Child Health Research Career Development Award

Louis J. Muglia, MD, PhD Co-Director, Perinatal Institute 513-803-7902 louis.muglia@cchmc.org

High Res

Louis J. Muglia, MD, PhD

Co-Director, Perinatal Institute

Director, Center for Prevention of Preterm Birth

Director, Division of Human Genetics

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-803-7902

Email louis.muglia@cchmc.org

Show All

Specialties

Pediatric endocrinology

Visit the Muglia Lab.

Biography

Dr. Muglia has pioneered the in vivo analyses of regulation of the endocrine stress response and the molecular pathways leading to birth using novel genetically altered mutant mice. These studies have elucidated the importance of corticotropin-releasing hormone, glucocorticoids, and prostaglandins in neuroendocrine modulation, behavior, and perinatal adaptation. These studies have evolved over the last decade to specifically focus on the mechanisms controlling the timing for birth in humans using genetics and comparative genomics. The composition of the biological clock metering the duration of human gestation remains a central question in reproductive biology. The goal of the Muglia Laboratory is to understand the molecular timing machinery comprising this biological clock to prevent or better treat human preterm labor and delivery.

Among Dr. Muglia’s achievements are more than 180 publications and many awards, including a Burroughs Wellcome Fund Career Development Award in the biomedical sciences, the Society of Pediatric Research Young Investigator Award, and election to the American Society for Clinical Investigation and Association of American Physicians. In 2010, Dr. Muglia was elected to fellow in the American Association for the Advancement of Science. He is an active member of the Society for Pediatric Research, Society for Neuroscience, and the Lawson Wilkins Pediatric Endocrine Society. Dr. Muglia currently serves as chair of the Board of Scientific Counselors for the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health. In 2013, Dr. Muglia was elected to membership in the Institute of Medicine of the National Academies.

BS: University of Michigan, Ann Arbor, MI, 1981.

PhD: University of Chicago, Chicago, IL, 1986.

MD: University of Chicago, Chicago, IL, 1988.

Plunkett J, Doniger S, Orabona G, Morgan T, Haataja R, Hallman M, Puttonen H, Menon R, Kuczynski E, Norwitz E, Victoria Snegovskikh V, Palotie A, Peltonen L, Fellman V, DeFranco EA, Chaudhari BP, McGregor TL, McElroy JJ, Oetjens MT, Teramo K, Boreck I, Fay J, Muglia L. An evolutionary genomic approach to identify genes involved in human birth timing. PLoS Genetics. 2011; 7: e1001365.

Muglia LJ, Katz M. The enigma of spontaneous preterm birth. N Engl J Med. 2010; 362: 529-535.

Kolber BJ, Boyle MP, Wieczorek L, Kelley CL, Kelley CL, Onwuzurike CC, Nettles SA, Vogt SK, Muglia LJ. Transient early-life forebrain corticotropin-releasing hormone elevation causes long-lasting anxiogenic and despair-like changes in mice. J Neurosci. 2010; 30: 2571-2581.

Plunkett J, Feitosa MF, Trusgnich M, Wangler MF, Palomar L, Kistka ZA-F, DeFranco EA, Shen TT, Stormo EAD, Puttonen H, Hallman M, Haataja R, Luukkonen A, Fellman V, Peltonen L, Palotie A, Daw EW, An P, Teramo K, Borecki I, Muglia LJ. Mother’s genome or maternally-inherited genes acting in the fetus influence gestational age in familial preterm birth. Human Heredity. 2009; 68: 209-219.

Kolber BJ, Roberts MS, Howell MP, Wozniak DF, Sands MS, Muglia LJ. Central amygdala glucocorticoid receptor action promotes fear-associated CRH activation and conditioning. Proc Natl Acad Sci USA. 2008; 105: 12004 - 12009.

Roizen J, Asada M, Tong M, Tai H-H, Muglia LJ. Preterm birth without progesterone withdrawal in 15-hydroxyprostaglandin dehydrogenase hypomorphic mice. Mol Endocrinol. 2008; 22: 105-112.

