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Menegatti, M.

Publications and source records attributed to Menegatti, M..

2 recordsLinked to original sources

Reading of ingroup politicians smiles triggers smiling in the corner of ones eyes

Capturing political support from spontaneous smile reactions detected in others faces can be used to gauge electorate preference. But will a smile elicited in the corner of ones eye while reading of a favored politician smiling indicate positive disposition and political support for target candidates? From an embodied simulation perspective, we tested whether reading of an ingroup or outgroup politician smiling would trigger morphologically different smiles in faces of readers. In a reading task in the laboratory, participants were presented with subject-verb phrases describing left and right-wing politicians smiling or frowning while their facial muscular reactions were measured via electromyography (EMG) recording from the zygomaticus major (ZM, lip puller muscle), orbicularis oculi (OO, eye corner muscle) and the corrugator supercili (CS, wrinkler of the eyebrows). We expected and found that participants responded with a smile detected at the lip puller (ZM) and eye corner (OO) facial muscles when exposed to portrayals of smiling politicians of same political orientation, and reported more positive emotions towards these latter. When reading about outgroup politicians smiling, there was a weaker activation of the lip corner (ZM) muscle and no activation of the eye corner (OO) muscle, while emotions reported towards outgroup politicians were significantly more negative. Also, a more enhanced frown response (CS) was found for ingroup compared to outgroup politicians frown expressions. Present findings suggest that a politicians smile may go a long way to influence electorates through both non-verbal and verbal pathways. They add another layer to our understanding of how language and social information shape embodied effects in a highly nuanced manner.

physiology↗

Analysis of factor V in zebrafish demonstrates minimal levels needed for hemostasis and risk stratifies human variants

In humans, coagulation factor V (F5) deficiency is a rare, clinically heterogeneous bleeding disorder, suggesting that genetic modifiers may contribute to disease expressivity. Complete loss of mouse F5 results in early lethality. Zebrafish possess many distinct advantages including high fecundity, optical clarity, external development, and homology with the mammalian hemostatic system, features that make it ideal for genetic studies. Our aim was to study the role of F5 in zebrafish through targeted mutagenesis, and apply the model to the study of human F5 variants. CRISPR-mediated genome editing of the zebrafish f5 locus was performed, generating mutants homozygous for a 49 base pair deletion in exon 4. Thrombus formation secondary to vascular endothelial injury was absent in f5-/- mutant embryos and larvae. Despite this severe hemostatic defect, homozygous mutants survived before succumbing to severe hemorrhage in adulthood. Human F5 variants of uncertain significance from patients with F5 deficiency were evaluated, and the causative mutations identified and stratified by their ability to restore thrombus formation in larvae. Analysis of these novel mutations demonstrates variable residual F5 function, with minimal activity being required to restore hemostasis. This in vivo evaluation may be beneficial for patients whose factor activity levels lack correlation with bleeding symptomatology. Furthermore, homozygous mutant embryos tolerate what is a severe and lethal defect in mammals, suggesting the possibility of species-specific factors enabling survival, and allowing further study not possible in the mouse. Identification of these factors or other genetic modifiers could lead to novel therapeutic modalities.\n\nKey PointsO_LIF5 mutant fish embryos tolerate symptoms lethal in mammals but succumb to bleeding in adulthood\nC_LIO_LIAnalysis of human variants demonstrate that all have some residual function and that minimal F5 activity is required to restore hemostasis\nC_LI

genetics↗