975 resultados para Multicarrier Modulation


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In this paper we propose the use of Discrete Cosine Transform Type-III (DCT3) for multicarrier modulation. There are two DCT3 (even and odd) and, for each of them, we derive the expressions for both prefix and suffix to be appended into each data symbol to be transmitted. Moreover, DCT3 are closely related to the corresponding inverse DCT Type-II even and odd. Furthermore, we give explicit expressions for the 1-tap per subcarrier equalizers that must be implemented at the receiver to perform the channel equalization in the frequency-domain. As a result, the proposed DCT3-based multicarrier modulator can be used as an alternative to DFT-based systems to perform Orthogonal Frequency-Division Multiplexing or Discrete Multitone Modulation

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A major limitation in any high-performance digital communication system is the linearity region of the transmitting amplifier. Nonlinearities typically lead to signal clipping. Efficient communication in such conditions requires maintaining a low peak-to-average power ratio (PAR) in the transmitted signal while achieving a high throughput of data. Excessive PAR leads either to frequent clipping or to inadequate resolution in the analog-to-digital or digital-to-analog converters. Currently proposed signaling schemes for future generation wireless communications suffer from a high PAR. This paper presents a new signaling scheme for channels with clipping which achieves a PAR as low as 3. For a given linear range in the transmitter's digital-to-analog converter, this scheme achieves a lower bit-error rate than existing multicarrier schemes, owing to increased separation between constellation points. We present the theoretical basis for this new scheme, approximations for the expected bit-error rate, and simulation results. (C) 2002 Elsevier Science (USA).

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This chapter considers the Multiband Orthogonal Frequency Division Multiplexing (MB- OFDM) modulation and demodulation with the intention to optimize the Ultra-Wideband (UWB) system performance. OFDM is a type of multicarrier modulation and becomes the most important aspect for the MB-OFDM system performance. It is also a low cost digital signal component efficiently using Fast Fourier Transform (FFT) algorithm to implement the multicarrier orthogonality. Within the MB-OFDM approach, the OFDM modulation is employed in each 528 MHz wide band to transmit the data across the different bands while also using the frequency hopping technique across different bands. Each parallel bit stream can be mapped onto one of the OFDM subcarriers. Quadrature Phase Shift Keying (QPSK) and Dual Carrier Modulation (DCM) are currently used as the modulation schemes for MB-OFDM in the ECMA-368 defined UWB radio platform. A dual QPSK soft-demapper is suitable for ECMA-368 that exploits the inherent Time-Domain Spreading (TDS) and guard symbol subcarrier diversity to improve the receiver performance, yet merges decoding operations together to minimize hardware and power requirements. There are several methods to demap the DCM, which are soft bit demapping, Maximum Likelihood (ML) soft bit demapping, and Log Likelihood Ratio (LLR) demapping. The Channel State Information (CSI) aided scheme coupled with the band hopping information is used as a further technique to improve the DCM demapping performance. ECMA-368 offers up to 480 Mb/s instantaneous bit rate to the Medium Access Control (MAC) layer, but depending on radio channel conditions dropped packets unfortunately result in a lower throughput. An alternative high data rate modulation scheme termed Dual Circular 32-QAM that fits within the configuration of the current standard increasing system throughput thus maintaining the high rate throughput even with a moderate level of dropped packets.

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El entorno aéreo es, a día de hoy, uno de los escenarios más complicados a la hora de establecer enlaces de comunicación fiables. Esto es debido, principalmente, a las altas velocidades a las que circulan los aviones, que propician una gran degradación del rendimiento des sistema si no se estima de forma continua el canal. Además el entorno aéreo es susceptible a sufrir muchos otros efectos que provocan la degradación de la señal, como la difracción, la reflexión, etc. Por este motivo en este proyecto se hace un estudio de dos escenarios típicos de vuelo: arrival (aterrizaje) y on route (vuelo en ruta). En el escenario on route los aviones circulan a más de el doble de velocidad que en el escenario arrival, de esta manera se podrá ver el efecto de sufrir un doppler mayor. Para realizar el estudio se utiliza un sistema multiportadora con solapamiento de subcanales, OFDM, y se toman inicialmente parámetros típicos de la tecnología WiMAX, que se variarán con el objetivo de mejorar el rendimiento del sistema.

