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.

The standard treatment for choledocholithiasis is to remove the stones by performing endoscopic retrograde cholangiopancreatography (ERCP). With various techniques such as basket extraction, balloon catheter extraction, mechanical lithotripsy, followed by endoscopic papillary sphincterotomy or endoscopic papillary balloon dilatation, the success rate of stone extraction is known to be over 90%. However, stone extraction can fail in cases with large common bile duct stones or biliary stricture. We report a case of impacted choledocholithiasis after conventional ERCP and mechanical lithotripsy treated with extracorporeal shock wave lithotripsy.

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.

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.