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In this paper, an intelligent weather conditions fuzzy adjustment based on spatial features (IWeCASF) is developed. It is indispensable for our regional soil moisture estimation approach, complementing a point estimation model of soil moisture from the literature. The point estimation model requires the weather conditions at the point where an estimate is made. Therefore, IWeCASF's aim is to determine these weather conditions. The procedure begins measuring them at only one checkpoint, called the primary checkpoint. The model determines the weather conditions anywhere within a region through image processing algorithms and fuzzy inference systems. The results are compared with the measurement records and with a spatial interpolation method. The performance is similar to or better than interpolation, especially in the rain, where the model developed is more accurate due to the certainty of replication. Additionally, IWeCASF does not require more than one measurement point. Therefore, it is a more appropriate approach to complement the point estimation model for enabling a regional soil moisture estimation. [ABSTRACT FROM AUTHOR]

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In this paper, an intelligent weather conditions fuzzy adjustment based on spatial features (IWeCASF) is developed. It is indispensable for our regional soil moisture estimation approach, complementing a point estimation model of soil moisture from the literature. The point estimation model requires the weather conditions at the point where an estimate is made. Therefore, IWeCASF’s aim is to determine these weather conditions. The procedure begins measuring them at only one checkpoint, called the primary checkpoint. The model determines the weather conditions anywhere within a region through image processing algorithms and fuzzy inference systems. The results are compared with the measurement records and with a spatial interpolation method. The performance is similar to or better than interpolation, especially in the rain, where the model developed is more accurate due to the certainty of replication. Additionally, IWeCASF does not require more than one measurement point. Therefore, it is a more appropriate approach to complement the point estimation model for enabling a regional soil moisture estimation.

Although there is a wealth of literature on improving the reading skills of EFL learners at Saudi universities, very little work has been done on struggling readers in lifelong and continuous learning programs. To address the issue, this study seeks to explore the needs of struggling learners in reading comprehension classes. Interviews were conducted with selected instructors from three Saudi universities to reflect on the challenges and problems faced by struggling readers, as well as their language needs. The instructors reported that the majority of EFL learners in lifelong and continuous learning programs have difficulty decoding monosyllabic and polysyllabic words. They also reported that around 15–20% of learners have difficulties identifying the English alphabet. They attributed the main challenges to poor linguistic knowledge, lack of self-esteem, and lack of motivation. In light of these results, the study proposed a computer-based model implemented through insessional support courses to help struggling readers with their reading courses and improve their reading performance. The proposed model addresses the linguistic needs of struggling readers and enhances their motivation and positive attitudes toward L2 learning. In-sessional support courses for struggling readers are supposed to have the potential to improve their vocabulary decoding and retention skills, as well as to enhance their working memory. The use of computers can promote the effectiveness of exploiting reading material in terms of pronunciation, vocabulary, use of words in different contexts, and comprehension. The findings of the study emphasize the significance of incorporating technology in EFL reading instruction. [ABSTRACT FROM AUTHOR]

Endothelial dysfunction is thought to underpin atherosclerotic cardiovascular disease. The most widely used in vivo test of endothelial function is flow-mediated dilation (FMD). However, the results of FMD may be subject to some confounding factors that are not fully understood. We investigated potential biophysical confounding factors that could cause a disassociation between FMD and true endothelial cell shear stress response (the release of endothelium-dependent relaxing factors in response to wall shear stress). Arterial hemodynamics during FMD was simulated using a novel computational modeling approach. The model included an endothelial response function relating changes in wall shear stress to changes in local vascular stiffness in the arm arteries and accounted for vascular stiffening with increasing blood pressure. The hemodynamic effects of cuff inflation and deflation were modeled by prescribing intraluminal arterial pressure changes and peripheral vasodilation. Evolution of arterial diameter and flow velocity during FMD was assessed by comparison against in vivo data. Our model revealed that vasoconstriction occurring immediately after cuff deflation is independent of endothelial response function and entirely caused by the change in transmural pressure along conduit arteries. Moreover, for the same endothelial response function model, FMD values increased exponentially with increasing peak flow velocity, decreased linearly with increasing arterial stiffness at a rate of 0.95%/MPa, and increased linearly with increasing central blood pressure at a rate of 0.22%/mmHg. Dependence of FMD on confounding factors, such as arterial stiffness and blood pressure, suggests that the current FMD test may not reflect the true endothelial cell response. NEW & NOTEWORTHY First, a novel computational model simulating arterial hemodynamaics during flow-mediated dilation (FMD) was proposed. Second, the model was used to explain why FMD may be influenced by endothelium-independent factors, showing that FMD results are 1) partly masked by the vasoconstriction due to the change in transmural pressure and 2) affected by physiological factors (i.e., arterial stiffness and arterial blood pressure) that are difficult to eliminate due to their multiple interactions. [ABSTRACT FROM AUTHOR]

