Pediatric Research (Pediatr Res)

Publisher: International Pediatric Research Foundation, Nature Publishing Group

Journal description

Pediatric Research publishes original papers on research into the diseases, disorders and development of children, extending from molecular biology to epidemiology. Use of theoretical models, animals, or in vitro techniques relevant to developmental biology or medicine are acceptable as are human studies.

Current impact factor: 2.84

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.84
2012 Impact Factor 2.673
2011 Impact Factor 2.7
2010 Impact Factor 2.803
2009 Impact Factor 2.607
2008 Impact Factor 2.604
2007 Impact Factor 2.839
2006 Impact Factor 2.619
2005 Impact Factor 2.875
2004 Impact Factor 2.875
2003 Impact Factor 3.064
2002 Impact Factor 3.382
2001 Impact Factor 3.289
2000 Impact Factor 2.794
1999 Impact Factor 2.671
1998 Impact Factor 3.098
1997 Impact Factor 2.661

Impact factor over time

Impact factor
Year

Additional details

5-year impact 2.90
Cited half-life 9.00
Immediacy index 0.63
Eigenfactor 0.02
Article influence 0.95
Website Pediatric Research website
Other titles Pediatric research
ISSN 0031-3998
OCLC 1761994
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Nature Publishing Group

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 6 months embargo
  • Conditions
    • Authors retain copyright
    • Published source must be acknowledged and DOI cited
    • Must link to publisher version
    • Publisher's version/PDF cannot be used
    • On author's personal website and institutional repository
    • If funding agency rules apply, authors may post authors version to their relevant funding body's archive, 6 months after publication
    • This policy is an exception to the default policies of 'Nature Publishing Group'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND: Activated leukocytes and infection are implicated in neonatal brain injury. Leukocyte surface receptors are increased in stroke models and may be targets for future adjunctive therapies. METHODS: Serial blood samples were analysed from preterm infants (n= 51; <32 weeks gestation) on day 0, 1, 2 and 7 of life. Monocyte and neutrophil activation were evaluated via flow cytometry at baseline and following endotoxin stimulation ex vivo by measuring CD11b (activation), Toll-Like Receptor 4 (TLR-4; endotoxin recognition) expression and intracellular reactive oxygen intermediate (ROI) production (function). RESULTS: Control Preterm infants with normal neuroimaging had elevated baseline CD11b and TLR-4 expression, and ROI production compared with adults as well as a robust immune response following endotoxin stimulation. Preterm infants with abnormal neuroimaging had increased neutrophil TLR-4 and ROI compared with all controls. CONCLUSIONS: Preterm infants have a robust immune response compared to adults. Increased TLR-4 expression in preterm infants with abnormal neuroimaging is similar to findings in adult stroke. In addition, ROI production may cause tissue injury. The modulation of these responses may be beneficial in preterm inflammatory disorders.
    Pediatric Research 03/2015; DOI:10.1038/pr.2015.66.
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    ABSTRACT: Nutrition and growth in early post-natal life have a role in future diseases. Our aim was to investigate adiponectin oligomers in AGA obese children with respect to type and duration of feeding in the first year of life. Adiponectin oligomers and cardiometabolic risk factors were measured in 113 AGA obese children, divided into group A (prolonged breast feeding, > 6 months), group B (short breast feeding; 1-6 months); group C (formula feeding from birth). All the parameters were similar among the groups. Adiponectin oligomers did not correlate with gestational age, months of breast feeding and time of weaning. Total and HMW adiponectin were differently distributed across gender and pubertal stages (p<0.02), being lower in males from the start of puberty. Pre-pregnancy BMI and at the end of the pregnancy were negatively associated (p<0.04) with total and MMW adiponectin in female and male offspring, respectively. Adiponectin oligomers and metabolic characteristics are similarly distributed in AGA obese children, irrespective of the type and duration of the feeding in the first year of life. Gender and mother's BMI in pregnancy are contributors to adiponectin regulation. Further studies will explain whether breast feeding protects against metabolic impairment later in life.Pediatric Research (2015); doi:10.1038/pr.2015.52.
