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An optimization technique based on the combination of optimization algorithm and sensitivity analysis is discussed. The technique allows reducing the number of optimized parameters during the optimization process, which consequently reduces the search space and time of optimization. This paper explains the principle, benefits, and future challenges of this technique and illustrates its utilization with numerical experiments and a typical example. The algorithm is implemented in the framework OptiLab that represents a part of the application Agros2D developed by me. [ABSTRACT FROM AUTHOR]

A magneto-thermal inverse problem, dealing with the optimal design of an induction heating device, is proposed as a benchmark. The coupled-field problem is analysed by means of a higher order finite element method. Then the optimal design problem is solved in terms of the Pareto front trading off two conflicting objective functions. [ABSTRACT FROM AUTHOR]

A magneto-thermal inverse problem, dealing with the optimal design of an induction heating device, is proposed as a benchmark. The coupled-field problem is analysed by means of a higher order finite element method. Then the optimal design problem is solved in terms of the Pareto front trading off two conflicting objective functions. [ABSTRACT FROM AUTHOR]

Induction heating of non-magnetic cylindrical billets is modeled. The billet rotates in static magnetic field generated by appropriately distributed permanent magnets. The mathematical model of the process consists of two second-order partial differential equations describing the distributions of magnetic and temperature fields. Its solution is solved numerically in the quasi-coupled formulation respecting all important non-linearities. The computations are carried out by the code Agros2-D, based on a fully adaptive higher-order finite element method. Some results are verified experimentally on an industrial prototype of the device. Presented are also other important results obtained by measurements. [ABSTRACT FROM AUTHOR]

Background and Objective Anti-apolipoprotein A-1 (anti-apo A-1) Ig G is a potential marker of atherosclerotic plaque vulnerability and cardiovascular complications. In patients with periodontitis the presence of anti-apo A-1 IgGs in serum and their association with atherosclerosis is unknown. Material and Methods One-hundred and thirty subjects with periodontal disease and 46 healthy subjects, matched for age and gender, participated in this study. Anti-apo A-1 Ig G, high-sensitivity C-reactive protein (hs CRP) and matrix metalloproteinase ( MMP) -2, -3, -8 and -9 were measured in serum samples. An ankle-brachial index ( ABI) value below 1.11 served as a surrogate marker of atherosclerosis. Predictive accuracies of biomarkers for abnormal ABI were determined using receiver-operating characteristics curves and logistic regression analyses. Results Compared with healthy controls, periodontitis patients showed lower median ABI values (1.10 vs. 1.15; p < 0.0001), a higher prevalence of anti-apo A-1 Ig G positivity (23.8% vs. 6.5%; p = 0.009) and higher concentrations of hs CRP (1.62 mg/L vs. 0.85 mg/L; p = 0.02) and MMP-9 (435 μg/mL vs. 283 μg/mL; p < 0.0001). In patients younger than 50 years of age ( n = 66), anti-apo A-1 Ig G was found to be the best predictor for an abnormal ABI (area under the curve = 0.63; p = 0.03). Anti-apo A-1 Ig G positivity increased the risk of having an abnormal ABI (odds ratio = 4.20; p = 0.04), independently of diabetes, smoking and body mass index. Conclusions Anti-apo A-1 Ig G positivity and atherosclerosis, as reflected by abnormal ABI, were more prevalent in periodontitis patients than in age- and gender-matched controls. In younger periodontitis patients, anti-apo A-1 Ig G was found to be the best predictor of atherosclerosis burden. [ABSTRACT FROM AUTHOR]

