Evaluating an Institutional Response to Generative Artificial Intelligence (GenAI): Applying Kotter’s Change Model and Sharing Lessons Learned for Educational Development

Copyright (c) 2023 Jackie Potter, Katharine Welsh, Laura MilneSince the launch of ChatGPT in November 2022, there has been a dawning understanding in the higher education sector of ways Generative artificial intelligence (GenAI) tools can challenge the traditional roles of academic teaching staff (e.g., Chan and Tsi, 2023) and support learning by students. For example, Mike Sharples in Sabzalieva and Valentini (2023) identifies ten roles that ChatGPT can play which would all support student learners. Media and sector concern has focused on whether GenAI use by students would disrupt the integrity of degrees and awards and there is a good deal of debate on how to adapt assessment, learning outcomes and curricula to reflect and reward unique human competences associated with a discipline or subject and embrace students’ use of GenAI. Educational development colleagues have been at the vanguard of leading higher education provider reactions and responses to the widespread availability and capabilities of GenAI. This case study reflects on a year of action to lead teaching staff and students as well as institutional policy and practice through a series of steps to enable rapid, proportionate and robust change. We apply Kotter’s (1996) eight stage change model to reflect on the activities, achievements and challenges to date. We do not purport to have finished but rather can see, one year in, that increasingly activity is more embedded into structures, routines, the practice of others, and our work as educational developers. We reflect forward too on the ways we will act next to ‘make change stick’ and on our own personal, professional journeys as educational change leaders, all of whom were new appointments in the educational development centre. We chart how we have been able to innovate and to lead complex educational change at pace

Reduced Interhemispheric Functional Connectivity in the Motor Cortex during Rest in Limb-Onset Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder of motor neurons that leads to paralysis and eventually death. There is evidence that atrophy occurs in the primary motor cortex (M1), but it is unclear how the disease affects the intrinsic connectivity of this structure. Thus, the goal of this study was to examine interhemispheric coupling of low frequency blood-oxygen-level dependent (BOLD) signal fluctuations in M1 using functional connectivity magnetic resonance imaging during rest. Because disease progression is rapid, high-functioning patients were recruited to assess neural changes in the relatively early stages of ALS. Twenty patients with limb-onset ALS participated in this study. A parceling technique was employed to segment both precentral gyri into multiple regions of interest (ROI), thus increasing sensitivity to detect changes that exist along discretely localized regions of the motor cortex. We report an overall systemic decrease in functional connectivity between right and left motor cortices in patients with limb-onset ALS. Additionally, we observed a pronounced disconnection between dorsal ROI pairs in the ALS group compared to the healthy control group. Furthermore, measures of limb functioning correlated with the connectivity data from dorsal ROI pairs in the ALS group, suggesting a symptomatic relationship with interhemispheric M1 connectivity

Using Virtual Markets to Program Global Behavior in Sensor Networks

This paper presents market-based macroprogramming (MBM), a new paradigm for achieving globally efficient behavior in sensor networks. Rather than programming the individual, low-level behaviors of sensor nodes, MBM defines a virtual market where nodes sell "actions" (such as taking a sensor reading or aggregating data) in response to global price information. Nodes take actions to maximize their own utility, subject to energy budget constraints. The behavior of the network is determined by adjusting the price vectors for each action, rather than by directly specifying local node actions, resulting in a globally efficient allocation of network resources. We present the market-based macro-programming paradigm, as well as several experiments demonstrating its value for a sensor network vehicle tracking application.Engineering and Applied Science

Detecting rare asymmetrically methylated cytosines and decoding methylation patterns in the honeybee genome

Context-dependent gene expression in eukaryotes is controlled by several mechanisms including cytosine methylation that primarily occurs in the CG dinucleotides (CpGs). However, less frequent non-CpG asymmetric methylation has been found in various cell types, such as mammalian neurons, and recent results suggest that these sites can repress transcription independently of CpG contexts. In addition, an emerging view is that CpG hemimethylation may arise not only from deregulation of cellular processes but also be a standard feature of the methylome. Here, we have applied a novel approach to examine whether asymmetric CpG methylation is present in a sparsely methylated genome of the honeybee, a social insect with a high level of epigenetically driven phenotypic plasticity. By combining strand-specific ultra-deep amplicon sequencing of illustrator genes with whole-genome methylomics and bioinformatics, we show that rare asymmetrically methylated CpGs can be unambiguously detected in the honeybee genome. Additionally, we confirm differential methylation between two phenotypically and reproductively distinct castes, queens and workers, and offer new insight into the heterogeneity of brain methylation patterns. In particular, we challenge the assumption that symmetrical methylation levels reflect symmetry in the underlying methylation patterns and conclude that hemimethylation may occur more frequently than indicated by methylation levels. Finally, we question the validity of a prior study in which most of cytosine methylation in this species was reported to be asymmetric

