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Background: In preterm newborns, neonatal respiratory distress syndrome (RDS) is among the main causes of respiratory failure and mortality. However, the effect of macrophage migration-inhibitory factor (MIF) on neonatal developmental lung disease is not well documented in the literature. Moreover, little is known about the effects of growth differentiation factor-15 (GDF-15) on lung maturity in preterm infants.Purpose: To evaluate serum MIF and GDF-15 levels in preterm infants with and without RDS and analyze the genetic profile of single nucleotide polymorphisms (SNPs) for MIF rs755622 G>C and GDF-15 rs4808793 C>GMethods: In this case-control study, 90 preterm newborns were categorized into 3 groups: group A included 30 preterm newborns with mild to moderate RDS, group B included 30 preterm newborns with severe RDS, and group C included 30 healthy preterm newborns. Enzyme-linked immunosorbent assay methods were used to measure serum MIF and GDF-15 levels. The MIF rs755622 G>C and GDF-15 rs4808793 C>G SNPs were analyzed by restriction fragment length polymorphism-polymerase chain reaction.Results: Significantly higher median MIF and GDF-15 blood levels were noted among neonates with severe RDS (17.32 μg/L and 3.19 pg/mL, respectively) versus those with mild to moderate RDS (5.50 μg/L and 0.71 pg/mL, respectively) (P<0.05 for both). A significantly higher frequency of a mutant C-allele of MIF rs755622 G>C was noted among cases (37.5%) versus controls (13.3%) (P=0.001; odds ratio [OR], 0.256; 95% confidence interval [CI], 0.112–0.589). A significantly higher frequency of a mutant G-allele of GDF-15 rs4808793 C>G SNPs was noted among cases (49.2%) versus controls (30%) (OR, 0.443; 95% CI, 0.229–0.856).Conclusion: These findings suggest that serum MIF and GDF-15 levels are strongly associated with RDS severity among preterm neonates. Moreover, polymorphisms of MIF and GDF-15 could be genetic risk factors for the development of neonatal RDS among preterm babies.

To determine the bacteriological pattern and antibiotic susceptibility of bacterial isolates causing neonatal sepsis in Qena University Hospitals and compare polymerase chain reaction (PCR) and blood culture results in a trial for rapid diagnosis. Blood samples from 75 clinically suspected cases of neonatal sepsis were subjected to identification of bacteria and determination of their antibiotic sensitivity through blood culture, and rapid detection of 16S rRNA and the uidA gene (to confirm the presence of ) by PCR from extracted bacterial DNA. Most patients were preterm (64%) and low birth weight (LBW) (68%). In total, 42.7% presented with early onset sepsis (EOS). LBW was significantly associated with EOS ( -value=0.03). Although the blood culture and PCR results were similar in EOS, the PCR results were significantly higher than those of blood culture in detecting bacteria (85.3% vs 68%, respectively, -value=0.001). Blood culture showed 100% specificity. The most common pathogen was (86.2%) in EOS and . (45.5%) in late-onset sepsis (LOS) ( -value=0.001 and 0.02, respectively). The most effective antibiotics against Gram-negative bacteria were ofloxacin, ciprofloxacin, imipenem, and amikacin, while vancomycin, oxacillin, and imipenem were the most effective antibiotics against Gram-positive bacteria. EOS was mainly caused by , while LOS was mainly caused by . The 16S rRNA PCR showed higher sensitivity with rapid and accurate diagnosis. Blood culture is the most suitable method for antimicrobial sensitivity testing.

