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: 2.31

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.314
2013 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

Additional details

5-year impact 2.86
Cited half-life 9.70
Immediacy index 0.60
Eigenfactor 0.02
Article influence 0.97
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

Publications in this journal

  • Catherine Monk · Michael K. Georgieff · Dongrong Xu · Xuejun Hao · Ravi Bansal · Hanna Gustafsson · Julie Spicer · Bradley S. Peterson ·
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    ABSTRACT: Background: Children prenatally exposed to inadequate iron have poorer motor and neurocognitive development. No prior study to our knowledge has assessed the influence of maternal prenatal iron intake on newborn brain tissue organization in full term infantsMethods:3(rd) trimester daily iron intake was obtained using the Automated SelfAdministered 24hour Dietary Recall with n=40 healthy pregnant adolescents (14-19 years old). Cord blood ferritin was collected in a subsample (n=16). Newborn (m=39 gestational weeks at birth; range 37-41) Neonatal MRI scans were acquired on a 3.0 Tesla MR Scanner. Diffusion Tensor Imaging (DTI) slices were acquired to measure the directional diffusion of water indexed by fractional anisotropy (FA). Results: Reported iron intake was inversely associated with newborn FA values (P ≤.0001) predominantly in cortical gray matter. FA findings were similar using cord blood ferritin values. Conclusion: Higher maternal prenatal iron intake accentuates, and lower intake attenuates, the normal age- related decline in FA values in gray matter, perhaps representing increasing dendritic arborization and synapse formation with higher iron intake. These DTI results suggest that typical variation in maternal iron outside the scope of standard clinical surveillance exerts subtle effects on infant brain development.Pediatric Research (2015); doi:10.1038/pr.2015.248.
    Pediatric Research 11/2015; DOI:10.1038/pr.2015.248
  • David J. Askenazi · Catherine Morgan · Stuart L. Goldstein · David T. Selewski · Marva M. Moxey-Mims · Paul L. Kimmel · Robert A. Star · Rosemary Higgins · Matthew Laughon ·
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    ABSTRACT: Survival rates in critically ill neonates have improved; yet, many sustain long-term morbidities, including chronic kidney disease (CKD). Premature infants are at high risk to develop acute kidney injury (AKI), and those with AKI are more likely to die. Growing evidence in pediatric, and adult cohorts suggest that AKI leads to CKD; however, this relationship has not been fully addressed in neonates. Besides AKI, other factors, such as premature delivery and intra-uterine growth retardation can themselves lead to CKD. As more critically ill premature infants and neonates with AKI live into adulthood, interventions to curb the CKD burden may have tremendous health and economic benefits.The neonatal AKI workshop sponsored by the National Institute of Health on April 9, 2013, provided a platform to discuss optimal ways to improve our understanding of the long-term renal consequences of CKD in sick neonates. This special article summarizes discussions addressing the feasibility to conduct large prospective multi-center studies in order to improve our understanding of the epidemiology and pathophysiology of CKD, and guide optimal follow-up recommendations for these infants. This report addresses: 1) Statement of the problem; 2) Key elements needed to conduct a long-term follow-up study; 3) Challenges; and 4) Opportunities.Pediatric Research (2015); doi:10.1038/pr.2015.241.
    Pediatric Research 11/2015; DOI:10.1038/pr.2015.241
  • Naureen Memon · Barry I Weinberger · Thomas Hegyi · Lauren M Aleksunes ·
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    ABSTRACT: Inherited disorders of hyperbilirubinemia may be caused by increased bilirubin production or decreased bilirubin clearance. Reduced hepatic bilirubin clearance can be due to defective 1) unconjugated bilirubin uptake and intrahepatic storage, 2) conjugation of glucuronic acid to bilirubin (e.g. Gilbert syndrome, Crigler-Najjar syndrome, Lucey-Driscoll syndrome, breast milk jaundice), 3) bilirubin excretion into bile (Dubin-Johnson syndrome), or 4) conjugated bilirubin re-uptake (Rotor syndrome). In this review, the molecular mechanisms and clinical manifestations of these conditions are described, as well as current approaches to diagnosis and therapy.Pediatric Research (2015); doi:10.1038/pr.2015.247.
    Pediatric Research 11/2015; DOI:10.1038/pr.2015.247
  • Theodore S. Nowicki · Jennifer L. Anderson · Noah Federman ·
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    ABSTRACT: Progress has slowed substantially in improving survival rates for pediatric sarcomas, particularly in refractory and metastatic disease. Significant progress has been made in the field of tumor vaccines for such malignancies, which target established tumor antigens. While tumor vaccines have demonstrated safety and improved survival rates, they are inadequate in mediating the regression of established tumor masses and metastases. Programmed cell death ligand 1 (PDL1) is a cell-surface protein induced in a number of adult malignancies. By acting on the corresponding T-cell receptor PD1, PDL1 is able to suppress cytotoxic T-cell-mediated tumor responses. Recent therapeutics blocking this interaction have shown promise in various adult cancers by restoring a functional T-cell response and by directing this response towards an activated, rather than regulatory T-cell phenotype. We shall discuss the current state of tumor vaccines targeting pediatric sarcomas, review PD1-PDL1 interactions and current therapies targeting these interactions in adult malignancies, and discuss recent studies in which tumor vaccines, combined with PDL1 blockades, produced superior tumor regression compared to the vaccine alone. These studies provide a compelling case for investigation of PDL1 expression and its inhibition in pediatric sarcomas, while continuing to utilize tumor vaccines in tandem to achieve superior clinical outcomes.Pediatric Research (2015); doi:10.1038/pr.2015.246.
