Pediatric Research (Pediatr Res )

Publisher: International Pediatric Research Foundation, Lippincott, Williams & Wilkins

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.

Impact factor 2.84

  • Hide impact factor history
     
    Impact factor
  • 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

Lippincott, Williams & Wilkins

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • Pre-print must be removed upon acceptance for publication
    • Post-print may be deposited in personal website or institutional repository
    • Publisher's version/PDF cannot be used
    • Must include statement that it is not the final published version
    • Published source must be acknowledged with full citation
    • Set statement to accompany deposit
    • Must link to publisher version
    • NIH authors will have their accepted manuscripts transmitted to PubMed Central on their behalf after a 12 months embargo (see policy for details)
    • Wellcome Trust and HHMI authors will have their accepted manuscripts transmitted to PubMed Central on their behalf after a 6 months embargo (see policy for details)
    • If the hybrid open access option is not available, RCUK authors articles will be released as Creative Commons Attirbution Non-Commercial No Derivatives after a 6 months
    • Publisher last reviewed on 10/04/2014
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Primary care pediatricians and a variety of specialist physicians strive to define an accurate diagnosis for children presenting with impairment of expressive speech and delay in achieving developmental milestones. Within the past two decades, a group of disorders featuring this presentation have been identified as cerebral creatine deficiency syndromes (CCDS). Patients with these disorders were initially discerned using proton magnetic resonance spectroscopy of the brain within a magnetic resonance imaging (MRI) examination. The objective of this review is to provide the clinician with an overview of the current information available on identifying and treating these conditions. We explain the salient features of creatine metabolism, synthesis and transport required for normal development. We propose diagnostic approaches for confirming a CCDS diagnosis. Finally, we describe treatment approaches for managing patients with these conditions.Pediatric Research (2014); doi:10.1038/pr.2014.203.
    Pediatric Research 12/2014;
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    ABSTRACT: Background Diseases of adulthood, such as diabetes and hypertension, may be related to changes during pregnancy, particularly in kidney. We hypothesized that acute kidney injury progresses more rapidly in cases of fetal programming.Methodsdiabetic dams' offspring were divided into: CC (controls, receiving vehicle); DC (diabetics, receiving vehicle); CA (controls receiving Folic Acid solution, 250 mg/kg); and DA (diabetics receiving Folic Acid solution). Renal function tests, morphometry, gene and protein expression of epithelial mesenchymal transition (EMT) markers was analyzed by qPCR and immunohistochemistry, respectively.ResultsCreatinine, urea, Bowman's space and EMT markers were increased in CA and DA groups. TGF-ß3, actin and fibronectin expression was higher in CA and DA, with significant increase in DA compared to CA 2-mo offspring. There was higher expression level of TGF-β1, TGF-β3, fibronectin, and vimentin in the offspring of diabetic dams at 5 months. Increases in TGF-β1 and TGF-β3 were more evident in the offspring of diabetic dams.Conclusions Fetal programming promotes remarkable changes in kidney morphology and function in offspring and renal failure progression may be faster in younger offspring of diabetic dams subjected to an additional injury.Pediatric Research (2014); doi:10.1038/pr.2014.205.
    Pediatric Research 12/2014;
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    ABSTRACT: Background Necrotizing enterocolitis (NEC) is an immature intestinal condition resulting in devastating intestinal inflammation due to unknown mechanisms. Evidence has suggested that intestinal maturation attenuates the severity of NEC and TLR4 has been suggested to play a critical role in its pathogenesis. We investigated whether maturational effects of TLR4 expression in immature colon might contribute to the development of NEC.MethodsTLR4 colonocyte expression was detected by immunofluorescence confocal microscopy. Interleukin-6 (IL-6) levels were assayed by an enzyme-linked immunosorbent assay (ELISA).ResultsTLR4 expression was high in fetal colonic epithelium in human and mouse, with earlier gestation having a higher surface/cytoplasm distribution. TLR4 remained high in mouse postnatal day 1 but the surface/cytoplasm distribution was reduced. TLR4 decreased in amount and then was expressed in crypts in the mature human and mouse colon. Hydrocortisone (HC) reduced the surface/cytoplasm distribution of TLR4 in human fetal colon. Elevated IL-6 levels in immature colon after LPS were attenuated by HC in human and mouse.Conclusions Expression, localization and signaling of TLR4 in colonic epithelium may be developmentally regulated. HC may accelerate the TLR developmental pathway change to an adult type which may account for its impact on TLR4 signaling.Pediatric Research (2014); doi:10.1038/pr.2014.207.
