Background: Left bundle branch block (LBBB) significantly increases the risk of left ventricular systolic dysfunction (LVSD) due to cardiac dyssynchrony. Although artificial intelligence–enabled electrocardiography (AI-ECG) mod‑ els show promise in detecting LVSD, their performance in LBBB patients remains underexplored. We hypothesized that an AI-ECG model clinically validated for detecting LVSD would accurately detect LVSD and predict future clinical outcomes in LBBB patients. Methods: In this retrospective multicenter study, 5,689 expert-validated LBBB ECGs collected from 2,813 patients between 2016 and 2024 were analyzed using a previously developed and validated AI-ECG model. LVSD was defined as an ejection fraction of ≤ 40%. Model performance was assessed using the area under the receiver operating char‑ acteristic curve (AUROC), the area under the precision-recall curve (AUPRC), sensitivity, and specificity. Patients were stratified into high- and low-risk groups based on a threshold that achieved 90% sensitivity. A Kaplan–Meier analysis was used to compare clinical outcomes. Results: Among the 2,813 LBBB patients (mean age, 70.7 years; male sex, 43.7%), hypertension and a history of heart failure were common. The AiTiALVSD model showed strong diagnostic performance for LVSD (AUROC, 0.930 [95% CI, 0.924–0.937]; AUPRC, 0.913 [95% CI, 0.902–0.923]; sensitivity, 0.979; specificity, 0.473). During the mean follow-up of 4.1 years, high-risk patients had significantly higher hazards than low-risk patients for all-cause mortality (adjusted hazard ratio [HR], 1.87; 95% CI, 1.53–2.28), implantable cardioverter defibrillator/cardiac resynchronization therapy implantation (adjusted HR, 15.2; 95% CI, 7.51–30.77), and cardiovascular hospitalization (adjusted HR, 1.11; 95% CI, 0.96–1.28). Conclusions AiTiALVSD effectively detects LVSD and stratifies long-term cardiovascular risk in LBBB patients, support‑ ing its clinical utility for early detection and patient management.

This report presents radiologic changes after clinical improvement in a patient with acute interstitial nephritis (AIN). A 45-year-old female patient was referred for decreased renal function. Eight months prior, she had undergone hysterectomy and received chemotherapy. At the start of chemotherapy, her baseline creatinine level was 0.55 mg/dL, which rose to 1.46 mg/dL. Multiple imaging modalities performed when decreased renal function was observed revealed bilateral renal enlargement with increased cortical attenuation on computed tomography (CT), cortical hyperechogenicity on ultrasonography, and diffusion restriction in the renal cortices on magnetic resonance imaging. A renal biopsy was performed, and AIN was diagnosed. Follow-up laboratory tests showed that kidney function had improved to normal levels, and CT at that time showed a reduction in the size of both kidneys. Radiologic changes can serve as clues for the diagnosis of AIN. This is the first report to confirm radiological changes after the clinical improvement of AIN, thereby providing novel information about the course of AIN.

This report presents radiologic changes after clinical improvement in a patient with acute interstitial nephritis (AIN). A 45-year-old female patient was referred for decreased renal function. Eight months prior, she had undergone hysterectomy and received chemotherapy. At the start of chemotherapy, her baseline creatinine level was 0.55 mg/dL, which rose to 1.46 mg/dL. Multiple imaging modalities performed when decreased renal function was observed revealed bilateral renal enlargement with increased cortical attenuation on computed tomography (CT), cortical hyperechogenicity on ultrasonography, and diffusion restriction in the renal cortices on magnetic resonance imaging. A renal biopsy was performed, and AIN was diagnosed. Follow-up laboratory tests showed that kidney function had improved to normal levels, and CT at that time showed a reduction in the size of both kidneys. Radiologic changes can serve as clues for the diagnosis of AIN. This is the first report to confirm radiological changes after the clinical improvement of AIN, thereby providing novel information about the course of AIN.

