DIGITAL VIDEO BROADCASTING VIA SATELLITE (DVB-S)

This paper provides a brief introduction to the DVB-S system based on [EN-300-421]. The DVB-S system provides directto-home (DTH) services for consumer integrated receiver decoders (IRD), as well as collective antenna systems (satellitemaster antenna television SMATV) and cable television head-end stations. The overview covers the physical layer thatcomprises adaptation, framing, coding, interleaving and modulation, and discusses error performance requirements toachieve quality of service (QoS) targets.Keywords: system provides direct-to-homey, satellite master antenna television and achieves quality of service

ADVANCED RECEIVER ARCHITECTURES IN RADIO-FREQUENCY APPLICATIONS

The general principles of several types of receivers fall under the two main headings of TRF (tuned radiofrequency) receivers, where the received signal is processed at the incoming frequency right up to the detector stage, and thesuperhet (supersonic heterodyne) receiver, where the incoming signal is translated (sometimes after some amplification atthe incoming frequency) to an intermediate frequency for further processing. There are however, a number of variants ofeach of these two main types. Regeneration (‘reaction’ or ‘tickling’) may be applied in a TRF receiver, to increase both itssensitivity and selectivity. This may be carried to the stage where the RF amplifier actually oscillates – either continuously,so that the receiver operates as a synchrodyne or homodyne, or intermittently, so that the receiver operates as a superregenerativereceiver, both of which have been described previously. The synchrodyne or homodyne may be consideredalternatively as a superhet, where the IF (intermediate frequency) is 0 Hz. In this paper we present the new type of receiverarchitectures which work in radiofrequencies.Keywords: Supersonic Heterodyne, Tuned Radio Frequency

Effect of remifentanil on mitochondrial oxygen consumption of cultured human hepatocytes

During sepsis, liver dysfunction is common, and failure of mitochondria to effectively couple oxygen consumption with energy production has been described. In addition to sepsis, pharmacological agents used to treat septic patients may contribute to mitochondrial dysfunction. This study addressed the hypothesis that remifentanil interacts with hepatic mitochondrial oxygen consumption. The human hepatoma cell line HepG2 and their isolated mitochondria were exposed to remifentanil, with or without further exposure to tumor necrosis factor-α (TNF-α). Mitochondrial oxygen consumption was measured by high-resolution respirometry, Caspase-3 protein levels by Western blotting, and cytokine levels by ELISA. Inhibitory κBα (IκBα) phosphorylation, measurement of the cellular ATP content and mitochondrial membrane potential in intact cells were analysed using commercial ELISA kits. Maximal cellular respiration increased after one hour of incubation with remifentanil, and phosphorylation of IκBα occurred, denoting stimulation of nuclear factor κB (NF-κB). The effect on cellular respiration was not present at 2, 4, 8 or 16 hours of incubation. Remifentanil increased the isolated mitochondrial respiratory control ratio of complex-I-dependent respiration without interfering with maximal respiration. Preincubation with the opioid receptor antagonist naloxone prevented a remifentanil-induced increase in cellular respiration. Remifentanil at 10× higher concentrations than therapeutic reduced mitochondrial membrane potential and ATP content without uncoupling oxygen consumption and basal respiration levels. TNF-α exposure reduced respiration of complex-I, -II and -IV, an effect which was prevented by prior remifentanil incubation. Furthermore, prior remifentanil incubation prevented TNF-α-induced IL-6 release of HepG2 cells, and attenuated fragmentation of pro-caspase-3 into cleaved active caspase 3 (an early marker of apoptosis). Our data suggest that remifentanil increases cellular respiration of human hepatocytes and prevents TNF-α-induced mitochondrial dysfunction. The results were not explained by uncoupling of mitochondrial respiration

Toll-like receptor-3-induced mitochondrial dysfunction in cultured human hepatocytes

Several studies have shown the presence of liver mitochondrial dysfunction during sepsis. TLR3 recognizes viral double-stranded RNA and host endogenous cellular mRNA released from damaged cells. TLR3 ligand amplifies the systemic hyperinflammatory response observed during sepsis and in sepsis RNA escaping from damaged tissues/cells may serve as an endogenous ligand for TLR3 thereby modulating immune responses. This study addressed the hypothesis that TLR3 might regulate mitochondrial function in cultured human hepatocytes. HepG2 cells were exposed to TLR-3 ligand (dsRNA--polyinosine-polycytidylic acid; Poly I:C) and mitochondrial respiration was measured. Poly I:C induced a reduction in maximal mitochondrial respiration of human hepatocytes which was prevented partially by preincubation with cyclosporine A (a mitochondrial permeability transition pore-opening inhibitor). Poly-I:C induced activation of NF-κB, and the mitochondrial dysfunction was accompanied by caspase-8 but not caspase-3 activation and by no major alterations in cellular or mitochondrial ultrastructure