Objectives: In alignment with the World Health Organization’s goal of eliminating hepatitis C, this study assessed the current treatment status and reasons for non-treatment among patients with hepatitis C in Jeonbuk State, Republic of Korea, to inform strategies for improving care engagement. Methods: Among 311 individuals diagnosed with hepatitis C and reported through the NationalNotifiable Infectious Disease Surveillance system between January 2023 and June 2024, 208 patients were surveyed after excluding those who had died or could not be contacted.Statistical analyses included the chi-square test, the Cochran-Armitage test for trend, and logistic regression. Results: Overall, 116 participants (55.8%) reported having received antiviral therapy. Among the 92 untreated individuals, the most common reason for non-treatment was the absence of symptoms (n = 23; 25.0%), followed by the burden of drug costs (n = 21; 22.8%). Conclusion These findings highlight suboptimal treatment uptake and key barriers that may hinder progress toward hepatitis C elimination. Expanding screening and strengthening linkage-to-care strategies, while addressing financial barriers, will be essential to achievingnational elimination targets.

Purpose: The chromodomain helicase DNA-binding (CHD) protein family comprises adenosine triphosphate-dependent chromatin remodelers that regulate chromatin structure and gene expression. Pathogenic CHD2 variants are associated with neurodevelopmental phenotypes, but these genotype–phenotype correlations remain unclear. This study aimed to delineate the clinical and genetic features of patients with CHD2-related disorders and to explore the associated genotype–phenotype relationships. Methods: Among 22 patients with pathogenic or likely pathogenic CHD2 variants identified using a customized 172-gene neurodevelopmental and epilepsy panel, 19 with sufficient clinical data were included. Demographic, clinical, neuroimaging, electroencephalographic, and genetic data were retrospectively reviewed. Results: Eighteen pathogenic or likely pathogenic variants were identified, including eight novel variants: nine nonsense (50.0%), five splice-site (27.8%), two missense (11.1%), and two exon deletions (11.1%). All patients had epilepsy, with a median age of seizure onset of 2.33 years. Comorbidities included global developmental delay (89.5%), intellectual disability (82.0%), and neuropsychiatric symptoms (47.4%). Seizure types were heterogeneous, with a predominance of generalized-onset seizures, and 13 patients (68.4%) achieved seizure freedom. Marked phenotypic variability was observed: two unrelated patients with the same truncating variant had different developmental and seizure-related profiles, a symptomatic child with an inherited exon 5 deletion contrasted with her asymptomatic father, and a patient with an exon 17–29 deletion exhibited relatively mild features. Conclusion Epilepsy was a consistent manifestation in this study and was accompanied by diverse developmental and neurobehavioral features, with substantial genotype–phenotype discordance. Further research on genotype–phenotype correlation is warranted.

Background/Aims: Spinal cord injury (SCI) frequently impairs defecation, severely affecting the quality of life. This study examines compensatory neural remodeling after SCI, focusing on basal colonic contractility, neural responses to electrical field stimulation, and alterations in excitatory cholinergic and inhibitory nitrergic pathways. Methods: Female Sprague–Dawley rats underwent either sham surgery or T10 spinal cord transection and were categorized into 3 groups: sham, 1-week post-SCI (acute), and 4-week post-SCI (chronic). Colonic contractility was assessed in an organ bath using electrical field stimulation in the presence of a nitric oxide synthase inhibitor. Neural protein expression was analyzed by immunofluorescence and Western blotting. Results: SCI produced region- and time-dependent impairments in colonic contractility, with distinct alterations in the proximal circular and longitudinal muscles across acute and chronic phases. Neural excitability shifted dynamically, showing enhanced excitatory activity in the proximal longitudinal muscle at 1-week and the distal circular muscle at 4-week post-SCI. Protein analysis revealed increased neuronal nitric oxide synthase in the proximal colon, decreasedsoluble guanylyl cyclase in the distal colon, upregulated muscarinic M3 receptor in the proximal colon, and reduced vaso-active intestinal peptide receptor 1 in both proximal and distal regions. Conclusion SCI induces spatiotemporal remodeling of excitatory and inhibitory neural pathways, contributing to colonic dysmotility and revealing potential targets for therapeutic intervention.

