Nahla Zaghloul, MD
Assistant Professor, Pediatrics

Contact:

PO Box 245073 Tucson, AZ 85724
Admin Office: 
(520) 626-6627

Division

About

Biography:
Nahla Zaghloul is a member of the Steele Children’s Research Center at the University of Arizona College of Medicine. She is an Assistant Professor of Pediatrics at the University of Arizona College of Medicine, and attending Neonatologist at Banner Diamond Children’s Medical Center. Her research interests involve improving outcome among premature infants with brain injury. She is a member of the American Academy of Pediatrics, American Academy of Perinatal Medicine, Society of Pediatric Research, and Society of Neuroscience.

Education

Medical School: 
Cairo University, Egypt - Completed 11/30/2003
Residency: 
Pediatrics, Stony Brook Children's Hospital, NY - Completed 06/30/2009
Fellowship: 
Neonatology, Cohen Children's Hospital, NY - Completed 06/30/2012

Clinical

Board Certification: 
American Board of Pediatrics
American Board of Pediatrics-Neonatal-Perinatal Medicine
Clinical Interests: 
Point of care ultrasound (POC-US) program in the NICU is a bedside tool for immediate diagnostic and therapeutic purposes. It has many great benefits: quick, focused and no ionizing radiation allowing timely lifesaving therapeutic interventions.
 
Neonatal Neuro-critical care program: Combining Neuro-monitoring and Neuro-imaging to provide optimal care for infants at risk or who had developed brain injury. This is a multi-disciplinary team of experts in neonatal neurology, neonatology, neuro-radiology, and developmental pediatrics, occupational and physical therapy. Our main goal is to the outcome of these vulnerable babies.

Research

Research Interests: 
 
Mission:
The Zaghloul lab investigated mechanism of neonatal brain injury and developing  targeted therapeutics.
The brain is the most energetically demanding organ of the body especially in premature infants. Premature infants are at increased risk of Periventricular leukomalacia (PVL) which is caused by hypoxic ischemic (HI) to the brain. HI causes an abrupt decline of brain’s fuel supply and mitochondrial generation of ATP. PVL further leads to neuronal death, hypomyelination and microglial activation. PVL is the most common cause of cerebral palsy in premature infant.
Targeted therapeutics for PVL at our lab mainly inhibit microglial activation while restoring mitochondrial integrity and function.
 

The challenge:
Premature infants are susceptibility to develop HI due to the pressure-passive circulation without autoregulation and the susceptibility of premyelinating oligodendrocytes (pre-OLs) to both reactive oxidative (ROS) and nitrative stress (RNS) and excitotoxicity caused by accumulation of injurious extracellular glutamate. Preterm infants have deficient antioxidant system. Infection and/or systemic inflammation, which are seen in neonates born with chorioamnionitis induce a systemic increase in pro-inflammatory cytokines. Microglia activation causes the release of pro-inflammatory cytokines and free radicals leading to pre-OLs loss and maturation arrest. This in turn leads to mitochondrial dysfunction and ATP loss.
 

The strategy:
The Zaghloul Group focuses on the role of microglial activation, inflammation, oxidative stress and mitochondrial dysfunction that acts synergistically to cause PVL.
By inhibiting microglial activation through various drug therapies, anti-inflammatory state, energy metabolism and redox homeostasis will be restored thus preventing ongoing degeneration and promoting regeneration. By developing novel preclinical animal models and testing anti-microglial therapeutics will soon translate to human clinical trials.
 

Innovations:
The Zaghloul lab established a neonate mouse HI model mimicking human PVL in symptomatology, pathogenesis, molecular and cellular mechanism and long term neurodevelopmental aspects. This model develops diplegia and cerebral palsy. It also mimics human PVL autopsy specimens in histopathology showing white matter loss leading to ventriculomegally, neuronal apoptosis, astrogliosis and microglial activation. Our animal model also survives long beyond the HI injury, allowing better long term monitoring.
We have discovered that using various drugs that inhibit microglial activation can lead to white matter regeneration and reversal of neuronal apoptosis.
 

