1,919 research outputs found

    Creation of two-dimensional coulomb crystals of ions in oblate Paul traps for quantum simulations

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    We develop the theory to describe the equilibrium ion positions and phonon modes for a trapped ion quantum simulator in an oblate Paul trap that creates two-dimensional Coulomb crystals in a triangular lattice. By coupling the internal states of the ions to laser beams propagating along the symmetry axis, we study the effective Ising spin-spin interactions that are mediated via the axial phonons and are less sensitive to ion micromotion. We find that the axial mode frequencies permit the programming of Ising interactions with inverse power law spin-spin couplings that can be tuned from uniform to r−3r^{-3} with DC voltages. Such a trap could allow for interesting new geometrical configurations for quantum simulations on moderately sized systems including frustrated magnetism on triangular lattices or Aharonov-Bohm effects on ion tunneling. The trap also incorporates periodic boundary conditions around loops which could be employed to examine time crystals.Comment: 17 pages, 8 figures, submitted to the journal EPJ Quantum Technology for the thematic Series on Quantum Simulation

    Care homes education: what can we learn?

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    Medical care received by care home residents can be variable. Initiatives, such as matron-led community teams, ensure a timely response to alerts about unwell residents. But early recognition of deterioration is vital in accessing this help. The aim of this project was to design and deliver an education programme for carers. It was hypothesised that the implementation of a teaching programme may result in improved medical care for residents. By understanding the enablers and barriers to implementing teaching, we hoped to identify the components of a successful teaching programme. Four care homes in Enfield received training on topics such as deterioration recognition over a 1-year period. The project was evaluated at 3, 6 and 9 months. Each evaluation comprised: pre-and-post-teaching questionnaires, focus groups, analysis of percentages of staff trained, review of overall and potentially avoidable, hospital admission rates. A Plan-Do-Study-Act cycle structure was used. The programme was well-received by carers, who gave examples of application of learning. Modules about conditions frequently resulting in hospital admission, or concerning real cases, demonstrated the best pre-and-post lesson change scores. However, the reach of the programme was low, with attendance rates between 5% and 28%. Overall, the percentage of staff trained in deterioration recognition ranged from 35% (care home one) to 12% (care home three). Hospital admissions reduced from 37 hospital admissions to 20 over the duration of the project. Potentially avoidable admissions reduced from 16 to 5. Proving causality to the intervention was difficult. Factors facilitating delivery of training included a flexible approach, an activity-based curriculum, alignment of topics with real cases and embedding key messages in every tutorial. Barriers included: time pressures, shift work, low attendance rates, inequitable perception of the value of teaching and IT issues. Care home factors impacting on delivery included: stability of management and internal communication systems.please ensure space here

    Conditioning bounds for traveltime tomography in layered media

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    This paper revisits the problem of recovering a smooth, isotropic, layered wave speed profile from surface traveltime information. While it is classic knowledge that the diving (refracted) rays classically determine the wave speed in a weakly well-posed fashion via the Abel transform, we show in this paper that traveltimes of reflected rays do not contain enough information to recover the medium in a well-posed manner, regardless of the discretization. The counterpart of the Abel transform in the case of reflected rays is a Fredholm kernel of the first kind which is shown to have singular values that decay at least root-exponentially. Kinematically equivalent media are characterized in terms of a sequence of matching moments. This severe conditioning issue comes on top of the well-known rearrangement ambiguity due to low velocity zones. Numerical experiments in an ideal scenario show that a waveform-based model inversion code fits data accurately while converging to the wrong wave speed profile

    Bodies, technologies and action possibilities: when is an affordance?

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    Borrowed from ecological psychology, the concept of affordances is often said to offer the social study of technology a means of re-framing the question of what is, and what is not, ‘social’ about technological artefacts. The concept, many argue, enables us to chart a safe course between the perils of technological determinism and social constructivism. This article questions the sociological adequacy of the concept as conventionally deployed. Drawing on ethnographic work on the ways technological artefacts engage, and are engaged by, disabled bodies, we propose that the ‘affordances’ of technological objects are not reducible to their material constitution but are inextricably bound up with specific, historically situated modes of engagement and ways of life

    Sit-to-Stand Transition Reveals Acute Fall Risk in Activities of Daily Living

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    Reciprocal regulation of PKA and rac signaling

