Heidi Chamberlain Shea, M.D.
Currently in Private Practice

Education

• 1990 (B.S.):  University of California, Davis, CA - Biological Sciences
• 1996 (M.D.):  Stritch School of Medicine, Loyola University of Chicago, Maywood, IL
• 2000 (Residency):  Indiana University, Indianapolis, IN - Medicine-Pediatrics (combined program)
• 2004 (Fellowship):  UT Southwestern, Dallas, TX - Pediatric/Adult Endocrinology (combined program)

Fellowship Honors

• 2001:  Outstanding Fellow Award, Children's Medical Center of Dallas, Dallas, TX

 Fellowship Research Summary
Research Type:  Basic
Mentor:  David W. Russell, Ph.D.
Titles:  Characterization of Knockout Mice Lacking 3ß-Hydroxy-D5-C27--Steroid Oxidoreductase and The Role of Small Heterodimer Partner (SHP) in Metabolism

The first project involved generating a knockout mouse for the C27-3ß hydroxysteroid dehydrogenase gene, which encodes an enzyme required for bile acid synthesis.  Her hypothesis was that the absence of this gene will provide an inducible model of neonatal cholestasis.  In addition to providing insight into childhood liver disease, this animal model will be useful in examining the effects of end-stage liver failure in adults.  As of this writing, she had successfully generated the desired mutant mice, and developed a special diet that allows the knockout mice to survive.  She is now expanding the colony and beginning to characterize lipid metabolism and liver disease in these mutant mice.

A second project involved an analysis of glucose metabolism in mice deficient in the nuclear receptor, small heterodimer partner (SHP).  SHP is known to repress the activities of several transcription factors, including the hepatocyte nuclear factors (HNF).  HNF proteins prevent maturity onset diabetes of the young (MODY).  In addition, SHP mutations in humans have been described in obese Japanese adolescents with Type II diabetes.  These patients provide insight into the potential phenotype of SHP knockout mice.  To initiate this project, she backcrossed the SHP mutation onto an isogenic background (C57BL/6).  Using these mice, she will now analyze the role of SHP in insulin resistance and obesity by conducting insulin tolerance and other metabolic experiments.  These studies will provide insight into the role SHP may play in glucose metabolism.

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 Michele R. Hutchison, M.D., Ph.D.
Currently Assistant Professor of Pediatrics at UT Southwestern

Education

• 1988 (B.A.):  Wellesley College, Wellesley, MA - Biochemistry, Political Science
• 1999 (M.D.):  UT Southwestern Medical Center, Dallas, TX
• 1999 (Ph.D.):  UT Southwestern Medical Center, Dallas, TX - Cell Biology
• 2002 (Residency):  Children's Medical Center of Dallas, Dallas, TX - Pediatrics
• 2004 (Fellowship):  UT Southwestern Medical Center, Dallas, TX -  Pediatric Endocrinology

Fellowship Honors

• 2003:  Recipient of the Pharmacia Endocrine Care Fellowship Fund Award

Fellowship Research Summary
Research Type:  Basic
Mentor:  Perrin C. White, M.D.
Title:  Examination of IGF-I and GH-Regulated Intracellular Signaling Pathway Relevant to Chondrocyte Differentiation in the Mammalian Growth Plate

Long bone growth in children is dependent on the constant and consistent development of chondrocytes at the growth plate. Epiphyseal chondrocytes achieve growth first through an increase in cell number, or proliferation, and then by the accumulation of glycogen which results in significant cellular hypertrophy. This ordered pattern of differentiation is regulated by a long list of both systemic and locally derived factors, not the least of which is growth hormone (GH). The “somatomedin hypothesis” was originally put forth to describe how systemic GH, by stimulating the hepatic production of insulin-like growth factor (IGF-I), positively affects long bone growth. More recent studies have suggested that GH acts locally at the growth plate, both directly and in an autocrine manner by stimulating IGF-I synthesis by the chondrocytes themselves. IGF-I is known to utilize protein kinase cascades in multiple different cell types, but surprisingly little is known about which intracellular signaling mechanisms are employed by GH and IGF-I in growth plate chondrocytes. We propose to study the role of the various mitogen-activated protein kinase (MAPK) pathways in the regulation of chondrocyte proliferation and hypertrophy by GH and IGF-I.

