468 research outputs found

    Risk groups for clinical complications of norovirus infections: an outbreak investigation.

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    Norovirus infections have been described as self-limiting diseases of short duration. An investigation of a norovirus outbreak in a university hospital provided evidence for severe clinical features in patients with several underlying diseases. Clinical outcomes of norovirus infection were defined. Risk-factor analysis targeting underlying diseases and medication was performed using multivariate analyses. In five outbreak wards, 84 patients and 60 nurses were infected (an overall attack rate of 32% in patients, and 76% in nurses). The causative agent was the new variant Grimsby virus. Severe clinical features, including acute renal failure, arrhythmia and signs of acute graft organ rejection in renal transplant patients, were observed in seven (8.3%) patients. In multivariate analyses, cardiovascular disease (OR 17.1, 95% CI 2.17-403) and renal transplant (OR 13.0, 95% CI 1.63-281) were risk-factors for a potassium decrease of >20%. Age >65 years (OR 11.6, 95% CI 1.89-224) was a risk-factor for diarrhoea lasting >2 days. Immunosuppression (OR 5.7, 95% CI 1.78-20.1) was a risk-factor for a creatinine increase of >10%. Norovirus infections in patients with underlying conditions such as cardiovascular disease, renal transplant and immunosuppressive therapy may lead to severe consequences typified by decreased potassium levels, increased levels of C-reactive protein and creatine phosphokinase. In the elderly, norovirus infection may lead to an increased duration of diarrhoea. Therefore patients at risk should be hospitalised early and monitored frequently. Strict preventional measures should be implemented as early as possible to minimise the risk of nosocomial outbreaks

    Vortical flow. Part 2. Flow past a sphere in a constant-diameter pipe

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    This paper describes an experimental and numerical investigation of concentrated vortex flow past a sphere in a constant-diameter pipe. As the swirl was increased at a fixed sphere Reynolds number of approximately 1100, the length of the mean downstream separation bubble decreased. For a small range of swirl intensity, an almost stagnant separation bubble formed on the upstream hemisphere. A further increase in swirl caused the bubble to become unstable and develop into an unsteady spiral disturbance. At very high swirl the downstream separation bubble was eliminated and an unsteady separation zone extended far upstream. Calculations of the vorticity field from surface fits to azimuthal and axial velocity data suggest that upstream separation is caused by the distortion of vortex filaments in the diverging flow approaching the sphere. Numerical solutions of steady inviscid axisymmetric flow past a sphere exhibit a fold in the vicinity of upstream separation. It is suggested that this accounts for the extreme sensitivity encountered in the experiments.T. W. Mattner, P. N. Joubert and M. S. Chon

    Vortical flow. Part 1. Flow through a constant-diameter pipe

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    This paper describes an exploration of the behaviour and properties of swirling flow through a constant-diameter pipe. The experiments reveal a complicated transition process as the swirl intensity [Omega] is increased at fixed pipe Reynolds number Re [approximate] 4900. For [Omega] [less-than-or-eq, slant] 1.09, the vortex was steady, laminar, axisymmetric, and developed slowly with streamwise distance. The upstream velocity profiles were similar to those commonly appearing in the literature in similar apparatus. Spiral vortex breakdown appeared in the test section for 1.09 [less-than-or-eq, slant] [Omega] [less-than-or-eq, slant] 1.31 and was associated with a localized transition from jet-like to wake-like mean axial velocity profiles. Further increase in [Omega] caused the breakdown to move upstream of the test section. Downstream, the core of the post-breakdown flow was unsteady and recovered toward jet-like profiles with streamwise distance. At [Omega] = 2.68, a global transition occurred in which the mean axial velocity profiles suddenly developed an annular axial velocity deficit. At the same time, disturbances began to appear in the outer flow. Further increase in [Omega] eventually led to an annulus of reversed axial flow and a completely unsteady vortex

    Derivative pricing under the possibility of long memory in the supOU stochastic volatility model

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    We consider the supOU stochastic volatility model which is able to exhibit long-range dependence. For this model we give conditions for the discounted stock price to be a martingale, calculate the characteristic function, give a strip where it is analytic and discuss the use of Fourier pricing techniques. Finally, we present a concrete specification with polynomially decaying autocorrelations and calibrate it to observed market prices of plain vanilla options

    Tailoring the Antibody Response to Aggregated Aß Using Novel Alzheimer-Vaccines

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    Recent evidence suggests Alzheimer-Disease (AD) to be driven by aggregated Aß. Capitalizing on the mechanism of molecular mimicry and applying several selection layers, we screened peptide libraries for moieties inducing antibodies selectively reacting with Aß-aggregates. The technology identified a pool of peptide candidates; two, AFFITOPES AD01 and AD02, were assessed as vaccination antigens and compared to Aβ1-6, the targeted epitope. When conjugated to Keyhole Limpet Hemocyanin (KLH) and adjuvanted with aluminum, all three peptides induced Aß-targeting antibodies (Abs). In contrast to Aß1-6, AD01- or AD02-induced Abs were characterized by selectivity for aggregated forms of Aß and absence of reactivity with related molecules such as Amyloid Precursor Protein (APP)/ secreted APP-alpha (sAPPa). Administration of AFFITOPE-vaccines to APP-transgenic mice was found to reduce their cerebral amyloid burden, the associated neuropathological alterations and to improve their cognitive functions. Thus, the AFFITOME-technology delivers vaccines capable of inducing a distinct Ab response. Their features may be beneficial to AD-patients, a hypothesis currently tested within a phase-II-study

    PET imaging of brain inflammation during early epileptogenesis in a rat model of temporal lobe epilepsy.

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    Background Recently, inflammatory cascades have been suggested as a target for epilepsy therapy. Positron emission tomography (PET) imaging offers the unique possibility to evaluate brain inflammation longitudinally in a non-invasive translational manner. This study investigated brain inflammation during early epileptogenesis in the post-kainic acid-induced status epilepticus (KASE) model with post-mortem histology and in vivo with [18F]-PBR111 PET. Methods Status epilepticus (SE) was induced (N = 13) by low-dose injections of KA, while controls (N = 9) received saline. Translocator protein (TSPO) expression and microglia activation were assessed with [125I]-CLINDE autoradiography and OX-42 immunohistochemistry, respectively, 7 days post-SE. In a subgroup of rats, [18F]-PBR111 PET imaging with metabolite-corrected input function was performed before post-mortem evaluation. [18F]-PBR111 volume of distribution (V t) in volume of interests (VOIs) was quantified by means of kinetic modelling and a VOI/metabolite-corrected plasma activity ratio. Results Animals with substantial SE showed huge overexpression of TSPO in vitro in relevant brain regions such as the hippocampus and amygdala (P < 0.001), while animals with mild symptoms displayed a smaller increase in TSPO in amygdala only (P < 0.001). TSPO expression was associated with OX-42 signal but without obvious cell loss. Similar in vivo [18F]-PBR111 increases in V t and the simplified ratio were found in key regions such as the hippocampus (P < 0.05) and amygdala (P < 0.01). Conclusion Both post-mortem and in vivo methods substantiate that the brain regions important in seizure generation display significant brain inflammation during epileptogenesis in the KASE model. This work enables future longitudinal investigation of the role of brain inflammation during epileptogenesis and evaluation of anti-inflammatory treatments. © 2012, Springer
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