    Pediatric Research 12/2014;
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    ABSTRACT: BackgroundPPHN is associated with decreased lung angiogenesis and impaired pulmonary vasodilatation at birth. Prostanoids are important modulators of vascular tone and angiogenesis. We hypothesized that altered levels of prostacyclin (PGI2), a potent vasodilator, and thromboxane (TXA2), a vasoconstrictor, contribute to impaired angiogenesis of pulmonary artery endothelial cells (PAEC) in PPHN.MethodsPAEC were isolated from fetal lambs with PPHN induced by prenatal ductus arteriosus constriction or sham operated controls. Expression and activity of PGI2 synthase (PGIS) and TXA2 synthase (TXAS), expression of cyclooxygenases 1 and 2 (COX-1 and COX-2) and the role of PGIS/TXAS alterations in angiogenesis were investigated in PAEC from PPHN and control lambs.ResultsPGIS protein and activity were decreased and PGIS protein tyrosine nitration was increased in PPHN PAEC. In contrast, TXAS protein and its stimulated activity were increased in PPHN PAEC. COX-1 and COX-2 proteins were decreased in PPHN PAEC. Addition of PGI2 improved in vitro tube formation by PPHN PAEC, whereas, indomethacin decreased tube formation by control PAEC. PGIS knockdown decreased the in vitro angiogenesis in control PAEC, whereas, TXAS knockdown increased the in vitro angiogenesis in PPHN PAEC.Conclusions Reciprocal alterations in PGI2 and TXA2 may contribute to impaired angiogenesis in PPHN.Pediatric Research (2014); doi:10.1038/pr.2014.209.
    Pediatric Research 12/2014;
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    ABSTRACT: Background In juvenile mammals, the epiphyses of long bones grow by chondrogenesis within the articular cartilage. A better understanding of the molecular mechanisms that regulate the growth of articular cartilage may give insight into the antecedents of joint disease, such as osteoarthritis.Methods We used laser-capture microdissection to isolate chondrocytes from the superficial, middle, and deep zones of growing tibial articular cartilage in the 1-wk old mouse and then investigated expression patterns by microarray. To identify molecular markers for each zone of the growing articular cartilage, we found genes showing zone-specific expression and confirmed by real-time PCR and in situ hybridization.ResultsBioinformatic analyses implicated ephrin receptor signaling, Wnt signaling, and BMP signaling in the spatial regulation of chondrocyte differentiation during growth. Molecular markers were identified for superficial (e.g. Cilp, Prg4), middle (Cxcl14, Tnn), and deep zone (Sfrp5, Frzb). Comparison between juvenile articular and growth plate cartilage revealed that the superficial-to-deep zone transition showed similarity with the hypertrophic-to-resting zone transition.Conclusions Laser capture microdissection combined with microarray analysis identified novel signaling pathways that are spatially regulated in growing mouse articular cartilage and revealed similarities between the molecular architecture of the growing articular cartilage and that of growth plate cartilage.Pediatric Research (2014); doi:10.1038/pr.2014.208.
