936 resultados para brain network


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The current study sought to identify the impact of whether teammates in a cooperative videogame were controlled by other humans (avatars) or by the game (agents). The impact on player experience was explored through both subjective questionnaire measures and brain wave activity measurement (electroencephalography). Play with human teammates was associated with a greater sense of relatedness, but less competence and flow than play with other computer-controlled teammates. In terms of brain activity, play with human teammates was associated with greater activity in the alpha, theta and beta power bands than play with computer-controlled teammates. Overall, the results suggest that play with human teammates involves greater cognitive activity in terms of 'mentalising' than play with computer-controlled teammates. Additionally, the associations between subjective measures of player experience and brain activity are described. Limitations of the current study are identified and key directions for future research are discussed.

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In this paper we have proposed and implemented a joint Medium Access Control (MAC) -cum- Routing scheme for environment data gathering sensor networks. The design principle uses node 'battery lifetime' maximization to be traded against a network that is capable of tolerating: A known percentage of combined packet losses due to packet collisions, network synchronization mismatch and channel impairments Significant end-to-end delay of an order of few seconds We have achieved this with a loosely synchronized network of sensor nodes that implement Slotted-Aloha MAC state machine together with route information. The scheme has given encouraging results in terms of energy savings compared to other popular implementations. The overall packet loss is about 12%. The battery life time increase compared to B-MAC varies from a minimum of 30% to about 90% depending on the duty cycle.

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Previous studies have shown that buffering packets in DRAM is a performance bottleneck. In order to understand the impediments in accessing the DRAM, we developed a detailed Petri net model of IP forwarding application on IXP2400 that models the different levels of the memory hierarchy. The cell based interface used to receive and transmit packets in a network processor leads to some small size DRAM accesses. Such narrow accesses to the DRAM expose the bank access latency, reducing the bandwidth that can be realized. With real traces up to 30% of the accesses are smaller than the cell size, resulting in 7.7% reduction in DRAM bandwidth. To overcome this problem, we propose buffering these small chunks of data in the on chip scratchpad memory. This scheme also exploits greater degree of parallelism between different levels of the memory hierarchy. Using real traces from the internet, we show that the transmit rate can be improved by an average of 21% over the base scheme without the use of additional hardware. Further, the impact of different traffic patterns on the network processor resources is studied. Under real traffic conditions, we show that the data bus which connects the off-chip packet buffer to the micro-engines, is the obstacle in achieving higher throughput.

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Stroke, ischemic or hemorrhagic, belongs among the foremost causes of death and disability worldwide. Massive brain swelling is the leading cause of death in large hemispheric strokes and is only modestly alleviated by available treatment. Thrombolysis with tissue plasminogen activator (TPA) is the only approved therapy in acute ischemic stroke, but fear of TPA-mediated hemorrhage is often a reason for withholding this otherwise beneficial treatment. In addition, recanalization of the occluded artery (spontaneously or with thrombolysis) may cause reperfusion injury by promoting brain edema, hemorrhage, and inflammatory cell infiltration. A dominant event underlying these phenomena seems to be disruption of the blood-brain barrier (BBB). In contrast to ischemic stroke, no widely approved clinical therapy exists for intracerebral hemorrhage (ICH), which is associated with poor outcome mainly due to the mass effect of enlarging hematoma and associated brain swelling. Mast cells (MCs) are perivascularly located resident inflammatory cells which contain potent vasoactive, proteolytic, and fibrinolytic substances in their cytoplasmic granules. Experiments from our laboratory showed MC density and their state of granulation to be altered early following focal transient cerebral ischemia, and degranulating MCs were associated with perivascular edema and hemorrhage. (I) Pharmacological MC stabilization led to significantly reduced ischemic brain swelling (40%) and BBB leakage (50%), whereas pharmacological MC degranulation raised these by 90% and 50%, respectively. Pharmacological MC stabilization also revealed a 40% reduction in neutrophil infiltration. Moreover, genetic MC deficiency was associated with an almost 60% reduction in brain swelling, 50% reduction in BBB leakage, and 50% less neutrophil infiltration, compared with controls. (II) TPA induced MC degranulation in vitro. In vivo experiments with post-ischemic TPA administration demonstrated 70- to 100-fold increases in hemorrhage formation (HF) compared with controls HF. HF was significantly reduced by pharmacological MC stabilization at 3 (95%), 6 (75%), and 24 hours (95%) of follow-up. Genetic MC deficiency again supported the role of MCs, leading to 90% reduction in HF at 6 and 24 hours. Pharmacological MC stabilization and genetic MC deficiency were also associated with significant reduction in brain swelling and in neutrophil infiltration. Importantly, these effects translated into a significantly better neurological outcome and lower mortality after 24 hours. (III) Finally, in ICH experiments, pharmacological MC stabilization resulted in significantly less brain swelling, diminished growth in hematoma volume, better neurological scores, and decreased mortality. Pharmacological MC degranulation produced the opposite effects. Genetic MC deficiency revealed a beneficial effect similar to that found with pharmacological MC stabilization. In sum, the role of MCs in these clinically relevant scenarios is supported by a series of experiments performed both in vitro and in vivo. That not only genetic MC deficiency but also drugs targeting MCs could modulate these parameters (translated into better outcome and decreased mortality), suggests a potential therapeutic approach in a number of highly prevalent cerebral insults in which extensive tissue injury is followed by dangerous brain swelling and inflammatory cell infiltration. Furthermore, these experiments could hint at a novel therapy to improve the safety of thrombolytics, and a potential cellular target for those seeking novel forms of treatment for ICH.

