SpineCreator: a Graphical User Interface for the Creation of Layered Neural Models.

There is a growing requirement in computational neuroscience for tools that permit collaborative model building, model sharing, combining existing models into a larger system (multi-scale model integration), and are able to simulate models using a variety of simulation engines and hardware platforms. Layered XML model specification formats solve many of these problems, however they are difficult to write and visualise without tools. Here we describe a new graphical software tool, SpineCreator, which facilitates the creation and visualisation of layered models of point spiking neurons or rate coded neurons without requiring the need for programming. We demonstrate the tool through the reproduction and visualisation of published models and show simulation results using code generation interfaced directly into SpineCreator. As a unique application for the graphical creation of neural networks, SpineCreator represents an important step forward for neuronal modelling

A type-2 fuzzy modelling framework for aircraft taxi-time prediction

Knowing aircraft taxi-time precisely a-priori is increasingly important for any airport management system. This work presents a new approach for estimating and characterising the taxi-time of an aircraft based on historical information. The approach makes use of the interval type-2 fuzzy logic system, which provides more robustness and accuracy than the conventional type-1 fuzzy system. To compensate for erroneous modelling assumptions, the error distribution of the model is further analysed and an error compensation strategy is developed. Results, when tested on a real data set for Manchester Airport (U.K.), show improved taxi-time accuracy and generalisation capability over a wide range of modelling assumptions when compared with existing fuzzy systems and linear regression-based methods

Simulation Training in U.K. General Aviation: An Undervalued Aid to Reducing Loss of Control Accidents

Analysis of data from 1,007 U.K. general aviation (GA) accidents demonstrates the predominant cause of accidents is loss of control, exacerbated by a lack of recent flying experience. These are long-standing problems that can be targeted effectively with simulation training. Discussion on training strategies in commercial aviation reinforces the logic of introducing simulation training for the GA pilot. Conclusions drawn affirm the notion that GA safety would benefit from implementation of regulated simulation training

0111i I ll III ACTUATOR PLACEMENT FOR ACTIVE SURGE CONTROL IN A MULTI-STAGE AXIAL COMPRESSOR

ABSTRACT. This paper describes an actuator placement methodology for the active control of purely onedimensional instabilities of a seven-stage axial compressor using an air bleeding strategy. In this theoretical study, using stage-by-stage non-linear modelling based on the conservation equations of mass, momentum, and energy, a scheduling LQR (Linear Quadratic Regulator) controller is designed for several actuator locations in a compressor from the first stage to the plenum. In this controller design, the LQR weighting matrices are selected so that the associated cost function includes only air bleeding mass flow leading to the minimisation of the air bleed. The LQR cost function represents a measure of the consumption of air bleeding and can be calculated analytically using the solution of an Algebraic Riccati Equation. From analysis of the cost at different compressor stages, the location of an air bleeding actuator is selected at the stage with the minimum cost. Finally, using an ACSL simulation program, the scheduling controller has been integrated with a non-lineat stage-by-stage model and the time response of the air bleeding mass flow at different locations has been obtained to confirm the results from the analytical approach. Results are presented to show actively stabilised compressor flow beyond the surge point where the air bleed is minimised. These results also indicate the preferred location of the actuator at the compressor downstream stages for both low and high compressor speeds

Co-ingestion of whey protein with a carbohydrate-rich breakfast boes not affect glycemia, insulinemia or subjective appetite following a subsequent meal in healthy males

We aimed to assess postprandial metabolic and appetite responses to a mixed-macronutrient lunch following prior addition of whey protein to a carbohydrate-rich breakfast. Ten healthy males (age: 24 ± 1 y; body mass index (BMI): 24.5 ± 0.7 kg/m2) completed three trials in a non-isocaloric, crossover design. A carbohydrate-rich breakfast (93 g carbohydrate; 1799 kJ) was consumed with (CHO+WP) or without (CHO) 20 g whey protein isolate (373 kJ), or breakfast was omitted (NB). At 180 minutes, participants consumed a mixed-macronutrient lunch meal. Venous blood was sampled at 15 minute intervals following each meal and every 30 minutes thereafter, while subjective appetite sensations were collected every 30 minutes throughout. Post-breakfast insulinaemia was greater after CHO+WP (time-averaged area under the curve (AUC0-180 min): 193.1 ± 26.3 pmol/L), compared to CHO (154.7 ± 18.5 pmol/L) and NB (46.1 ± 8.0 pmol/L; p < 0.05), with no difference in post breakfast (0-180 min) glycaemia (CHO+WP, 3.8 ± 0.2 mmol/L; CHO, 4.2 ± 0.2 mmol/L; NB, 4.2 ± 0.1 mmol/L; p = 0.247). There were no post lunch (0-180 min) effects of condition on glycaemia (p = 0.492), insulinaemia (p = 0.338) or subjective appetite (p > 0.05). Adding whey protein to a carbohydrate-rich breakfast enhanced the acute postprandial insulin response, without influencing metabolic or appetite responses following a subsequent mixed-macronutrient meal