This report presents radiologic changes after clinical improvement in a patient with acute interstitial nephritis (AIN). A 45-year-old female patient was referred for decreased renal function. Eight months prior, she had undergone hysterectomy and received chemotherapy. At the start of chemotherapy, her baseline creatinine level was 0.55 mg/dL, which rose to 1.46 mg/dL. Multiple imaging modalities performed when decreased renal function was observed revealed bilateral renal enlargement with increased cortical attenuation on computed tomography (CT), cortical hyperechogenicity on ultrasonography, and diffusion restriction in the renal cortices on magnetic resonance imaging. A renal biopsy was performed, and AIN was diagnosed. Follow-up laboratory tests showed that kidney function had improved to normal levels, and CT at that time showed a reduction in the size of both kidneys. Radiologic changes can serve as clues for the diagnosis of AIN. This is the first report to confirm radiological changes after the clinical improvement of AIN, thereby providing novel information about the course of AIN.

This report presents radiologic changes after clinical improvement in a patient with acute interstitial nephritis (AIN). A 45-year-old female patient was referred for decreased renal function. Eight months prior, she had undergone hysterectomy and received chemotherapy. At the start of chemotherapy, her baseline creatinine level was 0.55 mg/dL, which rose to 1.46 mg/dL. Multiple imaging modalities performed when decreased renal function was observed revealed bilateral renal enlargement with increased cortical attenuation on computed tomography (CT), cortical hyperechogenicity on ultrasonography, and diffusion restriction in the renal cortices on magnetic resonance imaging. A renal biopsy was performed, and AIN was diagnosed. Follow-up laboratory tests showed that kidney function had improved to normal levels, and CT at that time showed a reduction in the size of both kidneys. Radiologic changes can serve as clues for the diagnosis of AIN. This is the first report to confirm radiological changes after the clinical improvement of AIN, thereby providing novel information about the course of AIN.

This report presents radiologic changes after clinical improvement in a patient with acute interstitial nephritis (AIN). A 45-year-old female patient was referred for decreased renal function. Eight months prior, she had undergone hysterectomy and received chemotherapy. At the start of chemotherapy, her baseline creatinine level was 0.55 mg/dL, which rose to 1.46 mg/dL. Multiple imaging modalities performed when decreased renal function was observed revealed bilateral renal enlargement with increased cortical attenuation on computed tomography (CT), cortical hyperechogenicity on ultrasonography, and diffusion restriction in the renal cortices on magnetic resonance imaging. A renal biopsy was performed, and AIN was diagnosed. Follow-up laboratory tests showed that kidney function had improved to normal levels, and CT at that time showed a reduction in the size of both kidneys. Radiologic changes can serve as clues for the diagnosis of AIN. This is the first report to confirm radiological changes after the clinical improvement of AIN, thereby providing novel information about the course of AIN.

Purpose: Papillary thyroid carcinoma (PTC) is the most prevalent endocrine malignancy, and the global incidence has been steadily increasing over the years. Although PTC generally exhibits favorable prognosis, a subset of patients experiences aggressive progression and increased mortality. Current prognostic approaches, reliant on clinic-pathological factors, have limitations, underscoring the need for innovative biomarkers. MicroRNAs (miRs) have emerged as promising candidates due to their roles in cellular processes and cancer progression. Among them, the present study investigated the role of miR-18b in PTC, exploring its potential as a prognostic biomarker. Methods: Utilizing PTC cell lines (TPC1, K1), we examined miR-18b expression and its regulatory effects. The present study used web-based tools to predict the target of miR-18b and to investigate the prognostic impact of miR-18b on thyroid cancer. Results: Through a series of cell proliferation, invasion assay, gap closure, and colony formation assays, we identified that miR-18b suppresses PTC aggressiveness. Dual-luciferase assays confirmed that miR-18b directly targeted the 3’-untranslated region of CDK2 and suppressed the expression of CDK2. In addition, miR-18b significantly attenuates the interaction between cyclin A or cyclin E with cyclin-dependent kinase 2 according to co-immunoprecipitation assay.Western blotting of cell cycle proteins and flow cytometry revealed miR-18b–induced cell cycle arrest and apoptosis. Conclusion Our findings underscore miR-18b’s potential as a biomarker for predicting the prognosis of PTC and suggest that it functions through direct regulation of CDK2, influencing cell cycle dynamics. This study not only enhances our understanding of miR-18b in thyroid cancer but also highlights its potential in refining prognostic evaluations and therapeutic strategies.

