Rapid Implementation of Telecritical Care Support During a Pandemic: Lessons Learned During the Coronavirus Disease 2020 Surge in New York City.

Objectives: We describe the key elements for a New York City health system to rapidly implement telecritical care consultative services to a newly created ICU during the coronavirus disease 2020 patient surge.

Design: This was a rapid quality-improvement initiative using public health decrees, a HIPAA-compliant and device-agnostic telemedicine patform, and a group of out-of-state intensivist volunteers to enhance critical care support. Telecritical care volunteers initially provided on-demand consults but then shifted to round twice daily with housestaff in a 12-bed newly created ICU.

Transcription factor ets-2 plays an important role in the pathogenesis of pulmonary fibrosis.

Ets-2 is a ubiquitous transcription factor activated after phosphorylation at threonine-72. Previous studies highlighted the importance of phosphorylated ets-2 in lung inflammation and extracellular matrix remodeling, two pathways involved in pulmonary fibrosis. We hypothesized that phosphorylated ets-2 played an important role in pulmonary fibrosis, and we sought to determine the role of ets-2 in its pathogenesis.

Social disruption induces lung inflammation.

Social disruption (SDR) is a well-characterized mouse stressor that causes changes in immune cell reactivity in response to inflammatory stimuli. In this study, we found that SDR in the absence of an immune challenge induced pulmonary inflammation and increased pulmonary myeloperoxidase activity. The percentage of neutrophils within the lungs increased 2-fold after social disruption.

The role of inflammation in the pathogenesis of idiopathic pulmonary fibrosis.

The role of inflammation in idiopathic pulmonary fibrosis (IPF) is controversial. If inflammation were critical to the disease process, lung pathology would demonstrate an influx of inflammatory cells, and that the disease would respond to immunosuppression. Neither is true.

Important roles for macrophage colony-stimulating factor, CC chemokine ligand 2, and mononuclear phagocytes in the pathogenesis of pulmonary fibrosis.

Rationale: An increase in the number of mononuclear phagocytes in lung biopsies from patients with idiopathic pulmonary fibrosis (IPF) worsens prognosis. Chemokines that recruit mononuclear phagocytes, such as CC chemokine ligand 2 (CCL2), are elevated in bronchoalveolar lavage (BAL) fluid (BALF) from patients with IPF. However, little attention is given to the role of the mononuclear phagocyte survival and recruitment factor, macrophage colony-stimulating factor (M-CSF), in pulmonary fibrosis.