Deconstructivist Interaction Design: Interrogating Expression and Form

In this paper, we propose deconstructivist interaction design in order to facilitate the differentiation of an expressional vo- cabulary in interaction design. Based on examples that illus- trate how interaction design critically explores (i.e., decon- structs) its own expressional repertoire, we argue that there are commonalities with deconstructivist phases in related de- sign disciplines to learn from. Therefore, we draw on the role and characteristics of deconstructivism in the history of archi- tecture, graphic design, and fashion. Afterwards, we reflect on how interaction design is already a means of deconstruc- tion (e.g., in critical design). Finally, we discuss the potential of deconstructivism for form-giving practices, resulting in a proposal to extend interaction design’s expressional vocabu- lary of giving form to computational material by substantiat- ing a deconstructivist perspective.

Critical Ways of Making: Design Artefacts, De-Computation and Un-Crafting

This workshop intends to elaborate on new and emerging crit- ical approaches that aim to question the nature of contempo- rary computational artefacts. By interrogating interactive sys- tems from a perspective that is focussed on the arrangement of their constituent parts and the relations between them, we seek to challenge the constructive paradigms that might have led to those configurations. In particular, with this workshop we will introduce and further explore De-Computation as a methodology, and Un-Crafting as a method, both targeting a critical examination of contemporary computational arte- facts and the interaction paradigms they follow. Both De- Computation and Un-Crafting approach and explore possi- ble computational futures by critically examining the present. The workshop will include collaborative hands-on activities with reflection in practice and discussions around the topic. We are inviting interdisciplinary viewpoints that will enable us to further ground De-Computation and Un-Crafting in a diverse set of contexts

Parathyroid hormone and dietary phosphate provoke a lysosomal routing of the proximal tubular Na/Pi-cotransporter type II

Parathyroid hormone and dietary phosphate provoke a lysosomal routing of the proximal tubular Na/Pi-cotransporter type II.BackgroundA decrease of proximal tubular reabsorption of phosphate (Pi), which can be provoked by parathyroid hormone (PTH) or by a high Pi-diet, has been shown to correlate with a decrease of the number of type II Na/Pi-cotransporters residing in the brush border membrane. While both PTH and a high Pi-diet lead to an internalization of type II cotransporters, the further cellular routing of internalized cotransporters has not been established unequivocally.MethodsTo prevent lysosomal degradation, rats were treated with leupeptin prior to the injection of PTH or feeding acutely with a high Pi-diet. Kidney cortex were recovered and used for immunohistochemistry. In parallel, brush border membranes and lysosomes were isolated and analyzed by Western blotting.ResultsUnder both conditions (PTH and high Pi-diet), a strong overlap of internalized type II cotransporters with the late endosomes/lysosomes was observed by immunohistochemistry. In agreement, the content of type II Na/Pi-cotransporters was increased in lysosomes isolated from the corresponding tissues.ConclusionsThese results suggest that in proximal tubular cells type II Na/Pi-cotransporters internalized due to the action of PTH and acute high Pi-diet are routed to the lysosomes, and likely do not enter a recycling compartment

Elevated high-sensitivity troponin does not indicate the presence of coronary artery disease in patients presenting with supraventricular tachycardia

Background: Patients with supraventricular tachycardia (SVT) and patients with coronary artery disease (CAD) often present with similar symptoms (chest pain, shortness of breath), similar electrocar¬diographic changes and elevated high-sensitivity troponin (Tn). It is not clear whether troponin reflects critical CAD or is elevated due to other causes in patients presenting with SVT. The aim of this study was to assess the role of elevated troponin in patients presenting with SVT. Methods: Patients undergoing radiofrequency ablation (RFA) for SVT and simultaneous coronary an¬giography at the Heart Centre Lucerne, Switzerland between January 2010 and October 2014 were in¬cluded in this analysis. Significant CAD was defined as diameter-stenosis ≥ 75% in vessels > 2.0 mm. The level of Tn was compared between patients with the presence or absence of CAD on coronary angi¬ography. A Tn value of ≥ 0.014 μg/L was considered as elevated. Results: During the study period a total of 473 patients underwent RFA for SVT. The study population consisted of 326 patients (69%, mean age 60 ± 12 years) who underwent invasive coronary angiogra¬phy during the same session. The prevalence of significant CAD was 14% (45/326 patients). The highest prevalence of CAD was found in patients with atrial flutter (35%, 18/45 patients). Tn was elevated in 83% (10/12 patients) with significant CAD and in 47% (26/55 patients) without CAD. Conclusions: The prevalence of CAD is low in patients with SVT, which questions the role of routine invasive coronary angiography during RFA. Tn measurement did not reliably exclude or confirm CAD in these patients

