Akt phosphorylation, while upregulating glucose transporter type 4 expression, indicating enhanced glucose uptake. Among all treatments, ASC showed relatively greater efficacy compared to AS or C alone, suggesting a potential additive effect. CONCLUSION These findings demonstrate that ASC effectively modulates multiple metabolic pathways in adipocytes, including adipogenesis, lipogenesis, lipolysis, energy metabolism, and insulin signaling, to exert its anti-obesity effects.

Obesity is a major global health issue and a leading contributor to cardiovascular disease (CVD). While traditional research has emphasized diet and physical inactivity, psychological factors, particularly emotional eating, are increasingly recognized as important contributors to metabolic and cardiovascular health. Emotional eating, defined as eating in response to negative emotions, represents a maladaptive coping mechanism that promotes excessive caloric intake, visceral fat accumulation, and metabolic dysregulation. Chronic stress activates the hypothalamic-pituitary-adrenal axis, leading to increased cortisol secretion and appetite, while recurrent emotional eating behaviors reinforce this biological pathway and contribute to insulin resistance, dyslipidemia, hypertension, and systemic inflammation. Together, these mechanisms link psychological stress to cardiometabolic dysfunction and ultimately to increased CVD risk. Although direct evidence linking emotional eating to clinical CVD outcomes remains limited, accumulating evidence supports its role as a behavioral mediator connecting psychological stress, metabolic abnormalities, and cardiovascular risk. Effective management of emotional eating requires an integrated approach that combines cognitive behavioral therapy, mindfulness-based strategies, stress management, healthy lifestyle modification, and pharmacological treatment for obesity when indicated. Recognizing emotional eating as a modifiable behavioral risk factor may open new opportunities for early prevention and holistic management of CVD.

Major depressive disorder (MDD) is a psychiatric disorder that leads to reduced quality of life and poses a significant societal burden; however, its diagnosis still relies on subjective evaluation. Consequently, task-based functional magnetic resonance imaging (fMRI) has emerged as a crucial tool for exploring the neurobiological mechanisms of MDD and identifying objective biomarkers. This review systematically examines fMRI studies on cognitive dysfunction in patients with MDD, summarizing the representative tasks and associated functional abnormalities in neural circuits across three core domains: executive function, negative bias, and reward processing. Deficits in executive function manifest as inefficiency in the fronto-parietal network and failure to suppress the default mode network during n-back and Stroop tasks. Negative bias was identified through the Self-Referent Encoding Task and Autobiographical Memory Test, revealing hyperactivity in bottom-up emotional responses and failure of top-down regulation. In the domain of reward processing, studies using Monetary Incentive Delay and reinforcement learning tasks have consistently reported that blunted reward prediction error signals and hypoactivation of the thalamo-striatal-prefrontal circuitry are associated with anhedonia. By integrating these findings from task-based fMRI research, this review aimed to define the neurocognitive characteristics that distinguish MDD and provide practical guidance for future studies.

Purpose: This study aimed to explore the fear of cancer recurrence and unmet needs in triple negative breast cancer survivors. Methods: A cross-sectional descriptive design was used for this study. Data were collected from 331 triple negative breast cancer survivors using Fear of Cancer Recurrence Inventory (FCRI) and the Comprehensive Needs Assessment Tool in cancer (CNAT). In addition, descriptive statistics, a t-test, and one-way ANOVA were used for analysis. Results: Among triple-negative breast cancer survivors, 92.7% experienced fear of cancer recurrence, and 59.2% reported a severe fear of recurrence. The severity of fear of cancer recurrence differed significantly according to monthly household income (t=2.25, p=.025), cancer stage (F=4.26, p=.006), and recurrence history (t=-3.79, p<.001). Unmet needs were notably high, particularly in information and psychological problems. Furthermore, there were differences in unmet needs depending on the severity level of fear of cancer recurrence. Conclusion Most triple-negative breast cancer survivors experience fear of cancer recurrence, but management was found to be inadequate. Therefore, nursing interventions are needed to alleviate this fear. Additionally, unmet needs vary depending on the severity of the fear of cancer recurrence. It will be necessary to assess the fear of cancer recurrence among triple-negative breast cancer survivors and manage unmet needs according to its severity.