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This paper presents a new low-complexity multicarrier modulation (MCM) technique based on lattices which achieves a peak-to-average power ratio (PAR) as low as three. The scheme can be viewed as a drop in replacement for the discrete multitone (DMT) modulation of an asymmetric digital subscriber line modem. We show that the lattice-MCM retains many of the attractive features of sinusoidal-MCM, and does so with lower implementation complexity, O(N), compared with DMT, which requires O(N log N) operations. We also present techniques for narrowband interference rejection and power profiling. Simulation studies confirm that performance of the lattice-MCM is superior, even compared with recent techniques for PAR reduction in DMT.

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Nel campo della trasmissione di segnali alfanumerici è cresciuto sempre di più l’interesse riguardo alla trasmissione di segnali caratterizzati da più sottoportanti affiancate nel dominio della frequenza mediante modulazione multiportante (MC, multicarrier modulation). Si è dimostrato che OFDM è un’effettiva tecnica per "combattere" il problema del multipath-fading nei canali wirless. Il multipath-fading è una forma di distorsione di un segnale che giunge a destinazione sotto forma di un certo numero di repliche, sfasate nel tempo, originate dai vari percorsi che il segnale stesso può aver seguito durante la sua propagazione e sommantesi tra loro in ricezione; ogni replica inoltre, sarà soggetta ad un’attenuazione in generale diversa da quella subita dalle altre repliche. Ciò che si vuole realizzare è un sistema di trasmissione e ricezione dati alfanumerico tramite la modulazione OFDM tramite l’utilizzo di due dispositivi SDR. In particolare per la trasmissione del segnale viene utilizzato il dispositivo ADALM-PLUTO, ed è lasciata libera scelta nel trasmettere qualsiasi tipo di segnale alfanumerico, ovvero il numero di simboli OFDM può variare a discrezione dell’utente. Per la ricezione del segnale inviato è stato impiegato il dispositivo Noolec NESDR, e l’utente, qui, sarà invece obbligato a inserire il numero di simboli OFDM da dover ricevere per avere così una corretta decodifica del segnale.

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Multicarrier transmission such as OFDM (orthogonal frequency division multiplexing) is an established technique for radio transmission systems and it can be considered as a promising approach for next generation wireless systems. However, in order to comply with the demand on increasing available data rates in particular in wireless technologies, systems with multiple transmit and receive antennas, also called MIMO (multiple-input multiple-output) systems, have become indispensable for future generations of wireless systems. Due to the strongly increasing demand in high-data rate transmission systems, frequency non-selective MIMO links have reached a state of maturity and frequency selective MIMO links are in the focus of interest. In this field, the combination of MIMO transmission and OFDM can be considered as an essential part of fulfilling the requirements of future generations of wireless systems. However, single-user scenarios have reached a state of maturity. By contrast multiple users' scenarios require substantial further research, where in comparison to ZF (zero-forcing) multiuser transmission techniques, the individual user's channel characteristics are taken into consideration in this contribution. The performed joint optimization of the number of activated MIMO layers and the number of transmitted bits per subcarrier shows that not necessarily all user-specific MIMO layers per subcarrier have to be activated in order to minimize the overall BER under the constraint of a given fixed data throughput.

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The SLC8A1 gene, which encodes the Na(+)/Ca(2+) exchanger, plays a key role in calcium homeostasis. Our previous gene expression oligoarray data revealed SLC8A1 underexpression in penile carcinoma (PeCa). The aim of this study was to investigate whether the dysregulation of SLC8A1 expression is associated with apoptosis and cell proliferation in PeCa, via modulation of calcium concentration. The underlying mechanisms of SLC8A1 underexpression were also explored, focusing on copy number alteration and microRNA. Transcript levels of SLC8A1 gene and miR-223 were evaluated by quantitative PCR, comparing PeCa samples with normal glans tissues. SLC8A1 copy number was evaluated by microarray-based comparative genomic hybridization (array-CGH). Caspase-3 and Ki-67 immunostaining, as well as calcium distribution by Laser Ablation Imaging Inductively Coupled Plasma Mass Spectrometry [LA(i)-ICP-MS], were investigated in both normal and tumor samples. Confirming our previous data, SLC8A1 underexpression was detected in PeCa samples (P=0.001) and was not associated with gene copy number loss. In contrast, overexpression of miR-223 (P=0.002) was inversely correlated with SLC8A1 (P=0.015, r=-0.426), its putative repressor. In addition, SLC8A1 underexpression was associated with decreased calcium distribution, high Ki-67 and low caspase-3 immunoexpression in PeCa when compared with normal tissues. Down-regulation of the SLC8A1 gene, most likely mediated by its regulator miR-223, can lead to reduced calcium levels in PeCa and, consequently, to suppression of apoptosis and increased tumor cell proliferation. These data suggest that the miR-223-NCX1-calcium-signaling axis may represent a potential therapeutic approach in PeCa.