Adjunctive therapy with an oral H2S donor provides additional therapeutic benefit beyond SGLT2 inhibition in cardiometabolic heart failure with preserved ejection fraction

Background and Purpose: Sodium glucose cotransporter 2 inhibitors (SGLT2i) have emerged as a potent therapy for heart failure with preserved ejection fraction (HFpEF). Hydrogen sulphide (H2S), a well-studied cardioprotective agent, could be beneficial in HFpEF. SGLT2i monotherapy and combination therapy involving an SGLT2i and H2S donor in two preclinical models of cardiometabolic HFpEF was investigated. Experimental Approach: Nine-week-old C57BL/6N mice received L-NAME and a 60% high fat diet for five weeks. Mice were then randomized to either control, SGLT2i monotherapy or SGLT2i and H2S donor, SG1002, for five additional weeks. Ten-week-old ZSF1 obese rats were randomized to control, SGLT2i or SGLT2i and SG1002 for 8 weeks. SG1002 monotherapy was investigated in additional animals. Cardiac function (echocardiography and haemodynamics), exercise capacity, glucose handling and multiorgan pathology were monitored during experimental protocols. Key Results: SGLT2i treatment improved E/e′ ratio and treadmill exercise in both models. Combination therapy afforded increases in cardiovascular sulphur bioavailability that coincided with improved left end-diastolic function (E/e′ ratio), exercise capacity, metabolic state, cardiorenal fibrosis, and hepatic steatosis. Follow-up studies with SG1002 monotherapy revealed improvements in diastolic function, exercise capacity and multiorgan histopathology. Conclusions and Implications: SGLT2i monotherapy remediated pathological complications exhibited by two well-established HFpEF models. Adjunctive H2S therapy resulted in further improvements of cardiometabolic perturbations beyond SGLT2i monotherapy. Follow-up SG1002 monotherapy studies inferred an improved phenotype with combination therapy beyond either monotherapy. These data demonstrate the differing effects of SGLT2i and H2S therapy while also revealing the superior efficacy of the combination therapy in cardiometabolic HFpEF

Exercise Therapy Rescues Skeletal Muscle Dysfunction and Exercise Intolerance in Cardiometabolic HFpEF

Exercise intolerance, a hallmark of heart failure with preserved ejection fraction (HFpEF) exacerbated by obesity, involves unclear mechanisms related to skeletal muscle metabolism. In a “2-hit” model of HFpEF, we investigated the ability of exercise therapy (voluntary wheel running) to reverse skeletal muscle dysfunction and exercise intolerance. Using state-of-the-art metabolic cages and a multiomic approach, we demonstrate exercise can rescue dysfunctional skeletal muscle lipid and branched-chain amino acid oxidation and restore exercise capacity in mice with cardiometabolic HFpEF. These results underscore the importance of skeletal muscle metabolism to improve exercise intolerance in HFpEF

Exercise Therapy Rescues Skeletal Muscle Dysfunction and Exercise Intolerance in Cardiometabolic HFpEF

Exercise intolerance, a hallmark of heart failure with preserved ejection fraction (HFpEF) exacerbated by obesity, involves unclear mechanisms related to skeletal muscle metabolism. In a “2-hit” model of HFpEF, we investigated the ability of exercise therapy (voluntary wheel running) to reverse skeletal muscle dysfunction and exercise intolerance. Using state-of-the-art metabolic cages and a multiomic approach, we demonstrate exercise can rescue dysfunctional skeletal muscle lipid and branched-chain amino acid oxidation and restore exercise capacity in mice with cardiometabolic HFpEF. These results underscore the importance of skeletal muscle metabolism to improve exercise intolerance in HFpEF