Tunneling in Fractional Quantum Hall line junctions

We study the tunneling current between two counterpropagating edge modes described by chiral Luttinger liquids when the tunneling takes place along an extended region. We compute this current perturbatively by using a tunnel Hamiltonian. Our results apply to the case of a pair of different two-dimensional electron gases in the fractional quantum Hall regime separated by a barrier, e. g. electron tunneling. We also discuss the case of strong interactions between the edges, leading to nonuniversal exponents even in the case of integer quantum Hall edges. In addition to the expected nonlinearities due to the Luttinger properties of the edges, there are additional interference patterns due to the finite length of the barrier.Comment: 7 pages, RevTex, 12 figs, submitted to Phys Rev

Release of Intracellular Calcium Stores Facilitates Coxsackievirus Entry into Polarized Endothelial Cells

Group B coxsackieviruses (CVB) are associated with viral-induced heart disease and are among the leading causes of aseptic meningitis worldwide. Here we show that CVB entry into polarized brain microvasculature and aortic endothelial cells triggers a depletion of intracellular calcium stores initiated through viral attachment to the apical attachment factor decay-accelerating factor. Calcium release was dependent upon a signaling cascade that required the activity of the Src family of tyrosine kinases, phospholipase C, and the inositol 1,4,5-trisphosphate receptor isoform 3. CVB-mediated calcium release was required for the activation of calpain-2, a calcium-dependent cysteine protease, which controlled the vesicular trafficking of internalized CVB particles. These data point to a specific role for calcium signaling in CVB entry into polarized endothelial monolayers and highlight the unique signaling mechanisms used by these viruses to cross endothelial barriers

The impact of co-infections on fish: a review

International audienceAbstractCo-infections are very common in nature and occur when hosts are infected by two or more different pathogens either by simultaneous or secondary infections so that two or more infectious agents are active together in the same host. Co-infections have a fundamental effect and can alter the course and the severity of different fish diseases. However, co-infection effect has still received limited scrutiny in aquatic animals like fish and available data on this subject is still scarce. The susceptibility of fish to different pathogens could be changed during mixed infections causing the appearance of sudden fish outbreaks. In this review, we focus on the synergistic and antagonistic interactions occurring during co-infections by homologous or heterologous pathogens. We present a concise summary about the present knowledge regarding co-infections in fish. More research is needed to better understand the immune response of fish during mixed infections as these could have an important impact on the development of new strategies for disease control programs and vaccination in fish

ICAR: endoscopic skull‐base surgery

n/

Host responses to Renibacterium salmoninarum and specific components of the pathogen reveal the mechanisms of immune suppression and activation

During infection, Renibacterium salmoninarum survives within the pronephric macrophages of salmonid fish. Therefore, to study the initial phases of the interaction we infected macrophages with live bacteria and analysed the responses of host and pathogen. It was found that the expression of msa encoding the p57 antigen of R. salmoninarum, was constitutive, while the expression of hly and rsh, encoding haemolysins, and lysB and grp was reduced after infection. Macrophages showed a rapid inflammatory response in which the expression of interleukin-1β (IL-1β), major histocompatibility complex class II (MHC II), inducible cyclo-oxygenase (Cox-2), and inducible nitric oxide synthase (iNOS) was enhanced, but tumour necrosis factor-α (TNF-α) expression was greatly reduced initially and then increased. After 5 days, except for TNF-α and MHC II, expression returned to levels approaching those of uninfected macrophages. We propose that R. salmoninarum survives initial contact with macrophages by avoiding and/or interfering with TNF-α-dependent killing pathways. The effects of specific R. salmoninarum components were studied in vivo by injecting fish with DNA vaccine constructs expressing msa, hly, rsh, lysB, or grp. We found that msa reduced the expression of IL-1β, Cox-2, and MHC II but stimulated TNF-α while hly, rsh and grp stimulated MHC II but down-regulated TNF-α. Constructs expressing hly or lysB stimulated iNOS expression and additionally, lysB stimulated TNF-α. The results show how p57 suppresses the host immune system and suggest that the immune mechanisms for the containment of R. salmoninarum infections rely on MHC II- and TNF-α-dependent pathways. Moreover, prolonged stimulation of TNF-α may contribute to the chronic inflammatory pathology of bacterial kidney disease

TRPV3 control of uterine blood vessels

Introduction. Transient receptor potential vanilloid proteins (TRPV) represent a class of voltage-insensitive, non-selective cation channels with emerging roles in vascular biology. The hypothesis of this study was that changes in the expression of TRPV3 contributed to pregnancy-induced functional changes in rat uterine radial arteries. Aims. This study investigated the expression and function of TRPV3 in uterine radial arteries isolated from non-pregnant and twenty-day pregnant rats. Methods. TRPV3 mRNA and protein expression was assayed through quantitative and analytical PCR, immunofluorescence (IF) and Western blot analysis. Functional studies in isolated vessels were performed using pressure myography. Data were analysed utilizing GraphPad Prism 6.0 (). Results. IF studies suggested TRPV3 is primarily localized to the smooth muscle in uterine radial arteries from both pregnant and non-pregnant rats. Pregnancy increased TRPV3 mRNA expression in the arteries but protein assays yielded conflicting results suggesting post-translational modification. The TRPV3 activator carvacrol caused a concentration-dependent dilation of arteries which was not affected by pregnancy (pEC50 Non-preg 4.03 ± 0.08, n = 11; Preg 4.07 ± 0.1, n = 10). Inhibition of nitric oxide synthase or cGMP-dependent protein kinase (PKG) enhanced responses to carvacrol in arteries from nonpregnant rats only. In arteries from both non-pregnant and pregnant rats responses to carvacrol were prevented by TRAM-34 (1 µM), a blocker of the K+ channel KCa3.1. Discussion. Smooth muscle TRPV3 mediate dilation of rat uterine radial arteries through activation of KCa3.1, the intermediate-conductance Ca2+-sensitive K+ channel. Pregnancy increased expression of TRPV3 in the arteries, but this did not alter responses to the activator, carvacrol. TRPV3 activity in these vessels is inhibited by NO-cGMP-PKG, but this effect is lost in pregnancy (Murphy et al., 2016)