Research Team: 
Edward Abril
Research Specialist Senior and Lab Manger
Prisca Zimmerman
Research Specialist Senior

Publications

2019

Zaghloul, N., L. Watkins, J. Choi-Rosen, S. Perveen, and D. Kurepa, "The superiority of point of care ultrasound in localizing central venous line tip position over time.", Eur J Pediatr, vol. 178, issue 2, pp. 173-179, 2019 Feb. PMID: 30374753
Perveen, S., K. Ayasolla, N. Zagloul, H. Patel, K. Ochani, D. Orner, H. Benveniste, M. Salerno, P. Vaska, Z. Zuo, et al., "MIF inhibition enhances pulmonary angiogenesis and lung development in congenital diaphragmatic hernia.", Pediatr Res, vol. 85, issue 5, pp. 711-718, 2019 Apr. PMID: 30759452
Li, H-L., N. Zaghloul, I. Ahmed, A. Omelchenko, B. L. Firestein, H. Huang, and L. Collins, "Caffeine inhibits hypoxia-induced nuclear accumulation in HIF-1α and promotes neonatal neuronal survival.", Exp Neurol, vol. 317, pp. 66-77, 2019 Jul. PMID: 30822423

2018

Kurepa, D., N. Zaghloul, L. Watkins, and J. Liu, "Neonatal lung ultrasound exam guidelines.", J Perinatol, vol. 38, issue 1, pp. 11-22, 2018 01. PMID: 29144490

2017

Zaghloul, N., H. Patel, and M. Nagy Ahmed, "A model of Periventricular Leukomalacia (PVL) in neonate mice with histopathological and neurodevelopmental outcomes mimicking human PVL in neonates.", PLoS One, vol. 12, issue 4, pp. e0175438, 2017. PMCID: PMC5391059  PMID: 28406931
Zaghloul, N., M. E. Addorisio, H. A. Silverman, H. L. Patel, S. I. Valdés-Ferrer, K. R. Ayasolla, K. R. Lehner, P. S. Olofsson, M. Nasim, C. N. Metz, et al., "Forebrain Cholinergic Dysfunction and Systemic and Brain Inflammation in Murine Sepsis Survivors.", Front Immunol, vol. 8, pp. 1673, 2017. PMCID: PMC5736570  PMID: 29326685
Patel, H., N. Zaghloul, K. Lin, S. Fang Liu, E. J. Miller, and M. Ahmed, "Hypoxia-induced activation of specific members of the NF-kB family and its relevance to pulmonary vascular remodeling.", Int J Biochem Cell Biol, vol. 92, pp. 141-147, 2017 11. PMID: 28987523
Zaghloul, N., and M. Ahmed, "Pathophysiology of periventricular leukomalacia: What we learned from animal models.", Neural Regen Res, vol. 12, issue 11, pp. 1795-1796, 2017 Nov. PMCID: PMC5745826  PMID: 29239318

2016

Hand, I., N. Zaghloul, L. Barash, R. Parris, U. Aden, and H-L. Li, "Timing of Caffeine Therapy and Neonatal Outcomes in Preterm Infants: A Retrospective Study.", Int J Pediatr, vol. 2016, pp. 9478204, 2016. PMCID: PMC4875982  PMID: 27242907

2014

Zaghloul, N., H. Patel, C. Codipilly, P. Marambaud, S. Dewey, S. Frattini, P. T. Huerta, M. Nasim, E. J. Miller, and M. Ahmed, "Overexpression of extracellular superoxide dismutase protects against brain injury induced by chronic hypoxia.", PLoS One, vol. 9, issue 9, pp. e108168, 2014. PMCID: PMC4182464  PMID: 25268361

2012

Zaghloul, N., M. Nasim, H. Patel, C. Codipilly, P. Marambaud, S. Dewey, W. K. Schiffer, and M. Ahmed, "Overexpression of extracellular superoxide dismutase has a protective role against hyperoxia-induced brain injury in neonatal mice.", FEBS J, vol. 279, issue 5, pp. 871-81, 2012 Mar. PMID: 22240000
Ahmed, M. N., Y. Zhang, C. Codipilly, N. Zaghloul, D. Patel, M. Wolin, and E. J. Miller, "Extracellular superoxide dismutase overexpression can reverse the course of hypoxia-induced pulmonary hypertension.", Mol Med, vol. 18, pp. 38-46, 2012 Feb 10. PMCID: PMC3269642  PMID: 22045221