Gene expression analysis reveals a novel, integrated molecular mechanism for much of the pathogenesis of COVID-19 that provides therapeutic intervention points that can be addressed with existing approved pharmaceuticals.
The pain mediator bradykinin was found to sensitize spinal motoneurons by a direct postsynaptic action, questioning the role of motoneurons in the assessment of hyperalgesia since the withdrawal motor reflex is commonly used as a surrogate pain model.
Transcription changes in cells taken from bronchoalveolar fluid of COVID-19 patients indicate severe disruption of coagulation and fibrinolytic pathways in the lung and suggest similar processes in other organs.
Inflammatory pain, previously thought to result from increased activity in "pain" neurons, may in fact be due to wholesale changes in afferent output that includes increased and decreased activity that the brain interprets as pain.
The activation and membrane localization of the broadly-tuned noxious chemosensory cation channel TRPA1 are regulated by direct interactions with cholesterol via CRAC motifs in transmembane segments 2 and 4.
Pathological vessel leakage in mouse retinopathy models depends on VE-cadherin Y685 phosphorylation status, which in turn is regulated by a signaling cascade originating with VEGFR2 Y949 phosphorylation.