    Pediatric Research 12/2014;
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    ABSTRACT: Background Neonatal jaundice resulting from elevated unconjugated bilirubin (UCB) occurs in 60-80% of newborn infants. Although mild jaundice is generally considered harmless, little is known about its long-term consequences. Recent studies have linked mild bilirubin-induced neurological dysfunction (BIND) with a range of neurological syndromes, including attention deficit-hyperactivity disorder. The goal of this study was to measure BIND across the lifespan in the Gunn rat model of BIND.Methods Using a sensitive force plate actometer, we measured locomotor activity and gait in jaundiced (jj) Gunn rats versus their non-jaundiced (Nj) littermates. Data were analyzed for young adult (3-4 months), early middle-aged (9-10 months), and late middle-aged (17-20 months) male rats.Resultsjj rats exhibited lower body weights at all ages and a hyperactivity that resolved at 17-20 months of age. Increased propulsive force and gait velocity accompanied hyperactivity during locomotor bouts at 9-10 months in jj rats. Stride length did not differ between the two groups at this age. Hyperactivity normalized and gait deficits, including decreased stride length, propulsive force, and gait velocity, emerged in the 17-20-month-old jj rats.Conclusions These results demonstrate that, in aging, hyperactivity decreases with the onset of gait deficits in the Gunn rat model of BIND.Pediatric Research (2014); doi:10.1038/pr.2014.199.
    Pediatric Research 12/2014;
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    ABSTRACT: Background:To minimize secondary lung injury, ventilated preterm infants are extubated as soon as possible. To maximize extubation success, they are often placed in prone position. The effect of extubation and subsequent prone positioning on lung volumes is currently unknown.Methods:Changes in end-expiratory lung volume (ΔEELV), tidal volume (VT) and ventilation distribution were monitored during transition from endotracheal to nasal continuous positive airway pressure and following prone positioning using electrical impedance tomography. In addition, the continuous distending pressure (CDP) and oxygen need (FiO2) were recorded.Results:20 preterm infants (GA 28.7±1.7 wk) were included. Following extubation the CDP decreased from 7.9±0.5 to 6.0±0.2 cmH2O, while the FiO2 remained stable. Both ΔEELV and VT increased significantly (p<0.05) after extubation, without changing ventilation distribution. Prone positioning resulted in a further increase in ΔEELV (p<0.01) and a decrease in respiratory rate. VT remained stable but its distribution clearly shifted towards the ventral lung regions.Conclusion:Infants who are transitioned from invasive to non-invasive respiratory support are able to maintain their EELV and increase their VT. Prone positioning increases EELV and shifts tidal ventilation to the ventral lung regions. The latter suggests that infants should preferably be placed in prone position after extubation.Pediatric Research (2014); doi:10.1038/pr.2014.201.
    Pediatric Research 12/2014;
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    ABSTRACT: Background Ex-premature infants are at higher risk for hypertension and cardiovascular disease as adults, although the mechanisms underlying such increased risks are unknown. We hypothesize that postnatal exposure to intermittent hypoxia (IH) leads to cardiovascular dysfunction in adulthood with alterations of the renin-angiotensin pathway.Methods Neonatal mice were exposed to IH for 4 weeks. At the age of 3 months, various cardiovascular measurements were obtained.ResultsIH-exposed mice exhibited higher systolic blood pressure, impaired baroreflex responses, and decreased heart rate variability. Furthermore, IH-exposed mice manifested evidence of endothelial dysfunction, as shown by reduced reperfusion indices after tail vessel occlusion and impaired vasodilatory responses to acetylcholine. CD31+ endothelial cells isolated from mesenteric arteries of IH-exposed mice expressed higher levels of angiotensin-converting enzyme and reactive oxygen species; plasma angiotensin-II levels were also significantly higher in these animals. In addition, DNA methylation patterns of the Ace1 and the Agt genes in these cells were congruent with their expression patterns.Conclusion Our results suggest that exposures to postnatal IH alter the normal development of the renin-angiotensin system and promote the occurrence of cardiovascular dysfunction during adulthood in mice.Pediatric Research (2014); doi:10.1038/pr.2014.197.
