The positivity principle states that people learn better from instructors who display positive emotions rather than negative emotions. In two experiments, students viewed a short video lecture on a statistics topic in which an instructor stood next to a series of slides as she lectured and then they took either an immediate test (Experiment 1) or a delayed test (Experiment 2). In a between-subjects design, students saw an instructor who used her voice, body movement, gesture, facial expression, and eye gaze to display one of four emotions while lecturing: happy (positive/active), content (positive/passive), frustrated (negative/active), or bored (negative/passive). First, learners were able to recognize the emotional tone of the instructor in an instructional video lecture, particularly by more strongly rating a positive instructor as displaying positive emotions and a negative instructor as displaying negative emotions (in Experiments 1 and 2). Second, concerning building a social connection during learning, learners rated a positive instructor as more likely to facilitate learning, more credible, and more engaging than a negative instructor (in Experiments 1 and 2). Third, concerning cognitive engagement during learning, learners reported paying more attention during learning for a positive instructor than a negative instructor (in Experiments 1 and 2). Finally, concerning learning outcome, learners who had a positive instructor scored higher than learners who had a negative instructor on a delayed posttest (Experiment 2) but not an immediate posttest (Experiment 1). Overall, there is evidence for the positivity principle and the cognitive-affective model of e-learning from which it is derived.
BackgroundBasal-like breast cancer (BLBC) is associated with a poor clinical outcome; however, the mechanism of BLBC aggressiveness is still unclear. It has been shown that a linker histone functions as either a positive or negative regulator of gene expression in tumors. Here, we aimed to investigate the possible involvement and mechanism of HIST1H1B in BLBC progression.Experimental designWe analyzed multiple gene expression datasets to determine the relevance of HIST1H1B expression with BLBC. We employed quantitative real-time PCR, transwell assay, colony formation assay, and mammosphere assay to dissect the molecular events associated with the expression of HIST1H1B in human breast cancer. We studied the association of HIST1H1B with CSF2 by ChIP assay. Using tumorigenesis assays, we determine the effect of HIST1H1B expression on tumorigenicity of BLBC cells.ResultsHere, we show that the linker histone HIST1H1B is dramatically elevated in BLBC due to HIST1H1B copy number amplification and promoter hypomethylation. HIST1H1B upregulates colony-stimulating factor 2 (CSF2) expression by binding the CSF2 promoter. HIST1H1B expression promotes, whereas knockdown of HIST1H1B expression suppresses tumorigenicity. In breast cancer patients, HIST1H1B expression is positively correlated with large tumor size, high grade, metastasis and poor survival.ConclusionHIST1H1B contributes to basal-like breast cancer progression by modulating CSF2 expression, indicating a potential prognostic marker and therapeutic target for this disease.
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