The study aimed to compare the changes between IL-6 and oxidative stress marker with 8-hydroxy-2'-deoxyguanosine (8-OHdG) from serum and tracheal aspiration (TA) in VLBW preterm infants following development of BPD.
Infectious complications were retrospectively determined in 293 (233 African-American (AA), 57 Caucasian and 3 Hispanic) mechanically ventilated very low birth weight (VLBW) infants (<1500 grams at birth) who were genotyped for the IL-6-174 G/C, IL-10 -1082 G/A and CD14 -260 C/T single nucleotide polymorphisms (SNPs).
We determined the -159T mutation of the CD14 gene, the 896G mutation of the toll-like receptor 4 gene, the 3020insC mutation of the NOD2 gene (NOD2-3020insC), the IL-6174G/C promoter polymorphism (IL6-174G/C), and the mannose-binding lectin genotype and their association to the subsequent development of neonatal sepsis in a large cohort of very low birth weight (VLBW) infants.
The aim of this study was to evaluate whether functional polymorphisms of interleukin (IL)-1beta, IL-4 receptor alpha-chain (IL-4ra), IL-6, and IL-10 genes might be associated with the risk of NEC in VLBW infants.
We investigated whether genetic polymorphisms of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-10 genes leading to a more intense inflammatory response might predispose very low birth weight (VLBW) infants to the development of ARF in severe infection.
<b>Conclusion</b> We uncovered an association between IL-10 1082 gene variation and sepsis in VLBW infants but did not identify associations between neonatal sepsis and TNF-α 308 or IL-6 gene variation.
Infectious complications were retrospectively determined in 293 (233 African-American (AA), 57 Caucasian and 3 Hispanic) mechanically ventilated very low birth weight (VLBW) infants (<1500 grams at birth) who were genotyped for the IL-6 -174 G/C, IL-10-1082 G/A and CD14 -260 C/T single nucleotide polymorphisms (SNPs).
The IL-10 -1082 SNP was determined in 294 (235 African American, 56 Caucasian, and 3 Hispanic) mechanically ventilated very low birth weight (VLBW) infants and compared to outcome (death and/or development of BPD).
The aim of this study was to evaluate whether functional polymorphisms of interleukin (IL)-1beta, IL-4 receptor alpha-chain (IL-4ra), IL-6, and IL-10 genes might be associated with the risk of NEC in VLBW infants.
We investigated whether genetic polymorphisms of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-10 genes leading to a more intense inflammatory response might predispose very low birth weight (VLBW) infants to the development of ARF in severe infection.
<b>Conclusion</b> The CRP levels and heart rate both decreased, while the pH and base excess parameters of the blood gas analysis changed positively after pentoxifylline treatment in VLBW preterm neonates with nosocomial sepsis.
Our aim was to evaluate whether single nucleotide polymorphisms (SNPs) of CD14, TLR4, and CARD15 are associated with the risk of NEC in very low birth weight (VLBW) infants.
We determined the -159T mutation of the CD14 gene, the 896G mutation of the toll-like receptor 4 gene, the 3020insC mutation of the NOD2 gene (NOD2-3020insC), the IL-6 174G/C promoter polymorphism (IL6-174G/C), and the mannose-binding lectin genotype and their association to the subsequent development of neonatal sepsis in a large cohort of very low birth weight (VLBW) infants.
We have developed for the first time a mechanistic, target-mediated disposition model that provides novel insights into the mechanisms driving Epo PK in VLBW neonates.
Thirteen very low-birth-weight premature infants (<1500 g at birth), and 10 healthy adults received up to 4 intravenous doses of Epo that ranged from 10 to 500 U/kg.
No associations between storage duration and changes in the other analytes were observed.ConclusionTransfusion of RBCs into VLBW infants is associated with increased markers of hemolysis and the inflammatory chemokine MCP-1.
We determined the -159T mutation of the CD14 gene, the 896G mutation of the toll-like receptor 4 gene, the 3020insC mutation of the NOD2 gene (NOD2-3020insC), the IL-6 174G/C promoter polymorphism (IL6-174G/C), and the mannose-binding lectin genotype and their association to the subsequent development of neonatal sepsis in a large cohort of very low birth weight (VLBW) infants.