Publications Through Fellowship

• Wolfson AJ, Hutchison MR, Andrews JS, Merriam KJ. Effects of charcoal on dissociation kinetics of nuclear and cytosolic steroid-receptor complexes from hen oviduct. Journal of Receptor Research 1990; 10(3-4):137-148.
• Gama Sosa MA, Rosas DH, DeGasperi R, Morita E, Hutchison MR, Ruprecht RM. Negative regulation of the 5' long terminal repeat (LTR) by the 3' LTR in the murine proviral genome. Journal of Virology 1994; 68(4):2662-2670.
• Cobb MH, Xu S, Hepler JE, Hutchison M, Frost J, Robbins DJ. Regulation of the MAP kinase cascade. Cellular & Molecular Biology Research 1994; 40(3):253-256.
• Polverino A, Frost J, Yang P, Hutchison M, Neiman AM, Cobb MH et al. Activation of mitogen-activated protein kinase cascades by p21-activated protein kinases in cell-free extracts of Xenopus oocytes. Journal of Biological Chemistry 1995; 270(44):26067-26070.
• Frost JA, Xu S, Hutchison MR, Marcus S, Cobb MH. Actions of Rho family small G proteins and p21-activated protein kinases on mitogen-activated protein kinase family members. Molecular & Cellular Biology 1996; 16(7):3707-3713.
• Hutchison M, Berman KS, Cobb MH. Isolation of TAO1, a protein kinase that activates MEKs in stress-activated protein kinase cascades. Journal of Biological Chemistry 1998; 273(44):28625-28632.
• Chen Z, Hutchison M, Cobb MH. Isolation of the protein kinase TAO2 and identification of its mitogen-activated protein kinase/extracellular signal-regulated kinase kinase binding domain. Journal of Biological Chemistry 1999; 274(40):28803-28807.
• Berman, KS, Hutchison M, Avery L, Cobb MH. kin-18, a C. elegans protein kinase involved in feeding. Gene 2001; 279(2):137-147.

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Bassil M. Kublaoui, M.D., Ph.D.
Currently Assistant Professor of Pediatrics at UT Southwestern

Education

• 1990 (B.A.):  Rutgers University, New Brunswick, NJ - Biochemistry, Psychology
• 1997 (M.D.):  Boston University School of Medicine, Boston, MA
• 1999 (Ph.D.):  Boston University School of Medicine, Boston, MA - Biochemistry
• 2001 (Residency):  Harvard Medical School Affiliated Hospitals, Boston, MA - Medicine-Pediatrics (combined program)
• 2005 (Fellowship):  UT Southwestern, Dallas, TX - Pediatric/Adult Endocrinology (combined program)

 Fellowship Research Summary
Research Type:  Basic
Mentor:  Andrew R. Zinn, M.D., Ph.D.
Title:  Mutations of the SIM1 Gene Cause Obesity in Mice and Humans

SIM1 encodes a transcription factor and member of the bHLH-PAS family. It is expressed in the paraventricular nucleus (PVN) of the hypothalamus, a nucleus that is important in the central regulation of feeding and energy expenditure. The goal of this project is to characterize the relationship of SIM1 to other known regulators of feeding at the level of the PVN.

Aim 1. Characterize the expression pattern of genes known to regulate feeding and energy expenditure in the hypothalamus in Sim1 heterozygous mice.:

Sim1 heterozygote mice are obese and have elevated leptin levels. By evaluating the expression pattern of proopiomelanocortin (Pomc), neuropeptide Y (Npy), Agouti-related peptide (Agrp) and their receptors we may be able to gain insight into the mechanism by which Sim1 haploinsufficiency induces obesity.

Aim 2. Characterize the feeding, weight, and energy expenditure of Sim1 transgenic mice as well as the expression patterns of genes known to regulate feeding and energy expenditure in the hypothalamus.:

Sim1 transgenic mice may have a complementary phenotype to heterozygotes. By characterizing these mice we may be able to gain insight into the mechanism of Sim1 action in the hypothalamus.

Aim 3. Characterize the relationship between SIM1 and the melanocortin-4 receptor (MC4R) in hypothalamic cell lines and begin to define signaling pathways important for SIM1 regulation.:

Sim1 heterozygote mice have a similar phenotype to MC4R knockout mice, and both genes are expressed in the PVN. Also patients with mutations in SIM1 are similar to patients with mutations in the MC4R. Using cells that express both SIM1 and MC4R we aim to examine crosstalk between these two genes.