    Pediatric Research 03/2015; DOI:10.1038/pr.2015.52
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    ABSTRACT: Breastfeeding has been associated with improved cognitive development. This may be explained by polyunsaturated fatty acid (PUFA) content of breast milk, especially long-chain (LC) PUFA that are needed for postnatal brain growth. Using data from the French EDEN cohort, we aimed to study whether the PUFA content of colostrum may explain observed associations between breastfeeding duration and cognitive scores at 2 and 3 years. A total of 709 breastfed children with available data on PUFA composition of milk were assessed using parent-reported questionnaires for motor and language at 2 years of age, or global cognition at 3 years. Multiple linear regressions were used to examine associations between PUFA levels and child cognitive scores, after controlling for many confounders. We found no association between LCPUFA levels in colostrum and child development. However, levels of linoleic acid (LA) were negatively associated with motor and cognitive scores, independently of breastfeeding duration. Children breastfed with the highest levels of LA tended to score closer to the never breastfed children than children breastfed with the lowest levels of LA. Our findings suggest that too high levels of LA in colostrum are associated with poorer child development at 2 and 3 years.Pediatric Research (2015); doi:10.1038/pr.2015.50.
    Pediatric Research 03/2015; DOI:10.1038/pr.2015.50
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    ABSTRACT: Despite years of research, the etiologies of preterm birth remain unclear. In order to help generate new research hypotheses, this study explored spatial and temporal patterns of preterm birth in a large, total-population dataset. Data on 145 million U.S. births in 3,000 counties from the Natality Files of the National Center for Health Statistics for 1971-2011 were examined. State trends in early (<34 weeks) and late (34-36 weeks) preterm birth rates were compared. K-means cluster analyses were conducted to identify gestational age distribution patterns for all US counties over time. A weak association was observed between state trends in <34 weeks birth rates and the initial absolute <34 weeks birth rate. Significant associations were observed between trends in <34 weeks and 34-36 weeks birth rates and between white and African American <34 weeks births. Periodicity was observed in county-level trends in <34 weeks birth rates. Cluster analyses identified periods of significant heterogeneity and homogeneity in gestational age distributional trends for U.S. counties. The observed geographic and temporal patterns suggest periodicity and complex, shared influences among preterm birth rates in the United States. These patterns could provide insight into promising hypotheses for further research.Pediatric Research (2015); doi:10.1038/pr.2015.55.
    Pediatric Research 03/2015; DOI:10.1038/pr.2015.55
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    ABSTRACT: Preterm infants may inadvertently be exposed to lead from the pRBC transfusions with almost no or very limited data available. The aim of the study was to quantify this exposure in preterm infants ≤30 weeks gestational age (GA). Prospective cohort study, infants ≤30 weeks GA were eligible, infants < 23 weeks GA and known chromosomal diseases were excluded. Blood lead levels (BLLs) were obtained at birth, before and after each transfusion, and at discharge. BLLs were also obtained from the donor pRBC aliquot transfused. A linear mixed model analysis was done. Of 75 infants, 34 received a total of 126 pRBC transfusions. Each infant had an average of 3.7 transfusions. 92% of lead levels in the transfused aliquot were ≤ 5 mcg/dl, 6.8 % were between 6-8mcg/dl and 1 had a level of 56mcg/dl. Average total lead load was 1.3 mcg/dL. For each 1 mcg/dl increase in transfused pRBC lead level, infant's post-transfusion BLL increased by 0.20 mcg/dl, (95%CI: 0.07 mcg/dl, 0.33 mcg/dl; p=0.002) adjusting for GA and birth weight. No significant increase in discharge BLLs, which were similar for both transfused and non-transfused infants. Post-transfusion infant BLLs correlate significantly with the transfused pRBCs lead level.Pediatric Research (2015); doi:10.1038/pr.2015.53.
    Pediatric Research 03/2015; DOI:10.1038/pr.2015.53
