Recovering palladium and gold by peroxydisulfate-based advanced oxidation process.

Palladium (Pd) and gold (Au) are the most often used precious metals (PMs) in industrial catalysis and electronics. Green recycling of Pd and Au is crucial and difficult. Here, we report a peroxydisulfate (PDS)-based advanced oxidation process (AOPs) for selectively recovering Pd and Au from spent catalysts. The PDS/NaCl photochemical system achieves complete dissolution of Pd and Au. By introducing Fe(II), the PDS/FeCl2·4H2O solution functioned as Fenton-like system, enhancing the leaching efficiency without xenon (Xe) lamp irradiation. Electron paramagnetic resonance (EPR), 18O isotope tracing experiments, and density functional theory calculations revealed that the reactive oxidation species of SO4·-, ·OH, and Fe(IV)═O were responsible for the oxidative dissolution process. Lixiviant leaching and one-step electrodeposition recovered high-purity Pd and Au. Strong acids, poisonous cyanide, and volatile organic solvents were not used during the whole recovery, which enables an efficient and sustainable precious metal recovery approach and encourage AOP technology for secondary resource recycling.

Cuproptosis-associated ncRNAs predict breast cancer subtypes.

BACKGROUND: Cuproptosis is a novel copper-dependent mode of cell death that has recently been discovered. The relationship between Cuproptosis-related ncRNAs and breast cancer subtypes, however, remains to be studied. METHODS: The aim of this study was to construct a breast cancer subtype prediction model associated with Cuproptosis. This model could be used to determine the subtype of breast cancer patients. To achieve this aim, 21 Cuproptosis-related genes were obtained from published articles and correlation analysis was performed with ncRNAs differentially expressed in breast cancer. Random forest algorithms were subsequently utilized to select important ncRNAs and build breast cancer subtype prediction models. RESULTS: A total of 94 ncRNAs significantly associated with Cuproptosis were obtained and the top five essential features were chosen to build a predictive model. These five biomarkers were differentially expressed in the five breast cancer subtypes and were closely associated with immune infiltration, RNA modification, and angiogenesis. CONCLUSION: The random forest model constructed based on Cuproptosis-related ncRNAs was able to accurately predict breast cancer subtypes, providing a new direction for the study of clinical therapeutic targets.

Exploring the multifaceted role of GCN1: Implications in cellular responses and disease pathogenesis.

GCN1 is a highly conserved protein present widely across eukaryotes. As an upstream activator of protein kinase GCN2, GCN1 plays a pivotal role in integrated stress responses, such as amino acid starvation and oxidative stress. Through interaction with GCN2, GCN1 facilitates the activation of GCN2, thus initiating downstream signaling cascades in response to cellular stressors. In these contexts, the activation of GCN2 necessitates the presence and action of GCN1. Notably, GCN1 also operates as a ribosome collision sensor, contributing significantly to the translation quality control pathway. These discoveries offer valuable insights into cellular responses to internal stresses, vital for maintaining cellular homeostasis. Additionally, GCN1 exhibits the ability to regulate the cell cycle and suppress inflammation, among other processes, independently of GCN2. Our review outlines the structural characteristics and biological functions of GCN1, shedding light on its significant involvement in the onset and progression of various cancer and non-cancer diseases. Our work underscores the role of GCN1 in the context of drug therapeutic effects, hinting at its potential as a promising drug target. Furthermore, our work delves deep into the functional mechanisms of GCN1, promising innovative avenues for the diagnosis and treatment of diseases in the future. The exploration of GCN1's multifaceted roles not only enhances our understanding of its mechanisms but also paves the way for novel therapeutic interventions. The ongoing quest to unveil additional functions of GCN1 holds the promise of further enriching our comprehension of its mode of action.