942 resultados para Nerve-terminals
Resumo:
Neuromyelitis optica (NMO), or Devic's disease, is an idiopathic severe demyelinating disease that preferentially affects the optic nerve and spinal cord. Neuraxial anesthesia in women with multiple sclerosis is widely accepted, but reports of the use of neuraxial anesthesia in patients with NMO are scarce. We report the case of a morbidly obese primigravida undergoing a planned cesarean delivery at 32 weeks' gestation due to an acute exacerbation of NMO, managed with spinal anesthesia. Other than increased intraoperative hyperalgesia requiring inhaled nitrous oxide/oxygen, the mother experienced no apparent anesthetic-related complications.
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Recent emergence of human connectome imaging has led to a high demand on angular and spatial resolutions for diffusion magnetic resonance imaging (MRI). While there have been significant growths in high angular resolution diffusion imaging, the improvement in spatial resolution is still limited due to a number of technical challenges, such as the low signal-to-noise ratio and high motion artifacts. As a result, the benefit of a high spatial resolution in the whole-brain connectome imaging has not been fully evaluated in vivo. In this brief report, the impact of spatial resolution was assessed in a newly acquired whole-brain three-dimensional diffusion tensor imaging data set with an isotropic spatial resolution of 0.85 mm. It was found that the delineation of short cortical association fibers is drastically improved as well as the definition of fiber pathway endings into the gray/white matter boundary-both of which will help construct a more accurate structural map of the human brain connectome.
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Small bistratified cells (SBCs) in the primate retina carry a major blue-yellow opponent signal to the brain. We found that SBCs also carry signals from rod photoreceptors, with the same sign as S cone input. SBCs exhibited robust responses under low scotopic conditions. Physiological and anatomical experiments indicated that this rod input arose from the AII amacrine cell-mediated rod pathway. Rod and cone signals were both present in SBCs at mesopic light levels. These findings have three implications. First, more retinal circuits may multiplex rod and cone signals than were previously thought to, efficiently exploiting the limited number of optic nerve fibers. Second, signals from AII amacrine cells may diverge to most or all of the approximately 20 retinal ganglion cell types in the peripheral primate retina. Third, rod input to SBCs may be the substrate for behavioral biases toward perception of blue at mesopic light levels.
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Posttraumatic stress disorder (PTSD) affects the functional recruitment and connectivity between neural regions during autobiographical memory (AM) retrieval that overlap with default and control networks. Whether such univariate changes relate to potential differences in the contributions of the large-scale neural networks supporting cognition in PTSD is unknown. In the present functional MRI study, we employed independent-component analysis to examine the influence of the engagement of neural networks during the recall of personal memories in a PTSD group (15 participants) as compared to non-trauma-exposed healthy controls (14 participants). We found that the PTSD group recruited similar neural networks when compared to the controls during AM recall, including default-network subsystems and control networks, but group differences emerged in the spatial and temporal characteristics of these networks. First, we found spatial differences in the contributions of the anterior and posterior midline across the networks, and of the amygdala in particular, for the medial temporal subsystem of the default network. Second, we found temporal differences within the medial prefrontal subsystem of the default network, with less temporal coupling of this network during AM retrieval in PTSD relative to controls. These findings suggest that the spatial and temporal characteristics of the default and control networks potentially differ in a PTSD group versus healthy controls and contribute to altered recall of personal memory.
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Huntington's disease (HD) is a neurodegenerative disease caused by the expansion of a poly-glutamine (poly-Q) stretch in the huntingtin (Htt) protein. Gain-of-function effects of mutant Htt have been extensively investigated as the major driver of neurodegeneration in HD. However, loss-of-function effects of poly-Q mutations recently emerged as potential drivers of disease pathophysiology. Early synaptic problems in the excitatory cortical and striatal connections have been reported in HD, but the role of Htt protein in synaptic connectivity was unknown. Therefore, we investigated the role of Htt in synaptic connectivity in vivo by conditionally silencing Htt in the developing mouse cortex. When cortical Htt function was silenced, cortical and striatal excitatory synapses formed and matured at an accelerated pace through postnatal day 21 (P21). This exuberant synaptic connectivity was lost over time in the cortex, resulting in the deterioration of synapses by 5 weeks. Synaptic decline in the cortex was accompanied with layer- and region-specific reactive gliosis without cell loss. To determine whether the disease-causing poly-Q mutation in Htt affects synapse development, we next investigated the synaptic connectivity in a full-length knock-in mouse model of HD, the zQ175 mouse. Similar to the cortical conditional knock-outs, we found excessive excitatory synapse formation and maturation in the cortices of P21 zQ175, which was lost by 5 weeks. Together, our findings reveal that cortical Htt is required for the correct establishment of cortical and striatal excitatory circuits, and this function of Htt is lost when the mutant Htt is present.
