Shaping Social Media: Is Twitter an Equitable tool for Professional Development?

PURPOSE: Twitter has become a powerful tool for professional development in academia. However, studies from the general population suggest that racialized and gender biases disproportionately empower male and white users. We characterized the demographics of Twitter influencers in Canadian healthcare. METHODS: We used the Right Relevance Insight API algorithm to identify Twitter influencers in the healthcare, healthcare research, and health policy domains, and to generated normalized influencer scores based on user connections and engagement. We used facial recognition software to approximate the influencers' race and sex. RESULTS: The majority of influencers identified were white (84%) and/or male (60%). Males had significantly higher influencer scores than females (65.1 ± 8.0 vs. 61.2 ± 6.2, P < 0.05) in health policy. We did not identify any sex- or race-associated disparities among influencers in healthcare or healthcare research. CONCLUSION: Male users have significantly higher levels of influence in health policy on Twitter. Given the importance of Twitter as a tool for professional development, it is crucial that institutional leaders and policymakers are aware of potential inequities in user reach. Future studies should evaluate additional factors shaping user influence in healthcare on Twitter, with a focus on equity, diversity, and trustworthiness.

Hepatic mitochondrial bioenergetics in aged C57BL/6 mice exhibit delayed recovery from severe burn injury.

Severe burn injuries initiate a cascade of downstream events, culminating in multiple organ dysfunction, sepsis, and even death. The elderly are in particular vulnerable to such outcomes, due primarily to a scarcity of knowledge on trauma progression at the biomolecular level in this population. Mitochondria, the cellular powerhouses, have been increasingly scrutinized recently for their contribution to trauma outcomes. We hypothesized that elderly have a worse outcome compared to adult patients due to failed recovery of hepatic mitochondria. Using a murine model of burn injury, Seahorse respirometry and functional proteomic assays, we demonstrate the impact of thermal trauma on hepatic mitochondrial respiration in adult and aged mice. While the mitochondria in adults rebound from the initial insult within 7days of the injury, the older animals display delayed recovery of mitochondrial bioenergetics accompanied by uncoupling and an oxidative environment. This is associated with a state of increased protein oxidation and nitrosylation, along with increases in circulating mtDNA, a known damage-associated molecular pattern. These findings suggest that hepatic mitochondria fail to normalize after trauma in aged mice and we suggest that this cellular failure is associated with organ damage and subsequently increased morbidity and mortality in elderly burn patients.

A Case of Li-Fraumeni Associated Thymoma.

Thymomas are among the most common cancers of the anterior mediastinum. They rarely occur in patients with Li-Fraumeni syndrome (LFS), a hereditary syndrome that predisposes individuals to cancer and is characterized by mutations in the tumor suppressor encoding gene TP53. Here we describe a case of primary thymoma in a woman diagnosed with LFS. We cover the initial presentation and diagnosis, radiological findings, histopathological examination, and management of thymoma. In addition, we review p53 physiology and LFS pathophysiology to explore how TP53 expression might differ between the majority of thymomas and in thymomas associated with LFS. This altered pathophysiology may affect management and prognosis due to emerging evidence of increased resistance to conventional treatment, which suggests a need for close monitoring and consideration of novel treatment strategies such as programmed death-ligand 1 (PD-L1) inhibitors.

Adipose browning response to burn trauma is impaired with aging.

BACKGROUNDThe incidence of burn injuries in older patients is dramatically increasing as the population of older people grows. Despite the increased demand for elderly burn care, the mechanisms that mediate increased morbidity and mortality in older trauma patients are unknown. We recently showed that a burn injury invokes white adipose tissue browning that leads to a substantially increased hypermetabolic response associated with poor outcomes. Therefore, the aim of this study was to determine the effect of age on the metabolic adipose response of browning after a burn injury.METHODOne hundred and seventy patients with burn injury admitted to the Ross Tilley Burn Centre were prospectively enrolled and grouped by age as older (≥50 years) and young (≤35 years). Adipose tissue and sera were collected and analyzed for browning markers and metabolic state via histology, gene expression, and resting energy expenditure assays.RESULTSWe found that older patients with burn injury lacked the adipose browning response, as they showed significant reductions in uncoupling protein 1 (UCP1) expression. This failure of the browning response was associated with reduced whole-body metabolism and decreased survival in older patients with burn injury. Mechanistically, we found that the adipose of both aged patients after burn trauma and aged mice after a burn showed impairments in macrophage infiltration and IL-6, key immunological regulators of the browning process after a severe trauma.CONCLUSIONTargeting pathways that activate the browning response represents a potential therapeutic approach to improve outcomes after burn trauma for elderly patients.FUNDINGNIH (R01-GM087285-01), Canadian Institutes of Health Research (grant no. 123336), and Canada Foundation for Innovation Leaders Opportunity Fund (no. 25407).

Metformin adapts its cellular effects to bioenergetic status in a model of metabolic dysfunction.

Thermal injury induces a complex immunometabolic response, characterized by hyperglycemia, extensive inflammation and persistent hypermetabolism. It has been suggested that attenuation of the hypermetabolic response is beneficial for patient wellbeing. To that effect, metformin represents an attractive therapeutic agent, as its effects on glycemia, inflammation and bioenergetics can improve outcomes in burn patients. Therefore, we studied metformin and its effects on mitochondrial bioenergetics in a murine model of thermal injury. We set out to determine the impact of this agent on mitochondrial hypermetabolism (adult mice) and mitochondrial dysfunction (aged mice). Seahorse respirometry complimented by in-gel activity assays were used to elucidate metformin's cellular mechanism. We found that metformin exerts distinctly different effects, attenuating the hypermetabolic mitochondria of adult mice while significantly improving mitochondrial bioenergetics in the aged mice. Furthermore, we observed that these changes occur both with and without adenosine monophosphate kinase (AMPK) activation, respectively, and analyzed damage markers to provide further context for metformin's beneficial actions. We suggest that metformin has a dual role following trauma, acting via both AMPK-dependent and independent pathways depending on bioenergetic status. These findings help further our understanding of metformin's biomolecular effects and support the continued use of this drug in patients.