NELIN LABORATORY
The research focus in my laboratory is on the elucidation of the functional and mechanistic aspects of cellular uptake of L-arginine by the cationic amino acid transporters (CAT) and the role of CAT activities and expression in regulation of nitric oxide (NO) production in the lung. Furthermore, we are studying the regulation of nitric oxide synthase and arginase induction in models of pulmonary hypertension and lung injury to develop strategies to influence arginine metabolism inside of the cell. Experiments are carried out in cell culture systems and animal models using pharmacological and genetic manipulations with experimental end-points ranging from biochemical assays, protein and mRNA assays, to functional and physiological measurements. The long-term goals of these studies are to develop therapies that increase NO production by facilitating CAT-mediated L-arg uptake in pulmonary hypertensive diseases, and that decrease NO production by inhibiting CAT-mediated L-arg uptake in inflammatory lung diseases. |
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Faculty and Staff
Principal Investigator: Leif D. Nelin M.D.
e-mail: Leif.Nelin@nationwidechildrens.org |
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Corns, John
e-mail: John.Corns@nationwidechildrens.org |
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Cui, Hong Mei
e-mail: Hong Mei.Cui@nationwidechildrens.org |
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Jin, Yi
e-mail: Yi.Jin@nationwidechildrens.org |
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Nuthakki, Sushma
e-mail: Sushma.Nuthakki@nationwidechildrens.org |
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Stein, Melanie
e-mail: Melanie.Stein@nationwidechildrens.org |
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Stenger, Michael
e-mail: Michael.Stenger@nationwidechildrens.org |
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Toby, Inimary
e-mail: Inimary.Toby@nationwidechildrens.org |
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Trittman, Jennifer
e-mail: Jennifer.Trittman@nationwidechildrens.org |
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Trittmann, Jennifer
e-mail: Jennifer.Trittmann@nationwidechildrens.org |
BESNER LABORATORY
Dr. Besner's research centers around a growth factor known as heparin-binding EGF-like growth factor (HB-EGF), first identified by Besner et al. in 1990. The central theme of Dr. Besner's research involves the effect of HB-EGF as an intestinal cytoprotective agent. Multiple lines of evidence, both in vitro and in vivo, have been obtained in Dr. Besner's laboratory to support the ability of HB-EGF to protect the intestines from injury. HB-EGF plays a vital role in postischemic regeneration due to its mitogenic, chemoattractant, antiapoptotic and anti-inflammatory effects. In vitro, HB-EGF is a potent mitogen and chemoattractant agent for intestinal epithelial cell lines. In addition, it protects intestinal epithelial cells from necrosis and apoptosis, in part by decreasing reactive oxygen and nitrogen radical formation. In vivo, we have used several rodent models of intestinal injury to demonstrate the intestinal cytoptotective effects of HB-EGF. We have shown that HB-EGF protects the intestine in the face of intestinal ischemia/reperfusion injury, hemorrhagic shock and resuscitation and experimental necrotizing enterocolitits. The translational component of Dr. Besner's research involves a disease process known as neonatal necrotizing enterocolitis (NEC), which results in intestinal necrosis in newborn babies, especially those born prematurely. The long range goal of Dr. Besner's work is the prophylactic and therapeutic treatment of high-risk neonates with HB-EGF, in order to prevent and treat this often devastating disease. In addition to funding of Dr. Besner's work from the National Institutes of Health, Dr. Besner is working with industry to bring HB-EGF to the bedside in human clinical trials, expected to begin in 2009. |
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Faculty and Staff
Principal Investigator: Gail E. Besner, M.D.
e-mail: Gail.Besner@nationwidechildrens.org |
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Chen, Chun-Liang
e-mail: Chun-Liang.Chen@nationwidechildrens.org |
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Chen, Yan
e-mail: Yan.Chen@nationwidechildrens.org |
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Lagoa, Claudio
e-mail: Claudio.Lagoa@nationwidechildrens.org |
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Otabor, Iyore
e-mail: Iyore.Otabor@nationwidechildrens.org |
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Radulescu, Andrei
e-mail: Andrei.Radulescu@nationwidechildrens.org |
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Yu, David
e-mail: Xiaoyi.Yu@nationwidechildrens.org |
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Zhang, Hong-Yi
e-mail: Hong-Yi.Zhang@nationwidechildrens.org |
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Zhou, Yu
e-mail: Yu.Zhou@nationwidechildrens.org |
HALL LABORATORY
The focus of my research program is the regulation of the inflammatory response in critically ill children. We have ongoing clinical and translational protocols detailing the mechanisms and natural history of impairment of innate immune function (immunoparalysis) and adaptive immunity in the setting of severe sepsis, septic shock, and other forms of critical illness. The relationships between regulatory T cells, neuroendocrine dysfunction, and monocyte function with overall immune phenotype and clinical outcomes are all subjects of current interest. A specific example of this is our novel work exploring the role of the MEFV gene, coding for the protein pyrin which is known to be mutated in familial Mediterranean fever, in the regulation of the inflammatory response in monocytes during critical illness. |
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Faculty and Staff
Principal Investigator: Mark W. Hall, M.D.
e-mail: Mark.Hall@nationwidechildrens.org |
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Nateri, Jyotsna
e-mail: Jyotsna.Nateri@nationwidechildrens.org |
LIU LABORATORY
My laboratory is interested in the signal transduction pathways that control the innate immunity. Specifically, we are studying the signaling pathways that regulate the production of inflammatory cytokines. We have found that MAP kinase phosphatase (MKP)-1 plays a pivotal role in the restraint of the inflammatory responses in innate immune cells-by dephosphorylating p38 and JNK, MKP-1 deactivates the stress-activated MAP kinases and inhibits the production of pro-inflammatory cytokines. We hypothesize that defects in MKP-1 gene may sensitize host to inflammatory diseases. Currently, animal models are developed to test this hypothesis using genetics, biochemistry, and molecular biology techniques. Another research project in the laboratory is to understand the anti-inflammatory mechanism of triptolide, a compound isolated from an anti-rheumatic herb used for centuries in traditional Chinese medicine. The long term goals of these research projects are to understand the regulation of inflammation and to develop novel treatments for inflammatory diseases. |
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Faculty and Staff
Principal Investigator: Yusen Liu, Ph.D.
e-mail: Yusen.Liu@nationwidechildrens.org |
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Matta, Ronny
e-mail: Ronny.Matta@nationwidechildrens.org |
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Wang, Xianxi
e-mail: Xianxi.Wang@nationwidechildrens.org |
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Wang, Qingqing
e-mail: Qingqing.Wang@nationwidechildrens.org |
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Zhang, Nan
e-mail: Nan.Zhang@nationwidechildrens.org |
ROGERS LABORATORY
Premature infants are born with poorly developed respiratory systems and often require breathing assistance and supplemental oxygen for survival.The consequences of these life-saving therapies are often injury and permanent defects to the developing lungs. My laboratory is interested in identifying “biomarkers” as predictors of lung disease and understanding the mechanisms involved in both the injury and developmental defects that result from premature birth and oxygen therapies.We are currently involved studies to investigate the role of lipid oxidation products and their influence on inflammation in developmental models. |
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Faculty and Staff
Principal Investigator: Lynette Rogers, Ph.D.
e-mail: Lynette.Rogers@nationwidechildrens.org |
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Augustine, Molly
e-mail: Molly.Augustine@nationwidechildrens.org |
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Leonhart, Karen
e-mail: Karen.Leonhart@nationwidechildrens.org |
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Meng, Xiaomei
e-mail: Xiaomei.Meng@nationwidechildrens.org |
