252 research outputs found
A Hamiltonian description of finite-time singularity in Euler's fluid equations
The recently proposed low degree-of-freedom model of Moffat and Kimura [1,2]
for describing the approach to finite-time singularity of the incompressible
Euler fluid equations is investigated. The model assumes an initial
finite-energy configuration of two vortex rings placed symmetrically on two
tilted planes. The Hamiltonian structure of the inviscid limit of the model is
obtained. The associated noncanonical Poisson bracket [3] and two invariants,
one that serves as the Hamiltonian and the other a Casimir invariant, are
discovered. It is shown that the system is integrable with a solution that lies
on the intersection for the two invariants, just as for the free rigid body of
mechanics whose solution lies on the intersection of the kinetic energy and
angular momentum surfaces. Also, a direct quadrature is given and used to
demonstrate the Leray form for finite-time singularity in the model. To the
extent the Moffat and Kimura model accurately represents Euler's ideal fluid
equations of motion, we have shown the existence of finite-time singularity
Determination of the structure of Ne by full-microscopic framework
We perform the first quantitative analysis of the reaction cross sections of
Ne by C at 240 MeV/nucleon, using the double-folding model
(DFM) with the Melbourne -matrix and the deformed projectile density
calculated by the antisymmetrized molecular dynamics (AMD). To describe the
tail of the last neutron of Ne, we adopt the resonating group method
(RGM) combined with AMD. The theoretical prediction excellently reproduce the
measured cross sections of Ne with no adjustable parameters. The
ground state properties of Ne, i.e., strong deformation and a halo
structure with spin-parity , are clarified.Comment: 4 pages, 4 figures, 2 table
Deformation effect on total reaction cross sections for neutron-rich Ne-isotopes
Isotope-dependence of measured reaction cross sections in scattering of
Ne isotopes from C target at 240 MeV/nucleon is analyzed by
the double-folding model with the Melbourne -matrix. The density of
projectile is calculated by the mean-field model with the deformed Wood-Saxon
potential. The deformation is evaluated by the antisymmetrized molecular
dynamics. The deformation of projectile enhances calculated reaction cross
sections to the measured values.Comment: 6 pages, 4 figures, 2 table
Herpes simplex virus type 1 UL14 tegument protein regulates intracellular compartmentalization of major tegument protein VP16
<p>Abstract</p> <p>Background</p> <p>Herpes simplex virus type 1 (HSV-1) has a complicated life-cycle, and its genome encodes many components that can modify the cellular environment to facilitate efficient viral replication. The protein UL14 is likely involved in viral maturation and egress (Cunningham C. et al), and it facilitates the nuclear translocation of viral capsids and the tegument protein VP16 during the immediate-early phase of infection (Yamauchi Y. et al, 2008). UL14 of herpes simplex virus type 2 exhibits multiple functions (Yamauchi Y. et al, 2001, 2002, 2003).</p> <p>Methods</p> <p>To better understand the function(s) of UL14, we generated VP16-GFP-incorporated UL14-mutant viruses with either single (K51M) or triple (R60A, R64A, E68D) amino acid substitutions in the heat shock protein (HSP)-like sequence of UL14. We observed the morphology of cells infected with UL14-null virus and amino acid-substituted UL14-mutant viruses at different time points after infection.</p> <p>Results</p> <p>UL14(3P)-VP16GFP and UL14D-VP16GFP (UL14-null) viruses caused similar defects with respect to growth kinetics, compartmentalization of tegument proteins, and cellular morphology in the late phase. Both the UL14D-VP16GFP and UL14(3P)-VP16GFP viruses led to the formation of an aggresome that incorporated some tegument proteins but did not include nuclear-egressed viral capsids.</p> <p>Conclusions</p> <p>Our findings suggest that a cluster of charged residues within the HSP-like sequence of UL14 is important for the molecular chaperone-like functions of UL14, and this activity is required for the acquisition of functionality of VP16 and UL46. In addition, UL14 likely contributes to maintaining cellular homeostasis following infection, including cytoskeletal organization. However, direct interactions between UL14 and VP16, UL46, or other cellular or viral proteins remain unclear.</p
High hydrostatic pressure induces counterclockwise to clockwise reversals of the Escherichia coli flagellar motor.
