A noninvasive surfactant adsorption test predicting the need for surfactant therapy in preterm infants treated with continuous positive airway pressure

Objective: To determine the diagnostic accuracy of the surfactant adsorption test (SAT) as a predictor for the need for surfactant replacement therapy in neonates with respiratory distress syndrome (RDS). Study design Amniotic fluid samples were collected from 41 preterm neonates with RDS treated with continuous positive airway pressure (CPAP) and 15 healthy control term neonates. Purified porcine surfactant served as a further control. Lamellar bodies and lung ultrasound score were also measured in a subset of the neonates treated with CPAP. Surfactant was administered according to the European guidelines, and clinical data were collected prospectively. Surfactant activity was measured as adsorption at the air/liquid interface and given in relative fluorescent units (RFU). Results: Surfactant activity differed among native porcine surfactant (median, 4863 RFU; IQR, 4405-5081 RFU), healthy term neonates (median, 2680 RFU; IQR, 2069-3050 RFU), and preterm neonates with RDS (median, 442 RFU; IQR, 92-920 RFU; P < .0001). The neonates who failed CPAP had lower surfactant activity compared with those who did not fail CPAP (median, 92 RFU; IQR, 0-315 RFU vs 749 RFU; IQR, 360-974 RFU; P = .0002). Differences between groups were more evident beyond 20-30 minutes of fluorescence; the 30-minute time point showed the highest area under the curve (0.84; P < .001) and the best cutoff level (170 RFU; specificity, 72%; sensitivity, 96%) for the prediction of CPAP failure. Surfactant activity at 30 minutes was significantly correlated with lamellar bodies (r = 0.51, P = .006) and lung ultrasound score (r = -0.39, P = .013). Conclusion: This technique has the potential to be developed into a fast, simple-to-interpret clinical test. The SAT can reliably identify preterm infants with subsequent CPAP failure and shows promise as a screening test for surfactant replacement in preterm neonates

Additional file 1: Table S1. of Prognostic and therapeutic value of disruptor of telomeric silencing-1-like (DOT1L) expression in patients with ovarian cancer

The primer sequences used for PCR. (DOCX 15 kb

Additional file 6: Figure S4. of Prognostic and therapeutic value of disruptor of telomeric silencing-1-like (DOT1L) expression in patients with ovarian cancer

DOT1L regulates the transcription of G1 arrest genes CDK6 and CCND3 through H3K79 dimethylation. (a) and (b) RT-PCR detecting the change of primary G1 arrest genes, D-type cyclins (D1, D2, and D3), cyclin E, Cdks (2, 4, and 6) in mRNA levels in TOV21G cells knocking down of DOT1L with shDOT1L shRNAs lentiviral particles (a) and DOT1L inhibitors, EPZ004777 and SGC0946 (b) (P < 0.05, Student’s t test, data represented as mean±SD). (c) and (d) DOT1L transcriptionally regulates the expression of CDK6 (c) and CCND3 (d) through induction of H3K79 dimethylation in the binding regions of these genes. Chromatin immunoprecipitation (ChIP) PCR assays were performed in a loss-of-function system. TOV21G cells were transfected with shDOT1L shRNAs and shCON lentiviral particles, and ChIP assays using anti-DOT1L and anti-H3K79me2 antibodies were performed with ChIP primers targeting the binding regions of CDK6 and CCND3 (P < 0.05, Student’s t test, data represented as mean±SD). (TIF 815 kb