Publications Through Fellowship

• Kublaoui B, Lee J, Pilch PF. Dynamics of signaling during insulin-stimulated endocytosis of its receptor in adipocytes. Journal of Biological Chemistry 1995; 270(1):59-65.
• Liu H, Kublaoui B, Pilch PF, Lee J. Insulin activation of mitogen-activated protein (MAP) kinase and Akt is phosphatidylinositol 3-kinase-dependent in rat adipocytes. Biochemical & Biophysical Research Communications 2000; 274(3):845-851.
• Holder JL, Zhang L, Kublaoui BM, DiLeone RJ, Oz OK, Bair CH, Lee YH, Zinn AR. Sim1 gene dosage modulates the homeostatic feeding response to increase dietary fat in mice. American Journal of Physiology: Endocrinology and Metabolism 2004; 287(1):E105-E113.

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Mark Vanderwel, M.D.
Currently in Private Practice

Education

• 1993 (B.A.):  Macalester College, St. Paul, MN - Chemistry
• 1997 (M.D.):  Michigan State University College of Human Medicine, East Lansing, MI
• 2000 (Residency):  Carolinas Medical Center, Charlotte, NC - Pediatrics
• 2005 (Fellowship):  UT Southwestern, Dallas, TX - Pediatric Endocrinology

 Fellowship Research Summary
Research Type:  Clinical
Mentor:  Dana S. Hardin, M.D.
Title:  Metabolic Abnormalities in Hispanic Children with Cystic Fibrosis

Hispanic children with Cystic Fibrosis generally have a worsened course of disease than their non-Hispanic counterparts with cystic fibrosis (CF).  Unfortunately, the precise reasons why have not been determined.   The purpose of this study is to explore potential metabolic reasons for the worsened clinical status of Hispanic children with CF. We believe that the Hispanic heredity predisposes an individual toward insulin resistance, which in turn, causes high blood sugars occur at a younger age in Hispanics with CF.  We also hypothesize that Hispanic children with CF are also more likely to break down protein because of resistance to insulin in the liver, predisposing the child to a catabolic state that hinders muscle growth.

This study involves recruiting twelve Hispanic prepubertal children ages 7 to 12 and twelve Hispanic adolescents ages 15 to 17 from the CF Centers at University of Texas Southwestern and Baylor College of Medicine in Houston.  Information obtained from these subjects will be compared to 12 prepubertal and 12 adolescent Caucasian children with CF recruited from the same CF centers. Subjects will be categorized according to their ability to maintain normal blood sugars despite drinking a sugar-water solution, as well as their ability to produce, release and respond to insulin when stimulated by dextrose-containing IV fluids.  We will compare the information of socio-economic status and family history.  The patients’ current state of health will be characterized by measuring lung function and using a standard CF clinical rating developed by the NIH.  We will learn how Hispanic patients with CF metabolize carbohydrate and protein by using a non-radioactive label.  We will measure the patients’ ability to manufacture sugar by using a special Hydrogen molecule that they will drink with water.  Nutritional status will be determined by three day food journals, and intake will be compared to energy needs comparing caloric intake to the energy the patients use at rest.

Our proposed studies will provide better understanding of the origins of CF-related diabetes in children and will especially provide new understanding about Hispanic children with Cystic Fibrosis.

Publications Through Fellowship

• Vanderwel MR, Auchus RJ. Androgen Biosynthesis and Gene Defects. Encyclopedia of Endocrine Diseases. Academic Press., 2004: 201-209.

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Jennifer Shine Dyer, M.D.
Currently in Academic Medicine

Education

• 1995 (B.A.):  Texas Tech University, Lubbock, TX - English Literature
• 2000 (M.D.):  UT Health Science Center, San Antonio TX
• 2003 (Residency):  Children's Medical Center of Dallas, Dallas, TX - Pediatrics
• 2003 (Fellowship):  UT Southwestern, Dallas, TX - Pediatric Endocrinology

