Breaking the Screen: Interaction Across Touchscreen Boundaries in Virtual Reality for Mobile Knowledge Workers.

Virtual Reality (VR) has the potential to transform knowledge work. One advantage of VR knowledge work is that it allows extending 2D displays into the third dimension, enabling new operations, such as selecting overlapping objects or displaying additional layers of information. On the other hand, mobile knowledge workers often work on established mobile devices, such as tablets, limiting interaction with those devices to a small input space. This challenge of a constrained input space is intensified in situations when VR knowledge work is situated in cramped environments, such as airplanes and touchdown spaces. In this paper, we investigate the feasibility of interacting jointly between an immersive VR head-mounted display and a tablet within the context of knowledge work. Specifically, we 1) design, implement and study how to interact with information that reaches beyond a single physical touchscreen in VR; 2) design and evaluate a set of interaction concepts; and 3) build example applications and gather user feedback on those applications.Comment: 10 pages, 8 figures, ISMAR 202

ReconViguRation: Reconfiguring Physical Keyboards in Virtual Reality.

Physical keyboards are common peripherals for personal computers and are efficient standard text entry devices. Recent research has investigated how physical keyboards can be used in immersive head-mounted display-based Virtual Reality (VR). So far, the physical layout of keyboards has typically been transplanted into VR for replicating typing experiences in a standard desktop environment. In this paper, we explore how to fully leverage the immersiveness of VR to change the input and output characteristics of physical keyboard interaction within a VR environment. This allows individual physical keys to be reconfigured to the same or different actions and visual output to be distributed in various ways across the VR representation of the keyboard. We explore a set of input and output mappings for reconfiguring the virtual presentation of physical keyboards and probe the resulting design space by specifically designing, implementing and evaluating nine VR-relevant applications: emojis, languages and special characters, application shortcuts, virtual text processing macros, a window manager, a photo browser, a whack-a-mole game, secure password entry and a virtual touch bar. We investigate the feasibility of the applications in a user study with 20 participants and find that, among other things, they are usable in VR. We discuss the limitations and possibilities of remapping the input and output characteristics of physical keyboards in VR based on empirical findings and analysis and suggest future research directions in this area

Glutamate-system defects behind psychiatric manifestations in a familial hemiplegic migraine type 2 disease-mutation mouse model

Migraine is a complex brain disorder, and understanding the complexity of this prevalent disease could improve quality of life for millions of people. Familial Hemiplegic Migraine type 2 (FHM2) is a subtype of migraine with aura and co-morbidities like epilepsy/seizures, cognitive impairments and psychiatric manifestations, such as obsessive-compulsive disorder (OCD). FHM2 disease-mutations locate to the ATP1A2 gene encoding the astrocyte-located α(2)-isoform of the sodium-potassium pump (α(2)Na(+)/K(+)-ATPase). We show that knock-in mice heterozygous for the FHM2-associated G301R-mutation (α(2)(+/G301R)) phenocopy several FHM2-relevant disease traits e.g., by mimicking mood depression and OCD. In vitro studies showed impaired glutamate uptake in hippocampal mixed astrocyte-neuron cultures from α(2)(G301R/G301R) E17 embryonic mice, and moreover, induction of cortical spreading depression (CSD) resulted in reduced recovery in α(2)(+/G301R) male mice. Moreover, NMDA-type glutamate receptor antagonists or progestin-only treatment reverted specific α(2)(+/G301R) behavioral phenotypes. Our findings demonstrate that studies of an in vivo relevant FHM2 disease knock-in mouse model provide a link between the female sex hormone cycle and the glutamate system and a link to co-morbid psychiatric manifestations of FHM2

Up-regulation of endothelin type B receptors in the human internal mammary artery in culture is dependent on protein kinase C and mitogen-activated kinase signaling pathways