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BACKGROUND: Mechanical and in particular tactile allodynia is a hallmark of chronic pain in which innocuous touch becomes painful. Previous cholera toxin B (CTB)-based neural tracing experiments and electrophysiology studies had suggested that aberrant axon sprouting from touch sensory afferents into pain-processing laminae after injury is a possible anatomical substrate underlying mechanical allodynia. This hypothesis was later challenged by experiments using intra-axonal labeling of A-fiber neurons, as well as single-neuron labeling of electrophysiologically identified sensory neurons. However, no studies have used genetically labeled neurons to examine this issue, and most studies were performed on spinal but not trigeminal sensory neurons which are the relevant neurons for orofacial pain, where allodynia oftentimes plays a dominant clinical role. FINDINGS: We recently discovered that parvalbumin::Cre (Pv::Cre) labels two types of Aβ touch neurons in trigeminal ganglion. Using a Pv::CreER driver and a Cre-dependent reporter mouse, we specifically labeled these Aβ trigeminal touch afferents by timed taxomifen injection prior to inflammation or infraorbital nerve injury (ION transection). We then examined the peripheral and central projections of labeled axons into the brainstem caudalis nucleus after injuries vs controls. We found no evidence for ectopic sprouting of Pv::CreER labeled trigeminal Aβ axons into the superficial trigeminal noci-receptive laminae. Furthermore, there was also no evidence for peripheral sprouting. CONCLUSIONS: CreER-based labeling prior to injury precluded the issue of phenotypic changes of neurons after injury. Our results suggest that touch allodynia in chronic orofacial pain is unlikely caused by ectopic sprouting of Aβ trigeminal afferents.
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Inhibitory motor control is a core function of cognitive control. Evidence from diverse experimental approaches has linked this function to a mostly right-lateralized network of cortical and subcortical areas, wherein a signal from the frontal cortex to the basal ganglia is believed to trigger motor-response cancellation. Recently, however, it has been recognized that in the context of typical motor-control paradigms those processes related to actual response inhibition and those related to the attentional processing of the relevant stimuli are highly interrelated and thus difficult to distinguish. Here, we used fMRI and a modified Stop-signal task to specifically examine the role of perceptual and attentional processes triggered by the different stimuli in such tasks, thus seeking to further distinguish other cognitive processes that may precede or otherwise accompany the implementation of response inhibition. In order to establish which brain areas respond to sensory stimulation differences by rare Stop-stimuli, as well as to the associated attentional capture that these may trigger irrespective of their task-relevance, we compared brain activity evoked by Stop-trials to that evoked by Go-trials in task blocks where Stop-stimuli were to be ignored. In addition, region-of-interest analyses comparing the responses to these task-irrelevant Stop-trials, with those to typical relevant Stop-trials, identified separable activity profiles as a function of the task-relevance of the Stop-signal. While occipital areas were mostly blind to the task-relevance of Stop-stimuli, activity in temporo-parietal areas dissociated between task-irrelevant and task-relevant ones. Activity profiles in frontal areas, in turn, were activated mainly by task-relevant Stop-trials, presumably reflecting a combination of triggered top-down attentional influences and inhibitory motor-control processes.
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BACKGROUND: The development of a microcomputer-based device permits quick, simple, and noninvasive quantification of the respiratory sinus arrhythmia (RSA) during quiet breathing. METHODS AND RESULTS: We prospectively and serially measured the radionuclide left ventricular ejection fraction and the RSA amplitude in 34 cancer patients receiving up to nine monthly bolus treatments with doxorubicin hydrochloride (60 mg/m2). Of the eight patients who ultimately developed symptomatic doxorubicin-induced congestive heart failure, seven (87.5%) demonstrated a significant decline in RSA amplitude; five of 26 subjects without clinical symptoms of cardiotoxicity (19.2%) showed a similar RSA amplitude decline. On average, significant RSA amplitude decline occurred 3 months before the last planned doxorubicin dose in patients destined to develop clinical congestive heart failure. CONCLUSION: Overall, RSA amplitude abnormality proved to be a more specific predictor of clinically significant congestive heart failure than did serial resting radionuclide ejection fractions.
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CD4+CD25highFOXP3+ regulatory T (Treg) cells have recently been found at elevated levels in the peripheral blood of tuberculosis patients, compared to Mycobacterium tuberculosis latently infected (LTBI) healthy individuals and non-infected controls. Here, we show that CD4+CD25highFOXP3+ T lymphocytes can be expanded in vitro from peripheral blood mononuclear cells (PBMC) of LTBI individuals, but not of uninfected controls by incubating them with BCG in the presence of TGF-beta. These expanded cells from the PBMC of LTBI subjects expressed CTLA-4, GITR and OX-40, but were CD127low/- and have therefore the phenotype of Treg cells. In addition, they inhibited in a dose-dependant manner the proliferation of freshly isolated mononuclear cells in response to polyclonal stimulation, indicating that they are functional Treg lymphocytes. In contrast, incubation of the PBMC with BCG alone preferentially induced activated CD4+ T cells, expressing CD25 and/or CD69 and secreting IFN-gamma. These results show that CD4+CD25highFOXP3+ Treg cells can be expanded or induced in the peripheral blood of LTBI individuals in conditions known to predispose to progression towards active tuberculosis and may therefore play an important role in the pathogenesis of the disease.
