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CORE FACULTY: Professional Biography Arrow Read More Biographies
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Stephen Black, Ph.D. spacer
Stephen M. Black, Ph.D.
Regents Professor, OBGYN/Pediatrics
Phone:(706) 721-7860
Fax: (706) 721-9799
Email:sblack@gru.edu
Office: CB-3211B
Lab: CB-3201B
LinkedIn | StephenMBlack.com | About.me | Cardiovascular Discovery Institute

Research Interests

Research in the Black Laboratory focuses on the roles of reactive oxygen species (ROS) in cell signaling and how derangements in ROS generation underlie many pathologic states. These studies impact both ROS mediated signal transduction and nitric oxide synthase (NOS) structure-function biology and are of importance in a number of physiological processes. Clinically, these studies should be important in developing intervention directed at various pathophysiological disorders in which redox signaling is thought to play crucial roles. These include pulmonary and systemic hypertension, diabetes, renal failure, atherosclerosis, and stroke. The studies in the Black Laboratory are funded by a number of RO1 awards form the National Institutes of Health (NIH). In addition, the Black Lab has active collaborations with research groups at a number of universities including the University of California at San Francisco, University of California at Davis, Northwestern University in Chicago, German Heart Centre of the State of Bavaria, in Munich, Germany, Medical College of Wisconsin, and Hannover Medical School, Germany.

Current Projects

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) represent a continuum of progressive respiratory failure in the absence of left heart failure. ARDS patients represent a subset of ALI patients, distinguished by a greater severity. In ALI/ARDS, the integrity of the capillary barrier is compromised leading to increased vascular permeability and alveolar flooding. The only intervention that has shown a clear survival benefit is the use of low tidal volume mechanical ventilation. The incidence of ALI/ARDS is in the range of 59-79 per 100,000 people in the USA alone, threatening more than 150,000 lives annually. The mortality rate of patients with ARDS ranges from 34 to 58%. Despite new information about pathophysiology of ARDS, it continues to be associated with an unacceptably high mortality rate. Different therapeutic approaches are needed. Importantly, it has become clear that a multi-target approach is required to address the multiple pathways activated in ARDS.

The pathology of ALI/ARDS is so complex that a single project cannot hope to address all the relevant areas. Our PO1 is designed to focus on role played by the vascular endothelium in the progression of ALI/ARDS. The endothelium undergoes dramatic changes in response to the various stimuli associated with inflammation. Overall our research program is based on the premise that aberrant regulation of RhoA and Rac1 signaling leads to the disruption of the endothelial barrier and plays a key role in the development of ALI/ARDS and we are attempting to elucidate both new mechanisms by which the RhoA/Rac1 balance is disrupted during the development of ALI and to develop novel therapies to restoring the RhoA/Rac1 balance and repair the endothelial barrier.
Black Lab

Alterations in endothelial NO synthase (eNOS) expression and activity by reactive oxygen species
reactive oxygen species (ROS) are thought to play an important role in the development of endothelial dysfunction. Endothelial dysfunction relates to the inability of a blood vessel to expand properly with the result that blood flow is compromised. Endothelial dysfunction has been associated with a decrease in the activity of endothelial NOS (eNOS). We hypothesize that there is a link between high levels ROS and alterations in eNOS expression and activity. To test this hypothesis we are employing an integrated molecular and biochemical approach. We are delineating the signaling pathways that result in increased production of ROS. To evaluate these signaling pathways we are employing a number of techniques including immunoprecipitation, cellular protein kinase determination, and pharmacological inhibition. We are also utilizing the over-expression of wild type, dominant negative, and constitutively active mutant proteins from both mammalian and adenoviral expression systems to specifically target signaling molecules within the cell. In addition we are using fluorescent imaging analysis to quantitate the changes in ROS. We are also employing eNOS promoter-reporter constructs to determine the cis-elements through which ROS alter eNOS expression with the goal of identifying the trans-acting factors.

