Constructing and Characterising Solar Structure Models for Computational Helioseismology

In this paper, we construct background solar models that are stable against convection, by modifying the vertical pressure gradient of Model S (Christensen-Dalsgaard et al., 1996, Science, 272, 1286) relinquishing hydrostatic equilibrium. However, the stabilisation affects the eigenmodes that we wish to remain as close to Model S as possible. In a bid to recover the Model S eigenmodes, we choose to make additional corrections to the sound speed of Model S before stabilisation. No stabilised model can be perfectly solar-like, so we present three stabilised models with slightly different eigenmodes. The models are appropriate to study the f and p1 to p4 modes with spherical harmonic degrees in the range from 400 to 900. Background model CSM has a modified pressure gradient for stabilisation and has eigenfrequencies within 2% of Model S. Model CSM_A has an additional 10% increase in sound speed in the top 1 Mm resulting in eigenfrequencies within 2% of Model S and eigenfunctions that are, in comparison with CSM, closest to those of Model S. Model CSM_B has a 3% decrease in sound speed in the top 5 Mm resulting in eigenfrequencies within 1% of Model S and eigenfunctions that are only marginally adversely affected. These models are useful to study the interaction of solar waves with embedded three-dimensional heterogeneities, such as convective flows and model sunspots. We have also calculated the response of the stabilised models to excitation by random near-surface sources, using simulations of the propagation of linear waves. We find that the simulated power spectra of wave motion are in good agreement with an observed SOHO/MDI power spectrum. Overall, our convectively stabilised background models provide a good basis for quantitative numerical local helioseismology. The models are available for download from http://www.mps.mpg.de/projects/seismo/NA4/.Comment: 35 pages, 23 figures Changed title Updated Figure 1

Modeling the Subsurface Structure of Sunspots

While sunspots are easily observed at the solar surface, determining their subsurface structure is not trivial. There are two main hypotheses for the subsurface structure of sunspots: the monolithic model and the cluster model. Local helioseismology is the only means by which we can investigate subphotospheric structure. However, as current linear inversion techniques do not yet allow helioseismology to probe the internal structure with sufficient confidence to distinguish between the monolith and cluster models, the development of physically realistic sunspot models are a priority for helioseismologists. This is because they are not only important indicators of the variety of physical effects that may influence helioseismic inferences in active regions, but they also enable detailed assessments of the validity of helioseismic interpretations through numerical forward modeling. In this paper, we provide a critical review of the existing sunspot models and an overview of numerical methods employed to model wave propagation through model sunspots. We then carry out an helioseismic analysis of the sunspot in Active Region 9787 and address the serious inconsistencies uncovered by \citeauthor{gizonetal2009}~(\citeyear{gizonetal2009,gizonetal2009a}). We find that this sunspot is most probably associated with a shallow, positive wave-speed perturbation (unlike the traditional two-layer model) and that travel-time measurements are consistent with a horizontal outflow in the surrounding moat.Comment: 73 pages, 19 figures, accepted by Solar Physic

Bovine herpesvirus 1-induced apoptotic cell death: role of glycoprotein D

Bovine herpesvirus 1 (BHV-1) induces apoptotic cell death in peripheral blood mononuclear cells and in bovine B lymphoma (BL-3) cells. Attachment but not penetration of BHV-1 is necessary to induce apoptosis in target cells, suggesting that one or more BHV-1 envelope glycoproteins could be involved in the activation of the apoptotic process. In the present study, we demonstrate that, although BHV-1 virions devoid of glycoprotein D (BHV-1 gD-/-) still bind to BL-3 cells, they are no longer able to induce apoptosis. In contrast, virions that contain glycoprotein D (gD) in the viral envelope but do not genetically encode gD (BHV-1 gD-/+) induce a level of apoptosis comparable to that produced by wild-type (wt) BHV-1. In addition, monoclonal antibodies directed against gD, but not against gB or gC, strongly reduced the high levels of apoptosis induced by BHV-1. These observations demonstrate that the induction of apoptosis is directly due to BHV-1 viral particles harboring gD in the viral envelope. Interestingly, binding of affinity-purified gD to BL-3 cells did not induce apoptosis but inhibited the ability of wt BHV-1 to induce apoptosis. Altogether, these results provide evidence for the direct or indirect involvement of gD in the mechanism by which BHV-1 induces apoptosis