    Pediatric Research 12/2014;
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    ABSTRACT: Background Pediatric venous thromboembolism (VTE) is an increasingly common, difficult to diagnose problem. Clinical probability tools (CPT) for adults estimate VTE likelihood, but are not available for children. We hypothesized that a pediatric-specific CPT is feasible.Methods Radiology reports were utilized to identify children imaged for suspected VTE. Relevant signs, symptoms, and co-morbidity variables, identified from published literature, were extracted from corresponding medical records. Variables associated with pediatric VTE were incorporated into a multivariate logistic regression to create a pilot CPT which was confirmed on a separate cohort.Results389 subjects meeting inclusion criteria were identified: 91 with VTE and 298 without. Univariate analysis revealed male gender (OR 2.96; p<0.001), asymmetric extremity (OR 1.76; p=0.033), central venous catheter utilization and/or dysfunction (OR 2.51; p<0.001), and cancer (OR 2.35; p=0.014) as VTE predictive variables. Documentation of an alternate diagnosis was inversely related to VTE (OR 0.42; p=0.004). Receiver operating characteristic analysis of the derived CPT demonstrated reasonable ability to discriminate VTE probability in the training cohort (AUC 0.73; p<0.001) and moderate discrimination in a separate validation cohort of 149 children (AUC 0.64; p=0.011).ConclusionA pediatric-specific VTE CPT is feasible, would facilitate early diagnosis, and could lead to improved outcomes.Pediatric Research (2014); doi:10.1038/pr.2014.198.
    Pediatric Research 12/2014;
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    ABSTRACT: Background:Lung injury resulting from oxidative stress contributes to bronchopulmonary dysplasia (BPD) pathogenesis. Nuclear factor erythroid-2 related factor-2 (NFE2L2) regulates cytoprotective responses to oxidative stress by inducing enzymes containing anti-oxidant response elements (ARE). We hypothesized that ARE genetic variants will modulate susceptibility or severity of BPD in very low birth weight (VLBW) infants.Methods:Blood samples obtained from VLBW infants were used for genotyping variants in the SOD2, NFE2L2, GCLC, GSTP1, HMOX1 and NQO1 genes. SNPs were genotyped utilizing TaqMan probes (Applied Biosystems (ABI), Grand Island, NY), and data was analyzed using the ABI HT7900. Genetic dominance and recessive models were tested to determine associations between SNPs and BPD.Results:In our cohort (n=659), 284 infants had BPD; 135 of whom developed severe BPD. Presence of the hypomorphic NQO1 SNP (rs1800566) in a homozygous state was associated with increased BPD while presence of the NFE2L2 SNP (rs6721961) was associated with decreased severe BPD in the entire cohort and in Caucasian infants. In regression models that adjusted for epidemiological confounders, the NQO1 and the NFE2L2 SNPs were associated with BPD and severe BPD, respectively.Conclusion:Genetic variants in NFE2L2-ARE axis may contribute to the variance in liability to BPD observed in preterm infants. These results require confirmation in independent cohorts.Pediatric Research (2014); doi:10.1038/pr.2014.200.
    Pediatric Research 12/2014;
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    ABSTRACT: Background:Obesity is frequently complicated by comorbid conditions, yet how excess adipose contributes is poorly understood. Although adipocytes in obese individuals induce systemic inflammation via secreted cytokines, another potential mediator has recently been identified (i.e. adipocyte-derived exosomes). We hypothesized that adipocyte-derived exosomes contain mediators capable of activating end-organ inflammatory and fibrotic signaling pathways.Methods:We developed techniques to quantify and characterize exosomes shed by adipocytes from 7 obese (age: 12-17.5 years, BMI: 33-50 kg/m(2)) and 5 lean (age: 11-19 years, BMI: 22-25 kg/m(2)) subjects.Results:Abundant exosomal miRNAs, but no mRNAs, were detected. Comparison of obese vs. lean visceral adipose donors detected 55 differentially-expressed miRNAs (p<0.05; fold change≥|1.2|). qRT-PCR confirmed downregulation of miR-148b (ratio = 0.2 (95% confidence interval = 0.1, 0.6)) and miR-4269 (0.3 (0.1, 0.8)), and upregulation of miR-23b (6.2 (2.2, 17.8)) and miR-4429 (3.8 (1.1 to 13.4)). Pathways analysis identified TGF-ß signaling and Wnt/ ß-catenin signaling among the top canonical pathways expected to be altered with visceral adiposity based on projected mRNA targets for the 55 differentially expressed miRNAs. A select mRNA target was validated in vitro.Conclusion:These data show that visceral adipocytes shed exosomal-mediators predicted to regulate key end-organ inflammatory and fibrotic signaling pathways.Pediatric Research (2014); doi:10.1038/pr.2014.202.