<p>Abstract</p> <p>Background</p> <p>Up-regulation of vascular endothelin type B (ET_B) receptors is implicated in the pathogenesis of cardiovascular disease. Culture of intact arteries has been shown to induce similar receptor alterations and has therefore been suggested as a suitable method for, <it>ex vivo</it>, in detail delineation of the regulation of endothelin receptors. We hypothesize that mitogen-activated kinases (MAPK) and protein kinase C (PKC) are involved in the regulation of endothelin ET_Breceptors in human internal mammary arteries.</p> <p>Methods</p> <p>Human internal mammary arteries were obtained during coronary artery bypass graft surgery and were studied before and after 24 hours of organ culture, using <it>in vitro </it>pharmacology, real time PCR and Western blot techniques. Sarafotoxin 6c and endothelin-1 were used to examine the endothelin ET_Aand ET_Breceptor effects, respectively. The involvement of PKC and MAPK in the endothelin receptor regulation was examined by culture in the presence of antagonists.</p> <p>Results</p> <p>The endohtelin-1-induced contraction (after endothelin ET_Breceptor desensitization) and the endothelin ET_Areceptor mRNA expression levels were not altered by culture. The sarafotoxin 6c contraction, endothelin ET_Breceptor protein and mRNA expression levels were increased after organ culture. This increase was antagonized by; (1) PKC inhibitors (10 μM bisindolylmaleimide I and 10 μM Ro-32-0432), and (2) inhibitors of the p38, extracellular signal related kinases 1 and 2 (ERK1/2) and C-jun terminal kinase (JNK) MAPK pathways (10 μM SB203580, 10 μM PD98059 and 10 μM SP600125, respectively).</p> <p>Conclusion</p> <p>In conclusion, PKC and MAPK seem to be involved in the up-regulation of endothelin ET_Breceptor expression in human internal mammary arteries. Inhibiting these intracellular signal transduction pathways may provide a future therapeutic target for hindering the development of vascular endothelin ET_Breceptor changes in cardiovascular disease.</p

Activity-Dependent Calcium, Oxygen, and Vascular Responses in a Mouse Model of Familial Hemiplegic Migraine Type 1

Functional Genomics of Muscle, Nerve and Brain Disorder

Vascular endothelial growth factor in articular cartilage of healthy and osteoarthritic human knee joints

OBJECTIVE—To determine the levels of vascular endothelial growth factor (VEGF) mRNA and protein expression in normal and osteoarthritic (OA) human articular cartilage, and whether VEGF expression alters during the progression of OA.
METHODS—Sections from normal and OA human knee cartilage were immunotained with a polyclonal antibody recognising VEGF. In addition, total RNA was isolated from normal and osteoarthritic human knee cartilage and analysed by reverse transcriptase-polymerase chain reaction (RT-PCR) for VEGF mRNA expression.
RESULTS—VEGF was found to be present in normal and OA human knee cartilage in all cartilage layers. A significant increase of VEGF immunopositive chondrocytes to up to ~82% was detected in severe OA cartilage compared with normal articular cartilage (~56% of immunopositive chondrocytes). RT-PCR analysis showed the expression of VEGF also on the mRNA level.
CONCLUSIONS—VEGF is expressed by articular chondrocytes in normal and OA human knee cartilage. The percentage of VEGF immunopositive chondrocytes significantly increases in late stages of the disease. The VEGF transcript levels encoding all four isoforms shows a big variability in samples from different donors, suggesting a distinct regulation of the expression of the four VEGF isoforms in normal and OA cartilage.


Patellofemoral osteoarthritis after Insall's proximal realignment for recurrent patellar dislocation

PURPOSE: The aim of the present study was to retrospectively investigate the development of patellofemoral osteoarthritis after the historical Insall's proximal realignment for patellar stabilisation in patients with recurrent patellar dislocation. Furthermore, risk factors for recurrent patellar dislocation and for patellofemoral osteoarthritis development were evaluated. METHODS: Forty-two patients underwent patellofemoral stabilising surgery by the historic Insall's proximal realignment; they were evaluated with a mean follow-up period of 52 months. Plain radiography was used to document osteoarthritic changes by using the Iwano classification. MRIs obtained at the latest follow-up were evaluated for patellofemoral cartilage lesions. Univariate and multivariate logistic regression analyses were performed to evaluate the influence of trochlear dysplasia, tibial tubercle-trochlear groove distance and patellar height on redislocation. Pearson's χ (2) and the Spearman's correlation tests were used to assess a possible correlation between trochlear dysplasia and patellar dislocation, as well as between instability and development of patellofemoral osteoarthritis. RESULTS: At the latest follow-up, plain radiographs showed a significant increase in patellofemoral osteoarthritis (grades II-IV according to the Iwano classification) in 18 patients (43%) compared with 4 patients (10%) at the time of surgery (P = 0.001). Patellofemoral cartilage lesions (grades II-IV) were detected in 18 patients (43 %) on MRI. Nine patients (21%) had at least one incidence of redislocation at follow-up. Estimated redislocation-associated risk factors could not be determined. Trochlear dysplasia had a significant impact on patellofemoral osteoarthritis development (P = 0.001), whereas recurrent patellar instability had none (n.s.). CONCLUSION: Insall's proximal realignment technique leads to a significant progression of patellofemoral osteoarthritis. No risk factors for redislocation could be found; however, the presence of trochlear dysplasia did correlate with patellofemoral osteoarthritis. LEVEL OF EVIDENCE: IV