Angiogenesis, or the formation of new blood vessels, plays a central role in a number of physiologic and pathologic conditions, including wound healing, diabetic retinopathy, and solid tumor growth, and endothelial cells can be induced to mimic this process in vitro. Using a modification of the differential display method (Zimrin, A. B., Villeponteau, B., and Maciag, T. (1995) Biochem. Biophys. Res. Commun. 213, 630 -638), we isolated the human homolog of the Jagged ligand for the Notch receptor from human endothelial cells exposed to fibrin and demonstrate that the Jagged transcript, but not the Notch 1 or Notch 2 transcripts, are up-regulated by fibrin. Interestingly, the addition of an antisense Jagged oligomer to bovine microvascular endothelial cells grown on a collagen gel resulted in a marked increase in invasion and tube formation in the underlying gel in response to fibroblast growth factor. In contrast, no effect was observed on vascular endothelial growth factor-induced angiogenesis under identical conditions. These data suggest that Jagged-Notch signaling is able to regulate fibroblast growth factor-induced endothelial cell migration in vitro, an early event during angiogenesis in vivo.
Electronic performance support systems (EPSS) deliver relevant support information to users while they are performing tasks. The present study examined the effect of different types of EPSS on user performance, attitudes, system use and time on task. Employees at a manufacturing company were asked to complete a procedural software task and received support from either an intrinsic, extrinsic, external performance support system or no system at all. Results revealed significant differences on performance, attitudes and use between several treatment groups. The study suggests that providing any kind of EPSS to support task performance is better than having none at all. In addition, designers can improve user performance, attitudes and use by creating systems that integrate with the primary work interface.
Dysregulation of iron homeostasis is implicated in Alzheimer's disease (AD). In this pilot study, common variants of the apolipoprotein E (APOE) and HFE genes resulting in the iron overload disorder of hereditary hemochromatosis (C282Y, H63D and S65C) were evaluated as factors in sporadic AD in an Ontario sample in which folic acid fortification has been mandatory since 1998. Laboratory studies also were done to search for genetic effects on blood markers of iron status, red cell folates and serum B12. Participants included 58 healthy volunteers (25 males, 33 females) and 54 patients with probable AD (20 males, 34 females). Statistical analyses were interpreted at the 95% confidence level. Contingency table and odds ratio analyses supported the hypothesis that in females of the given age range, E4 significantly predisposed to AD in the presence but not absence of H63D. In males, E4 significantly predisposed to AD in the absence of H63D, and H63D in the absence of E4 appeared protective against AD. Among E4+ AD patients, H63D was associated with significant lowering of red cell folate concentration, possibly as the result of excessive oxidative stress. However, folate levels in the lowest population quartile did not affect the risk of AD. A model is presented to explain the experimental findings.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.