40 research outputs found
Parity-Violating Hydrodynamics in 2+1 Dimensions
We study relativistic hydrodynamics of normal fluids in two spatial
dimensions. When the microscopic theory breaks parity, extra transport
coefficients appear in the hydrodynamic regime, including the Hall viscosity,
and the anomalous Hall conductivity. In this work we classify all the transport
coefficients in first order hydrodynamics. We then use properties of response
functions and the positivity of entropy production to restrict the possible
coefficients in the constitutive relations. All the parity-breaking transport
coefficients are dissipationless, and some of them are related to the
thermodynamic response to an external magnetic field and to vorticity. In
addition, we give a holographic example of a strongly interacting relativistic
fluid where the parity-violating transport coefficients are computable.Comment: 39+1 page
Revealed fuzzy preferences
Bondareva O. Revealed fuzzy preferences. Working Papers. Institute of Mathematical Economics. Vol 183. Bielefeld: Center for Mathematical Economics; 1990
Generation of a Protective T-Cell Response Following Coronavirus Infection of the Central Nervous System Is Not Dependent on IL-12/23 Signaling
The functional role of IL-12 and IL-23 in host defense and disease following viral infection of the CNS was determined. Instillation of mouse hepatitis virus (MHV, a positive-strand RNA virus) into the CNS of mice results in acute encephalitis followed by a chronic immune-mediated demyelinating disease. Antibody-mediated blocking of either IL-23 (anti-IL-23p19) or IL-12 and IL-23 (anti-IL-12/23p40) signaling did not mute T-cell trafficking into the CNS or antiviral effector responses and mice were able to control viral replication within the brain. Therapeutic administration of either anti-IL-23p19 or anti-IL-12/23p40 to mice with viral-induced demyelination did not attenuate T-cell or macrophage infiltration into the CNS nor improve clinical disease or diminish white matter damage. In contrast, treatment of mice with anti-IL-12/23p40 or anti-IL-23p19 resulted in inhibition of the autoimmune model of demyelination, experimental autoimmune encephalomyelitis (EAE). These data indicate that (1) IL-12 and IL-23 signaling are dispensable in generating a protective T-cell response following CNS infection with MHV, and (2) IL-12 and IL-23 do not contribute to demyelination in a model independent of autoimmune T-cell–mediated pathology. Therefore, therapeutic targeting of IL-12 and/or IL-23 for the treatment of autoimmune diseases may offer unique advantages by reducing disease severity without muting protective responses following viral infection