Childhood unintentional injury: The impact of family income, education level, occupation status, and other measures of socioeconomic status. A systematic review.

INTRODUCTION: Unintentional injuries represent a substantial public health burden among children and adolescents, and previous evidence suggests that there are disparities in injury by socioeconomic status (SES). This paper reports on a systematic review of literature on injury rates among children and adolescents by measures of SES. METHODS: A systematic literature search was conducted using six electronic databases: MEDLINE, PsycINFO, CINAHL, HealthSTAR, EMBASE, and SportsDiscus. This review considered children ages 19 years and under and publications between 1997 and 2017-representing an update since the last systematic review examined this specific question. Fifty-four articles were summarized based on study and participant descriptions, outcome and exposure, statistical tests used, effect estimates, and overall significance. RESULTS: Most articles addressed risk factors across all injury mechanisms; however, some focused particularly on burns/scalds, road traffic injuries, falls/drowning cases, and playground/sports injuries. Other studies reported on specific injury types including traumatic dental injuries, traumatic brain injuries, and fractures. The studies were of moderate quality, with a median of 15.5 (95% confidence interval [CI]: 15.34 to 15.66) out of 19. Thirty-two studies found an inverse association between SES and childhood unintentional injury, three found a positive association while twenty were not significant or failed to report effect measures. CONCLUSION: Given the variability in definition of the exposure (SES) and outcome (injury), the results of this review were mixed; however, the majority of studies supported a relationship between low SES and increased injury risk. Public health practice must consider SES, and other measures of health equity, in childhood injury prevention programming, and policy.

Learning and memory function preserved by delayed A1 adenosine receptor agonist treatment following soman intoxication in rats and a humanized esterase mouse model.

Exposure to organophosphorus compounds, such as soman (GD), cause widespread toxic effects, sustained status epilepticus, neuropathology, and death. The A1 adenosine receptor agonist N-bicyclo-(2.2.1)-hept-2-yl-5'-chloro-5'-deoxyadenosine (ENBA), when given 1 min after GD exposure, provides neuroprotection and prevents behavioral impairments. Here, we tested the ability of ENBA at delayed treatment times to improve behavioral outcomes via a two-way active avoidance task in two male animal models, each consisting of saline and GD exposure groups. In a rat model, animals received medical treatments (atropine sulfate [A], 2-PAM [P], and midazolam [MDZ]) or AP + MDZ + ENBA at 15 or 30 min after seizure onset and were subjected to behavioral testing for up to 14 days. In a human acetylcholinesterase knock-in serum carboxylesterase knock-out mouse model, animals received AP, AP + MDZ, AP + ENBA, or AP + MDZ + ENBA at 15 min post seizure onset and were subjected to the behavioral task on days 7 and 14. In rats, the GD/AP + MDZ + ENBA group recovered to saline-exposed avoidance levels while the GD/AP + MDZ group did not. In mice, in comparison with GD/AP + MDZ group, the GD/AP + MDZ + ENBA showed decreases in escape latency, response latency, and pre-session crossings, as well as increases in avoidances. In both models, only ENBA-treated groups showed control level inter-trial interval crossings by day 14. Our findings suggest that ENBA, alone and as an adjunct to medical treatments, can improve behavioral and cognitive outcomes when given at delayed time points after GD intoxication.