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Martin, Camilia

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Martin

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Camilia

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Martin, Camilia

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2012 - 20187

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Author's Publications: search.filters.isAuthorOfPublication.9d5eb060-5ded-4d57-b2a9-da16223a2e2b

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Now showing 1 - 7 of 7
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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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    Short Course in the Microbiome
    (SAGE Publications, 2015) Falana, Kimberly; Knight, Rob; Martin, Camilia; Goldszmid, Romina; Greathouse, K. Leigh; Gere, Joanne; Young, Howard; Kuo, Winston Patrick
    Over the past decade, it has become evident that the microbiome is an important environmental factor that affects many physiological processes, such as cell proliferation and differentiation, behaviour, immune function and metabolism. More importantly, it may contribute to a wide variety of diseases, including cancer, inflammatory diseases, metabolic diseases and responses to pathogens. We expect that international, integrative and interdisciplinary translational research teams, along with the emergence of FDA-approved platforms, will set the framework for microbiome-based therapeutics and diagnostics. We recognize that the microbiome ecosystem offers new promise for personalized/precision medicine and targeted treatment for a variety of diseases. The short course was held as a four-session webinar series in April 2015, taught by pioneers and experts in the microbiome ecosystem, covering a broad range of topics from the healthy microbiome to the effects of an altered microbiome from neonates to adults and the long term effects as it is related to disease, from asthma to cancer. We have learned to appreciate how beneficial our microbes are in breaking down our food, fighting off infections and nurturing our immune system, and this information provides us with ideas as to how we can manipulate our microbiome to prevent certain diseases. However, given the variety of applications, there are scientific challenges, though there are very promising areas in reference to the clinical benefits of understanding more about our microbiome, whether in our gut or on our skin: the outlook is bright. A summary of the short course is presented as a meeting dispatch.
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    Non-invasive analysis of intestinal development in preterm and term infants using RNA-Sequencing
    (Nature Publishing Group, 2014) Knight, Jason M.; Davidson, Laurie A.; Herman, Damir; Martin, Camilia; Goldsby, Jennifer S.; Ivanov, Ivan V.; Donovan, Sharon M.; Chapkin, Robert S.
    The state and development of the intestinal epithelium is vital for infant health, and increased understanding in this area has been limited by an inability to directly assess epithelial cell biology in the healthy newborn intestine. To that end, we have developed a novel, noninvasive, molecular approach that utilizes next generation RNA sequencing on stool samples containing intact epithelial cells for the purpose of quantifying intestinal gene expression. We then applied this technique to compare host gene expression in healthy term and extremely preterm infants. Bioinformatic analyses demonstrate repeatable detection of human mRNA expression, and network analysis shows immune cell function and inflammation pathways to be up-regulated in preterm infants. This study provides incontrovertible evidence that whole-genome sequencing of stool-derived RNA can be used to examine the neonatal host epithelial transcriptome in infants, which opens up opportunities for sequential monitoring of gut gene expression in response to dietary or therapeutic interventions.
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    Early Nutrition and Weight Gain in Preterm Newborns and the Risk of Retinopathy of Prematurity
    (Public Library of Science, 2013) Vanderveen, Deborah; Martin, Camilia; Mehendale, Reshma; Allred, Elizabeth; Dammann, Olaf; Leviton, Alan
    Objective: To identify nutritional and weight gain limitations associated with retinopathy of prematurity (ROP) severity among very preterm newborns. Patients and Methods 1180 infants <28 weeks GA at birth with ROP examination results were grouped and analyzed by quartile of weekly total calorie, carbohydrate, protein, and lipid intake, as well as growth velocity between postnatal days 7 and 28 (adjusted for GA and birth weight Z-score). ROP was categorized by development of no, mild (
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    Review of Infant Feeding: Key Features of Breast Milk and Infant Formula
    (MDPI, 2016) Martin, Camilia; Ling, Pei-Ra; Blackburn, George L.
    Mothers’ own milk is the best source of nutrition for nearly all infants. Beyond somatic growth, breast milk as a biologic fluid has a variety of other benefits, including modulation of postnatal intestinal function, immune ontogeny, and brain development. Although breastfeeding is highly recommended, breastfeeding may not always be possible, suitable or solely adequate. Infant formula is an industrially produced substitute for infant consumption. Infant formula attempts to mimic the nutritional composition of breast milk as closely as possible, and is based on cow’s milk or soymilk. A number of alternatives to cow’s milk-based formula also exist. In this article, we review the nutritional information of breast milk and infant formulas for better understanding of the importance of breastfeeding and the uses of infant formula from birth to 12 months of age when a substitute form of nutrition is required.
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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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    Effects of Intestinal Microbiota on Brain Development in Humanized Gnotobiotic Mice
    (Nature Publishing Group UK, 2018) Lu, Jing; Lu, Lei; Yu, Yueyue; Cluette-Brown, Joanne; Martin, Camilia; Claud, Erika C.
    Poor growth in the Neonatal Intensive Care Unit is associated with an increased risk for poor neurodevelopmental outcomes for preterm infants, however the mechanism is unclear. The microbiome has increasingly been recognized as a modifiable environmental factor to influence host development. Here we explore the hypothesis that the microbiome influences both growth phenotype and brain development. A germ free mouse transfaunation model was used to examine the effects of preterm infant microbiotas known to induce either high growth or low growth phenotypes on postnatal brain development. The microbiome which induced the low growth phenotype was associated with decreases in the neuronal markers NeuN and neurofilament-L as well as the myelination marker MBP when compared to the microbiome associated with the high growth phenotype. Additionally, poor growth phenotype-associated microbiota was associated with increased neuroinflammation marked by increased Nos1, as well as alteration in IGF-1 pathway including decreased circulating and brain IGF-1, decreased circulating IGFBP3, and increased Igfbp3 brain mRNA expression. This study suggests that growth-associated microbiota can influence early neuron and oligodendrocyte development and that this effect may be mediated by effects on neuroinflammation and circulating IGF-1.