RESUMEN
BACKGROUND: A bloodstream infection (BSI) prognostic score applicable at the time of blood culture collection is missing. METHODS: In total, 4,327 patients with BSIs were included, divided into a derivation (80%) and a validation dataset (20%). Forty-two variables among host-related, demographic, epidemiological, clinical, and laboratory extracted from the electronic health records were analyzed. Logistic regression was chosen for predictive scoring. RESULTS: The 14-day mortality model included age, body temperature, blood urea nitrogen, respiratory insufficiency, platelet count, high-sensitive C-reactive protein, and consciousness status: a score of ≥ 6 was correlated to a 14-day mortality rate of 15% with a sensitivity of 0.742, a specificity of 0.727, and an area under the curve of 0.783. The 30-day mortality model further included cardiovascular diseases: a score of ≥ 6 predicting 30-day mortality rate of 15% with a sensitivity of 0.691, a specificity of 0.699, and an area under the curve of 0.697. CONCLUSIONS: A quick mortality score could represent a valid support for prognosis assessment and resources prioritizing for patients with BSIs not admitted in the intensive care unit.
RESUMEN
TNF-α (tumor necrosis factor-α) is a potent pro-inflammatory cytokine that regulates the permeability of blood and lymphatic vessels. The plasma concentration of TNF-α is elevated (> 1 pg/mL) in several pathologies, including rheumatoid arthritis, atherosclerosis, cancer, pre-eclampsia; in obese individuals; and in trauma patients. To test whether circulating TNF-α could induce similar alterations in different districts along the vascular system, three endothelial cell lines, namely HUVEC, HPMEC, and HCAEC, were characterized in terms of 1) mechanical properties, employing atomic force microscopy; 2) cytoskeletal organization, through fluorescence microscopy; and 3) membrane overexpression of adhesion molecules, employing ELISA and immunostaining. Upon stimulation with TNF-α (10 ng/mL for 20 h), for all three endothelial cells, the mechanical stiffness increased by about 50% with a mean apparent elastic modulus of E ~5 ± 0.5 kPa (~3.3 ± 0.35 kPa for the control cells); the density of F-actin filaments increased in the apical and median planes; and the ICAM-1 receptors were overexpressed compared with controls. Collectively, these results demonstrate that sufficiently high levels of circulating TNF-α have similar effects on different endothelial districts, and provide additional information for unraveling the possible correlations between circulating pro-inflammatory cytokines and systemic vascular dysfunction.
