Patients exposed to ⍺1-AR antagonists have reduced risks of mechanical ventilation and death in lower respiratory tract infection-related illnesses, highlighting the need for prospective trials assessing ⍺1-AR antagonists' effectiveness in COVID-19.
Biological aging processes and age-related diseases demonstrate sexual dimorphism where complex interactions between underlying aging mechanisms and sex chromosomes and hormones are seen in humans and animals.
Assessing plaque biomechanics by optical coherence tomography highlights the importance of the disrupting effects of plaque stress, bringing stress concentrations as the prime movers of plaque rupture back into clinical practice.
Experiments in a mouse model for Alzheimer’s disease using germ-free and conventionally housed animals reveal that microbiota-derived short-chain fatty acids promote the deposition of cerebral Aβ plaques.
A human experimental model for physiological glucocorticoid exposure and glucocorticoid withdrawal identifies a multi-omic cluster, including microRNA miR-122-5p and metabolites, associated with glucocorticoid-responsive genes.
Early postmortem autopsy of COVID-19 patients shows high viral loads and damage of the lung, although extrapulmonary cells demonstrate no injury, they contribute to inflammation, hyper-coagulation, and multiple organ dysfunction.