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This paper presents a genetic algorithm for finding a constrained minimum spanning tree. The problem is of relevance in the design of minimum cost communication networks, where there is a need to connect all the terminals at a user site to a terminal concentrator in a multipoint (tree) configuration, while ensuring that link capacity constraints are not violated. The approach used maintains a distinction between genotype and phenotype, which produces superior results to those found using a direct representation in a previous study.
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The diversity gains achievable in the generalised distributed antenna system with cooperative users (GDAS-CU) are considered. A GDAS-CU is comprised of M largely separated access points (APs) at one side of the link, and N geographically closed user terminals (UTs) at the other side. The UTs are collaborating together to enhance the system performance, where an idealised message sharing among the UTs is assumed. First, geometry-based network models are proposed to describe the topology of a GDAS-CU. The mean cross-correlation coefficients of signals received from non-collocated APs and UTs are calculated based on the network topology and the correlation models derived from the empirical data. The analysis is also extendable to more general scenarios where the APs are placed in a clustered form due to the constraints of street layout or building structure. Subsequently, a generalised signal attenuation model derived from several stochastic ray-tracing-based pathloss models is applied to describe the power-decaying pattern in urban built-up areas, where the GDAS-CU may be deployed. Armed with the cross-correlation and pathloss model preliminaries, an intrinsic measure of cooperative diversity obtainable from a GDAS-CU is then derived, which is the number of independent fading channels that can be averaged over to detect symbols. The proposed analytical framework would provide critical insight into the degree of possible performance improvement when combining multiple copies of the received signal in such systems.
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This is about politics and protest, or rather about a politics of protest, and of rebellion. But it is also about creativity and the way in which theory and practice combine within the context of the ‘productive/creative’ process. In this case the combination is explicit and can be traced along a clear trajectory. The following will set out the way in which the accompanying piece of music – a cover of the 1969 protest song Leaving on a Jet Plane by Peter, Paul & Mary - came into being. In doing so it will make reference to a number of theoretical ideas/concepts that fed into the productive process and/or appeared relevant postproduction. It will draw on various aspects of thought from Heidegger (Standing reserve, Enframing and Authenticity), Camus (The Rebel), Foucault (Luminosity), and Deleuze (Immanence, Difference and Repetition and The Fold). [From the Author].
Resumo:
Sediment contaminants were monitored in Milford Haven Waterway (MHW) since 1978 (hydrocarbons) and 1982 (metals), with the aim of providing surveillance of environmental quality in one of the UK’s busiest oil and gas ports. This aim is particularly important during and after large-scale investment in liquefied natural gas (LNG) facilities. However, methods inevitably have changed over the years, compounding the difficulties of coordinating sampling and analytical programmes. After a review by the MHW Environmental Surveillance Group (MHWESG), sediment hydrocarbon chemistry was investigated in detail in 2010. Natural Resources Wales (NRW) contributed their MHW data for 2007 and 2012, collected to assess the condition of the Special Area of Conservation (SAC) designated under the European Union Habitats Directive. Datasets during 2007-2012 have thus been more comparable. The results showed conclusively that a MHW-wide peak in concentrations of sediment polycyclic aromatic hydrocarbons (PAHs), metals and other contaminants occurred in late 2007. This was corroborated by independent annual monitoring at one centrally-located station with peaks in early 2008 and 2011. The spatial and temporal patterns of recovery from the 2007 peak, shown by MHW-wide surveys in 2010 and 2012, indicate several probable causes of contaminant trends, as follows: atmospheric deposition, catchment runoff, sediment resuspension from dredging, and construction of two LNG terminals and a power station. Adverse biological effects predictable in 2007 using international sediment quality guidelines, were independently tested by data from monitoring schemes of more than a decade duration in MHW (starfish, limpets), and in the wider SAC (grey seals). Although not proving cause and effect, many of these potential biological receptors showed a simultaneous negative response to the elevated 2007 contamination following intense dredging activity in 2006. Wetland bird counts were typically at a peak in the winter of 2005-2006 previous to peak dredging. In the following winter 2006-2007, shelduck in Pembroke River showed their lowest winter count, and spring 2007 was the largest ever drop in numbers of broods across MHW between successive breeding seasons. Wigeon counts in Pembroke River were again low in late 2012 after further dredging nearby. These results are strongly supported by PAH data reported previously from invertebrate bioaccumulation studies in MHW 2007-2010, themselves closely reflecting sediment