Noninvasive high-frequency oscillatory ventilation versus nasal continuous positive airway pressure in preterm infants with moderate-severe respiratory distress syndrome: A preliminary report.

OBJECTIVE: The aim of this study was to compare the effect of noninvasive high-frequency oscillatory ventilation (nHFOV) with nasal continuous positive airway pressure (nCPAP) in preterm infants with moderate-severe respiratory distress syndrome (RDS) after surfactant administration via INSURE (intubation, surfactant, extubation) method on the need for invasive mechanical ventilation (IMV). METHODS: A total of 81 infants with a gestational age (GA) of 28-34 weeks were eligible and were randomized to nCPAP (n = 42) or to nHFOV (n = 39). The need for IMV was the primary outcome. The incidence of bronchopulmonary dysplasia (BPD), occurrence of intraventricular hemorrhage (IVH), and air leaks, and mortality were considered as secondary outcomes. RESULT: A total 76 infants finally completed the study. The need for IMV was significantlylower in the nHFOV group compared with the nCPAP group(24.3% vs 56.4%, P < 0.01). The incidence of IVH, air leaks or BPD was similar between the two groups. In addition, the mortality rate was not statistically different. CONCLUSION: In this prospective, randomized controlled study, nHFOV significantly reduced the need for IMV as compared with nCPAP in preterm infants with moderate-severe RDS without increase in adverse effects.

Changes of positron emission tomography in newborn infants at different gestational ages, and neonatal hypoxic-ischemic encephalopathy.

Cerebral glucose metabolism was measured by (18)F-fluorodeoxyglucose position emission tomography in infants at different gestational ages and with neonatal hypoxic-ischemic encephalopathy. Thirty-six preterm and term infants at different gestational ages without brain injury were divided into four subgroups: ≤32 weeks (n = 4), 33-34 weeks (n = 5), 35-36 weeks (n = 12), and ≥37 weeks (n = 15). Twenty-four newborn infants with hypoxic-ischemic encephalopathy were divided into three subgroups: mild (n = 13), moderate (n = 7), and severe (n = 4). Cerebral glucose metabolism manifested a trend toward increase, and the structure of cranial (18)F-fluorodeoxyglucose positron emission tomography images became clear with increased gestational age, especially at ≥37 weeks. Uptakes of (18)F-fluorodeoxyglucose in the ≥37-week group were significantly higher than in the ≤32-week group (P < 0.01). Cerebral glucose metabolism changed significantly in neonatal hypoxic-ischemic encephalopathy, and was either unbalanced bilaterally or relatively low at all sites. Moreover, uptakes of (18)F-fluorodeoxyglucose were significantly lower in severe than in mild and medium hypoxic-ischemic encephalopathy (P < 0.05). Cerebral glucose metabolism, as measured by (18)F-fluorodeoxyglucose positron emission tomography, may prove useful for estimating brain development and injury in newborn infants, and its clinical values need further investigation.

Brain positron emission tomography in preterm and term newborn infants.

OBJECTIVE: To study the clinical values of positron emission tomography (PET) in preterm and term newborn infants through observing brain glucose metabolism by (18)F-fluorodeoxyglucose ((18)F-FDG) PET. METHOD: To observe the brain (18)F-FDG PET imaging in 9 term and 7 preterm newborn infants in the same condition after administration of 0.1 mCi/kg (18)F-FDG. RESULT: The brain (18)F-FDG PET imaging showed that the uptake of (18)F-FDG was relatively more in the thalamus, and less in the cerebral cortex in preterm and term newborn infants. The uptake of (18)F-FDG of cerebral cortex in preterm infants was less than that in term infants, so the structure of brain (18)F-FDG PET imaging was a little fainter in preterm neonates as compared with that in term newborns. CONCLUSION: (18)F-FDG PET imaging could show different glucose metabolisms of brain in preterm and term infants. Brain (18)F-FDG PET imaging might be a useful tool for estimating the brain function in newborn infants, and its clinical values need further investigation.

[Role of dendritic cells in the pathogenesis of asthma in children].

