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We present a 6-month-old boy with failure to thrive who was referred to the emergency department by his primary care doctor for leukocytosis and was found to be hypoxic with diffuse infiltrates on chest radiograph. Our patient was admitted and eventually diagnosed with Pneumocystis jirovecii
White matter of the brain and spinal cord is susceptible to anoxia, ischemia, trauma and autoimmune attack. Irreversible injury to this tissue can have serious consequences for the overall function of the CNS through disruption of signal transmission. Like neurons, central myelinated axons are
Effects of acute hypobaric hypoxia (1:30 hrs. at 190-200 mm Hg) on the autolytic changes in lipids of the gray and white substance of the brain were evaluated in an experiment with white rats. Total lipids (TL) in the autolysing segments of the brain of rats sacrificed immediately following the end
Axon function in the CNS has been reported to fail rapidly during anoxia, implying that there is no anaerobic capacity. This phenomenon was reassessed in rodent white matter using mouse or rat optic nerve. Axon function was semiquantitatively measured as area under the compound action potential.
We studied the effects of GABA on anoxia-induced injury in CNS white matter using optic nerves exposed to 60 min of anoxia. Injury was assessed by recording pre- and postanoxic compound action potentials (CAPs). GABA (1 microM) significantly increased postanoxic CAP recovery when applied 60 min
Successful axon function is vital to the overall performance of the central nervous system (CNS). White matter (WM) axons are dependent on constant supply of oxygen and glucose to transmit signals with high fidelity. The optic nerve is a pure WM tract composed of completely myelinated axons while
In 128 mature white rats (males) after adaptation for 1--45 days, to 4,000 m altitude (North-West Pamir, Glasier Fortambek), weight characteristics of the heart were estimated (capillary diameters, their network density per 1 mm2 of the section summing length and volume in 1 mm3 of the right and
Hypoxemia immediately following traumatic brain injury (TBI) has been observed to exacerbate injury. However, it remains unclear whether delayed hypoxemia beyond the immediate postinjury period influences white matter injury. In a retrospective clinical cohort of children aged 4-16 years admitted
Obstructive sleep apnoea is a highly prevalent disease characterised by repetitive upper airway collapse during sleep leading to intermittent hypoxia. Cardiometabolic complications of sleep apnoea have been mostly attributed to intermittent hypoxia. These consequences could be mediated through
Despite the advances in neonatal intensive care, the preterm brain remains vulnerable to white matter injury (WMI) and disruption of normal brain development (i.e., dysmaturation). Compared to severe cystic WMI encountered in the past decades, contemporary cohorts of preterm neonates experience
Irreversible anoxic injury of axons in the rat optic nerve requires the presence of extracellular Ca2+. To test the hypothesis that Ca2+ enters an intracellular compartment during anoxia we monitored [Ca2+]0 in this CNS white matter tract using ion-sensitive microelectrodes. Periods of anoxia