See Article by Al'Aref et al

Background The relative impact of right ventricular (RV) electromechanical dyssynchrony versus pulmonary regurgitation (PR) on exercise capacity and RV function after tetralogy of Fallot repair is unknown. We aimed to delineate the relative effects of these factors on RV function and exercise capacity. Methods and Results We retrospectively analyzed 81 children with tetralogy of Fallot repair using multivariable regression. Predictor parameters were electrocardiographic QRS duration reflecting electromechanical dyssynchrony and PR severity by cardiac magnetic resonance. The outcome parameters were exercise capacity (percentage predicted peak oxygen consumption) and cardiac magnetic resonance ejection fraction (RV ejection fraction). To understand the relative effects of RV dyssynchrony versus PR on exercise capacity and RV function, virtual patient simulations were performed using a closed‐loop cardiovascular system model (CircAdapt), covering a wide spectrum of disease severity. Eighty‐one patients with tetralogy of Fallot repair (median [interquartile range {IQR}] age, 14.48 [11.55–15.91] years) were analyzed. All had prolonged QRS duration (median [IQR], 144 [123–152] ms), at least moderate PR (median [IQR], 40% [29%–48%]), reduced exercise capacity (median [IQR], 79% [68%–92%] predicted peak oxygen consumption), and reduced RV ejection fraction (median [IQR], 48% [44%–52%]). Longer QRS duration, more than PR, was associated with lower oxygen consumption and lower RV ejection fraction. In a multivariable regression analysis, oxygen consumption decreased with both increasing QRS duration and PR severity. CircAdapt modeling showed that RV dyssynchrony exerts a stronger limiting effect on exercise capacity and on RV ejection fraction than does PR, regardless of contractile function. Conclusions In both patient data and computer simulations, RV dyssynchrony, more than PR, appears to be associated with reduced exercise capacity and RV systolic dysfunction in patients after TOF repair.

Introductory undergraduate courses present an opportunity to use disciplinary concepts in solving authentic problems. Making complex natural systems accessible to students through computer-based models allows them to practice making evidence-based predictions and communicate understanding. Despite the importance of modelling tools in formal classrooms, gaps exist in our understanding of how post-secondary students engage in computer-based modelling. Introductory courses, particularly in the hydrosciences, typically do not use these tools. This mixed methods study examines students' model-based reasoning about a water-related issue over two years in response to a flipped course model. Students in an introductory water course learned basic hydrologic content and used a computer-based water model to complete a project. Data came from a pre-/post-course assessment, student assignments, and student interviews. Results of quantitative and qualitative data analyses show that students in the revised version of the course (Year 2, n = 53) increased their understanding of core hydrology concepts and performed better on their evaluation of a computer-based water model, than students in the initial course (Year 1, n = 38). We tentatively attribute these observed changes to increased active learning opportunities surrounding computer-based modelling of water systems. Findings contribute to science literacy development, undergraduate science learning environment design, and undergraduate scientific modelling. [ABSTRACT FROM AUTHOR]

Background Ventricular tachyarrhythmias are often preceded by short sequences of premature ventricular complexes. In a previous study, a restitution‐based computational model predicted which sequences of stimulated premature complexes were most likely to induce ventricular fibrillation in canines in vivo. However, the underlying mechanism, based on discordant‐alternans dynamics, could not be verified in that study. The current study seeks to elucidate the mechanism by determining whether the spatiotemporal evolution of action potentials and initiation of ventricular fibrillation in in vitro experiments are consistent with model predictions. Methods and Results Optical mapping voltage signals from canine right‐ventricular tissue (n=9) were obtained simultaneously from the entire epicardium and endocardium during and after premature stimulus sequences. Model predictions of action potential propagation along a 1‐dimensional cable were developed using action potential duration versus diastolic interval data. The model predicted sign‐change patterns in action potential duration and diastolic interval spatial gradients with posterior probabilities of 91.1%, and 82.1%, respectively. The model predicted conduction block with 64% sensitivity and 100% specificity. A generalized estimating equation logistic‐regression approach showed that model‐prediction effects were significant for both conduction block (P