Three indole derivatives (1–3) and a diketopiperazine (4) were isolated from the ethyl acetate extract of Chromobacterium violaceum. Their structures were elucidated based on the analysis of NMR and HR-MS data and by comparing those in the previous literature. The antibacterial activities of the isolated compounds were evaluated against Gram-positive bacteria, including human pathogenic methicillin-resistant Staphylococcus aureus (MRSA), Lacticaseibacillus paracasei subsp. paracasei, and Brevibacterium epidermidis. Compound 1 exhibited moderate antibacterial activity against all the three strains with MIC values ranging from 8.58 to 34.3 μg/mL.

BACKGROUND/OBJECTIVES: UV radiation is a major factor contributing to DNA damage in skin cells, including stem cells and mesenchymal stem cells, leading to the depletion of these crucial cells. This study examined whether a mixture of Indian gooseberry and barley sprout (IB) could inhibit UVB irradiation and 3-isobutyl-1-methylxanthine (IBMX)-induced photoaging and oxidative stress in the skin using HaCaT, Hs27, and B16F10 cells.MATERIALS/METHODS: The moisturizing-related factors, the collagen synthesis-related c-Jun N-terminal kinase (JNK)/c-Fos/c-Jun/matrix metalloproteinases (MMPs) pathway, and the melanogenesis-related cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/cAMP-responsive binding protein (CREB)/melanocyte inducing transcription factor (MITF)/tyrosinase-related protein (TRP)/tyrosinase activation pathways were analyzed in vitro by an enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blot analysis. RESULTS: The IB complex increased the hyaluronic acid and sphingomyelin levels and the collagenase inhibitory activity, enhanced hydration-related factors, including collagen, hyaluronic acid synthase (HAS), elastin, long chain base subunit 1 (LCB1) (serine palmitoyltransferase; SPT), and delta 4-desaturase sphingolipid 1 (DEGS1), modulated the inflammatory cytokines levels, antioxidant enzyme activities and the NF-κB/MMPs/cyclooxygenase-2 (COX-2) pathway in UVB-irradiated HaCaT cells, and inhibited wrinkle formation by down-regulation of the JNK/c-Fos/c-Jun/MMP pathway and up-regulation of the transforming growth factor-β receptor I (TGFβR1)/small mothers against decapentaplegic homolog (Smad3)/procollagen type I pathway in UVB-irradiated Hs27 cells. Moreover, the IB complex prevented melanin production by down-regulating the PKA/CREB/MITF/TRP-1/TRP-2 pathway in IBMX-induced B16F10 cells. CONCLUSION These findings suggest that the IB complex has the potential to serve as a safeguard, shielding the skin from UVB radiation-induced photo-damage.

Tramadol is an opioid analog used to treat chronic and acute pain. Intradermal injections of tramadol at hundreds of millimoles have been shown to produce a local anesthetic effect. We used the whole-cell patch-clamp technique in this study to investigate whether tramadol blocks the sodium current in HEK293 cells, which stably express the pain threshold sodium channel Na v1.7 or the cardiac sodium channel Na v1.5. The half-maximal inhibitory concentration of tramadol was 0.73 mM for Na v1.7 and 0.43 mM for Na v1.5 at a holding potential of –100 mV. The blocking effects of tramadol were completely reversible. Tramadol shifted the steady-state inactivation curves of Na v1.7 and Na v1.5 toward hyperpolarization. Tramadol also slowed the recovery rate from the inactivation of Na v1.7 and Na v1.5 and induced stronger use-dependent inhibition. Because the mean plasma concentration of tramadol upon oral administration is lower than its mean blocking concentration of sodium channels in this study, it is unlikely that tramadol in plasma will have an analgesic effect by blocking Na v1.7 or show cardiotoxicity by blocking Na v1.5. However, tramadol could act as a local anesthetic when used at a concentration of several hundred millimoles by intradermal injection and as an antiarrhythmic when injected intravenously at a similar dose, as does lidocaine.

