Abstract Background Engineering self‐efficacy, or the belief in one's own capabilities to complete engineering tasks, has been shown to predict greater motivation, academic performance, and retention of engineering students. Investigating the types of experiences that influence engineering students' self‐efficacy can reveal ways to support students in their undergraduate engineering programs. Purpose/Hypothesis(es) The purpose of this study was to qualitatively examine how undergraduate engineering students describe the sources of their engineering self‐efficacy and whether patterns in students' responses differed by gender. Design/Method Participants ( N = 654) were undergraduate engineering students attending two public, land‐grant universities in the U.S. Open‐ended survey questions were used to identify the events, social experiences, and emotions that students described as relevant to their engineering self‐efficacy. Chi‐square analyses were used to investigate whether response patterns varied by gender. Results Students described enactive performances as their most salient source of self‐efficacy, but interesting insights also emerged about how engineering students draw from social and emotional experiences when developing their self‐efficacy. Women more often referred to social sources of self‐efficacy and reported fewer positive emotions than did men. Conclusion Findings suggest ways that educators can provide more targeted opportunities for students to develop their self‐efficacy in engineering.
The ‘perfect’ lens: Perfectionism and early adolescents' math self‐efficacy development
Abstract Background Self‐efficacy, or the beliefs learners hold about what they can do, develops largely from how learners perceive and interpret four main sources of information: mastery experiences, vicarious experiences, social persuasions and physiological and affective states. Although the relationship between these sources and self‐efficacy is well‐established, less is known about the factors that may influence how early adolescent learners perceive and interpret information from these sources. Aims The purpose of this study was to investigate how the predisposition of perfectionism might predict how learners perceive efficacy‐relevant information in the domain of math. Methods Using a correlational design, this study considered whether perfectionism was associated with how middle school students ( N = 1683) perceive information from the four hypothesized sources of self‐efficacy. Participants completed a paper‐based survey at two time points. Perfectionism was measured at Time 1. Self‐efficacy and its sources were measured at Time 2. Structural equation modelling techniques were used to examine the relationship between factors. Results and Conclusions Students who held themselves to high standards (i.e., greater self‐oriented perfectionism) reported higher levels of mastery experiences, vicarious experiences, social messages and self‐efficacy. Conversely, students who felt external pressure to be perfect (i.e., socially prescribed perfectionism) reported lower levels of mastery experiences, vicarious experiences and self‐efficacy, as well as higher levels of negative physiological and affective states. The relationship between perfectionism and self‐efficacy was partially mediated by students' perceptions of mastery. This study extends the current literature on the sources of math self‐efficacy in early adolescence by showing how a predisposition like perfectionism is associated with how adolescent learners perceive and interpret efficacy‐relevant information.
Niclosamide blocks autophagy via lysosomal dysfunction (663.18)
Niclosamide is a salicylanilide derivative used as antihelminthic agent. Recently, Nic has been screened out as an autophagy modulator by us and other groups and was identified to be a structurally distinct mTORC1 signaling inhibitor. In this work, we measured the long‐lived protein degradation activity and found Niclosamide could inhibit the autophagic process. To elucidate the inhibition of Niclosamide on autophagy, we further tested the lysosomal activity using DQ‐BSA assay and measured protease activity such as Cathepsin B and Cathepsin D with fluorescent substrates. The lower degradation of DQ‐BSA and decreased protease activity after Niclosamide treatments indicated the impaired lysosome function. In addition, both LC‐II and P62 proteins accumulated significantly when treated by Niclosamide suggesting the late stage of autophagy was blocked. The increased pH of lysosome and release of Cathepsins from lysosome to cytosol demonstrated that Niclosamide might affect lysosome resulted from lysosomal membrane permeabilization. Collectively, we firstly disclosed Niclosamide not only inhibited mTORC1 activity but also, as other well‐known lysosome inhibitors, strongly blocked autophagy via lysosomal dysfunction. Grant Funding Source : Supported by Guandong Provincial Natural Science Foundation, China (S2013010015876)
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)
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Abstract Reciprocal epithelial–mesenchymal interactions are pivotal in lung development, homeostasis, injury, and repair. Organoids have been used to investigate such interactions, but with a major focus on epithelial responses to mesenchyme and less attention to epithelial effects on mesenchyme. In the present study, we used nascent organoids composed of human and mouse lung epithelial and mesenchymal cells to demonstrate that healthy lung epithelium dramatically represses transcriptional, contractile, and matrix synthetic functions of lung fibroblasts. Repression of fibroblast activation requires signaling via the bone morphogenetic protein (BMP) pathway. BMP signaling is diminished after epithelial injury in vitro and in vivo, and exogenous BMP4 restores fibroblast repression in injured organoids. In contrast, inhibition of BMP signaling in healthy organoids is sufficient to derepress fibroblast matrix synthetic function. Our results reveal potent repression of fibroblast activation by healthy lung epithelium and a novel mechanism by which epithelial loss or injury is intrinsically coupled to mesenchymal activation via loss of repressive BMP signaling.
Adipocyte Mitochondrial Function Is Reduced in Human Obesity Independent of Fat Cell Size