Nucleus pulposus cell-mimicking nanoparticles for cell-specific HIF1A editing to modulate SASP-mediated disc inflammation via autophagy activation.

Traditional methods of plasmid delivery, including viral vectors, lipofection, and electroporation, are widely used for gene editing but have limitations, such as cellular toxicity, limited transfection efficiency in primary cells, and nonspecific side effects. Here, we report the development of nucleus pulposus cell (NPC)-mimicking nanoparticles (HIF1A@NNP) with an NPC membrane as the shell and pcDNA3.1-rHIF1A encapsulated in the core via extrusion.

CUR-PDT induces ferroptosis of RA-FLS via the Nrf2/xCT/GPX4 pathway to inhibit proliferation in rheumatoid arthritis.

Objective: Ferroptosis is a non-apoptotic cell death mechanism driven by reactive oxygen species (ROS) and iron. Its significance in inflammatory arthritis is well-established, but its role in rheumatoid arthritis (RA) remains uncertain. This study aimed to clarify the mechanisms through which curcumin-mediated photodynamic therapy (CUR-PDT) triggers ferroptosis in RA fibroblast-like synoviocytes (FLSs).

The value of targeted CXCR4 F-AlF-NOTA-pentixafor PET/CT for subtyping primary aldosteronism.

Objective: The study aimed to investigate the diagnostic value of F-AlF-NOTA-Pentixafor PET/CT in subtyping primary aldosteronism (PA).

Methods: This study enrolled 88 patients with PA or nonfunctional adenoma (NFA) for F-Pentixafor PET/CT scan. Of these, 20 patients underwent adrenal venous sampling (AVS), and 65 underwent adrenalectomy and postoperative follow-up.

The structural basis of the G protein-coupled receptor and ion channel axis.

Sensory neurons play an essential role in recognizing and responding to detrimental, irritating, and inflammatory stimuli from our surroundings, such as pain, itch, cough, and neurogenic inflammation. The transduction of these physiological signals is chiefly mediated by G protein-coupled receptors (GPCRs) and ion channels. The binding of ligands to GPCRs triggers a signaling cascade, recruiting G proteins or β-arrestins, which subsequently interact with ion channels (e.

Successful treatment with refractory myasthenia gravis that developed after allogeneic hematopoietic stem cell transplantation: two case reports.

Introduction: Myasthenia gravis (MG) is an autoimmune disorder caused by autoantibodies that target the neuromuscular junction, leading to muscle weakness and fatigability. Diagnosis is based on clinical presentation, confirmation of the presence of AChR-Ab, characteristic electromyography findings, and clinical improvement after administration of acetylcholinesterase inhibitors.MG is often associated with thymoma and other autoimmune diseases, but it is rare following allo-HSCT.