Kistka Z A-F, Palomar P, Lee KA, Boslaugh SE, Wangler MF, Cole FS, DeBaun MR, Muglia LJ. Racial disparity in the frequency of recurrence of preterm birth. Am J Obstet Gynecol. 2007; 196: 131.e1-131.e6.

Bethin KE, Nagai Y, Sladek R, Asada M, Sadovsky Y, Hudson TJ, Muglia LJ. Microarray analysis of uterine gene expression in mouse and human pregnancy. Mol Endocrinol. 2003; 17: 1454-1469.

Gross G, Imamura T, Luedke C, Vogt SK, Olson LM, Nelson DM, Sadovsky Y, Muglia LJ. Opposing actions of prostaglandins and oxytocin determine the onset of murine labor. Proc. Natl. Acad. Sci. USA. 1998; 95: 11871-11875.

Muglia LJ, Jacobson L, Dikkes P, Majzoub JA. Corticotropin-releasing hormone deficiency reveals major fetal but not adult glucocorticoid need. Nature. 1995; 373:427-432.

Grants

Maternal Temperament, Stress, Inflammation and Preterm Birth. Multi-PI. NIH/NICHD. Sep 2013-Aug 2017.

March of Dimes Prematurity Research Center Ohio Collaborative. Coordinating PI. March of Dimes. Jul 2013-Jun 2018.

Program Co-Directors

James E. Heubi, MD Director, Center for Clinical and Translational Science and Training 513-636-9776 sandra.geideman@cchmc.org

High Res

James E. Heubi, MD

Director, Center for Clinical and Translational Science and Training

Associate Dean, Clinical and Translational Research

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-9776

Fax 513-803-1039

Email sandra.geideman@cchmc.org

Show All

Clinical & Research Interests

Clinical

Pediatric gastroenterology; hepatology and nutrition; pediatric cholestatic liver disease

Research

Pediatric cholestatic liver disease; childhood bone disease; fat malabsorption

Biography

James Heubi, MD, is associate dean for clinical and translational research and professor of pediatrics at the University of Cincinnati College of Medicine. He is the director of the Center for Clinical and Translational Science and Training which is the vehicle by which the University of Cincinnati, Cincinnati Children’s Hospital Medical Center and the Veterans Administration Medical Center administer the NIH-funded, Clinical Translational Science Award and director of the Division of Gastroenterology, Hepatology and Nutrition at the Cincinnati Children’s Hospital Medical Center.

He has been an active clinical investigator with over 195 peer reviewed publications and was the long term program director for the NIH funded General Clinical Research Center. He is the principal investigator and co-investigator on NIH grants and participates is a local principal or co-investigator on two rare disease networks supported by the NIH.

His research interests include cholestatic liver disease in childhood and its complications, inborn errors of bile acid metabolism, bone disease in gastrointestinal and hepatobiliary disorders, fat absorption, and cholesterol absorption and metabolism.

MD: Indiana University School of Medicine, Indianapolis, IN, 1973.

Residency: James Whitcomb Riley Hospital for Children, Indiana University, Indianapolis, IN, 1973 to 1975.

Fellowship: Pediatric Gastroenterology, Children's Hospital Medical Center, Cincinnati, OH, 1979.

Certification: Pediatric Gastroenterology and Nutrition, 1990.

View PubMed Publications

Heubi JE, Setchell KDR, Jha P, Buckley D, Zhang W, Rosenthal P, Potter C, Horslen S, Suskind D. Treatment of bile acid amidation defects with glycocholic acid. Hepatology. 2015 Jan;61(1):268-274.

Setchell KDR, Heubi JE, Shah S, Lavine JE, Suskind D, Al-Edreesi M, Potter C, Russell DW, O’Connell NC, Wolfe B, Jha P, Zhang W, Bove KE, Knisely AS, Hofmann AF, Rosenthal P, Bull LN. Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. Gastroenterology. 2013 May;144(5):945-955.

