138 research outputs found

    Tracing Nitrogen in Volcanic and Geothermal Volatiles from the Nicaraguan Volcanic Front

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    We report new chemical and isotopic data from 26 volcanic and geothermal gases, vapor condensates, and thermal water samples, collected along the Nicaraguan volcanic front. The samples were analyzed for chemical abundances and stable isotope compositions, with a focus on nitrogen abundances and isotope ratios. These data are used to evaluate samples for volatile contributions from magma, air, air-saturated water, and the crust. Samples devoid of crustal contamination (based upon He isotope composition) but slightly contaminated by air or air-saturated water are corrected using N2/Ar ratios in order to obtain primary magmatic values, composed of contributions from upper mantle and subducted hemipelagic sediment on the down-going plate. Using a mantle endmember with d15N= 5&and N2/He = 100 and a subducted sediment component with d15N=+7& and N2/He = 10,500, the average sediment contribution to Nicaraguan volcanic and geothermal gases was determined to be 71%. Most of the gases were dominated by sediment-derived nitrogen, but gas from Volca´n Mombacho, the southernmost sampling location, had a mantle signature (46% from subducted sediment, or 54% from the mantle) and an affinity with mantle-dominated gases discharging from Costa Rica localities to the south. High CO2/N2 exc. ratios (N2 exc. is the N2 abundance corrected for contributions from air) in the south are similar to those in Costa Rica, and reflect the predominant mantle wedge input, whereas low ratios in the north indicate contribution by altered oceanic crust and/or preferential release of nitrogen over carbon from the subducting slab. Sediment-derived nitrogen fluxes at the Nicaraguan volcanic front, estimated by three methods, are 7.8 · 108 mol N/a from 3He flux, 6.9 · 108 mol/a from SO2 flux, and 2.1 · 108 and 1.3 · 109 mol/a from CO2 fluxes calculated from 3He and SO2, respectively. These flux results are higher than previous estimates for Central America, reflecting the high sediment-derived volatile contribution and the high nitrogen content of geothermal and volcanic gases in Nicaragua. The fluxes are also similar to but higher than estimated hemipelagic nitrogen inputs at the trench, suggesting addition of N from altered oceanic basement is needed to satisfy these flux estimates. The similarity of the calculated input of N via the trench to our calculated outputs suggests that little or none of the subducted nitrogen is being recycled into the deeper mantle, and that it is, instead, returned to the surface via arc volcanism

    Carbon export from mountain forests enhanced by earthquake-triggered landslides over millennia

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    Rapid ground accelerations during earthquakes can trigger landslides that disturb mountain forests and harvest carbon from soils and vegetation. Although infrequent over human timescales, these co-seismic landslides can set the rates of geomorphic processes over centuries to millennia. However, the long-term impacts of earthquakes and landslides on carbon export from the biosphere remain poorly constrained. Here, we examine the sedimentary fill of Lake Paringa, New Zealand, which is fed by a river draining steep mountains proximal to the Alpine Fault. Carbon isotopes reveal enhanced accumulation rates of biospheric carbon after four large earthquakes over the past ~1,100 years, probably reflecting delivery of soil-derived carbon eroded by deep-seated landslides. Cumulatively these pulses of earthquake-mobilized carbon represent 23 ± 5% of the record length, but account for 43 ± 5% of the biospheric carbon in the core. Landslide simulations suggest that 14 ± 5 million tonnes of carbon (MtC) could be eroded in each earthquake. Our findings support a link between active tectonics and the surface carbon cycle and suggest that large earthquakes can significantly contribute to carbon export from mountain forests over millennia

    Permutation branes and linear matrix factorisations

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    All the known rational boundary states for Gepner models can be regarded as permutation branes. On general grounds, one expects that topological branes in Gepner models can be encoded as matrix factorisations of the corresponding Landau-Ginzburg potentials. In this paper we identify the matrix factorisations associated to arbitrary B-type permutation branes.Comment: 43 pages. v2: References adde

