Objective To explore the pathogenesis of acute respiratory distress syndrome (ARDS) in fullterm newborns, and to assess the effect of pulmonary surfactant. Methods All full-term newboms were divided into two groups,with 50 cases in group A and 12 cases in group B. Compared to the treatment of group A,pulmonary surfactant was added to group B. The indicators of pH, PaO2, PaCO2, SaO2, HCO3- were compared between the two groups.Results The cure rate was 92% in group B , which was significant higher than that of 80% in group A( t = 3. 5,P < 0. 05 ). There were 42 cases of neonatal asphyxia (68%), 36 cases of asphyxia combined aspiration pneumonia (58% ) ,19 cases of cesarean section(31% ) ,6 cases of milk aspiration pneumonia (10% ) and 3 cases of infectious pneumonia (5 % ). The AUC was 0. 80,0. 76,0. 35,0. 83 and 0.74, respectively.Neonatal asphyxia, asphyxia combined aspiration pneumonia,milk aspiration pneumonia and infectious pneumonia were associated with ARDS in full-term newborns. PaO2 in group A and B was (78. 80 ± 8. 2 ) mm Hg and (87. 20 ± 8. 30) mm Hg, respectively (t = 4. 56, P < 0. 05 ). SaO2 in group A was (89. 50 ± 5.40) % ,which was significantly lower than that of (99. 63 ± 3. 30 ) % in group B (t = 5. 78, P < 0. 05). Conclusions There are various causes of ARDS in full-term newborns.Intensive clinical observation and continuous monitoring of blood oxygen saturation will be helpful to improve the efficiency of treatment Pulmonary surfactants can improve the efficiency in the treatment of ARDS in the full-term newboms.

OBJECTIVES: To investigate the effect of adriamycin (ADM), idelalisib or ADM and their combination on cell proliferation and intracellular concentration of ADM, and to explore the reversal effect of idelalisib on drug resistance to ADM. METHODS: The K562 and K562/ADM cells were respectively treated with ADM and idelalisib at different concentrations. The 50% inhibitory concentration (IC RESULTS: The cell survival rates were significantly decreased in a dose-dependent manner when the cells were treated with different doses of ADM (0.001-10.000 mg/L ). The IC CONCLUSIONS Idelalisib exerts effect on inhibition of the proliferation in myeloid leukemia K562 and K562/ADM cells, which may partially reverse the drug resistance of K562/ADM cells to ADM. The mechanisms for the effect of idelalisib may be related to increasing the accumulation of ADM and inducing the cell apoptosis in the K562 and K562/ADM cells.
ATP Binding Cassette Transporter, Subfamily B, Member 1 ; Cell Proliferation ; Doxorubicin/pharmacology* ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Humans ; K562 Cells ; Leukemia, Myeloid ; Purines ; Quinazolinones