Gonzales E, Gerhardt MF, Fabre M, Setchell KDR, Davit-Spraul A, Vincent I, Heubi JE, Bernard O, Jacquemin E. Oral cholic acid for hereditary defects of primary bile acid synthesis: a safe and effective long-term therapy. Gastroenterology. 2009 Oct;137(4):1310-1320.

Setchell KDR, Heubi JE, Bove KE, O’Connell NC, Brewsaugh T, Steinberg SJ, Moser A, Squires Jr RH. Liver disease caused by failure to racemize trihydroxycholestanocic acid: gene mutation and effect of bile acid therapy. Gastroenterology. 2003 Jan;124(1):217-232.

Oelkers P, Kirby LC, Heubi JE, Dawson PA. Primary bile acid malabsorption caused by mutations in the ileal sodi¬um-de¬pen¬dent bile acid transporter gene (SLC10A2). J Clin Invest. 1997 Apr 15;99(8):1880-1887.

Heubi JE, Hollis BW, Specker B, Tsang RC. Bone disease in chronic childhood cholestasis I. Vitamin D absorption and metabolism. Hepatology. 1989 Feb;9(2):258-264.

Setchell KDR, Suchy FJ, Welsh MB, Zimmer-Nechemias L, Heubi JE, Balistreri WF. Δ4-3-Oxosteroid 5B-reductase deficiency described in identical twins with neonatal hepatitis - A new inborn error in bile acid synthesis. J Clin Invest. 1988 Dec; 82(6):2148-2157.

Heubi JE, Daugherty CC, Partin JS, Partin JC, Schubert WK. Grade l Reye's Syndrome--outcome and predictors of progression to deeper coma grades. N Engl J Med. 1984 Dec 13;311(24):l539-1554.

Lichtenstein PK, Heubi JE, Daugherty CC, Farrell MK, Sokol RJ, Rothbaum RJ, Suchy FJ, Balistreri WF. Grade l Reye's Syndrome. A frequent cause of vomiting and liver dysfunction following varicella and upper respiratory tract infection. N Engl J Med. 1983 Jul;309(3):l33-139.

Heubi JE, Balistreri WF, Fondacaro JD, Partin JC, Schubert WK. Primary bile acid malabsorption: Defective in vitro ileal active bile acid transport. Gastroenterology. 1982 Oct;83(4):804-8ll.

Grants

Cincinnati Center for Clinical and Translational Science and Training. Principal Investigator. National Center for Advancing Translational Sciences/National Institutes of Health. Aug 2015-Mar 2019. UL1 TR000077-05.

Pediatric Gastroenterology and Nutrition Training Grant. Mentor. National Institute of Diabetes and Digestive and Kidney Diseases/ National Institutes of Health. Jul 2005-Jun 2020. T32 DK007727.

Clinical Center of Cholestatic Liver Disease in Children (CHILDREN). Co-Investigator. National Institute of Diabetes and Digestive and Kidney Diseases/ National Institutes of Health. Sep 2009-May 2019. U01 DK062497.

Sterol and Isoprenoid Diseases Consortium. Site Principal Investigator. Eunice Kennedy Shriver National Institute of Child Health and Human Development/National Institutes of Health. Sep 2009-Jul 2019. U54 HD061939.

Bone Mineral Accretion in Young Children. Co-Investigator. Eunice Kennedy Shriver National Institute of Child Health and Human Development/National Institutes of Health. Sep 2013-Jul 2018. R01 HD076321.

Short Term Medical Student Training Grant. Principal Investigator. National Institute of Diabetes and Digestive and Kidney Diseases/National Institutes of Health. Apr 2002-Mar 2019. T35 DK060444-11.

Jeffrey Robbins, PhD Executive Co-Director, Heart Institute 513-636-8098 jeffrey.robbins@cchmc.org

High Res

Jeffrey Robbins, PhD

Executive Co-Director, Heart Institute

Director, Molecular Cardiovascular Biology

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-8098

Email jeffrey.robbins@cchmc.org

Show All

Specialties

Structure function relationships for the contractile proteins; cardiac-specific gene manipulation in transgenic rabbits; the contractile protein myosin and human heart failure; molecular studies of human valve disease

Visit the Robbins Lab.

