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Van Marter, Linda

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Van Marter

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Linda

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Van Marter, Linda
Author's Publications: search.filters.isAuthorOfPublication.6562f360-05b1-4d75-b50f-beacc0f00027

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    Elevated protein concentrations in newborn blood and the risks of autism spectrum disorder, and of social impairment, at age 10 years among infants born before the 28th week of gestation
    (Nature Publishing Group UK, 2018) Korzeniewski, Steven J.; Allred, Elizabeth N.; O’Shea, T. Michael; Leviton, Alan; Kuban, Karl C. K.; Lee, Kathleen; McGovern, Anne; Gambardella, Jill; Ursprung, Susan; Ecklund, Ruth Blomquist Kristen; Bassan, Haim; Butler, Samantha; Duplessis, Adré; Hahn, Cecil; Limperopoulos, Catherine; Khwaja, Omar; Soul, Janet S.; Shah, Bhavesh; Christianson, Karen; Hampf, Frederick; Gilmore, Herbert; McQuiston, Susan; Martin, Camilia; Hallisey, Colleen; Hurley, Caitlin; Creixell, Miren; Share, Jane; Van Marter, Linda; Durfee, Sara; Insoft, Robert M.; Wilson, Jennifer G.; Pimental, Maureen; Westra, Sjirk; Krishnamoorthy, Kalpathy; Cole, Cynthia; Fiascone, John M.; Madden, Janet; Nylen, Ellen; McCauley, Anne Furey Roy; Church, Paige T.; Keller, Cecelia; Miller, Karen J.; Bednarek, Francis; Naples, Mary; Powers, Beth; Wellman, Jacqueline; Adair, Robin; Bream, Richard; Miller, Alice; Scheiner, Albert; Stine, Christy; Ehrenkranz, Richard; Williams, Joanne; Romano, Elaine; Miller, Cindy; Close, Nancy; Gordon, Debbie; Harold, Teresa; Specter, Barbara; Allred, Deborah; Dillard, Robert; Goldstein, Don; Hiatt, Deborah; Hounshell, Gail; Waldrep, Ellen; Washburn, Lisa; Welch, Cherrie D.; Engelke, Stephen C.; Moseley, Sherry; Pare, Linda; Smart, Donna; Wilson, Joan; Adler, Ira; Buckwald, Sharon; Helms, Rebecca; Kerkering, Kathyrn; MacGilvray, Scott S.; Resnik, Peter; Bose, Carl; Bose, Gennie; Fordham, Lynn A.; Bostic, Lisa; Marshall, Diane; Milowic, Kristi; Wereszczak, Janice; Poortenga, Mariel; Sutton, Dinah; Betz, Bradford W.; Bezinque, Steven L.; Junewick, Joseph; Burdo-Hartman, Wendy; Fagerman, Lynn; Lohr, Kim; Pastyrnak, Steve; Solomon, Carolyn; Cavenagh, Ellen; Caine, Victoria J.; Olomu, Nicholas; Price, Joan; Paneth, Nigel; Karna, Padmani; Lenski, Madeleine; Schreiber, Michael D.; Yoon, Grace; Feinstein, Kate; Caldarelli, Leslie; O’Connor, Sunila E.; Msall, Michael; Plesha-Troyke, Susan; Batton, Daniel; Kring, Beth; Brooklier, Karen; Oca, Melisa J.; Solomon, Katherine M.
    Among the 1 of 10 children who are born preterm annually in the United States, 6% are born before the third trimester. Among children who survive birth before the 28th week of gestation, the risks of autism spectrum disorder (ASD) and non-autistic social impairment are severalfold higher than in the general population. We examined the relationship between top quartile inflammation-related protein concentrations among children born extremely preterm and ASD or, separately, a high score on the Social Responsiveness Scale (SRS total score ≥65) among those who did not meet ASD criteria, using information only from the subset of children whose DAS-II verbal or non-verbal IQ was ≥70, who were assessed for ASD, and who had proteins measured in blood collected on ≥2 days (N = 763). ASD (N = 36) assessed at age 10 years is associated with recurrent top quartile concentrations of inflammation-related proteins during the first post-natal month (e.g., SAA odds ratio (OR); 95% confidence interval (CI): 2.5; 1.2–5.3) and IL-6 (OR; 95% CI: 2.6; 1.03–6.4)). Top quartile concentrations of neurotrophic proteins appear to moderate the increased risk of ASD associated with repeated top quartile concentrations of inflammation-related proteins. High (top quartile) concentrations of SAA are associated with elevated risk of ASD (2.8; 1.2–6.7) when Ang-1 concentrations are below the top quartile, but not when Ang-1 concentrations are high (1.3; 0.3–5.8). Similarly, high concentrations of TNF-α are associated with heightened risk of SRS-defined social impairment (N = 130) (2.0; 1.1–3.8) when ANG-1 concentrations are not high, but not when ANG-1 concentrations are elevated (0.5; 0.1–4.2).