. Keller P-F, Pagano S, Roux-Lombard P, Sigaud P, Rutschmann OT, Mach F, Hochstrasser D Vuilleumier N (Geneva University Hospitals, Geneva). Autoantibodies against apolipoprotein A-1 and phosphorylcholine for diagnosis of non-ST-segment elevation myocardial infarction. J Intern Med 2012; 271: 451-462. Objectives. To explore the diagnostic accuracies of anti-apolipoproteinA-1 (anti-ApoA-1) IgG and anti-phosphorylcholine (anti-PC) IgM alone, expressed as a ratio (anti-ApoA-1 IgG/anti-PC IgM), and combined with the Thrombolysis In Myocardial Infarction (TIMI) score for non-ST-segment elevation myocardial infarction (NSTEMI) (NSTEMI-TIMI score) to create a new diagnostic algorithm - the Clinical Autoantibody Ratio (CABR) score - for the diagnosis of NSTEMI and subsequent cardiac troponin I (cTnI) elevation in patients with acute chest pain (ACP). Methods. In this single-centre prospective study, 138 patients presented at the emergency department with ACP without ST-segment elevation myocardial infarction. Anti-ApoA-1 IgG and anti-PC IgM were assessed by enzyme-linked immunosorbent assay on admission. Post hoc determination of the CABR score cut-off was performed by receiver operating characteristics analyses. Results. The adjudicated final diagnosis was NSTEMI in 17% (24/138) of patients. Both autoantibodies alone were found to be significant predictors of NSTEMI diagnosis, but the CABR score had the best diagnostic accuracy [area under the curve (AUC): 0.88; 95% confidence interval (CI): 0.82-0.95]. At the optimal cut-off of 3.3, the CABR score negative predictive value (NPV) was 97% (95% CI: 90-99). Logistic regression analysis showed that a CABR score >3.3 increased the risk of subsequent NSTEMI diagnosis 19-fold (odds ratio: 18.7; 95% CI: 5.2-67.3). For subsequent cTnI positivity, only anti-ApoA-1 IgG and CABR score displayed adequate predictive accuracies with AUCs of 0.80 (95% CI: 0.68-0.91) and 0.82 (95% CI: 0.70-0.94), respectively; the NPVs were 95% (95% CI: 90-98) and 99% (95% CI: 94-100), respectively. Conclusion. The CABR score, derived from adding the anti-ApoA-1 IgG/anti-PC IgM ratio to the NSTEMI-TIMI score, could be a useful measure to rule out NSTEMI in patients presenting with ACP at the emergency department without electrocardiographic changes. [ABSTRACT FROM AUTHOR]

Abstract Si-SiC open cell foams with porosity >87% and high pore sizes (4-7 mm) are commonly employed as active zone in porous burners for heat radiation applications. In a porous burner, the solid porous body let the heat recirculate from the hot combustion products to the incoming reactants. The result is that the flame is confined within the foam, meaning high thermomechanical loadings on its constituent material. A set of commercial Si-SiC foams from the same production batch was aged with flat porous burners. Thermal cycles ramp-up, dwell and cooling, as well as burner set-up (power: 15 kW, fuel/air ratio: 1·5), were chosen based on previous experience. Before aging, each foam was first cut in bars ready for bending tests, reassembled into the burner foam configuration and operated. As produced and aged samples were physically, mechanically and chemically analysed and results compared. [ABSTRACT FROM AUTHOR]

1. Chlorhexidine digluconate has been used as a topical antiseptic in the treatment of acne vulgaris and periodontitis. The acute phase of these diseases involves neutrophilic infiltration. Neutrophil activation and recruitment to inflammatory sites are crucial in both protection against bacterial infection and the induction of hystotoxic damage. Activated neutrophils release several enzymes, including elastase and myeloperoxidase (MPO), which contribute to tissue injury via direct toxic actions, the generation of oxidants and inactivation of protective factors, such as α1-antitrypsin (α1-AT). In the present study, we investigated whether chlorhexidine can modulate neutrophil-mediated histotoxicity. 2. Human primary neutrophils were isolated from healthy donors. Inactivation of α1-AT by neutrophils or hypochlorous acid (HOCl) was evaluated by spectrophotometry and sodium dodecyl sulphate–polyacrylamide gel electrophoresis analysis of its capacity to complex with porcine pancreatic elastase (PPE). Neutrophil generation of HOCl, superoxide anion and MPO release were assessed spectrophometrically. 3. Chlorhexidine (0, 0.5, 1, 5 and 10 μmol/L) dose-dependently prevented HOCl-induced inactivation of α1-AT and reduced HOCl recovery from phorbol myristate acetate (PMA)-treated human neutrophils, but did not inhibit superoxide anion and MPO release. Chlorhexidine directly inhibited HOCl recovery from neutrophils and HOCl-induced inactivation of α1-AT in a cell-free assay. Accordingly, chlorhexidine reversed HOCl-mediated inhibition of α1-AT capacity to complex with PPE. 4. These data suggest that chlorhexidine prevents neutrophil-induced α1-AT inactivation via a direct inhibitory action on HOCl. Although highly speculative, the present study indicates that chlorhexidine may protect inflamed tissues not only through its antimicrobial properties, but also via a direct anti-inflammatory effect on neutrophil toxic products. [ABSTRACT FROM AUTHOR]

Changes in diagnostic criteria have impacted on the definition of the metabolic syndrome. The central aetiological importance of insulin resistance has lessened, while the role of other cardiovascular risk factors has progressively increased. Inflammatory mediators have also been identified as crucial targets for more selective therapies in metabolic syndrome. Among several pro-inflammatory factors, adiponectin has been shown to be associated with reduced cardiovascular risk in metabolic syndrome patients. Here, we review new therapeutic approaches, which could potentially increase adiponectin levels in metabolic syndrome. [ABSTRACT FROM AUTHOR]

The article discusses a study which assessed the oxidation processes of silicon-infiltrated silicon carbide (SiSiC) ceramic forms. Isothermal oxidation deals with the mechanisms of scale growth and oxidation rates, while cyclic oxidation investigates durability. The transition from passive to active oxidation starts at lower temperatures by decreasing the oxygen concentration.

