Molecularly Imprinted Magnetic Fluorescent Carbon Dots Using Polydopamine with Dual Functionality as a Monomer and Cross-Linking Agent for Selective Mefenamic Acid Detection.

This research presents a sustainable and efficient method for synthesizing polydopamine imprinted magnetic carbon dots (MCDs@PI), which were synthesized from wheat straw via hydrothermal carbonization. The carbon dots were magnetically functionalized using iron salts and coated with a polydopamine layer, where dopamine acted as a functional monomer as well as a cross-linker. The sensor demonstrated high selectivity and sensitivity for mefenamic acid, achieving a limit of detection of 2.

Rab4A-directed endosome traffic shapes pro-inflammatory mitochondrial metabolism in T cells via mitophagy, CD98 expression, and kynurenine-sensitive mTOR activation.

Activation of the mechanistic target of rapamycin (mTOR) is a key metabolic checkpoint of pro-inflammatory T-cell development that contributes to the pathogenesis of autoimmune diseases, such as systemic lupus erythematosus (SLE), however, the underlying mechanisms remain poorly understood. Here, we identify a functional role for Rab4A-directed endosome traffic in CD98 receptor recycling, mTOR activation, and accumulation of mitochondria that connect metabolic pathways with immune cell lineage development and lupus pathogenesis. Based on integrated analyses of gene expression, receptor traffic, and stable isotope tracing of metabolic pathways, constitutively active Rab4A exerts cell type-specific control over metabolic networks, dominantly impacting CD98-dependent kynurenine production, mTOR activation, mitochondrial electron transport and flux through the tricarboxylic acid cycle and thus expands CD4 and CD3CD4CD8 double-negative T cells over CD8 T cells, enhancing B cell activation, plasma cell development, antinuclear and antiphospholipid autoantibody production, and glomerulonephritis in lupus-prone mice.

Transition from TNF-Induced Inflammation to Death Signaling.

Tumor necrosis factor (TNF) plays a key role in inflammatory responses and in various cellular events such as apoptosis and necroptosis. The interaction of TNF with its receptor, TNFR1, drives the initiation of complex molecular pathways leading to inflammation and cell death. RARγ is released from the nucleus to orchestrate the formation of the cytosolic death complexes, and it is cytosolic RARγ that plays a pivotal role in switching TNF-induced inflammatory responses to RIPK1-initiated cell death.