Fellowship Honors

• 2004:  Recipient of Children’s Medical Center Dallas Clinical Research Advisory Committee’s Grant
• 2004:  Selected participant in Mead Johnson Nutritionals: 21st Interdisciplinary Neonatal Nutritional and Gastroenterology Symposium
• 2005:  Winning Team Member (Clinical College) - 3rd Annual Sherman M. Holvey Forum In Diabetes
• 2005:  Recipient of Genentech Center for Clinical Research in Endocrinology Fellowship Grant
• 2005:  Recipient of LWPES travel grant award for poster presentation at LWPES/ESPE meeting
• 2005:  Selected participant in the Endocrine Society 2nd Annual Clinical Investigators Workshop

National/International Fellowship Presentations

• 2004:  Mead Johnson Nutritionals: 21st Interdisciplinary Neonatal Nutritional and Gastroenterology Symposium
• 2005:  Selected for poster presentation at LWPES/ESPE Meeting in Lyon, France
• 2005:  The Endocrine Society 2nd Annual Clinical Investigators Workshop

Fellowship Research Summary
Research Type:  Clinical
Mentor:  Dana S. Hardin, M.D.
Title:  Metabolic Syndrome in Neonates

The Metabolic Syndrome (MSX) as defined in adults consists of abdominal obesity, dyslipidemia, hypertension, insulin resistance, and a proinflammatory and prothrombotic state resulting in increased risk of cardiovascular disease. Obesity is an ever-increasing problem in children and is associated with development of type 2 diabetes, hypertension, lipid abnormalities and sleep apnea.  Although these features appear similar to the MSX described in adults, the problem has not been well studied in the pediatric population.   It is likely that the definition and pathogenesis of MSX may change with age. Description of the evolving pathogenesis in children could lead to development of age-specific definitions, and targeting age-specific pathology could greatly impact clinical care.

We hypothesize that the MSX in children is associated with early presentation of peripheral and hepatic insulin resistance, but normal insulin secretion, and that progressive worsening of insulin resistance leads to defects of insulin secretion secondary to glucose toxicity.  We further hypothesize that fatty acid metabolism is abnormal leading to lipotoxic damage and further insulin resistance.  We propose cross-sectional metabolic studies to characterize the metabolic changes associated with MSX in defined age groups (infants, toddlers, prepubertal children and adolescents).  We will recruit 15 LGA, 15 AGA and 15 SGA infants and 15 MSX and 15 normals from ages: toddler, young children, prepubertal and adolescents recruited from the Children's Medical Center and Parkland Medical Centers in Dallas.

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Ellen C. Kaizer, M.D.
Currently Assistant Instructor of Pediatrics at UT Southwestern

Education

• 1996 (B.A.):  Washington University, St. Louis, MO - Biology, English
• 2000 (M.D.):  Creighton University School of Medicine, Omaha, NE
• 2003 (Residency):  University of Hospitals Cleveland, Rainbow Babies and Children's Hospital/Case Western University School of Medicine, Cleveland, OH - Pediatrics
• 2006 (Fellowship) UT Southwestern Medical Center, Dallas, TX - Pediatric Endocrinology

Fellowship Honors

• 2005: Recipient of Children’s Medical Center Dallas Clinical Research Advisory Committee’s Grant
• 2005:  Selected to attend the European Society for Pediatric Endocrinology Summer School for Fellows by the Lawson-Wilkins Pediatric Endocrine Society Awards Committee
• 2006:  Awarded Clinical Fellows Travel Grant from Endocrine Society to attend the 88^th Annual Endocrine Society Meeting
• 2006:  Recipient of Children’s Medical Center Dallas Clinical Research Advisory Committee’s Grant

Fellowship Research Summary
Research Type:  Translational
Mentor:  Perrin C. White, M.D.
Title:  Blood Gene Signatures in Pediatric Patients with Newly Diagnosed IDDM

The purpose of this research is to analyze the blood gene signatures of newly diagnosed juvenile diabetes patients.

Cytokines are key players in immunity and autoimmunity. Type I interferons (IFN-a/b), major effectors in response to viral infection, play a major role in Systemic Lupus Erythematosus (SLE), a prototype autoimmune disease characterized by a break of tolerance to nuclear components. TNF, a major factor in response to bacterial infection, plays a major role in Rheumatoid Arthritis. Immunity and autoimmunity can therefore be viewed as dynamic systems driven by opposite vectors, for example, IFN-a/b and TNF. When balanced, both cytokines synergize in protective immunity. When one of the cytokines prevails beyond a certain threshold, autoimmunity may occur. These cytokines will drive differentiation of distinct types of dendritic cells (DCs), for example an excess of TNF results in TNF-DCs, while excess of IFN-a/b leads to IFN-DCs. These different DCs will present different autoantigens leading to different autoimmune responses, i.e., IFN-DCs driving SLE and TNF-DCs driving Arthritis. Therefore, immunity can be viewed as a dynamic system driven by sets of opposite vectors like IFN-a/b/TNF and IFN-g/IL-4.

