Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The epidermal growth factor receptor (EGF-R) is perhaps the best studied member of tyrosine kinase receptors. Its inactivation by homologous recombination results in three different phenotypes ranging from peri-implantation lethality to postnatal lethality. The mildest form of EGF-R inactivation leads to epithelial immaturity and postnatal death due to respiratory failure and necrotizing enterocolitis-like lesions in the intestine. The defects seen in this 'postnatal lethality phenotype' manifest in the classical EGF-responsive organs (skin, intestine) and organs undergoing branching morphogenesis during development (lung, kidney, mammary gland, pancreas and prostate), and thus accord with the concept of EGF family members being important epithelial mitogens. The respiratory failure of the EGF-R (-/-) mice results from impaired branching of the alveolar tree and leads to decreased surface for gas exchange. Overall, the lung phenotype bears similarity to respiratory distress syndrome and bronchopulmonary dysplasia--the most common complications of prematurity in humans. Intestinal changes seen in the EGF-R (-/-) mice vary in severity, the end-point being severe mucosal lesions and necroses. These findings resemble those seen in necrotizing enterocolitis of premature babies, a serious intestinal problem in the neonate. Although deficient EGF-R function is not the reason for these prematurity-associated diseases it may nevertheless exacerbate them. Potential usage of EGF transforming growth factor-alpha in clinical work is discussed.
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PMID:Epidermal growth factor receptor in mice and men--any applications to clinical practice? 956 19

Spontaneous intestinal perforation (SIP) occurs commonly in extremely low birth weight (ELBW) infants. Our understanding of its etiologies has improved dramatically over the last decade. Included in this comprehension is an ongoing reconciliation of the iatrogenic risk factors, the microbiology, and the histopathology. The latter shows focal perforations with necrosis of the muscularis externa and no sign of ischemic damage (typically characterized by mucosal necrosis in the preterm bowel). Associations include extreme prematurity, early postnatal steroids (EPS), early use of indomethacin (EUI), and two common pathogens (Candida and Staphylococcus epidermis). Animal models of SIP suggest that all risk factors converge on a common collection of signaling pathways: those of nitric oxide synthases (NOS), insulin-like growth factors (IGFs), and epidermal growth factors (EGFs). Many of these factors skew trophism of the ileum (defined as thinning of the submucosa concomitant with hyperplasia of the muscosa). Global depletion of NOS is associated with disturbed intestinal motility and diminished transforming growth factor-alpha (TGF-alpha) in the muscularis externa. This constellation of insults seems to make the distal intestine vulnerable to perforation during recovery of motility.
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PMID:Understanding intestinal vulnerability to perforation in the extremely low birth weight infant. 1878 6