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Selective Channel (selective + channel)

Distribution by Scientific Domains
Engineering50%

Selected Abstracts

Optimum adaptive OFDM systems

EUROPEAN TRANSACTIONS ON TELECOMMUNICATIONS, Issue 3 2003
Lorenzo Piazzo
When Orthogonal Frequency Division Multiplexing (OFDM) is used to transmit information over a frequency selective channel, it is convenient to vary the power and the number of bits allocated to each subcarrier in order to optimize the system performance. In this paper, the three classical problems of transmission power minimization, error rate minimization and throughput maximization are investigated in a unified manner. The relations existing among these three problems are clarified and a precise definition of optimum system is given. A general and rigorous way to extend the solution of any of the three problems in order to obtain the solution of the other two is presented. This result is used to devise an efficient algorithm for the error rate minimization. Copyright © 2003 AEI. [source]

Agonist activation of arachidonate-regulated Ca2+ -selective (ARC) channels in murine parotid and pancreatic acinar cells

THE JOURNAL OF PHYSIOLOGY, Issue 3 2005
Olivier Mignen
ARC channels (arachidonate-regulated Ca2+ -selective channels) are a novel type of highly Ca2+ -selective channel that are specifically activated by low concentrations of agonist-induced arachidonic acid. This activation occurs in the absence of any depletion of internal Ca2+ stores (i.e. they are ,non-capacitative'). Previous studies in HEK293 cells have shown that these channels provide the predominant pathway for the entry of Ca2+ seen at low agonist concentrations where oscillatory [Ca2+]i signals are typically produced. In contrast, activation of the more widely studied store-operated Ca2+ channels (e.g. CRAC channels) is only seen at higher agonist concentrations where sustained ,plateau-type'[Ca2+]i responses are observed. We have now demonstrated the presence of ARC channels in both parotid and pancreatic acinar cells and shown that, again, they are specifically activated by the low concentrations of appropriate agonists (carbachol in the parotid, and both carbachol and cholecystokinin in the pancreas) that are associated with oscillatory [Ca2+]i signals in these cells. Uncoupling the receptor-mediated activation of cytosolic phospholipase A2 (cPLA2) with isotetrandrine reduces the activation of the ARC channels by carbachol and, correspondingly, markedly inhibits the [Ca2+]i signals induced by low carbachol concentrations, whilst those signals seen at high agonist concentrations are essentially unaffected. Interestingly, in the pancreatic acinar cells, activation by cholecystokinin induces a current through the ARC channels that is only approximately 60% of that seen with carbachol. This is consistent with previous reports indicating that carbachol-induced [Ca2+]i signals in these cells are much more dependent on Ca2+ entry than are the cholecystokinin-induced responses. [source]

Active measurements of a mimo WiMAX-OFDM based system in reverberation chambers

MICROWAVE AND OPTICAL TECHNOLOGY LETTERS, Issue 10 2010
Adil Belhouji
Abstract Electromagnetic reverberation chambers can be used for multiple-input multiple-output (MIMO) systems testing.Currently, the tests focus on parameters such as correlation, diversity gain, efficiency, etc., by using a vector network analyzer. In contrast with these passive tests, a novel way of MIMO systems characterization is described in this article. It consists on evaluating bit error rate (BER) levels of a MIMO WiMAX-OFDM system according to the Signal-to-Noise Ratio (SNR) by establishing an active link between the transmitter and the receiver. The measurement process is set up in a reverberation chamber, where multipath frequency selective channels are emulated. The obtained results are compared to a reference case with single-input single-output (SISO) to evaluate the real improvements made by the studied system. © 2010 Wiley Periodicals, Inc. Microwave Opt Technol Lett 52:2347,2352, 2010; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/mop.25465 [source]

Agonist activation of arachidonate-regulated Ca2+ -selective (ARC) channels in murine parotid and pancreatic acinar cells

THE JOURNAL OF PHYSIOLOGY, Issue 3 2005
Olivier Mignen
ARC channels (arachidonate-regulated Ca2+ -selective channels) are a novel type of highly Ca2+ -selective channel that are specifically activated by low concentrations of agonist-induced arachidonic acid. This activation occurs in the absence of any depletion of internal Ca2+ stores (i.e. they are ,non-capacitative'). Previous studies in HEK293 cells have shown that these channels provide the predominant pathway for the entry of Ca2+ seen at low agonist concentrations where oscillatory [Ca2+]i signals are typically produced. In contrast, activation of the more widely studied store-operated Ca2+ channels (e.g. CRAC channels) is only seen at higher agonist concentrations where sustained ,plateau-type'[Ca2+]i responses are observed. We have now demonstrated the presence of ARC channels in both parotid and pancreatic acinar cells and shown that, again, they are specifically activated by the low concentrations of appropriate agonists (carbachol in the parotid, and both carbachol and cholecystokinin in the pancreas) that are associated with oscillatory [Ca2+]i signals in these cells. Uncoupling the receptor-mediated activation of cytosolic phospholipase A2 (cPLA2) with isotetrandrine reduces the activation of the ARC channels by carbachol and, correspondingly, markedly inhibits the [Ca2+]i signals induced by low carbachol concentrations, whilst those signals seen at high agonist concentrations are essentially unaffected. Interestingly, in the pancreatic acinar cells, activation by cholecystokinin induces a current through the ARC channels that is only approximately 60% of that seen with carbachol. This is consistent with previous reports indicating that carbachol-induced [Ca2+]i signals in these cells are much more dependent on Ca2+ entry than are the cholecystokinin-induced responses. [source]