Objective: To evaluate the diagnostic performance of the “probable hepatocellular carcinoma (HCC)” category in the Korean Liver Cancer Association-National Cancer Center (KLCA-NCC) v2022 guidelines. Materials and Methods: This multicenter retrospective study included patients at risk of HCC who underwent gadoxetic acid-enhanced MRI between January 2015 and June 2018; a subgroup of these patients also underwent liver CT. Eligible patients had at least one non-cystic lesion (≥10 mm) with a reference standard. Four radiologists interpreted the images independently and the results were pooled. The performance of “definite HCC” and “probable HCC” together and “probable HCC” alone were compared between v2018 and v2022. Results: A total of 2,237 patients (1,666 men; mean age, 59 ± 11 years) with 2,445 lesions were included. In v2022, 1.5% (143/9,780) of the lesions were additionally categorized as “probable HCC” by four reviewers on MRI; among these, 104 lesions were not HCCs. Focal nodular hyperplasia (FNH) or FNH-like nodules constituted 90.4% (94/104) of the false positives. When “definite HCC” and “probable HCC” were combined, v2022 showed higher sensitivity (83.7% [5,670/6,776] vs. 83.1% [5,631/6,776]) but lower specificity (77.1% [2,316/3,004] vs. 80.6% [2,420/3,004]) than v2018 (P < 0.001). For “probable HCC” alone, v2022 showed a lower positive predictive value (PPV) than v2018 (64.1% [373/582] vs. 76.1% [334/439], P < 0.001). In v2022, lesions with non-rim arterial-phase hyperenhancement (APHE) showed a lower PPV than those without APHE (42.3% [91/215] vs. 76.8% [282/367], P < 0.001). In the CT subgroup (n = 1,590), 1.6% (99/6,360) of the lesions were reassessed as “probable HCC,” and its PPV was 83.8% (83/99) in v2022 whereas no lesions were classified as “probable HCC” under v2018. Conclusion The revised “probable HCC” category in the KLCA-NCC v2022 aligns with updates in the diagnostic flow, demonstrating acceptable performance on MRI and CT. Notably, FNH or FNH-like nodules can be misclassified as “probable HCC” when MRI is used.

Punica granatum L. has been widely used in traditional medicine and is known to contain bioactiveellagitannins with potential antidiabetic properties. The primary objective of this study was to develop and validate a reliable HPLC-DAD method for the quantitative analysis of major compounds isolated from stems and pericarpium of P. granatum, namely pedunculagin (1), flavogallonic acid (2), casuarinin (3), isocorilagin (4), methyl brevifolincarboxylate (5), eschweilenol C (6), ellagic acid-4-O-β-D-xylopyranoside (7), ellagic acid (8), and quercitrin (9), and to futher evaluate their α-glucosidase inhibitory activity. The analytical method demonstrated linearity with correlation coefficients (R²) exceeding 0.9991. The limits of detection (LOD) and limits of quantification (LOQ) ranged from 2.75 to 7.44 μg/mL and 8.33 to 22.54 μg/mL, respectively. Intra-day and inter-day precision showed relative standard deviation (RSD) values below 2.85% and 2.72%, while recovery values ranged from 96.87% to 107.72%, confirming the accuracy and reliability of the method.Quantitative results revealed that ellagitannins were the predominant constituents in both stems and pericarpium of P. granatum. Biological evaluation demonstrated that several isolated compounds exhibited strong αglucosidase inhibitory activity, with compounds 1–3 showing significantly stronger activity than the reference inhibitor acarbose. Enzyme kinetic studies and molecular docking analyses were conducted to clarify their inhibition mechanisms, revealing mixed, uncompetitive and competitive inhibition modes associated with binding to catalytic or allosteric sites of the enzyme. This study integrates quantitative analysis with mechanistic enzyme inhibition evaluation, providing a practical analytical tool for quality control of P. granatum and scientific evidence supporting its potential application in antidiabetic therapy.

Background: Rosacea is a chronic inflammatory disorder characterized by flushing, erythema, papules/pustules, and telangiectasia. Several clinical studies have investigated the efficacy of botulinum neurotoxin A (BoNT/A) in the treatment of rosacea, but its mechanism of action remains unclear. Objective: This study aims to examine the potential role of BoNT/A in a mouse model of rosacea-like skin lesions induced by the 37-amino acid C-terminal cathelicidin peptide (LL-37). Methods: Mice were randomly divided into 4 groups: Control, LL-37, LL-37 + BoNT/A, and LL-37 + dexamethasone. Results: BoNT/A treatment alleviated skin damage, reduced skin thickness, and decreased mast cell infiltration. Furthermore, BoNT/A improved redness score severity and redness area while enhancing skin barrier function by suppressing transepidermal water loss and increasing skin hydration. At the molecular level, BoNT/A decreased the mRNA levels of interleukin (IL)-6 and tumor necrosis factor-α, which are known as pro-inflammatory cytokines. It also downregulated the expression of pyrin domain-containing protein 3, caspase-1, and IL-1 beta in the LL-37-injected dorsal skin. Furthermore, BoNT/A prevented LL-37-mediated upregulation of neurovascular-associated factors, including CD31, transient receptor potential vanilloid 1, calcitonin-related polypeptide alpha, vascular endothelial growth factor, chymase 1, and tryptase alpha/beta 1. Conclusion These results indicate that BoNT/A effectively alleviates inflammatory and vascular responses in a rosacea mouse model, highlighting its potential as a promising preventive approach for rosacea.