Cardiac resynchronization therapy (CRT) is an effective treatment for heart failure (HF) patients with an electrical substrate pathology causing ventricular dyssynchrony. However 40-50% of patients do not respond to treatment. Cardiac modeling of the electrophysiology, electromechanics, and hemodynamics of the heart has been used to study mechanisms behind HF pathology and CRT response. Recently, multi-scale dyssynchronous HF models have been used to study optimal device settings and optimal lead locations, investigate the underlying cardiac pathophysiology, as well as investigate emerging technologies proposed to treat cardiac dyssynchrony. However the breadth of patient and experimental data required to create and parameterize these models and the computational resources required currently limits the use of these models to small patient numbers. In the future, once these technical challenges are overcome, biophysically based models of the heart have the potential to become a clinical tool to aid in the diagnosis and treatment of HF. [ABSTRACT FROM AUTHOR]

BackgroundStructural remodeling of human atria plays a key role in sustaining atrial fibrillation (AF), but insufficient quantitative analysis of human atrial structure impedes the treatment of AF. We aimed to develop a novel 3‐dimensional (3D) structural and computational simulation analysis tool that could reveal the structural contributors to human reentrant AF drivers. Methods and ResultsHigh‐resolution panoramic epicardial optical mapping of the coronary‐perfused explanted intact human atria (63‐year‐old woman, chronic hypertension, heart weight 608 g) was conducted during sinus rhythm and sustained AF maintained by spatially stable reentrant AF drivers in the left and right atrium. The whole atria (107×61×85 mm3) were then imaged with contrast‐enhancement MRI (9.4 T, 180×180×360‐μm3 resolution). The entire 3D human atria were analyzed for wall thickness (0.4–11.7 mm), myofiber orientations, and transmural fibrosis (36.9% subendocardium; 14.2% midwall; 3.4% subepicardium). The 3D computational analysis revealed that a specific combination of wall thickness and fibrosis ranges were primarily present in the optically defined AF driver regions versus nondriver tissue. Finally, a 3D human heart–specific atrial computer model was developed by integrating 3D structural and functional mapping data to test AF induction, maintenance, and ablation strategies. This 3D model reproduced the optically defined reentrant AF drivers, which were uninducible when fibrosis and myofiber anisotropy were removed from the model. ConclusionsOur novel 3D computational high‐resolution framework may be used to quantitatively analyze structural substrates, such as wall thickness, myofiber orientation, and fibrosis, underlying localized AF drivers, and aid the development of new patient‐specific treatments.

Aims: Anatomical re-entry is an important mechanism of ventricular tachycardia, characterized by circular electrical propagation in a fixed pathway. It's current investigative and therapeutic approaches are non-biological, rather unspecific (drugs), traumatizing (electrical shocks), or irreversible (ablation). Optogenetics is a new biological technique that allows reversible modulation of electrical function with unmatched spatiotemporal precision using light-gated ion channels. We therefore investigated optogenetic manipulation of anatomical re-entry in ventricular cardiac tissue. Methods and results: Transverse, 150-μm-thick ventricular slices, obtained from neonatal rat hearts, were genetically modified with lentiviral vectors encoding Ca2+-translocating channelrhodopsin (CatCh), a light-gated depolarizing ion channel, or enhanced yellow fluorescent protein (eYFP) as control. Stable anatomical re-entry was induced in both experimental groups. Activation of CatCh was precisely controlled by 470-nm patterned illumination, while the effects on anatomical re-entry were studied by optical voltage mapping. Regional illumination in the pathway of anatomical re-entry resulted in termination of arrhythmic activity only in CatCh-expressing slices by establishing a local and reversible, depolarization-induced conduction block in the illuminated area. Systematic adjustment of the size of the lightexposed area in the re-entrant pathway revealed that re-entry could be terminated by either wave collision or extinction, depending on the depth (transmurality) of illumination. In silico studies implicated source-sink mismatches at the site of subtransmural conduction block as an important factor in re-entry termination. Conclusions: Anatomical re-entry in ventricular tissue can be manipulated by optogenetic induction of a local and reversible conduction block in the re-entrant pathway, allowing effective re-entry termination. These results provide distinctively new mechanistic insight into re-entry termination and a novel perspective for cardiac arrhythmia management. [ABSTRACT FROM AUTHOR]

Objective: Over one hundred predictive models were defined in the past for head injury (HI) prognosis, but none of them have been widely used up to the present. The aim of this study is to predict the prognosis of isolated HI patients by simply using data from the first day after injury.Materials and Methods: Data of head injury patients in Trakya University Hospital between January 1996 and December 2006 were obtained from records. The age, gender, causes of HI, basic neurologic examination findings, radiologic findings and discharge status are examined.Results: Most of the data were simplified as absent (0) and present (1), and mortality rates for each groups were accepted weighted values. All data were processed statistically and two models were created. Model 1 with Glasgow Coma Scale (GCS) score predicted the mortality/vegetative event at a rate of 56.5%, and the conscious survival event at 98.7%. Model 2, without the GCS score, predicted the mortality/vegetative event at 55.1% rate and the conscious survival event at 99.2%.Conclusion: Both models could be used for informing the patient and relatives and helping them to understand the severity of HI in busy working conditions of emergency departments.

