A prediction model of military combat and training exposures on VA service-connected disability: a CENC study.

Background: Research has shown that number of and blast-related Traumatic Brain Injuries (TBI) are associated with higher levels of service-connected disability (SCD) among US veterans. This study builds and tests a prediction model of SCD based on combat and training exposures experienced during active military service.Methods: Based on 492 US service member and veteran data collected at four Department of Veterans Affairs (VA) sites, traditional and Machine Learning algorithms were used to identify a best set of predictors and model type for predicting %SCD ≥50, the cut-point that allows for veteran access to 0% co-pay for VA health-care services.Results: The final model of predicting %SCD ≥50 in veterans revealed that the best blast/injury exposure-related predictors while deployed or non-deployed were: 1) number of controlled detonations experienced, 2) total number of blast exposures (including controlled and uncontrolled), and 3) the total number of uncontrolled blast and impact exposures.Conclusions and Relevance: We found that the highest blast/injury exposure predictor of %SCD ≥50 was number of controlled detonations, followed by total blasts, controlled or uncontrolled, and occurring in deployment or non-deployment settings. Further research confirming repetitive controlled blast exposure as a mechanism of chronic brain insult should be considered.

Fetal alcohol exposure blocks full masculinization of the dorsolateral nucleus in rat spinal cord.

Male rats prenatally exposed to a combination of stress and ethanol show severely impaired ejaculatory patterns. This study examined two sexually dimorphic nuclei in the lumbar spinal cord implicated in the control of male copulatory reflexes in rats whose mothers were exposed to alcohol, to stress, or to both treatments during pregnancy. Alcohol exposure led to a marked decrease (22%) in the number of motor neurons in the dorsolateral nucleus (DLN) of the adult male offspring, but no significant change in cell count was detectable in the sexually dimorphic nucleus of the bulbocavernosus (SNB). The combination of alcohol and stress did not enhance the effect on the DLN above that produced by alcohol alone. Somal sizes in the DLN and SNB were not altered by any of the treatment conditions. Alcohol exposure probably leads to incomplete masculinization of the DLN in male rats by decreasing testicular steroidogenesis during the fetal stage(s) when sexual differentiation is ongoing in that CNS structure.