Role of reactive oxygen species in the development of pulmonary hypertension of the newborn (PPHN)
With the initiation of ventilation and oxygenation at birth, pulmonary vascular resistance decreases and pulmonary blood flow increases. There is evidence that increased endothelial NO synthase (eNOS) gene expression, eNOS activity, and NO production, contribute to these changes. However, in a number of clinical conditions, there is failure of the pulmonary circulation to undergo this normal transition to postnatal life, resulting in persistent pulmonary hypertension of the newborn (PPHN). PPHN complicates more than 5 in 1000 live births and up to 10% of admissions to intensive care units. PPHN causes substantial morbidity and mortality in otherwise normal term infants. It is known that newborns who die of PPHN have decreased endogenous NO production and an increase in circulating endothelin-1 (ET-1) levels. In addition these children have an increase in pulmonary arterial medial smooth muscle cell thickness and extension of muscle to normally non-muscular arteries. The anatomic changes in the pulmonary vessels in newborns with PPHN are thought to be intimately associated with the morbidity and mortality associated with PPHN. However, the mechanisms producing this abnormal smooth muscle cell (SMC) development and the reduction in eNOS gene expression and NO production are not well understood. Using whole animal models as well as cellular and molecular biological techniques we are elucidating the signaling mechanisms through which ET-1 alters SMC growth and elucidating how alterations in SMC signaling can alter gene expression in endothelial cells. We hope that these studies will lead to a better understanding of the mechanisms responsible for the development of PPHN that will in turn lead to improved treatment strategies for children born with pulmonary hypertension.

Biomechanical forces in vascular remodeling
Approximately 1% of children are born with a congenital heart defect, with half requiring medical and/or surgical treatment. Survival for these children has improved although substantial morbidity and mortality occurs even after corrective surgery. This is due, in part, to abnormal pulmonary vascular development. This abnormal vascular growth can persist even after surgical intervention establishes a normal pulmonary blood flow. The factors responsible for the altered pulmonary vascular growth in these children are not well understood. We are trying to understand how this process is regulated since a better understanding of this process could lead to treatment strategies that could [PHOTO]prevent the adverse consequences of CHD. We have developed a unique ovine model of CHD with increased pulmonary blood flow. In these lambs there is an increase in both the size and number of the pulmonary vessels by 4-weeks of age. The pulmonary circulation of these lambs is subjected to increased levels of blood flow resulting in increased exposure to the biomechanical forces, fluid shear stress and cyclic stretch. We are testing the hypothesis that the vascular remodeling observed in children with CHD, is due, at least in part, to biomechanical forces increasing the expression of growth factors in the lung that stimulate blood vessel growth.

Reactive oxygen species in perintal-hypoxia ischemia
Perinatal hypoxia-ischemia (HI) or "stroke" represents a long-standing, refractory public health problem. The neurologic sequelae of the severe form of this injury include mental retardation, epilepsy, cerebral palsy and blindness. Multiple lines of evidence have established the critical role of nitric oxide (NO) in HI-mediated brain injury in the newborn. In addition, data from our laboratory indicate that the developing brain is more vulnerable to HI injury than the mature brain, due to a deficiency in anti-oxidant enzyme capacity, resulting in a greater susceptibility to oxidative stress. However, how the oxidative stress and NO induced by HI interact to produce injury to the neonatal brain remains unresolved. Studies in the lab are trying to unravel the signaling pathways involved in this process. We are utilizing both whole animal models as well as primary neuronal cultures to investigate these events.

