111 research outputs found
Symmetries and Cluster Synchronization in Multilayer Networks
Real-world systems in epidemiology, social sciences, power transportation,
economics and engineering are often described as multilayer networks. Here we
first define and compute the symmetries of multilayer networks, and then study
the emergence of cluster synchronization in these networks. We distinguish
between independent layer symmetries which occur in one layer and are
independent of the other layers and dependent layer symmetries which involve
nodes in different layers. We study stability of the cluster synchronous
solution by decoupling the problem into a number of independent blocks and
assessing stability of each block through a Master Stability Function. We see
that blocks associated with dependent layer symmetries have a different
structure than the other blocks, which affects the stability of clusters
associated with these symmetries. Finally, we validate the theory in a fully
analog experiment in which seven electronic oscillators of three kinds are
connected with two kinds of coupling
Analysis of the putative role of CR1 in Alzheimer’s disease: Genetic association, expression and function
Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer's disease (AD). Recent large genome wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) in the C3b/C4b receptor (CR1 or CD35) that are associated with late onset AD. Here, anti-CR1 antibodies (Abs) directed against different epitopes of the receptor, were used to localize CR1 in brain, and relative binding affinities of the CR1 ligands, C1q and C3b, were assessed by ELISA. Most Abs tested stained red blood cells in blood vessels but showed no staining in brain parenchyma. However, two monoclonal anti-CR1 Abs labeled astrocytes in all of the cases tested, and this reactivity was preabsorbed by purified recombinant human CR1. Human brain-derived astrocyte cultures were also reactive with both mAbs. The amount of astrocyte staining varied among the samples, but no consistent difference was conferred by diagnosis or the GWAS-identified SNPs rs4844609 or rs6656401. Plasma levels of soluble CR1 did not correlate with diagnosis but a slight increase was observed with rs4844609 and rs6656401 SNP. There was also a modest but statistically significant increase in relative binding activity of C1q to CR1 with the rs4844609 SNP compared to CR1 without the SNP, and of C3b to CR1 in the CR1 genotypes containing the rs6656401 SNP (also associated with the larger isoform of CR1) regardless of clinical diagnosis. These results suggest that it is unlikely that astrocyte CR1 expression levels or C1q or C3b binding activity are the cause of the GWAS identified association of CR1 variants with AD. Further careful functional studies are needed to determine if the variant-dictated number of CR1 expressed on red blood cells contributes to the role of this receptor in the progression of AD, or if another mechanism is involved
Candidate members of an LFA-1 signaling complex on T cells identified by adhesion-activating monoclonal antibodies
C1q and C4b bind simultaneously to CR1 and additively support erythrocyte adhesion
Previously, we showed that soluble C1q bound specifically to CR1 on transfected cells. If the CR1-C1q interaction were to participate in immune complex clearance, then this interaction should support E adhesion. Using a tip plate adhesion assay, we found that immobilized C1q mediated adhesion of human E, E binding to C1q was specifically inhibited by polyclonal anti-CR1 Fab fragments, Intact C1 was not efficient as an adherence ligand until it was treated with EDTA or the C1 inhibitor to remove the C1r(2)C1s(2) complex from C1, leaving C1q, Titration of Clq alone, C4b alone, and C1q + C4b indicated that the two complement ligands were additive in their ability to support CR1-mediated adhesion of E. Analysis of binding to Immobilized CR1 using a BIAcore instrument documented that C1q, C4b, and C3b binding were independent events. Additionally, C1q-dependent binding of immune complexes and heat-aggregated IgG to E was documented. These experiments confirm that the immune adherence receptor in humans, CR1, is the single receptor for all of the opsonic ligands of complement, provide evidence for a single C1q binding site on LHR-D of CR1, and suggest that C1q may participate in immune clearanc
Concomitant regulation of LFA-1-mediated adhesion and cell growth in the J-lo1.3 Jurkat T cell clone
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