Dongyang People's Hospital

To compare the clinical value of video electroencephalography (VEEG) and routine electroencephalography (EEG) in diagnosing seizures that occur within 14 days of ischemic stroke onset.

A retrospective analysis of 140 ischemic stroke patients suspected of having epileptic seizures was conducted between April 2022 and April 2024. Seventy patients underwent EEG, while 70 underwent VEEG. Diagnostic performance within 24 hours was compared.

VEEG had a higher seizure detection rate (74.29% vs. 44.29%) and epileptiform discharge detection rate (90.00% vs. 50.00%), with a shorter time from stroke onset to the first seizure diagnosis (21.15 hours vs. 25.24 hours), as determined on the basis of either recorded EEG/VEEG events or confirmed clinical documentation. VEEG also revealed superior accuracy in distinguishing nonepileptic seizures (95.71% vs. 68.57%) and a higher success rate in localizing epileptic foci (80.00% vs. 40.00%). The detection rate of VEEG for localized epilepsy was greater (90.00% vs. 71.42%), and that of EEG for generalized epilepsy was greater (4.29% vs. 25.71%). The treatment adjustment rates were significantly higher in the VEEG group (57.14% vs. 30.00%). The monitoring duration for VEEG was longer (24 hours vs. 20-30 minutes for EEG), but the compliance rates were similar (98.57% vs. 92.68%).

VEEG offers superior diagnostic value over EEG in detecting seizures within 14 days of ischemic stroke onset, providing higher diagnostic accuracy, better differentiation between seizure types, and greater influence on treatment decisions.

Tecotabart vedotin (LM-302) is a novel antibody-drug conjugate (ADC) targeting CLDN18.2, a promising therapeutic target in gastrointestinal cancers. This phase 1/2 study evaluated the safety, pharmacokinetics, immunogenicity, and preliminary anti-tumor activity of tecotabart vedotin in patients with advanced solid tumors, with a focus on CLDN18.2-positive gastric/gastroesophageal junction (G/GEJ) cancer.

This open-label, multicenter study utilized a Bayesian adaptive design. Phase 1 enrolled patients with advanced solid tumors; phase 2 focused on CLDN18.2-positive G/GEJ, pancreatic, biliary tract cancer, or gastrointestinal tumors with low to moderate CLDN18.2 expression. Tecotabart vedotin was administered at 0.2-2.8 mg/kg every 3 weeks (Q3W) or 1.8-2.0 mg/kg every 2 weeks (Q2W). Primary endpoints included dose-limiting toxicities (DLTs) and safety in phase 1, and objective response rate (ORR) in phase 2. Secondary endpoints included safety, pharmacokinetics, immunogenicity, and other anti-tumor activity outcomes.

Overall, 153 patients received tecotabart vedotin (phase 1: 38; phase 2: 115). DLTs occurred in 5 patients at higher dose levels. The maximum tolerated dose was 2.4 mg/kg Q3W; recommended phase 2 doses were 1.8 mg/kg Q2W and 2.4 mg/kg Q3W. Among 52 evaluable patients with CLDN18.2-positive G/GEJ cancer receiving 1.8 mg/kg Q2W, ORR was 32.7 % (95 % confidence interval [CI] 20.3-47.1), with median progression-free survival of 4.9 months (95 % CI 2.7-6.9), and overall survival of 10.9 months (95 % CI 9.1-17.1). Adverse events were manageable and consistent with monomethyl auristatin E-based ADCs.

Tecotabart vedotin demonstrated encouraging anti-tumor activity and manageable safety in CLDN18.2-positive G/GEJ cancer, supporting further clinical development in gastrointestinal malignancies.

Liver fibrosis (LF) is a pathological condition that, if not controlled, can progress into liver sclerosis and malignant tumors. Ferroptosis has been comprehensively studied and found to improve LF by exacerbating hepatic cell ferroptosis. Ginsenoside RK1 (GRK1) is an essential component of ginseng with antifibrotic effects. However, the anti-LF mechanism of GRK1 remains elusive. The impact of GRK1 on LF was evaluated via RNA-sequence analysis of GRK1-treated hepatic stellate cells (HSC). Furthermore, a cellular thermal shift assay, drug affinity-responsive target stability, and molecular docking analyses were carried out to verify the interaction between GRK1 and HK2. The fibrosis indicators and histopathology assessment revealed that GRK1 substantially suppressed CCl₄-induced LF in mice. Moreover, GRK1 markedly improved malondialdehyde, lipid reactive oxygen species, and liver Fe²⁺ in CCl₄-stimulated mice. This study revealed that GRK1 targets HK2 in HSC-T6 cells to stimulate the ACSL4/LPCAT3/ALOX5 pathway, thereby inducing HSC ferroptosis and alleviating hepatic fibrosis.