Alveolar type II cells are main target of hyperoxia-induced lung injury. The authors investigated whether lysosomal protease, cathepsin B (CB), is activated in fetal alveolar type II cells in the transitional period from the canalicular to saccular stages during 65%-hyperoxia and whether CB is related to fetal alveolar type II cell (FATIIC) death secondary to hyperoxia. FATIICs were isolated from embryonic day 19 rats and exposed to 65%-oxygen for 24 h and 36 h. The cells exposed to room air were used as controls. Cell cytotoxicity was assessed by lactate dehydrogenase-release and flow cytometry, and apoptosis was analyzed by TUNEL assay and flow cytometry. CB activity was assessed by colorimetric assay, qRT-PCR and western blots. 65%-hyperoxia induced FATIIC death via necrosis and apoptosis. Interestingly, caspase-3 activities were not enhanced in FATIICs during 65%-hyperoxia, whereas CB activities were greatly increased during 65%-hyperoxia in a time-dependent manner, and similar findings were observed with qRT-PCR and western blots. In addition, the preincubation of CB inhibitor prior to 65%-hyperoxia reduced FATIIC death significantly. Our studies suggest that CB activation secondary to hyperoxia might have a relevant role in executing the cell death program in FATIICs during the acute stage of 65%-hyperoxia.
Among 312 rotavirus-positive samples collected from eight hospitals across South Korea during 2008 and 2009, the most prevalent circulating G genotype was G1 (35.9%), followed by G3 (24.7%), G2 (17.0%), G4 (7.7%), and G9 (2.6%). Notably, one unusual G11 lineage III strain-the first hypoendemic infection case in the world-was found. Of the P genotypes, P[8] (43.9%) was the most common, followed by P[6] (29.5%), P[4] (9.3%) and P[9] (0.6%). Determining G- and P-type combinations showed that G1P[8] was the most prevalent (20.5%), followed by G2P[6] (12.8%) and G3P[8] (12.8%). These findings provide new information concerning the current prevalence and spread of the rare G11 rotavirus.
Amyoplasia congenita is a diagnostic subgroup of children with arthrogryposis multiplex congenita (AMC). AMC is a relatively rare syndrome characterized by multiple joint contractures at birth. Amyoplasia congenita is the most common type of this syndrome with an occurrence rate of 1 in 10,000 live births, and mainly refers to the disorders with limb involvement. In this report, the author presents a premature baby with amyoplasia congenita, whose hips showed flexion, abduction, and external rotation contractures. The knees showed fixed extension contractures, so that his lower extremities were cylindrical with absent skin creases at birth.
Purpose: Lung injury imposed by hyperoxia is the most important cause of bronchopulmonary dysplasia (BPD) in premature lungs, and hyperoxia has the chief biological effect of inducing cell death. The objective of this study was to investigate the response of cell death in fetal alveolar type II cells (FATIICs) exposed to different concentrations of hyperoxia for 36 h. Methods: FATIICs were isolated on embryonic day 19 and exposed to 65%-or 85%-oxygen for 36 h. Cells in room air were used as controls. FACScan was performed in hyperoxic and control samples at 0/6/12/24/36 h, and the patterns of cell death were compared at each time point using flow-cytometry. Results: Cell necrosis as measured by selective propidium iodide staining increased significantly from 12 h of 65%-hyperoxia and 6 h of 85%-hyperoxia, respectively. Cell necrosis increased 1.6-fold, 3.0-fold and 4.6-fold after 12 h, 24 h, and 36 h, respectively during 65%-hyperoxia and increased by 2.4-fold, 3.1-fold, 6.3-fold, and 8.8-fold after 6 h, 12 h, 24 h, and 36 h, respectively during 85%-hyperoxia compared to controls. Apoptotic cells as measured by selective Annexin-V staining peaked at 1.3% at 24 h of 65%-hyperoxia and peaked at 1.2% at 6 h of 85%-hyperoxia, respectively and then decreased rapidly. Conclusion: This study shows that exposure to sublethal and lethal hyperoxia increases necrosis of FATIICs remarkably from the early stage of hyperoxia. These findings support the idea that short-term exposure to oxygen from birth may contribute to the evolution of "new" BPD in preterm lungs.
Purpose: To compare respiratory and clinical outcomes between the currently used strategy of Intubation, Surfactant, Extubation (InSurE) and nasal continuous positive airway pressure (NCPAP) and the alternative strategy of InSurE and nasal intermittent positive pressure ventilation (NIPPV) for the initial treatment of respiratory distress syndrome (RDS) in preterm newborns ≤32 weeks. Methods: Twenty-six comparable preterm infants with RDS were included in the study; 13 were randomized to NCPAP and 13 to NIPPV. In both groups, the InSurE procedure consisted of intubation, surfactant instillation and 2 h positive pressure ventilation followed by extubation, after which spontaneously breathing newborns were placed on NCPAP or NIPPV. Results: There were no differences in demographic characteristics or cardiorespiratory status among preterm infants enrolled in the study. The reinutation rate was lower among the infants treated with NIPPV than among those on NCPAP (8% vs. 46%, P<0.05) and the rate of aminophylline use between 4 and 7 days of age of was lower in the NIPPV group compared to the NCPAP group (8% vs. 30%, P<0.05). In addition, "InSurE with NIPPV" significantly reduced the overall duration of endotracheal ventilation and shortened the time to first feed compared to "InSurE with NCPAP". Conclusion: "InSurE with NIPPV" displayed therapeutic benefits as the initial treatment of preterm RDS when compared with the currently used ventilator strategy, "InSurE with NCPAP" by preventing re-intubation and shortening the duration of endotracheal ventilation.
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