Julia Nguyen

TL;DR: It is concluded that intravascular hemolysis in SCD releases heme that activates endothelial TLR4 signaling leading to WPB degranulation, NF-κB activation, and vaso-occlusion, and heme lethality.

TL;DR: It is concluded that transgenic sickle mice are good models to study vascular inflammation and the potential benefit of anti-inflammatory therapies to prevent vaso-occlusion in sickle cell disease.

TL;DR: It is shown that mice expressing HbS exhibit characteristics of pain observed in sickle cell disease patients, and neurochemical changes suggestive of nociceptor and glial activation, and cannabinoids attenuate pain in mice expressing hbS, indicating deep/musculoskeletal and cutaneous hyperalgesia.

TL;DR: It is shown that mast cell activation/degranulation contributes to sickle pain pathophysiology by promoting neurogenic inflammation and nociceptor activation via the release of substance P in the skin and dorsal root ganglion.

TL;DR: MOR may be associated with morphine-induced cancer progression, resulting in shorter survival, and Mast cell activation by morphine may contribute to increased cytokine and SP levels, leading to cancer progression and refractory pain.