418 research outputs found

    An associative memory for the on-line recognition and prediction of temporal sequences

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    This paper presents the design of an associative memory with feedback that is capable of on-line temporal sequence learning. A framework for on-line sequence learning has been proposed, and different sequence learning models have been analysed according to this framework. The network model is an associative memory with a separate store for the sequence context of a symbol. A sparse distributed memory is used to gain scalability. The context store combines the functionality of a neural layer with a shift register. The sensitivity of the machine to the sequence context is controllable, resulting in different characteristic behaviours. The model can store and predict on-line sequences of various types and length. Numerical simulations on the model have been carried out to determine its properties.Comment: Published in IJCNN 2005, Montreal, Canad

    From ARMS to brains - from the Acorn RISC machine to Spiking Neural Network Architecture

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    In May 2018, Prof Steve Furber CBE FRS FREng DFBCS FIET CITP CEng spoke to Manchester Branch BCS, the Chartered Institute for IT. This article is a summary of Prof Furber's contribution

    Meeting the design challenges of nano-CMOS electronics: an introduction to an upcoming EPSRC pilot project

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    The years of ‘happy scaling’ are over and the fundamental challenges that the semiconductor industry faces, at both technology and device level, will impinge deeply upon the design of future integrated circuits and systems. This paper provides an introduction to these challenges and gives an overview of the Grid infrastructure that will be developed as part of a recently funded EPSRC pilot project to address them, and we hope, which will revolutionise the electronics design industry

    A GPS-Less Localization and Mobility Modelling (LMM) System for Wildlife Tracking

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    Existing wildlife tracking solutions typically use sensor nodes with specialised facilities, such as long-range radio, solar array of cells and Global Positioning System (GPS). This introduces additional manufacturing cost, increased energy and memory consumptions and increased sensor node weight. This paper proposes a novel Localization and Mobility Modelling (LMM) system, that can carry out wildlife tracking by merely using low-cost, lightweight sensor nodes and using short-range peer-to-peer communication facilities only, i.e. without the need for any specialised facilities. This is done by using two computationally simple operations, which are: (i) aggregated data collections from sensor nodes via peer-to-peer communications in a distributed manner, and (ii) estimation of sensor nodes' movement traces using trilateration. The computational load placed on each sensor node is just that of data collection and aggregation, whereas movement traces estimation is carried out on a backend server, separated from the sensor nodes. In the design of the LMM system, we have: (i) carried out an empirical evaluation of different parameter value settings for data collection to develop a Multi-Zone Multi-Hierarchy (MZMH) communication structure, (ii) demonstrated a novel use of an Aggregation based Topology Learning (ATL) protocol for collecting sensor nodes' topology data using peer-to-peer multi-hop communications, and (iii) used a novel Location Estimation (LE) method for estimating sensor nodes' movement traces from the collected topology data. The evaluation results show that the LMM system can accurately estimate sensor nodes' movement traces but with significantly less energy and memory costs, demonstrating its cost-efficiency as compared to the related wildlife tracking solutions. © 2020 IEEE

    Three-dimensional MRI assessment of regional wall stress after acute myocardial infarction predicts postdischarge cardiac events

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    PURPOSE: To determine the prognostic significance of systolic wall stress (SWS) after reperfused acute myocardial infarction (AMI) using MRI. MATERIALS AND METHODS: A total of 105 patients underwent MRI 7.8 +/- 4.2 days after AMI reperfusion. SWS was calculated by using a three-dimensional (3D) MRI approach to left ventricular (LV) wall thickness and to the radius of curvature. Between hospital discharge and the end of follow-up, an average of 4.1 +/- 1.7 years after AMI, 19 patients experienced a major cardiac event, including cardiac death, nonfatal reinfarction or heart failure (18.3%). RESULTS: The results were mainly driven by heart failure outcome. In univariate analysis the following factors were predictive of postdischarge major adverse cardiac events: 1) at the time of AMI: higher heart rate, previous calcium antagonist treatment, in-hospital congestive heart failure, proximal left anterior descending artery (LAD) occlusion, a lower ejection fraction, higher maximal ST segment elevation before reperfusion, and ST segment reduction lower than 50% after reperfusion; 2) MRI parameters: higher LV end-systolic volume, lower ejection fraction, higher global SWS, higher SWS in the infarcted area (SWS MI) and higher SWS in the remote myocardium (SWS remote). In the final multivariate model, only SWS MI (odds ratio [OR]: 1.62; 95% confidence interval [CI]: 1.01-2.60; P = 0.046) and SWS remote (OR: 2.17; 95% CI: 1.02-4.65; P = 0.046) were independent predictors. CONCLUSION: Regional SWS assessed by means of MRI a few days after AMI appears to be strong predictor of postdischarge cardiac events, identifying a subset of at risk patients who could qualify for more aggressive management

