Memory Window Ratio Enhancement of p‑Type WSe₂ Memtransistors Using Dielectric GeSe₂ Nanosheets with Asymmetric Interfaces for Neuromorphic Computing

The emergence of 2D wide-bandgap semiconductor (WBGS) GeSe2 as charge-trapping dielectrics has helped realize superior devices by using an extremely simple device setup. However, the controllability of deep-gap-state defects in 2D GeSe2 poses a challenge due to the vulnerability and susceptibility of charge-trapping centers, resulting in various problems, i.e., small memory window and poor device durability during programming. Herein, we deliberately perform asymmetric interfacial oxidation to reinforce the memory performance based on the WSe2/Janus-GeSe2 van der Waals heterostructure, which exhibits a giant memory window ratio of 88.5% (70.8 V at ±40 V gate sweep range), high-room-temperature hole mobility of 15 cm2 V–1 s–1, and low nonlinearity factor close to 0 with regard to synaptic weight update characteristics. The information storage performance is excellent, owing to the interface rendered by asymmetric oxidation in the GeSe2 layer, providing an effective charge-trapping layer and atomically flat surface to enhance the mobility of the WSe2 channel. The controllable strategy helps to derive a simple design principle to realize high-performance 2D WBGS GeSe2-based memory and electrical synaptic devices with complex neural functions

ALOX5 deficiency contributes to bladder cancer progression by mediating ferroptosis escape

Abstract Ferroptosis is an iron-dependent form of regulated cell death driven by the lethal lipid peroxides. Previous studies have demonstrated that inducing ferroptosis holds great potential in cancer therapy, especially for patients with traditional therapy failure. However, cancer cells can acquire ferroptosis evasion during progression. To date, the therapeutic potential of inducing ferroptosis in bladder cancer (BCa) remains unclear, and whether a ferroptosis escape mechanism exists in BCa needs further investigation. This study verified that low pathological stage BCa cells were highly sensitive to RSL3-induced ferroptosis, whereas high pathological stage BCa cells exhibited obviously ferroptosis resistance. RNA-seq, RNAi-mediated loss-of-function, and CRISPR/Cas9 experiments demonstrated that ALOX5 deficiency was the crucial factor of BCa resistance to ferroptosis in vitro and in vivo. Mechanistically, we found that ALOX5 deficiency was regulated by EGR1 at the transcriptional level. Clinically, ALOX5 expression was decreased in BCa tissues, and its low expression was associated with poor survival. Collectively, this study uncovers a novel mechanism for BCa ferroptosis escape and proposes that ALOX5 may be a valuable therapeutic target and prognostic biomarker in BCa treatment