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    Activated G protein-coupled receptors (GPCRs) and receptor tyrosine kinases relay extracellular signals through spatial and temporal controlled kinase and GTPase entities. These enzymes are coordinated by multifunctional scaffolding proteins for precise intracellular signal processing. The cAMP-dependent protein kinase A (PKA) is the prime example for compartmentalized signal transmission downstream of distinct GPCRs. A-kinase anchoring proteins tether PKA to specific intracellular sites to ensure precision and directionality of PKA phosphorylation events. Here, we show that the Rho-GTPase Rac contains A-kinase anchoring protein properties and forms a dynamic cellular protein complex with PKA. The formation of this transient core complex depends on binary interactions with PKA subunits, cAMP levels and cellular GTP-loading accounting for bidirectional consequences on PKA and Rac downstream signaling. We show that GTP-Rac stabilizes the inactive PKA holoenzyme. However, β-adrenergic receptor-mediated activation of GTP-Rac–bound PKA routes signals to the Raf-Mek-Erk cascade, which is critically implicated in cell proliferation. We describe a further mechanism of how cAMP enhances nuclear Erk1/2 signaling: It emanates from transphosphorylation of p21-activated kinases in their evolutionary conserved kinase-activation loop through GTP-Rac compartmentalized PKA activities. Sole transphosphorylation of p21-activated kinases is not sufficient to activate Erk1/2. It requires complex formation of both kinases with GTP-Rac1 to unleash cAMP-PKA–boosted activation of Raf-Mek-Erk. Consequently GTP-Rac functions as a dual kinase-tuning scaffold that favors the PKA holoenzyme and contributes to potentiate Erk1/2 signaling. Our findings offer additional mechanistic insights how β-adrenergic receptor-controlled PKA activities enhance GTP-Rac–mediated activation of nuclear Erk1/2 signaling

    Antibody signatures in patients with histopathologically defined multiple sclerosis patterns

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    Early active multiple sclerosis (MS) lesions can be classified histologically into three main immunopathological patterns of demyelination (patterns I-III), which suggest pathogenic heterogeneity and may predict therapy response. Patterns I and II show signs of immune-mediated demyelination, but only pattern II is associated with antibody/complement deposition. In pattern III lesions, which include Baló's concentric sclerosis, primary oligodendrocyte damage was proposed. Serum antibody reactivities could reflect disease pathogenesis and thus distinguish histopathologically defined MS patterns. We established a customized microarray with more than 700 peptides that represent human and viral antigens potentially relevant for inflammatory demyelinating CNS diseases, and tested sera from 66 patients (pattern I n = 12; II n = 29; III n = 25, including 8 with Baló's), healthy controls, patients with Sjögren's syndrome and stroke patients. Cell-based assays were performed for aquaporin 1 (AQP1) and AQP4 antibody detection. No single peptide showed differential binding among study cohorts. Because antibodies can react with different peptides from one protein, we also analyzed groups of peptides. Patients with pattern II showed significantly higher reactivities to Nogo-A peptides as compared to patterns I (p = 0.02) and III (p = 0.02). Pattern III patients showed higher reactivities to AQP1 (compared to pattern I p = 0.002, pattern II p = 0.001) and varicella zoster virus (VZV, compared to pattern II p = 0.05). In patients with Baló's, AQP1 reactivity was also significantly higher compared to patients without Baló's (p = 0.04), and the former revealed distinct antibody signatures. Histologically, Baló's patients showed loss of AQP1 and AQP4 in demyelinating lesions, but no antibodies binding conformational AQP1 or AQP4 were detected. In summary, higher reactivities to Nogo-A peptides in pattern II patients could be relevant for enhanced axonal repair and remyelination. Higher reactivities to AQP1 peptides in pattern III patients and its subgroup of Baló's patients possibly reflect astrocytic damage. Finally, latent VZV infection may cause peripheral immune activation

    Serum peptide reactivities may distinguish neuromyelitis optica subgroups and multiple sclerosis

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    Objective: To assess in an observational study whether serum peptide antibody reactivities may distinguish aquaporin-4 (AQP4) antibody (Ab)–positive and -negative neuromyelitis optica spectrum disorders (NMOSD) and relapsing-remitting multiple sclerosis (RRMS). Methods: We screened 8,700 peptides that included human and viral antigens of potential relevance for inflammatory demyelinating diseases and random peptides with pooled sera from different patient groups and healthy controls to set up a customized microarray with 700 peptides. With this microarray, we tested sera from 66 patients with AQP4-Ab-positive (n = 16) and AQP4-Ab-negative (n = 19) NMOSD, RRMS (n = 11), and healthy controls (n = 20). Results: Differential peptide reactivities distinguished NMOSD subgroups from RRMS in 80% of patients. However, the 2 NMOSD subgroups were not well-discriminated, although those patients are clearly separated by their antibody reactivities against AQP4 in cell-based assays. Elevated reactivities to myelin and Epstein-Barr virus peptides were present in RRMS and to AQP4 and AQP1 peptides in AQP4-Ab-positive NMOSD. Conclusions: While AQP4-Ab-positive and -negative NMOSD subgroups are not well-discriminated by peptide antibody reactivities, our findings suggest that peptide antibody reactivities may have the potential to distinguish between both NMOSD subgroups and MS. Future studies should thus concentrate on evaluating peptide antibody reactivities for the differentiation of AQP4-Ab-negative NMOSD and MS
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