Background: There are inconsistent reports regarding the association between general anesthesia and adverse neurodevelopmental and behavioral disorders in children. Methods: This nationwide administrative cohort study included children born in Korea between 2008 and 2009, and followed until December 31, 2017. The cohort included 93,717 participants who received general anesthesia with endotracheal intubation (ETI) who were matched to unexposed subjects in a 1:1 ratio. General anesthesia was defined by National Health Insurance Service treatment codes with intratracheal anesthesia, and the index date was the first event of general anesthesia. The primary outcome was attention deficit hyperactive disorder (ADHD), which was defined as at least a principal diagnosis of 10th revision of the International Classification of Diseases code F90.X after the age of 72 months.Neurodevelopment, which was assessed using a developmental screening test (Korean-Ages and Stages Questionnaire [K-ASQ]), was a secondary outcome. The K-ASQ is performed annually from 1 to 6 years of age and consists of 5 domains. The association between general anesthesia and ADHD was estimated using a Cox hazard model, and its association with neurodevelopment was estimated using a generalized estimation equation, with control for multiple risk factors beyond 1 year after the index date. Results: The median age at the index date was 3.8 (95% confidence interval [CI], 1.7–5.8) years, and there were 57,625 (61.5%) men. During a mean follow-up period of 5 years, the incidence rate of ADHD was 42.6 and 27.7 per 10,000 person-years (PY) in the exposed and unexposed groups, respectively (absolute rate difference 14.9 [95% CI, 12.5–17.3] per 10,000 PY). Compared to the unexposed group, the exposed group had an increased risk of ADHD (adjusted hazard ratio, 1.41 [95% CI, 1.30–1.52]). In addition, a longer duration of anesthesia with ETI and more general anesthesia procedures with ETI were associated with greater risk of ADHD. General anesthesia with ETI was also associated with poorer results in the K-ASQ. Conclusion Administration of general anesthesia with ETI to children is associated with an increased risk of ADHD and poor results in a neurodevelopmental screening test.

Objective: Bone morphogenetic protein receptor type 2 (BMPR2) has been associated with radiographic changes in ankylosing spondylitis (AS), but further characterization of the cellular signaling pathway in osteoprogenitor (OP) is not clearly understood.The aim of this study was to investigate the expression of BMPR2 and bone morphogenetic protein 2 (BMP2)-mediated responsibility in AS. Methods: We collected 10 healthy control (HC) and 14 AS-OPs derived from facet joints. Subsequently, we then conducted RNA sequencing with two samples per group and selected BMP-related genes. Facet joint tissues and derived primary OPs were evaluated by validation of selected RNA sequencing data, immunohistochemistry, and comparison of osteogenic differentiation potential. Results: Based on RNA-sequencing analysis, we found that BMPR2 expression is higher in AS-OPs compared to in HC-OPs. We also validated the increased BMPR2 expression in facet joint tissues with AS and its derived OPs in messenger RNA and protein levels. Additionally, primary AS-OPs showed much greater response to osteogenic differentiation induced by BMP2 and a higher capacity for smad1/5/8-induced RUNX2 expression compared to HCs. Conclusion The expression of BMPR2 was found to be significantly increased in facet joint tissues of patients with AS. These findings suggest that BMPR2 may play a role in the BMP2-mediated progression of AS.

Purpose: We developed a comprehensive return to work (RTW) intervention covering physical, psycho-social and practical issues for patients newly diagnosed and evaluated its efficacy in terms of RTW. Materials and Methods: A multi-center randomized controlled trial was done to evaluate the efficacy of the intervention conducted at two university-based cancer centers in Korea. The intervention program comprised educational material at diagnosis, a face-to-face educational session at completion of active treatment, and three individualized telephone counseling sessions. The control group received other education at enrollment. Results: At 1-month post-intervention (T2), the intervention group was more likely to be working compared to the control group after controlling working status at diagnosis (65.4% vs. 55.9%, p=0.037). Among patients who did not work at baseline, the intervention group was 1.99-times more likely to be working at T2. The mean of knowledge score was higher in the intervention group compared to the control group (7.4 vs. 6.8, p=0.029). At the 1-year follow-up, the intervention group was 65% (95% confidence interval, 0.78 to 3.48) more likely to have higher odds for having work. Conclusion The intervention improved work-related knowledge and was effective in facilitating cancer patients’ RTW.