Background and Objectives: We evaluated 20-year trends in heart failure (HF) epidemiology in Korea to quantify changes in its burden from 2002 to 2023. Methods: A nationwide analysis was conducted using a random 50% sample from the Korean National Health Information Database linked to mortality records (2002–2023). HF was defined using diagnostic codes recorded as a primary or secondary condition. We calculated crude and age-standardized rates of prevalence, incidence, hospitalization, and mortality. Survival was assessed using the Kaplan–Meier method, stratified by inpatient versus outpatient diagnosis.Trends in heart transplantation and left ventricular assist device implantations were also examined. Results: By 2023, approximately 1,750,228 individuals had HF (3.41% prevalence). The age-standardized prevalence has more than doubled from 2002 to 2023. The crude incidence increased over time; the age-standardized incidence remained stable in men and declined in women.Hospitalization rates for any cause or secondary HF diagnoses have increased substantially, whereas primary HF hospitalization rates have remained relatively stable. The annual mortality rate in patients with HF was approximately 6.0% in 2023, being markedly higher in older adults.Although short-term survival has improved, particularly in hospitalized patients, long-term survival remains limited. Use of advanced therapies significantly increased. Conclusions The burden of HF in Korea has increased substantially over the past two decades, driven primarily by population aging and improved survival rather than increasing age-adjusted incidence. Despite therapeutic advances, hospitalization and long-term mortality rates remain high, highlighting the need for comprehensive HF strategies in aging societies.

Hormone receptor-positive (HR+) breast cancer is known for its potential to recur many years after initial treatment. Although most recurrences occur within the first 5–10 years, late recurrence, especially beyond 15 years of age, is rare and isolated cutaneous recurrence is even less frequently reported. However, awareness of the possibility of extremely late and subtle local recurrences in patients with HR+ breast cancer has gradually increased over time. Clinicians should remain vigilant for atypical cutaneous changes near previous surgical sites, even decades after the initial treatment, and consider biopsy in the absence of classic signs of recurrence. We report the case of a 56-year-old woman who experienced an isolated cutaneous recurrence nearly 20 years after mastectomy for HR+ breast cancer, presenting with only faint erythema.

Vitreous floaters are a common ophthalmic symptom caused by age-related vitreous degeneration, trauma, or other ocular conditions.Patients typically describe floaters as moving shadows or thread-like opacities in their visual field, which can cause significant visual and psychological discomfort. While most cases improve over time through natural neuroadaptation, some patients experience persistent symptoms that impact quality of life and seek active treatment. Despite various therapeutic attempts—including Nd:YAG vitreolysis, pharmacologic vitreolysis, and pars plana vitrectomy (PPV)—no standardized treatment guideline has been established. Among those proposed, PPV is the most direct method to remove floaters, but it poses considerable risks, including cataract formation, retinal tears, retinal detachment, and endophthalmitis. Additionally, its subjective efficacy raises concerns about inconsistent outcomes. This review explores the pathophysiology of vitreous changes leading to floaters and critically evaluates the efficacy and safety of PPV for floater treatment based on current literature and the results of a survey conducted by the Korean Retina Society. The survey indicates that most specialists prefer observation and patient counseling over surgery, citing high complication risks, limited benefits, and ethical concerns.Floater management should prioritize conservative approaches, and PPV should be considered only in highly selected cases following thorough evaluation and counseling. Continued research into safer and more effective treatments is essential for addressing this common yet complex clinical issue.

Objective: This study was performed to evaluate the efficacy and safety of lurasidone (160 mg/day) compared to quetiapine XR (QXR; 600 mg/day) in the treatment of acutely psychotic patients with schizophrenia. Methods: Patients were randomly assigned to 6 weeks of double-blind treatment with lurasidone 160 mg/day (n=105) or QXR 600 mg/day (n=105). Primary efficacy measure was the change from baseline to week 6 in Positive and Negative Syndrome Scale (PANSS) total score and Clinical Global Impressions severity (CGI-S) score. Adverse events, body measurements, and laboratory parameters were assessed. Results: Lurasidone demonstrated non-inferiority to QXR on the PANSS total score. Adjusted mean±standard error change at week 6 on the PANSS total score was -26.42±2.02 and -27.33±2.01 in the lurasidone and QXR group, respectively. The mean difference score was -0.91 (95% confidence interval -6.35–4.53). The lurasidone group showed a greater reduction in PANSS total and negative subscale on week 1 and a greater reduction in end-point CGI-S score compared to the QXR group. Body weight, body mass index, and waist circumference in the lurasidone group were reduced, with significantly lower mean change compared to QXR. Endpoint changes in glucose, cholesterol, triglycerides, and low-density lipoprotein levels were also significantly lower. The most common adverse drug reactions with lurasidone were akathisia and nausea. Conclusion Lurasidone 160 mg/day was found to be non-inferior to QXR 600 mg/day in the treatment of schizophrenia with comparable efficacy and tolerability. Adverse effects of lurasidone were generally tolerable, and beneficial effects on metabolic parameters can be expected.

