Spent Culture Medium from Virulent Borrelia burgdorferi Increases Permeability of Individually Perfused Microvessels of Rat Mesentery

Lyme disease is a common vector-borne disease caused by the spirochete Borrelia burgdorferi (Bb), which manifests as systemic and targeted tissue inflammation. Both in vitro and in vivo studies have shown that Bb-induced inflammation is primarily host-mediated, via cytokine or chemokine production that promotes leukocyte adhesion/migration. Whether Bb produces mediators that can directly alter the vascular permeability in vivo has not been investigated. The objective of the present study was to investigate if Bb produces a mediator(s) that can directly activate endothelial cells resulting in increases in permeability in intact microvessels in the absence of blood cells.The effects of cell-free, spent culture medium from virulent (B31-A3) and avirulent (B31-A) B. burgdorferi on microvessel permeability and endothelial calcium concentration, [Ca(2+)](i), were examined in individually perfused rat mesenteric venules. Microvessel permeability was determined by measuring hydraulic conductivity (Lp). Endothelial [Ca(2+)](i), a necessary signal initiating hyperpermeability, was measured in Fura-2 loaded microvessels. B31-A3 spent medium caused a rapid and transient increase in Lp and endothelial [Ca(2+)](i). Within 2-5 min, the mean peak Lp increased to 5.6+/-0.9 times the control, and endothelial [Ca(2+)](i) increased from 113+/-11 nM to a mean peak value of 324+/-35 nM. In contrast, neither endothelial [Ca(2+)](i) nor Lp was altered by B31-A spent medium.A mediator(s) produced by virulent Bb under culture conditions directly activates endothelial cells, resulting in increases in microvessel permeability. Most importantly, the production of this mediator is associated with Bb virulence and is likely produced by one or more of the 8 plasmid(s) missing from strain B31-A

Neurons Controlling Aplysia Feeding Inhibit Themselves by Continuous NO Production

Neural activity can be affected by nitric oxide (NO) produced by spiking neurons. Can neural activity also be affected by NO produced in neurons in the absence of spiking?Applying an NO scavenger to quiescent Aplysia buccal ganglia initiated fictive feeding, indicating that NO production at rest inhibits feeding. The inhibition is in part via effects on neurons B31/B32, neurons initiating food consumption. Applying NO scavengers or nitric oxide synthase (NOS) blockers to B31/B32 neurons cultured in isolation caused inactive neurons to depolarize and fire, indicating that B31/B32 produce NO tonically without action potentials, and tonic NO production contributes to the B31/B32 resting potentials. Guanylyl cyclase blockers also caused depolarization and firing, indicating that the cGMP second messenger cascade, presumably activated by the tonic presence of NO, contributes to the B31/B32 resting potential. Blocking NO while voltage-clamping revealed an inward leak current, indicating that NO prevents this current from depolarizing the neuron. Blocking nitrergic transmission had no effect on a number of other cultured, isolated neurons. However, treatment with NO blockers did excite cerebral ganglion neuron C-PR, a command-like neuron initiating food-finding behavior, both in situ, and when the neuron was cultured in isolation, indicating that this neuron also inhibits itself by producing NO at rest.Self-inhibitory, tonic NO production is a novel mechanism for the modulation of neural activity. Localization of this mechanism to critical neurons in different ganglia controlling different aspects of a behavior provides a mechanism by which a humeral signal affecting background NO production, such as the NO precursor L-arginine, could control multiple aspects of the behavior

Reducing systematic errors in time-frequency resolved mode number analysis

The present paper describes the effect of magnetic pick-up coil transfer functions on mode number analysis in magnetically confined fusion plasmas. Magnetic probes mounted inside the vacuum chamber are widely used to characterize the mode structure of magnetohydrodynamic modes, as, due to their relative simplicity and compact nature, several coils can be distributed over the vessel. Phase differences between the transfer functions of different magnetic pick-up coils lead to systematic errors in time- and frequency resolved mode number analysis. This paper presents the first in-situ, end-to-end calibration of a magnetic pick-up coil system which was carried out by using an in-vessel driving coil on ASDEX Upgrade. The effect of the phase differences in the pick-up coil transfer functions is most significant in the 50-250 kHz frequency range, where the relative phase shift between the different probes can be up to 1 radian (~60{\deg}). By applying a correction based on the transfer functions we found smaller residuals of mode number fitting in the considered discharges. In most cases an order of magnitude improvement was observed in the residuals of the mode number fits, which could open the way to investigate weaker electromagnetic oscillations with even high mode numbers

Solution of QCD⊗\otimesQED coupled DGLAP equations at NLO

In this work, we present an analytical solution for QCD$\otimes$QED coupled Dokshitzer-Gribov-Lipatov-Altarelli-Parisi (DGLAP) evolution equations at the leading order (LO) accuracy in QED and next-to-leading order (NLO) accuracy in perturbative QCD using double Laplace transform. This technique is applied to obtain the singlet, gluon and photon distribution functions and also the proton structure function. We also obtain contribution of photon in proton at LO and NLO at high energy and successfully compare the proton structure function with HERA data \cite{12} and APFEL results \cite{7}. Some comparisons also have been done for the singlet and gluon distribution functions with the MSTW results\cite{9}. In addition, the contribution of photon distribution function inside the proton has been compared with results of MRST \cite{11} and with the contribution of sea quark distribution functions which obtained by MSTW \cite{9} and CTEQ6M \cite{14}.Comment: 23 pages, 11 figur

Autaptic excitation contributes to bistability and rhythmicity in the neural circuit for feeding in Aplysia

The feeding circuit in Aplysia is a useful model system for studying the neuronal bases of cognitive functions such as sensory processing, generation of behavior, motivation, decision making, learning, and memory [1,2]. The goals of the present study are to develop a biologically-realistic model of the feeding circuit and to investigate the ways in which component processes contribute to circuit function. To begin, we developed a model of the central pattern generator (CPG) that mediates rhythmicity in the feeding circuit (Fig. ​(Fig.1A).1A). Simulations indicated that two positive-feedback loops (the B31 autapse and the synaptic interactions between B31 and B63) introduced bistability into the membrane potential of the B31 soma (Figures ​(Figures1B,1B, 1C1). In addition, simulations indicated that this plateau-like potential was the ‘deciding factor’ for initiating rhythmic activity (Fig. ​(Fig.1C).1C). Simulations also helped identify features of the model that warrant further empirical investigation; e.g., the simulated amplitude of the plateau-like potential was less than empirical observations

The bicrossed products of H4H_4 and H8H_8

Let $H_4$ and $H_8$ be the Sweedler's and Kac-Paljutkin Hopf algebras, respectively. In this paper we prove that any Hopf algebra which factorizes through $H_8$ and $H_4$ (equivalently, any bicrossed product between the Hopf algebras $H_8$ and $H_4$) must be isomorphic to one of the following four Hopf algebras: $H_8 \otimes H_4, H_{32,1}, H_{32,2}, H_{32,3}$. The set of all matched pair $(H_8, H_4, \triangleright, \triangleleft)$ is explicitly described, and then the associated bicrossed products is given by generators and relations