Background: The prevalence of diabetes mellitus and early-onset dementia (EOD), defined as dementia diagnosed at an age <65 years, is increasing worldwide, with significant socioeconomic implications. We investigated the association between diabetes, prediabetes, and EOD, focusing on the influence of diabetes duration on EOD risk. Methods: Using the Korean National Health Insurance Service database, we analyzed data from 1,979,509 patients aged 40–60 years who underwent health checkups in 2009. Patients were categorized into five groups: normal, impaired fasting glucose (IFG), newly diagnosed diabetes, diabetes duration <5 years, and diabetes duration ≥5 years. Cox proportional hazard models were used to estimate the adjusted hazard ratios (aHRs) for EOD after adjusting for demographic and clinical covariates. Results: During the observation period (mean 7.75 years), 8,921 patients with EOD were identified. The diabetes group demonstrated a significantly higher incidence of EOD compared to the normal group (aHR, 1.334; 95% confidence interval [CI], 1.226 to 1.451). EOD risk increased with longer diabetes duration, with the highest risk observed in patients with diabetes ≥5 years (aHR, 1.543; 95% CI, 1.368 to 1.741). No significant difference was observed between the IFG and normal groups (aHR, 0.989; 95% CI, 0.938 to 1.043). Additionally, the hypertension group exhibited a significantly higher incidence of EOD compared to the non-hypertension group (aHR, 1.364; 95% CI, 1.291 to 1.442). Conclusion Diabetes is independently associated with increased risk of EOD, and this risk increases with longer diabetes duration. This association remained significant regardless of the presence and duration of hypertension.

In patients with differentiated thyroid cancer (DTC), initial recurrence risk stratification based on clinical, histopathological, and perioperative data remains the key determinant for guiding management strategies during the first 1-2 years post-treatment. However, the adoption of ongoing risk stratification (ORS), which dynamically reassesses risk by integrating longitudinal clinical data and treatment response, enables more precise long-term prognostic assessment and facilitates highly individualized management. Building upon recent guidelines, the 2026 KTA guideline has been further refined by incorporating robust evidence from large-scale national cohorts and comprehensive systematic reviews. These updated recommendations outline contemporary concepts of ORS, risk-adapted TSH suppression targets, optimized surveillance modalities for recurrence detection, and disease-specific long-term follow-up strategies. Reflecting the paradigm shift toward de-escalated treatment, this revision integrates evolved perspectives on TSH suppression intensity, the clinical interpretation of thyroglobulin levels, and tailored follow-up intervals. These evidence-based recommendations aim to minimize unnecessary treatment and excessive surveillance in the large proportion of patients with excellent prognosis after initial therapy, while ensuring that each patient receives appropriately tailored and effective long-term management.

Purpose: This study aimed to develop and implement an antimicrobial stewardship education program for physician assistant nurses and to evaluate its effects on their knowledge and clinical performance. Methods: A quasi-experimental, single-group pre-post design was conducted with 50 physician assistant nurses at a university hospital in Seoul, Republic of Korea. The antimicrobial stewardship education program, developed using the ADDIE model, consisted of 12 sessions including lectures and case-based learning (CBL)-based discussions.Knowledge was measured before and immediately after the intervention, while performance was assessed pre-intervention and four weeks post-program. Data were analyzed using paired t-tests, Wilcoxon signed-rank tests, and analysis of covariance (ANCOVA). Results: Knowledge scores significantly improved from 44.65±7.45 to 58.50±10.11 (p<.001), and all subdomains showed significant increases (p<.001). Performance scores increased from 3.68±0.77 to 4.28±0.68 (p<.001). Knowledge gain did not differ significantly between the medical and surgical departments (p=.710). Likewise, after adjusting for pre-test scores, no significant difference in performance improvement was observed between the two departments (ANCOVA, p=.170). These results indicate that the program was effective across both departments regardless of their characteristics. Conclusion The antimicrobial stewardship education program improved both knowledge and performance among physician assistant nurses. This program may contribute to the standardization of antimicrobial stewardship education and to appropriate antimicrobial use and the reduction of antimicrobial resistance.

