Citations

Abstract Problem Statement Communication failures in critical care contribute to preventable medical errors, impaired team performance, and unsafe care environments. Despite recognition of its importance, communication training for fellows remains inconsistent across hierarchical (ICU) and non-hierarchical (research/QI) environments. This variability limits fellows’ ability to adapt communication strategies, affecting clinical decision making and collaboration. Existing curricula often lack experiential rehearsal and cross-context transfer, leaving trainees underprepared to communicate across settings. Targeted Needs Assessment A pre-course focused assessment of critical care fellows at a single center revealed heterogeneity in formal communication training and confidence in applying communication strategies across team structures. Peer feedback identified gaps in negotiation, nonverbal cue recognition, and role clarity. Primary Goal Equip critical care fellows to communicate with intentional presence and professionalism across hierarchical and non-hierarchical clinical settings. Objectives Implement a one-day curriculum aligned with ACGME Critical Care Medicine milestones and CCF HRO (High Reliability Organization) principles. - Demonstrate effective active listening and closed-loop communication - Identify and respond to verbal and nonverbal cues - Exhibit leadership behaviors promoting psychological safety - Adapt communication strategies across team structures Educational Strategies and Curriculum Design Curriculum planning involved interdisciplinary meetings between critical care faculty, simulation education specialists, curriculum leads, and improvisation specialist. Design aligned with adult learning and simulation best practices. The curriculum integrated three educational approaches 1) Improvisational communication training emphasizing inclusive language and nonverbal cue awareness 2) Narrative reflection and professional identity formation 3) High fidelity simulation using communication-intensive ICU and non-ICU scenarios. Simulation scenarios included a) Dual patient respiratory failure and cardiac arrest requiring role assignment and closed-loop communication b) Plane crash survival lab requiring group consensus without assigned leadership Implementation and Learner Evaluation Eleven of twelve critical care medicine fellows participated. Pre and post-course surveys assessing communication confidence across settings were completed by all participants. Faculty observation rubrics assessed communication behaviors. Key Outcomes/Results (see graphs) Substantial increases in communication confidence were observed across hierarchical ICU and non-hierarchical environments. Fellows agreed that communication competency should be a required component of training. High impact elements included a) Improvisational communication techniques integrated with simulation b) Nonverbal communication awareness c) Adoption of inclusive language d) Psychological safety e) Improved professionalism and interdisciplinary communication consistency Conclusion and Next Steps This improvisation-enhanced simulation curriculum improved fellows’ confidence communicating across hierarchical and non-hierarchical settings. Next steps include incorporating cognitive load management training; the curriculum is adaptable to external audiences and supports organizational HRO principles. This abstract is funded by: N/A

AbstractObjectiveThe most promising facial region for inducing pan‐facial effects is the temporal region. The temple displays signs of facial aging itself which include temporal volume loss and increased visibility of the temporal crest, the temporal vasculature, the lateral orbital rim, and the upper zygomatic arch. The objective of this article is to provide a detailed review of temple anatomy pertaining to routinely performed temporal injection techniques, their expected esthetic outcomes as well as the intendant advantages, disadvantages, and procedure pearls.Materials and MethodsThis narrative review is based on the clinical experience of the authors treating the temporal region for esthetic purposes. The postulated outcome of each technique was observed during the routine clinical practice of the authors.ResultsThe temporal region is based on a bony platform consisting of the parietal, frontal, sphenoid, and temporal bones. The overlying soft tissues are arranged in layers which contain the temporal neurovascular structures. The temporal soft tissues consist of 10 parallel layers which vary in their thickness depending on age‐related influences. Six different techniques will be addressed, which include subdermal and interfascial techniques for volumizing, low and high supraperiosteal techniques for volumizing, and supraauricular and temporal lifting techniques.ConclusionThis narrative provides a detailed anatomic overview of the temporal region and describes each commonly performed injection technique with respect to anatomy, esthetic outcome, as well as potential pearls and pitfalls. It is hoped that the description contained herein may guide esthetic practitioners toward safer and more natural outcomes when treating the face.