Current Grant Support

STATUS: P.I.
FUNDING AGENCY: National Heart, Lung, and Blood Institute
TITLE OF AWARD: Endothelial Barrier Protection and Repair in Acute Lung Injury
TYPE OF AWARD: PO1
PERIOD OF SUPPORT: July 10, 2011-June 30, 2016. TOTAL DIRECT COSTS: $7,575,000
STATUS: Co-Investigator (P.I. Jeffrey Fineman, MD)
FUNDING AGENCY: National Heart, Lung, and Blood Institute
TITLE OF AWARD: Perinatal Pulmonary Hypertension: Developmental Mediators
TYPE OF AWARD: RO1
PERIOD OF SUPPORT: April 15, 2013-March 30, 2017. TOTAL DIRECT COSTS: $1,871,384
STATUS: Co-Investigator (P.I. Ganesh Konduri, MD)
FUNDING AGENCY: National Heart, Lung, and Blood Institute
TITLE OF AWARD: Regulatory Pulmonary Circulation in Fetus and Newborn
TYPE OF AWARD: RO1
PERIOD OF SUPPORT: April 1, 2010-March 31, 2015
TOTAL DIRECT COSTS: $80,000
STATUS: Co-Investigator (P.I. Rudolf Lucas, Ph.D.)
FUNDING AGENCY: National Heart, Lung, and Blood Institute
TITLE OF AWARD: Protective Activity of the Lectin-Like Domain of TNF in Permeability Edema
TYPE OF AWARD: RO1
PERIOD OF SUPPORT: April 1, 2010-March 31, 2014 TOTAL DIRECT COSTS: $1,000,000

Honors and Awards

  • 2010: Regents' Professor
  • 2007: Distinguished Faculty Award for Basic Science Research, School of Medicine
  • 2006: NHLBI Board of Scientific Counselors
  • 2004-2006: Co-Chair AHA Lung, Respiration/Resuscitation Study Section
  • 1990: MRC Fellowship
  • 1986: Imperial Cancer Research Fund Bursars Award

Invited Speaker

  • 2011: Paris Centre de recherche Cardiovasculaire (PARCC), Paris, France
  • 2011: University Alabama Birmingham
  • 2011: European Society for Microcirculation (EMS)/German Society of Microcirculation and Vascular Biology (GfMVB), Munich
  • 2010: Gynecological Endocrinology World Congress, Florence, Italy
  • 2009: Pediatric Cardiology, Munich, Germany
  • 2009: LeDucq Symposium, Paris, France
  • 2006: Pediatric Developmental Biology Seminar Series, UC San Francisco
  • 2006: First International Symposium on Cardiovascular Biology, Prague, Czech Republic
  • 2006: German Microvascular Society Annual Meeting
  • 2006: University of Dundee, Center of Biomedical Research, Dundee, UK
  • 2005: CDC International Endothelium Conference, Crete, Greece
  • 2005: Vera Moulton Wall Center for Pulmonary Vascular Disease, Stanford University
  • 2004: Ruff Club
  • 2004: Peroxynitrite 2004, Konstanz, Germany.
  • 2004: IEEE Annual Meeting, San Francisco CA
  • 2003: Children's Memorial Hospital Research Seminar Series
  • 2003: Neonatology Research Seminar Series, UC San Francisco
  • 2003: Division of Critical Care Medicine Seminar Series, UC San Francisco
  • 2001: University of Edinburgh, Cardiovascular Research Institute
  • 2001: Children's Hospital Oakland Research Institute
  • 2001: Perinatal Biology Center, Loma Linda University
  • 2000: SUNY Buffalo, Department of Pediatrics

Selected Publications

Aggarwal S, Dimitropoulou C, Lu Q, Black SM, Sharma S. Glutathione supplementation attenuates lipopolysaccharide-induced mitochondrial dysfunction and apoptosis in a mouse model of acute lung injury. Front Physiol. 2012;3:161.

Sharma S, Sun X, Kumar S, Rafikov R, Aramburo A, Kalkan G, Tian J, Rehmani I, Kallarackal S, Fineman JR, Black SM. Preserving mitochondrial function prevents the proteasomal degradation of GTP cyclohydrolase I. Free Radic Biol Med. 2012 53:216-29.

Nadtochiy SM, Zhu Q, Urciuoli W, Rafikov R, Black SM, Brookes PS. Nitroalkenes confer acute cardioprotection via adenine nucleotide translocase 1. J Biol Chem. 2012 287:3573-80.

