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Contribution: Interactive learning tools with multiple learning support functionalities are nonexistent in power engineering education. An interactive learning tool for supporting student learning in power engineering is shown to improve analytical skills of students. Background: Power network architectures are becoming increasingly complex, requiring the development of educational tools to familiarize students with challenging engineering problems associated with these emerging architectures. Interactive functionalities offered by existing learning tools are inadequate to achieve the learning objectives of the evolving power engineering curriculum. Intended Outcomes: It is expected to improve students' conceptual understanding and analytical skill base by recognizing the correct base-values and actual ratings of power system devices in per-unit calculations, hence students will able to score high marks in exams. Application Design: It is essential to assess the knowledge level of the student for creating effective learning exercises. The proposed interactive learning tools first assess the student's knowledge level, then based on the results create a specific exercise giving a network model, and a unique set of parameters. The tools include solving assistance with three support-levels; in each level more information is provided to assist with solution process enabling students to recognize specific mistakes in their calculations. Once a given exercise is successfully completed, the student is prompted to undertake more challenging exercises, which will assist their progressive cognitive development. Findings: The average mark for the per-unit calculation question in the MST was improved by ˜40% after implementing the proposed learning tool, demonstrating its effectiveness.

Transport infrastructure investments constitute 31% of the world's capital investments. However, there is a significant gap between the demand for large-scale transport infrastructure and investments in such infrastructure. An investigation into the causes of the above gap brings to light the inefficiencies of the current capital deployment practices throughout the project life cycle that result in additional expenditure over the optimal investments. This paper aims to review the existing body of knowledge on capital deployment efficiencies of large-scale transport infrastructure investments. The review looks into the causes of inefficiencies and practices applied for efficiency enhancement. Pareto analysis is used to prioritise the causes, and a cause and effect diagram is drawn to identify the root causes for inefficiencies. Finally, practices applied in different stages of the project life cycle are discussed. Based on these findings, a decision support outline is suggested to enhance the efficiency of each identified cause. The findings of this study provide an important foundation to set up a strategic approach to improve capital deployment efficiency of large-scale transport infrastructure investments. Accordingly, a strategic approach is proposed in policy, organisation, and project level activities to improve the capital deployment efficiency of large-scale transportation infrastructure investments in developing countries. Existing studies primarily focus on the technological advancements, without focusing on healthier governance practices. Therefore, it is essential to address the technical advancement and better governance practices to get the best value for investments. Further research is suggested on the application of a strategic approach in different types of projects. • Pareto analysis and causes and effect diagram indicated causes affect the transport infrastructure investment projects. • Analysis of issues affected the capital inefficiencies of the project life cycle in transport infrastructure investments. • Decision support matrix is proposed to reduce the effects of the inefficacies throughout the project life cycle. • Application of the best practice framework for policy, organisation and project level practices are discussed. [ABSTRACT FROM AUTHOR]

An abstract of the study "Metabolic Modulation With Perhexiline in Chronic Heart Failure," by L. Lee and colleagues is presented.

This article focuses on a study related to augmentation of glucose metabolism with perhexiline in non-ischaemic heart failure. Chronic heart failure (CHF) is a major cause of morbidity and mortality. Additional effective therapies ore needed. Glucose metabolism is more oxygen efficient than free fatty acid metabolism at generating AIP. Treatment with perhexiline leads to an improvement in the heart failure syndrome in DCM even in the absence of ischaemia. This could be linked to the observed improvement in skeletal muscle energetics. Metabolic modulation could represent a potential future treatment strategy for CHF.

We describe a rare case of syncope caused by complete atrioventricular (AV) block on upright posture. The index case is a 72-year-old man who presented with recurrent syncopal episodes without a significant postural drop on presentation. During his admission we demonstrated reproducible AV block on standing for 15 s., (2014 BMJ Publishing Group Ltd.)

We report on an elderly lady with a large hiatus hernia presenting with presyncope and syncope associated with large meals. Though left atrial filling and mitral inflow was unimpaired, this case is interesting since the symptoms resolved with adjustment to meal size.

