The “cushion effect” revisited:

Background: It is known the pattern and severity of injuries sustained during a motor vehicle accident depend on many variables. An interesting avenue for research is obesity as a positive or negative modifier for injury distribution patterns in MVA. We hypothesize that body mass index (BMI) will influence MVC related injury patterns. Methods: We queried STRAC data for DHR - Edinburg for the years 2014 to 2018 using CPT codes for MVC/MVA, IS \u3e 8, age 15 - 64. Interactions between injury location, BMI, seatbelt and gender were analyzed. Results: We had 191 detailed crashes, we found increasing age to be protective for abdomen and pelvis (OR .94), increasing BMI to be predisposing for extremity injuries (OR 1.06) and increasing BMI and female gender together to be protecting for head and neck injury (OR .98). Patient without abdominal injuries were younger with lower BMI. However sample size small (46). Conclusion: BMI seems to have an exacerbating effect on extremity injuries and a protective effect for head and neck injuries driven predominantly by females. We believe this likely due to increase in momentum effect of each appendage and a decrease in torque of neck. Age seems to be a protective and we believe this is primarily due to hormonal deposition of adipose tissue. Overall it remains important to maintain a high index of suspicion when dealing with MVC triage patients and treat each individually

INFLUENCE OF BIOLOGICAL SEX ON SOCIAL BEHAVIOR, INDIVIDUAL RECOGNTION, AND NON-ASSOCIATIVE LEARNING IN THE ADULT GRAY SHORT-TAILED OPOSSUM (MONODELPHIS DOMESTICA)

Social behavior is critical for relationship formation and is influenced by myriad environmental and individual factors. Basic and preclinical research typically relies on rodent models to identify the mechanisms that underlie behavior; however, it is important to use non-rodent models as well. A major objective of the present study was to test the hypothesis that biological sex and social experience modulate the expression of social behavior in the adult gray short-tailed opossum (Monodelphis domestica), a non-traditional model. We also investigated the non-associative learning abilities of these animals. Following a period of social isolation, animals of both sexes were paired with a non-familiar, same-sex partner for 10 minutes on three different occasions, with 24-hour inter-trial intervals. We are the first research group to find significant sex differences in submissive and nonsocial behaviors in Monodelphis. Females displayed significantly higher durations of nonsocial behavior that increased over trials. Males were more aggressive; their latencies to the first attack and submissive behavior decreased over trials whereas these latencies increased for females; males’ duration of submissive behavior increased over trials whereas it decreased for females. A different group of subjects habituated in response to repeated presentations to neutral odors and dishabituated in response to novel odors. In addition, both males and females demonstrated the ability to form social memories in a standard individual (social) recognition test. Our results contribute to the characterization of this marsupial species, an important first step in developing it as a model of complex social behaviors

EP₂ receptor antagonism reduces peripheral and central hyperalgesia in a preclinical mouse model of endometriosis

Endometriosis is an incurable gynecological disorder characterized by debilitating pain and the establishment of innervated endometriosis lesions outside the uterus. In a preclinical mouse model of endometriosis we demonstrated overexpression of the PGE2-signaling pathway (including COX-2, EP2, EP4) in endometriosis lesions, dorsal root ganglia (DRG), spinal cord, thalamus and forebrain. TRPV1, a PGE2-regulated channel in nociceptive neurons was also increased in the DRG. These findings support the concept that an amplification process occurs along the pain neuroaxis in endometriosis. We then tested TRPV1, EP2, and EP4 receptor antagonists: The EP2 antagonist was the most efficient analgesic, reducing primary hyperalgesia by 80% and secondary hyperalgesia by 40%. In this study we demonstrate reversible peripheral and central hyperalgesia in mice with induced endometriosis

Age- and hormone-regulation of opioid peptides and synaptic proteins in the rat dorsal hippocampal formation

Circulating estrogen levels and hippocampal-dependent cognitive functions decline with aging. Moreover, the responses of hippocampal synaptic structure to estrogens differ between aged and young rats. We recently reported that estrogens increase levels of post-synaptic proteins, including PSD-95, and opioid peptides leu-enkephalin and dynorphin in the hippocampus of young animals. However, the influence of ovarian hormones on synaptic protein and opioid peptide levels in the aging hippocampus is understudied. Here, young (3–5 mo old), middle-aged (9–12 mo old), and aged (about 22 mo old) female rats were ovariectomized for 4 weeks and then subcutaneously implanted with a silastic capsule containing vehicle or 17β-estradiol. After 48 hours, rats were subcutaneously injected with progesterone or vehicle and sacrificed one day later. Coronal sections through the dorsal hippocampus were processed for quantitative peroxidase immunohistochemistry of leu-enkephalin, dynorphin, synaptophysin, and PSD-95. With age, females showed opposing changes in leu-enkephalin and dynorphin levels in the mossy fiber pathway, particularly within the hilus, and regionally specific changes in synaptic protein levels. 17β-estradiol, with or without progesterone, altered leu-enkephalin levels in the dentate gyrus and synaptophysin levels in the CA1 of young but not middle-aged or aged females. Additionally, 17β-estradiol decreased synaptophysin levels in the CA3 of middle-aged females. Our results support and extend previous findings indicating 17β-estradiol modulation of hippocampal opioid peptides and synaptic proteins while demonstrating regional and age-specific effects. Moreover, they lend credence to the “window of opportunity” hypothesis during which hormone replacement can modulate hippocampal structure and circuitry to improve cognitive outcomes

Ectopic HCN4 expression drives mTOR-dependent epilepsy in mice

A cAMP-dependent mechanism mediates seizures in mTOR disorders due to the ectopic expression of HCN4 channels in diseased neurons.</jats:p