Our current understanding of the pathophysiology of atherosclerosis suggests a prominent role for immune responses from its initiation through its complications. Given the increasing prevalence of cardiovascular risk factors worldwide, there is an urgent need to better understand the underlying mechanisms to improve current treatment protocols. A growing body of evidence suggests that endocannabinoid signalling plays a critical role in the pathogenesis of atherogenesis and its clinical manifestations. Blocking CB1 receptors has been shown to mediate not only weight reduction, but also several cardiometabolic effects in rodents and humans, indicating a potential relevance for the process of atherosclerosis. Activation of CB2 receptors with Δ9-tetrahydrocannabinol (THC) has been shown to inhibit atherosclerotic plaque progression in mice, mainly by inhibiting macrophage recruitment. Endocannabinoids released from endothelial cells, macrophages or platelets, reduce hypertension in rodents, a major risk factor for atherosclerosis. In addition, anandamide inhibits inflammatory gene expression in endothelial cells, and consequently monocyte adhesion. Conversely, endocannabinoids might also mediate pro-atherosclerotic effects by inducing platelet activation. In conclusion, the precise role of the endocannabinoid system during atherosclerosis is not yet understood. Whether increased endocannabinoid signalling is associated with disease progression and increased risk of acute thrombotic events remains to be determined. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a chronic inflammatory disease that is the primary cause of myocardial infarction and stroke, which occur after sudden thrombotic occlusion of an artery. A growing body of evidence suggests that cannabinoid signalling plays a fundamental role in atherosclerosis development and its clinical manifestations. Thus, CB2 receptors are protective in myocardial ischaemia/reperfusion and implicated in the modulation of chemotaxis, which is crucial for the recruitment of leukocytes during inflammation. Delta-9-Tetrahydrocannabinol (THC)-mediated activation has been shown to inhibit atherosclerotic plaque progression in a CB2 dependent manner. Although CB1 and CB2 expression has been reported on platelets, their involvement in thrombus formation is still controversial. While several reports suggest that CB1 receptors may have a relevant role in neuroprotection after ischaemic stroke, recent studies show the protective effects in various forms of neuroprotection are not related to CB1 stimulation, and a protective role of CB1 blockade has also been reported. In addition, vascular and myocardial CB1 receptors contribute to the modulation of blood pressure and heart rate. It is tempting to suggest that pharmacological modulation of the endocannabinoid system is a potential novel therapeutic strategy in the treatment of atherosclerosis. For these purposes, it is important to better understand the complex mechanisms of endocannabinoid signalling and potential consequences of its pharmacological modulation, as it may have both pro- and anti-atherosclerotic effects. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a complex inflammatory disease involving cellular migration and interaction. Vascular injury in response to different cardiovascular risk factors enhances endothelial dysfunction, which in turn promotes the expression of inflammatory markers and transendothelial leukocyte migration. Recruitment of leukocytes from the blood stream into the vessel intima is a crucial step for the development of the disease. Recent findings have highlighted the role of chemokines, chemokine receptors, adhesion molecules, and gap junctions in this process by acting as chemoattractant, adhesive, or intercellular communication molecules. In this short review, we summarize new data concerning the different steps from leukocyte arrest to transendothelial migration and discuss potential new therapeutic approaches concerning these processes. [ABSTRACT FROM AUTHOR]

Clopidogrel and statins are frequently coadministered in patients with ischemic heart diseases. Recent reports suggested that clopidogrel's effectiveness in inhibiting adenosine diphosphate (ADP)-induced platelets aggregation is attenuated by co-administration of certain statins. The objective of the present study was to define which statin might interfere with the antiaggregation property of clopidogrel. We designed a pharmacokinetic study and tested ex vivo platelet function on 21 healthy volunteers who received clopidogrel and all currently commercially available statins: rosuvastatin [10 mg o.d.], simvastatin [20 mg o.d.], fluvastatin [80 mg o.d.], pravastatin [40 mg o.d.], and atorvastatin [20 mg o.d.]. Each statin was administered for 7 days followed by 1 week of wash-out period with clopidogrel treatment alone. Detection of the statins in the plasma was performed on all blood samples, using HPLC analytical method. All individuals, except one, were responders to clopidogrel with inhibition of ex vivo ADP induced platelet aggregation. All statins, except pravastatin, were detectable in the plasma at the end of each treatment period in all patients, and no statin was detectable after any of the wash-out periods. Clopidogrel was significantly less efficient to prevent platelet aggregation when coadministrated with simvastatin or fluvastatin. No difference was observed in clopidogrel efficacy when coadministered with rosuvastatin, pravastatin or atorvastatin. This is the first study investigating clopidogrel-statin interactions on ex vivo platelet function with all commercially available statins and which were administered to the same individuals. It demonstrates in healthy volunteers that at the doses used in this study, simvastatin and fluvastatin, but not atorvastatin, pravastatin or rosuvastatin interfere with the anti-aggregation effect of clopidogrel. Eur J Clin Invest 2005; 35 (8): 476 –481 [ABSTRACT FROM AUTHOR]

