Several case reports have been filed regarding the latent presentation of hemorrhagic pheochromocytomas in the trauma setting; however, few patients have been found to exhibit these symptoms in the absence of a tumor. In this report, we discuss a patient who sustained blunt abdominal trauma leading to the development of an adrenal hemorrhage and his unexpected sequelae of symptoms. Discovery of the source of the patient's symptoms was delayed secondary to multiple comorbidities in the critical care setting and work-up for other sources such as infection and agitation. Hypertensive urgency was confirmed to be of adrenal etiology with measurement of persistently elevated plasma and urine metanephrines during the hospital course. The patients hypertensive urgency was successfully managed with the use of antisympathomimetics including an esmolol drip, clonidine, and eventually tapered dose of metoprolol. Symptoms improved over time, and repeat CT imaging weeks later showed resolution of the hematoma. Review of literature reveals only one other case of adrenal hemorrhage after blunt force trauma resulting in hemorrhagic psuedotumor. To our knowledge, this is the second such case ever presented. This case is discussed along with the presentation, diagnostic work-up, and treatment of a critically ill patient with an adrenal hemorrhage masked as a pseudotumor.

Every year 2.8 million Americans suffer a traumatic brain injury (TBI). Despite the prevalence and debilitating consequences of TBI, effective treatment options are scarce due to the limited understanding of the neurobiological effects of injury, especially in acute phases when the cellular processes leading to neuropathology are first initiated. To identify changes in neural function and cerebral blood flow (CBF) that might account for TBI-induced cognitive and sensory deficits, we took a multidisciplinary approach, examining synaptic function, cortical activity patterns, and microvascular hemodynamics. we used a weight drop model in mice to induce mild TBI, the most common form in humans, and focused on responses within the first hours of injury where existing data are particularly limited. For synaptic function, we measured excitatory and inhibitory input onto pyramidal cells in the piriform cortex with whole-cell recordings in acute brain slices. Increased excitation appeared at one hour but excitatory-inhibitory balance was reestablished by 48 hours, highlighting the importance of studying rapid-onset injury responses. We also compared neural activity before and after TBI using in vivo two-photon calcium imaging of pyramidal cells in visual cortex. While neural activity substantially decreased in most cells one hour after injury, a minority of cells showed hyperactivation or prolonged increases in intracellular calcium, again indicating major physiological disturbances during immediate post-injury phases. Finally, we measured in vivo changes in CBF throughout the cortical microvasculature with laser speckle contrast imaging and optical coherence tomography, tracking injury effects up to three weeks after TBI. CBF and capillary flow were dramatically reduced within minutes and remained suppressed for over one hour. As neurons’ high energetic needs require a constant supply of glucose and oxygen from local vasculature, decreased CBF likely contributes to altered neural activity and loss of ion homeostasis and thus potentially cognitive and sensory deficits after TBI. Our results reveal that even mild injury creates rapid, pronounced, and heterogeneous alterations in neural activity and capillary flow. The transient nature of these effects suggests that the first two hours after injury may be a key window for delivering interventions, and that restoring CBF may reduce damage due to metabolic stress.

The present study aims to examine which maladaptive and Big Five personality traits, as well as which lower order facets, are related to symptoms specific to PTSD (i.e., intrusions and avoidance). Unique effects were isolated by controlling for nonspecific general depression that occurs in the disorder but is not specific to it. 707 undergraduate students were administered a self-report online survey to assess their personality, trauma history, PTSD and mood symptoms. Additionally, data from 536 9/11 World Trade Center (WTC) responders who have been administered personality, PTSD, and mood surveys as part of a longitudinal study were analyzed. As expected, neuroticism was highly correlated with PTSD, but had fewer associations with PTSD dimensions after controlling for depression. Trust and agreeableness emerged as important, being negatively related to PTSD, while most maladaptive personality domains and facets were positively related to PTSD (perceptual dysregulation had the highest association). Other traits, such as antagonism and openness, were not significantly related to PTSD. There is growing evidence that clinical interventions can change personality traits; the present study provides new personality targets for intervention that are uniquely related to PTSD.

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Keratins are fibrous structural proteins found in human hair that have been used to develop bioactive and biocompatible constructs for a wide variety of tissue engineering and healthcare applications. Their ubiquity, capacity for self-assembly, ease of use and versatility in blended materials, and ability to modulate cell behavior and promote tissue ingrowth have made keratins well-suited for the development of regenerative therapies. In particular, keratins have demonstrated bioactivity in both in-vivo and in-vitro studies, by altering immune and stem cell phenotype and function and promoting an anti-inflammatory/wound healing environment. This work seeks to build on previous research by investigating the ability of low and high molecular weight keratins to augment anti-inflammatory primary macrophage phenotypes and examining the influence of keratin biomaterials on cellular and inflammatory mechanisms in two models of injury and disease. Rodent models of blast induced neurotrauma (BINT) and severe osteoporosis were used to inform the development of 2D and 3D in-vitro models of macrophage/endothelial cell injury and osteogenic differentiation respectively. Keratin biomaterials exhibited some potential to alter macrophage and endothelial cell dynamics following blast, specifically by promoting anti-inflammatory (M2c-like) macrophage polarization and diminishing endothelial cell injury responses (i.e. endothelial glycocalyx shedding). A more clinically relevant model of osteoporosis found that stem cells harvested from older, osteoporotic animals demonstrated limited proliferative and bone differentiation potential compared to healthy cells. However, 3D constructs (especially keratin-based materials) were able to enhance calcification and osteogenic gene expression of diseased cells. These results highlight the complexity of macrophage phenotypic switching and cellular dynamics in these systems. However, keratin-based therapeutics may prove useful for facilitating tissue regeneration and limiting detrimental inflammatory and cellular responses in various models of injury and disease. / Ph. D.

Yes / Background: Depression is a common psychiatric problem following traumatic brain injury (TBI) with reported prevalence rates of 30-77% in the first year post-TBI. Given the negative influence of post-TBI depression on cognition, interpersonal, social, physical and occupational functioning; early initiation of pharmacotherapy to prevent post-TBI depression has been considered. This systematic review will synthesize the available evidence from published studies on the effectiveness and harms of pharmacotherapy for the secondary prevention of post-TBI depression. Method: Studies published before November 2017 were reviewed. Six databases were searched, with additional searching of key additional documents. Studies meeting inclusion criteria were evaluated for methodological quality. Results: Six articles addressing five studies met inclusion criteria. Study designs included three randomised controlled trials (RCT), two retrospective cohorts and one case-control. Prophylactic pharmacotherapy included antidepressants, beta-blockers and statins. In one RCT, the number-needed-to-treat with sertraline to prevent one case of depression post-TBI at 24 weeks was 5.9 (95%CI: 3.1-71.1). Prescribing beta-blockers prior to TBI reduced the depression risk regardless of the specific brain trauma. TBI patients with pre-existing hyperlipidemia not treated with statins had an increased depression risk compared to those without hyperlipidemia. Conclusion: Early initiation of sertraline prophylaxis in nondepressed TBI patients shows promise to reduce the odds of post-TBI depression developing. However, in the absence of rigorous study of tolerability, existing data are insufficient to recommend sertraline prophylaxis. Optimal timing and treatment duration with identification of patients most likely to benefit from prophylaxis require further consideration. Dedicated prospective studies assessing the effects of beta-blockers and statins on post-TBI depression are required. / The Transport Accident Commission (TAC), through the Institute for Safety, Compensation and Recovery Research (ISCRR) at Monash University, provided funding for this review.