Risk factors for the failure of the InSure method in very preterm infants with respiratory distress syndrome / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the risk factors for the failure of the InSure method in very preterm infants with respiratory distress syndrome (RDS).</p><p><b>METHODS</b>Seventy-one very preterm infants with RDS treated with InSure method were enrolled. These infants were categorized into two groups: InSure success (42 cases) and InSure failure (29 cases). The differences in basic information were compared between the two groups, and logistic regression analysis was used to identify the risk factors for InSure failure.</p><p><b>RESULTS</b>The failure rate of the InSure method was 41%. The failure group were much lower in the birth weight, the antenatal steroids utilization rate and the vaginal delivery rate than the success group (P<0.05). The incidence of patent ductus arteriosus in the failure group was significantly higher than in the success group (P<0.05). PaO2, PaO2/FiO2 and PaO2/PAO2 in the failure group were significantly lower than in the success group (P<0.05). PaCO2 in the failure group was much higher than in the success group (P<0.05). Further logistic regression analysis showed that birth weight <1 150 g (OR=22.240 95%CI=2.124-232.901), PaCO2>54 mm Hg(OR=9.360, 95%CI=1.958-44.741, and PaO2/FiO2 <195 (OR=6.570, 95%CI=1.027-42.003), were the independmend risk factors for InSure failure. Furthermore, the duration of oxygen therapy, the total time of hospitalization and the incidence of BPD in the failure group were much longer and higher than in the success group (P<0.05).</p><p><b>CONCLUSIONS</b>Low birth weight, elevated PaCO2 and low PaO2/PiO2 ratio are the risk factors for the failure of the InSure method in very preterm infants.</p>

Expression of IL-8, SP-A and TGF-beta1 in bronchoalveolar lavage fluid of neonates with bronchopulmonary dysplasia / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the expression of interleukin 8 (IL-8), surfactant protein-A (SP-A) and transforming growth factor beta1 (TGF-beta1) in bronchoalveolar lavage fluid (BALF) of neonates with bronchopulmonary dysplasia (BPD).</p><p><b>METHODS</b>Thirty neonates with BPD and 30 gestational age-, gender-, and birth weight-matched neonates without BPD (control group) were enrolled from December 2007 to October 2009. Non-brochoscopic bronchoalveolar lavage was performed. The levels of IL-8, SP-A and TGF-beta1 in BALF were measured using ELISA.</p><p><b>RESULTS</b>The levels of TGF beta1 (47+/-15 microg/mL vs 34+/-13 microg/mL) and IL-8 (54+/-16 microg/mL vs 28+/-13 microg/mL) in the BPD group were significantly higher than those in the control group (P<0.01). In contrast, the contents of SP-A in the BPD group were significantly lower than those in the control group (35+/-16 microg/mL vs 42+/-14 microg/mL;P<0.05).</p><p><b>CONCLUSIONS</b>The increased expression of TGF-beta1 and IL-8 in BALF may be involved in abnormal lung development and maturation in neonates with BPD. The low expression of SP-A in the BPD group suggests that the exogenous SP-A administration may be an option for the treatment of BPD.</p>

Effect of basic fibroblast growth factor on expression of protein and mRNA of bone morphogenetic protein 4 in hypoxic-ischemic brain damage in newborn rats / 中华儿科杂志

<p><b>OBJECTIVE</b>To investigate the effect of basic fibroblast growth factor(bFGF) on expression of protein and mRNA of bone morphogenetic protein 4 in hypoxic-ischemic brain damage (HIBD) in newborn rats.</p><p><b>METHOD</b>One hundred and twenty 7 days old neonatal rats were randomly divided into control group, hypoxic-ischemic brain damage and interventional group of bFGF, each having forty neonatal rats. After HIBD model was established, bFGF was given to interventional group by peritoneal injection for 5 continuous days. Every group was randomly divided into 7 days, 14 days, 21 days and 28 days group, according to the time of sacrifice. BMP4 protein in hippocampus was determined with immunohistochemical method. Messenger RNA of BMP4 were determined with in situ hybridization. Apoptosis of nerve cell was determined with TUNEL. Intergroup or intragroup comparisons were performed with analysis of variance.</p><p><b>RESULT</b>On the days 7 and 14, expression of BMP4 protein in hippocampus was higher in interventional group of bFGF than in HIBD while expression of BMP4 protein in interventional group of bFGF and HIBD was lower on day 7 than on day 14. Expression of BMP4 protein on the days 21 and 28 had no significant difference among three groups. mRNA expression of BMP4 in interventional group of bFGF and HIBD was significantly higher in hippocampus than in control group. On the day 14, BMP4 mRNA in hippocampus widely expressed in HIBD while BMP4 mRNA only expressed in CA1 in interventional group of bFGF. Expression of BMP4 mRNA in hippocampus on the affected side decreased from the time of killing on 28th day while there was no significant change in interventional group of bFGF. Apoptosis of neural cells at the time of sacrifice on day 7 was lower in interventional group of bFGF than that in HIBD group (F=9.010, P<0.01). Apoptotic neural cells was higher in bFGF and HIBD groups at the time of killing on days 14, 21 and 28 than that on day 7 but that the bFGF group had less apoptotic neural cells than HIBD group (F=9.202, 7.932, 14.985, P<0.01).</p><p><b>CONCLUSIONS</b>bFGF has a neurorestoration effect, which promotes expression of BMP4 protein and BMP4 mRNA in hippocampus of HIBD and inhibit apoptosis of neural cells.</p>

Intra-amniotic administration of pulmonary surfactant improves lung ultrastructural pathology and enhances surfactant protein A expression in fetal rabbits with intrauterine infection / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the effect of intra-amniotic administration of pulmonary surfactant (PS) on the lung ultrastructure and expression of surfactant protein A (SP-A) in fetal rabbit with intrauterine infection.</p><p><b>METHODS</b>Intra-amniotic PS injection was administered in a rabbit model of premature rupture of membrane and intrauterine infection induced by intrauterine colibacillus injection on the gestational days 24 and 26 days. The lung ultrastructural changes in the fetal rabbits were observed using electron microscope, and the expression of SP-A was measured with immunohistochemical staining and Western blotting 19.5 h after the PS administration.</p><p><b>RESULTS</b>alveolar type I cell (AT I), alveolar type II cell (AT II). In fetal rabbits with intrauterine colibacillus injection, inflammatory cell infiltration was observed in the pulmonary alveolus, bronchus lumens and intracytoplasm irrespective of PS administration. Compared with those in normal fetal rabbits, the number of alveolar type II cells (AT II) in the lung tissue decreased in fetal rabbits with intrauterine infection, and vacuolization of the lamellar bodies occurred with evidence of cell apoptosis; PS administration resulted in increased number of the AT II cells and lamellar bodies and reduced the cell apoptosis. The expression of SP-A was significantly lower in the infection group than in normal control group (P<0.05), but comparable between the PS group and the control group (P>0.05).</p><p><b>CONCLUSION</b>Changes in pulmonary alveolar ultrastructure and decreased expression of SP-A occur in fetal rabbits after intrauterine infection, and intra-amniotic administration of PS can alleviate these changes to promote lung maturation.</p>