Bridging the gap: scenario-based design as a solution for delayed access to users

Scenario-based design (Carroll & Rosson, 2002) is a Human-Computer Interaction methodology for considering the needs of potential users, without their direct input. Scenario-based design gives the interface designer the ability to create scenarios of use, along with postulations on the various types of users, expressed in the form of personas (Grudin & Pruitt, 2002). These scenarios and personas can be useful in the context of a design project, where real world issues preclude the direct involvement of users at a critical stage. By ‘walking through’ informal narrative descriptions in the form of a story, scenario-based design focuses on human activity rather than technology. We propose that scenario-based design can be utilised to fill gaps in a collaborative project, where, due to circumstances beyond the control of the designer, other parties have not provided vital information before the prototyping stage. Scenario-based design can allow us, as designers, to consider the needs of our potential users when circumstances mean that we would not otherwise be able to. While different disciplines utilise proprietary project management methods, scenario-based design bridges gaps between practice-specific epistemologies, allowing contributions from different fields to feed the project at any stage of its progress. This paper details our early reflections as designers working on an ARC Linking Grant-funded, interdisciplinary project to redesign a bushfire warning website. We explain that scenario-based design can act as a catalyst, to ‘kick-start’ a project where, due to various factors, timing or resources means that direct contact with users is not always possible

Tunneling anisotropic magnetoresistance in multilayer-(Co/Pt)/AlOx/Pt structures

We report observations of tunneling anisotropic magnetoresitance (TAMR) in vertical tunnel devices with a ferromagnetic multilayer-(Co/Pt) electrode and a non-magnetic Pt counter-electrode separated by an AlOx barrier. In stacks with the ferromagnetic electrode terminated by a Co film the TAMR magnitude saturates at 0.15% beyond which it shows only weak dependence on the magnetic field strength, bias voltage, and temperature. For ferromagnetic electrodes terminated by two monolayers of Pt we observe order(s) of magnitude enhancement of the TAMR and a strong dependence on field, temperature and bias. Discussion of experiments is based on relativistic ab initio calculations of magnetization orientation dependent densities of states of Co and Co/Pt model systems.Comment: 4 pages, 5 figures, to be published in Phys. Rev. Let

Production and optical properties of liquid scintillator for the JSNS2^{2} experiment

The JSNS$^{2}$ (J-PARC Sterile Neutrino Search at J-PARC Spallation Neutron Source) experiment will search for neutrino oscillations over a 24 m short baseline at J-PARC. The JSNS$^{2}$ inner detector will be filled with 17 tons of gadolinium-loaded liquid scintillator (LS) with an additional 31 tons of unloaded LS in the intermediate $\gamma$-catcher and outer veto volumes. JSNS$^{2}$ has chosen Linear Alkyl Benzene (LAB) as an organic solvent because of its chemical properties. The unloaded LS was produced at a refurbished facility, originally used for scintillator production by the RENO experiment. JSNS$^{2}$ plans to use ISO tanks for the storage and transportation of the LS. In this paper, we describe the LS production, and present measurements of its optical properties and long term stability. Our measurements show that storing the LS in ISO tanks does not result in degradation of its optical properties.Comment: 7 pages, 4 figures

Mitochondrial and apoptotic neuronal death signaling pathways in cerebral ischemia

AbstractMitochondria play important roles as the powerhouse of the cell. After cerebral ischemia, mitochondria overproduce reactive oxygen species (ROS), which have been thoroughly studied with the use of superoxide dismutase transgenic or knockout animals. ROS directly damage lipids, proteins, and nucleic acids in the cell. Moreover, ROS activate various molecular signaling pathways. Apoptosis-related signals return to mitochondria, then mitochondria induce cell death through the release of pro-apoptotic proteins such as cytochrome c or apoptosis-inducing factor. Although the mechanisms of cell death after cerebral ischemia remain unclear, mitochondria obviously play a role by activating signaling pathways through ROS production and by regulating mitochondria-dependent apoptosis pathways

Cholestenoic acid, an endogenous cholesterol metabolite, is a potent γ-secretase modulator.

