Background: Catecholamines play a crucial role in muscle biogenesis, but their persistent elevation is linked to muscle wasting, which is poorly understood. This study aimed to investigate the association between catecholamine levels and age-related muscle loss. Methods: This retrospective study evaluated the plasma levels of two catecholamines, metanephrine and normetanephrine, and the clinical characteristics of 830 patients with adrenal incidentaloma on computed tomography (CT). Cross-sectional CT data at the L3 lumbar vertebrae were used to measure muscle areas. In vitro studies on C2C12 myotubes were conducted to examine β-adrenergic receptor signaling pathways and their role in myogenesis. Results: Men had significantly higher mean metanephrine levels of 0.17 nmol/L and normetanephrine levels of 0.63 nmol/L than women (P<0.05). Total abdominal muscle area was negatively correlated with catecholamine levels in both men and women, with the strongest negative correlation between normetanephrine levels and total abdominal muscle area in men (r=–0.31, P<0.001). Similarly, the strongest negative correlation between visceral fat area and metanephrine was observed in men (r=–0.25, P=0.004). Clenbuterol, a β-adrenergic receptor agonist, inhibited myogenesis, including myotube formation by extracellular signal-regulated kinase (ERK) suppression in C2C12 myoblasts. Conversely, β-blockers increased myogenesis via increasing ERK phosphorylation in C2C12 cells. These findings suggest that β-adrenergic modulation influences skeletal muscle differentiation, with ERK phosphorylation. Conclusion Catecholamine levels are associated with age, sex, muscle mass, and fat mass. Monitoring catecholamine levels, particularly in older men and in individuals with reduced muscle mass, may help manage age-related muscle loss and lead to individualized treatment strategies.

Background and Objectives: Clinical characteristics and outcomes in acute heart failure (AHF) vary by phenotype. We assessed phenotype-specific features, treatment patterns, and outcomes in a nationwide Korean cohort. Methods: The Korean Heart Failure III registry prospectively enrolled 7,351 AHF admissions at 47 hospitals. Among 6,777 patients with available left ventricular ejection fraction (EF), phenotypes were defined as heart failure with reduced EF (HFrEF, ≤40%), mildly reduced EF (HFmrEF,41–49%), or preserved EF (HFpEF, ≥50%). The primary endpoint was a 12-month composite of all-cause death or heart transplantation, evaluated from index admission and, among hospital survivors, from discharge. We used inverse probability weighting (multinomial generalized boosted models with stabilized, trimmed weights) and weighted Cox proportional-hazards models to estimate hazard ratios (HRs). Results: Phenotype distribution was 58.9% HFrEF, 13.6% HFmrEF, and 27.5% HFpEF. Crude 12-month composite rates from index admission were 13.4% (HFrEF), 12.7% (HFmrEF), and 16.8% (HFpEF). After weighting, from index admission, HFmrEF (HR, 0.892; 95% confidence interval [CI], 0.731–1.088) and HFpEF (HR, 1.101; 95% CI, 0.939–1.291) did not differ from HFrEF; from discharge, HFpEF had modestly higher risk (HR, 1.207; 95% CI, 1.008–1.445) whereas HFmrEF did not (HR, 1.039; 95% CI, 0.844–1.279). Hyponatremia and chronic kidney disease were consistent adverse markers, while angiotensin-converting enzyme inhibitor/ angiotensin II receptor blocker use at discharge was protective. Conclusions Across the EF spectrum, phenotypes showed distinct profiles and risk. Postdischarge risk was modestly higher in HFpEF, supporting phenotype-tailored care and systematic discharge optimization in Korean patients with AHF.

Idiopathic pulmonary fibrosis (IPF) is characterized by maladaptive epithelial–mesenchymal crosstalk and progressive extracellular matrix accumulation, whereas currently available antifibrotic agents merely decelerate functional decline.This study investigated whether exosomes derived from human mesenchymal stem cells derived from embryonic stem cells (ESC-MSCs) restore epithelial stress responses and attenuate fibrotic remodeling. Human IPF lung transcriptomes were integrated with a bleomycin-induced murine model analyzed by RNA sequencing and protein signaling, together with cigarette smoke extract-induced injury in A549 epithelial cells. ESC-MSCs-derived exosomes exhibited typical morphology and size distribution, enrichment of tetraspanins, and absence of endoplasmic reticulum contamination, consistent with high-purity preparations. Across human IPF and bleomycin-injured lungs, transcriptomic profiling revealed prominent enrichment of extracellular matrix and cytoskeletal gene programs, whereas mitogen-activated protein kinase (MAPK) and Smad families displayed only modest alterations at the mRNA level. In vivo administration of exosomes during the fibrotic remodeling phase, via either intravenous or intratracheal delivery, resulted in improved body weight, reduced lung weight-to-body weight ratios, and decreased collagen deposition and Ashcroft scores. These structural and functional improvements were accompanied by suppression of profibrotic and mesenchymal markers and selective attenuation of activator protein-1 (AP-1) activity. In epithelial injury models, ESC-MSCs-derived exosomes enhanced cell viability, restored redox homeostasis, and constrained stress-induced mesenchymal gene expression and MAPK phosphorylation in both co-treatment and post-treatment settings. Collectively, these data support an epithelial-centered mechanism in which ESC-MSCs-derived exosomes re-establish oxidative balance and selectively restrict AP-1-driven stress signaling, thereby secondarily limiting extracellular matrix accumulation and fibrotic remodeling.

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.

