Nonaxisymmetric simulations of the Princeton magnetorotational instability experiment with insulating and conducting axial boundaries.

Stability and nonlinear evolution of rotating magnetohydrodynamic flows in the Princeton magnetorotational instability (MRI) experiment are examined using three-dimensional non-axisymmetric simulations. In particular, the effect of axial boundary conductivity on a free Stewartson-Shercliff layer (SSL) is numerically investigated using the spectral finite-element Maxwell and Navier Stokes (SFEMaNS) code. The free SSL is established by a sufficiently strong magnetic field imposed axially across the differentially rotating fluid with two rotating rings enforcing the boundary conditions. Numerical simulations show that the response of the bulk fluid flow is vastly different in the two different cases of insulating and conducting end caps. We find that, for the insulating end caps, there is a transition from stability to instability of a Kelvin-Helmholtz-like mode that saturates at an azimuthal mode number m=1, whereas for the conducting end caps, the reinforced coupling between the magnetic field and the bulk fluid generates a strong radially localized shear in the azimuthal velocity resulting in axisymmetric Rayleigh-like modes even at reduced thresholds for the axial magnetic field. For reference, three-dimensional nonaxisymmetric simulations have also been performed in the MRI unstable regime to compare the modal structures.

Effects of axial boundary conductivity on a free Stewartson-Shercliff layer.

The effects of axial boundary conductivity on the formation and stability of a magnetized free Stewartson-Shercliff layer (SSL) in a short Taylor-Couette device are reported. As the axial field increases with insulating endcaps, hydrodynamic Kelvin-Helmholtz-type instabilities set in at the SSLs of the conducting fluid, resulting in a much reduced flow shear. With conducting endcaps, SSLs respond to an axial field weaker by the square root of the conductivity ratio of endcaps to fluid. Flow shear continuously builds up as the axial field increases despite the local violation of the Rayleigh criterion, leading to a large number of hydrodynamically unstable modes. Numerical simulations of both the mean flow and the instabilities are in agreement with the experimental results.

Discovery of mouse spleen signaling responses to anthrax using label-free quantitative phosphoproteomics via mass spectrometry.

Inhalational anthrax is caused by spores of the bacterium Bacillus anthracis (B. anthracis), and is an extremely dangerous disease that can kill unvaccinated victims within 2 weeks. Modern antibiotic-based therapy can increase the survival rate to ∼50%, but only if administered presymptomatically (within 24-48 h of exposure). To discover host signaling responses to presymptomatic anthrax, label-free quantitative phosphoproteomics via liquid chromatography coupled to mass spectrometry was used to compare spleens from uninfected and spore-challenged mice over a 72 h time-course. Spleen proteins were denatured using urea, reduced using dithiothreitol, alkylated using iodoacetamide, and digested into peptides using trypsin, and the resulting phosphopeptides were enriched using titanium dioxide solid-phase extraction and analyzed by nano-liquid chromatography-Linear Trap Quadrupole-Orbitrap-MS(/MS). The fragment ion spectra were processed using DeconMSn and searched using both Mascot and SEQUEST resulting in 252,626 confident identifications of 6248 phosphopeptides (corresponding to 5782 phosphorylation sites). The precursor ion spectra were deisotoped using Decon2LS and aligned using MultiAlign resulting in the confident quantitation of 3265 of the identified phosphopeptides. ANOVAs were used to produce a q-value ranked list of host signaling responses. Late-stage (48-72 h postchallenge) Sterne strain (lethal) infections resulted in global alterations to the spleen phosphoproteome. In contrast, ΔSterne strain (asymptomatic; missing the anthrax toxin) infections resulted in 188 (5.8%) significantly altered (q<0.05) phosphopeptides. Twenty-six highly tentative phosphorylation responses to early-stage (24 h postchallenge) anthrax were discovered (q<0.5), and ten of these originated from eight proteins that have known roles in the host immune response. These tentative early-anthrax host response signaling events within mouse spleens may translate into presymptomatic diagnostic biomarkers of human anthrax detectable within circulating immune cells, and could aid in the identification of pathogenic mechanisms and therapeutic targets.