RESUMO
Spontaneous neuronal network activity is essential in development of central and peripheral circuits, yet whether this is a feature of enteric nervous system development has yet to be established. Using ex vivo gastrointestinal (GI) motility assays with unbiased computational analyses, we identify a previously unknown pattern of spontaneous neurogenic GI motility. We further show that this motility is driven by cholinergic signaling, which may inform GI pharmacology for preterm patients.
RESUMO
During a traumatic brain injury (TBI), there is an injection of glial fibrillary acidic protein (GFAP) from the brain into the bloodstream through a lesion in the blood-brain barrier (BBB). In the blood, a bio controller responds by up-regulating Immunoglobulin G (IgG) production into the bloodstream to remove the excess protein. Here, we model the concentrations over time of GFAP and IgG in the bloodstream following a mild TBI. We apply these dynamics to repeated traumas that aggravate the recovery process, as well as increasing the severity of injury. Both show substantially elevated and prolonged GFAP levels. This research and model is clinically relevant in that it could lead to the analyzation of GFAP levels in the brain through methods as simple as a blood draw. This information can be used to predict the extent of brain lesions as well as help understand the recovery process that the brain takes when having undergone a TBI.