Leaders\u27 roles in creating and sustaining collective genius

This study examined leaders’ roles in fostering collective genius innovation within one private elementary school, including managing the paradoxes of innovation. Based on content analysis of eleven participants, this study found that teamwork, clear student learning outcomes emphasizing individualized learning, design thinking, and a growth mindset, all impacted willingness to innovate. To develop conditions for collective genius, leaders again focus on teamwork as well as being relational. In terms of their management of the six innovative paradoxes, the school leaders tend to balance their affirmation of the individual and the group, support staff and parents, focus on experimentation and learning, improvisation, patience, and bottom-up initiatives

Using mlearning in the education of radiation science students

Radiation science is a highly visual field that is constantly evolving due to technological advances. Technology has significantly improved almost all aspects of the field over the past 10-15 years. These advances in technology have also played a significant role in the education of radiation science students didactically and clinically. The enormous increase in the capabilities of information technology provides the opportunity for educators to dramatically change their way of teaching.1 mLearning or mobile learning involves the use of mobile devices (i.e. personal digital assistants, smart phones, iPhones, iTouch, iPad, laptops and tablets) to enhance teaching and learning. The most significant advantage of mLearning is the mobility of the technology which allows for unlimited, immediate and continuous access to course materials. The goal of this initial research is to discuss the implementation of mobile learning, specifically through the use of the Apple iTouch, into the education of radiation science students

Platelet endothelial cell adhesion molecule-1 inhibits platelet response to thrombin and von Willebrand factor by regulating the internalization of glycoprotein Ib via AKT/glycogen synthase kinase-3/dynamin and integrin αIIbβ3

OBJECTIVE: Platelet endothelial cell adhesion molecule-1 (PECAM-1) regulates platelet response to multiple agonists. How this immunoreceptor tyrosine-based inhibitory motif-containing receptor inhibits G protein-coupled receptor-mediated thrombin-induced activation of platelets is unknown. APPROACH AND RESULTS: Here, we show that the activation of PECAM-1 inhibits fibrinogen binding to integrin αIIbβ3 and P-selectin surface expression in response to thrombin (0.1-3 U/mL) but not thrombin receptor-activating peptides SFLLRN (3×10(-7)-1×10(-5) mol/L) and GYPGQV (3×10(-6)-1×10(-4) mol/L). We hypothesized a role for PECAM-1 in reducing the tethering of thrombin to glycoprotein Ibα (GPIbα) on the platelet surface. We show that PECAM-1 signaling regulates the binding of fluorescein isothiocyanate-labeled thrombin to the platelet surface and reduces the levels of cell surface GPIbα by promoting its internalization, while concomitantly reducing the binding of platelets to von Willebrand factor under flow in vitro. PECAM-1-mediated internalization of GPIbα was reduced in the presence of both EGTA and cytochalasin D or latrunculin, but not either individually, and was reduced in mice in which tyrosines 747 and 759 of the cytoplasmic tail of β3 integrin were mutated to phenylalanine. Furthermore, PECAM-1 cross-linking led to a significant reduction in the phosphorylation of glycogen synthase kinase-3β Ser(9), but interestingly an increase in glycogen synthase kinase-3α pSer(21). PECAM-1-mediated internalization of GPIbα was reduced by inhibitors of dynamin (Dynasore) and glycogen synthase kinase-3 (CHIR99021), an effect that was enhanced in the presence of EGTA. CONCLUSIONS: PECAM-1 mediates internalization of GPIbα in platelets through dual AKT/protein kinase B/glycogen synthase kinase-3/dynamin-dependent and αIIbβ3-dependent mechanisms. These findings expand our understanding of how PECAM-1 regulates nonimmunoreceptor signaling pathways and helps to explains how PECAM-1 regulates thrombosis

Platelet endothelial cell adhesion molecule-1 regulates collagen-stimulated platelet function by modulating the association of phosphatidylinositol 3-kinase with Grb-2-associated binding protein-1 and linker for activation of T cells

