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To determine donor cornea contamination rate and to determine factors associated with cornea contamination. To assess the effect of hospitalization, intensive care unit (ICU) time, and antibiotic use on corneal contamination rate. To determine the spectrum of the contaminating microorganisms. The contamination rate of 212 corneas, obtained by enucleation from April 2014 to January 2015 in a single eye bank, was assessed retrospectively according to age, sex, cause of death, systemic antibiotic use, hospitalization time, ICU time, mechanical ventilation (MV), death to enucleation interval (DEI), enucleation to processing interval (EPI), and corneal epithelial exposure grading. The relative risk (RR) and adjusted RR with a 95% confidence interval were calculated using IBM-SPSS 20.0. The contamination rate was 35.6% (n = 75). On multivariate analysis, ICU stay of 4 days or longer and enucleation to processing interval (EPI) greater than 7.4 h (RR 1.58, CI 0.96–2.60, P = 0.06) were associated with donor cornea contamination. Corneal contamination risk was highest from 4 to 6 days at the ICU (RR 3.40, CI 1.54–7.51, P

Naringenin is a biologically active analgesic, anti-inflammatory, and antioxidant flavonoid. Naringenin targets in inflammation-induced articular pain remain poorly explored. The present study investigated the cellular and molecular mechanisms involved in the analgesic/anti-inflammatory effects of naringenin in zymosan-induced arthritis. Mice were pre-treated orally with naringenin (16.7–150 mg/kg), followed by intra-articular injection of zymosan. Articular mechanical hyperalgesia and oedema, leucocyte recruitment to synovial cavity, histopathology, expression/production of pro- and anti-inflammatory mediators and NFκB activation, inflammasome component expression, and oxidative stress were evaluated. Naringenin inhibited articular pain and oedema in a dose-dependent manner. The dose of 50 mg/kg inhibited leucocyte recruitment, histopathological alterations, NFκB activation, and NFκB-dependent pro-inflammatory cytokines (TNF-α, IL-1β, and IL-33), and preproET-1 mRNA expression, but increased anti-inflammatory IL-10. Naringenin also inhibited inflammasome upregulation (reduced Nlrp3, ASC, caspase-1, and pro-IL-1β mRNA expression) and oxidative stress (reduced gp91phox mRNA expression and superoxide anion production, increased GSH levels, induced Nrf2 protein in CD45+ hematopoietic recruited cells, and induced Nrf2 and HO-1 mRNA expression). Naringenin presents analgesic and anti-inflammatory effects in zymosan-induced arthritis by targeting its main physiopathological mechanisms. These data highlight this flavonoid as an interesting therapeutic compound to treat joint inflammation, deserving additional pre-clinical and clinical studies.