Levothyroxine overdose is uncommon in adults and often presents with variable clinical severity, ranging from overt thyrotoxicosis to an entirely asymptomatic course. We report the case of a 47-year-old woman with a history of total thyroidectomy who intentionally ingested 10 mg of levothyroxine along with supratherapeutic doses of zolpidem and clonazepam at once in a suicide attempt. She presented three days later without adrenergic or gastrointestinal symptoms. Laboratory tests revealed markedly elevated free thyroxine and total triiodothyronine with suppressed thyroid stimulating hormone. She was treated with propranolol for heart rate control and empirical hydrocortisone in case of adrenal insufficiency. She remained asymptomatic with gradual biochemical improvement and normalization of thyroid function on follow-up. The protective effect of co-ingested supratherapeutic doses of gamma-aminobutyric acid (GABA)-ergic agents suggests a potential role for anti-anxiety medications in mitigating severe adrenergic symptoms in endogenous thyrotoxicosis, such as Graves’ disease.

Purpose: This study aimed to evaluate the correlation between bladder outlet obstruction (BOO) and bladder trabeculation in patients with benign prostatic hyperplasia (BPH). Methods: We analyzed data from consecutive BPH patients from July 2014 to June 2024, who underwent urodynamic study (UDS) and cystourethroscopy. The results of free uroflowmetry, filling cystometry, and pressure-flow study were analyzed to evaluate functional parameters. For anatomical parameters, bladder trabeculation grade, lateral lobe protrusion of prostate, and bladder neck elevation (BNE) measured in cystourethroscopy were used. BOO was defined as the BOO index of 40 or higher in UDS. Bladder trabeculation was graded using our previous studies. Results: Among total of 1,452 BPH patients, 1,028 patients had trabeculation on cystoscopy. Age, serum prostate-specific antigen, postvoid residual, total prostate volume, transition zone volume, terminal type detrusor overactivity, detrusor pressure at the maximal flow rate, bladder contractility index (BCI), and BOO index increased according to increase in bladder trabeculation. Multivariable logistic analysis showed that bladder trabeculation was significantly associated with age (odds ratio [OR], 1.05; P<0.001), kissing sign (OR, 1.55; P=0.007), BNE (OR, 1.76; P<0.001), detrusor overactivity (OR, 1.88; P=0.002), BCI (OR, 1.01; P=0.037), BOO (OR, 2.27; P<0.001). BOO had the greatest correlation with bladder trabeculation. In addition, BOO index showed a positive correlation (r=0.39, P<0.001) with bladder trabeculation. BOO index well distinguished between moderate trabeculation of grade 2 or higher in receiver operating characteristic analysis (area under curve=0.72, P<0.001). Conclusions Our results showed that the severity of BOO is positively associated with the severity of bladder trabeculation.

Background: Although various surface modifications enhance titanium (Ti) implant osseointegration, achieving rapid bone formation comparable to native healing remains challenging. Current strategies primarily focus on micro-scale topography, often overlooking the critical role of macroscopic three-dimensional (3D) architecture in osteoconduction. Methods: We hypothesized that mimicking native bone’s porous architecture is key to accelerating osseointegration. First, we verified the impact of structural continuity by comparing standard Ti implants with decellularized bone grafts in a mouse calvaria defect model. Subsequently, we developed a biomimetic polycaprolactone (PCL)-based 3D architectural cover (Cover-type) and evaluated its osseointegration efficacy in a rat femur model against conventional Ti implants. Results: The mouse study confirmed that decellularized bone integrated significantly faster than Ti, highlighting the necessity of 3D continuity. In the rat model, micro-computed tomography analysis indicated a clear trend of increased bone formation in the Cover-type group, though statistical significance was limited by sample size. However, histological analysis confirmed a statistically significant enhancement in bone-to-implant contact compared to controls (P<0.05). The PCL structure served as a scaffold for cell migration, effectively bridging the implant-bone gap. Conclusions These findings suggest that providing a bone-like 3D environment via a PCL cover may enhance histological osseointegration, rather than relying solely on surface chemistry.

Purpose: Triple-negative breast cancer (TNBC) is a frequent phenotype of BRCA-mutanttumors. Tumors with BRCAness may show characteristics of BRCA-mutant tumors and respond to similar treatments. Next-generation sequencing is an efficient and cost-effective method for simultaneously sequencing multiple cancer susceptibility genes, surpassing conventional Sanger testing. Methods: A total of 148 women with TNBC were recruited from December 2015 to November 2018, as part of a sub-analysis based on the PEARLY trial data. Of them, 103 patients received neoadjuvant chemotherapy (NCT). The targeted genes related to hereditary cancers were sequenced using the 65-gene germline next-generation sequencing (gNGS) panel pathogenic and likely pathogenic variants (P&LPs) were determined by Sanger sequencing. We examined the occurrence of pathologic complete remission (ypCR) in patients with P&LPs. Results: The patients’ median age was 47 years (range, 27–69 years). Twenty (13.7%) of 148 patients had P&LP in six genes, including BARD1 (n = 2), BRCA1 (n = 9), BRCA2 (n = 5), CHEK2 (n = 1), RAD51C (n = 1), and RAD51D (n = 2). Among the 103 patients with NCT, 43 (41.7%) achieved ypCR (P&LPs; 9 individuals vs. non-variants; 34 individuals). Among the 103 patients with NCT, 14 (9.3%) had P&LPs. Nine of 14 patients with P&LPs, including BARD1 (n = 2), BRCA1 (n = 4), BRCA2 (n = 1), RAD51C (n = 1), and RAD51D (n = 1), achieved ypCR, showing a trend toward statistical significance (p = 0.066). Conclusion Germline P&LP mutations in TNBC patients can be detected by gNGS. This panel test can identify BRCA and BRCAness mutations that may predict ypCR in TNBC.

suggest that some reproductive factors associated with BC differ across ethnicities and time trends, perhaps due to the prevalence of reproductive factors and the baseline hazard of BC.