ABSTRACT
Dental task trainer simulators using haptics (virtual touch) offers a cost-effective method of teaching certain clinical skills. The purpose of this study is to evaluate students' performance in removing artificial caries after training with either a haptic dental chair simulator with virtual reality or a traditional dental chair simulator with a mannequin head. Cluster Randomized Controlled Trials in two cohorts, both Year 1 dental students. Students taught using traditional dental chair simulators were compared with students taught using haptic-based simulators on their ability to cut a cavity in a plastic tooth following training. Across both cohorts, there was no difference in the quality of cavity cut, though students' technique differed across the two simulator groups in some respects. No difference was seen across both cohorts in the quality of cavity cut for a simple preparation, though students in the haptic condition performed less well in the more demanding task. Moreover, students in the haptic group were also less likely to be perceived to be 'holding the instrument appropriately'. These findings suggest further investigation is needed into the differences in handling of instruments and level of clinical task difficulty between the simulators.
ABSTRACT
This study examined the expression of the platelet collagen receptor glycoprotein VI (GPVI) in megakaryocyte cell lines and primary megakaryocytes by reverse transcriptase-polymerase chain reaction and by flow cytometry and ligand blotting using the snake venom toxin convulxin. Expression of GPVI is increased in the megakaryoblastic cell lines HEL and CMK on differentiation with the phorbol ester phorbol 12-myristate 13-acetate (PMA), along with the Fc receptor gamma-chain (FcR gamma-chain). The increase in GPVI expression is associated with marked potentiation of tyrosine phosphorylation and Ca(++) elevation in response to convulxin. Syk, linker for activated T cells, and phospholipase C gamma 2 (PLC gamma 2) are among the proteins tyrosine phosphorylated on convulxin stimulation in PMA-differentiated HEL cells. Studies on primary murine megakaryocytes grown in vitro confirmed that GPVI is up-regulated in parallel with functional activation, assessed by measurement of [Ca(++)](i), during differentiation. The results demonstrate that expression of GPVI is up-regulated along with the FcR gamma-chain during differentiation of megakaryocytes. (Blood. 2000;96:2740-2745)
Subject(s)
Gene Expression Regulation, Developmental , Lectins, C-Type , Megakaryocytes/metabolism , Platelet Membrane Glycoproteins/biosynthesis , Animals , Blood Platelets/metabolism , Calcium Signaling/drug effects , Cell Differentiation/drug effects , Cell Line/drug effects , Cell Line/metabolism , Crotalid Venoms/pharmacology , Flow Cytometry , Gene Expression Regulation, Developmental/drug effects , Humans , Megakaryocytes/cytology , Megakaryocytes/drug effects , Mice , Platelet Membrane Glycoproteins/genetics , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Receptors, IgG/biosynthesis , Receptors, IgG/genetics , Reverse Transcriptase Polymerase Chain Reaction , Tetradecanoylphorbol Acetate/pharmacology , Tumor Cells, Cultured/drug effects , Up-Regulation/drug effectsABSTRACT
Platelet endothelial cell adhesion molecule-1 (CD31) is a 130-kDa glycoprotein receptor present on the surface of platelets, neutrophils, monocytes, certain T-lymphocytes, and vascular endothelial cells. CD31 is involved in adhesion and signal transduction and is implicated in the regulation of a number of cellular processes. These include transendothelial migration of leukocytes, integrin regulation, and T-cell function, although its function in platelets remains unclear. In this study, we demonstrate the ability of the platelet agonists collagen, convulxin, and thrombin to induce tyrosine phosphorylation of CD31. Furthermore, we show that this event is independent of platelet aggregation and secretion and is accompanied by an increase in surface expression of CD31. A kinase capable of phosphorylating CD31 was detected in CD31 immunoprecipitates, and its activity was increased following activation of platelets. CD31 tyrosine phosphorylation was reduced or abolished by the Src family kinase inhibitor PP2, suggesting a role for these enzymes. In accordance with this, each of the Src family members expressed in platelets, namely Fyn, Lyn, Src, Yes, and Hck, was shown to co-immunoprecipitate with CD31. The involvement of Src family kinases in this process was confirmed through the study of mouse platelets deficient in Fyn.
