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Being digitally competent is an imperative requirement for the 21st century university teacher, a fact recognized by both the literature and policymakers. Although this topic has been addressed in different reviews and critical studies recently, none of them have systematically and explicitly addressed the factors that explain, or are explained by, the digital competencies of university teachers. Examples of these factors include, among others, demographic, professional and psychological aspects of university teachers, as well as very specific digital competencies. The present study seeks to close this gap through a systematic mapping of the literature published until 2021 in journals indexed by Scopus and Web of Science (WOS). Based on the selection of 53 primary studies, we characterized the literature and summarized the main results reported so far. The analysis allowed us to conclude the following: (1) there is a growing number of contributions aimed at understanding the acquisition of digital competencies, especially from external factors; (2) European, and more specifically Spanish, university teachers from multiple disciplines are the most studied population; (3) most studies adopted quantitative approaches to explain but not prove causality; (4) there is a great heterogeneity of relationships and results that explain the digital competencies of university professors. The implications of these results are discussed with a view to identifying the gaps that provide scope for future research.

Evaluating digital competencies has become a topic of growing interest in recent years. Although several reviews and studies have summarized the main elements of progress and shortcomings in this area, some issues are yet to be explored. Very little information is available about the ways of ensuring the validity and reliability of the instrument used. This study addresses this issue through systematic mapping covering the period from January 2015 to July 2020. Based on 88 primary studies, we conclude that a growing number of studies have emerged over the years; most of them are based on European university students in social science programs; the quality of the journals where they were published is low; and the instruments used are mostly questionnaires and ad-hoc surveys that measure the various dimensions of digital competence based on participants' perceptions. Out of the eight possible types of quality assessment, studies commonly report only four (one in the case of reliability and three in the case of validity). More than 50% of the studies do not provide evidence of having assessed the reliability and validity at the same time. Although participant discipline resulted in a significantly association with the practice of reporting reliability and validity assessments, no specific dimension explained such association. A non-parametric multivariate analysis reveals, among other interesting patterns, that the practice of not reporting quality assessments is more present in studies where participants belong to the fields of Engineering and Technology, Health Sciences, and Humanities.

To better understand radiation-induced organ dysfunction at both high and low doses, it is critical to understand how endothelial cells (ECs) respond to radiation. The impact of irradiation (IR) on ECs varies depending on the dose administered. High doses can directly damage ECs, leading to EC impairment. In contrast, the effects of low doses on ECs are subtle but more complex. Low doses in this study refer to radiation exposure levels that are below those that cause immediate and necrotic damage. Mitochondria are the primary cellular components affected by IR, and this study explored their role in determining the effect of radiation on microvascular endothelial cells. Human dermal microvascular ECs (HMEC-1) were exposed to varying IR doses ranging from 0.1 Gy to 8 Gy (~0.4 Gy/min) in the AFRRI 60-Cobalt facility. Results indicated that high doses led to a dose-dependent reduction in cell survival, which can be attributed to factors such as DNA damage, oxidative stress, cell senescence, and mitochondrial dysfunction. However, low doses induced a small but significant increase in cell survival, and this was achieved without detectable DNA damage, oxidative stress, cell senescence, or mitochondrial dysfunction in HMEC-1. Moreover, the mitochondrial morphology was assessed, revealing that all doses increased the percentage of elongated mitochondria, with low doses (0.25 Gy and 0.5 Gy) having a greater effect than high doses. However, only high doses caused an increase in mitochondrial fragmentation/swelling. The study further revealed that low doses induced mitochondrial elongation, likely via an increase in mitochondrial fusion protein 1 (Mfn1), while high doses caused mitochondrial fragmentation via a decrease in optic atrophy protein 1 (Opa1). In conclusion, the study suggests, for the first time, that changes in mitochondrial morphology are likely involved in the mechanism for the radiation dose-dependent effect on the survival of microvascular endothelial cells. This research, by delineating the specific mechanisms through which radiation affects endothelial cells, offers invaluable insights into the potential impact of radiation exposure on cardiovascular health. [ABSTRACT FROM AUTHOR]

Copyright of Opuntia Brava is the property of Universidad de Ciencias Pedagogicas de Las Tunas, Centro de Documentacion e Informacion Pedagogica and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista de Estudios Políticos is the property of Centro de Estudios Politicos y Constitucionales and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Opuntia Brava is the property of Universidad de Ciencias Pedagogicas de Las Tunas, Centro de Documentacion e Informacion Pedagogica and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Dysregulation of cholesterol homeostasis is associated with many diseases such as cardiovascular disease and cancer. Liver X receptors (LXRs) are major upstream regulators of cholesterol homeostasis and are activated by endogenous cholesterol metabolites such as 27-hydroxycholesterol (27HC). LXRs and various LXR ligands such as 27HC have been described to influence several extra-hepatic biological systems. However, disparate reports of LXR function have emerged, especially with respect to immunology and cancer biology. This would suggest that, similar to steroid nuclear receptors, the LXRs can be selectively modulated by different ligands. Here, we use RNA-sequencing of macrophages and single-cell RNA-sequencing of immune cells from metastasis-bearing murine lungs to provide evidence that LXR satisfies the 2 principles of selective nuclear receptor modulation: (1) different LXR ligands result in overlapping but distinct gene expression profiles within the same cell type, and (2) the same LXR ligands differentially regulate gene expression in a highly context-specific manner, depending on the cell or tissue type. The concept that the LXRs can be selectively modulated provides the foundation for developing precision pharmacology LXR ligands that are tailored to promote those activities that are desirable (proimmune), but at the same time minimizing harmful side effects (such as elevated triglyceride levels). [ABSTRACT FROM AUTHOR]

Copyright of Comprendre: Revista Catalana de Filosofía is the property of Herder Editorial S.L. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista de Estudios Políticos is the property of Centro de Estudios Politicos y Constitucionales and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)