Abstract The molecular mechanisms underlying the initiation of innate and adaptive proallergic Th2-type responses in the airways are not well understood. IL-33 is a new member of the IL-1 family of molecules that is implicated in Th2-type responses. Airway exposure of naive mice to a common environmental aeroallergen, the fungus Alternaria alternata, induces rapid release of IL-33 into the airway lumen, followed by innate Th2-type responses. Biologically active IL-33 is constitutively stored in the nuclei of human airway epithelial cells. Exposing these epithelial cells to A. alternata releases IL-33 extracellularly in vitro. Allergen exposure also induces acute extracellular accumulation of a danger signal, ATP; autocrine ATP sustains increases in intracellular Ca2+ concentration and releases IL-33 through activation of P2 purinergic receptors. Pharmacological inhibitors of purinergic receptors or deficiency in the P2Y2 gene abrogate IL-33 release and Th2-type responses in the Alternaria-induced airway inflammation model in naive mice, emphasizing the essential roles for ATP and the P2Y2 receptor. Thus, ATP and purinergic signaling in the respiratory epithelium are critical sensors for airway exposure to airborne allergens, and they may provide novel opportunities to dampen the hypersensitivity response in Th2-type airway diseases such as asthma.

The hepatocyte is especially vulnerable to injury due to its central role in xenobiotic metabolism including drugs and alcohol, participation in lipid and fatty acid metabolism, its unique role in the enterohepatic circulation of bile acids, the widespread prevalence of hepatotropic viruses, and its existence within a milieu of innate immune responding cells. Apoptosis and necrosis are the most widely recognized forms of hepatocyte cell death. The hepatocyte displays many unique features regarding cell death by apoptosis. It is quite susceptible to death receptor-mediated injury, and its death receptor signaling pathways involve the mitochondrial pathway for efficient cell killing. Also, death receptors can trigger lysosomal disruption in hepatocytes which further promote cell and tissue injury. Interestingly, hepatocytes are protected from cell death by only two anti-apoptotic proteins, Bcl-x L and Mcl-1, which have nonredundant functions. Endoplasmic reticulum stress or the unfolded protein response contributes to hepatocyte cell death during alterations of lipid and fatty acid metabolism. Finally, the current information implicating RIP kinases in necrosis provides an approach to more fully address this mode of cell death in hepatocyte injury. All of these processes contributing to hepatocyte injury are discussed in the context of potential therapeutic strategies.

Abstract Eosinophils are multifunctional leukocytes involved in various inflammatory processes, as well as tissue remodeling and immunoregulation. During inflammation and infection, injured cells and damaged tissues release uric acid and monosodium urate (MSU) crystals as important endogenous danger signals. Uric acid is also implicated in the immunogenic effects of an authentic Th2 adjuvant, aluminum hydroxide. Eosinophils often localize at sites of Th2-type chronic inflammation; therefore, we hypothesized that eosinophils may react to endogenous danger signals. We found that human eosinophils migrate toward soluble uric acid and MSU crystals in a gradient-dependent manner. Eosinophils incubated with MSU crystals, but not those incubated with uric acid solution, produced elevated levels of IL-6 and IL-8/CXCL8. Other cytokines and chemokines, including IL-1β, IL-10, IL-17, IFN-γ, CCL2, CCL3, CCL4, TNF-α, G-CSF, GM-CSF, fibroblast growth factor, vascular endothelial growth factor, and TGF-β, were also produced by eosinophils incubated with MSU crystals. Eosinophils exposed to MSU crystals rapidly (i.e., within 1 min of exposure) released ATP into the extracellular milieu. Importantly, this autocrine ATP was necessary for eosinophils to produce cytokines in response to MSU crystals, and P2 nucleotide receptors, in particular P2Y2, are likely involved in this positive feedback loop. Finally, at higher concentrations, MSU crystals promoted P2R-dependent release of a granule protein (eosinophil-derived neurotoxin) and cell death. Thus, human eosinophils may respond to particulate damage-associated endogenous danger signals. These responses by eosinophils to tissue damage may explain the self-perpetuating nature of chronic inflammation in certain human diseases, such as asthma.

Abstract Studies have shown that the immune system can recognize self-antigens under conditions (eg, cell injury) in which the self-tissue might elaborate immune-activating endogenous danger signals. Uric acid (UA) is an endogenous danger signal recently identified to be released from dying cells. Prior work has shown that UA activates immune effectors of both the innate and adaptive immune system, including neutrophils and cytotoxic T-cell immunity. However, it was unclear whether UA could enhance antibody immunity, which was examined in this study. When added to dying tumor cells or with whole protein antigen, UA increased IgG1-based humoral immunity. Further, UA blocked growth of tumor in subsequent tumor challenge experiments, which depended on CD4, but not CD8, T cells. Sera derived from UA-treated animals enhanced tumor growth, suggesting it had little role in the antitumor response. UA did not signal for T-cell expansion or altered tumor-infiltrating leukocyte populations. Consistent with the lack of T-cell expansion, when applied to dendritic cells, UA suppressed T-cell growth factors but up-regulated B cell–activating cytokines. Understanding the nature of endogenous danger signals released from dying cells may aid in a better understanding of mechanisms of immune recognition of self.