    De novo atrial fibrillation as an independent prognostic marker after ST-segment elevation myocardial infarction: Results from the RIMA registry

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    BACKGROUND: Atrial fibrillation (AF) is common in ST-segment elevation myocardial infarction (STEMI), but its influence on prognosis remains controversial. AIM: We examined the 1-year prognostic value of AF in STEMI, distinguishing patients with prior AF from patients with de novo AF. METHODS: Between January 2004 and December 2015, 3173 STEMI patients were enrolled in the RIMA registry (Registre des Infarctus en Maine Anjou). They were divided into 3 groups: (1) AF-free patients; (2) patients with known prior AF; and (3) patients with de novo AF during hospitalization (including admission). We defined 3 primary outcomes at 1-year post-discharge: cardiovascular mortality, readmission for heart failure (HF), and stroke. Temporal onset of de novo AF was also studied. RESULTS: A total 158 patients (5%) had prior AF, and 278 (8.8%) presented de novo AF. Prior AF patients were significantly older [81 (73;86) years] with more comorbidities, but de novo AF patients presented with a greater creatine kinase peak and lower left ventricular ejection fraction [LVEF=44 (35;50)% for de novo AF vs 50 (40;55)% for prior AF, p<0.001]. At 1-year follow-up, cardiovascular mortality was higher in cases of AF (13.5% for prior AF vs 9.2% for de novo AF, compared with 2.4% for AF-free patients, p<0.001). After adjustments, only de novo AF was correlated with cardiovascular mortality (hazard ratio 2.49; 95% CI 1.32-4.67; p=0.004), but both types of AF were correlated with readmission for HF. There was no significant difference in respect of stroke between prior AF, de novo AF, and AF-free (2.2%, 0.5%, and 0.8%, respectively, p=0.327). Finally, outcomes did not differ between AF occurring <24h after admission (n=127) and de novo AF occurring within ≄24h (n=151). CONCLUSION: De novo AF was independently associated with 1-year cardiovascular mortality. It should not be considered as an intercurrent event of STEMI, but rather as a strong prognostic marker

    Microparticle release in remote ischemic conditioning mechanism

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    Remote ischemic conditioning (RCond) induced by short periods of ischemia and reperfusion of an organ or tissue before myocardial reperfusion is an attractive strategy of cardioprotection in the context of acute myocardial infarction. Nonetheless, its mechanism remains unknown. A humoral factor appears to be involved, although its identity is currently unknown. We hypothesized that the circulating microparticles (MPs) are the link between the remote tissue and the heart. MPs from rats and healthy humans undergoing RCond were characterized. In rats, RCond was induced by 10 min of limb ischemia. In humans, RCond was induced by three cycles of 5-min inflation and 5-min deflation of a blood-pressure cuff. In the second part of the study, rats underwent 40 min myocardial ischemia followed by 2 h reperfusion. Infarct size was measured and compared among three groups of rats: 1) myocardial infarction alone (MI) (n = 6); 2) MI + RCond started 20 min after coronary ligation (n = 6); and 3) MI + injection of RCond-derived rat MPs (MI + MPs) (n = 5). MPs from endothelial cells (CD54(+) and CD146(+) for rats and humans, respectively) and procoagulant MPs (Annexin V(+)) markedly increased after RCond, both in rats and humans. RCond reduced infarct size (24.4 ± 5.9% in MI + RCond vs. 54.6 ± 4.7% in MI alone; P < 0.01). Infarct size did not decrease in MI + MPs compared with MI alone (50.2 ± 6.4% vs. 54.6 ± 4.7%, not significantly different). RCond increased endothelium-derived and procoagulant MPs in both rats and humans. However, MP release did not appear to be a biological vector of RCond in our model

    RISK and SAFE signaling pathway interactions in remote limb ischemic perconditioning in combination with local ischemic postconditioning

