Emergence of Artificial Intelligence and Machine Learning Models in Sudden Cardiac Arrest: A Comprehensive Review of Predictive Performance and Clinical Decision Support.

Sudden cardiac death/sudden cardiac arrest (SCD/SCA) is an increasingly prevalent cause of mortality globally, particularly in individuals with preexisting cardiac conditions. The ambiguous premortem warnings and the restricted interventional window related to SCD account for the complexity of the condition. Current reports suggest SCD to be accountable for 20% of all deaths hence accurately predicting SCD risk is an imminent concern. Traditional approaches for predicting SCA, particularly "track-and-trigger" warning systems have demonstrated considerable inadequacies, including low sensitivity, false alarms, decreased diagnostic liability, reliance on clinician involvement, and human errors. Artificial intelligence (AI) and machine learning (ML) models have demonstrated near-perfect accuracy in predicting SCA risk, allowing clinicians to intervene timely. Given the constraints of current diagnostics, exploring the benefits of AI and ML models in enhancing outcomes for SCA/SCD is imperative. This review article aims to investigate the efficacy of AI and ML models in predicting and managing SCD, particularly targeting accuracy in prediction.

An axon-T cell feedback loop enhances inflammation and axon degeneration.

Inflammation is closely associated with many neurodegenerative disorders. Yet, whether inflammation causes, exacerbates, or responds to neurodegeneration has been challenging to define because the two processes are so closely linked. Here, we disentangle inflammation from the axon damage it causes by individually blocking cytotoxic T cell function and axon degeneration. We model inflammatory damage in mouse skin, a barrier tissue that, despite frequent inflammation, must maintain proper functioning of a dense array of axon terminals. We show that sympathetic axons modulate skin inflammation through release of norepinephrine, which suppresses activation of γδ T cells via the ß2 adrenergic receptor. Strong inflammatory stimulation-modeled by application of the Toll-like receptor 7 agonist imiquimod-causes progressive γδ T cell-mediated, Sarm1-dependent loss of these immunosuppressive sympathetic axons. This removes a physiological brake on T cells, initiating a positive feedback loop of enhanced inflammation and further axon damage.

Programmed Cell Death Modifies Neural Circuits and Tunes Intrinsic Behavior.

Programmed cell death is a common feature of animal development. During development of the C. elegans hermaphrodite, programmed cell death (PCD) removes 131 cells from stereotyped positions in the cell lineage, mostly in neuronal lineages. Blocking cell death results in supernumerary "undead" neurons. We find that undead neurons can be wired into circuits, can display activity, and can modify specific behaviors. The two undead RIM-like neurons participate in the RIM-containing circuit that computes movement. The addition of these two extra neurons results in animals that initiate fewer reversals and lengthens the duration of those reversals that do occur. We describe additional behavioral alterations of cell-death mutants, including in turning angle and pharyngeal pumping. These findings reveal that, like too much PCD, too little PCD can modify nervous system function and animal behavior.