    Pediatric Research 11/2015; DOI:10.1038/pr.2015.246
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    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: 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; 77(6). DOI:10.1038/pr.2015.55
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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; 77(6). DOI:10.1038/pr.2015.46
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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; 77(6). DOI:10.1038/pr.2015.53
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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; 77(6). DOI:10.1038/pr.2015.44
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    ABSTRACT: Background: The α2-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 naive (uninjured) neonatal Lewis rats to provide acute (25 µg/kg, ×1) or prolonged (25 µg/kg three times daily, ×2 or ×4 d) 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 30 °C 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 03/2015; 77(6). DOI:10.1038/pr.2015.45
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    ABSTRACT: Background: Postconditioning (PostC) with mild hypoxia shortly after a neonatal hypoxic-ischemic (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 h) on postnatal day 7 and 24 h later, pups were exposed to hypoxic PostC (8% O2 for 1 h/day for 5 d) 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 toward 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 03/2015; 77(6). DOI:10.1038/pr.2015.47
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    ABSTRACT: Background: Stem cells or inhaled nitric oxide (iNO) are reported to improve lung structures in bronchopulmonary dysplasia (BPD) models. We hypothesized that combined iNO and transplanted endothelial progenitor cells (EPCs) might restore lung structure in rats after neonatal hyperoxia. Methods: Litters were separated into eight groups: room air, hyperoxia, hyperoxia + iNO, hyperoxia + iNO + L-NAME, hyperoxia + EPCs, hyperoxia + EPCs + L-NAME, hyperoxia + EPCs + iNO, and hyperoxia + EPCs + iNO + L-NAME. Litters were exposed to hyperoxia from the 21st day, then, sacrificed. EPCs were injected on the 21st day. L-NAME was injected daily for 7 d from the 21st day. Serum vascular endothelial growth factor (VEGF), radial alveolar count (RAC), VIII factor, EPCs engraftment, lung VEGF, VEGFR2, endothelial nitric oxide (eNOS) and SDF-1 expression, and NO production were examined. Results: Hyperoxia exposure led to air space enlargement, loss of lung capillaries, and low expression of VEGF and eNOS. Transplanted EPCs, when combined with iNO, had significantly increased engraftment in lungs, compared to EPCs alone, upon hyperoxia exposure. There was improvement in alveolarization, microvessel density, and upregulation of VEGF and eNOS proteins in the hyperoxia-exposed EPCs with iNO group, compared to hyperoxia alone. Conclusion: Combined EPCs and iNO improved lung structures after neonatal hyperoxia. This was associated with the upregulation of VEGF and eNOS expression.
    Pediatric Research 03/2015; 77(6). DOI:10.1038/pr.2015.39
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    ABSTRACT: Background: Intrauterine growth restriction (IUGR) is a frequent complication of pregnancy defined as a restriction of fetal growth. The objective of this work was to improve the knowledge on the pathophysiology of IUGR using a genome-wide method of expression analysis. Methods: We analyzed differentially expressed genes in pooled placental tissues from vascular IUGR (four pools of three placentas) and normal pregnancies (four pools of three placentas) using a long nucleotide microarray platform (Nimblegen). We first did a global bioinformatics analysis based only on P value without any a priori. We secondly focused on "target" genes among the most modified ones. Finally, reverse transcription quantitative polymerase chain reaction (RT-qPCR) was performed on an extended panel of tissue samples (n = 62) on selected "target". Results: We identified 636 modified genes among which 206 were upregulated (1.5 and higher; P < 0.05). Groups of patients were classified unambiguously. Genes involved in mitochondrial function and oxidative phosphorylation were decreased affecting three out of five complexes of the respiratory chain of the mitochondria, and thus energy production and metabolism. Among the most induced genes, we identified LEP, IGFBP1, and RBP4. Conclusion: Complementary studies on the role and function of LEP, IGFBP1, and RBP4 in IUGR pathophysiology and also in fetal programming remain necessary.
    Pediatric Research 03/2015; 77(6). DOI:10.1038/pr.2015.40
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    ABSTRACT: Background: Phlebotomy-induced anemia (PIA) is common in preterm infants. The hippocampus undergoes rapid differentiation during late fetal/early neonatal life and relies on adequate oxygen and iron to support oxidative metabolism necessary for development. Anemia shortchanges these two critical substrates, potentially altering hippocampal development and function. Methods: PIA (hematocrit <25%) was induced in neonatal mice pups from postnatal day (P)3 to P14. Neurochemical concentrations in the hippocampus were determined using in vivo (1)H NMR spectroscopy at 9.4T and compared with control animals at P14. Gene expression was assessed using quantitative real-time polymerase chain reaction (qRT-PCR). Results: PIA decreased brain iron concentration, increased hippocampal lactate and creatine concentrations, and decreased phosphoethanolamine (PE) concentration and the phosphocreatine/creatine ratio. Hippocampal transferrin receptor (Tfrc) gene expression was increased, while the expression of calcium/calmodulin-dependent protein kinase type IIα (CamKIIα) was decreased in PIA mice. Conclusion: This clinically relevant model of neonatal anemia alters hippocampal energy and phospholipid metabolism and gene expression during a critical developmental period. Low target hematocrits for preterm neonates in the neonatal intensive care unit (NICU) may have potential adverse neural implications.
    Pediatric Research 03/2015; 77(6). DOI:10.1038/pr.2015.41