UNLABELLED: Dendritic cells (DC) are very potent antigen-presenting cells (APC) with a unique ability to activate naive T cells to induce the differentiation of TH1/TH2. Monocytes can develop into DC in the presence of different cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-4. DCs are thought to play a key role in the initiation and maintenance of T cell immunity to inhaled antigens. While the density of DC within the bronchial mucosa is increased in asthma, there is little information currently available concerning the effects of DC in asthmatic children. OBJECTIVE: To investigate the role of dendritic cells in the pathogenesis of acute attack of asthma in children. METHODS: Thomas' method was adopted. The adherent precursors of DC were isolated from peripheral blood of asthmatic children in acute attack stage and healthy controls. The adherent cells were induced with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-4 (IL-4) and tumor necrosis factor-alpha (TNF-alpha) to DC in vitro. The expression of the surface molecules CD80, CD86, HLA-DR etc. on the DC was examined by fluorescent activated cell sorter (FACS). And the ability to secret IL-10, IL-12 and their potentials to stimulate the proliferative reaction of DC inductive self T- lymphocyte were observed. RESULTS: The results showed that in asthmatic children's acute attack stage, self T- lymphocyte proliferative reaction induced by DC was remarkably increased compared with normal control subjects (P < 0.01). At the same time, the asthmatic children in acute attack stage had remarkably decreased the ability to secret IL-10 compared with normal control subjects (P < 0.01), while the ability to secret IL-12 remarkably decreased compared with normal control subjects (P < 0.01); meanwhile, the HLA-DR and co-stimulating factor CD86(B(7-2)) expressed by DCs remarkably increased in the asthmatic children in acute attack stage compared with normal control subjects (P < 0.01). CONCLUSION: DC possibly plays a vital role in the immunological mechanism of asthma by means of inducing the differentiation of TH1/TH2, that is DC may be the key factor in initiating the airway allergic reaction and the possible mechanism may involve interleukins (especially IL-10 and IL-12, etc.) secreted by DCs.

[Activation of nuclear factor kappa B in newborn rats sepsis].

OBJECTIVE: The aim of the study is to explore the effect of NF-kappa B signal pathway in neonatal sepsis so as to provide the experimental base for corresponding clinical treatment of the sepsis, in which NF-kappa B is taken as the target. METHODS: The sepsis model was established in newborn rats by giving Staphylococcus aureus subcutaneously: (1) The electrophoretic mobility shift assay (EMSA) was used to observe the activity of NF-kappa B in the lungs and the livers in newborn rats with Staphylococcus aureus sepsis. (2) Immunohistochemical method was used to observe the activity of NF-kappa B P56 in newborn rats with Staphylococcus aureus sepsis. (3) The anti-oxidant pyrrolidine dithiocarbamate (PDTC) was used to observe its effect on NF-kappa B activities of liver and lungs and on the activity of splenic NF-kappa B P56 in newborn rats with Staphylococcus aureus sepsis. RESULTS: In newborn rats with Staphylococcus aureus sepsis, the NF-kappa B activity in lungs was enhanced at the 1st hour and reached to the peak level at the 3rd hour; then, it was weakened gradually and at the 24th hour faded away. The activity of the liver NF-kappa B was also activated and peaked at the 4th hour; then, it was gradually weakened and at the 24th hour faded away. The positive expression of splenic NF-kappa B P56 began to be intensified at the 1st hour (12.0 +/- 3.7), peaked at the 3rd hour (51.4 +/- 5.9) and showed insignificant differences at the 24th hour (3.4 +/- 1.4) as compared with the sepsis group. PDTC had an inhibitive effect on the activities of liver NF-kappa B and lung NF-kappa B and on the positive expression of splenic NF-kappa B P56 used in the dosage of 50-200 mg/kg. The larger the dosage was used, the more intensified inhibitive effect could be obtained. In the dosage of 200 mg/kg, the inhibitive effect was the most intensified. CONCLUSIONS: (1) In newborn rats with Staphylococcus aureus sepsis, the NF-kappa B of lungs, liver and spleen were activated, and all indicate a peak. (2) The anti-oxidant PDTC can inhibit NF-kappa B activity in a dose-effect fashion in newborn rats with Staphylococcus aureus sepsis.