Apelin peptides mediate beneficial effects on the cardiovascular system and are being targeted as potential new drugs. However, apelin peptides have extremely short biological half-lives, and improved understanding of apelin peptide metabolism may lead to the discovery of biologically stable analogues with therapeutic potential. We examined the ability of angiotensin-converting enzyme 2 (ACE2) to cleave and inactivate pyr-apelin 13 and apelin 17, the dominant apelin peptides. Computer-assisted modeling shows a conserved binding of pyr-apelin 13 and apelin 17 to the ACE2 catalytic site. In ACE2 knockout mice, hypotensive action of pyr-apelin 13 and apelin 17 was potentiated, with a corresponding greater elevation in plasma apelin levels. Similarly, pharmacological inhibition of ACE2 potentiated the vasodepressor action of apelin peptides. Biochemical analysis confirmed that recombinant human ACE2 can cleave pyr-apelin 13 and apelin 17 efficiently, and apelin peptides are degraded slower in ACE2-deficient plasma. The biological relevance of ACE2-mediated proteolytic processing of apelin peptides was further supported by the reduced potency of pyr-apelin 12 and apelin 16 on the activation of signaling pathways and nitric oxide production from endothelial cells. Importantly, although pyr-apelin 13 and apelin 17 rescued contractile function in a myocardial ischemia-reperfusion model, ACE2 cleavage products, pyr-apelin 12 and 16, were devoid of these cardioprotective effects. We designed and synthesized active apelin analogues that were resistant to ACE2-mediated degradation, thereby confirming that stable apelin analogues can be designed as potential drugs. We conclude that ACE2 represents a major negative regulator of apelin action in the vasculature and heart. [ABSTRACT FROM AUTHOR]

Background: The National Institutes of Health Stroke Scale (NIHSS) was not intended to be used to determine the stroke's vascular distribution. The aim of this study was to develop, assess the reliability, and validate a computer algorithm based on the NIHSS for this purpose.Methods: Two cohorts of patients with ischemic stroke having similar distributions of Oxfordshire localizations (total anterior, partial anterior, lacunar, and posterior circulation) based on neuroimaging were identified. The first cohort (n = 40) was used to develop a computer algorithm for vascular localization using a modified version of the NIHSS (NIHSS-Localization [NIHSS-Loc]) that included the laterality of selected deficits; the second (n = 20) was used to assess the reliability of algorithm-based localizations compared to those of 2 vascular neurologists. The validity of the algorithm-based localizations was assessed in comparison to neuroimaging. Agreement was assessed using the unweighted kappa (κ) statistic.Results: Agreement between the 2 raters using the standard NIHSS was slight to moderate (κ = .36, 95% confidence interval [CI] .10-.61). Inter-rater agreement significantly improved to the substantial to almost perfect range using the NIHSS-Loc (κ = .88, 95% CI .73-1.00). Agreement was perfect when the 2 raters entered the data into the NIHSS-Loc computer algorithm (κ = 1.00, 95% CI 1.00-1.00). Agreement between the algorithm localization and neuroimaging results was fair to moderate (κ = .59, 95% CI .35-.84) and not significantly different from the localizations of either rater using the NIHSS-Loc.Conclusion: A computerized, modified version of the standard NIHSS can be used to reliably and validly assign the vascular distribution of an acute ischemic stroke. [ABSTRACT FROM AUTHOR]

