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Faizah N Bhatti

TitleProf,Asst
InstitutionUniversity of Oklahoma Health Sciences Center
DepartmentDept of Pediatrics
Address1200 Everett Dr
Oklahoma City OK 73104-5047
Phone405/271-5215
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    Collapse Biography 
    Collapse education and training
    The Aga Khan University Medical College, Karachi, PakistanMBBS11/1998Medicine and Surgery
    Penn State College of Medicine, Hershey PAMS12/2011Health Evaluation Sciences
    Penn State Milton S. Hershey Medical Center, Hershey PAFellowship 12/2010Neonatology
    Penn State Milton S. Hershey Medical Center, Hershey PAResidency09/2007Pediatrics
    Georgetown University Medical Center, Washington DCFellowship06/04Cell Biology
    Collapse awards and honors
    2017 - PresElected member, Society for Pediatric Research
    2017 - PresCo-Chair Communications Committee, Society for Pediatric Research
    2014Young Faculty Award, Southern Society for Pediatric Research
    2013Awarded Attendance, AAMC Early Women Faculty Professional Development
    2013Basic Science Young Investigator Award, Southern Society for Pediatric Research
    2012Trainee Mentor Award, Department of Pediatrics, OUHSC
    2012AlconEarly Career Clinician-Scientist Research Award, Association for Research in Vision and Ophthalmology
    2011Travel Award, Association for Research in Vision and Ophthalmology
    2012Finalist, Basic Science Young Investigator Award, Southern Society for Pediatric Research

    Collapse Overview 
    Collapse overview
    With training in medical sciences as well as cell and molecular biology, Dr. Faizah Bhatti has pursued a track of translational/basic science research. Dr. Bhatti’s medical degree was completed at the Aga Khan University in Pakistan in 1998. She then completed a cell biology post-doctoral fellowship at Georgetown University, followed by residency training in pediatrics and an academic fellowship in neonatal medicine, both at the Penn State University Medical Center. During fellowship, Dr. Bhatti became interested in the biology of surfactant proteins and in their role as inflammatory mediators. She continued her work when she was recruited to the Children’s Hospital at OUHSC as a clinician scientist in 2011. Dr. Bhatti holds academic appointments in the Department of Pediatrics, Ophthalmology and the Oklahoma Center for Neurosciences. Collaborating with retinal, brain and immune experts, she is an independently funded clinician scientist studying inflammatory vascular biology. Her background and training give her an understanding of both the clinical relevance as well as the methodology needed to scientifically address clinical complications of extreme prematurity.

    Dr. Bhatti examines the biological and molecular roles of inflammatory mediators on vascular development, structure and function in both retinal as well as cerebral vascular beds. Simultaneously, she utilizes clinical data on preterm infants to study associations between inflammation, sepsis, growth and retinopathy in premature infants. She is a principal investigator/sub-PI for several clinical trials involving therapeutics and clinical aspects of ROP in the neonatal subjects at OUHSC. She has trained several residents, fellows and students in her lab program, several of whom who gone on to pursue academic fellowships and have contributed to the publications from their research program. Dr. Bhatti is committed to caring for premature babies and finding cures based on sound evidence and science.


    Collapse Research 
    Collapse research activities and funding
    RR 022262     (Bhatti F)Jun 16, 2006 - Jan 5, 2011
    K30-NIH Clinical Research Curricula for Physicians and Medical Students
    Risk Factors for Surgical Necrotizing Enterocolitis
    Role: Principal Investigator

    RR017703-10     (Bhatti F)Jul 1, 2011 - Jun 30, 2012
    NIH/NCRR COBRE Promising Junior Investigator Award
    The role of SP-A in Oxygen Induced Retinopathy
    Role Description: The goal of this study is to determine the relationship between age and lung function, and the local expression of SP-A as a determinant of the severity of retinopathy in mice. If successful, this study would allow us to develop better diagnosis and prediction of ROP in premature infants, and would identify a potential target pathway to develop new therapies to prevent ROP disease. This is desperately needed since the best current therapy leaves patience severely visually impaired.
    Role: Principal Investigator