Biography

Jeff Robbins CV (.pdf)

Gupta MK, Robbins J. Post-translational control of cardiac hemodynamics through myosin binding protein C. Pflugers Arch: European journal of physiology. 2014 Feb;466(2):231-6.

Mun JY, Previs MJ, Yu HY, Gulick J, Tobacman LS, Beck Previs S, Robbins J, Warshaw DM, Craig R. Myosin-binding protein C displaces tropomyosin to activate cardiac thin filaments and governs their speed by an independent mechanism. Proc Natl Acad Sci U S A. 2014 Feb 11;111(6):2170-5.

Sandri M, Robbins J. Proteotoxicity: An underappreciated pathology in cardiac disease. J Mol Cell Cardiol. 2014 Jun;71c:3-10.

Wang X, Robbins J. Proteasomal and lysosomal protein degradation and heart disease. J Mol Cell Cardiol. 2014 Jun;71c:16-24.

James J, Robbins J. Ablating a cardiac protein: Causality at last. Circ Res. 2013;112:1415-1419.

Razzaque MA, Gupta M, Osinska H, Gulick J, Blaxall BC, Robbins J. An endogenously produced fragment of cardiac myosin-binding protein C is pathogenic and can lead to heart failure. Circ Res. 2013 Aug 16;113(5):553-61.

Gupta MK, Gulick J, James J, Osinska H, Lorenz JN, Robbins J. Functional dissection of myosin binding protein C phosphorylation. J Mol Cell Cardiol. 2013;64C:39-50.

Bhuiyan MS, Pattison JS, Osinska H, James J, Gulick J, McLendon PM, Hill JA, Sadoshima J, Robbins J. Enhanced autophagy ameliorates cardiac proteinopathy. J Clin Invest. 2013;123(12):5284-97.

Pattison JS, Robbins J. Desmin and heart disease. In: Kavallaris M, ed. Cytoskeleton and human disease. New York, NY: Humana Press; 2012:411-424.

Bhuiyan MS, Gulick J, Osinska H, Gupta M, Robbins J. Determination of the critical residues responsible for cardiac myosin binding protein C's interactions. J Mol Cell Cardiol. 2012;53:838-847.

Grants

Cardiac Signaling in the Normal and Abnormal Heart. Principal Investigator. National Heart, Lung, and Blood Institute. Sep 2013-May 2018. #P01 HL69779.

Proteotoxicity: an underappreciated factor in cardiac disease. North American Coordinator. Leducq Transatlantic Alliance For Cardiovascular Disease. 2011-2016.

Marc E. Rothenberg, MD, PhD Director, Division of Allergy and Immunology 513-803-0257 marc.rothenberg@cchmc.org

High Res

Marc E. Rothenberg, MD, PhD

Director, Division of Allergy and Immunology

Director, Cincinnati Center for Eosinophilic Disorders

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-803-0257

Fax 513-636-3310

Email marc.rothenberg@cchmc.org

Show All

Clinical & Research Interests

Visit the Rothenberg Lab.

Clinical

Eosinophilia; eosinophilic disorders; asthma; allergy; food allergy

Research

Eosinophils; chemokines

Biography

Visit the Rothenberg Lab website.

Dr. Rothenberg is director of the Division of Allergy and Immunology at Cincinnati Children's Hospital Medical Center and tenured professor of pediatrics at Cincinnati Children’s within the University of Cincinnati College of Medicine. He graduated summa cum laude with highest honors in chemistry and biochemistry from Brandeis University. He then completed the MD/PhD program at Harvard Medical School under Dr. Frank Austen, conducting studies on eosinophil hematopoiesis, as he developed the first culture system for human eosinophils. After completing residency at Children’s Hospital, Boston, Dr. Rothenberg did a fellowship in allergy/immunology and hematology at Children’s Hospital. Dr. Rothenberg did post-doctorate training with Dr. Philip Leder, Harvard Medical School, where he cloned the eotaxin chemokine. After being faculty at Harvard Medical School for one year, he came to the University of Cincinnati and Cincinnati Children's, where he has helped build a top program in research, and his division is a leader in allergy and immunology.