Aims Acute ischemia is a major cause of sudden arrhythmic death, further promoted by potassium current blockers. Macro-reentry around the ischemic region and early afterdepolarizations (EADs) caused by electrotonic current have been suggested as potential mechanisms in animal and isolated cell studies. However, ventricular and human-specific arrhythmia mechanisms and their modulation by repolarization reserve remain unclear. The goal of this paper is to unravel multiscale mechanisms underlying the modulation of arrhythmic risk by potassium current (I Kr ) block in human ventricles with acute regional ischemia. Methods and results A human ventricular biophysically-detailed model, with acute regional ischemia is constructed by integrating experimental knowledge on the electrophysiological ionic alterations caused by coronary occlusion. Arrhythmic risk is evaluated by determining the vulnerable window (VW) for reentry following ectopy at the ischemic border zone. Macro-reentry around the ischemic region is the main reentrant mechanism in the ischemic human ventricle with increased repolarization reserve due to the ATP-sensitive potassium current (I K(ATP) ) activation. Prolongation of refractoriness by 4% caused by 30% I Kr reduction counteracts the establishment of macro-reentry and reduces the VW for reentry (by 23.5%). However, a further decrease in repolarization reserve (50% I Kr reduction) is less anti-arrhythmic despite further prolongation of refractoriness. This is due to the establishment of transmural reentry enabled by electrotonically-triggered EADs in the ischemic border zone. EADs are produced by L-type calcium current (I CaL ) reactivation due to prolonged low amplitude electrotonic current injected during the repolarization phase. Conclusions Electrotonically-triggered EADs are identified as a potential mechanism facilitating intramural reentry in a regionally-ischemic human ventricles model with reduced repolarization reserve. [ABSTRACT FROM AUTHOR]

Aims: Premature ventricular complexes (PVCs) due to spontaneous calcium (Ca) release (SCR) events at the cell level can precipitate ventricular arrhythmias. However, the mechanistic link between SCRs and PVC formation remains incompletely understood. The aim of this study was to investigate the conditions under which delayed afterdepolarizations resulting from stochastic subcellular SCR events can overcome electrotonic source-sink mismatch, leading to PVC initiation. Methods and results: A stochastic subcellular-scale mathematical model of SCR was incorporated in a realistic model of the rabbit ventricles and Purkinje system (PS). Elevated levels of diastolic sarcoplasmic reticulum Ca2+ (CaSR) were imposed until triggered activity was observed, allowing us to compile statistics on probability, timing, and location of PVCs. At CaSR= 1500 µmol/L PVCs originated in the PS. When SCR was incapacitated in the PS, PVCs also emerged in the ventricles, but at a higher CaSR (=1550 µmol/L) and with longer waiting times. For each model configuration tested, the probability of PVC occurrence increased from 0 to 100% within a well-defined critical CaSR range; this transition was much more abrupt in organ-scale models (~50 µmol/L CaSR range) than in the tissue strand (~100 µmol/L) or single-cell (~450 µmol/L) models. Among PVCs originating in the PS, ~68% were located near Purkinje-ventricular junctions (<1 mm). Conclusion: SCR events overcome source-sink mismatch to trigger PVCs at a critical CaSR threshold. Above this threshold, PVCs emerge due to increased probability and reduced variability in timing of SCR events, leading to significant diastolic depolarization. Sites of lower electronic load, such as the PS, are preferential locations for triggering. [ABSTRACT FROM AUTHOR]

Geometric Factors in Voltage Mapping Background Voltage mapping is an important tool for characterizing proarrhythmic electrophysiological substrate, yet it is subject to geometric factors that influence bipolar amplitudes and thus compromise performance. The aim of this study was to characterize the impact of catheter orientation on the ability of bipolar amplitudes to accurately discriminate between healthy and diseased tissues. Methods and Results We constructed a 3-dimensional, in silico, bidomain model of cardiac tissue containing transmural lesions of varying diameter. A planar excitation wave was stimulated and electrograms were sampled with a realistic catheter model at multiple positions and orientations. We carried out validation studies in animal experiments of acute ablation lesions mapped with a clinical mapping system. Bipolar electrograms sampled at higher inclination angles of the catheter with respect to the tissue demonstrated improvements in both sensitivity and specificity of lesion detection. Removing low-voltage electrograms with concurrent activation of both electrodes, suggesting false attenuation of the bipolar electrogram due to alignment with the excitation wavefront, had little effect on the accuracy of voltage mapping. Conclusions Our results demonstrate possible mechanisms for the impact of catheter orientation on voltage mapping accuracy. Moreover, results from our simulations suggest that mapping accuracy may be improved by selectively controlling the inclination of the catheter to record at higher angles with respect to the tissue. [ABSTRACT FROM AUTHOR]

