Profiles
Tushar A. Shah, MD
Faculty Appointments
Assistant Professor of Pediatrics
Assistant Professor of Microbiology and Molecular Cell Biology
Office Hours
OFFICE
Children's Hospital of The King's Daughters
Division of Neonatology
601 Children's Lane, Norfolk, VA 23507
Phone: 757-668-7456
Medical Education
Topiwala National Medical College, Mumbai University
Residency
Metrohealth Medical Center/Case Western Reserve University
Fellowship
Cincinnati Children's Hospital Medical Center - Neonatology
Emory University - Epidemiology
Board Certifications
American Board of Pediatrics
Neonatal-Perinatal Medicine
Lab Location
EV Williams Hall/Depart. of Pediatrics
855 W Brambleton Ave., Norfolk, VA 23510
(757) 668-6498
Email: Shahta@evms.edu
Research Interests
Role of Complement Modulation in a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy.
Brain injury resulting from neonatal asphyxia (hypoxic-ischemic encephalopathy, [HIE]) has an incidence of 1-2 per 1000 live births, with up to 60% mortality and 25% of survivors left with a significant disability. The complement system, an extremely potent inflammatory cascade of the immune system, which is critical for phagocytic cell recruitment and direct cell lysis, has been shown to play a major role in the pathogenesis of HIE in animal models and human studies. Although therapeutic hypothermia has been demonstrated to improve survival and neurodevelopment in newborns with HIE, if offers only an 11% reduction in risk of death or disability, a decrease from 58% to 47%. Modulation of complement activation may be a viable adjunct to therapeutic hypothermia for improving neurological outcomes in HIE.
Using the Vannucci neonatal rat model of brain hypoxia-ischemia, our lab is investigating:
- The role of complement activation in HIE
- The effect of therapeutic hypothermia on complement activation
- The effect of complement modulation in HIE using a novel inhibitor of the classical complement pathway, PIC1
Current Projects
Research Support
Commonwealth Health Research Board - Role of Novel Complement inhibitor in improving neurological outcomes in an animal model of Neonatal Hypoxic Ischemic Encephalopathy.
Presentations and Scholarships
Publications
Xia H, Ren X, Bolte CS, Ustiyan V, Zhang Y, Shah TA, Kalin TV, Whitsett JA, Kalinichenko VV. Foxm1 Regulates Resolution of Hyperoxic Lung Injury in Newborns. Am J Respir Cell Mol Biol. 2014 Oct 2.
Shah TA, Mauriello CT, Hair PS, Sandhu A, Stolz MP, Bass WT, Krishna NK, Cunnion KM. Clinical hypothermia temperatures increase complement activation and cell destruction via the classical pathway. J Transl Med. 2014 Jun 24;12(1):181.
Shah TA, Mauriello CT, Hair PS, Sharp JA, Kumar PS, Lattanzio FA, Werner AL, Whitley PH, Maes LA Cunnion KM, Krishna NK. Complement inhibition significantly decreases red blood cell lysis in a rat model of acute intravascular hemolysis. Transfusion. 2014 Nov;54(11):2892-900.
Ren X, Shah TA, Ustiyan V, Zhang Y, Shinn J, Chen G, Whitsett JA, Kalin TV, Kalinichenko VV. FOXM1 Promotes Allergen-Induced Goblet Cell Metaplasia and Pulmonary Inflammation. Mol Cell Biol. 2013 Jan; 33(2):371-86
Shah TA, Meinzen-Derr J, Schibler KR. Hospital and Neurodevelopmental Outcomes of Extremely Low Birth Weight Infants with Necrotizing Enterocolitis”. J Perinatol. 2012 Jul; 32(7):552-8
Slaughter JL, Pakrashi T, Jones DE, South AP, Shah TA. Echocardiographic Detection of Pulmonary Hypertension in Extremely Low Birth Weight Infants with Bronchopulmonary Dysplasia Requiring Prolonged Positive Pressure Ventilation. J Perinatol. 2011 Oct; 31(10):635-40.
Ren X, Zhang Y, Snyder J, Cross ER, Shah TA, Kalin TV, Kalinichenko VV. Forkhead box M1 transcription factor is required for macrophage recruitment during liver repair. Mol Cell Biol. 2010 Nov; 30(22):5381-93.
Shah TA, Hillman NH, Nitsos I, Polglase GR, Pillow JJ, Newnham JP, Jobe AH, Kallapur SG. Pulmonary and Systemic Expression of Monocyte Chemotactic Proteins in Preterm Sheep Fetuses Exposed to LPS Induced Chorioamnionitis. Pediatr Res. 2010 Sep; 68(3):210-5.
