Behind the scenes: Impact of virtual backgrounds in educational videos on visual processing and learning outcomes

The increasing use of instructional videos in educational settings has emphasized the need for a deeper understanding of their design requirements. This study investigates the impact of virtual backgrounds in educational videos on students' visual information processing and learning outcomes.  Participants aged 14-17 (N=47) were randomly assigned to one of three conditions: a video with a neutral, authentic, or off-topic background. Their prior knowledge and working memory capacity (WMC) were measured before watching the video, and eye tracking data was collected during the viewing. Learning outcomes and student experiences were assessed after viewing. The eye tracking data revealed that a neutral background was the least distracting, allowing students to pay better attention to relevant parts of the video. Students found the off-topic background most distracting, but the negative effect on learning outcomes was not statistically significant. In contrast to expectations, no positive effect was observed for the authentic background. Furthermore, WMC had a significant impact on visual information processing and learning outcomes. These findings suggest that educators should consider using neutral backgrounds in educational videos, particularly for learners with lower WMC. Consequently, this research underscores the significance of careful design considerations in the creation of instructional videos

It is all in the surv-eye: can eye tracking data shed light on the internal consistency in self-report questionnaires on cognitive processing strategies?

Although self-report questionnaires are widely used, researchers debate whether responses to these types of questionnaires are valid representations of the respondent’s actual thoughts and beliefs. In order to provide more insight into the quality of questionnaire data, we aimed to gain an understanding of the processes that impact the completion of self-report questionnaires. To this end, we explored the process of completing a questionnaire by monitoring the eye tracking data of 70 students in higher education. Specifically, we examined the relation between eye movement measurements and the level of internal consistency demonstrated in the responses to the questionnaire. The results indicated that respondents who look longer at an item do not necessarily have more consistent answering behaviour than respondents with shorter processing times. Our findings indicate that eye tracking serves as a promising tool to gain more insight into the process of completing self-report questionnaires

A20 deficiency sensitizes pancreatic beta cells to cytokine-induced apoptosis in vitro but does not influence type 1 diabetes development in vivo

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

The effects of summarization and factual retrieval practice on text comprehension and text retention in elementary education

When reading a text in school, the goal is both text comprehension and text retention. We examined the effects of the learning strategies summarization and factual retrieval practice on third- and fourth-grade pupils’ text comprehension and retention of factual knowledge from a text, using restudy as a control condition. The experiment was conducted in an authentic classroom setting, with teachers executing the experiment using original course materials. In 2016, 57 regular third- and fourth-grade pupils (M = 9.04 years old) read three different texts, and each applied three different learning strategies (summarization, retrieval practice and restudy, which were counterbalanced across texts) in subsequent practice sessions. After a 2-week delay, a final test was administered. The learning strategy summarization had a larger positive effect on text comprehension than factual retrieval practice, but had a similar effect compared to restudy. The learning strategy factual retrieval practice had a larger positive effect on text retention than both summarization and restudy. Implications for educational practice are discussed

A20 deficiency in myeloid cells protects mice from diet-induced obesity and insulin resistance due to increased fatty acid metabolism

Obesity-induced inflammation is a major driving force in the development of insulin resistance, type 2 diabetes (T2D), and related metabolic disorders. During obesity, macrophages accumulate in the visceral adipose tissue, creating a low-grade inflammatory environment. Nuclear factor kappa B (NF-kappa B) signaling is a central coordinator of inflammatory responses and is tightly regulated by the anti-inflammatory protein A20. Here, we find that myeloid-specific A20-deficient mice are protected from diet-induced obesity and insulin resistance despite an inflammatory environment in their metabolic tissues. Macrophages lacking A20 show impaired mitochondrial respiratory function and metabolize more palmitate both in vitro and in vivo. We hypothesize that A20-deficient macrophages rely more on palmitate oxidation and metabolize the fat present in the diet, resulting in a lean phenotype and protection from metabolic disease. These findings reveal a role for A20 in regulating macrophage immunometabolism

Two distinct ubiquitin-binding motifs in A20 mediate its anti-inflammatory and cell-protective activities

Protein ubiquitination regulates protein stability and modulates the composition of signaling complexes. A20 is a negative regulator of inflammatory signaling, but the molecular mechanisms involved are ill understood. Here, we generated Tnfaip3 gene-targeted A20 mutant mice bearing inactivating mutations in the zinc finger 7 (ZnF7) and ZnF4 ubiquitin-binding domains, revealing that binding to polyubiquitin is essential for A20 to suppress inflammatory disease. We demonstrate that a functional ZnF7 domain was required for recruiting A20 to the tumor necrosis factor receptor 1 (TNFR1) signaling complex and to suppress inflammatory signaling and cell death. The combined inactivation of ZnF4 and ZnF7 phenocopied the postnatal lethality and severe multiorgan inflammation of A20-deficient mice. Conditional tissue-specific expression of mutant A20 further revealed the key role of ubiquitin-binding in myeloid and intestinal epithelial cells. Collectively, these results demonstrate that the anti-inflammatory and cytoprotective functions of A20 are largely dependent on its ubiquitin-binding properties. van Loo and colleagues provide insights into the action of the anti-inflammatory protein A20. The ZnF7 and ZnF4 ubiquitin-binding domains of A20 are both required to suppress inflammatory signaling and cell death; however, these zinc fingers operate via distinct mechanisms