Phyllodes tumors are rare biphasic fibroepithelial breast neoplasms classified as benign, borderline, or malignant. Despite their rarity, malignant variants carry higher risks of recurrence and metastasis. This review synthesizes current evidence on their clinical, histopathological, and molecular characteristics, including treatment strategies and prognostic factors, emphasizing tailored management. We performed a comprehensive literature review to summarize knowledge on clinical presentation, imaging, histopathological features, surgical treatment, adjuvant therapy, and outcomes. Recent genomic and molecular research was also evaluated to identify future directions. Persistent challenges include a lack of consensus on optimal surgical margins, adjuvant radiotherapy, and follow-up protocols, highlighting the need for larger, high-quality studies. Advances in molecular profiling suggest potential for targeted therapies, especially in aggressive or metastatic cases. Due to clinical heterogeneity and the limited accuracy of core biopsies, definitive grading based on surgical histopathology remains essential for treatment planning. This review offers an updated perspective on phyllodes tumor management, identifies critical gaps, and suggests priorities for future research.

Soft tissue sarcomas (STSs), a diverse group of mesenchymal malignancies, are characterized primarily by copy-number alterations rather than a high tumor mutation burden. In this study, we sought to identify expression-based biomarkers in complex karyotype STS (CKS) with CDK4-amplification to support improved therapeutic strategies. Using transcriptome data from National Cancer Center (NCC)-CKS samples, we selected genes whose expression levels were more than two-fold higher or less than half in tumor tissues compared with normal tissues. These genes were further filtered by CDK4-amplification status, resulting in 30 candidates, which were refined to 14 differentially expressed genes (DEGs) based on false discovery rate (FDR) significance. Bioinformatics analyses revealed enriched pathways and gene–gene networks related to redox regulation and growth-factor–driven signal transduction, indicating metabolic alterations that may promote tumor survival in CDK4-amplified CKS. A subset of the 14 genes demonstrated prognostic significance in CDK4-amplified patients from the TCGA cohort. Additionally, immune cell marker analysis showed associations between CDK4-amplification and innate immune cell signatures. Together, our findings identify promising therapeutic and prognostic targets linked to CDK4-amplification in CKS. These biomarkers warrant further investigation and may ultimately contribute to improved clinical outcomes for patients with CKS.

This study aimed to develop a predictive model for the early identification of patients at risk of sepsis, using routinely available clinical information and laboratory test results collected during the initial phase of patient care. Methods: This retrospective analysis included electronic medical records of 22,400 adult patients who presented with suspected infection to a tertiary care university hospital in Korea between January 2013 and May 2024. Patients were classified according to Systemic Inflammatory Response Syndrome (score ≥ 2) or Quick Sequential Organ Failure Assessment (score ≥ 2), in combination with sepsis-related International Classification of Diseases, 10th revision codes. Four different machine learning models were trained and validated using five-fold cross-validation. In addition, Shapley additive explanations analysis was performed to interpret the contribution and clinical relevance of key predictive variables. Results: Among the evaluated models, CatBoost demonstrated the strongest predictive performance. Notably, platelet distribution width, alveolar–arterial oxygen difference, procalcitonin, and the arterial/alveolar oxygen ratio consistently emerged as major predictors. Importantly, several variables that did not reach statistical significance in univariate analysis nevertheless contributed substantially to overall model performance, highlighting the importance of complex, multidimensional interactions among clinical factors. Conclusion: These findings indicate that a model based on simple, routinely collected clinical data can achieve high predictive accuracy and strong generalizability. Such a tool may support early clinical decision-making by multidisciplinary teams, including nurses, across diverse real-world care settings. Further prospective studies are warranted to validate its clinical utility and to assess its potential effects on patient outcomes.