Pierce GL, Jablonski KL, Walker AE, Seibert SM, Devan AE, Black SM, Sharma S, Seals DR. Tetrahydrobiopterin Supplementation Enhances Carotid Artery Compliance in Healthy Older Men: A Pilot Study. Am J Hypertens. 2012 Jun 7. doi: 10.1038/ajh.2012.70. [Epub ahead of print].

Lu Q, Wainwright MS, Harris VA, Aggarwal S, Hou Y, Rau T, Poulsen DJ, Black SM.Increased NADPH oxidase-derived superoxide is involved in the neuronal cell death induced by hypoxia-ischemia in neonatal hippocampal slice cultures. Free Radic Biol Med. 2012 Jun 19. [Epub ahead of print].

Sun X, Fratz S, Sharma S, Hou Y, Rafikov R, Kumar S, Rehmani I, Tian J, Smith A, Schreiber C, Reiser J, Naumann S, Haag S, Hess J, Catravas JD, Patterson C, Fineman JR, Black SM. CHIP-Dependent GTP Cyclohydrolase I Degradation in Lambs with Increased Pulmonary Blood Flow. Am J Respir Cell Mol Biol. 2011 45:163-71.

Tian J, Fratz S, Hou Y, Lu Q, Gorlach A, Hess J, Schreiber C, Datar SA, Oishi PE, Nechtman J, Podolsky R, She JX, Fineman JR, Black SM. Delineating the angiogenic gene expression profile prior to pulmonary vascular remodeling in a lamb model of congenital heart disease. Physiol Genomics. 2011 43:87-98.

Fratz, S, Fineman JR, Gorlach A, Sharma, S, Oishi, P, Schreiber C, Keitzman, C. Adatia, I, Hess J, Black, SM. Pulmonary Vascular Remodelling: Early Determinants in Congenital Heart Disease And Potential New Therapeutic Treatment Strategies. Circulation. 2011 123: 916-23.

Aggarwal S, Gross CM, Kumar S, Datar S, Oishi P, Kalka G, Schreiber C, Fratz S, Fineman JR, Black SM. Attenuated vasodilatation in lambs with endogenous and exogenous activation of cGMP signaling: Role of protein kinase G nitration. J Cell Physiol. 2011 226:3104-13.

Ganapathy PS, White RE, Ha Y, Bozard BR, McNeil PL, Caldwell RW, Kumar S, Black SM, Smith SB. The Role of N-Methyl-D-Aspartate Receptor Activation in Homocysteine-Induced Death of Retinal Ganglion Cells. Invest Ophthalmol Vis Sci. 2011 52:5515-24.

Aggarwal S, Rafikov R, Gross CM, Kumar S, Pardo D, Black SM. Purification and functional analysis of protein kinase G-1? using a bacterial expression system. Protein Expr Purif. 2011 79:271-76.

Hartney T, Birari R, Venkataraman S, Villegas L, Martinez M, Black SM, Stenmark KR, Nozik-Grayck E. Xanthine oxidase-derived ROS upregulate Egr-1 via ERK1/2 in PA smooth muscle cells; model to test impact of extracellular ROS in chronic hypoxia. PLoS One. 2011 6:e27531.

Rafikov R, Fonseca FV, Kumar S, Pardo D, Darragh C, Elms S, Fulton D, Black SM. eNOS activation and NO function: structural motifs responsible for the posttranslational control of endothelial nitric oxide synthase activity. J Endocrinol. 2011 210:271-84.

Pandey D, Gratton JP, Rafikov R, Black SM, Fulton D. Calcium/Calmodulin- dependent Kinase II mediates the Phosphorylation and Activation of NADPH Oxidase 5.Mol Pharmacol. 2011 80:407-15.

Aggarwal S, Gross C, Fineman JR, Black SM. Oxidative stress and the development of endothelial dysfunction in congenital heart disease with increased pulmonary blood flow: lessons from the neonatal lamb. Trends Cardiovasc Med. 2010 20:238-46.

