Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intraventricular hemorrhage (IVH) in premature infants may be related to the immaturity of the vascular bed in the germinal matrix. We measured six hemostatic parameters whose alterations may represent an additional risk factor for IVH in preterm infants. On postnatal day 1 there were differences between plasminogen activator inhibitor-1 (PAI-1) activity and antigen, of both full-term and preterm infants with and without IVH (P < 0.05). Preterms with IVH were different to both full-terms and preterms without IVH. No difference was observed in plasma concentrations of fibrinogen, plasminogen and von Willebrand factor. Plasma concentrations of antithrombin III were significantly higher in full-term infants than in preterm infants. The difference between the platelet counts of preterm infants with and without IVH was not significant (P > 0.05). Elevation of crosslinked fibrin degradation products (XDP), determined by the SimpliRED D-dimer test, correlated in four out of five premature infants with the diagnosis of IVH by ultrasonography. No elevation of D-dimer XDP was observed in premature infants without IVH (11/12) and full-term infants (6/6). In conclusion, a hypercoagulable state, indicated by a rise in D-dimer XDP, may be initiated by some types of trauma to fragile blood vessels of the preterm infants who develop IVH. This hypercoagulability is further exacerbated by the increased release of PAI-1 leading to suppressed fibrinolysis.
 ...
PMID:Intraventricular haemorrhage in preterm infants: evidence of suppressed fibrinolysis. 873 35

Pancreatic acini and islets are believed to differentiate from common ductal precursors through a process requiring various growth factors. Epidermal growth factor receptor (EGF-R) is expressed throughout the developing pancreas. We have analyzed here the pancreatic phenotype of EGF-R deficient (-/-) mice, which generally die from epithelial immaturity within the first postnatal week. The pancreata appeared macroscopically normal. The most striking feature of the EGF-R (-/-) islets was that instead of forming circular clusters, the islet cells were mainly located in streak-like structures directly associated with pancreatic ducts. Based on BrdU-labelling, proliferation of the neonatal EGF-R (-/-) beta-cells was significantly reduced (2.6+/-0.4 versus 5.8+/-0.9%, P<0.01) and the difference persisted even at 7-11 days of age. Analysis of embryonic pancreata revealed impaired branching morphogenesis and delayed islet cell differentiation in the EGF-R (-/-) mice. Islet development was analyzed further in organ cultures of E12.5 pancreata. The proportion of insulin-positive cells was significantly lower in the EGF-R (-/-) explants (27+/-6 versus 48+/-8%, P<0.01), indicating delayed differentiation of the beta cells. Branching of the epithelium into ducts was also impaired. Matrix metalloproteinase (MMP-2 and MMP-9) activity was reduced 20% in EGF-R (-/-) late-gestation pancreata, as measured by gelatinase assays. Furthermore, the levels of secreted plasminogen activator inhibitor-1 (PAI-1) were markedly higher, while no apparent differences were seen in the levels of active uPA and tPa between EGF-R (-/-) and wild-type pancreata. Our findings suggest that the perturbation of EGF-R-mediated signalling can lead to a generalized proliferation defect of the pancreatic epithelia associated with a delay in beta cell development and disturbed migration of the developing islet cells as they differentiate from their precursors. Upregulated PAI-1 production and decreased gelatinolytic activity correlated to this migration defect. An intact EGF-R pathway appears to be a prerequisite for normal pancreatic development.
 ...
PMID:Impaired migration and delayed differentiation of pancreatic islet cells in mice lacking EGF-receptors. 1082 60