Channelled Waves in Anisotropic Mesh Metamaterials

Channelled waves in 2-D periodic anisotropic L-C mesh metamaterials have been investigated. Circuit simulation and the newly developed analytical model of a unit cell have demonstrated full qualitative agreement for both lossless and lossy cases. Isofrequencies for a lattice unit cell and the circuit simulations of finite meshes have shown that propagating waves are channelled from a point source as pencil beams which can travel only along specific trajectories. The beam direction varies with frequency, and at the resonance frequency, the phase and group velocities of the travelling wave are orthogonal. The effect of losses was explored, and it was shown that losses cause qualitative changes of the channelled wave type. It was proven that the channelled waves do not follow the laws of geometrical optics (Snell's law, specular reflection, etc.) at the interfaces of L-C meshes but are governed by the conditions of phase synchronism and impedance matching. Only in the special case of dual L-C and C-L meshes with the interface parallel to the axis of rectangular grid excited at the resonance frequency (X=1) do the channels follow the trajectories of optical rays. A planar mesh test cell has been designed and used for retrieving the unit cell L-C parameters from the S-parameter measurements.

Differential effects of reduced glycoprotein VI levels on activation of murine platelets by glycoprotein VI ligands

We have investigated the effects of decreased levels of the complex between glycoprotein VI (GPVI) and the Fc receptor gamma-chain (FcRgamma) on responses to collagen and GPVI-specific ligands in murine platelets. We show that levels of GPVI-FcRgamma of the order of 50 % and 20 % of wild-type levels caused 2- and 5-fold shifts to the right respectively in the dose-response curve for aggregation in response to collagen, the snake toxin convulxin and the monoclonal antibody JAQ1. In addition, there is a delay in the onset of aggregation in response to collagen. In contrast, the stimulation of protein tyrosine phosphorylation by collagen (as measured after 150 s) and adhesion to a collagen-coated surface under static conditions were unaffected in platelets with 50 % and 20 % of wild-type levels of GPVI. In contrast, responses to a collagen-related peptide (CRP), made up of repeat glycine-proline-hydroxyproline motifs, were markedly inhibited and abolished in platelets expressing 50 % and 20 % of wild-type levels of GPVI respectively. We suggest that the marked effect of a reduction in GPVI levels on the CRP-induced activation of platelets is due to the multivalent nature of CRP and the fact that GPVI is its sole receptor on platelets. Thus it appears that the interaction of CRP with GPVI is determined by a combination of affinity and avidity. The observation that collagen does not behave like CRP in platelets expressing reduced levels of GPVI, even in the combined presence of blocking antibodies against integrin alpha2beta1 and GPV, suggests that collagen has a greater affinity than CRP for GPVI, and/or that other receptors are involved in its binding to platelets. The clinical significance of these results is discussed.

Distinct roles of GPVI and integrin alpha(2)beta(1) in platelet shape change and aggregation induced by different collagens

1 Various platelet membrane glycoproteins have been proposed as receptors for collagen, in some cases as receptors For specific collagen types. In this study we have compared the ability of a range of collagen types to activate platelets.