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    Local ischemic postconditioning (IPost) and remote ischemic perconditioning (RIPer) are promising methods to decrease ischemia–reperfusion (I/R) injury. We tested whether the use of the two procedures in combination led to an improvement in cardioprotection through a higher activation of survival signaling pathways. Rats exposed to myocardial I/R were allocated to one of the following four groups: Control, no intervention at myocardial reperfusion; IPost, three cycles of 10-s coronary artery occlusion followed by 10-s reperfusion applied at the onset of myocardial reperfusion; RIPer, 10-min limb ischemia followed by 10-min reperfusion initiated 20 min after coronary artery occlusion; IPost+RIPer, IPost and RIPer in combination. Infarct size was significantly reduced in both IPost and RIPer (34.25 ± 3.36 and 24.69 ± 6.02%, respectively) groups compared to Control (54.93 ± 6.46%, both p < 0.05). IPost+RIPer (infarct size = 18.04 ± 4.86%) was significantly more cardioprotective than IPost alone (p < 0.05). RISK pathway (Akt, ERK1/2, and GSK-3ÎČ) activation was enhanced in IPost, RIPer, and IPost+RIPer groups compared to Control. IPost+RIPer did not enhance RISK pathway activation as compared to IPost alone, but instead increased phospho-STAT-3 levels, highlighting the crucial role of the SAFE pathway. In IPost+RIPer, a SAFE inhibitor (AG490) abolished cardioprotection and blocked both Akt and GSK-3ÎČ phosphorylations, whereas RISK inhibitors (wortmannin or U0126) abolished cardioprotection and blocked STAT-3 phosphorylation. In our experimental model, the combination of IPost and RIPer improved cardioprotection through the recruitment of the SAFE pathway. Our findings also indicate that cross talk exists between the RISK and SAFE pathways

    Innovative learning at The University of Edinburgh

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    The activities available to civil engineering students during the University of Edinburgh's innovative learning week in 2012 were examined. The academic staff proposed a wide range of possible activities and student participation was optional. Popular activities were those with a ‘hands-on’ element: making or doing something. The practical activities offered included designing and building trebuchets, relaying railway permanent way on a heritage railway, practical workshops on engineering in international development and learning to juggle. These activities suggested that heuristic learning by trial and error was likely to enhance the visualisation skills that contribute to good engineering design. Further, the linking of achievement to purposeful practice rather than innate talent could inform teaching methods in the future. They also showed that in some cases safety culture messages were still not fully assimilated by students

    Myocardial reperfusion injury management: erythropoietin compared with postconditioning

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    Ischemic postconditioning (IPost) and erythropoietin (EPO) have been shown to attenuate myocardial reperfusion injury using similar signaling pathways. The aim of this study was to examine whether EPO is as effective as IPost in decreasing postischemic myocardial injury in both Langendorff-isolated-heart and in vivo ischemia-reperfusion rat models. Rat hearts were subjected to 25 min ischemia, followed by 30 min or 2 h of reperfusion in the isolated-heart study. Rats underwent 45 min ischemia, followed by 24 h of reperfusion in the in vivo study. In both studies, the control group (n = 12; ischemia-reperfusion only) was compared with IPost (n = 16; 3 cycles of 10 s reperfusion/10 s ischemia) and EPO (n = 12; 1,000 IU/kg) at the onset of reperfusion. The following resulted. First, in the isolated hearts, IPost or EPO significantly improved postischemic recovery of left ventricular developed pressure. EPO induced better left ventricular developed pressure than IPost at 30 min of reperfusion (73.18 ± 10.23 vs. 48.11 ± 7.92 mmHg, P < 0.05). After 2 h of reperfusion, the infarct size was significantly lower in EPO-treated hearts compared with IPost and control hearts (14.36 ± 0.60%, 19.11 ± 0.84%, and 36.21 ± 4.20% of the left ventricle, respectively; P < 0.05). GSK-3ÎČ phosphorylation, at 30 min of reperfusion, was significantly higher with EPO compared with IPost hearts. Phosphatidylinositol 3-kinase and ERK1/2 inhibitors abolished both EPO- and IPost-mediated cardioprotection. Second, in vivo, IPost and EPO induced an infarct size reduction compared with control (40.5 ± 3.6% and 28.9 ± 3.1%, respectively, vs. 53.7 ± 4.3% of the area at risk; P < 0.05). Again, EPO decreased significantly more infarct size and transmurality than IPost (P < 0.05). In conclusion, with the use of our protocols, EPO showed better protective effects than IPost against reperfusion injury through higher phosphorylation of GSK-3ÎČ
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