The Future of Making: Where Industrial and Personal Fabrication Meet

This one-day workshop seeks to reflect on the notion of fab- rication in both personal and industrial contexts. Although these contexts are very distinct in their economical and polit- ical vision, they share important characteristics (e.g., users interacting with specific fabrication equipment and tools). The workshop topic spans from personal fabrication to (au- tomated) production, from applied to theoretical considera- tions, from user requirements to design as a crafting practice. We will address changes in production that affect humans, e.g., from mass production to Do-It-Yourself (DIY) produc- tion, in order to discuss findings and lessons learned for in- dividual and collective production workplaces of the future. We aim to explore the intersections between different dimen- sions and processes of production ranging all the way from hobbyist to professional making. Furthermore, the workshop will critically reflect on current developments and their conse- quences on personal, societal, and economical levels includ- ing questions of the reorganization of work and labor, inno- vation cultures, and politics of participation.

Open design at the intersection of making and manufacturing

This one-day workshop aims to consider the opportunities for HCI at the intersection of maker culture and professional, industrial manufacturing. In particular, we are interested in exploring how the concept of “open design” could help support productive interactions between professional manufacturers and non-professional makers. Our proposal builds on momentum established by previous related workshops (including one at CHI2016) and aims to respond critically to several key industry and government reports published in 2015-2016 on the ‘maker movement’

Prevalence and potential relevance of hyperuricemia in pediatric kidney transplant recipients—a CERTAIN registry analysis

Background: Asymptomatic hyperuricemia is frequently observed in pediatric kidney transplant recipients; symptomatic hyperuricemia, however, is a rare complication. Only few data are available in this patient population. We, therefore, investigated the prevalence of hyperuricemia and its association with kidney transplant function and blood pressure in a multicenter cohort of pediatric kidney transplant recipients. Methods: This is a retrospective, observational multicenter registry study. All pediatric kidney transplant recipients in the CERTAIN database with at least one documented serum uric acid level and a follow-up of 5 years posttransplant were eligible. We identified 151 patients with 395 measurements of serum uric acid. We calculated the prevalence of hyperuricemia, analyzed potential risk factors and clinical consequences such as elevated blood pressure and reduced estimated glomerular filtration rate (eGFR). Statistical analysis was performed using IBM SPSS Statistics 26. Results: One hundred and ten of 395 (27.8%) serum uric acid levels were above 416 µmol/L (7.0 mg/dL), defined as the upper limit of normal. Univariate analysis showed a significant (p = .026) inverse association of serum uric acid with eGFR overtime. There was no significant association of serum uric acid concentrations with body mass index (z-score), blood pressure (z-score), or sex. No episodes of gout were documented. Conclusion: This study shows that hyperuricemia is present in a considerable number of patients sometime after pediatric kidney transplantation and is associated with lower eGFR. Whether hyperuricemia contributes to faster decline of graft function or to the overall cardiovascular risk of these patients remains to be elucidated. Keywords: gout; long-term outcome; pediatric kidney transplantation; uric acid; uric acid-lowering therapy

A linkage study of candidate loci in familial Parkinson's Disease

BACKGROUND: Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease. Most cases are sporadic, however familial cases do exist. We examined 12 families with familial Parkinson's disease ascertained at the Movement Disorder clinic at the Oregon Health Sciences University for genetic linkage to a number of candidate loci. These loci have been implicated in familial Parkinson's disease or in syndromes with a clinical presentation that overlaps with parkinsonism, as well as potentially in the pathogenesis of the disease. METHODS: The examined loci were PARK3, Parkin, DRD (dopa-responsive dystonia), FET1 (familial essential tremor), BDNF (brain-derived neurotrophic factor), GDNF (glial cell line-derived neurotrophic factor), Ret, DAT1 (the dopamine transporter), Nurr1 and Synphilin-1. Linkage to the α-synuclein gene and the Frontotemporal dementia with parkinsonism locus on chromosome 17 had previously been excluded in the families included in this study. Using Fastlink, Genehunter and Simwalk both parametric and model-free non-parametric linkage analyses were performed. RESULTS: In the multipoint parametric linkage analysis lod scores were below -2 for all loci except FET1 and Synphilin-1 under an autosomal dominant model with incomplete penetrance. Using non-parametric linkage analysis there was no evidence for linkage, although linkage could not be excluded. A few families showed positive parametric and non-parametric lod scores indicating possible genetic heterogeneity between families, although these scores did not reach any degree of statistical significance. CONCLUSIONS: We conclude that in these families there was no evidence for linkage to any of the loci tested, although we were unable to exclude linkage with both parametric and non-parametric methods

