The role of emotions in educational processes: the conceptions of teacher educators.

The research shows that a very important part of initial teacher education is to reformulate the beliefs that student teachers bring with them from their school experience. These beliefs, which are intuitive in nature, deal with different educational topics and one area that is currently of great importance, due to the emotional turn that the educational system is experiencing, are the beliefs that student teachers hold about the role of emotions in educational processes. In a world full of views that portray emotions as discrete states that are separate from cognitive processes, it is a priority for initial teacher development to train future teachers to hold conceptions that consider the deep emotional-cognitive integration that exists in the human brain. At the same time, this process requires teacher educators (hereafter referred to as TEs) who hold conceptions on this topic that are aligned with the most current scientific knowledge on the subject. However, we do not know how the conceptions that TEs maintain on this topic are, since, until now, research on conceptions has focused on other types of educational topics. Considering the foregoing, this study aimed to evaluate the conceptions that TEs have on this topic, using a questionnaire of dilemmas that was applied to 68 TEs from different universities. The results obtained show that the TEs maintain perspectives on the role of emotions in the teaching and learning processes that oscillate between dualism and emotional-cognitive integration. In addition, it was found that TEs' perspectives tend to be more integrative when considering attitudinal learning than when considering verbal learning. Finally, the study shows that maintaining integrative perspectives is more difficult when educational situations involve emotions of positive valence that may constitute an obstacle for teaching and learning. The results are discussed, and a series of reflections are elaborated in order to analyze to what extent the beliefs held by TEs are adequate as a cognitive basis for reformulating the conceptions held by student teachers on this issue.

Beijing's central role in global artificial intelligence research.

Nations worldwide are mobilizing to harness the power of Artificial Intelligence (AI) given its massive potential to shape global competitiveness over the coming decades. Using a dataset of 2.2 million AI papers, we study inter-city citations, collaborations, and talent migrations to uncover dependencies between Eastern and Western cities worldwide. Beijing emerges as a clear outlier, as it has been the most impactful city since 2007, the most productive since 2002, and the one housing the largest number of AI scientists since 1995. Our analysis also reveals that Western cities cite each other far more frequently than expected by chance, East-East collaborations are far more common than East-West or West-West collaborations, and migration of AI scientists mostly takes place from one Eastern city to another. We then propose a measure that quantifies each city's role in bridging East and West. Beijing's role surpasses that of all other cities combined, making it the central gateway through which knowledge and talent flow from one side to the other. We also track the center of mass of AI research by weighing each city's geographic location by its impact, productivity, and AI workforce. The center of mass has moved thousands of kilometers eastward over the past three decades, with Beijing's pull increasing each year. These findings highlight the eastward shift in the tides of global AI research, and the growing role of the Chinese capital as a hub connecting researchers across the globe.

Palmitic acid control of ciliogenesis modulates insulin signaling in hypothalamic neurons through an autophagy-dependent mechanism.

Palmitic acid (PA) is significantly increased in the hypothalamus of mice, when fed chronically with a high-fat diet (HFD). PA impairs insulin signaling in hypothalamic neurons, by a mechanism dependent on autophagy, a process of lysosomal-mediated degradation of cytoplasmic material. In addition, previous work shows a crosstalk between autophagy and the primary cilium (hereafter cilium), an antenna-like structure on the cell surface that acts as a signaling platform for the cell. Ciliopathies, human diseases characterized by cilia dysfunction, manifest, type 2 diabetes, among other features, suggesting a role of the cilium in insulin signaling. Cilium depletion in hypothalamic pro-opiomelanocortin (POMC) neurons triggers obesity and insulin resistance in mice, the same phenotype as mice deficient in autophagy in POMC neurons. Here we investigated the effect of chronic consumption of HFD on cilia; and our results indicate that chronic feeding with HFD reduces the percentage of cilia in hypothalamic POMC neurons. This effect may be due to an increased amount of PA, as treatment with this saturated fatty acid in vitro reduces the percentage of ciliated cells and cilia length in hypothalamic neurons. Importantly, the same effect of cilia depletion was obtained following chemical and genetic inhibition of autophagy, indicating autophagy is required for ciliogenesis. We further demonstrate a role for the cilium in insulin sensitivity, as cilium loss in hypothalamic neuronal cells disrupts insulin signaling and insulin-dependent glucose uptake, an effect that correlates with the ciliary localization of the insulin receptor (IR). Consistently, increased percentage of ciliated hypothalamic neuronal cells promotes insulin signaling, even when cells are exposed to PA. Altogether, our results indicate that, in hypothalamic neurons, impairment of autophagy, either by PA exposure, chemical or genetic manipulation, cause cilia loss that impairs insulin sensitivity.

Mechanobiology of Autophagy: The Unexplored Side of Cancer.

Proper execution of cellular function, maintenance of cellular homeostasis and cell survival depend on functional integration of cellular processes and correct orchestration of cellular responses to stresses. Cancer transformation is a common negative consequence of mismanagement of coordinated response by the cell. In this scenario, by maintaining the balance among synthesis, degradation, and recycling of cytosolic components including proteins, lipids, and organelles the process of autophagy plays a central role. Several environmental stresses activate autophagy, among those hypoxia, DNA damage, inflammation, and metabolic challenges such as starvation. In addition to these chemical challenges, there is a requirement for cells to cope with mechanical stresses stemming from their microenvironment. Cells accomplish this task by activating an intrinsic mechanical response mediated by cytoskeleton active processes and through mechanosensitive protein complexes which interface the cells with their mechano-environment. Despite autophagy and cell mechanics being known to play crucial transforming roles during oncogenesis and malignant progression their interplay is largely overlooked. In this review, we highlight the role of physical forces in autophagy regulation and their potential implications in both physiological as well as pathological conditions. By taking a mechanical perspective, we wish to stimulate novel questions to further the investigation of the mechanical requirements of autophagy and appreciate the extent to which mechanical signals affect this process.

Palmitic acid reduces the autophagic flux in hypothalamic neurons by impairing autophagosome-lysosome fusion and endolysosomal dynamics.

High-fat diet (HFD)-induced obesity is associated with increased cancer risk. Long-term feeding with HFD increases the concentration of the saturated fatty acid palmitic acid (PA) in the hypothalamus. We previously showed that, in hypothalamic neuronal cells, exposure to PA inhibits the autophagic flux, which is the whole autophagic process from the synthesis of the autophagosomes, up to their lysosomal fusion and degradation. However, the mechanism by which PA impairs autophagy in hypothalamic neurons remains unknown. Here, we show that PA-mediated reduction of the autophagic flux is not caused by lysosomal dysfunction, as PA treatment does not impair lysosomal pH or the activity of cathepsin B.Instead, PA dysregulates autophagy by reducing autophagosome-lysosome fusion, which correlates with the swelling of endolysosomal compartments that show areduction in their dynamics. Finally, because lysosomes undergo constant dynamic regulation by the small Rab7 GTPase, we investigated the effect of PA treatment on its activity. Interestingly, we found PA treatment altered the activity of Rab7. Altogether, these results unveil the cellular process by which PA exposure impairs the autophagic flux. As impaired autophagy in hypothalamic neurons promotes obesity, and balanced autophagy is required to inhibit malignant transformation, this could affect tumor initiation, progression, and/or response to therapy of obesity-related cancers.