12 research outputs found

    Modelling the rapid near-surface expansion of gas slugs in low-viscosity magmas.

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    The ascent of large gas bubbles (slugs) in vertical cylindrical conduits and low-viscosity magmas is simulated using 1D mathematical and 3D computational fluid dynamic (CFD) models. Following laboratory evidence, the 1D model defines a constant rise velocity for the slug base and allows gas expansion to accelerate the slug nose through the overlying fluid during ascent. The evolution of rapidly expanding gas slugs observed in laboratory experiments is reproduced well and, at volcano scales, predicts at-surface overpressures of several atmospheres without requiring any initial overpressure at depth. The near-surface dynamics increase slug nose velocities through the overlying magma by a factor of c. 2.5 and the gas expansion results in pre-burst magma surface velocities of c. 35m s21. To examine pressure distributions and the forces exerted on a conduit, 3D CFD simulations were carried out. At volcano scales, the vertical single forces during final slug ascent to the surface are c. 106 N, two orders of magnitude smaller than those associated with verylong-period seismic events at Stromboli. This supports a previous interpretation of these events in which they are generated by gas slugs flowing through changes in conduit geometry, rather than being the direct result of slug eruption processes

    Degassing at low magma-viscosity volcanoes : quantifying the transition between passive bubble-burst and Strombolian eruption.

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    At many volcanoes, low magma-viscosities allow persistent degassing over a range of styles from explosive Strombolian activity to gas ‘puffing’ and passive degassing. It is generally accepted that Strombolian eruptions reflect the bursting of large bubbles (gas slugs) at the magma surface and that relatively quiescent ‘puffing’ indicates the presence of significantly smaller bubbles or slugs. Here, we address this qualitative range and derive a dimensionless parameter, P*slim, to quantify and distinguish different regimes of ‘burst vigour’. For P*slim ≀ 1, ‘passive’ activity is anticipated and measurable parameters such as infrasonic amplitude will be small. For P⁎slimN1, bursting slugs will be energetic, and surface effects are anticipated to increase with increasing P*slim. Various physical parameters recorded during laboratory experiments and simulated through numerical models are shown to demonstrate the same trends when parameterised by P*slim. Hence, P*slim provides a straightforward relationship between changes in measurable surface effects and the system's subsurface physical parameters and, for energetic activity of a particular system, burst effects are shown to be proportional to the square root of the gas mass involved. Effect magnitudes are also shown to be a function of atmospheric pressure and application of P*slim parameterisation to planetary scenarios produces results in line with our current understanding of planetary volcanism

    Additional file 1: Figure S1. of A 26-hour system of highly sensitive whole genome sequencing for emergency management of genetic diseases

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    Screen-shots demonstrating the functionality of SSAGA. A. The clinical feature entry page. Synonyms for each feature are entered in the top left box. Upon entry, a list of matching HPO terms is displayed. The appropriate HPO term is selected and added to the patientñ€™s feature list in the box on the right. This is performed for each clinical feature. In this case, patient CMH672ref, the patient had 11 clinical features that included neonatal seizures and a characteristic facies. B. Upon clicking the ñ€˜Get Diagnosisñ€™ button, the list of all matching diseases is generated. In this case, the differential diagnosis had 1,136 rows, representing 597 genes, of which 222 matched two or more clinical features. (PDF 240 kb

    APOE is a potential modifier gene in an autosomal dominant form of frontotemporal dementia (IBMPFD)

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    PurposeInclusion-body myopathy, Paget's disease of bone and frontotemporal dementia is an adult-onset autosomal dominant illness (IBMPFD) caused by mutations in the valosin-containing protein (VCP) on chromosome 9p21.1-p12. The penetrance of the gene is 82% for myopathy, 49% for Paget's disease, but may be as low as 30% for frontotemporal dementia. Modifier genes could account for decreased frontotemporal dementia penetrance. In this study apolipoprotein-E (APOE) was evaluated for this role in IBMPFD families based on its known modifier effect in Alzheimer's disease.MethodsFrom a database of 231 members of 15 families, 174 had APOE genotype available for analysis. Logistic regressions on APOE genotype and frontotemporal dementia were performed, using appropriate covariates.Results and conclusionFTD was associated with APOE 4 genotype (P=0.0002), myopathy (P=0.0006), and age (P=0.01), but not microtubule associated protein tau (MAPT) H2 haplotype (P=0.5) or gender (0.09) after adjustment for membership in pedigrees with at least one APOE 4 genotype. These data suggest a potential link between APOE 4 genotype and the specific form of frontotemporal dementia found in IBMPFD. The molecular basis of this link bears further investigation. We did not observe an association of frontotemporal dementia and H2 MAPT haplotype
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