Background/Aims: The etiology of irritable bowel syndrome (IBS) is associated with intestinal mucosal barrier damage. However, changes in the tight junction (TJ) proteins in IBS have not been fully elucidated. This study aimed to evaluate TJ protein changes in IBS patients and the relationship between aging and disease severity. Methods: Thirty-six patients with IBS fulfilling the Rome IV criteria and twenty-four controls were included. To evaluate the change of TJ in the colonic mucosa, quantitative reverse transcription polymerase chain reaction, western blot, and immunohistochemistry (IHC) were performed, respectively. Results: The entire IBS group (n = 36) exhibited decreased levels of claudin-1 and -2 mRNA compared to the control group (n = 24), with statistical significance (p < 0.05). Additionally, in western blot analyses, both claudin-1 and ZO-1 levels were significantly reduced in the IBS group compared to the control group (n = 24) (p < 0.05). IHC analysis further revealed that ZO-1 expression was significantly lower in the IBS group than in the control group (p < 0.001). This trend of reduced ZO-1 expression was also observed in the moderate-to-severe IBS subgroup (p < 0.001). Significantly, ZO-1 expression was notably lower in both the young- (p = 0.036) and old-aged (p = 0.039) IBS groups compared to their respective age-matched control groups. Subtype analysis indicated a more pronounced decrease in ZO-1 expression with advancing age. Conclusions ZO-1 expression was especially decreased in the aged IBS group. These results suggest that ZO-1 might be the prominent TJ protein causing IBS in the aging population.

Granular cell tumor is a rare disease, and it is even rarer in the male breast. Although it is typically a benign tumor, due to its features and image findings, it can be easily misdiagnosed and managed as a malignant tumor. Therefore, the extent of the surgery can inappropriately be expanded. To avoid misdiagnosis and overtreatment, surgeons must perform a careful evaluation. We describe a case of a granular cell tumor of the male breast treated with mastectomy.

Background: Bladder cancer is characterized by frequent mutations, which provide potential therapeutic targets for most patients. The effectiveness of emerging personalized therapies depends on an accurate molecular diagnosis, for which the accurate estimation of the neoplastic cell percentage (NCP) is a crucial initial step. However, the established method for determining the NCP, manual counting by a pathologist, is time-consuming and not easily executable. Methods: To address this, artificial intelligence (AI) models were developed to estimate the NCP using nine convolutional neural networks and the scanned images of 39 cases of urinary tract cancer. The performance of the AI models was compared to that of six pathologists for 119 cases in the validation cohort. The ground truth value was obtained through multiplexed immunofluorescence. The AI model was then applied to 41 cases in the application cohort that underwent next-generation sequencing testing, and its impact on the copy number variation (CNV) was analyzed. Results: Each AI model demonstrated high reliability, with intraclass correlation coefficients (ICCs) ranging from 0.82 to 0.88. These values were comparable or better to those of pathologists, whose ICCs ranged from 0.78 to 0.91 in urothelial carcinoma cases, both with and without divergent differentiation/ subtypes. After applying AI-driven NCP, 190 CNV (24.2%) were reclassified with 66 (8.4%) and 78 (9.9%) moved to amplification and loss, respectively, from neutral/minor CNV. The neutral/minor CNV proportion decreased by 6%. Conclusions These results suggest that AI models could assist human pathologists in repetitive and cumbersome NCP calculations.

Purpose: Vascular endothelial growth factor tyrosine kinase inhibitors (TKIs) have been the standard of care for advanced and metastatic clear cell renal cell carcinoma (ccRCC). However, the therapeutic effect of TKI monotherapy remains unsatisfactory given the high rates of acquired resistance to TKI therapy despite favorable initial tumor response. Materials and Methods: To define the TKI-resistance mechanism and identify new therapeutic target for TKI-resistant ccRCC, an integrative differential gene expression analysis was performed using acquired resistant cohort and a public dataset. Sunitinib-resistant RCC cell lines were established and used to test their malignant behaviors of TKI resistance through in vitro and in vivo studies. Immunohistochemistry was conducted to compare expression between the tumor and normal kidney and verify expression of pathway-related proteins. Results: Integrated differential gene expression analysis revealed increased interferon-induced transmembrane protein 3 (IFITM3) expression in post-TKI samples. IFITM3 expression was increased in ccRCC compared with the normal kidney. TKI-resistant RCC cells showed high expression of IFITM3 compared with TKI-sensitive cells and displayed aggressive biologic features such as higher proliferative ability, clonogenic survival, migration, and invasion while being treated with sunitinib. These aggressive features were suppressed by the inhibition of IFITM3 expression and promoted by IFITM3 overexpression, and these findings were confirmed in a xenograft model. IFITM3-mediated TKI resistance was associated with the activation of TRAF6 and MAPK/AP-1 pathways. Conclusions These results demonstrate IFITM3-mediated activation of the TRAF6/MAPK/AP-1 pathways as a mechanism of acquired TKI resistance, and suggest IFITM3 as a new target for TKI-resistant ccRCC.

Purpose: Tyrosine kinase inhibitors (TKI) targeting vascular endothelial growth factor receptor (VEGFR) signaling pathways have been used for metastatic clear cell renal cell carcinoma (mCCRCC), but resistance to the drug develops in most patients. We aimed to explore the underlying mechanism of the TKI resistance with regard to programmed death-ligand 1 (PD-L1) and to investigate signaling pathway associated with the resistant mechanism. Materials and Methods: To determine the mechanism of resistance, 10 mCCRCC patients from whom tumor tissues were harvested at both the pretreatment and the TKI-resistant post-treatment period were included as the discovery cohort, and their global gene expression profiles were compared. A TKI-resistant renal cancer cell line was established by long-term treatment with sunitinib. Results: Among differentially expressed genes in the discovery cohort, increased PD-L1 expression in post-treatment tissues was noted in four patients. Pathway analysis showed that PD-L1 expression was positively correlated with the mammalian target of rapamycin (mTOR) signaling pathway. The TKI-resistant renal cancer cells showed increased expression of PD-L1 and mTOR signaling proteins and demonstrated aggressive tumoral behaviour. Treatment with mTOR inhibitors down-regulated PD-L1 expression and suppressed aggressive tumoral behaviour, which was reversed with stimulation of the mTOR pathway. Conclusion These results showed that PD-L1 expression may be increased in a subset of VEGFR-TKI–resistant mCCRCC patients via the mTOR pathway.