Amplitude-modulation characteristics of power-combining Class-E amplifier with finite choke

Power back-off performances of a new variant power-combining Class-E amplifier under different amplitude-modulation schemes such as continuous wave (CW), envelope elimination and restoration (EER), envelope tracking (ET) and outphasing are for the first time investigated in this study. Finite DC-feed inductances rather than massive RF chokes as used in the classic single-ended Class-E power amplifier (PA) resulted from the approximate yet effective frequency-domain circuit analysis provide the wherewithal to increase modulation bandwidth up to 80% higher than the classic single-ended Class-E PA. This increased modulation bandwidth is required for the linearity improvement in the EER/ET transmitters. The modified output load network of the power-combining Class-E amplifier adopting three-harmonic terminations technique relaxes the design specifications for the additional filtering block typically required at the output stage of the transmitter chain. Qualitative agreements between simulation and measurement results for all four schemes were achieved where the ET technique was proven superior to the other schemes. When the PA is used within the ET scheme, an increase of average drain efficiency of as high as 40% with respect to the CW excitation was obtained for a multi-carrier input signal with 12 dB peak-to-average power ratio. © 2011 The Institution of Engineering and Technology.

Power back-off behaviour of high-efficiency power-combining Class-E amplifier

Power back-off performances of the modified power-combining Class-E amplifier under different amplitudemodulation schemes such as envelope elimination and restoration (EER) and envelope tracking (ET) are experimentally assessed in this paper. The modified output load network adopting three-harmonic terminations technique eliminates the need for additional lossy filtering section in the transmitter chain. Small dc-feed inductances rather than massive RF chokes as in the classic Class-E amplifier are used so as to increase the modulation bandwidth and therefore improve the linearity of the EER transmitter. High efficiency over a wide dynamic range using amplitude modulation through drain-voltage control (EER) was achieved and this agrees well with the Class-E theoretical prediction. When the PA was used within the ET scheme, an increase of average drain efficiency of as high as 40% with respect to the CW excitation was obtained for a multi-carrier input signal with 12dB peak-to-average power ratio. © 2011 Institut fur Mikrowellen.

Role of IP(3) in modulation of spontaneous activity in pacemaker cells of rabbit urethra.

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]

Modulation of contractile function through NPY receptors during development of cardiomyocyte hypertrophy.

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.