Electronic Phenotyping of Urinary Tract Infections as a Silver Standard Label for Machine Learning.

This study explored the efficacy of electronic phenotyping in data labeling for machine learning with a focus on urinary tract infections (UTIs). We contrasted labels from electronic phenotyping against previously published labels such as urine culture positivity. In comparison, electronic phenotyping showed the potential to enhance specificity in UTI labeling while maintaining similar sensitivity and was easily scaled for application to a large dataset suitable for machine learning, which we used to train and validate a machine learning model. Electronic phenotyping offers a valuable method for machine learning label generation in healthcare, with potential benefits for patient care and antimicrobial stewardship. Further research will expand its application and optimize techniques for increased performance.

Pro-inflammatory and anti-inflammatory T cells in giant cell arteritis.

Giant cell arteritis is an autoimmune disease defined by explicit tissue tropism to the walls of medium and large arteries. Pathognomic inflammatory lesions are granulomatous in nature, emphasizing the functional role of CD4T cells and macrophages. Evidence for a pathogenic role of antibodies and immune complexes is missing. Analysis of T cell populations in giant cell arteritis, both in the tissue lesions and in the circulation, has supported a model of broad, polyclonal T cell activation, involving an array of functional T cell lineages. The signature of T cell cytokines produced by vasculitic lesions is typically multifunctional, including IL-2, IFN-γ, IL-17, IL-21, and GM-CSF, supportive for a general defect in T cell regulation. Recent data describing the lack of a lymph node-based population of anti-inflammatory T cells in giant cell arteritis patients offers a fresh look at the immunopathology of this vasculitis. Due to defective CD8+NOX2+ regulatory T cells, giant cell arteritis patients appear unable to curtail clonal expansion within the CD4T cell compartment, resulting in widespread CD4T cell hyperimmunity. Why unopposed expansion of committed CD4 effector T cells would lead to invasion of the walls of medium and large arteries needs to be explored in further investigations.