In preterm newborns, neonatal respiratory distress syndrome (RDS) is among the main causes of respiratory failure and mortality. However, the effect of macrophage migration inhibitory factor (MIF) on neonatal developmental lung disease is not well documented in the literature. Moreover, little is known about the effects of growth differentiation factor-15 (GDF-15) on lung maturity in preterm infants.BackgroundIn preterm newborns, neonatal respiratory distress syndrome (RDS) is among the main causes of respiratory failure and mortality. However, the effect of macrophage migration inhibitory factor (MIF) on neonatal developmental lung disease is not well documented in the literature. Moreover, little is known about the effects of growth differentiation factor-15 (GDF-15) on lung maturity in preterm infants.To evaluate serum MIF and GDF-15 levels in preterm infants with and without RDS and analyze the genetic profile of single nucleotide polymorphisms (SNPs) for MIF rs755622 G>C and GDF-15 rs4808793 C>G.PurposeTo evaluate serum MIF and GDF-15 levels in preterm infants with and without RDS and analyze the genetic profile of single nucleotide polymorphisms (SNPs) for MIF rs755622 G>C and GDF-15 rs4808793 C>G.In this case-control study, 90 preterm newborns were categorized into three groups: group A included 30 preterm newborns with mild-to-moderate RDS, group B included 30 preterm newborns with severe RDS, and group C included 30 healthy preterm newborns. Enzyme-linked immunosorbent assay methods were used to measure serum MIF and GDF-15 levels. The MIF rs755622 G>C and GDF-15 rs4808793 C>G SNPs were analyzed by restriction fragment length polymorphism-polymerase chain reaction.MethodsIn this case-control study, 90 preterm newborns were categorized into three groups: group A included 30 preterm newborns with mild-to-moderate RDS, group B included 30 preterm newborns with severe RDS, and group C included 30 healthy preterm newborns. Enzyme-linked immunosorbent assay methods were used to measure serum MIF and GDF-15 levels. The MIF rs755622 G>C and GDF-15 rs4808793 C>G SNPs were analyzed by restriction fragment length polymorphism-polymerase chain reaction.Significantly higher median MIF and GDF-15 blood levels were noted among neonates with severe RDS (17.32 µg/L and 3.19 pg/mL, respectively) versus those with mild to moderate RDS (5.5 µg/L and 0.71 pg/mL, respectively) (p <0.05 for both). A significantly higher frequency of a mutant C-allele of MIF rs755622 G>C was noted among cases (37.5%) versus controls (13.3%) (p=0.001; odds ratio, 0.256; 95% confidence interval, 0.112-0.589). A significantly higher frequency of a mutant G-allele of GDF-15 rs4808793 C>G SNPs was noted among cases (49.2%) versus controls (30%) (odds ratio, 0.443; 95% confidence interval, 0.229-0.856).ResultsSignificantly higher median MIF and GDF-15 blood levels were noted among neonates with severe RDS (17.32 µg/L and 3.19 pg/mL, respectively) versus those with mild to moderate RDS (5.5 µg/L and 0.71 pg/mL, respectively) (p <0.05 for both). A significantly higher frequency of a mutant C-allele of MIF rs755622 G>C was noted among cases (37.5%) versus controls (13.3%) (p=0.001; odds ratio, 0.256; 95% confidence interval, 0.112-0.589). A significantly higher frequency of a mutant G-allele of GDF-15 rs4808793 C>G SNPs was noted among cases (49.2%) versus controls (30%) (odds ratio, 0.443; 95% confidence interval, 0.229-0.856).These findings suggest that serum MIF and GDF-15 levels are strongly associated with RDS severity among preterm neonates. Moreover, polymorphisms of MIF and GDF-15 could be genetic risk factors for the development of neonatal RDS among preterm babies.ConclusionThese findings suggest that serum MIF and GDF-15 levels are strongly associated with RDS severity among preterm neonates. Moreover, polymorphisms of MIF and GDF-15 could be genetic risk factors for the development of neonatal RDS among preterm babies.

Background: Pediatric patients infected with coronavirus disease 2019 (COVID-19) have unique clinical characteristics. Tumor necrosis factor (TNF) is a proinflammatory cytokine that greatly contributes to tumor pathogenesis.Purpose: To describe the presenting characteristics of COVID-19 infection among pediatric patients, and investigate the possible role of the TNF-α signaling pathway.Methods: This prospective case-control study included 50 Egyptian pediatric patients with COVID-19 and 50 healthy controls. Clinical, laboratory, and radiological assessments were performed. Serum TNF-alpha (TNF-α), TNF-α-converting enzyme (TACE), and angiotensin-converting enzyme 2 (ACE2) were measured using enzyme-linked immunosorbent assay. ACE (I/D) (rs4646994), ACE2 rs2285666, and TNF-α-308G/A single nucleotide polymorphisms (SNPs) were performed using conventional polymerase chain reaction techniques with or without restriction fragment length polymorphism.Results: The median age was 1 year (interquartile range [IQR], 0.31–2.50 years) in the case group and 1.45 years (IQR, 1.00–3.00) in the control group. The main presenting symptoms were fever (92%), dry cough (74%), and dyspnea (72%). The lymphocytic count was normal in 14 patients (28%), decreased in 16 patients (32%), and increased in 20 patients (40%) of the case group. Positive chest computed tomography finding of COVID-19 infection were demonstrated among 40% of patients using COVID-19 Reporting and Data System categories (ground-glass opacity with or without consolidations in the lungs). There were significant increased serum TACE and TNF-α with decreased ACE2 levels among cases versus controls (P< 0.001). The GG genotype and G allele of the TNF-α-308G/A SNP were significantly higher in patients than in controls (P<0.05 for both), with insignificant differences in genotype and allelic frequencies in the ACE (I/D) (rs4646994) and ACE2 rs2285666 SNPs.Conclusion: The TNF signaling pathway was significantly activated in pediatric COVID-19 infection. Only the TNF-α-308G/A SNP was significantly associated with pediatric COVID-19 infection.