95 resultados para electro-optic modulation

em QUB Research Portal - Research Directory and Institutional Repository for Queen's University Belfast


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The electro-optic response of a cell consisting of a thin layer of liquid crystal deposited onto gold nanorods embedded in thin film alumina with a transparent top electrode has been investigated. For p-polarized light incident from the liquid crystal side, the extinction peak associated with the nanorod longitudinal plasmon resonance is completely suppressed. The peak could be recovered by applying an external electric field parallel to the long axis of the nanorods. No extinction peak suppression is observed when the light was incident from the nanorod side of the cell. The effect is explained by polarization properties of liquid crystal.

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The nonlinear amplitude modulation of electrostatic waves propagating in a collisionless two-component plasma consisting of negative and positive species of equal mass and absolute charge is investigated. Pair-ion (e.g., fullerene) and electron-positron (e-p) plasmas (neglecting recombination) are covered by this description. Amplitude perturbation oblique to the direction of propagation of the wave has been considered. Two distinct linear electrostatic modes exist, namely an acoustic lower mode and Langmuir-type optic-type upper one. The behavior of each of these modes is examined from the modulational stability point of view. The stability criteria are investigated, depending on the electrostatic carrier wave number, the angle theta between the modulation and propagation directions, and the positron-to-electron temperature ratio sigma. The analysis shows that modulated electrostatic wavepackets associated to the lower (acoustic) mode are unstable, for small values of carrier wave number k (i.e., for large wavelength lambda) and for finite (small) values of the angle theta (yet stable for higher theta), while those related to the upper (optic-like) mode are stable for large values of the angle theta only, in the same limit, yet nearly for all values of sigma. These results are of relevance in astrophysical contexts (e.g., in pulsar environments), where e-p plasmas are encountered, or in pair fullerene-ion plasmas, in laboratory. (c) 2006 American Institute of Physics.

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Isolated interstitial ("pacemaker") cells from rabbit urethra were examined using the perforated-patch technique. Under voltage clamp at -60 mV, these cells fired large spontaneous transient inward currents (STICs), averaging -860 pA and >1 s in duration, which could account for urethral pacemaker activity. Spontaneous transient outward currents (STOCs) were also observed and fell into two categories, "fast" (1 s in duration). The latter were coupled to STICs, suggesting that they shared the same mechanism, while the former occurred independently at faster rates. All of these currents were abolished by cyclopiazonic acid, caffeine, or ryanodine, suggesting that they were activated by Ca(2+) release. When D-myo-inositol 1,4,5-trisphosphate (IP(3))-sensitive stores were blocked with 2-aminoethoxydiphenyl borate, the STICs and slow STOCs were abolished, but the fast STOCs remained. In contrast, the fast STOCs were more nifedipine sensitive than the STICs or the slow STOCs. These results suggest that while fast STOCs are mediated by a mechanism similar to STOCs in smooth muscle, STICs and slow STOCs are driven by IP(3). These results support the hypothesis that pacemaker activity in the urethra is driven by the IP(3)-sensitive store. PMID: 11287348 [PubMed - indexed for MEDLINE]

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Severity of left ventricular hypertrophy (LVH) correlates with elevated plasma levels of neuropeptide Y (NPY) in hypertension. NPY elicits positive and negative contractile effects in cardiomyocytes through Y(1) and Y(2) receptors, respectively. This study tested the hypothesis that NPY receptor-mediated contraction is altered during progression of LVH. Ventricular cardiomyocytes were isolated from spontaneously hypertensive rats (SHRs) pre-LVH (12 weeks), during development (16 weeks), and at established LVH (20 weeks) and age-matched normotensive Wistar Kyoto (WKY) rats. Electrically stimulated (60 V, 0.5 Hz) cell shortening was measured using edge detection and receptor expression determined at mRNA and protein level. The NPY and Y(1) receptor-selective agonist, Leu(31)Pro(34)NPY, stimulated increases in contractile amplitude, which were abolished by the Y(1) receptor-selective antagonist, BIBP3226 [R-N(2)-(diphenyl-acetyl)-N-(4-hydroxyphenyl)methyl-argininamide)], confirming Y(1) receptor involvement. Potencies of both agonists were enhanced in SHR cardiomyocytes at 20 weeks (2300- and 380-fold versus controls). Maximal responses were not attenuated. BIBP3226 unmasked a negative contraction effect of NPY, elicited over the concentration range (10(-12) to 3 x 10(-9) M) in which NPY and PYY(3-36) attenuated the positive contraction effects of isoproterenol, the potencies of which were increased in cardiomyocytes from SHRs at 20 weeks (175- and 145-fold versus controls); maximal responses were not altered. Expression of NPY-Y(1) and NPY-Y(2) receptor mRNAs was decreased (55 and 69%) in left ventricular cardiomyocytes from 20-week-old SHRs versus age-matched WKY rats; parallel decreases (32 and 80%) were observed at protein level. Enhancement of NPY potency, producing (opposing) contractile effects on cardiomyocytes together with unchanged maximal response despite reduced receptor number, enables NPY to contribute to regulating cardiac performance during compensatory LVH.