Wiseman DA, Sharma S, Black SM. Elevated zinc induces endothelial apoptosis via disruption of glutathione metabolism: role of the ADP translocator. Biometals. 2010 23:19-30.

Church JE, Qian J, Kumar S, Black SM, Venema RC, Papapetropoulos A, Fulton DJ Inhibition of endothelial nitric oxide synthase by the lipid phosphatase PTEN. Vascul Pharmacol. 2010 52:191-8.

Sharma S, Smith A, Kumar S, Aggarwal S, Rehmani I, Snead C, Harmon C, Fineman J, Fulton D, Catravas JD, Black SM. Mechanisms of nitric oxide synthase uncoupling in endotoxin-induced acute lung injury: Role of asymmetric dimethylarginine. Vascul Pharmacol. 2010 52:182-90.

Kondrikov D, Fonseca FV, Elms S, Fulton D, Black SM, Block ER, Su Y. {beta}-actin association with endothelial NO synthase modulates NO and superoxide generation from the enzyme. 2010 J Biol Chem. 285:4319-4327.

Kumar S, Sud N, Fonseca FV, Hou Y, Black SM. Shear stress stimulates nitric oxide signaling in pulmonary arterial endothelial cells via a reduction in catalase activity: role of protein kinase C delta. Am J Physiol Lung Cell Mol Physiol. 2010 298:L105-L1116.

Fonseca FV, Ravi K, Wiseman D, Tummala M, Harmon C, Ryzhov V, Fineman JR, Black SM. Mass spectroscopy and molecular modeling predict endothelial nitric oxide synthase dimer collapse by hydrogen peroxide through zinc tetrathiolate metal-binding site disruption. DNA Cell Biol. 2010 29:149-160.

Hamacher J, Stammberger U, Roux J, Kumar S, Yang G, Xiong C, Schmid RA, Fakin RM, Chakraborty T, Hossain HM, Pittet JF, Wendel A, Black SM, Lucas R. The lectin-like domain of tumor necrosis factor improves lung function after rat lung transplantation--potential role for a reduction in reactive oxygen species generation. Crit Care Med. 2010 38:871-878.

Umapathy NS, Fan Z, Zemskov EA, Alieva IB, Black SM, Verin AD. Molecular mechanisms involved in adenosine-induced endothelial cell barrier enhancement. Vascul Pharmacol. 2010 52:199-206.

Catravas JD, Snead C, Dimitropoulou C, Chang AS, Lucas R, Verin AD, Black SM. Harvesting, identification and barrier function of human lung microvascular endothelial cells. Vascul Pharmacol. 2010 52:175-81.

Xiong C, Yang G, Kumar S, Aggarwal S, Leustik M, Snead C, Hamacher J, Fischer B, Umapathy NS, Hossain H, Wendel A, Catravas JD, Verin AD, Fulton D, Black SM, Chakraborty T, Lucas R. The lectin-like domain of TNF protects from listeriolysin-induced hyperpermeability in human pulmonary microvascular endothelial cells - A crucial role for protein kinase C-alpha inhibition. Vascul Pharmacol. 2010 52:207-13.

Black SM. New insights into acute lung injury. Vascul Pharmacol. 2010 52:171-4

Tian J, Hou Y, Lu Q, Wiseman DA, Fonsesca F, Elms S, Fulton DJ, Black SM. A novel role for caveolin-1 in regulating endothelial nitric oxide synthase activation in response to H2O2 and shear stress. Free Radic Biol Med. 2010 49: 159-70.

Sharma S, Kumar S, Wiseman DA, Kallarackal S, Ponnala S, Elgaish M, Fineman JR, Black SM. Perinatal changes in superoxide generation in the ovine lung: Alterations associated with increased pulmonary blood flow. Vascul Pharmacol. 2010 53:38-52.

