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.

Liver fibrosis arises from chronic hepatic injury and remains a major clinical challenge due to the lack of effective therapies.Although G-protein-coupled receptor 119 (GPR119) has been explored as a metabolic target in type 2 diabetes, its role in liver fibrogenesis is not well understood. In this study, the protein and mRNA expression of GPR119 were detected in mouse primary hepatic stellate cells (HSCs) using immunostaining and reverse transcriptase-polymerase chain reaction. The anti-fibrotic activities of GPR119 agonists were assessed in primary HSCs, LX-2 cells, and a carbon tetrachloride (CCl₄)–induced mouse model of liver fibrosis. Treatment with the GPR119 agonists MBX-2982 and GSK1292263 inhibited HSC activation, suppressed transforming growth factor-β1 (TGFβ1)–induced Smad2/3 phosphorylation, and reduced the expression of fibrogenic genes. In vivo, oral administration of MBX-2982 attenuated collagen accumulation and decreased hepatic α-smooth muscle actin and TGFβ expression in CCl₄-treated mice. Mechanistically, MBX-2982 activated AMP-activated protein kinase (AMPK), and pharmacological inhibition of AMPK reversed its anti-fibrogenic effects. MBX-2982 further reduced Smad3 acetylation by disrupting the interaction between Smad3 and p300 and promoting AMPK-dependent proteasomal degradation of p300. These results identify GPR119 as a regulator of HSC activation and highlight GPR119 agonists as promising therapeutic candidates for liver fibrosis.

Objectives: Allergic rhinitis (AR) is a chronic inflammation of the nasal mucosa triggered by environmental allergens. Although its pathophysiology has been extensively investigated, the influence of environmental aggravating factors—particularly combined pollutant exposure—remains insufficiently characterized. This study aimed to assess the impact of coexposure to PM2.5, formaldehyde, and Zn on allergic inflammation in a murine AR model and to delineate the associated immunological and histopathological responses. Methods: Female BALB/c mice were sensitized with ovalbumin (OVA) and challenged intranasally to induce AR. On days 21–24, the mice were exposed to PM2.5, formaldehyde, and Zn, either individually or in combination with OVA. Allergic symptoms were evaluated through behavioral observation, while immune responses were assessed by analyzing nasal and bronchoalveolar lavage fluids (NALF and BALF), serum immunoglobulin levels, nasal histopathology, and cytokine profiles. Results: Combined exposure to PM2.5, formaldehyde, and Zn significantly intensified allergic inflammation compared with single exposures. Coexposure to PM2.5 and Zn led to synergistic increases in total and OVA-specific immunoglobulin E levels, eosinophilic infiltration, nasal rubbing, sneezing, and Th2/Th17 cytokine levels in NALF and BALF. Histological analysis demonstrated epithelial thickening and goblet cell hyperplasia after combined exposure. Other combinations, including PM2.5 with formaldehyde, also produced additive or modestly amplified inflammatory responses. Conclusions Coexposure to PM2.5, formaldehyde, and Zn aggravated allergic inflammation in an OVA-induced murine model, with PM2.5+Zn yielding the strongest synergistic effects. These findings emphasize the role of pollutant–pollutant interactions in allergic airway diseases and highlight the need for further research to clarify long-term health effects and relevance to human disease.

Purpose: The Korean Oral Biobank Network (KOBN) collects, stores, and provides oral samples for research. Quality control (QC) of biospecimens is necessary to ensure that they meet the basic prerequisites before being sent to researchers. This study presents the standard operating procedures (SOPs) for the QC of biospecimens. Methods: QC methods using molecular genetic techniques according to sample types, including teeth, blood, oral soft tissue, oral tissue-derived cells, saliva, mouth rinse solution, dental plaque, and gingival crevicular fluid, are described in detail. Results: The KOBN established SOP for oral biospecimen QC and assessment methods. Conclusions To ensure a stable supply of high-quality biospecimens for researchers, regular QC checks should be carried out according to the SOP following the specifications of the Korea Biobank Network under the Korea Disease Control and Prevention Agency.

Dental clinicians and researchers have recently recommended oral microbial examinations to more accurately diagnose and treat oral diseases, including periodontitis and dental caries. Theoretical and experimental evidence suggests that oral microbiota may also be associated with non-oral diseases, such as gastrointestinal and extra-gastrointestinal diseases. This review highlights studies demonstrating microbial alterations in the oral cavity associated with malignant tumors including gastric, colorectal, esophageal, and lung cancers, implying that these alterations may serve as early indicators for non-invasive diagnosis and risk assessment of cancer development. Furthermore, we addressed the implications of oral microbial co-occurrence with malignant tumors, such as Streptococcus anginosus, Fusobacterium nucleatum, and Veillonella parvula, which are recognized as tumor-enriched oral pathogens involved in the development and progression of cancers in the stomach, colon, and lungs, respectively. Notably, we explored the immune and inflammatory mechanisms underlying reciprocal interactions between oral microbiota and tumors, underscoring that targeting these mechanistic pathways can contribute to preventing cancer development.

Dental clinicians and researchers have recently recommended oral microbial examinations to more accurately diagnose and treat oral diseases, including periodontitis and dental caries. Theoretical and experimental evidence suggests that oral microbiota may also be associated with non-oral diseases, such as gastrointestinal and extra-gastrointestinal diseases. This review highlights studies demonstrating microbial alterations in the oral cavity associated with malignant tumors including gastric, colorectal, esophageal, and lung cancers, implying that these alterations may serve as early indicators for non-invasive diagnosis and risk assessment of cancer development. Furthermore, we addressed the implications of oral microbial co-occurrence with malignant tumors, such as Streptococcus anginosus, Fusobacterium nucleatum, and Veillonella parvula, which are recognized as tumor-enriched oral pathogens involved in the development and progression of cancers in the stomach, colon, and lungs, respectively. Notably, we explored the immune and inflammatory mechanisms underlying reciprocal interactions between oral microbiota and tumors, underscoring that targeting these mechanistic pathways can contribute to preventing cancer development.

Background: Single room isolation with contact precautions is widely regarded as a fundamental strategy to prevent the transmission of multidrug-resistant organisms (MDROs). However, its implementation demands substantial resources, limiting its universal application to all MDROs. In this study, we assessed the effect of discontinuing single room isolation for vancomycin-resistant Enterococcus (VRE). Methods: This is a retrospective, observational study conducted at a single 750-bed tertiary center. We conducted an interrupted time series analysis to compare incidence rates and trends of new-onset VRE colonization and bacteremia during the one year before and after the strategy change on January 1, 2023. Results: Single-room occupancy decreased from 79.7% pre-intervention to 23.6% postintervention (P < 0.001). The incidence rate of new-onset VRE colonization was 0.452 and 0.535 per 1,000 patient-days in the pre- and post-intervention periods, respectively, with no statistically significant difference (P = 0.202). However, there was a slightly increasing trend (0.036 [95% confidence interval, −0.002, 0.074] increase per month, P = 0.066). The new-onset VRE bacteremia incidence rate was not differed in incidence (0.060 and 0.055, P= 0.571) or trend (P = 0.720). Conclusion Our study suggests that discontinuing single-room isolation for VRE patients may not affect the incidence of new-onset VRE bacteremia, but caution is needed due to the potential increase in colonization.