STE20 kinase TAOK3 regulates type 2 immunity and metabolism in obesity

Healthy adipose tissue (AT) contains ST2(+) Tregs, ILC2s, and alternatively activated macrophages that are lost in mice or humans on high caloric diet. Understanding how this form of type 2 immunity is regulated could improve treatment of obesity. The STE20 kinase Thousand And One amino acid Kinase-3 (TAOK3) has been linked to obesity in mice and humans, but its precise function is unknown. We found that ST2(+) Tregs are upregulated in visceral epididymal white AT (eWAT) of Taok3(-/-) mice, dependent on IL-33 and the kinase activity of TAOK3. Upon high fat diet feeding, metabolic dysfunction was attenuated in Taok3(-/-) mice. ST2(+) Tregs disappeared from eWAT in obese wild-type mice, but this was not the case in Taok3(-/-) mice. Mechanistically, AT Taok3(-/-) Tregs were intrinsically more responsive to IL-33, through higher expression of ST2, and expressed more PPAR & gamma; and type 2 cytokines. Thus, TAOK3 inhibits adipose tissue Tregs and regulates immunometabolism under excessive caloric intake. Maes et al. reveal an unexpected role of TAOK3 in regulating ST2(+) regulatory T cells in mouse adipose tissue. Absence of TAOK3 sustains Tregs in obesity and improves metabolic dysfunction

The hepatocyte IKK:NF-κB axis promotes liver steatosis by stimulating <i>de novo</i> lipogenesis and cholesterol synthesis

OBJECTIVE: Obesity-related chronic inflammation plays an important role in the development of Metabolic Associated Fatty Liver Disease (MAFLD). Although the contribution of the pro-inflammatory NF-κB signaling pathway to the progression from simple steatosis to non-alcoholic steatohepatitis (NASH) is well-established, its role as an initiator of hepatic steatosis and the underlying mechanism remains unclear. Here, we investigated the hypothesis that the hepatocytic NF-κB signaling pathway acts as a metabolic regulator, thereby promoting hepatic steatosis development. METHODS: A murine model expressing a constitutively active form of IKKβ in hepatocytes (Hep-IKKβca) was used to activate hepatocyte NF-κB. In addition, IKKβca was also expressed in hepatocyte A20-deficient mice (IKKβca;A20(LKO)). A20 is an NF-κB-target gene that inhibits the activation of the NF-κB signaling pathway upstream of IKKβ. These mouse models were fed a sucrose-rich diet for 8 weeks. Hepatic lipid levels were measured and using [1–(13)C]-acetate de novo lipogenesis and cholesterol synthesis rate were determined. Gene expression analyses and immunoblotting were used to study the lipogenesis and cholesterol synthesis pathways. RESULTS: Hepatocytic NF-κB activation by expressing IKKβca in hepatocytes resulted in hepatic steatosis without inflammation. Ablation of hepatocyte A20 in Hep-IKKβca mice (IKKβca;A20(LKO) mice) exacerbated hepatic steatosis, characterized by macrovesicular accumulation of triglycerides and cholesterol, and increased plasma cholesterol levels. Both De novo lipogenesis (DNL) and cholesterol synthesis were found elevated in IKKβca;A20(LKO) mice. Phosphorylation of AMP-activated kinase (AMPK) - a suppressor in lipogenesis and cholesterol synthesis - was decreased in IKKβca;A20(LKO) mice. This was paralleled by elevated protein levels of hydroxymethylglutaryl-CoA synthase 1 (HMGCS1) and reduced phosphorylation of HMG-CoA reductase (HMGCR) both key enzymes in the cholesterol synthesis pathway. Whereas inflammation was not observed in young IKKβca;A20(LKO) mice sustained hepatic NF-κB activation resulted in liver inflammation, together with elevated hepatic and plasma cholesterol levels in middle-aged mice. CONCLUSIONS: The hepatocytic IKK:NF-κB axis is a metabolic regulator by controlling DNL and cholesterol synthesis, independent of its central role in inflammation. The IKK:NF-κB axis controls the phosphorylation levels of AMPK and HMGCR and the protein levels of HMGCS1. Chronic IKK-mediated NF-κB activation may contribute to the initiation of hepatic steatosis and cardiovascular disease risk in MAFLD patients

Epithelial HMGB1 delays skin wound healing and drives tumor initiation by priming neutrophils for NET formation

Regenerative responses predispose tissues to tumor formation by largely unknown mechanisms. High-mobility group box 1 (HMGB1) is a danger-associated molecular pattern contributing to inflammatory pathologies. We show that HMGB1 derived from keratinocytes, but not myeloid cells, delays cutaneous wound healing and drives tumor formation. In wounds of mice lacking HMGB1 selectively in keratinocytes, a marked reduction in neutrophil extracellular trap (NET) formation is observed. Pharmacological targeting of HMGB1 or NETs prevents skin tumorigenesis and accelerates wound regeneration. HMGB1-dependent NET formation and skin tumorigenesis is orchestrated by tumor necrosis factor (TNF) and requires RIPK1 kinase activity. NETs are present in the microenvironment of keratinocyte-derived tumors in mice and lesional and tumor skin of patients suffering from recessive dystrophic epidermolysis bullosa, a disease in which skin blistering predisposes to tumorigenesis. We conclude that tumorigenicity of the wound microenvironment depends on epithelial-derived HMGB1 regulating NET formation, thereby establishing a mechanism linking reparative inflammation to tumor initiation