OBJECTIVES In clinical practice, maximum diameter is used as a criterion to estimate aneurysm-rupture risk; however, it is only a general indicator and its value becomes difficult to estimate in the thoracic segment. Improved understanding of aortic aneurysm complexity and biomechanics is needed to achieve advancements in surgical repair techniques. The objective of this study was to determine the maximum wall stress by using imaging-derived data and a specific probabilistic design integrated into finite element (FE) analysis. METHODS Computed tomography images of thoracic aortic aneurysms from our database were analysed and the main morphological features were identified by means of a specific automatic routine. Morphological data were used to develop an idealized finite element library of thoracic aortic arch models. Sensitivity analyses were performed by using the geometrical parameters as input variables for a statistical wall stress assessment. Numerical results were compared with those obtained from deterministic analysis on patient-specific three-dimensional reconstructions. RESULTS The results showed that in small aneurysms, wall stress values similar to those of large aneurysms can be obtained if a significant eccentricity is achieved. In small aneurysms, the peak stress is primarily affected by the eccentricity of the bulge [correlation coefficient (CC) = 0.86], while for diameters in the range of 50–60 mm, the CC is 0.43 for the eccentricity and 0.72 for the maximum diameter. CONCLUSIONS The stress distribution in small aneurysms may contribute to the pathogenesis of aortic rupture and dissections. Our method can provide a novel and efficient procedure for generating computational models to estimate the wall stress in a comparative multivariate manner. [ABSTRACT FROM PUBLISHER]

Objective: To translate the individual abdominal aortic aneurysm (AAA) patient's biomechanical rupture risk profile to risk-equivalent diameters, and to retrospectively test their predictability in ruptured and non-ruptured aneurysms. Methods: Biomechanical parameters of ruptured and non-ruptured AAAs were retrospectively evaluated in a multicenter study. General patient data and high resolution computer tomography angiography (CTA) images from 203 non-ruptured and 40 ruptured aneurysmal infrarenal aortas. Three-dimensional AAA geometries were semi-automatically derived from CTA images. Finite element (FE) models were used to predict peak wall stress (PWS) and peak wall rupture index (PWRI) according to the individual anatomy, gender, blood pressure, intra-luminal thrombus (ILT) morphology, and relative aneurysm expansion. Average PWS diameter and PWRI diameter responses were evaluated, which allowed for the PWS equivalent and PWRI equivalent diameters for any individual aneurysm to be defined. Results: PWS increased linearly and PWRI exponentially with respect to maximum AAA diameter. A size-adjusted analysis showed that PWS equivalent and PWRI equivalent diameters were increased by 7.5 mm (p = .013) and 14.0 mm (p < .001) in ruptured cases when compared to non-ruptured controls, respectively. In non-ruptured cases the PWRI equivalent diameters were increased by 13.2 mm (p < .001) in females when compared with males. Conclusions: Biomechanical parameters like PWS and PWRI allow for a highly individualized analysis by integrating factors that influence the risk of AAA rupture like geometry (degree of asymmetry, ILT morphology, etc.) and patient characteristics (gender, family history, blood pressure, etc.). PWRI and the reported annual risk of rupture increase similarly with the diameter. PWRI equivalent diameter expresses the PWRI through the diameter of the average AAA that has the same PWRI, i.e. is at the same biomechanical risk of rupture. Consequently, PWRI equivalent diameter facilitates a straightforward interpretation of biomechanical analysis and connects to diameter-based guidelines for AAA repair indication. PWRI equivalent diameter reflects an additional diagnostic parameter that may provide more accurate clinical data for AAA repair indication. [Copyright &y& Elsevier]

With the development of concrete technology, fillers are widely used in high performance concrete to improve its properties. Among them, limestone powder is popularly added in self-compacting concrete to gain good flowability. However, by lack of experimental data, several materials properties after the addition of limestone powder are still not sure, which actually yield some uncertainty for the further use of limestone powder in cement-based materials. In this study, by employing computer-based model, the microstructure of self-compacting cement paste containing limestone as filler is simulated and further used to investigate the role of limestone in hardening materials. To gain this goal, thermometric isothermal conduction calorimetry, thermal analysis and backscattered electron image acquisition were applied to understand the hydration kinetics with the addition of limestone filler. After that, a computational materials model based on HYMOSTRUC was developed to simulate the formation of microstructure in materials containing limestone powder. The predictive ability of the model was validated with the experimental test results. Then the developed model was employed to investigate the influence of several variables, such as water to cement ratio, limestone filler content and fineness, on the microstructure formation in hardening materials. The numerical experiments show that the addition of limestone filler could result in a denser microstructure at the initial hydration stage. With the proceeding of hydration, the limestone powder has a decreasing influence on the microstructure, and could obstruct somewhat the formation of a denser microstructure at later hydration stage. And it is found that computer-based modelling is an effective method to provide insights into the material behaviour, by relieving researchers from numerous repeated experiments. [ABSTRACT FROM AUTHOR]

