2 research outputs found
Meta-Analysis of Experimental Manipulations: Some Factors Affecting the Velten Mood Induction Procedure
Manipulation validity may be influenced by many factors, including specific aspects of experimental procedure. Meta-analysis is an ideal tool for assessing factors that influence manipulations because it is capable of equating, combining, and gauging the impact of different experimental procedures on a given manipulation. This use of meta-analysis is demonstrated by meta-analyzing experiments employing the Velten mood manipulation. This manipulation has been criticized for creating experimental demand. Procedures relevant to experimental demand include whether an honest or deceptive cover story is used and whether a self-report or non-self-report manipulation check measure is used. Effect sizes are smaller when a deceptive (vs. honest) cover story is used and when a non-self-report (vs. self-report) manipulation check measure is used. Discussion concerns how the Velten manipulation may be compromised and how meta-analysis may be employed to evaluate factors influencing manipulation validity.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/68937/2/10.1177_0146167291173013.pd
Rapid stimulation of tyrosine phosphorylation signals downstream of G-protein-coupled receptors for thromboxane A(2) in human platelets
Signals ensuing from trimeric G-protein-coupled receptors synergize to induce platelet activation. At low doses, the thromboxane A(2) analogue U46619 does not activate integrin αIIbβ3 or trigger platelet aggregation, but it induces shape changes. In the present study, we addressed whether low doses of U46619 trigger tyrosine phosphorylation independently of integrin αIIbβ3 activation and ADP secretion, and synergize with adrenaline (epinephrine) to induce aggregation in acetylsalicylic acid (aspirin)-treated platelets. Low doses of U46619 triggered tyrosine phosphorylation of different proteins, including FAK (focal adhesion kinase), Src and Syk, independently of signals ensuing from integrin αIIbβ3 or ADP receptors engaged by secreted ADP. The G(12/13)-mediated Rho/Rho-kinase pathway was also increased by low doses of U46619; however, this pathway was not upstream of tyrosine phosphorylation, because this occurred in the presence of the Rho-kinase inhibitor Y-27632. Although low doses of U46619 or adrenaline alone were unable to trigger platelet aggregation and integrin αIIbβ3 activation, the combination of the two stimuli effectively induced these responses. PP2, a tyrosine kinase inhibitor, and Y-27632 inhibited platelet activation induced by low doses of U46619 plus adrenaline and, when used in combination, totally suppressed this platelet response. In addition, the two inhibitors selectively blocked tyrosine kinases and the Rho/Rho-kinase pathway respectively. These findings suggest that both tyrosine phosphorylation and the Rho/Rho-kinase pathway are required to activate platelet aggregation via G(12/13) plus G(z) signalling