Objective: To investigate the longitudinal association between sarcopenia and depressive symptoms in community-dwellingolder adults, focusing on sex-specific differences. Methods: This 2-year prospective study utilized data from the Korean Frailty and Aging Cohort Study. We included 1,366participants (700 men, 666 women) aged 70-84 years who were free of depressive symptoms (Short Geriatric Depression Scale-Korean [SGDS-K]<8) at baseline. Sarcopenia status (no sarcopenia, sarcopenia, severe sarcopenia) was defined by the AsianWorking Group for Sarcopenia 2019 criteria. Multivariate logistic regression analysis was performed to assess the association be-tween baseline sarcopenia and incident depressive symptoms (SGDS-K≥8) at follow-up, adjusting for covariates. Results: After adjustment, baseline severe sarcopenia was significantly associated with a higher risk of incident depression (adjusted odds ratio [aOR]=3.040, 95% confidence interval [CI]=1.494-6.188). In the sex-stratified analysis, this association remained robust only in men (aOR=3.344, 95% CI=1.332-8.395), but was not statistically significant in women (aOR=2.490, 95% CI=0.699-8.872, p=0.159). Conclusion Severe sarcopenia independently predicts for 2-year development of depressive symptoms, particularly amongolder Korean men. These findings highlight a significant sex difference in the temporal relationship between sarcopenia and de-pression for older men.

Purpose: We aimed to compare the final adult height (FAH) of male patients with central precocious puberty (CPP) after treatment with a gonadotropin-releasing hormone agonist (GnRHa). Specifically, we compared FAH with the target height (TH) and the predicted adult height (PAH) before and after GnRHa treatment to quantify height gain and identify predictive factors. Methods: We retrospectively reviewed the medical records of 92 male patients with CPP and known FAH after GnRHa treatment at the Department of Pediatrics of Severance Children’s Hospital between January 2000 and June 2024. Results: The mean duration of GnRHa treatment was 2.7±1.3 years. A significant 1.1±0.9 years narrowing was observed in the difference between bone age (BA) and chronological age (CA) during treatment (P<0.001). TH was 172.4±3.4 cm. FAH was 173.6±6.4 cm. FAH was greater than TH by 1.2±5.9 cm (P=0.047). PAH before and after treatment was 179.9±8.1 and 181.2±7.4 cm, respectively. PAH was increased by 1.3±4.9 cm (P=0.012) after treatment. As the PAH standard deviation score (SDS) before GnRHa treatment increased, FAH tended to exceed TH. In contrast, higher testosterone levels before treatment are associated with FAH falling below TH. A longer duration of treatment and taller TH are associated with an FAH SDS greater than height SDS before treatment. Conversely, a greater weight SDS, BA–CA difference, and testis size before treatment are associated with FAH SDS being less than height SDS before GnRHa treatment. Conclusion GnRHa treatment improved FAH and inhibited bone maturation in male patients with CPP.