    Pediatric Research 12/2014;
  • Pediatric Research 12/2014; 76(6):571-6.
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    ABSTRACT: Background Hyperoxic reoxygenation following hypoxia increases the expression of inflammatory genes in the neonatal mouse brain. We have therefore compared the temporal profile of 44 a priori selected genes after hypoxia and hyperoxic or normoxic reoxygenation.Methods Postnatal day 7 mice were subjected to 2 hours of hypoxia (8% O2) and 30 min reoxygenation with 60% or 21% O2. After 0 h to 72 h observation, mRNA and protein were examined in hippocampus and striatum.ResultsThere were significantly higher gene expression changes in six genes after hyperoxic compared to normoxic reoxygenation. Three genes had a generally higher expression throughout the observation period: The inflammatory genes Hmox1 (mean difference 0.52, 95% CI 0.151.01) and Tgfb1 (mean diff 0.099, CI 0.0030.194), and the transcription factor Nfkb1 (mean difference 0.049, CI 0.0110.087). The inflammatory genes Cxcl10 and Il1b, and the DNA repair gene Neil3, had a higher gene expression change after hyperoxic reoxygenation at one time point only. Nineteen genes involved in inflammation, transcription regulation, apoptosis, angiogenesis, and glucose transport had significantly different gene expression changes with time in all intervention animals.Conclusion We confirm that hyperoxic reoxygenation induces a stronger inflammatory gene response than reoxygenation in air.Pediatric Research (2014); doi:10.1038/pr.2014.193.
    Pediatric Research 11/2014;
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    ABSTRACT: Background Specific probiotics prevent NEC. A mixture of lactobacilli and bifidobacteria (Infloran) was highly effective in Asian very low birth weight (VLBW) infants. We analyzed the effect of Infloran on NEC, NEC severity and the influence of enteral feedings (breast milk vs. formula) on NEC prevention in a cohort of European VLBW infants.Methods Infloran was implemented for routine use at our department. VLBW infants receiving probiotics were prospectively followed (2010-12) and compared to historic controls (2008-9). Data on NEC, neonatal morbidity, feeding tolerance, and descriptive parameters on NEC cases were analyzed.ResultsInfloran had no statistically significant impact on NEC (controls: 24/233 (10.3%), probiotics: 16/230 (7%); P=0.2). However, NEC was significantly reduced in infants of the probiotics group who were fed any breast milk (20/179 (11.2%) vs. 10/183 (5.5%); P=0.027), whereas it was ineffective in infants exclusively fed formula (4/54 (7.4%) vs. 6/44 (13.6%); P=0.345). Occurrence of severe NEC (IIIB), time until full feeds and gastric residuals were similar.Conclusions Infloran was of lower efficacy in a European VLBW cohort and showed a reduction of NEC only in infants fed breast milk. Future studies should investigate the influence of feeding formula or breast milk on the effect of probiotics.Pediatric Research (2014); doi:10.1038/pr.2014.192.
    Pediatric Research 11/2014;
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    ABSTRACT: The global burden of kidney disease is increasing, and several etiologies first begin in childhood. Risk factors for pediatric kidney disease are common in Africa, but data regarding its prevalence are lacking. We completed a systematic review of community-based studies describing the prevalence of proteinuria, hematuria, abnormal imaging, or kidney dysfunction among children in sub-Saharan Africa. Medline and Embase were searched. Five hundred twenty-three references were reviewed. Thirty-two references from 9 countries in sub-Saharan Africa were included in the qualitative synthesis. The degree of kidney damage and abnormal imaging varied widely: proteinuria 32.5% (2.2%-56.0%); hematuria 31.1% (0.6%-67.0%); hydronephrosis 11.3% (0.0%-38.0%), hydroureter 7.5% (0.0%-26.4%), major kidney abnormalities 0.1% (0.0%-0.8%). Serum creatinine was reported in four studies with insufficient detail to identify the prevalence renal dysfunction. A majority of the studies were performed in Schistosoma haematobium endemic areas. A lower prevalence of kidney disease was observed in the few studies from non-endemic areas. Published data on pediatric kidney disease in sub-Saharan Africa is highly variable and dependent on S. haematobium prevalence. More community-based studies are needed to describe the burden of pediatric kidney disease, particularly in regions where S. haematobium infection is non-endemic.Pediatric Research (2014); doi:10.1038/pr.2014.189.