Faculty Appointments
Assistant Professor of Pediatrics
Assistant Professor of Microbiology and Molecular Cell Biology
Office Hours
OFFICE
Children's Hospital of The King's Daughters
Division of Neonatology
601 Children's Lane, Norfolk, VA 23507
Phone: 757-668-7456
Medical Education
Topiwala National Medical College, Mumbai University
Residency
Metrohealth Medical Center/Case Western Reserve University
Fellowship
Cincinnati Children's Hospital Medical Center - Neonatology
Emory University - Epidemiology
Board Certifications
American Board of Pediatrics
Neonatal-Perinatal Medicine
Lab Location
EV Williams Hall/Depart. of Pediatrics
855 W Brambleton Ave., Norfolk, VA 23510
(757) 668-6498
Email: Shahta@evms.edu
Research Interests
Role of Complement Modulation in a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy.
Brain injury resulting from neonatal asphyxia (hypoxic-ischemic encephalopathy, [HIE]) has an incidence of 1-2 per 1000 live births, with up to 60% mortality and 25% of survivors left with a significant disability. The complement system, an extremely potent inflammatory cascade of the immune system, which is critical for phagocytic cell recruitment and direct cell lysis, has been shown to play a major role in the pathogenesis of HIE in animal models and human studies. Although therapeutic hypothermia has been demonstrated to improve survival and neurodevelopment in newborns with HIE, if offers only an 11% reduction in risk of death or disability, a decrease from 58% to 47%. Modulation of complement activation may be a viable adjunct to therapeutic hypothermia for improving neurological outcomes in HIE.
Using the Vannucci neonatal rat model of brain hypoxia-ischemia, our lab is investigating:
- The role of complement activation in HIE
- The effect of therapeutic hypothermia on complement activation
- The effect of complement modulation in HIE using a novel inhibitor of the classical complement pathway, PIC1
Current Projects
Research Support
Commonwealth Health Research Board - Role of Novel Complement inhibitor in improving neurological outcomes in an animal model of Neonatal Hypoxic Ischemic Encephalopathy.
Presentations and Scholarships
Publications
Xia H, Ren X, Bolte CS, Ustiyan V, Zhang Y, Shah TA, Kalin TV, Whitsett JA, Kalinichenko VV. Foxm1 Regulates Resolution of Hyperoxic Lung Injury in Newborns. Am J Respir Cell Mol Biol. 2014 Oct 2.
Shah TA, Mauriello CT, Hair PS, Sandhu A, Stolz MP, Bass WT, Krishna NK, Cunnion KM. Clinical hypothermia temperatures increase complement activation and cell destruction via the classical pathway. J Transl Med. 2014 Jun 24;12(1):181.
Shah TA, Mauriello CT, Hair PS, Sharp JA, Kumar PS, Lattanzio FA, Werner AL, Whitley PH, Maes LA Cunnion KM, Krishna NK. Complement inhibition significantly decreases red blood cell lysis in a rat model of acute intravascular hemolysis. Transfusion. 2014 Nov;54(11):2892-900.
Ren X, Shah TA, Ustiyan V, Zhang Y, Shinn J, Chen G, Whitsett JA, Kalin TV, Kalinichenko VV. FOXM1 Promotes Allergen-Induced Goblet Cell Metaplasia and Pulmonary Inflammation. Mol Cell Biol. 2013 Jan; 33(2):371-86
Shah TA, Meinzen-Derr J, Schibler KR. Hospital and Neurodevelopmental Outcomes of Extremely Low Birth Weight Infants with Necrotizing Enterocolitis”. J Perinatol. 2012 Jul; 32(7):552-8
Slaughter JL, Pakrashi T, Jones DE, South AP, Shah TA. Echocardiographic Detection of Pulmonary Hypertension in Extremely Low Birth Weight Infants with Bronchopulmonary Dysplasia Requiring Prolonged Positive Pressure Ventilation. J Perinatol. 2011 Oct; 31(10):635-40.
Ren X, Zhang Y, Snyder J, Cross ER, Shah TA, Kalin TV, Kalinichenko VV. Forkhead box M1 transcription factor is required for macrophage recruitment during liver repair. Mol Cell Biol. 2010 Nov; 30(22):5381-93.
Shah TA, Hillman NH, Nitsos I, Polglase GR, Pillow JJ, Newnham JP, Jobe AH, Kallapur SG. Pulmonary and Systemic Expression of Monocyte Chemotactic Proteins in Preterm Sheep Fetuses Exposed to LPS Induced Chorioamnionitis. Pediatr Res. 2010 Sep; 68(3):210-5.