Melissa D. Halpern

ORCID: 0000-0003-0871-3235
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About
Contact & Profiles
Research Areas
  • Infant Nutrition and Health
  • Pediatric Hepatobiliary Diseases and Treatments
  • Neonatal Respiratory Health Research
  • Clinical Nutrition and Gastroenterology
  • Digestive system and related health
  • Viral gastroenteritis research and epidemiology
  • Child Nutrition and Water Access
  • T-cell and B-cell Immunology
  • Drug Transport and Resistance Mechanisms
  • Child Nutrition and Feeding Issues
  • Monoclonal and Polyclonal Antibodies Research
  • Gut microbiota and health
  • Immune Response and Inflammation
  • Infant Health and Development
  • Diet and metabolism studies
  • Systemic Lupus Erythematosus Research
  • Barrier Structure and Function Studies
  • Mast cells and histamine
  • Gastrointestinal disorders and treatments
  • Diabetes and associated disorders
  • Growth Hormone and Insulin-like Growth Factors
  • Cleft Lip and Palate Research
  • Probiotics and Fermented Foods
  • Immune Cell Function and Interaction
  • Breastfeeding Practices and Influences

University of Arizona
2007-2024

Children's Center
2010

Duke University Hospital
1995-1998

Duke Medical Center
1995-1998

Durham VA Medical Center
1995-1996

University of North Carolina at Chapel Hill
1992-1994

Technion – Israel Institute of Technology
1985

University of California, Berkeley
1970

Necrotizing enterocolitis (NEC) is the most common gastrointestinal disease of prematurely born infants. Maternal milk plays an important protective role against NEC development and major source epidermal growth factor (EGF) for neonates. The aim this study was to examine effect orally administered EGF on incidence in a neonatal rat model. Newborn rats were artificially fed either with factor-free substitute (RMS) or RMS supplemented 500 ng/ml (RMS+EGF). Experimental induced by exposure...

10.1152/ajpgi.00196.2001 article EN AJP Gastrointestinal and Liver Physiology 2002-01-01

Necrotizing enterocolitis (NEC) is the most common intestinal disease of premature infants. Although increased mucosal permeability and altered epithelial structure have been associated with many disorders, role barrier function in NEC pathogenesis currently unknown. We investigated structural functional changes a rat model NEC. In addition, effect EGF treatment on was evaluated. Premature rats were divided into three groups: dam fed (DF), formula (NEC), or supplemented 500 ng/ml (NEC +...

10.1152/ajpgi.00090.2006 article EN AJP Gastrointestinal and Liver Physiology 2006-06-24

Neonatal necrotizing enterocolitis (NEC) is a major cause of morbidity and mortality in premature infants. Oral administration probiotics has been suggested as promising strategy for prevention NEC. However, little known about the mechanism(s) probiotic-mediated protection against The aim this study was to evaluate effects Bifidobacterium bifidum treatment on development NEC, cytokine regulation, intestinal integrity rat model Premature rats were divided into three groups: dam fed (DF), hand...

10.1152/ajpgi.00141.2009 article EN AJP Gastrointestinal and Liver Physiology 2009-08-28

The intestinal epithelial barrier plays an important role in maintaining host health. Breakdown of function is known to play a many diseases such as infectious enteritis, idiopathic inflammatory bowel disease, and neonatal diseases. Recently, increasing research has demonstrated the importance understanding how develops premature neonate order develop strategies promote its maturation. Optimizing thought be key preventing necrotizing enterocolitis. In this review, we will first summarize...

10.1080/21688370.2014.1000707 article EN Tissue Barriers 2015-01-22

Necrotizing enterocolitis (NEC) is a devastating intestinal disease of neonates, and clinical studies suggest the beneficial effect probiotics in NEC prevention. Recently, we have shown that administration Bifidobacterium bifidum protects against rat model. Intestinal apoptosis can be suppressed by activation cyclooxygenase-2 (COX-2) increased production prostaglandin E(2) (PGE(2)). The present study investigates B. on model an epithelial cell line (IEC-6), as mechanism protection mucosal...

10.1152/ajpgi.00131.2010 article EN AJP Gastrointestinal and Liver Physiology 2010-08-12

Necrotizing enterocolitis (NEC) is a devastating intestinal disease of premature infants. Although end-stage NEC characterized histopathologically as extensive necrosis, apoptosis may account for the initial loss epithelium before full development disease. We have previously shown that epidermal growth factor (EGF) reduces incidence in rat model. EGF has been to protect enterocytes from apoptosis, mechanism EGF-mediated protection against not known. The aim this study was investigate if...

10.1152/ajpgi.00172.2004 article EN AJP Gastrointestinal and Liver Physiology 2004-11-05

Necrotizing enterocolitis (NEC) is the most common gastrointestinal disease of premature infants. However, despite significant morbidity and mortality, etiology pathogenesis NEC are poorly understood. Evidence suggests that ileal proinflammatory mediators such as IL-18 contribute to pathology associated with this disease. In addition, we have previously shown upregulation TNF-alpha in liver correlated severity a neonatal rat model NEC. With use NEC, evaluated incidence damage along...