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    ABSTRACT: Bronchopulmonary dysplasia (BPD) is one of the leading causes of morbidity and mortality in babies born prematurely, yet there is no curative treatment.In recent years, a number of inhibitors against TGFβ signaling have been tested for their potential to prevent neonatal injury associated with hyperoxia, which is a contributing factor of BPD. In this study we assessed the contribution of activin A - a member of the TGFβ superfamily - to the development of hyperoxia induced lung injury in neonatal mice. We placed newborn C57Bl6 mouse pups in continuous hyperoxia (85% O2) to mimic many aspects of BPD including alveolar simplification and pulmonary inflammation. The pups were administered activin A receptor type IIB-Fc antagonist (ActRIIB-Fc) at 5mg/kg or follistatin at 0.1mg/kg on postnatal days 4, 7, 10 and 13. Treatment with ActRIIB-Fc and follistatin protected against hyperoxia-induced growth retardation. ActRIIB-Fc also reduced pulmonary leukocyte infiltration, normalised tissue: airspace ratio and increased septal crest density. These findings were associated with reduced phosphorylation of Smad3 and decreased MMP-9 activity. This study suggests that activin A signaling may contribute to the pathology of bronchopulmonary dysplasia.Pediatric Research (2015); doi:10.1038/pr.2015.46.
    Pediatric Research 03/2015; DOI:10.1038/pr.2015.46
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    ABSTRACT: Background:Heme Oxygenase 1 (HO1) catalyzes heme degradation, and offers protection for several organs, including the kidney. Genetic polymorphisms of HO-1 are associated with poor clinical outcomes in several populations.Methods:Population: We prospectively enrolled 117 premature infants (birth weight ≤1200 gm. or post gestational age ≤31 weeks) and evaluated 2 DNA genetic variants proximal to the promoter region of HO-1 (GT(n) repeats, and -413T>A SNP). We evaluated how these polymorphisms affect 2 clinical outcomes i) AKI - rise in serum creatinine (SCr) ≥ 0.3 mg/dl or ≥ 150-200% from lowest previous value, ii) bronchopulmonary dysplasia (BPD) defined as receipt of oxygen at 36 weeks post menstrual age (PMA) / mortality.Results:AKI occurred in 34/ 117 (29%) of neonates; 12/117 (10%) died; 29/105 (28%) survivors had BPD. Neonates with TT genotype at 413T>A before the HO-1 promoter had higher rates of AKI (p<0.05). There was no difference in number of GT(n) repeats and clinical outcomes.Conclusions:We did not find an association between the GT(n) tandem repeat of HO-1 and AKI nor BPD/mortality. However, infants with TT genotype of the 413T>A genetic alteration had lower incidence of AKI. Further studies using larger cohorts are needed to better understand these relationships.Pediatric Research (2015); doi:10.1038/pr.2015.44.
    Pediatric Research 03/2015; DOI:10.1038/pr.2015.44
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    ABSTRACT: Background:Postconditioning (PostC) with mild hypoxia shortly after a neonatal hypoxic-ischaemic (HI) brain injury can reduce brain damage however, the mechanisms underlying this protection are not known. We hypothesize that hypoxic PostC reduces brain markers of glial activity, inflammation and apoptosis following HI injury.Methods:Sprague Dawley rat pups were exposed to right common carotid artery occlusion and hypoxia (7% oxygen, 3 hours) on postnatal day 7 and 24 hours later, pups were exposed to hypoxic PostC (8% O2 for 1 hour/day for 5 days) or kept at ambient conditions for the same duration. HI+N pups demonstrated ~10% loss in ipsilateral brain tissue which was rescued with HI+PostC. To investigate the cellular responses, markers of astrocytes, microglia, inflammation, and caspase 3 activity were examined using immunohistochemistry and enzyme-linked immunosorbent assay.Results:PostC reduced the area of astrocyte staining compared to HI+N. There was also a shift in microglial morphology towards a primed state in both PostC groups. Protein levels of interleukin-1β and caspase 3 were elevated in HI+N brains and reduced by PostC.Conclusion:This is the first demonstration that PostC can reduce glial activity, inflammatory mediators and cell death after a neonatal HI brain injury.Pediatric Research (2015); doi:10.1038/pr.2015.47.
    Pediatric Research 03/2015; DOI:10.1038/pr.2015.47