Long-term effects of an inpatient weight-loss program in obese children and the role of genetic predisposition-rationale and design of the LOGIC-trial

<p>Abstract</p> <p>Background</p> <p>The prevalence of childhood obesity has increased worldwide, which is a serious concern as obesity is associated with many negative immediate and long-term health consequences. Therefore, the treatment of overweight and obesity in children and adolescents is strongly recommended. Inpatient weight-loss programs have shown to be effective particularly regarding short-term weight-loss, whilst little is known both on the long-term effects of this treatment and the determinants of successful weight-loss and subsequent weight maintenance.</p> <p>The purpose of this study is to evaluate the short, middle and long-term effects of an inpatient weight-loss program for children and adolescents and to investigate the likely determinants of weight changes, whereby the primary focus lies on the potential role of differences in polymorphisms of adiposity-relevant genes.</p> <p>Methods/Design</p> <p>The study involves overweight and obese children and adolescents aged 6 to 19 years, who participate in an inpatient weight-loss program for 4 to 6 weeks. It started in 2006 and it is planned to include 1,500 participants by 2013. The intervention focuses on diet, physical activity and behavior therapy. Measurements are taken at the start and the end of the intervention and comprise blood analyses (DNA, lipid and glucose metabolism, adipokines and inflammatory markers), anthropometry (body weight, height and waist circumference), blood pressure, pubertal stage, and exercise capacity. Physical activity, dietary habits, quality of life, and family background are assessed by questionnaires. Follow-up assessments are performed 6 months, 1, 2, 5 and 10 years after the intervention: Children will complete the same questionnaires at all time points and visit their general practitioner for examination of anthropometric parameters, blood pressure and assessment of pubertal stage. At the 5 and 10 year follow-ups, blood parameters and exercise capacity will be additionally measured.</p> <p>Discussion</p> <p>Apart from illustrating the short, middle and long-term effects of an inpatient weight-loss program, this study will contribute to a better understanding of inter-individual differences in the regulation of body weight, taking into account the role of genetic predisposition and lifestyle factors.</p> <p>Trial Registration</p> <p><a href="http://www.clinicaltrials.gov/ct2/show/NCT01067157">NCT01067157</a>.</p

When RON MET TAM in Mesothelioma: All Druggable for One, and One Drug for All?

Malignant pleural mesothelioma (MPM) is an aggressive inflammatory cancer with a poor survival rate. Treatment options are limited at best and drug resistance is common. Thus, there is an urgent need to identify novel therapeutic targets in this disease in order to improve patient outcomes and survival times. MST1R (RON) is a trans-membrane receptor tyrosine kinase (RTK), which is part of the c-MET proto-oncogene family. The only ligand recognized to bind MST1R (RON) is Macrophage Stimulating 1 (MST1), also known as Macrophage Stimulating Protein (MSP) or Hepatocyte Growth Factor-Like Protein (HGFL). In this study, we demonstrate that the MST1-MST1R (RON) signaling axis is active in MPM. Targeting this pathway with a small molecule inhibitor, LCRF-0004, resulted in decreased proliferation with a concomitant increase in apoptosis. Cell cycle progression was also affected. Recombinant MST1 treatment was unable to overcome the effect of LCRF-0004 in terms of either proliferation or apoptosis. Subsequently, the effect of an additional small molecular inhibitor, BMS-777607 (which targets MST1R (RON), MET, Tyro3, and Axl) also resulted in a decreased proliferative capacity of MPM cells. In a cohort of MPM patient samples, high positivity for total MST1R by IHC was an independent predictor of favorable prognosis. Additionally, elevated expression levels of MST1 also correlated with better survival. This study also determined the efficacy of LCRF-0004 and BMS-777607 in xenograft MPM models. Both LCRF-0004 and BMS-777607 demonstrated significant anti-tumor efficacy in vitro, however BMS-777607 was far superior to LCRF-0004. The in vivo and in vitro data generated by this study indicates that a multi-TKI, targeting the MST1R/MET/TAM signaling pathways, may provide a more effective therapeutic strategy for the treatment of MPM as opposed to targeting MST1R alone