Surfactant protein C (SP-C) is an important constituent of lung surfactant (LS) and, along with SP-B, is included in exogenous surfactant replacement therapies for treating respiratory distress syndrome (RDS).
By balancing these features in one mimic, a novel analogue was created that emulates SP-C's in vitro surface activity while overcoming many of the challenges related to natural SP-C. Peptoid-based analogues hold great potential for use in a synthetic, biomimetic LS formulation for treating RDS.
Recently the first synthetic surfactant that contains analogues of the two hydrophobic surfactant proteins B (SP-B) and SP-C entered clinical trials for the treatment of neonatal RDS.
In neonates, elevated SP-D levels in cord blood and on day 1 have been associated with prenatal risk factors and with an increased risk of respiratory distress syndrome and infections.
Compared with healthy newborn rabbits, the mRNA and protein expression levels of miR-200a and IL-10 in the blood of newborn rabbits with RDS decreased significantly (p<0.05), while β-catenin increased markedly (p<0.05).
One hundred child patients with NRDS in Linyi Central Hospital were collected according to the diagnostic criteria for RDS in the Pediatrics, and randomly divided into the treatment group (n=50) and the control group (n=50) based on different therapeutic methods.
Intra-amniotic exposure to proinflammatory cytokines such as interleukin-1 (IL-1) correlates with a decreased incidence of respiratory distress syndrome (RDS) in infants following premature birth.
We observed the need for CPAP in three neonates (1%), respiratory distress syndrome (RDS) in three neonates (1%), transient tachypnea of the newborn (TTN) in two neonates (1%), need for resuscitation at birth in one neonate (0.5%), and apnea in one neonate (0.5%).
Intra-amniotic exposure to proinflammatory cytokines such as interleukin-1 (IL-1) correlates with a decreased incidence of respiratory distress syndrome (RDS) in infants following premature birth.
However, the potential role of miR-34a in the regulation of pulmonary endothelial dysfunction, vascular injury, and endothelial cells (ECs) apoptosis in acute lung injury (ALI)/acute lung respiratory distress syndrome is largely unknown.
Individuals with PCD caused by mutations in <i>RSPH1</i> (radial spoke head 1 homolog) have been reported to have a milder phenotype than other individuals with PCD, as evidenced by a lower incidence of neonatal respiratory distress, higher nasal nitric oxide concentrations, and better lung function.
One hundred child patients with NRDS in Linyi Central Hospital were collected according to the diagnostic criteria for RDS in the Pediatrics, and randomly divided into the treatment group (n=50) and the control group (n=50) based on different therapeutic methods.
However, when we restricted the analysis to the studies that adjust for Gestational Age, in order to exclude the influence of prematurity, we found that HCA reduced the risk of respiratory distress syndrome (RR 0.57, CI 95% 0.35-0.93) and it did not affect the development of Bronchopulmonary Dysplasia (RR 0.99, CI 0.76-1.3).
Compared with those in normal tissues, the expression of miR-26a in lung tissues of neonatal rats with RDS was significantly decreased (p<0.05), while the expression of GSK-3β messenger RNAs (mRNAs) was notably increased (p<0.01), and the GSK-3β expression was negatively correlated with the miR-26a expression (r=-0.6693, p=0.0064).
Compared with healthy newborn rabbits, the mRNA and protein expression levels of miR-200a and IL-10 in the blood of newborn rabbits with RDS decreased significantly (p<0.05), while β-catenin increased markedly (p<0.05).
Compared with healthy newborn rabbits, the mRNA and protein expression levels of miR-200a and IL-10 in the blood of newborn rabbits with RDS decreased significantly (p<0.05), while β-catenin increased markedly (p<0.05).