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This report summarises the development of an Unmanned Aerial System and an integrated Wireless Sensor Network (WSN), suitable for the real world application in remote sensing tasks. Several aspects are discussed and analysed to provide improvements in flight duration, performance and mobility of the UAV, while ensuring the accuracy and range of data from the wireless sensor system.

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We compute the throughput obtained by a TCP connection in a UMTS environment. For downloading data at a mobile terminal, the packets of each TCP connection are stored in separate queues at the base station (node B). Also due to fragmentation of the TCP packets into Protocol Data Units (PDU) and link layer retransmissions of PDUs there can be significant delays at the queue of the node B. In such a scenario the existing models of TCP may not be sufficient. Thus, we provide a new approximate TCP model and also obtain new closed-form expressions of mean window size. Using these we obtain the throughput of a TCP connection which matches with simulations quite well.

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The polymer-amorphous carbon composites show a negative magnetoconductance which varies as B-2 at low fields which changes to B-1/2 at sufficiently high fields. The magnetoconductance gives the evidence of electron-electron interaction in composites whose conductivity follows thermal fluctuation induced tunneling and falls in the critical regime. (c) 2006 Elsevier B.V. All rights reserved.

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Carotid atherosclerotic disease is a major cause of stroke, but it may remain clinically asymptomatic. The factors that turn the asymptomatic plaque into a symptomatic one are not fully understood, neither are the subtle effects that a high-grade carotid stenosis may have on the brain. The purpose of this study was to evaluate brain microcirculation, diffusion, and cognitive performance in patients with a high-grade stenosis in carotid artery, clinically either symptomatic or asymptomatic, undergoing carotid endarterectomy (CEA). We wanted to find out whether the stenoses are associated with diffusion or perfusion abnormalities of the brain or variation in the cognitive functioning of the patients, and to what extent the potential findings are affected by CEA, and compare the clinically symptomatic and asymptomatic subjects as well as strictly healthy controls. Coagulation and fibrinolytic parameters were compared with the rate microembolic signals (MES) in transcranial Doppler (TCD) and the macroscopic appearance of stenosing plaques in surgery. Patients (n=92) underwent CEA within the study. Blood samples pertaining to coagulation and fibrinolysis were collected before CEA, and the subjects underwent repeated TCD monitoring for MES. A subpopulation (n= 46) underwent MR imaging and repeated neuropsychological examination (preoperative, as well 4 and 100 days after CEA). In MRI, the average apparent diffusion coefficients were higher in the ipsilateral white matter (WM), and altough the interhemispheric difference was abolished by CEA, the levels remained higher than in controls. Symptomatic stenoses were associated with more sluggish perfusion especially in WM, and lower pulsatility of flow in TCD. All patients had poorer cognitive performance than healthy controls. Cognitive functions improved as expected by learning effect despite transient postoperative worsening in a few subjects. Improvement was greater in patients with deepest hypoperfusion, primarily in executive functions. Symptomatic stenoses were associated with higher hematocrit and tissue plasminogen activator antigen levels, as well as higher rate of MES and ulcerated plaques, and better postoperative improvement of vasoreactivity and pulsatility. In light of the findings, carotid stenosis is associated with differences in brain diffusion, perfusion, and cognition. The effect on diffusion in the ipsilateral WM, partially reversible by CEA, may be associated with WM degeneration. Asymptomatic and symptomatic subpopulations differ from each other in terms of hemodynamic adaptation and in their vascular physiological response to removal of stenosis. Although CEA may be associated with a transient cognitive decline, a true improvement of cognitive performance by CEA is possible in patients with the most pronounced perfusion deficits. Mediators of fibrinolysis and unfavourable hemorheology may contribute to the development of a symptomatic disease in patients with a high-grade stenosis.

