Social media interaction, the university brand and recruitment performance

yesCommentators and academics now refer to Higher Education (HE) as a market and the language of the market frames and describes the sector. Considerable competition for students exists and the marketplace is global as institutions compete for students not just from their own country, but from the lucrative international market. Universities are aware of the importance of their reputations, but to what extent are they utilizing branding activity to deal with such competitive threats? Can institutions with lower reputational capital compete for students by increasing their brand presence? This study provides evidence from research into social media related branding activity from 56 UK universities and considers the impact of this activity, in particular social media interaction and social media validation, on performance in terms of student recruitment. The results demonstrate a positive effect for the use of social media on brand performance, especially when an institution attracts a large number of Likes on Facebook and a high number of Followers on Twitter. A particularly strong and positive effect results when universities use social media interactively

Role of microRNAs in the age-associated decline of pancreatic beta cell function in rat islets

This is a freely-available open access publication. Please cite the published version which is available via the DOI link in this record.AIMS/HYPOTHESIS: Ageing can lead to reduced insulin sensitivity and loss of pancreatic beta cell function, predisposing individuals to the development of diabetes. The aim of this study was to assess the contribution of microRNAs (miRNAs) to age-associated beta cell dysfunction. METHODS: The global mRNA and miRNA profiles of 3- and 12-month-old rat islets were collected by microarray. The functional impact of age-associated differences in miRNA expression was investigated by mimicking the observed changes in primary beta cells from young animals. RESULTS: Beta cells from 12-month-old rats retained normal insulin content and secretion, but failed to proliferate in response to mitotic stimuli. The islets of these animals displayed modifications at the level of several miRNAs, including upregulation of miR-34a, miR-124a and miR-383, and downregulation of miR-130b and miR-181a. Computational analysis of the transcriptomic modifications observed in the islets of 12-month-old rats revealed that the differentially expressed genes were enriched for miR-34a and miR-181a targets. Indeed, the induction of miR-34a and reduction of miR-181a in the islets of young animals mimicked the impaired beta cell proliferation observed in old animals. mRNA coding for alpha-type platelet-derived growth factor receptor, which is critical for compensatory beta cell mass expansion, is directly inhibited by miR34a and is likely to be at least partly responsible for the effects of this miRNA. CONCLUSIONS/INTERPRETATION: Changes in the level of specific miRNAs that occur during ageing affect the proliferative capacity of beta cells. This might reduce their ability to expand under conditions of increased insulin demand, favouring the development of type 2 diabetes.Swiss National Science FoundationFondation Francophone pour la Recherche sur le DiabèteWellcome Trust Senior Investigator AwardMRC Programme GrantRoyal Society Wolfson Research Merit AwardWellcome Trust project gran

Learning safely from error: Reconsidering the ethics of simulation-based medical education through ethnography

‘Human factors’ is an influential rationale in the UK national health service to understand mistakes, risk and safety. Although there have been studies examining its implications in workplaces, there has been little investigation of how it is taught, as a form of professional morality. This article draws on an observational study of human factors teaching in four hospital simulation centres in London, UK. Its main argument is that the teaching of human factors is realised through an identification and positive evaluation of ‘non-technical skills’ and the espousal of ‘non-judgemental’ pedagogy, both of which mean that mistakes cannot be made. Professional solidarity is then maintained on the absence of mistakes. We raise questions about the ethics of this teaching. The study is situated within a history of ethnographic accounts of medical mistakes, to explore the relationship between claims to professional knowledge and claims about failure

Coloring Mixed and Directional Interval Graphs

A mixed graph has a set of vertices, a set of undirected egdes, and a set ofdirected arcs. A proper coloring of a mixed graph $G$ is a function $c$ thatassigns to each vertex in $G$ a positive integer such that, for each edge $uv$in $G$, $c(u) \ne c(v)$ and, for each arc $uv$ in $G$, $c(u) mixed graph$G$, the chromatic number$\chi(G)$is the smallest number ofcolors in any proper coloring of$G$. A directional interval graph is a mixedgraph whose vertices correspond to intervals on the real line. Such a graph hasan edge between every two intervals where one is contained in the other and anarc between every two overlapping intervals, directed towards the interval thatstarts and ends to the right. Coloring such graphs has applications in routing edges in layered orthogonalgraph drawing according to the Sugiyama framework; the colors correspond to thetracks for routing the edges. We show how to recognize directional intervalgraphs, and how to compute their chromatic number efficiently. On the otherhand, for mixed interval graphs, i.e., graphs where two intersecting intervalscan be connected by an edge or by an arc in either direction arbitrarily, weprove that computing the chromatic number is NP-hard.<br

Beiträge zur Kenntnis der Vanadinverbindungen

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Limited impact on glucose homeostasis of leptin receptor deletion from insulin- or proglucagon-expressing cells

Aims/hypothesis The adipose tissue-derived hormone leptin plays an important role in the maintenance of body weight and glucose homeostasis. Leptin mediates its effects by interaction with leptin receptors (LepRb), which are highly expressed in the hypothalamus and other brain centres, and at lower levels in the periphery. Previous studies have used relatively promiscuous or inefficient Cre deleter strains, respectively, to explore the roles of LepR in pancreatic β and α cells. Here, we use two newly-developed Cre lines to explore the role of leptin signalling in insulin and proglucagon-expressing cells. Methods Leptin receptor expression was measured in isolated mouse islets and highly-purified islet cells by RNASeq and quantitative RT-PCR. Mice lacking leptin signalling in pancreatic β, or in α and other proglucagon-expressing cells, were generated using Ins1Cre- or iGluCre-mediated recombination respectively of flox'd leptin receptor alleles. In vivo glucose homeostasis, changes in body weight, pancreatic histology and hormone secretion from isolated islets were assessed using standard techniques. Results Leptin receptor mRNA levels were at or below the level of detection in wild-type adult mouse isolated islets and purified cells, and leptin signalling to Stat3 phosphorylation was undetectable. Whereas male mice further deleted for leptin receptors in β cells exhibited no abnormalities in glucose tolerance up to 16 weeks of age, females transiently displayed improved glucose tolerance at 8 weeks (11.2 ± 3.2% decrease in area under curve; p < 0.05), and improved (39.0 ± 13.0%, P < 0.05) glucose-stimulated insulin secretion in vitro. No differences were seen between genotypes in body weight, fasting glucose or β/α cell ratio. Deletion of LepR from α-cells, a minority of β cells, and a subset of proglucagon-expressing cells in the brain, exerted no effects on body weight, glucose or insulin tolerance, nor on pancreatic hormone secretion assessed in vivo and in vitro. Conclusions/interpretation The use here of a highly selective Cre recombinase indicates that leptin signalling plays a relatively minor, age- and sex-dependent role in the control of β cell function in the mouse. No in vivo role for leptin receptors on α cells, nor in other proglucagon-expressing cells, was detected in this study