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We tested the hypothesis that chronic pain development (pain chronification) and ongoing chronic pain (chronic pain) reduce the activity and induce plastic changes in an endogenous analgesia circuit, the ascending nociceptive control. An important mechanism mediating this form of endogenous analgesia, referred to as capsaicin-induced analgesia, is its dependence on nucleus accumbens μ-opioid receptor mechanisms. Therefore, we also investigated whether pain chronification and chronic pain alter the requirement for nucleus accumbens μ-opioid receptor mechanisms in capsaicin-induced analgesia. We used an animal model of pain chronification in which daily subcutaneous prostaglandin E2 (PGE2) injections into the rat's hind paw for 14 days, referred to as the induction period of persistent hyperalgesia, induce a long-lasting state of nociceptor sensitization referred to as the maintenance period of persistent hyperalgesia, that lasts for at least 30 days following the cessation of the PGE2 treatment. The nociceptor hypersensitivity was measured by the shortening of the time interval for the animal to respond to a mechanical stimulation of the hind paw. We found a significant reduction in the duration of capsaicin-induced analgesia during the induction and maintenance period of persistent mechanical hyperalgesia. Intra-accumbens injection of the μ-opioid receptor selective antagonist Cys(2),Tyr(3),Orn(5),Pen(7)amide (CTOP) 10 min before the subcutaneous injection of capsaicin into the rat's fore paw blocked capsaicin-induced analgesia. Taken together, these findings indicate that pain chronification and chronic pain reduce the duration of capsaicin-induced analgesia, without affecting its dependence on nucleus accumbens μ-opioid receptor mechanisms. The attenuation of endogenous analgesia during pain chronification and chronic pain suggests that endogenous pain circuits play an important role in the development and maintenance of chronic pain.

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BACKGROUND: Spontaneously hypertensive rats develop left ventricular hypertrophy, increased blood pressure and blood pressure variability, which are important determinants of heart damage, like the activation of renin-angiotensin system. AIMS: To investigate the effects of the time-course of hypertension over 1) hemodynamic and autonomic patterns (blood pressure; blood pressure variability; heart rate); 2) left ventricular hypertrophy; and 3) local and systemic Renin-angiotensin system of the spontaneously hypertensive rats. METHODS: Male spontaneously hypertensive rats were randomized into two groups: young (n=13) and adult (n=12). Hemodynamic signals (blood pressure, heart rate), blood pressure variability (BPV) and spectral analysis of the autonomic components of blood pressure were analyzed. LEFT ventricular hypertrophy was measured by the ratio of LV mass to body weight (mg/g), by myocyte diameter (μm) and by relative fibrosis area (RFA, %). ACE and ACE2 activities were measured by fluorometry (UF/min), and plasma renin activity (PRA) was assessed by a radioimmunoassay (ng/mL/h). Cardiac gene expressions of Agt, Ace and Ace2 were quantified by RT-PCR (AU). RESULTS: The time-course of hypertension in spontaneously hypertensive rats increased BPV and reduced the alpha index in adult spontaneously hypertensive rats. Adult rats showed increases in left ventricular hypertrophy and in RFA. Compared to young spontaneously hypertensive rats, adult spontaneously hypertensive rats had lower cardiac ACE and ACE2 activities, and high levels of PRA. No change was observed in gene expression of Renin-angiotensin system components. CONCLUSIONS: The observed autonomic dysfunction and modulation of Renin-angiotensin system activity are contributing factors to end-organ damage in hypertension and could be interacting. Our findings suggest that the management of hypertensive disease must start before blood pressure reaches the highest stable levels and the consequent established end-organ damage is reached.