In the present study, we investigated the effects of basal and intra-arterial infusion of bradykinin on unstressed forearm vascular volume (a measure of venous tone) and blood flow in healthy volunteers (n=20) and in chronic heart failure patients treated with ACEIs [ACE (angiotensin-converting enzyme) inhibitors] (n=16) and ARBs (angiotensin receptor blockers) (n=14). We used radionuclide plethysmography to examine the effects of bradykinin and of the bradykinin antagonists B9340 [B1 (type 1)/B2 (type 2) receptor antagonist] and HOE140 (B2 antagonist). Bradykinin infusion increased unstressed forearm vascular volume in a similar dose-dependent manner in healthy volunteers and ARB-treated CHF patients (healthy volunteers maximum 12.3+/-2.1%, P<0.001 compared with baseline; ARB-treated CHF patients maximum 9.3+/-3.3%, P<0.05 compared with baseline; P=not significant for difference between groups), but the increase in unstressed volume in ACEI-treated CHF patients was higher (maximum 28.8+/-7.8%, P<0.001 compared with baseline; P<0.05 for the difference between groups). In contrast, while the increase in blood flow in healthy volunteers (maximum 362+/-9%, P<0.001) and in ACEI-treated CHF patients (maximum 376+/-12%, P<0.001) was similar (P=not significant for the difference between groups), the increase in ARB-treated CHF patients was less (maximum 335+/-7%, P<0.001; P<0.05 for the difference between groups). Infusion of each receptor antagonist alone similarly reduced basal unstressed volume and blood flow in ACEI-treated CHF patients, but not in healthy volunteers or ARB-treated CHF patients. In conclusion, bradykinin does not contribute to basal venous tone in health, but in ACEI-treated chronic heart failure it does. In ARB-treated heart failure, venous responses to bradykinin are preserved but arterial responses are reduced compared with healthy controls. Bradykinin-mediated vascular responses in both health and heart failure are mediated by the B2, rather than the B1, receptor.

The nongenomic effects of aldosterone in disease states associated with endothelial dysfunction may differ from those in healthy subjects. The effects of locally infused aldosterone on the forearm blood flow and volume were studied in optimally treated patients with chronic heart failure (CHF). At baseline and after incremental intrabrachial aldosterone, forearm blood flow was assessed using conventional strain gauge plethysmography, and forearm venous volume was assessed by radionuclide plethysmography. Constriction of the resistance vasculature of the forearm without significant effect on forearm venous capacitance was demonstrated in response to aldosterone in patients treated for CHF.

Aims: Alpha-lipoic acid (ALA) is a thiol compound with antioxidant properties used in the treatment of diabetic polyneuropathy. ALA may also improve arterial function, but there have been scant human trials examining this notion. This project aimed to investigate the effects of oral and intra-arterial ALA on changes in systemic and regional haemodynamics, respectively., Methods: In study 1, 16 healthy older men aged 58 +/- 7 years (mean +/- SD) received 600 mg of ALA or placebo, on two occasions 1 week apart, in a randomized cross-over design. Repeated measures of peripheral and central haemodynamics were then obtained for 90 min. Central blood pressure and indices of arterial stiffness [augmentation index (AIx) and estimated aortic pulse wave velocity] were recorded non-invasively using pulse wave analysis. Blood samples obtained pre- and post-treatments were analysed for erythrocyte antioxidant enzyme activity, plasma nitrite and malondialdehyde. In study 2 the effects of incremental cumulative doses (0.5, 1.0, 1.5 and 2.0 mg ml(-1) min(-1)) of intra-arterial ALA on forearm blood flow (FBF) were assessed in eight healthy subjects (aged 31 +/- 5 years) by conventional venous occlusion plethysmography., Results: There were no significant changes on any of the central or peripheral haemodynamic measures after either oral or direct arterial administration of ALA. Plasma ALA was detected after oral supplementation (95% confidence intervals 463, 761 ng ml(-1)), but did not alter cellular or plasma measures of oxidative stress., Conclusions: Neither oral nor intra-arterial ALA had any effect on regional and systemic haemodynamics or measures of oxidative stress in healthy men.

