The role of atrial natriuretic peptide to attenuate inflammation in a mouse skin wound and individually perfused rat mesenteric microvessels.

We tested the hypothesis that the anti-inflammatory actions of atrial natriuretic peptide (ANP) result from the modulation of leukocyte adhesion to inflamed endothelium and not solely ANP ligation of endothelial receptors to stabilize endothelial barrier function. We measured vascular permeability to albumin and accumulation of fluorescent neutrophils in a full-thickness skin wound on the flank of LysM-EGFP mice 24 h after formation. Vascular permeability in individually perfused rat mesenteric microvessels was also measured after leukocytes were washed out of the vessel lumen. Thrombin increased albumin permeability and increased the accumulation of neutrophils. The thrombin-induced inflammatory responses were attenuated by pretreating the wound with ANP (30 min). During pretreatment ANP did not lower permeability, but transiently increased baseline albumin permeability concomitant with the reduction in neutrophil accumulation. ANP did not attenuate acute increases in permeability to histamine and bradykinin in individually perfused rat microvessels. The hypothesis that anti-inflammatory actions of ANP depend solely on endothelial responses that stabilize the endothelial barrier is not supported by our results in either individually perfused microvessels in the absence of circulating leukocytes or the more chronic skin wound model. Our results conform to the alternate hypothesis that ANP modulates the interaction of leukocytes with the inflamed microvascular wall of the 24 h wound. Taken together with our previous observations that ANP reduces deformability of neutrophils and their strength of attachment, rolling, and transvascular migration, these observations provide the basis for additional investigations of ANP as an anti-inflammatory agent to modulate leukocyte-endothelial cell interactions

Group 2 Innate Lymphoid Cells Are Redundant in Experimental Renal Ischemia-Reperfusion Injury.

Acute kidney injury (AKI) can be fatal and is a well-defined risk factor for the development of chronic kidney disease. Group 2 innate lymphoid cells (ILC2s) are innate producers of type-2 cytokines and are critical regulators of homeostasis in peripheral organs. However, our knowledge of their function in the kidney is relatively limited. Recent evidence suggests that increasing ILC2 numbers by systemic administration of recombinant interleukin (IL)-25 or IL-33 protects against renal injury. Whilst ILC2s can be induced to protect against ischemic- or chemical-induced AKI, the impact of ILC2 deficiency or depletion on the severity of renal injury is unknown. Firstly, the phenotype and location of ILC2s in the kidney was assessed under homeostatic conditions. Kidney ILC2s constitutively expressed high levels of IL-5 and were located in close proximity to the renal vasculature. To test the functional role of ILC2s in the kidney, an experimental model of renal ischemia-reperfusion injury (IRI) was used and the severity of injury was assessed in wild-type, ILC2-reduced, ILC2-deficient, and ILC2-depleted mice. Surprisingly, there were no differences in histopathology, collagen deposition or mRNA expression of injury-associated (Lcn2), inflammatory (Cxcl1, Cxcl2, and Tnf) or extracellular matrix (Col1a1, Fn1) factors following IRI in the absence of ILC2s. These data suggest the absence of ILC2s does not alter the severity of renal injury, suggesting possible redundancy. Therefore, other mechanisms of type 2-mediated immune cell activation likely compensate in the absence of ILC2s. Hence, a loss of ILC2s is unlikely to increase susceptibility to, or severity of AKI

Impact of spin-orbit coupling on quantum Hall nematic phases

Anisotropic charge transport is observed in a two-dimensional (2D) hole system in a perpendicular magnetic field at filling factors nu=7/2, nu=11/2, and nu=13/2 at low temperature. In stark contrast, the transport at nu=9/2 is isotropic for all temperatures. Isotropic hole transport at nu=7/2 is restored for sufficiently low 2D densities or an asymmetric confining potential. The density and symmetry dependences of the observed anisotropies suggest that strong spin-orbit coupling in the hole system contributes to the unusual transport behavior.Comment: 4 pages, 4 figure

On a Cahn--Hilliard--Darcy system for tumour growth with solution dependent source terms

We study the existence of weak solutions to a mixture model for tumour growth that consists of a Cahn--Hilliard--Darcy system coupled with an elliptic reaction-diffusion equation. The Darcy law gives rise to an elliptic equation for the pressure that is coupled to the convective Cahn--Hilliard equation through convective and source terms. Both Dirichlet and Robin boundary conditions are considered for the pressure variable, which allows for the source terms to be dependent on the solution variables.Comment: 18 pages, changed proof from fixed point argument to Galerkin approximatio

Composite Fermion Wavefunctions Derived by Conformal Field Theory

The Jain theory of hierarchical Hall states is reconsidered in the light of recent analyses that have found exact relations between projected Jain wavefunctions and conformal field theory correlators. We show that the underlying conformal theory is precisely given by the W-infinity minimal models introduced earlier. This theory involves a reduction of the multicomponent Abelian theory that is similar to the projection to the lowest Landau level in the Jain approach. The projection yields quasihole excitations obeying non-Abelian fractional statistics. The analysis closely parallels the bosonic conformal theory description of the Pfaffian and Read-Rezayi states.Comment: 4 pages, 1 figur

Specific heat and validity of quasiparticle approximation in the half-filled Landau level

We calculate the specific heat of composite fermion system in the half-filled Landau level. Two different methods are used to examine validity of the quasiparticle approximation when the two-body interaction is given by $V(q) = V_0 / q^{2-\eta}$ ($1 \le \eta \le 2$). The singular part of the specific heat is calculated from the free energy of the gauge field, which is compared with the specific heat calculated from the quasiparticle approximation via the singular self-energy correction due to the gauge field fluctuations. It turns out that two results are in general different and they coincide only for the case of the Coulomb interaction ($\eta = 1$). This result supports the fact that the quasiparticle approximation is valid only for the case of the Coulomb interaction. It is emphasized that this result is obtained by looking at a gauge-invariant quantity -- the specific heat.Comment: 8 pages, Revte

Influence of gauge-field fluctuations on composite fermions near the half-filled state

Taking into account the transverse gauge field fluctuations, which interact with composite fermions, we examine the finite temperature compressibility of the fermions as a function of an effective magnetic field $\Delta B = B - 2 n_e hc/e$ ($n_e$ is the density of electrons) near the half-filled state. It is shown that, after including the lowest order gauge field correction, the compressibility goes as ${\partial n \over \partial \mu} \propto e^{- \Delta \omega_c / 2 T} \left ( 1 + {A (\eta) \over \eta - 1} {(\Delta \omega_c)^{2 \over 1 + \eta} \over T} \right )$ for $T \ll \Delta \omega_c$, where $\Delta \omega_c = {e \Delta B \over mc}$. Here we assume that the interaction between the fermions is given by $v ({\bf q}) = V_0 / q^{2 - \eta} \ (1 \le \eta \le 2)$, where $A (\eta)$ is a $\eta$ dependent constant. This result can be interpreted as a divergent correction to the activation energy gap and is consistent with the divergent renormalization of the effective mass of the composite fermions.Comment: Plain Tex, 24 pages, 5 figures available upon reques