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Genetic and environmental factors affect white matter connectivity in the normal brain, and they also influence diseases in which brain connectivity is altered. Little is known about genetic influences on brain connectivity, despite wide variations in the brain's neural pathways. Here we applied the 'DICCCOL' framework to analyze structural connectivity, in 261 twin pairs (522 participants, mean age: 21.8 y ± 2.7SD). We encoded connectivity patterns by projecting the white matter (WM) bundles of all 'DICCCOLs' as a tracemap (TM). Next we fitted an A/C/E structural equation model to estimate additive genetic (A), common environmental (C), and unique environmental/error (E) components of the observed variations in brain connectivity. We found 44 'heritable DICCCOLs' whose connectivity was genetically influenced (α2>1%); half of them showed significant heritability (α2>20%). Our analysis of genetic influences on WM structural connectivity suggests high heritability for some WM projection patterns, yielding new targets for genome-wide association studies.

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The metabolic syndrome and type 1 diabetes are associated with brain alterations such as cognitive decline brain infarctions, atrophy, and white matter lesions. Despite the importance of these alterations, their pathomechanism is still poorly understood. This study was conducted to investigate brain glucose and metabolites in healthy individuals with an increased cardiovascular risk and in patients with type 1 diabetes in order to discover more information on the nature of the known brain alterations. We studied 43 20- to 45-year-old men. Study I compared two groups of non-diabetic men, one with an accumulation of cardiovascular risk factors and another without. Studies II to IV compared men with type 1 diabetes (duration of diabetes 6.7 ± 5.2 years, no microvascular complications) with non-diabetic men. Brain glucose, N-acetylaspartate (NAA), total creatine (tCr), choline, and myo-inositol (mI) were quantified with proton magnetic resonance spectroscopy in three cerebral regions: frontal cortex, frontal white matter, thalamus, and in cerebellar white matter. Data collection was performed for all participants during fasting glycemia and in a subgroup (Studies III and IV), also during a hyperglycemic clamp that increased plasma glucose concentration by 12 mmol/l. In non-diabetic men, the brain glucose concentration correlated linearly with plasma glucose concentration. The cardiovascular risk group (Study I) had a 13% higher plasma glucose concentration than the control group, but no difference in thalamic glucose content. The risk group thus had lower thalamic glucose content than expected. They also had 17% increased tCr (marker of oxidative metabolism). In the control group, tCr correlated with thalamic glucose content, but in the risk group, tCr correlated instead with fasting plasma glucose and 2-h plasma glucose concentration in the oral glucose tolerance test. Risk factors of the metabolic syndrome, most importantly insulin resistance, may thus influence brain metabolism. During fasting glycemia (Study II), regional variation in the cerebral glucose levels appeared in the non-diabetic subjects but not in those with diabetes. In diabetic patients, excess glucose had accumulated predominantly in the white matter where the metabolite alterations were also the most pronounced. Compared to the controls values, the white matter NAA (marker of neuronal metabolism) was 6% lower and mI (glia cell marker) 20% higher. Hyperglycemia is therefore a potent risk factor for diabetic brain disease and the metabolic brain alterations may appear even before any peripheral microvascular complications are detectable. During acute hyperglycemia (Study III), the increase in cerebral glucose content in the patients with type 1 diabetes was, dependent on brain region, between 1.1 and 2.0 mmol/l. An every-day hyperglycemic episode in a diabetic patient may therefore as much as double brain glucose concentration. While chronic hyperglycemia had led to accumulation of glucose in the white matter, acute hyperglycemia burdened predominantly the gray matter. Acute hyperglycemia also revealed that chronic fluctuation in blood glucose may be associated with alterations in glucose uptake or in metabolism in the thalamus. The cerebellar white matter appeared very differently from the cerebral (Study IV). In the non-diabetic men it contained twice as much glucose as the cerebrum. Diabetes had altered neither its glucose content nor the brain metabolites. The cerebellum seems therefore more resistant to the effects of hyperglycemia than is the cerebrum.

