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The Hackam lab focuses on the cell and molecular biology governing the environmental cues that regulate normal maturation of the host, and how failed mucosal adaptation leads to disease in premature infants. We have focused extensively on the pathogenesis of necrotizing enterocolitis (NEC), which is a major disease that affects premature infants, and have proposed a unifying hypothesis which states that the development of NEC results from the inappropriate activation of the innate immune receptor toll like receptor 4 (TLR4) on the intestinal epithelium, which is expressed at high levels in the premature versus full-term neonate, reflecting the role that TLR4 plays in normal intestinal stem cell development and differentiation. Using transgenic mouse models as well as experimental models in piglets, we have focused on the mechanisms by which envioronmental cues induce injury to the intestinal stem cells, and how signals released from the damaged neonatal gut can induce disease in other organs, including the lung and the developing brain, which are particularly susceptible to disease in the premature host.
The Hackam lab focuses on the cell and molecular biology governing the environmental cues that regulate normal maturation of the host, and how failed mucosal adaptation leads to disease in premature infants. We have focused extensively on the pathogenesis of necrotizing enterocolitis (NEC), which is a major disease that affects premature infants, and have proposed a unifying hypothesis which states that the development of NEC results from the inappropriate activation of the innate immune receptor toll like receptor 4 (TLR4) on the intestinal epithelium, which is expressed at high levels in the premature versus full-term neonate, reflecting the role that TLR4 plays in normal intestinal stem cell development and differentiation. Using transgenic mouse models as well as experimental models in piglets, we have focused on the mechanisms by which envioronmental cues induce injury to the intestinal stem cells, and how signals released from the damaged neonatal gut can induce disease in other organs, including the lung and the developing brain, which are particularly susceptible to disease in the premature host.
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论文共 239 篇作者统计合作学者相似作者
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Gut microbesno. 1 (2023): 2221470
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Chhinder P. Sodhi,Raheel Ahmad,William B. Fulton,Carla M. Lopez, Benjamin O. Eke,Daniel Scheese, Johannes W. Duess,Steve N. Steinway,Zachariah Raouf,Hannah Moore,Koichi Tsuboi,Maame Efua Sampah,
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGYno. 1 (2023): G23-G41
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The journal of trauma and acute care surgeryno. 3 (2023): 361-367
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