10.1152/ajpgi.00408.2005 article EN AJP Gastrointestinal and Liver Physiology 2005-11-04

Necrotizing enterocolitis (NEC) is a devastating intestinal disease of premature infants. Epidermal growth factor (EGF) one the most promising candidates in NEC prophylaxis. Autophagy regulates cell homeostasis, but uncontrolled activation autophagy may lead to cellular injury. The aim was evaluate effects EGF on epithelial cells and rat model measure patients. Intestinal (IEC-6) were used study effect autophagy. Protein levels Beclin 1 LC3II measured epithelium both vivo vitro models....

10.1152/ajpgi.00076.2010 article EN AJP Gastrointestinal and Liver Physiology 2010-06-11

Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency of premature infants, but its etiology remains unclear. We have previously shown that mucin 2 (Muc2) positive goblet cells are significantly decreased in NEC. also ileal bile acids (BAs) increased during development this disease. Because BAs can affect mucins, we hypothesized elevated contribute to Muc2 experimental The role NEC was evaluated Winnie +/+ mice, a strain produces aberrant Muc2. and trefoil factor 3...

10.1371/journal.pone.0027191 article EN cc-by PLoS ONE 2011-12-05

Background Gastrointestinal barrier immaturity predisposes preterm infants to necrotizing enterocolitis (NEC). Intraepithelial lymphocytes (IEL) bearing the unconventional T cell receptor (TCR) γδ (γδ IEL) maintain intestinal integrity and prevent bacterial translocation in part through production of interleukin (IL) 17. Objective We sought study development IEL ileum human examine their role NEC pathogenesis. defined ontogeny proportions murine intestine subjected tcrδ−/− mice experimental...

10.1371/journal.pone.0099042 article EN cc-by PLoS ONE 2014-06-06

Necrotizing enterocolitis (NEC) is a common and devastating gastrointestinal disease of premature infants. Along with pathological effects in the ileum, severe NEC often accompanied by mutisystem organ failure, including liver failure. The aim this study was to determine changes hepatic cytokines inflammatory mediators experimental NEC. well-established neonatal rat model used study, morphology, numbers Kupffer cells (KC), gene expression, histological localization IL-18, TNF-α, inducible...

10.1152/ajpgi.00353.2002 article EN AJP Gastrointestinal and Liver Physiology 2003-04-01

Background Necrotizing enterocolitis (NEC) is the most common gastrointestinal disease of premature infants. We have shown in previous studies that proinflammatory interleukin-18 and interleukin-12 are up-regulated ileum rats with experimental NEC epidermal growth factor (EGF) reduces development disease. Here we investigated whether protective effects EGF a result changes ileal interleukin-18, and/or antiinflammatory interleukin-10. Methods Newborn were artificially fed either...

10.1097/00005176-200301000-00024 article EN Journal of Pediatric Gastroenterology and Nutrition 2003-01-01

Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease predominantly of prematurely born infants, characterized in its severest from by extensive hemorrhagic inflammatory necrosis the distal ileum and proximal colon. Proinflammatory cytokines have been implicated development NEC, we previously shown that IL-18 significantly elevated well-established neonatal rat model NEC. To determine whether contributes to intestinal pathology subjected knockout mice protocol used...

10.1152/ajpgi.00168.2007 article EN AJP Gastrointestinal and Liver Physiology 2007-10-19

ABSTRACT Background: Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease of prematurely born infants. Epidermal growth factor (EGF) and heparin‐binding EGF‐like (HB‐EGF) have protective effects against intestinal injury. The aim this study was to compare the effect oral administration HB‐EGF, EGF, or both on incidence NEC in neonatal rat model. Materials Methods: Premature rats were fed by hand exposed asphyxia cold stress develop NEC. Four diets used: formula (NEC),...

10.1097/mpg.0b013e3181788618 article EN Journal of Pediatric Gastroenterology and Nutrition 2008-07-01

Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency of premature infants. Previously, we showed that luminal bile acids (BAs) are increased and correlated with disease development apical sodium-dependent BA transporter (ASBT), which transports BAs from ileal lumen into enterocytes, upregulated in rats NEC. We hypothesized intraenterocyte, rather than luminal, associated NEC upregulation ASBT may be a mechanism by this occurs. Neonatal or without inhibitor SC-435,...

10.1152/ajpgi.00242.2010 article EN AJP Gastrointestinal and Liver Physiology 2010-08-27

Microbial DNA has multiple immune effects including the capacity to induce polyclonal B cell activation and cytokine production in normal mice. We recently described accelerated induction of anti-DNA Abs NZB/NZW mice immunized with Escherichia coli (EC) dsDNA; paradoxically these developed less renal disease than unimmunized or calf thymus DNA. postulated that alterations induced by bacterial may play a key role protection. To determine effect on mice, we measured serum levels, culture...

10.4049/jimmunol.161.8.3890 article EN The Journal of Immunology 1998-10-15
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