Objective-Develop a clinically relevant model of pediatric asphyxial cardiopulmonary arrest in rats. Design-Prospective interventional study. Setting-University research laboratory.Subjects-Post-natal day (PND) 16-18 rats.Interventions-Anesthetized rats were endotracheally intubated and mechanically ventilated, and vascular catheters were inserted. Vecuronium was administered and the ventilator was disconnected from the rats for 8 min, whereupon rats were resuscitated with epinephrine, sodium bicarbonate, and chest compressions until spontaneous circulation returned. Shams underwent all procedures except asphyxia.Measurements and Main Results-Asphyxial arrest typically occurred by 1 min after the ventilator was disconnected. Return of spontaneous circulation typically occurred <30 sec after resuscitation. An isoelectric electroencephalograph was observed for 30 min after asphyxia and rats remained comatose for 12-24 h. Survival rate in rats after asphyxia was 75%. Motor function measured using beam balance and inclined plane tests was impaired on d 1 and 2, but recovered by d 3, in rats after asphyxia vs. sham injury (n=9/group; P<0.05). Spatial memory acquisition measured using the Morris-water maze on d 7-14 and 28-35 was also impaired in rats after asphyxia vs. sham injury (total latency 379±28 vs. 501±40 sec, respectfully; n=9/group; P<0.05). CA1 hippocampal neuron survival after asphyxia was 39-43% (n=9/group; P<0.001 vs. sham). DNA fragmentation was detected in CA1 hippocampal neurons bilaterally in separate rats on d 3-7 after asphyxia (n=3-4/group). Neurodegeneration detected using Fluorojade-B was seen in bilateral CA1 hippocampi and layer III cortical neurons 3-7 d after asphyxia, with persistent neurodegeneration in CA1 hippocampus detected up to 5 wks after asphyxia. Evidence of DNA or cellular injury was not detected in sham rats.

Heme oxygenase 1 (HO-1) is an enzyme important in the catabolism of heme that is induced under conditions of oxidative stress. HO-1 degradation of heme yields biliverdin, bilirubin, carbon monoxide and iron. HO-1 is thought to serve a protective antioxidant function, and upregulation of HO-1 has been demonstrated in experimental models of neurodegeneration, subarachnoid hemorrhage, cerebral ischemia and traumatic brain injury (TBI). We measured HO-1 concentration in cerebral spinal fluid samples from 48 infants and children following TBI and 7 control patients by ELISA. Increased HO-1 was seen in TBI versus control patients – mean 2.75 ± 0.63, peak 4.17 ± 0.96 ng/ml versus control (<0.078 ng/ml, not detectable) (p< 0.001). Increased HO-1 concentration was associated with increased injury severity and unfavorable neurological outcome (both p < 0.05). Increased HO-1 concentration was independently associated with younger age; however, statistical analysis could not rule out the possibility that the effect of age was related to inflicted TBI from child abuse. HO-1 increases after TBI and appears to be more prominent in infants compared with older children after injury.

Beliefs in scientifically unsubstantiated ideas were investigated with a study that contrasted college students' attitudes toward paranormal phenomena before and after exposure to skeptical arguments concerning these events. Specifically, students enrolled in 2 sections of a psychological statistics course were exposed to illustrations of statistical concepts that were either paranormal-themed or not, with a 3rd group of participants completing a class that focused on the critical analysis of believer-and skeptic-based ideas surrounding paranormal phenomena. Results revealed that skepticism increased, over time, only when direct exposure to paranormal phenomena was included in one's course work. Results are discussed in terms of the educational and societal implications for encouraging skepticism of scientifically questionable claims.