Traumatic brain injury causes early aggregation of beta-amyloid peptides and NOTCH3 reduction in vascular smooth muscle cells of leptomeningeal arteries.

Traumatic brain injury (TBI) often leads to impaired regulation of cerebral blood flow, which may be caused by pathological changes of the vascular smooth muscle cells (VSMCs) in the arterial wall. Moreover, these cerebrovascular changes may contribute to the development of various neurodegenerative disorders such as Alzheimer's-like pathologies that include amyloid beta aggregation. Despite its importance, the pathophysiological mechanisms responsible for VSMC dysfunction after TBI have rarely been evaluated.

Long-term administration of paroxetine increases cortical EEG beta and gamma band activities in healthy awake rats.

Understanding the electrophysiological properties of antidepressant medications is important to resolve the response heterogeneity of these drugs in clinical practice. Administration of paroxetine, a selective serotonin reuptake inhibitor, has been shown to increase serotonin levels that affect cortical activities in healthy subjects. However, the extent to which cortical oscillations can be altered by ongoing administration of paroxetine is not known.

A Classification for Gastric Outlet Obstruction in Childhood: Extending Beyond Infantile Hypertrophic Pyloric Stenosis.

Background/aims:  Gastric outlet obstruction (GOO) is a rare condition in childhood, with the exception of infantile hypertrophic pyloric stenosis (IHPS). However, no classification exists from a pediatric gastroenterologist's perspective.

Materials And Methods:  The patients with a diagnosis of GOO between 2009 and 2020 were reviewed retrospectively.

Neutralization of Interleukin 1-beta is associated with preservation of thalamic capillaries after experimental traumatic brain injury.

Introduction: Traumatic brain injury to thalamo-cortical pathways is associated with posttraumatic morbidity. Diffuse mechanical forces to white matter tracts and deep grey matter regions induce an inflammatory response and vascular damage resulting in progressive neurodegeneration. Pro-inflammatory cytokines, including interleukin-1β (IL-1β), may contribute to the link between inflammation and the injured capillary network after TBI.

Impaired oligodendrogenesis in the white matter of aged mice following diffuse traumatic brain injury.

Senescence is a negative prognostic factor for outcome and recovery following traumatic brain injury (TBI). TBI-induced white matter injury may be partially due to oligodendrocyte demise. We hypothesized that the regenerative capacity of oligodendrocyte precursor cells (OPCs) declines with age.