Objectives: This study sought to test the hypothesis that “virtual” electrophysiological studies (EPS) on an anatomic platform generated by 3-dimensional magnetic resonance imaging reconstruction of the left ventricle can reproduce the reentrant circuits of induced ventricular tachycardia (VT) in a porcine model of myocardial infarction. Background: Delayed-enhancement magnetic resonance imaging has been used to characterize myocardial infarction and “gray zones,” which are thought to reflect heterogeneous regions of viable and nonviable myocytes. Methods: Myocardial infarction by coronary artery occlusion was induced in 8 pigs. After a recovery period, 3-dimensional cardiac magnetic resonance images were obtained from each pig in vivo. Normal areas, gray zones, and infarct cores were classified based on voxel intensity. In the computer model, gray zones were assigned slower conduction and longer action potential durations than those for normal myocardium. Virtual EPS was performed and compared with results of actual in vivo programmed stimulation and noncontact mapping. Results: The left ventricular volumes ranged from 97.8 to 166.2 cm3, with 4.9% to 17.5% of voxels classified as infarct zones. Six of the 7 pigs in which VT developed during actual EPS were also inducible with virtual EPS. Four of the 6 pigs that had simulated VT had reentrant circuits that approximated the circuits seen with noncontact mapping, whereas the remaining 2 had similar circuits but propagating in opposite directions. Conclusions: This initial study demonstrates the feasibility of applying a mathematical model to magnetic resonance imaging reconstructions of the left ventricle to predict VT circuits. Virtual EPS may be helpful to plan catheter ablation strategies or to identify patients who are at risk of future episodes of VT. [ABSTRACT FROM AUTHOR]

Objective: Over one hundred predictive models were defined in the past for head injury (HI) prognosis, but none of them have been widely used up to the present. The aim of this study is to predict the prognosis of isolated HI patients by simply using data from the first day after injury. Materials and Methods: Data of head injury patients in Trakya University Hospital between January 1996 and December 2006 were obtained from records. The age, gender, causes of HI, basic neurologic examination findings, radiologic findings and discharge status are examined. Results: Most of the data were simplified as absent (0) and present (1), and mortality rates for each groups were accepted weighted values. All data were processed statistically and two models were created. Model 1 with Glasgow Coma Scale (GCS) score predicted the mortality/vegetative event at a rate of 56.5%, and the conscious survival event at 98.7%. Model 2, without the GCS score, predicted the mortality/vegetative event at 55.1% rate and the conscious survival event at 99.2%. Conclusion: Both models could be used for informing the patient and relatives and helping them to understand the severity of HI in busy working conditions of emergency departments. [ABSTRACT FROM AUTHOR]

Endothelial dysfunction is thought to underpin atherosclerotic cardiovascular disease. The most widely used in vivo test of endothelial function is flow-mediated dilation (FMD). However, the results of FMD may be subject to some confounding factors that are not fully understood. We investigated potential biophysical confounding factors that could cause a disassociation between FMD and true endothelial cell shear stress response (the release of endothelium-dependent relaxing factors in response to wall shear stress). Arterial hemodynamics during FMD was simulated using a novel computational modeling approach. The model included an endothelial response function relating changes in wall shear stress to changes in local vascular stiffness in the arm arteries and accounted for vascular stiffening with increasing blood pressure. The hemodynamic effects of cuff inflation and deflation were modeled by prescribing intraluminal arterial pressure changes and peripheral vasodilation. Evolution of arterial diameter and flow velocity during FMD was assessed by comparison against in vivo data. Our model revealed that vasoconstriction occurring immediately after cuff deflation is independent of endothelial response function and entirely caused by the change in transmural pressure along conduit arteries. Moreover, for the same endothelial response function model, FMD values increased exponentially with increasing peak flow velocity, decreased linearly with increasing arterial stiffness at a rate of 0.95%/MPa, and increased linearly with increasing central blood pressure at a rate of 0.22%/mmHg. Dependence of FMD on confounding factors, such as arterial stiffness and blood pressure, suggests that the current FMD test may not reflect the true endothelial cell response. NEW & NOTEWORTHY First, a novel computational model simulating arterial hemodynamics during flow-mediated dilation (FMD) was proposed. Second, the model was used to explain why FMD may be influenced by endothelium-independent factors, showing that FMD results are 1 ) partly masked by the vasoconstriction due to the change in transmural pressure and 2 ) affected by physiological factors (i.e., arterial stiffness and arterial blood pressure) that are difficult to eliminate due to their multiple interactions.