Cytokine imbalances leading to abnormal immune responses can be detected using microarray technology. We have reported that peripheral blood mononuclear cell RNA from pediatric patients suffering from SLE and Juvenile Arthritis are characterized by the expression of unique gene signatures. We now propose that pediatric patients with new onset Insulin Dependent Diabetes Mellitus (IDDM) will also display unique blood gene signatures as a result of being exposed to unique cytokines.

Publications Through Fellowship

• Ressler C, Tatake JG, Kaizer E, Putnam DH. Neurotoxins in a vetch food: stability to cooking and removal of γ-glutamyl-β-cyanoalanine and β-cyanoalanine and acute toxicity from common vetch (vicia sativa l.) legumes. Journal of Agricultural Food Chemistry 1997; 45(1):189-194.
• Borel MJ, Williams PE, Jabbour K, Levenhagen D, Kaizer E, Flakoll PJ. Parenteral glutamine infusion alters insulin-mediated glucose metabolism. Journal of Parenteral & Enteral Nutrition 1998; 22(5):280-285.
• Kachur SP, Khatib RA, Kaizer E, Fox SS, Abdulla SM, Bloland PB. Adherence to antimalarial combination therapy with sulfadoxine-pyrimethamine and artesunate in rural Tanzania. American Journal of Tropical Medicine and Hygiene 2004; 71(6):715-722.

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Soumya Adhikari, M.D. 
Currently Assistant Professor of Pediatrics at UT Southwestern

Licensure

Physician, Texas

Board Certifications

• General Pediatrics, American Board of Pediatrics

Education

• 1996 (B.S.):  University of Florida, Gainesville, FL - Chemistry
• 2001 (M.D.):  University of Miami Medical School, Miami, FL
• 2004 (Residency):  Children's Medical Center of Dallas/UT Southwestern, Dallas, TX - Pediatrics
• 2007 (Fellowship):  UT Southwestern, Dallas, TX -  Pediatric Endocrinology

Other Positions and Honors

Former Positions

• 1995-1997:  Research Assistant, Department of Pharmacology, University of Florida College of Medicine, Gainesville, FL

Honors

• 1996:  Graduated with Highest Honors in Chemistry, University of Florida, Gainesville, FL
• 1999-2000:  Research Fellowship, American Heart Association
• 2004:  White Hat Award (Resident of the Year), Children's Medical Center of Dallas, Dallas, TX
• 2005:  Fellow of the Year, Children's Medical Center of Dallas, Dallas, TX

Bibliography

Research

Patient Care

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Y. Annie Wang, M.D. 
Currently Assistant Professor of Pediatrics at UT Southwestern

Licensure

• Physician, Texas

Board Certifications

• General Pediatrics, American Board of Pediatrics

Education

• 1995 (B.A.):  Hendrix College, Conway, AR - Biology
• 1999 (M.D.):  University of Arkansas for Medical Sciences, Little Rock, AR
• 2002 (Residency):  Wake Forest University Baptist Medical Center, Winston-Salem, NC - Pediatrics
  
• 2007 (Fellowship):  UT Southwestern, Dallas, TX -  Pediatric Endocrinology

Other Positions and Honors

Former Positions

• 2002-2003:  Jr. Faculty/Pediatric Chief Resident, Brenner Children's Hospital/Wake Forest University Health Sciences, Winston-Salem, NC
• 2003-2004:  Part-time Pediatrician, International Family Clinic (Private Practice) Burlington, NC

Honors

• 1995:  Graduated Cum Laude, Graduated with Distinction in Biology, Hendrix College, Conway, AR
• Dean's Office Scholarship, University of Arkansas for Medical Sciences, Little Rock, AR

Research

Patient Care

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Jill Ann Goldfarb, M.D.

