Medical Science Building (MSB) 185 South Orange Avenue Room F546 Newark, NJ 07101 Phone: (973) 972-9835
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Medical Expertise
Neonatal-Perinatal Medicine, including prematurity, hypoxic ischemic encephalopathy, multiple congenital anomalies and congenital heart disease
Hospital Affiliation
University Hospital, Newark
INSURANCE PARTICIPATION
Insurance Participation: with Provider Number (where applicable) The information below is subject to change and should not be relied upon until after
it is verified with the insurance company. In addition, psychiatric providers should
be contacted directly for information on their participation with managed care and
insurance companies.
Dr. Feldman was born about 15 minutes from Rutgers University-NJMS. He attended college at Yeshiva University, graduating with honors in 2005 and completed medical school at New York College of Osteopathic Medicine graduating with honors in 2009. Dr. Feldman completed Pediatrics residency at UMDNJ-NJMS in 2012 and Neonatal ?Perinatal Medicine Fellowship at New York Medical College in 2015, serving as chief fellow from 2014-2015. Dr. Feldman?s research interests include the transition from fetal to neonatal life in premature infants and the impact of genetics on various neonatal outcomes. He has presented extensively on the association of genetic variation and neonatal morbidities, being awarded the Eastern Society of Pediatric Research (ESPR) Meritorious Research Award in 2015.
Education
DO, 2009, New York College Osteopathic Medicine BA, 2004, Yeshiva University
Feldman A, DeBenedictis B, Alpan G, Kase J. Morbidity and Mortality Associate with Rewarming Hypothermic Very Low Birth Weight Infants. Journal of Neonatal-Perinatal Medicine, Preliminary acceptance March 2015.
La Gamma E, Feldman A, Mintzer J, Alpan G. Transfusion Related Acute Gut Injury (TRAGI):
The Role of Red Blood Cell Storage. Neoreviews. 2015; 16:7, e420-430.
Perez J, Feldman A, Alpan G. Treating Hypoxic Ischemic Encephalopathy Hypothermia. Neoreviews. 2015; 16:7, e413-419.
Feldman A, Kirtok N. High Flow Nasal Cannula: A Review of the Data. The Perinatal Gazette ? Newsletter of the Regional Perinatal Center, Maria Fareri Children?s Hospital at Westchester Medical Center. 2014 July; 14 (2): 1 ? 4.
AP2 beta Single Nucleotide Polymorphism associated with PDA in VLBW infants
The ductus arteriosus (DA) is a neural crest derived vascular conduit between the pulmonary artery and the aorta that develops by seven weeks of gestation. In the non-breathing fetus, the DA diverts vascular flow from the pulmonary to the systemic circulation. Following cessation of umbilical venous flow and the initiation of ventilation, pulmonary vascular resistance falls, directing vascular flow to the lungs, augmenting systemic perfusion pressures, and decreasing flow across the DA. In preterm newborns, the DA often fails to constrict-either functionally or anatomically-resulting in a differential pressure gradient between the systemic and pulmonary circulations, which favors increased pulmonary circulation and decreased perfusion of systemic vascular beds distal to the PDA.
Genetic foundations account for a high proportion of the variance in PDA outcome in preterm infants. Amongst the candidate genes, TFAP2? has been found to be a vital mediator of oxygen induced ductal vasoconstriction in a mouse model. Ductal epithelial cell expression of AP2? has been shown to upregulate expression of a number of genes, including hypoxia inducible factor 2a (HIF2a) and endothelin-1 (ET-1) from adjacent ductal smooth tissue. In the absence of TFAP2? (knockout mice), the HIF2a and ET-1 expression are not enhanced resulting in persistent PDA and early death.
Mutations of a highly conserved AP2? block that extends from the intronic region between exons one and two to beyond the end of the gene have been associated with syndromic and nonsyndromic causes of PDA. To date, in term infants, eleven disease causing mutations (of both introns and exons) in this region have been reported. Similarly, in a study of preterm infants <32 weeks gestational age, genome wide association studies have identified a strong association of genetic variation in the TFAP2? gene and PDA. We hypothesize that single nucleotide polymorphisms (SNPs) of the TFAP2? gene in this block are associated with the persistence of PDAs in ELBW infants.