American journal of respiratory and critical care medicine
-
Am. J. Respir. Crit. Care Med. · Jul 2020
Association of Pre-Morbid Blood Pressure with Vasopressor Infusion Duration in Patients with Shock.
Rationale: Guidelines for vasopressor titration suggest a universal target-mean arterial pressure (MAP) >65 mm Hg. The implications for patients with premorbid low/high blood pressure are unknown. Objectives: To investigate the relationship between premorbid blood pressure and vasopressor duration for patients with shock. ⋯ After adjustment, premorbid low admissions had longer vasopressor use (median, 1.35 d vs. 1.04 d for normal; hazard ratio for discontinuation vs. normal, 0.78 [0.73-0.85]; P < 0.001) and premorbid high admissions had shorter use (median, 0.84 d; hazard ratio, 1.22 [1.12-1.33]; P < 0.001). Premorbid low admissions had longer adjusted length of stay and higher adjusted mortality than premorbid normal admissions. Conclusions: Premorbid blood pressure was inversely associated with vasopressor duration.
-
Am. J. Respir. Crit. Care Med. · Jul 2020
A Network of Sputum MicroRNAs is Associated with Neutrophilic Airway Inflammation in Asthma.
Rationale: MicroRNAs are potent regulators of biologic systems that are critical to tissue homeostasis. Individual microRNAs have been identified in airway samples. However, a systems analysis of the microRNA-mRNA networks present in the sputum that contribute to airway inflammation in asthma has not been published. ⋯ Multiple microRNAs in the nely module correlated with two mRNA modules enriched for TLR (Toll-like receptor) and T-helper cell type 17 (Th17) signaling and endoplasmic reticulum stress. hsa-miR-223-3p was a key regulator of the TLR and Th17 pathways in the sputum of subjects with asthma. Conclusions: This study of sputum microRNA and mRNA expression from patients with asthma demonstrates the existence of microRNA networks and genes that are associated with features of asthma severity. Among these, hsa-miR-223-3p, a neutrophil-derived microRNA, regulates TLR/Th17 signaling and endoplasmic reticulum stress.