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There is a growing movement in education to address concepts of sustainability across the curriculum. The English Language Arts curriculum is about reading the word and the world (Freire, 1993) and therefore is a natural place to begin reading, writing and discussing issues of global importance. A holistic view of English education through the lens of sustainability re-affirms curriculum design as living, organic, and in tune with our changing world. According to our university's Institute for Sustainability (http://www.uwrf.edu/sustain/overview.html), the core concept of sustainability moves from one that is solely environmental, to one "Based on the collective data and trend analysis across ecologic, social, and economic contexts, it is now consciously more of an 'attempt to avoid unsustainability'." The interdisciplinary nature of this definition, makes it easier for educators to address this concept in curriculum. This year-long action research study traces the journey of two teacher educators working with both primary and secondary pre-service teachers to redesign curriculum with a focus on English education through the lens of sustainability. Findings suggest that integrating sustainability issues into the English curriculum empowers pre-service teachers with confidence and knowledge of best practices supporting an ethical stance emphasising the socially humane objective of teaching children. (Contains 6 figures.)

Introduction AngiotensinII (AngII) is a critical factor in arterial re-modelling induced by intrinsic (e.g., hypertension) and extrinsic (e.g., revascularization procedure) vascular injury by virtue of its ability to actively promote [...], Release of angiotensin II (AngII) after vascular injury promotes tissue repair by stimulating phenotypic modulation of smooth muscle cells, which enables cell proliferation and migration. This process requires cytoskeleton remodeling, which involves cortactin, a scaffold protein that is phosphorylated by Src kinase in response to Ang II. Since insulin-like growth factor (IGF)-1 receptor transactivation mediates intracellular signals originating from the AngII type 1 ([AT.sup.1]) receptor in a Src kinase-dependent manner, we examined whether IGF-1 receptor transactivation was also required for cortactin phosphorylation. Treatment of quiescent smooth muscle cells with Ang II resulted in both cortactin phosphorylation and its translocation to the plasma membrane. Both events were prevented by 1-(1,1-dimethylethyl)-1-(4-methylphenyl)1H- pyrazolo(3,4-d)pyrimidin-4-amine (PP1), a Src kinase inhibitor, and by AG1024, an inhibitor of the IGF-1 receptor tyrosine kinase. Additionally, PP1 and AG1024 blocked the association of cortactin with actin-related protein (Arp) 3, an actin nucleation factor. These results indicate that Src kinase and the IGF-1 receptor kinase are necessary for activating cortactin. Phosphorylation of Src kinase in Ang II-treated cells was subsequently examined and was shown to be prevented by AG1024. Furthermore, Src kinase phosphorylation was blocked by inhibitors of protein kinase C (PKC), but not by inhibitors of phosphatidylinositol (PI) 3-kinase. These data establish that IGF-1 receptor transactivation is required for Src kinase-mediated cortactin phosphorylation and cytoskeletal reorganization in response to Ang II. Key words: smooth muscle, angiotensin, cytoskeleton, cortactin, Src kinase, IGF-1 receptor. Resume : La secretion d'angiotensine II (AngII) consecutive a une lesion vasculaire favorise la reparation des tissus en stimulant la modulation pheenotypique des fibres musculaires lisses, ce qui rend possible la proliferation et la migration des cellules. A cette fin, il faut remodeler le cytosquelette par l'entree en action de la cortactine, une proteine d'eechafaudage phosphorylee par la Src-kinase en reponse a l'AngII. Puisque la transactivation du recepteur du facteur de croissance 1 analogue a l'insuline (IFG-1) transmet les signaux intracellulaires issus du recepteur AngII [AT.sup.1] comme le ferait une Src-kinase, nous voulons verifier si la transactivation du recepteur IGF-1 est aussi requise pour la phosphorylation de la cortactine. Le traitement de cellules musculaires lisses quiescentes au moyen de l'Ang II suscite la phosphorylation de la cortactine et sa translocation dans la membrane plasmique. Les deux phenomenes sont contres par le PP1, un inhibiteur de la Src-kinase et par l'AG1024, un inhibiteur de la tyrosine kinase sur le recepteur de l'IGF-1. En outre, le PP1 et l'AG1024 bloquent l'association de la cortactine avec l'Arp3, un facteur de nucleation de l'actine. D'apres ces observations, la Src-kinase et la kinase du recepteur de l'IGF-1 sont essentielles a l'activation de la cortactine. D'apres nos analyses subsequentes, l'AG1024 inhibe la phosphorylation de la Src-kinase des cellules traiteees au moyen de l'AngII. De plus, la phosphorylation de la Src-kinase est contree par des inhibiteurs de la PKC, ce qui n'est pas le cas de la P13-kinase. La transactivation du recepteur de l'IGF-1 est donc essentielle a la phosphorylation de la cortactine mediee par la Src-kinase et pour la reorganisation du cytosquelette en reeponse a l'AngII. Mots-cles: muscle lisse, angiotensine, cytosquelette, cortactine, Src-kinase, recepteur de l'IGF-1. [Traduit par la Redaction]

Cytokeratins are not present in the vascular smooth muscle cells (VSMCs) of normal arteries, but they are detectable in the VSMCs of atherosclerotic lesions. A correlation between cytokeratin expression and [...]

Background. It is hypothesized that normal weight individuals develop diabetes through different pathophysiological mechanisms and that methods of prevention may differ in the absence of overweight/obesity. In this study, we compared the effect of lifestyle health coaching (LHC) on fasting plasma glucose (FPG) in normal weight, overweight, and obese US adults with prediabetes. Methods. Subjects were 1358 individuals who completed baseline and follow-up evaluations as part of an LHC program (follow-up = ~6 months). Participants were stratified, based on baseline body mass index (BMI), into normal weight (n = 129), overweight (n = 345), and obese (n = 884) cohorts. LHC included counseling, predominantly via telehealth, on exercise and nutrition. Results. BMI decreased (P <.001) in the overweight and obese participants but was unchanged in the normal weight participants. FPG decreased (P <.001) in all 3 cohorts, and the magnitude of decrease did not differ significantly among cohorts. FPG decreased to <5.6 mmol/L in 58.1%, 49.3%, and 41.4% of the normal weight, overweight, and obese participants, respectively. Conclusions. To our knowledge, this study is the first outside of Asia to show that LHC is as effective in managing FPG in normal weight adults with prediabetes versus those who are overweight/obese. [ABSTRACT FROM AUTHOR]