    Nail lacquer films’ surface energies and in vitro water-resistance and adhesion do not predict their in vivo residence

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    The in vivo residence of nail lacquers (which are ideal topical drug carriers for the treatment of nail diseases) determines their frequency of application, and is thereby expected to influence patient adherence and success of treatment. Thus in vitro measurements to indicate lacquers’ in vivo residence are routinely conducted during formulation development. However the literature on in vitro-in vivo correlations is severely limited. Thus, the aim of the work discussed in this paper was to investigate correlations between in vivo residence and in vitro film resistance to water, in vitro film adhesion and surface energy of lacquer films. In vivo measurements were conducted on fingernails in six volunteers. Seven commercially available nail lacquers were tested in commonly-used measurements. Correlations between in vivo residence and in vitro water resistance and adhesion were found to be extremely poor. The surface energies of the lacquer films (which were between 33 and 39 mJ/m2) were also not predictive of in vivo residence. High density polyethylene (HDPE) sheet – whose surface energy was determined to be similar to that of the human nailplate – was found to be a suitable model for the nailplate (when investigating surface energy) and was used in a number of experiments

    Irish cardiac society - Proceedings of annual general meeting held 20th & 21st November 1992 in Dublin Castle

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    Study of the lineshape of the chi(c1) (3872) state

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    A study of the lineshape of the chi(c1) (3872) state is made using a data sample corresponding to an integrated luminosity of 3 fb(-1) collected in pp collisions at center-of-mass energies of 7 and 8 TeV with the LHCb detector. Candidate chi(c1)(3872) and psi(2S) mesons from b-hadron decays are selected in the J/psi pi(+)pi(-) decay mode. Describing the lineshape with a Breit-Wigner function, the mass splitting between the chi(c1 )(3872) and psi(2S) states, Delta m, and the width of the chi(c1 )(3872) state, Gamma(Bw), are determined to be (Delta m=185.598 +/- 0.067 +/- 0.068 Mev,)(Gamma BW=1.39 +/- 0.24 +/- 0.10 Mev,) where the first uncertainty is statistical and the second systematic. Using a Flatte-inspired model, the mode and full width at half maximum of the lineshape are determined to be (mode=3871.69+0.00+0.05 MeV.)(FWHM=0.22-0.04+0.13+0.07+0.11-0.06-0.13 MeV, ) An investigation of the analytic structure of the Flatte amplitude reveals a pole structure, which is compatible with a quasibound D-0(D) over bar*(0) state but a quasivirtual state is still allowed at the level of 2 standard deviations

    Measurement of the CKM angle γγ in B±DK±B^\pm\to D K^\pm and B±Dπ±B^\pm \to D π^\pm decays with DKS0h+hD \to K_\mathrm S^0 h^+ h^-

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    A measurement of CPCP-violating observables is performed using the decays B±DK±B^\pm\to D K^\pm and B±Dπ±B^\pm\to D \pi^\pm, where the DD meson is reconstructed in one of the self-conjugate three-body final states KSπ+πK_{\mathrm S}\pi^+\pi^- and KSK+KK_{\mathrm S}K^+K^- (commonly denoted KSh+hK_{\mathrm S} h^+h^-). The decays are analysed in bins of the DD-decay phase space, leading to a measurement that is independent of the modelling of the DD-decay amplitude. The observables are interpreted in terms of the CKM angle γ\gamma. Using a data sample corresponding to an integrated luminosity of 9fb19\,\text{fb}^{-1} collected in proton-proton collisions at centre-of-mass energies of 77, 88, and 13TeV13\,\text{TeV} with the LHCb experiment, γ\gamma is measured to be (68.75.1+5.2)\left(68.7^{+5.2}_{-5.1}\right)^\circ. The hadronic parameters rBDKr_B^{DK}, rBDπr_B^{D\pi}, δBDK\delta_B^{DK}, and δBDπ\delta_B^{D\pi}, which are the ratios and strong-phase differences of the suppressed and favoured B±B^\pm decays, are also reported

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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