BackgroundAmyloid-β (Aβ) 42 has been implicated as the initiating molecule in the pathogenesis of Alzheimer's disease (AD); thus, therapeutic strategies that target Aβ42 are of great interest. γ-Secretase modulators (GSMs) are small molecules that selectively decrease Aβ42. We have previously reported that many acidic steroids are GSMs with potencies ranging in the low to mid micromolar concentration with 5β-cholanic acid being the most potent steroid identified GSM with half maximal effective concentration (EC50) of 5.7 μM.ResultsWe find that the endogenous cholesterol metabolite, 3β-hydroxy-5-cholestenoic acid (CA), is a steroid GSM with enhanced potency (EC50 of 250 nM) relative to 5β-cholanic acid. CA i) is found in human plasma at ~100-300 nM concentrations ii) has the typical acidic GSM signature of decreasing Aβ42 and increasing Aβ38 levels iii) is active in in vitro γ-secretase assay iv) is made in the brain. To test if CA acts as an endogenous GSM, we used Cyp27a1 knockout (Cyp27a1-/-) and Cyp7b1 knockout (Cyp7b1-/-) mice to investigate if manipulation of cholesterol metabolism pathways relevant to CA formation would affect brain Aβ42 levels. Our data show that Cyp27a1-/- had increased brain Aβ42, whereas Cyp7b1-/- mice had decreased brain Aβ42 levels; however, peripheral dosing of up to 100 mg/kg CA did not affect brain Aβ levels. Structure-activity relationship (SAR) studies with multiple known and novel CA analogs studies failed to reveal CA analogs with increased potency.ConclusionThese data suggest that CA may act as an endogenous GSM within the brain. Although it is conceptually attractive to try and increase the levels of CA in the brain for prevention of AD, our data suggest that this will not be easily accomplished

Glycaemic status, insulin resistance, and risk of infection-related mortality:a cohort study

Importance: the impact of non-diabetic hyperglycaemia and insulin resistance on infection-related mortality risk remains unknown.Objective: we investigated the association of glycaemic status and insulin resistance with infection-related mortality in individuals with and without diabetes.Design: cohort study based on Kangbuk Samsung Health Study and national death records.Participants: about 666 888 Korean adults who underwent fasting blood measurements including glucose, glycated haemoglobin (HbA1c), and insulin during health-screening examinations were followed for up to 15.8 years.Main outcome and measures: infection-related mortality, therefore we used Cox proportional hazards regression analyses to estimate hazard ratios (HRs) and 95% CIs for infection-related mortality. Vital status and infection-related mortality were ascertained through national death records. Variable categories were created based on established cut-offs for glucose and HbA1c levels and homeostatic model assessment of insulin resistance (HOMA-IR) quintiles.Results: during a median follow-up of 8.3 years, 313 infectious disease deaths were dentified. The associations of glucose and HbA1c levels with infection-related mortality were J-shaped (P for quadratic trend&lt;.05). The multivariable-adjusted HR (95% CIs) for infection-related mortality comparing glucose levels &lt;5, 5.6-6.9, and ≥7.0 mmol/L to 5.0–5.5 mmol/L (the reference) were 2.31 (1.47–3.64), 1.65 (1.05–2.60), and 3.41 (1.66–7.00), respectively. Among individuals without diabetes, the multivariable-adjusted HR for infection-related mortality for insulin resistance (HOMA-IR ≥75th centile versus &lt;75th centile) was 1.55 (1.04–2.32).Conclusions and relevance: both low and high glycaemic levels and insulin resistance were independently associated with increased infection-related mortality risk, indicating a possible role of abnormal glucose metabolism in increased infection-related mortality.<br/

Eosinophilic gastroenteritis as a cause of non-Helicobacter pylori, non-gastrotoxic drug ulcers in children

Abstract Background While Helicobacter pylori (H. pylori) ulcers has declined recently, H. pylori-negative and/or gastrotoxic drug-negative peptic ulcers (HNGN-PU) has increased. This study aimed to analyze the etiology of peptic ulcers in children and the differences in clinical, laboratory, endoscopic, and histopathologic findings of peptic ulcers according to etiology, including eosinophilic gastroenteritis (EoGE). Methods In total, 255 children (157 boys and 98 girls) with peptic ulcers were recruited. The subjects were categorized into 5 groups according to the etiology of the ulcer: 1) H. pylori infection (n = 51); 2) gastrotoxic drugs (n = 18); 3) idiopathic (n = 144); 4) systemic disease (n = 23); 5) EoGE (n = 19). Clinical data were reviewed and analyzed retrospectively. Results Age at diagnosis, ulcer recurrence, atopic dermatitis history, white blood cell count, blood eosinophil count, platelet count, serum albumin level, iron level, erythrocyte sedimentation rate, and C-reactive protein level differed significantly among the 5 groups (all p < 0.05). Regarding endoscopic findings, multiple ulcers and gastric mucosal nodularity differed among the 5 groups (all p < 0.05). When comparing the EoGE ulcer group with the others, EoGE group revealed older ages (p = 0.022), higher rates of ulcer recurrence (p = 0.018), atopic dermatitis history (p = 0.001), and both blood and tissue eosinophilia (both p = 0.001). Conclusions EoGE ulcers constituted 10.2% of HNGN-PU in pediatric patients. In children with HNGN-PU, peripheral eosinophilia, ulcer recurrence, and atopic dermatitis history might imply EoGE, necessitating thorough investigation of tissue eosinophils during endoscopic biopsy. Trial registration A total of 255 children was retrospectively registered between between July 2003 and April 2017