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The dorsal raphe nucleus (DRN) is the origin of ascending serotonergic projections and is considered to be an important component of the brain circuit that mediates anxiety- and depression-related behaviors. A large fraction of DRN serotonin-positive neurons contain nitric oxide (NO). Disruption of NO-mediated neurotransmission in the DRN by NO synthase inhibitors produces anxiolytic- and antidepressant-like effects in rats and also induces nonspecific interference with locomotor activity. We investigated the involvement of the 5-HT1A autoreceptor in the locomotor effects induced by NO in the DRN of male Wistar rats (280-310 g, N = 9-10 per group). The NO donor 3-morpholinosylnomine hydrochloride (SIN-1, 150, and 300 nmol) and the NO scavenger S-3-carboxy-4-hydroxyphenylglycine (carboxy-PTIO, 0.1-3.0 nmol) were injected into the DRN of rats immediately before they were exposed to the open field for 10 min. To evaluate the involvement of the 5-HT1A receptor and the N-methyl-D-aspartate (NMDA) glutamate receptor in the locomotor effects of NO, animals were pretreated with the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, 8 nmol), the 5-HT1A receptor antagonist N-(2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl)-N-2-pyridinyl-cyclohexanecarboxamide maleate (WAY-100635, 0.37 nmol), and the NMDA receptor antagonist DL-2-amino-7-phosphonoheptanoic acid (AP7, 1 nmol), followed by microinjection of SIN-1 into the DRN. SIN-1 increased the distance traveled (mean ± SEM) in the open-field test (4431 ± 306.1 cm; F7,63 = 2.44, P = 0.028) and this effect was blocked by previous 8-OH-DPAT (2885 ± 490.4 cm) or AP7 (3335 ± 283.5 cm) administration (P < 0.05, Duncan test). These results indicate that 5-HT1A receptor activation and/or facilitation of glutamate neurotransmission can modulate the locomotor effects induced by NO in the DRN.

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To determine the effects of saturated and unsaturated fatty acids in phosphatidylcholine (PC) on macrophage activity, peritoneal lavage cells were cultured in the presence of phosphatidylcholine rich in saturated or unsaturated fatty acids (sat PC and unsat PC, respectively), both used at concentrations of 32 and 64 µM. The treatment of peritoneal macrophages with 64 µM unsat PC increased the production of hydrogen peroxide by 48.3% compared to control (148.3 ± 16.3 vs 100.0 ± 1.8%, N = 15), and both doses of unsat PC increased adhesion capacity by nearly 50%. Moreover, 64 µM unsat PC decreased neutral red uptake by lysosomes by 32.5% compared to the untreated group (67.5 ± 6.8 vs 100.0 ± 5.5%, N = 15), while both 32 and 64 µM unsat PC decreased the production of lipopolysaccharide-elicited nitric oxide by 30.4% (13.5 ± 2.6 vs 19.4 ± 2.5 µM) and 46.4% (10.4 ± 3.1 vs 19.4 ± 2.5 µM), respectively. Unsat PC did not affect anion production in non-stimulated cells or phagocytosis of unopsonized zymosan particles. A different result pattern was obtained for macrophages treated with sat PC. Phorbol 12-miristate 13-acetate-elicited superoxide production and neutral red uptake were decreased by nearly 25% by 32 and 64 µM sat PC, respectively. Sat PC did not affect nitric oxide or hydrogen peroxide production, adhesion capacity or zymosan phagocytosis. Thus, PC modifies macrophage activity, but this effect depends on cell activation state, fatty acid saturation and esterification to PC molecule and PC concentration. Taken together, these results indicate that the fatty acid moiety of PC modulates macrophage activity and, consequently, is likely to affect immune system regulation in vivo.

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Nutritional substances associated to some hormones enhance liver regeneration when injected intraperitoneally, being denominated hepatotrophic factors (HF). Here we verified if a solution of HF (glucose, vitamins, salts, amino acids, glucagon, insulin, and triiodothyronine) can revert liver cirrhosis and how some extracellular matrices are affected. Cirrhosis was induced for 14 weeks in 45 female Wistar rats (200 mg) by intraperitoneal injections of thioacetamide (200 mg/kg). Twenty-five rats received intraperitoneal HF twice a day for 10 days (40 mL·kg-1·day-1) and 20 rats received physiological saline. Fifteen rats were used as control. The HF applied to cirrhotic rats significantly: a) reduced the relative mRNA expression of the genes: Col-α1 (-53%), TIMP-1 (-31.7%), TGF-β1 (-57.7%), and MMP-2 (-41.6%), whereas Plau mRNA remained unchanged; b) reduced GGT (-43.1%), ALT (-17.6%), and AST (-12.2%) serum levels; c) increased liver weight (11.3%), and reduced liver collagen (-37.1%), regenerative nodules size (-22.1%), and fibrous septum thickness. Progranulin protein (immunohistochemistry) and mRNA (in situ hybridization) were found in fibrous septa and areas of bile duct proliferation in cirrhotic livers. Concluding, HF improved the histology and serum biochemistry of liver cirrhosis, with an important reduction of interstitial collagen and increased extracelullar matrix degradation by reducing profibrotic gene expression.