995 resultados para phylogenetic signal


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Traditional chemometrics techniques are augmented with algorithms tailored specifically for the de-noising and analysis of femtosecond duration pulse datasets. The new algorithms provide additional insights on sample responses to broadband excitation and multi-moded propagation phenomena.

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The dependency of the blood oxygenation level dependent (BOLD) signal on underlying hemodynamics is not well understood. Building a forward biophysical model of this relationship is important for the quantitative estimation of the hemodynamic changes and neural activity underlying functional magnetic resonance imaging (fMRI) signals. We have developed a general model of the BOLD signal which can model both intra- and extravascular signals for an arbitrary tissue model across a wide range of imaging parameters. The model of the BOLD signal was instantiated as a look-up-table (LuT), and was verified against concurrent fMRI and optical imaging measurements of activation induced hemodynamics. Magn Reson Med, 2008. © 2008 Wiley-Liss, Inc.

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The calcium (Ca) concentration of plant shoot tissues varies systematically between angiosperm orders. The phylogenetic variation in the shoot concentration of other mineral nutrients has not yet been described at an ordinal level. The aims of this study were (1) to quantify the shoot mineral concentration of different angiosperm orders, (2) to partition the phylogenetic variation in shoot mineral concentration between and within orders, (3) to determine if the shoot concentration of different minerals are correlated across angiosperm species, and (4) to compare experimental data with published ecological survey data on 81 species sampled from their natural habitats. Species, selected pro rata from different angiosperm orders, were grown in a hydroponic system under a constant external nutrient regime. Shoots of 117 species were sampled during vegetative growth. Significant variation in shoot carbon (C), calcium (Ca), potassium (K), and magnesium (Mg) concentration occurred between angiosperm orders. There was no evidence for systematic differences in shoot phosphorus (P) or organic-nitrogen (N) concentration between orders. At a species level, there were strong positive correlations between shoot Ca and Mg concentration, between shoot P and organic-N concentration, and between shoot K concentration and shoot fresh weight:dry weight ratio. Shoot C and cation concentration correlated negatively at a species level. Species within the Poales and the Caryophyllales had distinct shoot mineralogies in both the designed experiment and in the ecological survey.

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This paper presents an in-depth critical discussion and derivation of a detailed small-signal analysis of the Phase-Shifted Full-Bridge (PSFB) converter. Circuit parasitics, resonant inductance and transformer turns ratio have all been taken into account in the evaluation of this topology’s open-loop control-to-output, line-to-output and load-to-output transfer functions. Accordingly, the significant impact of losses and resonant inductance on the converter’s transfer functions is highlighted. The enhanced dynamic model proposed in this paper enables the correct design of the converter compensator, including the effect of parasitics on the dynamic behavior of the PSFB converter. Detailed experimental results for a real-life 36V-to-14V/10A PSFB industrial application show excellent agreement with the predictions from the model proposed herein.1

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This paper discusses ECG signal classification after parametrizing the ECG waveforms in the wavelet domain. Signal decomposition using perfect reconstruction quadrature mirror filter banks can provide a very parsimonious representation of ECG signals. In the current work, the filter parameters are adjusted by a numerical optimization algorithm in order to minimize a cost function associated to the filter cut-off sharpness. The goal consists of achieving a better compromise between frequency selectivity and time resolution at each decomposition level than standard orthogonal filter banks such as those of the Daubechies and Coiflet families. Our aim is to optimally decompose the signals in the wavelet domain so that they can be subsequently used as inputs for training to a neural network classifier.

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The susceptibility of a catchment to flooding is affected by its soil moisture prior to an extreme rainfall event. While soil moisture is routinely observed by satellite instruments, results from previous work on the assimilation of remotely sensed soil moisture into hydrologic models have been mixed. This may have been due in part to the low spatial resolution of the observations used. In this study, the remote sensing aspects of a project attempting to improve flow predictions from a distributed hydrologic model by assimilating soil moisture measurements are described. Advanced Synthetic Aperture Radar (ASAR) Wide Swath data were used to measure soil moisture as, unlike low resolution microwave data, they have sufficient resolution to allow soil moisture variations due to local topography to be detected, which may help to take into account the spatial heterogeneity of hydrological processes. Surface soil moisture content (SSMC) was measured over the catchments of the Severn and Avon rivers in the South West UK. To reduce the influence of vegetation, measurements were made only over homogeneous pixels of improved grassland determined from a land cover map. Radar backscatter was corrected for terrain variations and normalized to a common incidence angle. SSMC was calculated using change detection. To search for evidence of a topographic signal, the mean SSMC from improved grassland pixels on low slopes near rivers was compared to that on higher slopes. When the mean SSMC on low slopes was 30–90%, the higher slopes were slightly drier than the low slopes. The effect was reversed for lower SSMC values. It was also more pronounced during a drying event. These findings contribute to the scant information in the literature on the use of high resolution SAR soil moisture measurement to improve hydrologic models.

