No abstract

Aim Improved survival after cardiac arrest has placed greater emphasis on neurologic resuscitation. The purpose of this pilot study was to evaluate the relationship between cerebrovascular autoregulation and neurologic outcomes after pediatric cardiac arrest. Methods Children resuscitated from cardiac arrest had autoregulation monitoring during the first 72 hours after return of circulation with an index derived from near-infrared spectroscopy in a pilot study. The range of mean arterial blood pressure (MAP) with optimal vasoreactivity (MAPOPT) was identified. The area under the curve (AUC) of the time spent with MAP below MAPOPT and MAP deviation below MAPOPT was calculated. Neurologic outcome measures included placement of a new tracheostomy or gastrostomy, death from a primary neurologic etiology (brain death or withdrawal of support for neurologic futility), and change in the Pediatric Cerebral Performance Category score (ΔPCPC). Results Thirty-six children were monitored. Among children who did not require extracorporeal membrane oxygenation (ECMO), children who received a tracheostomy/gastrostomy had greater AUC during the second 24 hours after resuscitation than those who did not (P=0.04; n=19). Children without ECMO who died from a neurologic etiology had greater AUC during the first 48 hours than did those who lived or died from cardiovascular failure (P=0.04; n=19). AUC below MAPOPT was not associated with ΔPCPC when children with or without ECMO were analyzed separately. Conclusions Deviation from the blood pressure with optimal autoregulatory vasoreactivity may predict poor neurologic outcomes after pediatric cardiac arrest. This experimental autoregulation monitoring technique may help individualize blood pressure management goals after resuscitation.

In the world of artificial intelligence (AI), there is an endless stream of developing technologies which will soon be at the forefront of medicine and dermatology. In the field of cosmetic dermatology, several promising modalities involving AI are in development. The development of virtual planning for aesthetic treatments such as injectable dermal fillers and neuromodulators, and the use of robotics in the automation of laser treatment may soon revolutionize a dermatologist's ability to optimize treatments and aesthetic outcomes. In addition, these technologies will empower patients to choose customized skin and hair care products based on analysis of their personal features. Artificial intelligence is a method of making a computer, software, or robot think intelligently. It involves creating algorithms to classify, analyze, and make predictions from data. AI has become increasingly complex, using artificial neural networks, machine learning, and deep learning to uncover complex associations. Artificial neural networks (ANN) are structured to mimic the signaling that takes place in the human brain. The networks are composed of multiple nodes

Pharmacologic inactivation or genetic deletion of adenosine A 2A receptors protects ischemic neurons in adult animals, but studies in neonatal hypoxia-ischemia (H-I) are inconclusive. The present study in neonatal piglets examined the hypothesis that A 2A receptor signaling after reoxygenation from global H-I contributes to injury in highly vulnerable striatal neurons where A 2A receptors are enriched. A 2A receptor immunoreactivity was detected in striatopallidal neurons. In nonischemic piglets, direct infusion of the selective A 2A receptor agonist CGS 21680 through microdialysis probes into putamen increased phosphorylation of N-methyl-D-aspartic acid (NMDA) receptor NR1 subunit and Na þ ,K þ -ATPase selectively at protein kinase A (PKA)-sensitive sites. In ischemic piglets, posttreatment with SCH 58261, a selective A 2A receptor antagonist, improved early neurologic recovery and preferentially protected striatopallidal neurons. SCH 58261 selectively inhibited the ischemia-induced phosphorylation of NR1, Na þ ,K þ -ATPase, and cAMP-regulated phosphoprotein 32 KDa (DARPP32) at PKA-sensitive sites at 3 hours of recovery and improved Na þ ,K þ -ATPase activity. SCH 58261 also suppressed ischemia-induced protein nitration and oxidation. Thus, A 2A receptor activation during reoxygenation contributes to the loss of a subpopulation of neonatal putamen neurons after H-I. Its toxic signaling may be related to DARPP32-dependent phosphorylation of PKA-sensitive sites on NR1 and Na þ ,K þ -ATPase, thereby augmenting excitotoxicity-induced oxidative stress after reoxygenation.