    Pediatric Research 11/2014;
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    ABSTRACT: Background Deficiencies in vitamin D directly impact children's health and place minority and obese youth at risk for a range of health issues. The Institute of Medicine (IOM) Committee to Review Dietary Reference Intakes for Vitamin D and Calcium has set both a required daily allowance (RDA) for vitamin D supplementation and a population-wide sufficiency target for the biomarker of vitamin D status, serum 25-hydroxyvitamin D (25(OH)D). However, new research suggests that the RDA is not sufficient to meet the target biomarker status for individuals who are heavy or who have dark skin. Our objective was to provide appropriate daily vitamin D supplementation levels for these individuals.Methods Using data derived from the National Health and Nutrition Examination Survey (NHANES) and a recently-published dosing formula, we calculated the required supplemental dose of vitamin D to meet the IOM target in children and adolescents.ResultsTo be sure that 95% of the target population meets the IOM's population-wide biomarker target, some individuals require a daily dose of up to 2,000 IUs of supplemental vitamin D.Conclusions Health professionals should work with their patients to encourage life-long vitamin D supplement use at a dosage sufficient to obtain adequate 25(OH)D levels.Pediatric Research (2014); doi:10.1038/pr.2014.190.
    Pediatric Research 11/2014;
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    ABSTRACT: Pseudotumor cerebri syndrome (PTCS) is defined by the presence of elevated intracranial pressure (ICP) in the setting of normal brain parenchyma and cerebrospinal fluid (CSF). Headache, vision changes, and papilledema are common presenting features. Up to 10% of appropriately treated patients may experience permanent visual loss. The mechanism(s) underlying PTCS is unknown. PTCS occurs in association with a variety of conditions, including kidney disease, obesity, and adrenal insufficiency, suggesting endocrine and/or metabolic derangements may occur. Recent studies suggest that fluid and electrolyte balance in renal epithelia is regulated by a complex interaction of metabolic and hormonal factors; these cells share many of the same features as the choroid plexus cells in the CNS responsible for regulation of CSF dynamics. Thus, we posit that similar factors may influence CSF dynamics in both types of fluid-sensitive tissues. Specifically, we hypothesize that, in patients with PTCS, mitochondrial metabolites (glutamate, succinate) and steroid hormones (cortisol, aldosterone) regulate CSF production and/or absorption. In this integrated mechanism review, we consider the clinical and molecular evidence for each metabolite and hormone in turn. We illustrate how related intracellular signaling cascades may converge in the choroid plexus, drawing on evidence from functionally similar tissues.Pediatric Research (2014); doi:10.1038/pr.2014.188.
    Pediatric Research 11/2014;
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    ABSTRACT: Background Chronic rhinosinusitis (CRS) is characterized by mucous overproduction and submucosal gland hyperplasia. The global protein profile of sinonasal secretions in pediatric CRS has not been studied. We hypothesized that MUC5B, a glandular mucin, would be relatively increased in CRS secretions compared to other mucins.Methods Secretions were collected at Children's National Health System (Children's National) from CRS patients undergoing sinus surgery and from control patients without CRS undergoing craniofacial procedures. Proteins were extracted, digested to peptides, and analyzed by mass spectometry. Fold change significance was calculated using the QSpec algorithm. Western blot analysis was performed to validate proteomic findings.ResultsIn total, 294 proteins were identified. Although both MUC5B and MUC5AC were identified in a majority of samples, the relative abundance of MUC5B was found to be significantly higher (p < 0.05). Western blot data validated these findings. Other proteins with the highest significant positive-fold change in CRS samples were BP1 fold-containing family A member 1, chitinase-3-like protein 1, plastin-2, serpin 10, and BP1 fold-containing family B member 1.Conclusion Overall our data demonstrates an increase of MUC5B abundance in the sinus secretions of pediatric patients with CRS.Pediatric Research (2014); doi:10.1038/pr.2014.187.
    Pediatric Research 11/2014;