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We consider a dense, ad hoc wireless network confined to a small region, such that direct communication is possible between any pair of nodes. The physical communication model is that a receiver decodes the signal from a single transmitter, while treating all other signals as interference. Data packets are sent between source-destination pairs by multihop relaying. We assume that nodes self-organise into a multihop network such that all hops are of length d meters, where d is a design parameter. There is a contention based multiaccess scheme, and it is assumed that every node always has data to send, either originated from it or a transit packet (saturation assumption). In this scenario, we seek to maximize a measure of the transport capacity of the network (measured in bit-meters per second) over power controls (in a fading environment) and over the hop distance d, subject to an average power constraint. We first argue that for a dense collection of nodes confined to a small region, single cell operation is efficient for single user decoding transceivers. Then, operating the dense ad hoc network (described above) as a single cell, we study the optimal hop length and power control that maximizes the transport capacity for a given network power constraint. More specifically, for a fading channel and for a fixed transmission time strategy (akin to the IEEE 802.11 TXOP), we find that there exists an intrinsic aggregate bit rate (Theta(opt) bits per second, depending on the contention mechanism and the channel fading characteristics) carried by the network, when operating at the optimal hop length and power control. The optimal transport capacity is of the form d(opt)((P) over bar (t)) x Theta(opt) with d(opt) scaling as (P) over bar (1/eta)(t), where (P) over bar (t) is the available time average transmit power and eta is the path loss exponent. Under certain conditions on the fading distribution, we then provide a simple characterisation of the optimal operating point.

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The JoMeC Network project had three key objectives. These were to: 1. Benchmark the pedagogical elements of journalism, media and communication (JoMeC) programs at Australian universities in order to develop a set of minimum academic standards, to be known as Threshold Learning Outcomes (TLOs), which would applicable to the disciplines of Journalism, Communication and/or Media Studies, and Public Relations; 2. Build a learning and teaching network of scholars across the JoMeC disciplines to support collaboration, develop leadership potential among educators, and progress shared priorities; 3. Create an online resources hub to support learning and teaching excellence and foster leadership in learning and teaching in the JoMeC disciplines. In order to benchmark the pedagogical elements of the JoMeC disciplines, the project started with a comprehensive review of the disciplinary settings of journalism, media and communication-related programs within Higher Education in Australia plus an analysis of capstone units (or subjects) offered in JoMeC-related degrees. This audit revealed a diversity of degree titles, disciplinary foci, projected career outcomes and pedagogical styles in the 36 universities that offered JoMeC-related degrees in 2012, highlighting the difficulties of classifying the JoMeC disciplines collectively or singularly. Instead of attempting to map all disciplines related to journalism, media and communication, the project team opted to create generalised TLOs for these fields, coupled with detailed TLOs for bachelor-level qualifications in three selected JoMeC disciplines: Journalism, Communication and/or Media Studies, and Public Relations. The initial review’s outcomes shaped the methodology that was used to develop the TLOs. Given the complexity of the JoMeC disciplines and the diversity of degrees across the network, the project team deployed an issue-framing process to create TLO statements. This involved several phases, including discussions with an issue-framing team (an advisory group of representatives from different disciplinary areas); research into accreditation requirements and industry-produced materials about employment expectations; evaluation of learning outcomes from universities across Australia; reviews of scholarly literature; as well as input from disciplinary leaders in a variety of forms. Draft TLOs were refined after further consultation with industry stakeholders and the academic community via email, telephone interviews, and meetings and public forums at conferences. This process was used to create a set of common TLOs for JoMeC disciplines in general and extended TLO statements for the specific disciplines of Journalism and Public Relations. A TLO statement for Communication and/or Media Studies remains in draft form. The Australian and New Zealand Communication Association (ANZCA) and Journalism Education and Research Association of Australian (JERAA) have agreed to host meetings to review, revise and further develop the TLOs. The aim is to support the JoMeC Network’s sustainability and the TLOs’ future development and use.

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The purpose of this study was to compare the neuropsychological performance of two frontal dysexecutive phenotypes - disinhibited&' syndrome (DS) and &'apathetic&' syndrome (AS) following a traumatic brain injury in a non-western population, Oman. Methods: The study compared the performance of DS and AS in neuropsychological measures including those tapping into verbal reasoning ability/working memory/attention planning/goal-directed behavior and affective ranges. Results: The present analysis showed that DS and AS participants did not differ on indices measuring working memory/attention and affective ranges. However, the two cohorts differed significantly in measures of planning/goal-directed behaviour. Conclusion: This study lays the groundwork for further scrutiny in delineating the different characteristics of what has been previously labelled as frontal dysexecutive phenotype. This study indicates that DS and AS are marked with specific neuropsychological deficits.