Noninvasive Monitoring of Changes in Cerebral Hemodynamics During Prolonged Field Care for Hemorrhagic Shock and Hypoxia-Induced Injuries With Portable Diffuse Optical Sensors.

Introduction: Achieving simultaneous cerebral blood flow (CBF) and oxygenation measures, specifically for point-of-care injury monitoring in prolonged field care, requires the implementation of appropriate methodologies and advanced medical device design, development, and evaluation. The near-infrared spectroscopy (NIRS) method measures the absorbance of light whose attenuation is related to cerebral blood volume and oxygenation. By contrast, diffuse correlation spectroscopy (DCS) allows continuous noninvasive monitoring of microvascular blood flow by directly measuring the degree of light scattering because of red blood cell (RBC) movement in tissue capillaries.

Epidermal Growth Factor Receptor Inhibition Reverses Cellular and Transcriptomic Alterations Induced by Hypoxia in the Neonatal Piglet Brain.

Acute hypoxia (HX) causes extensive cellular damage in the developing human cerebral cortex. We found increased expression of activated-EGFR in affected cortical areas of neonates with HX and investigated its functional role in the piglet, which displays a highly evolved, gyrencephalic brain, with a human-like maturation pattern. In the piglet, HX-induced activation of EGFR and Ca/calmodulin kinase IV (CaMKIV) caused cell death and pathological alterations in neurons and glia.

Noninvasive monitoring of brain edema after hypoxia in newborn piglets.

BackgroundDevelopment of cerebral edema after brain injury carries a high risk for brain damage and death. The present study tests the ability of a noninvasive cerebral edema monitoring system that uses near-infrared spectroscopy (NIRS) with water as the chromophore of interest to detect brain edema following hypoxia.MethodsVentilated piglets were exposed to hypoxia for 1 h, and then returned to normal oxygen levels for 4 h.

Effect of sustained postnatal systemic inflammation on hippocampal volume and function in mice.

Background: Premature infants are at risk for persistent neurodevelopmental impairment. Children born preterm often exhibit reduced hippocampal volumes that correlate with deficits in working memory. Perinatal inflammation is associated with preterm birth and brain abnormalities.

Steroids and injury to the developing brain: net harm or net benefit?

Deleterious effects result from both glucocorticoid insufficiency and excess glucocorticoid tissue exposure in the developing brain. Accumulating evidence suggests a net benefit of postnatal glucocorticoid therapy when administered shortly after the first week of life to premature infants with early and persistent pulmonary dysfunction, particularly in those with evidence of relative adrenal insufficiency. The decision to treat with steroids should ensure maximum respiratory benefit at the lowest possible neurologic risk, while avoiding serious systemic complications.

Maternal glucocorticoid exposure alters tight junction protein expression in the brain of fetal sheep.

We examined the expression of tight junction (TJ) proteins in the cerebral cortex, cerebellum, and spinal cord of fetuses after maternal treatment with single and multiple courses of dexamethasone. Ewes received either single courses of four 6-mg dexamethasone or placebo injections every 12 h for 48 h between 104 and 107 days or the same treatment once a week between 76-78 and 104-107 days of gestation. TJ protein expression was determined by Western immunoblot analysis on tissue harvested at 105-108 days of gestation.

Na+, K+-ATPase activity and subunit isoform protein abundance: effects of antenatal glucocorticoids in the frontal cerebral cortex and renal cortex of ovine fetuses.

We examined the effects of single and multiple maternal glucocorticoid courses on cerebral cortical (CC) and renal cortical (RC) Na(+),K(+)-ATPase activity and protein isoform abundance in fetal sheep. Ewes received four dexamethasone or placebo injections in the single course (SC) groups, and the same treatment once a week for five-weeks in the multiple course (MC) groups. CC Na(+),K(+)-ATPase a(2)-abundance was higher (P<0.

Effects of maternal antenatal glucocorticoid treatment on apoptosis in the ovine fetal cerebral cortex.

We examined the effects of single and multiple maternal glucocorticoid courses on apoptosis in the cerebral cortices of ovine fetuses (CC). Ewes received single dexamethasone or placebo courses at 104-106 or 133-135 days or multiple courses between 76-78 and 104-106 days gestation. In the single-course groups, ewes received four 6 mg dexamethasone or placebo injections every 12 hr for 48 hr.

Effects of maternal treatment with corticosteroids on tight junction protein expression in the cerebral cortex of the ovine fetus with and without exposure to in utero brain ischemia.

Maternal treatment with corticosteroids reduces blood-brain barrier permeability in premature ovine fetuses and the incidence of intraventricular hemorrhage in premature infants. We tested the hypothesis that maternally administered corticosteroids increase the expression of tight junction (TJ) proteins in the cerebral cortex of ovine fetuses with and without exposure to in utero brain ischemia. Fetuses at 80% of gestation were studied 18 h after the last of four 4-6 mg dexamethasone or placebo injections were given over 48 h to ewes.

Aortic dissection in a neonate: case report and review of the literature.

We report a case of aortic dissection causing hypertension in a neonate, which occurred following iatrogenic intimal injury during umbilical arterial cannulation. The intimal flap was diagnosed by color Doppler sonography, and treated by conservative management with complete spontaneous healing of the intimal injury.

Bone mineralization in newborns whose mothers received magnesium sulphate for tocolysis of premature labour.

Prolonged maternal magnesium sulphate infusion therapy for tocolysis of premature labour may result in secondary fetal hypermagnesaemia, which has been associated with bony abnormalities in the newborn. We report on four infants, members of two twin pregnancies, who were exposed to prolonged fetal hypermagnesaemia. Three of the infants, all appropriate for gestational age, showed abnormal radiological findings consisting of abnormal mineralisation of long-bone metaphyses owing to fetal hypermagnesaemia.