Background: Platelet activation by collagen depends on signals transduced by the glycoprotein (GP)VI–Fc receptor (FcR)-chain collagen receptor complex, which involves recruitment of phosphatidylinositol 3-kinase (PI3K) to phosphorylated tyrosines in the linker for activation of T cells (LAT). An interaction between the p85 regulatory subunit of PI3K and the scaffolding molecule Grb-2-associated binding protein-1 (Gab1), which is regulated by binding of the Src homology 2 domain-containing protein tyrosine phosphatase-2 (SHP-2) to Gab1, has been shown in other cell types to sustain PI3K activity to elicit cellular responses. Platelet endothelial cell adhesion molecule-1 (PECAM-1) functions as a negative regulator of platelet reactivity and thrombosis, at least in part by inhibiting GPVI–FcR-chain signaling via recruitment of SHP-2 to phosphorylated immunoreceptor tyrosine-based inhibitory motifs in PECAM-1. Objective: To investigate the possibility that PECAM-1 regulates the formation of the Gab1–p85 signaling complexes, and the potential effect of such interactions on GPVI-mediated platelet activation in platelets. Methods: The ability of PECAM-1 signaling to modulate the LAT signalosome was investigated with immunoblotting assays on human platelets and knockout mouse platelets. Results: PECAM-1-associated SHP-2 in collagen-stimulated platelets binds to p85, which results in diminished levels of association with both Gab1 and LAT and reduced collagen-stimulated PI3K signaling. We therefore propose that PECAM-1-mediated inhibition of GPVI-dependent platelet responses result, at least in part, from recruitment of SHP-2–p85 complexes to tyrosine-phosphorylated PECAM-1, which diminishes the association of PI3K with activatory signaling molecules, such as Gab1 and LAT

Sheep Updates 2008 - part 2

This session covers eleven papers from different authors: The Sheep Room 1. Analgesia for Surgical Husbandry Procedures in Sheep and Other Livestock, Dr Meredith L. Sheil, Animal Ethics Pty Ltd, Associate Sydney University Faculty of Veterinary Science The Wool Enterprise 2. Unmulsed sheep - implications for chemical use, Di Evans & Brown Besier, Department of Agriculture and Food WA 3. Are Damara and Dorper sheep better adapted than Merinos to nutritional stress? - Growth rates, Tim Scanlon1, Andre Martinho de Almeida2, Johan Greeff1, Tanya Kilminster1, John Milton3, Chris Oldham1, Department of Agriculture and Food WA1, Instituto de Investigacao Cientifica Tropical, Lisbon, Portugal2, University of Western Australia3 4. Are Damara and Dorper sheep better adapted than Merinos to nutritional stress? - Carcass attributes, Tanya Kilminster1, Andre Martinho de Almeida2, Johan Greeff1, John Milton3, Chris Oldham1, Tim Scanlon1, Department of Agriculture and Food WA1, Instituto de Investigacao Cientifica Tropical, Lisbon, Portugal2, University of Western Australia3 The Beef Room 5. Benefits of matching animal requirements with pasture feed supply and animal supply market requirements, B.L. McIntyre, Department of Agriculture and Food Western Australia, 6. Optimal grazing for beef, Alison Wheatley, Beef farmer Winnejup, John Lucey, Department of Agriculture and Food, Western Australia 7. Grain Introduction in commercial cattle feedlots, Fiona Jones1,2, Nick Costa2, 1 Department of Agriculture and Food WA and 2 Murdoch University. Mixed Systems 8. Confinement feeding stock in mixed enterprises, John Milton, The University of Western Australia & Independent Lab Services The Sheep Enterprise 9. Making More than Sheep, Ed Riggall, Australian Wool Innovation and Meat & Livestock Australia 10. Sheep Cost of Production - the enemy is at the gate!, JRL (Bob) Hall, JRL Hall & Co 11. Australian lamb - high yielding good to eat, Robin Jacob1, Dave Pethick2, Dave Hopkins3 and Graham Gardner2, 1Department of Agrcultre and Food WA, 2Murdoch University, 3NSW Department of Primary Industrie

Farnesoid X receptor and liver X receptor ligands initiate formation of coated platelets

The liver X receptors (LXRs) and farnesoid X receptor (FXR) have been identified in human platelets. Ligands of these receptors have been shown to have nongenomic inhibitory effects on platelet activation by platelet agonists. This, however, seems contradictory with the platelet hyper-reactivity that is associated with several pathological conditions that are associated with increased circulating levels of molecules that are LXR and FXR ligands, such as hyperlipidemia, type 2 diabetes mellitus, and obesity. We, therefore, investigated whether ligands for the LXR and FXR receptors were capable of priming platelets to the activated state without stimulation by platelet agonists. Treatment of platelets with ligands for LXR and FXR converted platelets to the procoagulant state, with increases in phosphatidylserine exposure, platelet swelling, reduced membrane integrity, depolarization of the mitochondrial membrane, and microparticle release observed. Additionally, platelets also displayed features associated with coated platelets such as P-selectin exposure, fibrinogen binding, fibrin generation that is supported by increased serine protease activity, and inhibition of integrin αIIbβ3. LXR and FXR ligand-induced formation of coated platelets was found to be dependent on both reactive oxygen species and intracellular calcium mobilization, and for FXR ligands, this process was found to be dependent on cyclophilin D. We conclude that treatment with LXR and FXR ligands initiates coated platelet formation, which is thought to support coagulation but results in desensitization to platelet stimuli through inhibition of αIIbβ3 consistent with their ability to inhibit platelet function and stable thrombus formation in vivo