Exposure to social stress is an important risk factor for comorbid affective disorders and problem alcohol use. To better understand mechanisms involved in social stress-induced affective disorder and alcohol use co-morbidity, we studied the effects of adolescent social stress on anxiety- and depression-like behaviors and binge-like ethanol consumption. Male and female C57BL/6J mice were exposed to chronic variable social stress (CVSS) or control conditions throughout adolescence (postnatal days, PND, 25–59) and then tested for anxiety-like behavior in the elevated plus maze and a novel open field environment, or depression-like behavior using the forced swim test on PND 64–66. Mice were then tested for binge-like ethanol consumption using the Drinking-in-the-Dark model. Male and female mice exposed to adolescent CVSS had increased adult anxiety-like behavior and increased locomotor adaptation to a novel environment. Further, CVSS mice consumed significantly more ethanol, but not saccharin, than controls. Despite group differences in both anxiety-like behavior and ethanol consumption, there was no relationship between these outcomes within individual mice. These data suggest that exposure to adolescent social stress is an important risk factor for later alcohol use and affective behaviors, but that social stress does not necessarily dictate co-morbidity of these outcomes.

Spatial abilities allow animals to retain and cognitively manipulate information about their spatial environment and are dependent upon neural structures that mature during adolescence. Exposure to stress in adolescence is thought to disrupt neural maturation, possibly compromising cognitive processes later in life. We examined whether exposure to chronic unpredictable stress in adolescence affects spatial ability in late adulthood. We evaluated spatial learning, reference and working memory, as well as long-term retention of visuospatial cues using a radial arm water maze. We found that stress in adolescence decreased the rate of improvement in spatial learning in adulthood. However, we found no overall performance impairments in adult reference memory, working memory, or retention caused by adolescent-stress. Together, these findings suggest that adolescent-stress may alter the strategy used to solve spatial challenges, resulting in performance that is more consistent but is not refined by incorporating available spatial information. Interestingly, we also found that adolescent-stressed rats showed a shorter latency to begin the water maze task when re-exposed to the maze after an overnight delay compared with control rats. This suggests that adolescent exposure to reoccurring stressors may prepare animals for subsequent reoccurring challenges. Overall, our results show that stress in adolescence does not affect all cognitive processes, but may affect cognition in a context-dependent manner.

Neurosurgery has benefited from innovations as a result of military conflict. The volume and complexity of injuries sustained on the battlefield require medical teams to triage, innovate, and practice beyond their capabilities in order to treat wartime injuries. The neurosurgeons who practiced in the Pacific Command (PACOM) during World War II, the Korean War, and the War in Vietnam built upon field operating room knowledge and influenced the logistics of treating battle-injured patients in far-forward environments. Modern-day battles are held on new terrain, and the military neurosurgeon must adapt. War in the PACOM uniquely presented significant obstacles due to geographic isolation, ultimately accelerating the growth and adaptability of military neurosurgery and medical evacuation. The advancements in infrastructure and resource mobilization made during PACOM conflicts continue to inform modern-day practices and provide insight for future conflicts. In this historical article, the authors review the development and evolution of neurosurgical care, forward surgical teams, and mobile field hospitals with surgical capabilities through US conflicts in the PACOM.

Exposure to explosions often causes morbidity as waves of over‐pressure and under‐pressure shear interstitial tissue and cause traumatic damage including severe hemorrhage. Respiratory tissues are most at risk due to their proximity to free gas volumes that rapidly and severely contract or expand during blast‐induced pressure changes. Unfortunately, we have no medical interventions that can prevent or limit pressure‐induced blast damage to tissues. Perhaps such protective technology can be modeled from the respiratory tissue of diving animals that are naturally adapted for pressure changes. Our goal is to characterize any respiratory injuries resulting from postmortem blast pressure exposures. 5 species of freshly dead dolphins (n= 8) and porpoises (n =6) were obtained from naturally occurring strandings were artificially exposed to blast pressures postmortem. Gross observations were made during a necropsy, and respiratory tract tissues were then harvested and processed for histological examination. Blast pressure exposure levels were not revealed to enable unbiased observations. Results indicate that many specimens show dark reddish discoloration of variable intensities that may be evidence of blast‐induced trauma. Discoloration was found in the lungs (dark, striped pattern correlating with intercostal spaces between ribs), larynx (above and below palatopharyngeal sphincter), trachea (uniform throughout lumen), and nasal region (visualized only in areas of sloughed lining). Gas containing tissues may exhibit damage due to dramatic compression/expansion to accommodate changing gas volumes. Abrupt edges to discoloration patches indicate protection, possibly conferred by contact with adjacent tissues. Discoloration patterns are consistent in location but have variable intensity, perhaps reflecting different degrees of exposure. Specimens exhibited variable levels of damage to the same organs, perhaps indicating a correlation with received blast pressures. These differences may also indicate a level of resistance to blast damage of tissues that have mechanisms to compensate for pressure changes. Tissue compensation is likely limited to pressure exposures that correspond to naturally occurring diving pressures. Pressures that exceed these levels are presumed to overwhelm tissue compensatory mechanisms. This information may be useful in setting critical exposure limits to prevent harm to odontocetes in the vicinity of a blast event. Further, It is hoped that a discovery of pressure mitigating structures in dolphins can inspire the design of new protective devices for use by people exposed to blast forces.

No abstract