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    ABSTRACT: Background:The alpha2-adrenergic agonist dexmedetomidine (DEX) is increasingly used for prolonged sedation of critically ill neonates, but there are currently no data evaluating possible consequences of prolonged neonatal DEX exposure. We evaluated the pharmacokinetics and histological consequences of neonatal DEX exposure.Methods:DEX was administered (s.c.) to naïve (uninjured) neonatal Lewis rats to provide acute (25 µg/kg, x1) or prolonged (25 µg/kg three times daily, x2 or x4 days) exposure. Therapeutic hypothermia was simulated using a water-cooled blanket. Cranial temperatures were measured using an infrared thermometer. DEX concentrations were measured by LC-MS in plasma and homogenized brainstem tissue for pharmacokinetic analysis. Cortex, cerebellum and brainstem were evaluated for evidence of inflammation or injury.RESULTS:Prolonged neonatal DEX exposure was not associated with renal or brain pathology or indices of gliosis, macrophage activation, or apoptosis in either hypothermic or control rats. Plasma and brain DEX concentrations were tightly correlated. DEX peaked within 15 min in brain and reduced cranial temperature from 32 to 30ºC within 30 min after injection in cooled rats.CONCLUSION:Prolonged DEX treatment in neonatal rats was not associated with abnormal brain histology. These data provide reassuring preliminary results for using DEX with therapeutic hypothermia to treat near-term brain injury.Pediatric Research (2015); doi:10.1038/pr.2015.45.
    Pediatric Research 03/2015; DOI:10.1038/pr.2015.45
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    ABSTRACT: Background To develop serum creatinine (s[Cr]) reference ranges for VLBW infants from birth to 34-36 wk post menstrual age (PMA).Methods Retrospectively identified sample of 218 appropriate-for-GA VLBW infants without risk factors for renal impairment, classified into one of three GA groups: 25-27 wk, 28-29 wk, 30-33 wk. We observed three phases s[Cr] change (initial, decline, and equilibrium), whose characteristics varied by GA group. We used mixed-effects regression models to estimate mean and upper 95(th) prediction interval of s[Cr] for each GA group from birth to 34-36 wk PMA.ResultsIn phase 1, s [Cr] increased after birth, then returned slowly to baseline. The duration of phase 1 and the magnitude of s[Cr] rise decreased with increasing GA. In phase 2, s [Cr] declined abruptly at a rate that increased with GA. A gradual transition to Phase 3, steady state equilibrium with similar s[Cr] among GA groups, began at approximately 34-36 wk PMA. We constructed GA group-specific nomograms depicting s[Cr] behavior across the 3 phases.Conclusion Reference ranges derived from a sample of infants without risk factors for renal impairment provide a context for quantitative interpretation of s[Cr] trends in VLBW infants.Pediatric Research (2015); doi:10.1038/pr.2015.25.
    Pediatric Research 02/2015; DOI:10.1038/pr.2015.25
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    ABSTRACT: Background Smith-Lemli-Opitz syndrome (SLOS) is a rare disease caused by biallelic mutation in the 7-dehydrocholesterol (7DHC) reductase gene. High oxidizability of 7DHC and the appearance of small-sized low-density lipoprotein (LDL) subfractions indicate increased endogenous oxidative stress that is counterbalanced by natural antioxidant defense mechanisms including the high-density lipoprotein (HDL)-associated paraoxonase-1 (PON1) enzyme. PON1 prevents lipoproteins from oxidative modifications; however, PON1 activity and the distribution of lipoprotein subfractions have not been studied in SLOS.Methods7DHC levels and PON1 arylesterase activities were measured spectrophotometrically in eleven SLOS patients and ten healthy children. Lipoprotein subfractions were detected by polyacrylamide gel electrophoresis.ResultsCompared to controls, there was a shift towards the small-dense LDL subfraction and the large HDL subfraction in SLOS. PON1 arylesterase activity was significantly decreased in SLOS patients and correlated negatively with the proportion of small-dense LDL subfraction and the proportion of large HDL subfraction. Significant positive correlations were detected between PON1 arylesterase activity and the ratios of intermediate and small HDL subfractions.Conclusions Decreased PON1 activity and the deleterious shift in the distribution of lipoprotein subfractions may contribute to the impaired antioxidant status observed in SLOS. Monitoring of serum PON1 arylesterase activity may be a complementary biomarker in SLOS.Pediatric Research (2015); doi:10.1038/pr.2015.33.
    Pediatric Research 02/2015; DOI:10.1038/pr.2015.33