3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, have been described as the principal and the most effective class of drug to reduce serum cholesterol levels. Statin therapies have been shown to reduce cardiovascular events, including myocardial infarction, stroke, and death, significantly, by altering vascular atherosclerosis development in patients with or without coronary artery disease symptoms. Extensive use of statins has led to the increase of some undesirable effects that are heavily counterbalanced by the benefits. Indeed, pleiotropic effects extend far beyond cholesterol reduction and involve non-lipid-related mechanisms that modify endothelial functions, immunoinflammatory responses, smooth muscle cell activation, proliferation and migration, atherosclerotic plaque stability, and thrombus formation. In this review, we describe in detail the targets and mechanisms of action of statins. [ABSTRACT FROM AUTHOR]

Objective: To study prospectively if, when plasma creatine kinase (CK) and plasma myoglobin are elevated, the origin of these abnormalities is cardiac or not, by measuring cardio-specific troponin T (cTT).Method: Fifteen patients with acute severe bronchial asthma (ASBA) were prospectively studied in the intensive care unit (ICU) with continuous electrocardiograph (ECG). Plasma CK, CK-MB, myoglobin and cTT were measured at 0, 4, 8, 12, 16 and 20 h in the ICU.Results: Five out of 15 ASBA patients had elevated CK, four of them presenting with an increase in CK-MB. Plasma cTT was normal in every patient, including those with CK and/or myoglobin elevation. At admission to the ICU, myoglobin and CK were positively correlated (r = 0.760; p < 0.001). No patient was intubated. There was no difference in clinical signs or symptoms, medical history, laboratory values or ECG in patients with or without CK elevation.Conclusion: Patients admitted to an ICU for ASBA may present with an elevation of plasma CK, CK-MB and myoglobin not related to any heart injury. CK and CK-MB are not good markers of myocardial injury in ASBA patients due to the multitude of potential confounders. Therefore, troponin should be measured instead. [ABSTRACT FROM AUTHOR]

Chest pain with normal coronary angiograms is a relatively common syndrome. The mode of presentation of this syndrome includes patients with syndrome X and patients with an acute myocardial infarction and angiographically normal coronary arteries. Different mechanisms have been proposed to elucidate the exact cause and to explain the various clinical presentations in these patients. Abnormalities of pain perception and the presence of oesophageal dysmotility have all been reported in patients with syndrome X. In situ thrombosis or embolization with subsequent clot lysis and recanalization, coronary artery spasm, cocaine abuse, and viral myocarditis have been described as potential mechanisms responsible for an acute myocardial infarction in patients with angiographically normal coronary arteries. Recent data suggest that both microvascular and epicardial endothelial dysfunction may play an important role in the pathophysiological mechanism of the syndrome of stable angina or acute myocardial infarction with normal coronary arteries. [ABSTRACT FROM AUTHOR]

Background For several years, acute coronary syndromes have been perceived as causing the most hospital admissions, and even hospital mortality. The syndrome of unstable angina frequently progresses to acute myocardial infarction but its pathogenesis is poorly understood, and prognosis determination is still problematic. We tested the hypothesis that measurement of the C-reactive protein in patients admitted for chest pain could be a marker for acute coronary syndromes. Methods and Results We studied 110 patients admitted with suspected ischaemic heart disease, but without elevated serum creatine-kinase levels at the time of hospital admission. Patients were subsequently divided into two groups based on their final diagnosis: group 1 comprised patients with unstable angina; group 2 patients with acute myocardial infarction. We measured the C-reactive protein at the time of hospital admission. The concentration of C-reactive protein was elevated in 59% of the patients with a final diagnosis of acute myocardial infarction, and in 5% of the patients with a final diagnosis of unstable angina, (P<0·001). Conclusion This study indicates that C-reactive protein levels measured at the time of admission in patients with suspected ischaemic heart disease could be a marker for acute coronary syndromes, and helpful in identifying patients at high risk for acute myocardial infarction. Measurement of C-reactive protein may have practical clinical significance in the management of patients hospitalized for suspected acute coronary syndromes. [ABSTRACT FROM PUBLISHER]

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