Background The relative impact of right ventricular ( RV ) electromechanical dyssynchrony versus pulmonary regurgitation ( PR ) on exercise capacity and RV function after tetralogy of Fallot repair is unknown. We aimed to delineate the relative effects of these factors on RV function and exercise capacity. Methods and Results We retrospectively analyzed 81 children with tetralogy of Fallot repair using multivariable regression. Predictor parameters were electrocardiographic QRS duration reflecting electromechanical dyssynchrony and PR severity by cardiac magnetic resonance. The outcome parameters were exercise capacity (percentage predicted peak oxygen consumption) and cardiac magnetic resonance ejection fraction (RV ejection fraction). To understand the relative effects of RV dyssynchrony versus PR on exercise capacity and RV function, virtual patient simulations were performed using a closed-loop cardiovascular system model (CircAdapt), covering a wide spectrum of disease severity. Eighty-one patients with tetralogy of Fallot repair (median [interquartile range { IQR} ] age, 14.48 [11.55-15.91] years) were analyzed. All had prolonged QRS duration (median [IQR], 144 [123-152] ms), at least moderate PR (median [IQR], 40% [29%-48%]), reduced exercise capacity (median [IQR], 79% [68%-92%] predicted peak oxygen consumption), and reduced RV ejection fraction (median [IQR], 48% [44%-52%]). Longer QRS duration, more than PR , was associated with lower oxygen consumption and lower RV ejection fraction. In a multivariable regression analysis, oxygen consumption decreased with both increasing QRS duration and PR severity. CircAdapt modeling showed that RV dyssynchrony exerts a stronger limiting effect on exercise capacity and on RV ejection fraction than does PR , regardless of contractile function. Conclusions In both patient data and computer simulations, RV dyssynchrony, more than PR , appears to be associated with reduced exercise capacity and RV systolic dysfunction in patients after TOF repair.

Objectives: To compare registry and electronic health record (EHR) data mining approaches for cohort ascertainment in patients with pediatric pulmonary hypertension (PH) in an effort to overcome some of the limitations of registry enrollment alone in identifying patients with particular disease phenotypes.Study Design: This study was a single-center retrospective analysis of EHR and registry data at Boston Children's Hospital. The local Informatics for Integrating Biology and the Bedside (i2b2) data warehouse was queried for billing codes, prescriptions, and narrative data related to pediatric PH. Computable phenotype algorithms were developed by fitting penalized logistic regression models to a physician-annotated training set. Algorithms were applied to a candidate patient cohort, and performance was evaluated using a separate set of 136 records and 179 registry patients. We compared clinical and demographic characteristics of patients identified by computable phenotype and the registry.Results: The computable phenotype had an area under the receiver operating characteristics curve of 90% (95% CI, 85%-95%), a positive predictive value of 85% (95% CI, 77%-93%), and identified 413 patients (an additional 231%) with pediatric PH who were not enrolled in the registry. Patients identified by the computable phenotype were clinically distinct from registry patients, with a greater prevalence of diagnoses related to perinatal distress and left heart disease.Conclusions: Mining of EHRs using computable phenotypes identified a large cohort of patients not recruited using a classic registry. Fusion of EHR and registry data can improve cohort ascertainment for the study of rare diseases.Trial Registration: ClinicalTrials.gov: NCT02249923. [ABSTRACT FROM AUTHOR]

Background Ventricular tachyarrhythmias are often preceded by short sequences of premature ventricular complexes. In a previous study, a restitution-based computational model predicted which sequences of stimulated premature complexes were most likely to induce ventricular fibrillation in canines in vivo. However, the underlying mechanism, based on discordant-alternans dynamics, could not be verified in that study. The current study seeks to elucidate the mechanism by determining whether the spatiotemporal evolution of action potentials and initiation of ventricular fibrillation in in vitro experiments are consistent with model predictions. Methods and Results Optical mapping voltage signals from canine right-ventricular tissue (n=9) were obtained simultaneously from the entire epicardium and endocardium during and after premature stimulus sequences. Model predictions of action potential propagation along a 1-dimensional cable were developed using action potential duration versus diastolic interval data. The model predicted sign-change patterns in action potential duration and diastolic interval spatial gradients with posterior probabilities of 91.1%, and 82.1%, respectively. The model predicted conduction block with 64% sensitivity and 100% specificity. A generalized estimating equation logistic-regression approach showed that model-prediction effects were significant for both conduction block ( P<1×10 -15 , coefficient 44.36) and sustained ventricular fibrillation ( P=0.0046, coefficient, 1.63) events. Conclusions The observed sign-change patterns favored discordant alternans, and the model successfully identified sequences of premature stimuli that induced conduction block. This suggests that the relatively simple discordant-alternans-based process that led to block in the model may often be responsible for ventricular fibrillation onset when preceded by premature beats. These observations may aid in developing improved methods for anticipating block and ventricular fibrillation.