Providing person-centered care for patients with complex healthcare needs: A qualitative study

Background People with chronic conditions have complex healthcare needs that lead to challenges for adequate healthcare provision. Current healthcare services do not always respond adequately to their needs. A modular perspective, in particular providing visualization of the modular service architecture, is promising for improving the responsiveness of healthcare services to the complex healthcare needs of people with chronic conditions. The modular service architecture provides a comprehensive representation of the components and modules of healthcare provision. In this study, we explore this further in a qualitative multiple case study on healthcare provision for children with Down syndrome in the Netherlands. Methods Data collection for four cases involved 53 semi-structured interviews with healthcare professionals and 21 semi-structured interviews with patients (the parents of children with Down syndrome as proxy). In addition, we gathered data by means of practice observations and analysis of relevant documents. The interviews were audio-recorded, transcribed verbatim and analyzed utilizing the Miles and Huberman approach. Results Our study shows that the perspectives on healthcare provision of professionals and patients differ substantially. The visualization of the modular service architecture that was based on the healthcare professionals’ perspective provided a complete representation of (para)medical outcomes relevant to the professionals’ own discipline. In contrast, the modular service architecture based on the patients’ perspective, which we define as a person-centered modular service architecture, provided a representation of the healthcare service that was primarily based on functional outcomes and the overall wellbeing of the patients. Conclusion Our study shows that visualization of the modular service architecture can be a useful tool to better address the complex needs and requirements of people with a chronic condition. We suggest that a person-centered modular service architecture that focuses on functional outcomes and overall wellbeing, enables increased responsiveness of healthcare services to people with complex healthcare needs and provision of truly person-centered care

Decreased STARD10 expression is associated with defective insulin secretion in humans and mice

Genetic variants near ARAP1 (CENTD2) and STARD10 influence type 2 diabetes (T2D) risk. The risk alleles impair glucose-induced insulin secretion and, paradoxically but characteristically, are associated with decreased proinsulin:insulin ratios, indicating improved proinsulin conversion. Neither the identity of the causal variants nor the gene(s) through which risk is conferred have been firmly established. Whereas ARAP1 encodes a GTPase activating protein, STARD10 is a member of the steroidogenic acute regulatory protein (StAR)-related lipid transfer protein family. By integrating genetic fine-mapping and epigenomic annotation data and performing promoter-reporter and chromatin conformational capture (3C) studies in β cell lines, we localize the causal variant(s) at this locus to a 5 kb region that overlaps a stretch-enhancer active in islets. This region contains several highly correlated T2D-risk variants, including the rs140130268 indel. Expression QTL analysis of islet transcriptomes from three independent subject groups demonstrated that T2D-risk allele carriers displayed reduced levels of STARD10 mRNA, with no concomitant change in ARAP1 mRNA levels. Correspondingly, β-cell-selective deletion of StarD10 in mice led to impaired glucose-stimulated Ca2+ dynamics and insulin secretion and recapitulated the pattern of improved proinsulin processing observed at the human GWAS signal. Conversely, overexpression of StarD10 in the adult β cell improved glucose tolerance in high fat-fed animals. In contrast, manipulation of Arap1 in β cells had no impact on insulin secretion or proinsulin conversion in mice. This convergence of human and murine data provides compelling evidence that the T2D risk associated with variation at this locus is mediated through reduction in STARD10 expression in the β cell

Corporate environmental responsibility and criminology

This article addresses corporate environmental responsibility (CER) and aims to present a criminological analysis of it. We studied the opinion of a number of principle actors involved in CER in Europe in order to determine how they perceive it in terms of its definition, aetiology and approaches. For each of these dimensions we relate back to a criminological framework to ascertain how it is positioned in the green criminological debate. We start out by providing information on what corporate environmental responsibility is and how it relates to corporate social responsibility and sustainable development. Then we outline the theoretical framework in accordance with the three central themes for the criminological analysis of CER: definition, aetiology and approaches. We also explain the method that was used (semi-structured interviews). Next, we present the results according to the same threefold structure. Finally we discuss these results in a last part, which is divided in two. First, we look at the challenges that the criminological perspective poses for CER in terms of definition, aetiology and approaches. The second part of the discussion turns the question around and wonders how CER could contribute to greening criminology

Evaluation of two interaction techniques for visualization of dynamic graphs

Several techniques for visualization of dynamic graphs are based on different spatial arrangements of a temporal sequence of node-link diagrams. Many studies in the literature have investigated the importance of maintaining the user's mental map across this temporal sequence, but usually each layout is considered as a static graph drawing and the effect of user interaction is disregarded. We conducted a task-based controlled experiment to assess the effectiveness of two basic interaction techniques: the adjustment of the layout stability and the highlighting of adjacent nodes and edges. We found that generally both interaction techniques increase accuracy, sometimes at the cost of longer completion times, and that the highlighting outclasses the stability adjustment for many tasks except the most complex ones.Comment: Appears in the Proceedings of the 24th International Symposium on Graph Drawing and Network Visualization (GD 2016