His research is focused on molecular analysis of allergic inflammation, primarily on the molecular pathogenesis of eosinophilic esophagitis. His laboratory takes a multi-disciplinary approach including the development of preclinical murine models: genetics, genomics, molecular immunology, and biochemistry. Dr. Rothenberg’s awards include the 2007 E Mead Johnson Award from the Society of Pediatric Research, 2010 National Institutes of Health MERIT Award, and being elected an American Association for the Advancement of Science fellow. He is a member of the American Society for Clinical Investigation, American Academy of Pediatrics, and Society for Pediatric Radiology. His publications number over 300. He has served on review panels for journals/grant agencies including National Institutes of Health (NIH), Burroughs Trust, and Medical Research Council of the United Kingdom. He served for four years on the Advisory Council of National Institute of Allergy and Infectious Disease. He has been associate editor of the Journal of Allergy and Clinical Immunology since 2004. His research has been supported by sources including the NIH, Human Frontier Science Program Organization, Burroughs Wellcome Fund, Dana Foundation, and Department of Defense.

MD, PhD: Harvard Medical School, Cambridge, MA, 1990.

Residency: Pediatrics, Children's Hospital, Boston, MA, 1991-1992.

Fellowship: Immunology / Allergy, Children's Hospital, Boston, MA, 1992-1994; Hematology / Oncology, Children's Hospital and Dana Farber Cancer Institute, Boston, MA, 1992-1995.

Certification: National Board of Medical Examiners, 1991; Board of Registration in Medicine, MA, 1992; American Board of Pediatrics, 1995, 2001, 2008; Ohio State Medical Board, 1997; American Board of Allergy and Immunology, 1997, 2006.

Butz BK, Wen T, Gleich GJ, Furuta GT, Spergel J, King E, Kramer RE, Collins MH, Stucke E, Mangeot C, Jackson WD, O'Gorman M, Abonia JP, Pentiuk S, Putnam PE, Rothenberg ME. Efficacy, dose reduction, and resistance to high-dose fluticasone in patients with eosinophilic esophagitis. Gastroenterology. 2014 Aug;147(2):324:33.e5.

Sherrill JD, Kc K, Wu D, Djukic Z, Caldwell JM, Stucke EM, Kemme KA, Costello MS, Mingler MK, Blanchard C, Collins MH, Abonia JP, Putnam PE, Dellon ES, Orlando RC, Hogan SP, Rothenberg ME. Desmoglein-1 regulates esophageal epithelial barrier function and immune responses in eosinophilic esophagitis. Mucosal Immunol. 2014 May;7(3):718-29.

Wen T, Stucke EM, Grotjan TM, Kemme KA, Abonia JP, Putnam PE, Franciosi JP, Garza JM, Kaul A, King EC, Collins MH, Kushner JP, Rothenberg ME. Molecular diagnosis of eosinophilic esophagitis by gene expression profiling. Gastroenterology. 2013 Dec;145(6):1289-99.

Wen T, Besse JA, Mingler MK, Fulkerson PC, Rothenberg ME. Eosinophil adoptive transfer system to directly evaluate pulmonary eosinophil trafficking in vivo. Proc Natl Acad Sci U S A. 2013 Apr 9;110(15):6067-72.

Lu TX, Sherrill JD, Wen T, Plassard AJ, Besse JA, Abonia JP, Franciosi JP, Putnam PE, Eby M, Martin LJ, Aronow BJ, Rothenberg ME. MicroRNA signature in patients with eosinophilic esophagitis, reversibility with glucocorticoids, and assessment as disease biomarkers. J Allergy Clin Immunol. 2012 Apr;129(4):1064-75.e9.