Hsu JH, Oishi PE, Wiseman DA, Hou Y, Chikovani O, Datar S, Sajti E, Johengen MJ, Harmon C, Black SM, Fineman JR. Nitric Oxide Alterations Following Acute Ductal Constriction In The Fetal Lamb: A Role For Superoxide. Am J Physiol Lung Cell Mol Physiol. 2010 98: L880-L887.

Alieva IB, Zemskov EA, Kireev II, Gorshkov BA, Wiseman DA, Black SM, Verin AD. Microtubules growth rate alteration in human endothelial cells. J Biomed Biotechnol. 2010;2010:671536. Epub 2010 Apr 26.

Rossi NF, Maliszewska-Scislo M, Chen H, Black SM, Sharma S, Ravikov R, Augustyniak RA.Neuronal nitric oxide synthase within paraventricular nucleus: blood pressure and baroreflex in two-kidney, one-clip hypertensive rats. Exp Physiol. 2010 95:845-57.

Ali MI, Ketsawatsomkron P, Belin de Chantelemele EJ, Mintz JD, Muta K, Salet C, Black SM, Tremblay ML, Fulton DJ, Marrero MB, Stepp DW. (2009) Deletion of Protein Tyrosine Phosphatase 1b Improves Peripheral Insulin Resistance and Vascular Function in Obese, Leptin-Resistant Mice via Reduced Oxidant Tone. Circ Res. 105(10):1013-2.

Tian J, Smith A, Nechtman J, Podolsky R, Aggarwal S, Snead C, Kumar S, Elgaish M, Oishi PE, Goerlach A, Fratz S, Hess J, Catravas JD, Verin AD, Fineman JR, She JX, Black SM. (2009) Effect of PPAR{gamma} Inhibition on Pulmonary Endothelial Cell Gene Expression: Gene Profiling In Pulmonary Hypertension. Physiol Genomics. 40:48-60.

Sharma S, Kumar S, Sud N, Wiseman DA, Tian J, Rehmani I, Datar S, Oishi P, Fratz S, Venema RC, Fineman JR, Black SM. (2009) Alterations in lung arginine metabolism in lambs with pulmonary hypertension associated with increased pulmonary blood flow. Vascular Pharmacol. 51:359-64.


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Education and Training

University of California, San Francisco,
Postdoctoral Training, 1991-1993.
Molecular Endocrinology

University of Edinburgh, Scotland,
Postdoctoral Training, 1989-1990.
Molecular Endocrinology

University of Edinburgh, Scotland,
Ph. D., 1986-1989.
Molecular Pharmacology

University of Edinburgh , Scotland
B.Sc.(Honors) 1982- 1986.
Molecular Biology

Research Experience & Academic Appointments

Professor - Obstetrics & Gynecology, Medical College of Georgia, 04/2006-present.

Professor - Biomedical & Pharmaceutical Sciences, University of Montana, 06/2005-03/2006.

Associate Professor - Molecular Pharmacology, University of Washington, 07/2003-03/2006.

Associate Professor - Biomedical & Pharmaceutical Sciences, University of Montana, 07/2003-06/2005.

Associate Professor - Pediatrics & Molecular Pharamcology, Northwestern University, 03/1999-06/2003.

Assistant Professor - Pediatrics University of California, San Francisco, 10/1994-02/1999.

Research Chemist - Pharmaceutical Chemistry, University of California, San Francisco, 03/1993-09/1994.

Administrative Appointments

College of Graduate Studies' Graduate Council, 2012.

Basic Science Director - Cardiovascular Discovery Institute (CVDI), 2008-present.

Chief of Pulmonary Vascular Disease Program, 2007-present.

COBRE Group Leader - University of Montana, 07/2004-04/2006.

Director of Vascular Biology - St. Patrick Hospital, 07/2003-04/2006.

Research Director - Division of Neonatology, Northwestern University 03/1999-06/2003.

Laboratory Director - Child Health Research Center, University of California, San Francisco, 07/1997-02/1999.