Learning through assessment

This book aims to contribute to the discourse of learning through assessment within a self-directed learning environment. It adds to the scholarship of assessment and self-directed learning within a face-to-face and online learning environment. As part of the NWU Self-Directed Learning Book Series, this book is devoted to scholarship in the field of self-directed learning, focusing on ongoing and envisaged assessment practices for self-directed learning through which learning within the 21st century can take place. This book acknowledges and emphasises the role of assessment as a pedagogical tool to foster self-directed learning during face-to-face and online learning situations. The way in which higher education conceptualises teaching, learning and assessment has been inevitably changed due to the COVID- 19 pandemic, and now more than ever we need learners to be self-directed in their learning. Assessment plays a key role in learning and, therefore, we have to identify innovative ways in which learning can be assessed, and which are likely to become the new norm even after the pandemic has been brought under control. The goal of this book, consisting of original research, is to assist with the paradigm shift regarding the purpose of assessment, as well as providing new ideas on assessment strategies, methods and tools appropriate to foster self-directed learning in all modes of delivery

Learning through assessment

This book aims to contribute to the discourse of learning through assessment within a self-directed learning environment. It adds to the scholarship of assessment and self-directed learning within a face-to-face and online learning environment. As part of the NWU Self-Directed Learning Book Series, this book is devoted to scholarship in the field of self-directed learning, focusing on ongoing and envisaged assessment practices for self-directed learning through which learning within the 21st century can take place. This book acknowledges and emphasises the role of assessment as a pedagogical tool to foster self-directed learning during face-to-face and online learning situations. The way in which higher education conceptualises teaching, learning and assessment has been inevitably changed due to the COVID- 19 pandemic, and now more than ever we need learners to be self-directed in their learning. Assessment plays a key role in learning and, therefore, we have to identify innovative ways in which learning can be assessed, and which are likely to become the new norm even after the pandemic has been brought under control. The goal of this book, consisting of original research, is to assist with the paradigm shift regarding the purpose of assessment, as well as providing new ideas on assessment strategies, methods and tools appropriate to foster self-directed learning in all modes of delivery

Identification of a Novel β-Cell Glucokinase (GCK) Promoter Mutation (−71G>C) That Modulates GCK Gene Expression Through Loss of Allele-Specific Sp1 Binding Causing Mild Fasting Hyperglycemia in Humans

OBJECTIVE: Inactivating mutations in glucokinase (GCK) cause mild fasting hyperglycemia. Identification of a GCK mutation has implications for treatment and prognosis; therefore, it is important to identify these individuals. A significant number of patients have a phenotype suggesting a defect in glucokinase but no abnormality of GCK. We hypothesized that the GCK beta-cell promoter region, which currently is not routinely screened, could contain pathogenic mutations; therefore, we sequenced this region in 60 such probands. RESEARCH DESIGN AND METHODS: The beta-cell GCK promoter was sequenced in patient DNA. The effect of the identified novel mutation on GCK promoter activity was assessed using a luciferase reporter gene expression system. Electrophoretic mobility shift assays (EMSAs) were used to determine the impact of the mutation on Sp1 binding. RESULTS: A novel -71G>C mutation was identified in a nonconserved region of the human promoter sequence in six apparently unrelated probands. Family testing established cosegregation with fasting hyperglycemia (> or = 5.5 mmol/l) in 39 affected individuals. Haplotype analysis in the U.K. family and four of the Slovakian families demonstrated that the mutation had arisen independently. The mutation maps to a potential transcriptional activator binding site for Sp1. Reporter assays demonstrated that the mutation reduces promoter activity by up to fourfold. EMSAs demonstrated a dramatic reduction in Sp1 binding to the promoter sequence corresponding to the mutant allele. CONCLUSIONS: A novel beta-cell GCK promoter mutation was identified that significantly reduces gene expression in vitro through loss of regulation by Sp1. To ensure correct diagnosis of potential GCK-MODY (maturity-onset diabetes of the young) cases, analysis of the beta-cell GCK promoter should be included

Cellular characterisation of the GCKR P446L variant associated with type 2 diabetes risk

Aims/hypothesis Translation of genetic association signals into molecular mechanisms for diabetes has been slow. The glucokinase regulatory protein (GKRP; gene symbol GCKR) P446L variant, associated with inverse modulation of glucose- and lipid-related traits, has been shown to alter the kinetics of glucokinase (GCK) inhibition. As GCK inhibition is associated with nuclear sequestration, we aimed to determine whether this variant also alters the direct interaction between GKRP and GCK and their intracellular localisation. Methods Fluorescently tagged rat and human wild-type (WT)- or P446L-GCKR and GCK were transiently transfected into HeLa cells and mouse primary hepatocytes. Whole-cell and nuclear fluorescence was quantified in individual cells exposed to low- or high-glucose conditions (5.5 or 25 mmol/l glucose, respectively). Interaction between GCK and GKRP was measured by sensitised emission-based fluorescence resonance energy transfer (FRET) efficiency