Rothenberg ME, Spergel JM, Sherrill JD, Annaiah K, Martin LJ, Cianferoni A, Gober L, Kim C, Glessner J, Frackelton E, Thomas K, Blanchard C, Liacouras C, Verma R, Aceves S, Collins MH, Brown-Whitehorn T, Putnam PE, Franciosi JP, Chiavacci RM, Grant SF, Abonia JP, Sleiman PM, Hakonarson H. Common variants at 5q22 associate with pediatric eosinophilic esophagitis. Nat Genet. 2010 Apr;42(4):289-91.

Rothenberg ME, Klion AD, Roufosse FE, Kahn JE, Weller PF, Simon HU, Schwartz LB, Rosenwasser LJ, Ring J, Griffin EF, Haig AE, Frewer PI, Parkin JM, Gleich GJ; Mepolizumab HEC Study Group. Treatment of patients with the hypereosinophilic syndrome with mepolizumab. N Engl J Med. 2008 Mar 20;358(12):1215-28.

Blanchard C, Wang N, Stringer KF, Mishra A, Fulkerson PC, Abonia JP, Jameson SC, Kirby C, Konikoff MR, Collins MH, Cohen MB, Akers R, Hogan SP, Assa'ad AH, Putnam PE, Aronow BJ, Rothenberg ME. Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis. J Clin Invest. 2006 Feb;116(2):536-47.

Hogan SP, Mishra A, Brandt EB, Royalty MP, Pope SM, Zimmermann N, Foster PS, Rothenberg ME. A pathological function for eotaxin and eosinophils in eosinophilic gastrointestinal inflammation. Nat Immunol. 2001 Apr;2(4):353-60.

Mishra A, Hogan SP, Brandt EB, Rothenberg ME. An etiological role for aeroallergens and eosinophils in experimental esophagitis. J Clin Invest. 2001 Jan;107(1):83-90.

Grants

NICHHD Pediatric Center for Gene Expression and Developmental Sciences. Training Director. National Institutes of Health. Dec 2011–Nov 2016. K12 HD028827.

Epithelial Genes in Allergic Inflammation. Co-Investigator. National Institutes of Health. Sep 2011–Aug 2016. U19 AI070235.

Eosinophil:M2 Macrophage:CCL11 Axis in Experimental Colitis and Pediatric Corticosteroid Resistant Ulcerative Colitis. Co-Investigator. National Institutes of Health. Apr 2012–Mar 2016. R01 DK090119-01A1.

The Expression and Function of Paired Immunoglobulin-like Receptor B in Eosinophils. Co-Principal Investigator. U.S. - Israel Binational Science Foundation. Oct 2012–Sep 2016. #201144.

Arnold W. Strauss, MD Associate Director for External Relations and Strategic Projects, Cincinnati Children's Research Foundation 513-636-2942 arnold.strauss@cchmc.org

Jeffrey A. Whitsett, MD Co-Director, Perinatal Institute 513-803-2790 jeffrey.whitsett@cchmc.org

High Res

Jeffrey A. Whitsett, MD

Co-Director, Perinatal Institute

Chief, Section of Neonatology, Perinatal and Pulmonary Biology

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-803-2790

Fax 513-636-7868

Email jeffrey.whitsett@cchmc.org

Show All

Specialties

Cystic fibrosis research; lung morphogenesis; control of gene expression in the respiratory epithelium; gene delivery and therapy

Visit the Whitsett Lab.

Biography

Dr. Whitsett's laboratory discovered surfactant proteins B and C, cloned the genes encoding the surfactant proteins A, B, C, and D, Scgb1a1, TTF-1 and others and utilized transgenic mouse models to delete and mutate these genes in transgenic mice. They identified transcriptional networks regulating lung morphogenesis and perinatal lung maturation contributing to the understanding of the roles of TTF-1, CEBPα, SOX2, SOX17, FOXA1, FOXA2, FOXA3, SPDEF, KLF5, CDC42 and others using both in vitro and in vivo methods. They identified multiple transcription factors regulating goblet cell differentiation airway epithelial cells including critical role of SPDEF, FOXA3 and airway goblet cells controlling innate immunity. They produced transgenic mouse models for conditional deletion and expression of genes involved in lung development, disease, and repair. They have generated transgenic models of pulmonary adenocarcinoma and explored the role of transcription factors mediating pulmonary adenocarcinoma in vivo and in vitro. They utilized RNA-Seq, microarray, Chip-Seq in the application of Nex-Gen sequencing and bioinformatics to identify and understand networks involved in the regulation of lung development and disease using clinical sample, as well as in vitro and in vivo models.