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The detection of physiological signals from the motor system (electromyographic signals) is being utilized in the practice clinic to guide the therapist in a more precise and accurate diagnosis of motor disorders. In this context, the process of decomposition of EMG (electromyographic) signals that includes the identification and classification of MUAP (Motor Unit Action Potential) of a EMG signal, is very important to help the therapist in the evaluation of motor disorders. The EMG decomposition is a complex task due to EMG features depend on the electrode type (needle or surface), its placement related to the muscle, the contraction level and the health of the Neuromuscular System. To date, the majority of researches on EMG decomposition utilize EMG signals acquired by needle electrodes, due to their advantages in processing this type of signal. However, relatively few researches have been conducted using surface EMG signals. Thus, this article aims to contribute to the clinical practice by presenting a technique that permit the decomposition of surface EMG signal via the use of Hidden Markov Models. This process is supported by the use of differential evolution and spectral clustering techniques. The developed system presented coherent results in: (1) identification of the number of Motor Units actives in the EMG signal; (2) presentation of the morphological patterns of MUAPs in the EMG signal; (3) identification of the firing sequence of the Motor Units. The model proposed in this work is an advance in the research area of decomposition of surface EMG signals.

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Studiesthat use prolonged periods of sensory stimulation report associations between regional reductions in neural activity and negative blood oxygenation level-dependent (BOLD) signaling. However, the neural generators of the negative BOLD response remain to be characterized. Here, we use single-impulse electrical stimulation of the whisker pad in the anesthetized rat to identify components of the neural response that are related to “negative” hemodynamic changes in the brain. Laminar multiunit activity and local field potential recordings of neural activity were performed concurrently withtwo-dimensional optical imaging spectroscopy measuring hemodynamic changes. Repeated measurements over multiple stimulation trials revealed significant variations in neural responses across session and animal datasets. Within this variation, we found robust long-latency decreases (300 and 2000 ms after stimulus presentation) in gammaband power (30 – 80 Hz) in the middle-superficial cortical layers in regions surrounding the activated whisker barrel cortex. This reduction in gamma frequency activity was associated with corresponding decreases in the hemodynamic responses that drive the negative BOLD signal. These findings suggest a close relationship between BOLD responses and neural events that operate over time scales that outlast the initiating sensory stimulus, and provide important insights into the neurophysiological basis of negative neuroimaging signals.

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Tribe Merremieae, as currently circumscribed, comprise c. 120 species classified in seven genera, the largest of which (Merremia) is morphologically heterogeneous. Previous studies, with limited sampling, have suggested that neither Merremieae nor Merremia are monophyletic. In the present study, the monophyly of Merremia and its allied genera was re-assessed, sampling 57 species of Merremieae for the plastid matK, trnL–trnF and rps16 regions and the nuclear internal transcribed spacer (ITS) region. All genera of Merremieae and all major morphotypes in Merremia were represented. Phylogenetic analyses resolve Merremieae in a clade with Ipomoeae, Convolvuleae and Daustinia montana. Merremia is confirmed as polyphyletic and a number of well-supported and morphologically distinct clades in Merremieae are recognized which accommodate most of the species in the tribe. These provide a framework for a generic revision of the assemblage.

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We present a data-driven mathematical model of a key initiating step in platelet activation, a central process in the prevention of bleeding following Injury. In vascular disease, this process is activated inappropriately and causes thrombosis, heart attacks and stroke. The collagen receptor GPVI is the primary trigger for platelet activation at sites of injury. Understanding the complex molecular mechanisms initiated by this receptor is important for development of more effective antithrombotic medicines. In this work we developed a series of nonlinear ordinary differential equation models that are direct representations of biological hypotheses surrounding the initial steps in GPVI-stimulated signal transduction. At each stage model simulations were compared to our own quantitative, high-temporal experimental data that guides further experimental design, data collection and model refinement. Much is known about the linear forward reactions within platelet signalling pathways but knowledge of the roles of putative reverse reactions are poorly understood. An initial model, that includes a simple constitutively active phosphatase, was unable to explain experimental data. Model revisions, incorporating a complex pathway of interactions (and specifically the phosphatase TULA-2), provided a good description of the experimental data both based on observations of phosphorylation in samples from one donor and in those of a wider population. Our model was used to investigate the levels of proteins involved in regulating the pathway and the effect of low GPVI levels that have been associated with disease. Results indicate a clear separation in healthy and GPVI deficient states in respect of the signalling cascade dynamics associated with Syk tyrosine phosphorylation and activation. Our approach reveals the central importance of this negative feedback pathway that results in the temporal regulation of a specific class of protein tyrosine phosphatases in controlling the rate, and therefore extent, of GPVI-stimulated platelet activation.