Objective: Natriuretic peptides (NPs) reduce central venous pressure in patients with chronic heart failure (cHF) despite attenuation of arterial, renal, and humoral effects. This suggests a preserved venodilator response. This study had 4 aims: to compare the venodilator effects of human NPs in patients with cHF; to assess the contribution of basal ANP and BNP levels to regulation of forearm vascular volume (FVV); to test the hypothesis that venous ANP responsiveness is preserved in cHF; and to assess the involvement of endothelial nitric oxide-synthase (eNOS) in NP-induced vascular effects., Methods and Results: Venous and arterial forearm vascular responses to incremental intra-arterial doses of ANP, Urodilatin, BNP, CNP, or the ANP receptor antagonist A71915 were studied in 53 patients and 11 controls. ANP receptor antagonism reduced FVV by 4.4%+/-1.2% (P<0.05). The forearm blood flow (FBF) response to ANP was significantly blunted in patients versus controls (P<0.01), whereas FVV increased similarly in both groups (maximum 14.7% and 13.4%, both P<0.001). The eNOS blockade reduced ANP-induced FBF changes in controls but not in patients (P<0.05), whereas similar reductions in FVV changes were seen in groups (both P<0.001)., Conclusions: In cHF venous, but not arterial, ANP responsiveness is preserved. Arterial endothelial dysfunction may contribute to NP resistance.

Objective: To date, the contribution of basal atrial natriuretic peptide (ANP) levels to resting vascular function in humans is unknown. In the present study we sought to investigate the role of ANP in regulating regional vascular volume and venous tone in healthy subjects., Methods and Results: We used radionuclide plethysmography to examine the effects of ANP and the ANP-receptor antagonist A71915 on forearm vascular volume. Creating pressure/volume relations, we determined changes in vascular volume, compliance, and tone. Performing dose-ranging studies, we additionally assessed the potency and specificity of A71915 in the forearm resistance vasculature. Equilibrium blood pool scintigraphy was then used to assess the effects of systemic administration of A71915 on regional intestinal vascular volume. Infusion of ANP increased forearm vascular volume in a dose-dependent manner (maximum 20%; P<0.001), exerting a maximum venodilating effect at plasma levels similar to that seen in heart failure. A71915 increased venous tone, thereby decreasing vascular volume by 9.6+/-1.1%, P<0.001 (forearm), and 2.6+/-0.5%, P=0.01 (intestinal beds). At an infusion ratio of 50:1, A71915 almost completely abolished the effects of ANP on forearm blood flow., Conclusions: ANP locally regulates regional vascular volume and tone without affecting compliance.

Objectives: Systemic infusions of aldosterone cause an acute increase in systemic vascular resistance (SVR) in healthy subjects. It is not clear whether this is due to a direct effect on the vasculature or the result of increased sympathetic tone. We investigated the short-term effects of locally infused aldosterone on the forearm resistance bed., Methods: In this dose response study, we assessed the effects of incremental doses (10, 50, 100 ng/minute) of intrabrachial aldosterone on forearm blood flow (FBF), using conventional strain gauge plethysmography. Arterial blood pressure was monitored continuously, using finger photo- plethysmography. Forearm vascular resistance (FVR) was calculated. FBF and FVR were also measured in the non-infused arm. Changes in FBF and FVR in the infused arm were corrected for those occurring in the control arm., Results: Plasma aldosterone levels in the venous effluent of the infused arm increased in a dose-dependent fashion, from 113.3+/-17.9 pg/ml at baseline to 297.8+/-51.8 pg/ml at 10 ng/minute (p=<0.01), 743.9+/-105.9 pg/ml at 50 ng/min (p=<0.001 vs. baseline) and 1230.6+/-73.7 pg/ml at 100 ng/min (p=<0.0005 vs. baseline). Plasma concentrations of aldosterone in the control arm did not change significantly vs. baseline. The corrected FBF (+4.1+/-10.3%) and corrected FVR (+4.3+/-11.3%) did not change significantly even at peak infusion rates., Conclusions: Local intra-arterial infusion of aldosterone had no acute effect on forearm resistance vessels in healthy male volunteers.