Tushar A. Shah, MD

Assistant Professor

Pediatrics: Neonatology


Children's Hospital of The King's Daughters

757.668.7000


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:

  1. The role of complement  activation in HIE
  2. The effect of therapeutic hypothermia on complement activation
  3. 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:

  1. The role of complement  activation in HIE
  2. The effect of therapeutic hypothermia on complement activation
  3. 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.

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