Axial Mode Helical Antennas

The radiation characteristics of helical antennas operating in the axial mode are evaluated on the basis of the theoretical current distributions and are verified by experimental work. A comparison between monofilar helix and bifilar helix antennas is made, and a helical antenna with a parasitic helix (HAP) is proposed in order to enhance the power gain. It is found that the gain of the HAP in which the parasitic helix is wound from a point diametrically opposite to that of one and onehalf turns of the driven helix is about 1 dB higher than that of the monofilar helix. The ratio of the frequency band in which the HAP radiates a circularly polarized wave within an axial ratio of 3 dB is calculated to be 1:l.g

Analysis of Polarization Splitters Composed of Multilayer Thin-Film Waveguides Using the Beam-Propagation Method Based on Yee’s Mesh

Multilayer thin-film waveguides (MTFWs) are analyzed using the beam-propagation method based on Yee\u27s mesh. The birefringence properties of the MTFW are demonstrated by the eigenmode analysis based on the imaginary-distance procedure. Taking advantage of the birefringence, a polarization splitter composed of two parallel MTFWs is proposed. Calculation shows that a short device length of 270 mum is obtainable with crosstalks of -33.5 dB for the quasi-transverse-electric mode and -20.7 dB for the quasi-transverse-magnetic mode. A crossing-type polarization splitter is also developed, and the device length is further reduced to 120 mum

PKA Phosphorylation Dissociates FKBP12.6 from the Calcium Release Channel (Ryanodine Receptor) Defective Regulation in Failing Hearts

AbstractThe ryanodine receptor (RyR)/calcium release channel on the sarcoplasmic reticulum (SR) is the major source of calcium (Ca2+) required for cardiac muscle excitation-contraction (EC) coupling. The channel is a tetramer comprised of four type 2 RyR polypeptides (RyR2) and four FK506 binding proteins (FKBP12.6). We show that protein kinase A (PKA) phosphorylation of RyR2 dissociates FKBP12.6 and regulates the channel open probability (Po). Using cosedimentation and coimmunoprecipitation we have defined a macromolecular complex comprised of RyR2, FKBP12.6, PKA, the protein phosphatases PP1 and PP2A, and an anchoring protein, mAKAP. In failing human hearts, RyR2 is PKA hyperphosphorylated, resulting in defective channel function due to increased sensitivity to Ca2+-induced activation

Rapid electrical stimulation of contraction modulates gap junction protein in neonatal rat cultured cardiomyocytes Involvement of mitogen-activated protein kinases and effects of angiotensin ii-receptor antagonist

ObjectivesThe aim of this study was to investigate the effects of rapid electrical stimulation (RES) of contraction on the expression of connexin (Cx)43 gap junction in neonatal rat cultured ventricular myocytes and the consequent changes of conduction properties.BackgroundThe expression and distribution of gap junctions in cardiac muscle can be changed readily under a variety of pathological conditions because of dynamic turnover of Cxs. The effects of RES of contraction on gap junction remodeling are not well understood.MethodsNeonatal rat ventricular myocytes cultured for five days were subjected to RES (field stimulation) at 3.0 Hz for up to 120 min.ResultsRapid electrical stimulation resulted in a significant upregulation of Cx43 (by ∼1.5-fold in protein and by ∼1.9-fold in messenger ribonucleic acid at 60 min). Immunoreactive signal of Cx43 was also increased. Angiotensin II (AngII) content was increased significantly by RES >15 min. Phosphorylated forms of extracellular signal-regulated protein kinase (ERK), c-Jun NH2-terminal kinases, and p38 mitogen-activated protein kinases (MAPKs) were all increased dramatically by RES with peaks at 5 ∼ 60 min. Propagation of excitation was visualized by extracellular potential mapping by using a multiple electrode array system. Conduction velocity was increased significantly by RES for 60 to 90 min (25% ∼ 27% increase). Treatment of myocytes with losartan (100 nmol/l) prevented most of these effects of RES; RES-induced upregulation of Cx43 was also prevented by specific inhibitors for ERK and p38 MAPKs.ConclusionsA short-term RES causes upregulation of Cx43 in cardiomyocytes and a concomitant increase of conduction velocity, mainly through an autocrine action of AngII to activate ERK and p38 MAPKs