Exploring affective design for physical controls

Physical controls such as knobs, sliders, and buttons are experiencing a revival as many computing systems progress from personal computing architectures towards ubiquitous computing architectures. We demonstrate a process for measuring and comparing visceral emotional responses of a physical control to performance results of a target acquisition task. In our user study, participants experienced mechanical and rendered friction, inertia, and detent dynamics as they turned a haptic knob towards graphical targets of two different widths and amplitudes. Together, this process and user study provide novel affect- and performance-based design guidance to developers of physical controls for emerging ubiquitous computing environments. Our work bridges extensive human factors work in mechanical systems that peaked in the 1960’s, to contemporary trends, with a goal of integrating mechatronic controls into emerging ubiquitous computing systems. Author Keywords Haptic display, physical control, design process, affect

Social Touch

Interpersonal or social touch is an intuitive and powerful way to express and communicate emotions, comfort a friend, bond with teammates, comfort a child in pain, and soothe someone who is stressed. If there is one thing that the current pandemic is showing us, it is that social distancing can make some people crave physical interaction through social touch. The notion of “skin-hunger” has become tangible for many.Social touch differs at a functional and anatomical level from discriminative touch, and has clear effects at physiological, emotional, and behavioural levels. Social touch is a topic in psychology (perception, emotion, behaviour), neuroscience (neurophysiological pathways), computer science (mediated touch communication), engineering (haptic devices), robotics (social robots that can touch), humanities (science and technology studies), and sociology (the social implications of touch). Our current scientific knowledge of social touch is scattered across disciplines and not yet adequate for the purpose of meeting today's challenges of connecting human beings through the mediating channel of technology

Critical Role of the Pleckstrin Homology and Cysteine-rich Domains in Vav Signaling and Transforming Activity

Vav family proteins are members of the Dbl family of guanine nucleotide exchange factors and activators of Rho family small GTPases. In addition to the Dbl homology (DH) domain important for guanine nucleotide exchange factor catalytic function, all Dbl family proteins contain an adjacent pleckstrin homology (PH) domain that serves to regulate DH domain activity. Although the role of the PH domain in Vav function has been evaluated extensively, its precise role and whether it serves a distinct role in different Vav proteins remain unresolved. Additionally, the precise role of an adjacent cysteine-rich domain (CRD) in regulating DH domain function is also unclear. In this study, we evaluated the contribution of these putative protein-protein or protein-lipid interaction domains to Vav signaling and transforming activity. In contrast to previous observations, we found that the PH domain is critical for Vav transforming activity. Similarly, the CRD was also essential and served a function distinct from that of the PH domain. Although mutation of either domain reduced Vav membrane association, addition of plasma membrane targeting sequences to either the CRD or PH domain mutant proteins did not restore Vav transforming activity. This result contrasts with other Dbl family proteins, where a membrane targeting sequence alone was sufficient to restore the loss of function caused by mutation of the PH domain. Furthermore, green fluorescent protein fusion proteins containing the PH domain or CRD, or both, failed to target to the plasma membrane, suggesting that these two domains also serve regulatory functions independent of promoting membrane localization. Finally, we found that phosphatidylinositol 3-kinase activation may promote Vav membrane association via phosphatidylinositol 3,4,5-triphosphate binding to the PH domain

Households’ responses to spousal job loss: ‘all change’ or ‘carry on as usual’?

Economic theory suggests that when a primary earner within a couple loses their job, one potential response is for the secondary earner to seek additional paid work to bolster their household finances. The empirical quantitative evidence regarding any such ‘added worker effect’ is mixed, and, to investigate why this might be, the article explores processes behind couples’ responses to job loss. Drawing on in-depth qualitative interviews conducted with a purposive sample selected from the Understanding Society Innovation Panel, the analysis examines: (a) anticipation surrounding job loss and job search responses; (b) the extent to which couples adopt long- or short-term labour market perspectives; and (c) whether couples seek to preserve their established division of paid and unpaid labour or re-configure their joint labour supply. Findings indicate that the use of additional spousal labour is only one response among many alternatives and it is typically invoked in cases of serious financial hardship. </jats:p