Purpose: Skeletal muscle, accounting for approximately 40% of the total body mass, plays a critical role in movement, postural support, and metabolic homeostasis. Muscle mass is determined by the balance between protein synthesis and degradation, which is closely regulated by the mitochondrial function. Mitochondrial dysfunctions contribute to muscle loss by promoting oxidative stress and cellular damage. This study examined the effects of masutakeside I, a lignan glycoside derived from Styrax japonicus, on the mitochondrial function and muscle differentiation in C2C12 myoblasts. Methods: C2C12 myoblasts differentiated into myotubes in the presence of masutakeside I (0–10 ng/mL). Myogenic differentiation was assessed by myosin heavy chain (MHC) immunofluorescence, and multinucleated myotubes and relative diameters were quantified.The mitochondrial function was evaluated by measuring the mitochondrial reactive oxygen species (ROS), mitochondrial mass, and mitochondrial membrane potential using MitoSOX, MitoTracker Green, and JC-1 staining, respectively. Gene expression related to muscle differentiation, protein degradation, and the mitochondrial life cycle was analyzed using quantitative reverse transcription polymerase chain reaction. Results: Masutakeside I significantly increased the number of multinucleated (≥ 5 nuclei) MHC-positive myotubes and relative myotube diameter compared to the control. In addition, masutakeside I upregulated the myogenic markers, including phosphoinositide 3-kinase and MHC isoforms (Myh2, Myh4, and Myh7), while significantly downregulating protein degradation–related genes, including mothers against decapentaplegic homolog 2/3, forkhead box protein O1, atrogin-1, and muscle RING finger-1. Masutakeside I modulated the mRNA expression of the mitochondrial function and mitophagy-related markers, suggesting its potential involvement in mitochondrial quality control. Consistent with these effects, the mitochondrial ROS levels decreased, whereas mitochondrial mass and membrane potential increased. Conclusion These findings suggest that masutakeside I modulates the markers related to myogenic differentiation, muscle protein degradation, and mitochondrial function.

Background: Despite advancements in laboratory animal facility management, pinworm infections remain a persistent issue in immunodeficient mouse colonies. Rapid diagnosis and treatment are crucial to mitigating potential scientific and economic consequences. Effective control requires both the administration of anthelmintic agents and rigorous environmental decontamination. However, the safety and efficacy of these treatments in genetically modified mouse models remains uncertain.Case presentation Aspiculuris tetraptera infestation was identified in multiple immunodeficient mouse models housed in a laboratory facility. Diagnosis was confirmed through fecal flotation for egg detection and necropsy for adult worm examination in the large intestines. Mice received three subcutaneous ivermectin injections at two-week intervals, coupled with environmental decontamination using ivermectin spray for four consecutive weeks. Following treatment, all colonies tested negative for A. tetraptera without any mortality. Conclusions A combination of subcutaneous ivermectin injection and environmental spray application effectively eradicated A. tetraptera infestation in immunodeficient mouse colonies. The treatment protocol led to the complete elimination of eggs and adult worms, offering a practical strategy for managing pinworm infections in genetically modified mouse models. Limitations include the small sample size, and the lack of a comprehensive evaluation of physiological and metabolic safety in immunodeficient mice. Further validation will be required to confirm the broader applicability of this approach.

Arterial thrombosis remains a leading cause of cardiovascular morbidity and mortality despite widespread use of dual antiplatelet therapy (DAPT) with aspirin and P2Y12 inhibitors. Although these agents reduce ischemic events, their efficacy is counterbalanced by dose-dependent bleeding and their inability to distinguish pathological platelet activation from physiological hemostasis.Recent advances in platelet biology have shifted therapeutic development toward hemostasis-sparing antiplatelet strategies— approaches designed to selectively inhibit thrombosis while preserving baseline hemostatic function. These strategies target upstream adhesion receptors (GPVI, GPIb–vWF, CLEC-2) and receptor-proximal intracellular signaling nodes (SYK, BTK, PI3Kβ, PLCγ2, NADPH oxidases) that are preferentially engaged under high-shear or strongly prothrombotic conditions. Early-phase clinical and translational studies of such agents demonstrate antithrombotic efficacy with minimal impact on bleeding time, supporting their mechanistic selectivity. In parallel, contemporary clinical practice increasingly utilizes individualized risk assessment, platelet function testing, and genetic profiling to tailor treatment intensity. This integration of mechanism-selective agents with patient-specific risk evaluation forms the basis of precision-based thrombosis prevention, a framework aimed at aligning the duration and depth of platelet inhibition with the dynamic balance between ischemic and bleeding risk. Together, these developments mark a paradigm shift from broad platelet suppression toward rational, context-adaptive, and safer antiplatelet therapy.