Dr. Whitsett has a long interest in training both in the clinical setting in “Neonatology” and in “Pulmonary Biology” and has contributed to the direct training of more than 80 graduate or post-graduate students in his laboratory. The scope of his work is represented in several recent reviews. Initial discoveries from his laboratory provided early insights into the genes and proteins critical for surfactant function including ABCA3, SFTPC, SFTPB, SFTPA, SFTPD.

MD: Columbia University, New York, NY, 1973.

Residency: Pediatrics, Mt. Sinai Hospital, New York City, 1974 to 1976.

Fellowship: Neonatology, Children's Hospital Medical Center, University of Cincinnati College of Medicine, 1976 to 1977.

View PubMed Publications

Davies ER, Kelly JFC, Howarth PH, Wilson DI, Holgate ST, Davies DE, Whitsett JA, Haitchi HM. Soluble ADAM33 initiates airway remodeling to promote susceptibility for allergic asthma in early life. JCI Insight. 2016;1:e87632.

Ustiyan V, Zhang Y, Perl A-KT, Whitsett JA, Kalin TV, Kalinichenko VV. ß-Catenin and Kras/Foxm1 Signaling Pathway are Critical to Restrict Sox9 in Basal Cells During Pulmonary Branching Morphogenesis. Dev Dyn. 2016;245:590-604.

Guo M, Wang H, Potter SS, Whitsett JA, Xu Y. SINCERA: A pipeline for single-cell RNA-Seq profiling analysis. PLoS Comput Biol. 2015;11:e1004575.

Kamath-Rayne BD, Du Y, Hughes M, Wagner EA, Muglia LJ, DeFranco EA, Whitsett JA, Salomonis N, Xu Y. Systems biology evaluation of cell-free amniotic fluid transcriptome of term and preterm infants to detect fetal maturity. BMC Med Genomics. 2015;8:67.

Du Y, Guo M, Whitsett JA, Xu Y. ‘LungGENS’: a web-based tool for mapping single-cell gene expression in the developing lung. Thorax. 2015;70:1092-1094.

Snowball J, Ambalavanan M, Whitsett J, Sinner D. Endodermal Wnt signaling is required for tracheal cartilage formation. Dev Biol. 2015;405:56-70.

Wakata K, Tsuchiya T, Tomoshige K, Takagi K, Yamasaki N, Matsumoto K, Miyazaki T, Nanashima A, Whitsett JA, Maeda Y, Nagayasu T. A favorable prognostic marker for EGFR mutant non-small cell lung cancer: immunohistochemical analysis of MUC5B. BMJ Open. 2015;5:e008366.

Ishida N, Fukazawa T, Maeda Y, Yamatsuji T, Kato K, Matsumoto K, Shimo T, Takigawa N, Whitsett JA, Naomoto Y. A novel P13K inhibitor iMDK suppresses non-small cell lung Cancer cooperatively with a MEK inhibitor. Exp Cell Res. 2015;335:197-206.

Rajavelu P, Chen G, Xu Y, Kitzmiller JA, Korfhagen TR, Whitsett JA. Airway epithelial SPDEF integrates goblet cell differentiation and pulmonary Th2 inflammation. J Clin Invest. 2015;125:2021-2031.

Snowball J, Ambalavanan M, Cornett B, Lang R, Whitsett J, Sinner D. Mesenchymal Wnt signaling promotes formation of sternum and thoracic body wall. Dev Biol. 2015;401:264-275.

Grants