Background/Aims: To determine the association between evolutionary changes in metabolic dysfunction-associated steatotic liver disease (MASLD) status and the risk of hepatocellular carcinoma (HCC) in a nationwide population-based cohort. Methods: Information on study participants was derived from the Korea National Health Insurance Service database. The study population consisted of 5,080,410 participants who underwent two consecutive biennial health screenings between 2009 and 2012. All participants were followed up until HCC, death, or 31 December 2020. The association of evolutionary changes in MASLD status, as assessed by the fatty liver index and cardiometabolic risk factors, including persistent non-MASLD, resolved MASLD, incident MASLD, and persistent MASLD, with HCC risk was evaluated using multivariable-adjusted Cox proportional hazards regression. Results: Among the 5,080,410 participants with 39,910,331 person-years of follow-up, 4,801 participants developed HCC. The incidence of HCC in participants with resolved, incident, and persistent MASLD was approximately 2.2-, 2.3-, and 4.7-fold higher, respectively, than that in those with persistent non-MASLD among the Korean adult population. When stratifying the participants according to the evolutionary change in MASLD status, persistent (adjusted hazard ratio [aHR], 2.94; 95% confidence interval [CI], 2.68–3.21; P<0.001), incident (aHR, 1.85; 95% CI, 1.63–2.10; P<0.001), and resolved MASLD (aHR, 1.33; 95% CI, 1.18–1.50; P<0.001) had an increased risk of HCC compared to persistent non-MASLD. Conclusions The evolutionary changes in MASLD were associated with the differential risk of HCC independent of metabolic risk factors and concomitant medications, providing additional information on the risk of HCC stratification in patients with MASLD.

Background: Recent diabetes management guidelines recommend that sodium-glucose cotransporter 2 inhibitors (SGLT2is) or glucagon-like peptide 1 receptor agonists (GLP-1RAs) with proven cardiovascular benefits should be prioritized for combination therapy in patients with type 2 diabetes mellitus (T2DM) and established cardiovascular disease (CVD). This study was aimed at evaluating SGLT2i or GLP-1RA usage rates and various related factors in patients with T2DM and established CVD. Methods: We enrolled adults with T2DM aged ≥30 years who were hospitalized due to established CVD from January 2019 to May 2020 at 13 secondary and tertiary hospitals in Korea in this retrospective observational study. Results: Overall, 2,050 patients were eligible for analysis among 2,107 enrolled patients. The mean patient age, diabetes duration, and glycosylated hemoglobin level were 70.0 years, 12.0 years, and 7.5%, respectively. During the mean follow-up duration of 9.7 months, 25.7% of the patients were prescribed SGLT2is after CVD events. However, only 1.8% were prescribed GLP-1RAs. Compared with SGLT2i non-users, SGLT2i users were more frequently male and obese. Furthermore, they had a shorter diabetes duration but showed worse glycemic control and better renal function at the time of the event. GLP-1RA users had a longer duration of diabetes and worse glycemic control at the time of the event than GLP-1RA non-users. Conclusion The SGLT2i or GLP-1RA prescription rates were suboptimal in patients with T2DM and established CVD. Sex, body mass index, diabetes duration, glycemic control, and renal function were associated with the use of these agents.

One of the notable adverse effects of sodium-glucose cotransporter 2 (SGLT2) inhibitor is diabetic ketoacidosis (DKA) often characterized by euglycemia. In this retrospective review of patients with DKA from 2015 to 2023, 21 cases of SGLT2 inhibitorassociated DKA were identified. Twelve (57.1%) exhibited euglycemic DKA (euDKA) while nine (42.9%) had hyperglycemic DKA (hyDKA). More than 90% of these cases were patients with type 2 diabetes mellitus. Despite similar age, sex, body mass index, and diabetes duration, individuals with hyDKA showed poorer glycemic control and lower C-peptide levels compared with euDKA. Renal impairment and acidosis were worse in the hyDKA group, requiring hemodialysis in two patients. Approximately one-half of hyDKA patients had concurrent hyperosmolar hyperglycemic state. Common symptoms included nausea, vomiting, general weakness, and dyspnea. Seizure was the initial manifestation of DKA in two cases. Infection and volume depletion were major contributors, while carbohydrate restriction and inadequate insulin treatment also contributed to SGLT2 inhibitor-associated DKA. Despite their beneficial effects, clinicians should be vigilant for SGLT2 inhibitor risk associated with DKA.