Dr. Paul Cook, chief of the Division of Infectious Diseases at East Carolina Univesity’s Brody School of Medicine, began enrolling patients June 1 in a clinical trial investigating a new treatment aimed at preventing and shortening the duration of Acute Respiratory Distress Syndrome (ARDS). ARDS is a characteristic of COVID-19 that occurs when fluid builds up in the lungs and prevents oxygen from entering the bloodstream.
Mechanistically, RNA sequencing revealed that resolvin D1 induced a transcriptional program in macrophages characteristic of a pro-revascularization phenotype. Vascularization of ischemic skeletal muscle, as well as cutaneous wounds, was impaired in mice with myeloid-specific deficiency of Alx/Fpr2, and this was associated with altered expression of pro-revascularization genes in skeletal muscle and macrophages isolated from skeletal muscle.
[Proceedings of the National Academy of Sciences of the United States of America]
Endothelial dysfunction was determined by flow-mediated dilatationd asymmetric dimethylarginine (ADMA) levels. Serum ADMA, high sensitive C-reactive protein, serum PTX3, malondialdehyde, Cu/Zn-superoxide dismutase, glutathione peroxidase levels and FMD were studied in baseline and after 12 weeks of Morinda citrifolia, omega-3 and extract with Alaskan blueberry.
Scientists observed that Tie2-expressing macrophages prevented apoptosis of b.End3 cells, but promoted their migration, proliferation and tube formation via VEGF, extracellular signal-regulated kinase and v-akt murine thymoma viral oncogene-dependent signaling pathways.