         (Bhatti F)Jul 1, 2012 - Jun 30, 2013
    Knights Templar Eye Foundation
    The Role of Collectin Surfactant Proteins in Retinal Development and Neoproliferation
    Role Description: Retinopathy of prematurity relates to proliferative retinopathy in preterm neonates. Varying tensions of oxygen induce VEGF and IGF mediated vaso-obliteration followed by neoproliferation in the retina. Several clinical studies now show that merely limiting oxygen exposure does not eliminate retinopathy of prematurity, and that sepsis and inflammation are being recognized as important risk factors for this disease. Surfactant protein A (SP-A) is a lipid associated, innate immunity collectin protein. Preterm infants with deficiency of SP-A are at risk for pulmonary morbidity and systemic pathology. Downstream signaling pathways include TLR-2, TLR-4, NF-?B as well as TNFa. Stimuli such as LPS are known to up regulate SP-A expression. We now understand that angiogenesis in the retina may be impacted by inflammation. Preliminary data from our laboratory shows that SP-A is expressed in the developing retina and that the retina of SP-A-/- mice have diminished overall thickness when compared to wild type. In addition, flat mounts of retinal tissue show that retinal blood vessels are not as well developed and may be leaking CD31 marked cells. We therefore hypothesize that adequate SP-A expression may be critical to normal development of retinal structures including retinal vasculature. Developmentally, infants develop chronic inflammatory lung disease of prematurity, as well as retinopathy of prematurity at the same gestational age. Therefore, SP-A may play a crucial role in the pathogenesis of ROP. This is important to understand, as our best current therapies leave babies visually impaired at best, and this will help us design better targeted therapies prior to the onset of neoproliferation.
    Role: Principal Investigator

         (Bhatti F)Jul 1, 2014
    Department of Pediatrics, OUHSC
    Allelic Variants of Surfactant Protein A In Neonates With Proliferative Retinopathy: Population Based Study of Allelic Variants of Surfactant Protein A in Premature Infants
    Role Description: The goal is to examine the association of haplotypes of SP-A and SP-D with severity of ROP and to establish population specific prediction algorithms of ROP and lung disease using haplotype analysis
    Role: Principal Investigator

         (Bhatti F)Mar 16, 2015 - Jan 15, 2016
    Shire Human Genetic Therapies, Inc
    Determination of the rhIGF-1/rhIGFBP-3 Dose, Administered as a Continuous Infusion, Required to Establish and Maintain Longitudinal Serum IGF-1 Levels Within Physiological Levels in Premature Infants, to Prevent Retinopathy of Prematurity. A Phase 2, Randomized Controlled, Assessor-Blind, Dose-confirming, Pharmacokinetic, Safety and Efficacy, Multicenter Study
    Role Description: An International Multi center randomized controlled trial to compare the severity of retinopathy of prematurity (ROP) among treated infants with an untreated control population, while confirming the dose of rhIGF-1/rhIGFBP-3 is safe and efficacious.
    Role: Site PI

    EVA-18976-00     (Bhatti F)Jul 1, 2017 - Dec 31, 2017
    Shire Inc, Evidera
    Caregiver Burden of Extreme Prematurity
    Role Description: The primary objective of this study is to gain a comprehensive understanding of the caregiver burden of extreme prematurity from having a child born at < 28 weeks gestational age. The caregiver burden of extreme prematurity will be specifically characterized by emotional, physical, financial, and quality of life impacts experienced by the primary caregiver.
    Role: Site PI

    Collapse Bibliographic 
    Collapse selected publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
    List All   |   Timeline
    1. Vieira F, Kung JW, Bhatti F. Structure, genetics and function of the pulmonary associated surfactant proteins A and D: The extra-pulmonary role of these C type lectins. Ann Anat. 2017 May; 211:184-201. PMID: 28351530.
      View in: PubMed
    2. Gurwin J, Tomlinson LA, Quinn GE, Ying GS, Baumritter A, Binenbaum G. A Tiered Approach to Retinopathy of Prematurity Screening (TARP) Using a Weight Gain Predictive Model and a Telemedicine System. JAMA Ophthalmol. 2017 Jan 05. PMID: 28056115.
      View in: PubMed
    3. Binenbaum G, Tomlinson LA. Postnatal Growth and Retinopathy of Prematurity Study: Rationale, Design, and Subject Characteristics. Ophthalmic Epidemiol. 2017 Feb; 24(1):36-47. PMID: 27996334.
      View in: PubMed
    4. Bhatti F, Ball G, Hobbs R, Linens A, Munzar S, Akram R, Barber AJ, Anderson M, Elliott M, Edwards M. Pulmonary surfactant protein a is expressed in mouse retina by Müller cells and impacts neovascularization in oxygen-induced retinopathy. Invest Ophthalmol Vis Sci. 2014 Nov 18; 56(1):232-42. PMID: 25406276; PMCID: PMC4290564.
    5. Gu X, Reagan A, Yen A, Bhatti F, Cohen AW, Elliott MH. Spatial and temporal localization of caveolin-1 protein in the developing retina. Adv Exp Med Biol. 2014; 801:15-21. PMID: 24664676; PMCID: PMC4311519.
    6. Noutsios GT, Silveyra P, Bhatti F, Floros J. Exon B of human surfactant protein A2 mRNA, alone or within its surrounding sequences, interacts with 14-3-3; role of cis-elements and secondary structure. Am J Physiol Lung Cell Mol Physiol. 2013 Jun 01; 304(11):L722-35. PMID: 23525782; PMCID: PMC3680765.
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