The bacterial flagellar motor is a reversible rotary machine that rotates a left-handed helical filament, allowing bacteria to swim toward a more favorable environment. The direction of rotation reverses from counterclockwise (CCW) to clockwise (CW), and vice versa, in response to input from the chemotaxis signaling circuit. CW rotation is normally caused by binding of the phosphorylated response regulator CheY (CheY-P), and strains lacking CheY are typically locked in CCW rotation. The detailed mechanism of switching remains unresolved because it is technically difficult to regulate the level of CheY-P within the concentration range that produces flagellar reversals. Here, we demonstrate that high hydrostatic pressure can induce CW rotation even in the absence of CheY-P. The rotation of single flagellar motors in Escherichia coli cells with the cheY gene deleted was monitored at various pressures and temperatures. Application of >120 MPa pressure induced a reversal from CCW to CW at 20°C, although at that temperature, no motor rotated CW at ambient pressure (0.1 MPa). At lower temperatures, pressure-induced changes in direction were observed at pressures of <120 MPa. CW rotation increased with pressure in a sigmoidal fashion, as it does in response to increasing concentrations of CheY-P. Application of pressure generally promotes the formation of clusters of ordered water molecules on the surfaces of proteins. It is possible that hydration of the switch complex at high pressure induces structural changes similar to those caused by the binding of CheY-P
Ground-state properties of neutron-rich Mg isotopes
We analyze recently-measured total reaction cross sections for 24-38Mg
isotopes incident on 12C targets at 240 MeV/nucleon by using the folding model
and antisymmetrized molecular dynamics(AMD). The folding model well reproduces
the measured reaction cross sections, when the projectile densities are
evaluated by the deformed Woods-Saxon (def-WS) model with AMD deformation.
Matter radii of 24-38Mg are then deduced from the measured reaction cross
sections by fine-tuning the parameters of the def-WS model. The deduced matter
radii are largely enhanced by nuclear deformation. Fully-microscopic AMD
calculations with no free parameter well reproduce the deduced matter radii for
24-36Mg, but still considerably underestimate them for 37,38Mg. The large
matter radii suggest that 37,38Mg are candidates for deformed halo nucleus. AMD
also reproduces other existing measured ground-state properties (spin-parity,
total binding energy, and one-neutron separation energy) of Mg isotopes.
Neutron-number (N) dependence of deformation parameter is predicted by AMD.
Large deformation is seen from 31Mg with N = 19 to a drip-line nucleus 40Mg
with N = 28, indicating that both the N = 20 and 28 magicities disappear. N
dependence of neutron skin thickness is also predicted by AMD.Comment: 15 pages, 13 figures, to be published in Phys. Rev.
Immunization with a highly attenuated replication-competent herpes simplex virus type 1 mutant, HF10, protects mice from genital disease caused by herpes simplex virus type 2
Genital herpes is an intractable disease caused mainly by herpes simplex virus (HSV) type 2 (HSV-2), and is a major concern in public health. A previous infection with HSV type 1 (HSV-1) enhances protection against primary HSV-2 infection to some extent. In this study, we evaluated the ability of HF10, a naturally occurring replication-competent HSV-1 mutant, to protect against genital infection in mice caused by HSV-2. Subcutaneous inoculation of HF10-immunized mice against lethal infection by HSV-2, and attenuated the development of genital ulcer diseases. Immunization with HF10 inhibited HSV-2 replication in the mouse vagina, reduced local inflammation, controlled emergence of neurological dysfunctions of HSV-2 infection, and increased survival. In HF10-immunized mice, we observed rapid and increased production of interferon-γ in the vagina in response to HSV-2 infection, and numerous CD4+ and a few CD8+ T cells localized to the infective focus. CD4+ T cells invaded the mucosal subepithelial lamina propria. Thus, the protective effect of HF10 was related to induction of cellular immunity, mediated primarily by Th1 CD4+ cells. These data indicate that the live attenuated HSV-1 mutant strain HF10 is a promising candidate antigen for a vaccine against genital herpes caused by HSV-2
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