Lung injury and STAT1 deficit induce EGFR overexpression in SARS-CoV-2 infection. A phase I/II trial was done to evaluate the safety and preliminary effect of nimotuzumab, an anti-EGFR antibody, in COVID-19 patients. Patients received from one to three infusions together with other drugs included in the national guideline.
View Article and Find Full Text PDFIntroduction: SARS-CoV-2 infection can produce endothelial injury and microvascular damage, one cause of the multiorgan failure associated with COVID-19. Cerebrovascular endothelial damage increases the risk of stroke in COVID-19 patients, which makes prompt diagnosis important. Endothelial dysfunction can be evaluated by using transcranial Doppler ultrasound to study cerebral hemodynamic reserve, but there are few of these studies in patients with COVID-19, and the technique is not included in COVID-19 action and follow-up guidelines nationally or internationally.
View Article and Find Full Text PDFIn COVID-19, EGFR production is upregulated in the alveolar epithelial cells. EGFR overexpression further activates STAT-3 and increases lung pathology. The EGFR pathway is also one of the major nodes in pulmonary fibrosis.
View Article and Find Full Text PDFBackground: Health care-associated infection (HAI) represent a global health problem with an increase in hospital stays, deaths, and monetary costs. Recipients of solid organ transplants are a population at risk. The objectives of the study were to characterize the incidence of HAI in renal and hepatic transplant recipients as well as to compare them with the population without transplants in intensive care units (ICU).
View Article and Find Full Text PDF