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    Early Blood Gas Predictors of Bronchopulmonary Dysplasia in Extremely Low Gestational Age Newborns
    (Hindawi Publishing Corporation, 2014) Sriram, Sudhir; Condie, Joy; Schreiber, Michael D.; Batton, Daniel G.; Shah, Bhavesh; Bose, Carl; Laughon, Matthew; Van Marter, Linda; Allred, Elizabeth; Leviton, Alan
    Aim. To determine among infants born before the 28th week of gestation to what extent blood gas abnormalities during the first three postnatal days provide information about the risk of bronchopulmonary dysplasia (BPD). Methods:. We studied the association of extreme quartiles of blood gas measurements (hypoxemia, hyperoxemia, hypocapnea, and hypercapnea) in the first three postnatal days, with bronchopulmonary dysplasia, among 906 newborns, using multivariable models adjusting for potential confounders. We approximated NIH criteria by classifying severity of BPD on the basis of the receipt of any O2 on postnatal day 28 and at 36 weeks PMA and assisted ventilation. Results:. In models that did not adjust for ventilation, hypoxemia was associated with increased risk of severe BPD and very severe BPD, while infants who had hypercapnea were at increased risk of very severe BPD only. In contrast, infants who had hypocapnea were at reduced risk of severe BPD. Including ventilation for 14 or more days eliminated the associations with hypoxemia and with hypercapnea and made the decreased risk of very severe BPD statistically significant. Conclusions:. Among ELGANs, recurrent/persistent blood gas abnormalities in the first three postnatal days convey information about the risk of severe and very severe BPD.
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    Insulin‐like growth factor 1 has multisystem effects on foetal and preterm infant development
    (John Wiley and Sons Inc., 2016) Hellström, Ann; Ley, David; Hansen‐Pupp, Ingrid; Hallberg, Boubou; Löfqvist, Chatarina; Van Marter, Linda; van Weissenbruch, Mirjam; Ramenghi, Luca A.; Beardsall, Kathryn; Dunger, David; Hård, Anna‐Lena; Smith, Lois
    Abstract Poor postnatal growth after preterm birth does not match the normal rapid growth in utero and is associated with preterm morbidities. Insulin‐like growth factor 1 (IGF‐1) axis is the major hormonal mediator of growth in utero, and levels of IGF‐1 are often very low after preterm birth. We reviewed the role of IGF‐1 in foetal development and the corresponding preterm perinatal period to highlight the potential clinical importance of IGF‐1 deficiency in preterm morbidities. Conclusion: There is a rationale for clinical trials to evaluate the potential benefits of IGF‐1 replacement in very preterm infants.
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    Vitamin D status among preterm and full-term infants at birth
    (Nature Publishing Group, 2013) Burris, Heather H.; Van Marter, Linda; McElrath, Thomas; Tabatabai, Patrik; Litonjua, Augusto A.; Weiss, Scott; Christou, Helen
    Background: Risk factors for maternal vitamin D deficiency and preterm birth overlap but the distribution of 25-hydroxyvitamin D (25(OH)D) levels among preterm infants is not known. We aimed to determine associations between 25(OH)D levels and gestational age. Methods: We measured umbilical cord plasma levels of 25(OH)D from 471 infants born at Brigham and Women’s Hospital in Boston. We used generalized estimating equations to determine whether preterm (<37 weeks’ gestation) or very preterm (<32 weeks’ gestation) infants had greater odds of 25(OH)D levels < 20 ng/ml than more mature infants. We adjusted for potential confounding by season of birth, maternal age, race, marital status and singleton or multiple gestation. Results: Mean cord plasma 25(OH)D level was 34.0 ng/ml (range 4.1 to 95.3, and SD 14.1). Infants born before 32 weeks’ gestation had increased odds of 25(OH)D levels < 20 ng/ml in unadjusted (OR 2.2, 95% CI 1.1, 4.3) and adjusted models (OR 2.4, 95% CI 1.2, 5.3) compared to more mature infants. Conclusion: Infants born < 32 weeks’ gestation are at higher risk than more mature infants for low 25(OH)D levels. Further investigation of the relationships between low 25(OH)D levels and preterm birth and its sequelae is thus warranted.