Some inequalities for the Tutte polynomial

We prove that the Tutte polynomial of a coloopless paving matroid is convex along the portions of the line segments x+y=p lying in the positive quadrant. Every coloopless paving matroids is in the class of matroids which contain two disjoint bases or whose ground set is the union of two bases of M*. For this latter class we give a proof that T_M(a,a) <= max {T_M(2a,0), T_M(0,2a)} for a >= 2. We conjecture that T_M(1,1) <= max {T_M(2,0), T_M(0,2)} for the same class of matroids. We also prove this conjecture for some families of graphs and matroids.Comment: 17 page

The Neuromodulator Adenosine Regulates Oligodendrocyte Migration at Motor Exit Point Transition Zones

During development, oligodendrocyte progenitor cells (OPCs) migrate extensively throughout the spinal cord. However, their migration is restricted at transition zones (TZs). At these specialized locations, unique glial cells in both zebrafish and mice play a role in preventing peripheral OPC migration, but the mechanisms of this regulation are not understood. To elucidate the mechanisms that mediate OPC segregation at motor exit point (MEP) TZs, we performed an unbiased small-molecule screen. Using chemical screening and in vivo imaging, we discovered that inhibition of A2a adenosine receptors (ARs) causes ectopic OPC migration out of the spinal cord. We provide in vivo evidence that neuromodulation, partially mediated by adenosine, influences OPC migration specifically at the MEP TZ. This work opens exciting possibilities for understanding how OPCs reach their final destinations during development and identifies mechanisms that could promote their migration in disease

Émile Bernard. Au-delà de Pont-Aven

La personnalité et l’œuvre d’Émile Bernard constituent un véritable « cas » dans l’histoire de l’art moderne, susceptible en cela d’intéresser au premier chef les historiens de l’art. Voilà en effet un homme qui a fréquenté quelques-uns uns des plus grands artistes de son temps, Gauguin, Van Gogh, Toulouse-Lautrec, Cézanne, un homme qui a été au cœur des recherches avant-gardistes du groupe de Pont-Aven, qui a eu affaire aux grands marchands parisiens, Le Barc de Bouteville et Ambroise Vollard, et qui décide à un moment donné de se tourner résolument vers le passé pour essayer de retrouver ce qu’il croit définitivement perdu : la foi et le métier des maîtres anciens, pour tenir un discours de plus en plus réactionnaire sur les arts de son temps et renier les expériences de sa jeunesse. Si l’on ne saurait dire la part prise par le dépit de se sentir injustement méconnu dans cette singulière décision, il est certain qu’elle causa la mise à l’écart de l’artiste dans l’histoire canonique de la peinture du XXe siècle. L’exposition que présente aujourd’hui l’INHA porte précisément sur ce point, en s’efforçant d’éclairer tout le parcours d’Émile Bernard et en mettant en évidence, auprès de trois tableaux (dont un bel Autoportrait), l’un des points incontestablement forts de sa création, son œuvre magistral de graveur et de lithographe, notamment comme illustrateur de livres

The complex interplay between kidney injury and inflammation

Abstract Acute kidney injury (AKI) has gained significant attention following patient safety alerts about the increased risk of harm to patients, including increased mortality and hospitalization. Common causes of AKI include hypovolaemia, nephrotoxic medications, ischaemia and acute glomerulonephritis, although in reality it may be undetermined or multifactorial. A period of inflammation either as a contributor to the kidney injury or resulting from the injury is almost universally seen. This article was compiled following a workshop exploring the interplay between injury and inflammation. AKI is characterized by some degree of renal cell death through either apoptosis or necrosis, together with a strong inflammatory response. Studies interrogating the resolution of renal inflammation identify a whole range of molecules that are upregulated and confirm that the kidneys are able to intrinsically regenerate after an episode of AKI, provided the threshold of damage is not too high. Kidneys are unable to generate new nephrons, and dysfunctional or repeated episodes will lead to further nephron loss that is ultimately associated with the development of renal fibrosis and chronic kidney disease (CKD). The AKI to CKD transition is a complex process mainly facilitated by maladaptive repair mechanisms. Early biomarkers mapping out this process would allow a personalized approach to identifying patients with AKI who are at high risk of developing fibrosis and subsequent CKD. This review article highlights this process and explains how laboratory models of renal inflammation and injury assist with understanding the underlying disease process and allow interrogation of medications aimed at targeting the mechanistic interplay.</jats:p