Astrocytic responses to high glucose impair barrier formation in cerebral microvessel endothelial cells.

Hyperglycemic conditions are prodromal to blood-brain barrier (BBB) impairment. The BBB comprises cerebral microvessel endothelial cells (CMECs) that are surrounded by astrocytic foot processes. Astrocytes express high levels of gap junction connexin 43 (Cx43), which play an important role in autocrine and paracrine signaling interactions that mediate gliovascular cross talk through secreted products.

Effect of high glucose condition on glucose metabolism in primary astrocytes.

In the brain, glucose enters astrocytes through glucose transporter (GLUT1) and either enters glycolysis or the glycogen shunt. Astrocytes meet the energy needs of neurons by building up and breaking down their glycogen supply. High glucose exposure causes astrocyte dysregulation, but its effects on glucose metabolism are relatively unknown.

High glucose conditioned neonatal astrocytes results in impaired mitogenic activity in cerebral microvessel endothelial cells in co-culture.

Angiogenesis is a highly complex and coordinated process in the brain. Under normal conditions, it is a vital process in growth and development, but under adverse conditions such as diabetes mellitus, it can lead to severe pathology. Astrocytes are a key constituent of the neurovascular unit and contribute to cerebral function, not only bridging the gap between metabolic supplies from blood vessels to neurons, but also regulating angiogenesis.

Gastroschisis Complicated by Septo-Optic Dysplasia: Two Distinct Anomalies with a Common Origin.

Introduction Gastroschisis is considered to be an isolated abdominal wall defect that is infrequently associated with other anomalies. Case This case describes an infant with gastroschisis who developed refractory shock after an uncomplicated surgery for bowel atresia. He was found to have adrenal insufficiency secondary to septo-optic dysplasia with panhypopituitarism.