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    Hemopexin in severe inflammation and infection: mouse models and human diseases
    (BioMed Central, 2015) Lin, Tian; Maita, Dayana; Thundivalappil, Sujatha R; Riley, Frank E; Hambsch, Jasmin; Van Marter, Linda; Christou, Helen; Berra, Lorenzo; Fagan, Shawn; Christiani, David; Warren, H Shaw
    Introduction: Cell-free plasma hemoglobin is associated with poor outcome in patients with sepsis. Extracellular hemoglobin and secondarily released heme amplify inflammation in the presence of microbial TLR ligands and/or endogenous mediators. Hemopexin, a plasma protein that binds heme with extraordinary affinity, blocks these effects and has been proposed as a possible treatment approach to decrease inflammation in critically ill patients. Methods: We studied mouse models of endotoxemia, burn wound infections and peritonitis in order to assess if a repletion strategy for hemopexin might be reasonable. We also measured hemopexin in small numbers of three patient populations that might be logical groups for hemopexin therapy: patients with sepsis and ARDS, patients with severe burns, and premature infants. Results: Despite severe disease, mean plasma hemopexin levels were increased above baseline in each murine model. However, plasma hemopexin levels were decreased or markedly decreased in many patients in each of the three patient populations. Conclusions: Potentially different behavior of hemopexin in mice and humans may be important to consider when utilizing murine models to represent acute human inflammatory diseases in which heme plays a role. The findings raise the possibility that decreased hemopexin could result in insufficiently neutralized or cleared heme in some patients with ARDS, burns, or in premature infants who might be candidates to benefit from hemopexin administration. Electronic supplementary material The online version of this article (doi:10.1186/s13054-015-0885-x) contains supplementary material, which is available to authorized users.
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    Innate immune activation in neonatal tracheal aspirates suggests endotoxin-driven inflammation
    (Nature Publishing Group, 2012) Nathe, Katheryn; Mancuso, Christy J.; Parad, Richard; Van Marter, Linda; Martin, Camilia; Stoler-Barak, Liat; Philbin, Victoria J.; Phillips, Michele F.; Palmer, Christine D.; Levy, Ofer
    Background:: Tracheal aspirates (TAs) from critically ill neonates accumulate bacterial endotoxin and demonstrate mobilization of endotoxin-binding proteins, but the potential bioactivity of endotoxin in TAs is unknown. We characterized innate immune activation in TAs of mechanically ventilated neonates. Methods: Innate immune activation in TAs of mechanically ventilated neonates was characterized using a targeted 84-gene quantitative real-time (qRT) PCR array. Protein expression of cytokines was confirmed by multiplex assay. Expression and localization of the endotoxin-inducible antimicrobial protein Calgranulin C (S100A12) was assessed by flow cytometry. Endotoxin levels were measured in TA supernatants using the Limulus amoebocyte lysate assay. Results:: Analyses by qRT-PCR demonstrated expression of pattern recognition receptors, Toll-like receptor-nuclear factor κB and inflammasome pathways, cytokines/chemokines and their receptors, and anti-infective proteins in TA cells. Endotoxin positivity increased with postnatal age. As compared with endotoxin-negative TAs, endotoxin-positive TAs demonstrated significantly greater tumor necrosis factor (TNF), interleukin (IL)-6, IL-10, and serpin peptidase inhibitor, clade E, member 1 (SERPINE1) mRNA, and IL-10, TNF, and IL-1β protein. Expression of S100A12 protein was localized to TA neutrophils. Conclusion:: Correlation of endotoxin with TA inflammatory responses suggests endotoxin bioactivity and the possibility that endotoxin antagonists could mitigate pulmonary inflammation and its sequelae in this vulnerable population.
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    Perturbation of Gene Expression of the Chromatin Remodeling Pathway in Premature Newborns at Risk for Bronchopulmonary Dysplasia
    (BioMed Central, 2007) Cohen, Jennifer Naomi; Van Marter, Linda; Sun, Yao; Allred, Elizabeth; Leviton, Alan; Kohane, Isaac
    Background: One-third to one-half of all infants born before the 28th week of gestation develop bronchopulmonary dysplasia (BPD). Inflammatory regulators appear to be involved in the pathogenesis of BPD, possibly beginning in fetal life. To evaluate the feasibility of using expression profiling in umbilical cord tissue to discover molecular signatures for developmental staging and for determining risk of BPD, we conducted a cross-sectional study of infants born at less than 28 weeks of gestation (n = 54). Sections of umbilical cord were obtained at birth from 20 infants who later developed BPD and from 34 of their peers who did not develop BPD. Results: Umbilical cord expression profiles at birth exhibited systematic differences in bioenergetic pathways with respect to gestational age. Infants who subsequently developed BPD had distinct signatures involving chromatin remodeling and histone acetylation pathways, which have previously been implicated in several adult onset lung diseases. These findings are consistent with prior work on inflammatory processes and bioenergetics in prematurity. Conclusion: This study of gene expression of the newborn umbilical cord implicates the chromatin remodeling pathways in those premature infants who subsequently develop BPD. Larger sample sizes will be required to generate prognostic markers from umbilical cord profiles.