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The small G protein Ras has been implicated in hypertrophy of cardiac myocytes. We therefore examined the activation (GTP loading) of Ras by the following hypertrophic agonists: phorbol 12-myristate 13-acetate (PMA), endothelin-1 (ET-1), and phenylephrine (PE). All three increased Ras.GTP loading by 10-15-fold (maximal in 1-2 min), as did bradykinin. Other G protein-coupled receptor agonists (e.g. angiotensin II, carbachol, isoproterenol) were less effective. Activation of Ras by PMA, ET-1, or PE was reduced by inhibition of protein kinase C (PKC), and that induced by ET-1 or PE was partly sensitive to pertussis toxin. 8-(4-Chlorophenylthio)-cAMP (CPT-cAMP) did not inhibit Ras.GTP loading by PMA, ET-1, or PE. The association of Ras with c-Raf protein was increased by PMA, ET-1, or PE, and this was inhibited by CPT-cAMP. However, only PMA and ET-1 increased Ras-associated mitogen-activated protein kinase kinase 1-activating activity, and this was decreased by PKC inhibition, pertussis toxin, and CPT-cAMP. PMA caused the rapid appearance of phosphorylated (activated) extracellular signal-regulated kinase in the nucleus, which was inhibited by a microinjected neutralizing anti-Ras antibody. We conclude that PKC- and Gi-dependent mechanisms mediate the activation of Ras in myocytes and that Ras activation is required for stimulation of extracellular signal-regulated kinase by PMA.

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Studies in non-cardiomyocytic cells have shown that phosphorylation of the Bcl-2 family protein Bad on Ser-112, Ser-136 and Ser-155 decreases its pro-apoptotic activity. Both phenylephrine (100 microM) and the cell membrane-permeating cAMP analog, 8-(4-chlorophenylthio)-cAMP (100 microM), protected against 2-deoxy-D-glucose-induced apoptosis in neonatal rat cardiac myocytes as assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). In cardiac myocytes, phenylephrine primarily stimulates the alpha-adrenoceptor, but, at high concentrations (100 microM), it also increases the activity of the cAMP-dependent protein kinase, protein kinase A (PKA) through the beta-adrenoceptor. Phenylephrine (100 microM) promoted rapid phosphorylation of Bad(Ser-112) and Bad(Ser-155), though we were unable to detect phosphorylation of Bad(Ser-136). Phosphorylation of Bad(Ser-112) was antagonized by either prazosin or propranolol, indicating that this phosphorylation required stimulation of both alpha(1)- and beta-adrenoceptors. Phosphorylation of Bad(Ser-155) was antagonized only by propranolol and was thus mediated through the beta-adrenoceptor. Inhibitor studies and partial purification of candidate kinases by fast protein liquid chromatography showed that the p90 ribosomal S6 kinases, p90RSK2/3 [which are activated by the extracellular signal-regulated kinases 1 and 2 (ERK1/2)] directly phosphorylated Bad(Ser-112), whereas the PKA catalytic subunit directly phosphorylated Bad(Ser-155). However, efficient phosphorylation of Bad(Ser-112) also required PKA activity. These data suggest that, although p90RSK2/3 phosphorylate Bad(Ser-112) directly, phosphorylation of this site is enhanced by phosphorylation of Bad(Ser-155). These phosphorylations potentially diminish the pro-apoptotic activity of Bad and contribute to the cytoprotective effects of phenylephrine and 8-(4-chlorophenylthio)-cAMP.

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Cardiac hypertrophy, an important adaptational response, is associated with up-regulation of the immediate early gene, c- jun, which encodes the c-Jun transcription factor. c-Jun may feed back to up-regulate its own transcription and, since the c-Jun N-terminal kinase (JNK) family of mitogen-activated protein kinases (MAPKs) phosphorylate c-Jun(Ser-63/73) to increase its transactivating activity, JNKs are thought to be the principal factors involved in c- jun up-regulation. Hypertrophy in primary cultures of cardiac myocytes is induced by endothelin-1, phenylephrine or PMA, probably through activation of one or more of the MAPK family. These three agonists increased c- jun mRNA with the rank order of potency of PMA approximately endothelin-1>phenylephrine. Up-regulation of c- jun mRNA by endothelin-1 was attenuated by inhibitors of protein kinase C (GF109203X) and the extracellular signal-regulated kinase (ERK) cascade (PD98059 or U0126), but not by inhibitors of the JNK (SP600125) or p38-MAPK (SB203580) cascades. Hyperosmotic shock (0.5 M sorbitol) powerfully activates JNKs, but did not increase c- jun mRNA. These data suggest that ERKs, rather than JNKs, are required for c- jun up-regulation. However, endothelin-1 and phenylephrine induced greater up-regulation of c-Jun protein than PMA and phosphorylation of c-Jun(Ser-63/73) correlated with the level of c-Jun protein. Up-regulation of c-Jun protein by endothelin-1 was attenuated by inhibitors of protein kinase C and the ERK cascade, probably correlating with a primary input of ERKs into transcription. In addition, SP600125 inhibited the phosphorylation of c-Jun(Ser-63/73), attenuated the increase in c-Jun protein induced by endothelin-1 and increased the rate of c-Jun degradation. Thus whereas ERKs are the principal MAPKs required for c- jun transcription, JNKs are necessary to stabilize c-Jun for efficient up-regulation of the protein.