Grant Review Activity

Placenta & Neonatology study section (member) 2009-2014
AHA Vascular Bio BP CT (Chair) 2011-2013
RFA, HL-11032 Utilization of Human Lung Tissue Resource for Vascular Research (Chair) 2011-2012
Board of Scientific Counselors NHLBI 2006-2011
National Heart, Lung, and Blood Institute Board of Scientific Counselors (BSC) 2007-2011:
National Heart, Lung, and Blood Institute Ad Hoc Review, Challenge Awards, Special Emphasis Panel. 2008-2011:
American Heart Association Peer Review. 2008-2011
National Heart, Lung, and Blood Institute Study Section. 2009-2011
External Reviewer for Austrian Science Fund 2010
Grants in Lung Diseases (co-chair) 2010
RFA HL11-006, Next Generation Genetic Association Studies (U01) 2010
AHA Region I Vascular Wall Biology 2009
Placenta & Neonatology study section (AdHoc) 2009
ZRG1 EMNR-D Special Emphasis Panel 2009
ARRA GO RC2 Special Review Committee 2009
ZRG1 EMNR-D Special Emphasis Panel 2009
National Heart, Lung, and Blood Institute Pregnancy and Perinatal Study Section. 2009:
Lung, Respiration/Resuscitation Study Section (member) 2008
Peer Reviewed Medical Research Program (PRMRP) 2008
External Reviewer for Austrian Science Fund 2008
NHLBI K99/R00 Review Panel 2008
Alberta Heritage Foundation for Medical Research 2008
AHA Southeastern Affiliates
Pulmonar Hypertension Review Panel
NHLBI Translational Program Project
RO3 Grant Reviews

National Committees

2011: American Heart Association.
2010- present Society for Free Radical Biology & Medicine Lifetime Achievement Committee
Member
2009: German Pediatric Cardiology Annual Meeting (Session Chair)
2009: Society for Free Radical Biology & Medicine Discovery Award Selection Committee
2009-present Society for Free Radical Biology & Medicine Nominations/Leadership Development Committee
2005- Society of Free Radical Biology & Medicine Junior Investigator Judge
2005: CDC International Endothelium Conference, Crete, Greece (Session Chair)
2005- Society for Free Radical Biology & Medicine Annual Meeting Abstract Reviewer
2004: Pediatric Academic Societies, Annual meeting, San Francisco, CA, Session Chair
2004: Society for Free Radical Biology & Medicine Annual meeting, St. Thomas, Session
Chair
2003: Pediatric Academic Societies, Annual meeting, Seattle, WA, Session Chair

Society Memberships

1998-present - Society for Pediatric Research.
1999-present - American Heart Association
2000-present - Society for Neuroscience.
2000-present - Nitric Oxide Society.
2000-present - Oxygen Society
2001-present - American Physiological Society
2002-present - American Society for Cell Biology
2002-present - Society for Free Radical Biology & Medicine
2009-present - European Society for Paediatric Research
2009-present - American Thoracic Society
2009-present - Endocrine Society
2011-present - European Respiratory Society

Laboratory

Saurabh Aggarwal Saurabh Aggarwal, Ph.D., Postdoctoral Fellow
Sridevi Dasarathy Sridevi Dasarathy, Research Assistant
Valerie Harris Valerie Harris, Research Associate
Yali Hou Yali Hou, Research Associate
Sanjiv Kumar Sanjiv Kumar, Ph.D., Assistant Research Scientist
Ruslan Rafikov Ruslan Rafikov, Ph.D., Postdoctoral Fellow
Olga Rafikova Olga Rafikova, Ph.D., Postdoctoral Fellow
Shruti Sharma Shruti Sharma, Ph.D., Research Scientist
Sun Xutong Sun Xutong, Research Associate

Administrative Staff

Leslie Alexander Leslie Alexander, Research Manager
Kathy Brouse Kathy Brouse, CVDI Office Associate
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