Currently in Private Practice

Licensure

• Physician, Texas

Education

• 1996 (B.A.):  University of Arizona, Tucson, AZ - Biochemistry, French
• 2002 (M.D.):  University of Colorado Health Sciences Center, Denver, CO
• 2005 (Residency):  Children's Medical Center of Dallas/UT Southwestern, Dallas, TX - Pediatrics
• 2008 (Fellowship):  UT Southwestern, Dallas, TX -  Pediatric Endocrinology

Other Positions and Honors

Former Positions

• 1993-1995:  Research Assistant, Neonatology, University of Arizona
• 1996-1997:  Research Assistant, Neonatology/Cardiology, Harvard
• 1997-1998:  Research Assistant, Barbara Davis Center for Childhood Diabetes

Honors

• 1991-1995:  Regent’s Scholarship (full tuition), University of Arizona
• 1993-1995:  Accepted to the Undergraduate Biology Research Program, University of Arizona
• 1995:  Graduated Magna Cum Laude with Honors in Biochemistry

Other Responsibilities

• 1998-2002:  Student Oversight Committee for Primary Care and Embryology
• 1998-2002:  Pediatrics Club
• 1998-2002:  Sickle Cell Buddy Club

Memberships

• 2002:  American Academy of Pediatrics

Bibliography

Research

Patient Care

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Shuchi Shah, M.D. 
Currently in Private Practice

Licensure

• Physician, Texas

Board Certifications

• General Pediatrics, American Board of Pediatrics

Education

• 1998 (B.S.):  Duke University, Durham, NC - Biochemical/Electrical Engineering
• 2002 (M.D.):  Wake Forest University School of Medicine, Winston-Salem, NC
• 2005 (Residency):  Children's Medical Center of Dallas/UT Southwestern, Dallas, TX - Pediatrics
• 2008 (Fellowship):  UT Southwestern, Dallas, TX -  Pediatric Endocrinology

Other Positions and Honors

Honors

• 1994-1998:  Benjamin N. Duke Leadership Scholarship
• 1998:           Cum Laude Graduate
• 1998-2001:  Medical School Class Secretary
• 1998-2002:  Medical Student Alumni Council
• 2001-2002:  Senior Medical Class Vice President

Bibliography

Research

Patient Care

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Nicole S. Barnes, M.D. 

Education

• 1997 (B.S.):  University of Kentucky, Lexington, KY - Biology
• 2002 (M.D.):  University of Louisville School of Medicine, Louisville, KY
• 2006 (Residency):  Morehouse School of Medicine Pediatric Residency Program - Pediatrics
• 2009 (Fellowship):  UT Southwestern, Dallas, TX -  Pediatric Endocrinology

Other Positions and Honors

Former Positions

• 2005-2006:  Chief Resident of Continuity Clinic

Other Responsibilities

• 2002-2003:  Lectured students regarding careers in medical research , Institution of Clinical Research and Community Outreach, Louisville, KY

Memberships

• American Academy of Pediatrics
• American Medical Association, Educational Committee Member

Research

Mentor: Michele R. Hutchison, M.D., Ph.D.

Natural history of Type 2 diabetes in children

Research

Patient Care

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Kathryn M. Sumpter, M.D.
Currently Assistant Professor of Pediatrics at UT Southwestern

Licensure

• Physician, Texas

Education

• 1997 (B.A.):  Rice University, Houston, TX - Biochemistry, French
• 2003 (M.D.):  UT Southwestern, Dallas, TX
• 2006 (Residency):  Children's Medical Center of Dallas/UT Southwestern, Dallas, TX - Pediatrics
• 2009 (Fellowship):  UT Southwestern, Dallas, TX -  Pediatric Endocrinology

Other Positions and Honors

Honors

• 1996:  Phi Lambda Upsilon (National Chemistry Honor Society)
• 1997:  Phi Beta Kappa
• 1997:  James B. Walker Award for Outstanding Seniors in Biochemistry, Rice University, Houston, TX
• 1997:  Summa Cum Laude, Rice University, Houston, TX
• 2003:  Iatros Award, UT Southwestern Medical School Graduating Class
• 2003:  Alpha Omega Alpha
• 2007:  Teaching Fellow of the Year

Memberships

• 2003:  American Academy of Pediatrics

Fellowship Research

Mentors:  Perrin C. White, M.D. and Soumya Adhikari, M.D.

Anti-inflammatory therapy w/anakinra in children with newly diagnosed Type I diabetes.

Research

Patient Care

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