Investigating the possibilities of using patient-generated health data in emergency care: an explorative study

AbstractIt is well known that emergency departments (EDs) are exposed to human errors and unintended events due to large patient flow, high work pressure and overload of information. Strategies for providing efficient and effective health care are therefore imperative, and health information technologies are suggested to be one of the solutions. This study sought to investigate if the use of patient-generated health data gathered through a digital patient questionnaire and visualised as a patient-generated journal (PGJ v.1.0) has the potential to improve the care delivered in EDs.MethodsUsing a mixed-method approach, the PGJ (v.1.0) was investigatedfrom key stakeholders’ perspectives. First, we examined the PGJ from a patient perspective via participant observation (n = 18) and interviews (n = 18), supported by statistical data from the PGJ (n = 56). Second, we used questionnaires to explore the physicians’ perspectives (n = 9). Lastly, two interviews were conducted with healthcare leaders from the ED. The data were compared and analysed using descriptive statistics and hermeneutic analysis.Results From the findings, it appears that patients in need of urgent care accept the use of patient-generated data, and patients highly favoured being active in their patient pathway. However, the system needed some adjustments to fit the patients’abilities in urgent situations.The physicians expressed mixed attitudes towards the PGJ: the majority agreed that the system needed some adjustments in order for the full benefits to be gained, but thought that it had potential to improve their work processes when fully developed.Conclusions This study concludes that the use of patient-generated data is well accepted by patients in an urgent setting, and that the PGJ has the potential to improve quality of care in patient pathways by adding value to patient flows as well as clinical workflows. The concept of utilising patient-generated health data in emergency care should therefore be further developed and investigated

Recent Advances and Prospects in the Differentiation of Pancreatic Cells From Human Embryonic Stem Cells

Recent studies with human embryonic stem (hES) cells have established new protocols for substantial generation of pancreatic progenitors from definitive endoderm. These findings add to the efficient derivation of definitive endoderm, which is controlled by Wnt and Nodal pathways, and delineate a step forward in the quest for alternative β-cell sources. It also indicates that critical refining of the available strategies might help define a universal protocol for pancreatic differentiation applicable to several cell lines, therefore offering the possibility for transplantation of immune-matched or patient-specific hES–derived β-cells. We appraise here the fundamental role that bone morphogenetic protein, fibroblast growth factor, and retinoid signaling play during pancreas development, and describe a fundamental emergence of their combination in recent studies that generated pancreatic cells from hES cells. We finally enumerate some prospects that might improve further differentiation of the progenitor cells into functional β-cells needed in diabetes cell therapy

FGF10 maintains distal lung bud epithelium and excessive signaling leads to progenitor state arrest, distalization, and goblet cell metaplasia

<p>Abstract</p> <p>Background</p> <p>Interaction with the surrounding mesenchyme is necessary for development of endodermal organs, and Fibroblast growth factors have recently emerged as mesenchymal-expressed morphogens that direct endodermal morphogenesis. The fibroblast growth factor 10 (<it>Fgf10</it>) null mouse is characterized by the absence of lung bud development. Previous studies have shown that this requirement for <it>Fgf10 </it>is due in part to its role as a chemotactic factor during branching morphogenesis. In other endodermal organs <it>Fgf10 </it>also plays a role in regulating differentiation.</p> <p>Results</p> <p>Through gain-of-function analysis, we here find that FGF10 inhibits differentiation of the lung epithelium and promotes distalization of the embryonic lung. Ectopic expression of FGF10 in the lung epithelium caused impaired lung development and perinatal lethality in a transgenic mouse model. Lung lobes were enlarged due to increased interlobular distance and hyperplasia of the airway epithelium. Differentiation of bronchial and alveolar cell lineages was inhibited. The transgenic epithelium consisted predominantly of proliferating progenitor-like cells expressing Pro-surfactant protein C, TTF1, PEA3 and Clusterin similarly to immature distal tip cells. Strikingly, goblet cells developed within this arrested epithelium leading to goblet cell hyperplasia.</p> <p>Conclusion</p> <p>We conclude that FGF10 inhibits terminal differentiation in the embryonic lung and maintains the distal epithelium, and that excessive levels of FGF10 leads to metaplastic differentiation of goblet cells similar to that seen in chronic inflammatory diseases.</p

Genome-scale mechanistic modeling of signaling pathways made easy: a Bioconductor / cytoscape / web server framework for the analysis of omic data

Genome-scale mechanistic models of pathways are gaining importance for genomic data interpretation because they provide a natural link between genotype measurements (transcriptomics or genomics data) and the phenotype of the cell (its functional behavior). Moreover, mechanistic models can be used to predict the potential effect of interventions, including drug inhibitions. Here, we present the implementation of a mechanistic model of cell signaling for the interpretation of transcriptomic data as an R/Bioconductor package, a Cytoscape plugin and a web tool with enhanced functionality which includes building interpretable predictors, estimation of the effect of perturbations and assessment of the effect of mutations in complex scenarios

Fibroblast growth factor 10 represses premature cell differentiation during establishment of the intestinal progenitor niche

Spatio-temporal regulation of the balance between cell renewal and cell differentiation is of vital importance for embryonic development and adult homeostasis. Fibroblast growth factor signaling relayed from the mesenchyme to the epithelium is necessary for progenitor maintenance during organogenesis of most endoderm-derived organs, but it is still ambiguous whether the signal is exclusively mitogenic. Furthermore, the downstream mechanisms are largely unknown. In order to elucidate these questions we performed a complementary analysis of fibroblast growth factor 10 (Fgf10), gain-of-function and loss-of-function in the embryonic mouse duodenum, where the progenitor niche is clearly defined and differentiation proceeds in a spatially organized manner. In agreement with a role in progenitor maintenance, FGF10 is expressed in the duodenal mesenchyme during early development while the cognate receptor FGFR2b is expressed in the epithelial progenitor niche. Fgf10 gain-of-function in the epithelium leads to spatial expansion of the progenitor niche and repression of cell differentiation, while loss-of-function results in premature cell differentiation and subsequent epithelial hypoplasia. We conclude that FGF10 mediated mesenchymal-to-epithelial signaling maintains the progenitor niche in the embryonic duodenum primarily by repressing cell differentiation, rather than through mitogenic signaling. Furthermore, we demonstrate that FGF10-signaling targets include ETS-family transcription factors, which have previously been shown to regulate epithelial maturation and tumor progression. (C) 2010 Elsevier Inc. All rights reserved