Diastolic dysfunction and left atrial volume A population-based study

ObjectivesWe examined the association between diastolic function and left atrial volume indexed to body surface area (LAVi) in a population-based study.BackgroundAtrial enlargement has been suggested as a marker of the severity and duration of diastolic dysfunction (DD). However, the association between DD and atrial enlargement and their individual prognostic implications in the population is poorly defined.MethodsA cross-sectional sample of Olmsted County, Minnesota, residents ≥45 years of age (n = 2,042) underwent comprehensive Doppler echocardiography and medical record review.ResultsThe LAVi increased with worsening DD: 23 ± 6 ml/m2(normal), 25 ± 8 ml/m2(grade I DD), 31 ± 8 ml/m2(grade II DD), 48 ± 12 ml/m2(grades III to IV DD). In bivariate analyses, age, left ventricular mass index, and DD grade were positively associated, whereas female gender and ejection fraction (EF) were inversely associated with LAVi (p < 0.001 for all). When controlling for age, gender, cardiovascular (CV) disease, EF, and left ventricular mass, grade II DD was associated with a 24%, and grade III to IV DD was associated with a 62% larger LA volume (p < 0.0001 for both). The area under the receiver-operator characteristic curve for LAVi to detect grade I, grade II, or grade III to IV DD was 0.57, 0.81, and 0.98, respectively. Both DD and LAVi were predictive of all-cause mortality, but when controlling for DD, LAVi was not an independent predictor of mortality.ConclusionsThese data suggest that DD contributes to LA remodeling. Indeed, DD is a stronger predictor of mortality; presumably it better reflects the impact of CV disease within the general population

CDC42 and FGD1 Cause Distinct Signaling and Transforming Activities

Activated forms of different Rho family members (CDC42, Rac1, RhoA, RhoB, and RhoG) have been shown to transform NIH 3T3 cells as well as contribute to Ras transformation. Rho family guanine nucleotide exchange factors (GEFs) (also known as Dbl family proteins) that activate CDC42, Rac1, and RhoA also demonstrate oncogenic potential. The faciogenital dysplasia gene product, FGD1, is a Dbl family member that has recently been shown to function as a CDC42-specific GEF. Mutations within theFGD1locus cosegregate with faciogenital dysplasia, a multisystemic disorder resulting in extensive growth impairments throughout the skeletal and urogenital systems. Here we demonstrate that FGD1 expression is sufficient to cause tumorigenic transformation of NIH 3T3 fibroblasts. Although both FGD1 and constitutively activated CDC42 cooperated with Raf and showed synergistic focus-forming activity, both quantitative and qualitative differences in their functions were seen. FGD1 and CDC42 also activated common nuclear signaling pathways. However, whereas both showed comparable activation of c-Jun, CDC42 showed stronger activation of serum response factor and FGD1 was consistently a better activator of Elk-1. Although coexpression of FGD1 with specific inhibitors of CDC42 function demonstrated the dependence of FGD1 signaling activity on CDC42 function, FGD1 signaling activities were not always consistent with the direct or exclusive stimulation of CDC42 function. In summary, FGD1 and CDC42 signaling and transformation are distinct, thus suggesting that FGD1 may be mediating some of its biological activities through non-CDC42 targets

Human Multidrug-Resistant Salmonella Newport Infections, Wisconsin, 2003–2005

We conducted a retrospective study of Salmonella Newport infections among Wisconsin residents during 2003–2005. Multidrug resistance prevalence was substantially greater in Wisconsin than elsewhere in the United States. Persons with multidrug-resistant infections were more likely than persons with susceptible infections to report exposure to cattle, farms, and unpasteurized milk

UGT1A1 sequence variants and bilirubin levels in early postnatal life: a quantitative approach

<p>Abstract</p> <p>Background</p> <p>Fundamental to definitively identifying neonates at risk of developing significant hyperbilirubinemia is a better understanding of the genetic factors associated with early bilirubin rise. Previous genetic studies have focused on the UGT1A1 gene, associating common variation in the coding or promoter regions with qualitative assessments of bilirubin (i.e. significantly elevated or not). These studies have had conflicting results and limited success. We chose to approach the problem by focusing on the quantitative (absolute) change in bilirubin levels early in post-natal life. We apply this approach to the UGT1A1 gene - exploring the contribution of both rare and common variants to early bilirubin changes.</p> <p>Methods</p> <p>We sequenced the exons, PBREM, 5'-, and 3'- regions of the UGT1A1 gene in 80 otherwise healthy term neonates who had repeat bilirubin levels measured within the first five days of life.</p> <p>Results</p> <p>Three novel coding variants were observed, but there was no clear relationship between rare coding variants and bilirubin rise. Adjusted linear regression models fit to evaluate the relationship between changing bilirubin levels and common UGT1A1variants found that among 39 neonates whose bilirubin was resampled within 33 hours, individuals homozygous for the mutant allele of a 3'UTR SNP had significantly smaller changes in bilirubin (P = 0.003) than individuals carrying the wild-type allele.</p> <p>Conclusions</p> <p>Collectively, rare UGT1A1 coding variants do not appear to play a prominent role in determining early bilirubin levels; however common variants in the 3' UTR of UGT1A1 may modulate the early bilirubin rise. A quantitative approach to evaluating early bilirubin kinetics provides a more robust framework in which to better understand the genetics of neonatal hyperbilirubinemia.</p