999 resultados para Trellis-code modulation
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Considers Sampling, Pulse Amplitude Modulation, Multiple Access, Quantisation, Pulse Coded Modulation, Manchester Line Coding, Amplitude Modulation, Double SideBand Suppressed Carrier Modulation, Quadrature Amplitude Modulation and M-ary Shift Keying.
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Bilingualism is reported to re-structure executive control networks, but it remains unknown which aspects of the bilingual experience cause this modulation. This study explores the impact of three code-switching types on executive functions: (1) alternation of languages, (2) insertion of lexicon of one language into grammar of another, (3) dense code-switching with co-activation of lexicon and grammar. Current models hypothesise that they challenge different aspects of the executive system because they vary in the extent and scope of language separation. Two groups of German-English bilinguals differing in dense code-switching frequency participated in a flanker task under conditions varying in degree of trial-mixing and resulting demands to conflict-monitoring. Bilinguals engaging in more dense code-switching showed inhibitory advantages in the condition requiring most conflict-monitoring. Moreover, dense code-switching frequency correlated positively with monitoring skills. This suggests that the management of co-activated languages during dense code-switching engages conflict-monitoring and that the consolidation processes taking place within co-activated linguistic systems involve local inhibition. Code-switching types requiring greater degrees of language separation may involve more global forms of inhibition. This study shows that dense code-switching is a key experience shaping bilinguals’ executive functioning and highlights the importance of controlling for participants’ code-switching habits in bilingualism research.
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This letter presents an analytical model for evaluating the Bit Error Rate (BER) of a Direct Sequence Code Division Multiple Access (DS-CDMA) system, with M-ary orthogonal modulation and noncoherent detection, employing an array antenna operating in a Nakagami fading environment. An expression of the Signal to Interference plus Noise Ratio (SINR) at the output of the receiver is derived, which allows the BER to be evaluated using a closed form expression. The analytical model is validated by comparing the obtained results with simulation results.
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The following thesis presents results obtained from both numerical simulation and laboratory experimentation (both of which were carried out by the author). When data is propagated along an optical transmission line some timing irregularities can occur such as timing jitter and phase wander. Traditionally these timing problems would have been corrected by converting the optical signal into the electrical domain and then compensating for the timing irregularity before converting the signal back into the optical domain. However, this thesis posses a potential solution to the problem by remaining completely in the optical domain, eliminating the need for electronics. This is desirable as not only does optical processing reduce the latency effect that their electronic counterpart have, it also holds the possibility of an increase in overall speed. A scheme was proposed which utilises the principle of wavelength conversion to dynamically convert timing irregularities (timing jitter and phase wander) into a change in wavelength (this occurs on a bit-by-bit level and so timing jitter and phase wander can be compensated for simultaneously). This was achieved by optically sampling a linearly chirped, locally generated clock source (the sampling function was achieved using a nonlinear optical loop mirror). The data, now with each bit or code word having a unique wavelength, is then propagated through a dispersion compensation module. The dispersion compensation effectively re-aligns the data in time and so thus, the timing irregularities are removed. The principle of operation was tested using computer simulation before being re-tested in a laboratory environment. A second stage was added to the device to create 3R regeneration. The second stage is used to simply convert the timing suppressed data back into a single wavelength. By controlling the relative timing displacement between stage one and stage two, the wavelength that is finally produced can be controlled.
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The rapidly increasing demand for cellular telephony is placing greater demand on the limited bandwidth resources available. This research is concerned with techniques which enhance the capacity of a Direct-Sequence Code-Division-Multiple-Access (DS-CDMA) mobile telephone network. The capacity of both Private Mobile Radio (PMR) and cellular networks are derived and the many techniques which are currently available are reviewed. Areas which may be further investigated are identified. One technique which is developed is the sectorisation of a cell into toroidal rings. This is shown to provide an increased system capacity when the cell is split into these concentric rings and this is compared with cell clustering and other sectorisation schemes. Another technique for increasing the capacity is achieved by adding to the amount of inherent randomness within the transmitted signal so that the system is better able to extract the wanted signal. A system model has been produced for a cellular DS-CDMA network and the results are presented for two possible strategies. One of these strategies is the variation of the chip duration over a signal bit period. Several different variation functions are tried and a sinusoidal function is shown to provide the greatest increase in the maximum number of system users for any given signal-to-noise ratio. The other strategy considered is the use of additive amplitude modulation together with data/chip phase-shift-keying. The amplitude variations are determined by a sparse code so that the average system power is held near its nominal level. This strategy is shown to provide no further capacity since the system is sensitive to amplitude variations. When both strategies are employed, however, the sensitivity to amplitude variations is shown to reduce, thus indicating that the first strategy both increases the capacity and the ability to handle fluctuations in the received signal power.
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Recently, polynomial phase modulation (PPM) was shown to be a power- and bandwidth-efficient modulation format. These two characteristics are in high demand nowadays specially in mobile applications, where devices with size, weight, and power (SWaP) constraints are common. In this paper, we propose implementing a full-diversity quasiorthogonal space-time block code (QOSTBC) using polynomial phase signals as modulation format. QOSTBCs along with PPM are used in order to improve the power efficiency of communication systems with four transmit antennas. We obtain the optimal PPM constellations that ensure full diversity and maximize the QOSTBC's minimum coding gain distance. Simulation results show that by using QOSTBCs along with a properly selected PPM constellation, full diversity in flat fading channels and thus low BER at high signal-to-noise ratios (SNR) can be ensured. More importantly, it is also shown that QOSTBCs using PPM achieve a better error performance than those using conventional modulation formats.
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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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Universidade Estadual de Campinas . Faculdade de Educação Física
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Universidade Estadual de Campinas . Faculdade de Educação Física
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Universidade Estadual de Campinas . Faculdade de Educação Física
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Universidade Estadual de Campinas . Faculdade de Educação Física
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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.