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    ABSTRACT: Background Three risk factors are associated with hemorrhagic forms of encephalopathy of prematurity (EP): (i) prematurity, (ii) in utero ischemia (IUI) or perinatal ischemia, and (iii) mechanical ventilation. We hypothesized that IUI would induce an angiogenic response marked by activation of vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9), the latter degrading vascular basement membrane and increasing vulnerability to raised intravenous pressure during positive pressure mechanical ventilation.Methods We studied a rat model of hemorrhagic-EP characterized by periventricular hemorrhages in which a 20-min episode of IUI is induced at E19, pups are born naturally at E21-22, and on P0, are subjected to a 20-min episode of positive pressure mechanical ventilation. Tissues were studied by H&E staining, immunolabeling, immunoblot and zymography.ResultsMechanical ventilation of rat pups 2-3 days after 20-min IUI caused widespread hemorrhages in periventricular tissues. IUI resulted in upregulation of VEGF and MMP-9. Zymography confirmed significantly elevated gelatinase activity. MMP-9 activation was accompanied by severe loss of MMP-9 substrates, collagen IV and laminin, in microvessels in periventricular areas.Conclusions Our findings are consistent with the hypothesis that positive pressure mechanical ventilation of the newborn in the context of recent prenatal ischemia/hypoxia can predispose to periventricular hemorrhages.Pediatric Research (2015); doi:10.1038/pr.2015.34.
    Pediatric Research 02/2015; DOI:10.1038/pr.2015.34
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    ABSTRACT: Background Angiotensin (ANG) II is involved in experimental hyperoxia-induced lung fibrosis. Angiotensin Converting Enzyme-2 (ACE-2) degrades ANG II and is thus protective, but is downregulated in adult human and experimental lung fibrosis. Hyperoxia is a known cause of chronic fibrotic lung disease in neonates, but the role of ACE-2 in neonatal lung fibrosis is unknown. We hypothesized that ACE-2 in human fetal lung cells might be downregulated by hyperoxic gas.Methods Fetal human lung fibroblast IMR90 cells were exposed to hyperoxic (95% O2/5% CO2) or normoxic (21% O2/5% CO2) gas in vitro. Cells and culture media were recovered separately for assays of ACE-2 enzymatic activity, mRNA and immunoreactive protein.ResultsHyperoxia decreased ACE-2 immunoreactive protein and enzyme activity in IMR90 cells (both p<0.01), but did not change ACE-2 mRNA. ACE-2 protein was increased in the cell supernatant, suggesting protease-mediated ectodomain shedding. TAPI-2, an inhibitor of TNF-α Converting Enzyme (TACE/ADAM17), prevented both the decrease in cellular ACE-2 and the increase in soluble ACE-2 (both p<0.05).Conclusions These data show that ACE-2 is expressed in fetal human lung fibroblasts but is significantly decreased by hyperoxic gas. They also suggest that hyperoxia decreases ACE-2 through a shedding mechanism mediated by ADAM17/TACE.Pediatric Research (2015); doi:10.1038/pr.2015.27.
    Pediatric Research 02/2015; DOI:10.1038/pr.2015.27
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    ABSTRACT: BackgroundNEC, an intestinal inflammatory disease affecting premature infants, is associated with low regulatory T (Treg) to effector T (Teff) cell ratios. We recently demonstrated that heme oxygenase-1 (HO-1) deficiency leads to increased NEC development. Here, we investigated the effects of HO-1 on T cell proportions in a murine NEC-like injury model.Methods Intestinal injury was induced in 7d-old WT or HO-1 heterozygous (Het) pups by p.o. formula-feeding every 4h for 24-78h and exposures to 5%O2. Controls remained breastfed. HO-1 was induced in WT pups by administering heme pre-injury induction. Lamina propria T cells were identified by flow cytometry. For adoptive transfer studies, WT splenic/thymic Tregs were injected i.p. into Het pups 12-24h pre-induction.ResultsHet mice showed increased intestinal injury and decreased Treg/Teff ratios. Genes for pattern recognition (TLR4, C-reactive protein, MyD88) and neutrophil recruitment increased in Het pups after NEC induction. Inducing intestinal HO-1 decreased NEC scores and incidence, and increased Treg/Teff ratios. Moreover, adoptive transfer of Tregs from WT to Het pps decreased NEC scores and incidence and restored Treg/Teff ratios.ConclusionsHO-1 can change Treg proportions in the lamina propria of young mice under inflammatory conditions, which might, in part, confer partial intestinal protection.Pediatric Research (2015); doi:10.1038/pr.2015.22.
    Pediatric Research 02/2015; DOI:10.1038/pr.2015.22