236 research outputs found

    Thermoelectric magnetohydrodynamic control of melt pool dynamics and microstructure evolution in additive manufacturing

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    Large thermal gradients in the melt pool from rapid heating followed by rapid cooling in metal additive manufacturing generate large thermoelectric currents. Applying an external magnetic field to the process introduces fluid flow through thermoelectric magnetohydrodynamics. Convective transport of heat and mass can then modify the melt pool dynamics and alter microstructural evolution. As a novel technique, this shows great promise in controlling the process to improve quality and mitigate defect formation. However, there is very little knowledge within the scientific community on the fundamental principles of this physical phenomenon to support practical implementation. To address this multiphysics problem that couples the key phenomena of melting/solidification, electromagnetism, hydrodynamics, heat and mass transport, the lattice Boltzmann method for fluid dynamics was combined with a purpose-built code addressing solidification modelling and electromagnetics. The theoretical study presented here investigates the hydrodynamic mechanisms introduced by the magnetic field. The resulting steady-state solutions of modified melt pool shapes and thermal fields are then used to predict the microstructure evolution using a cellular automata based grain growth model. The results clearly demonstrate that the hydrodynamic mechanisms and, therefore, microstructure characteristics are strongly dependent on magnetic field orientation

    Modulating Meltpool Dynamics and Microstructure using Thermoelectric Magnetohydrodynamics in Additive Manufacturing

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    Meltpool modulation in Selective Laser Remelting Additive Manufacturing via an oscillating magnetic field generates Thermoelectric Magnetohydrodynamics (TEMHD) flow. Numerical predictions show that the resulting microstructure can be significantly altered. A multi-scale numerical model captures the meso-scale melt pool dynamics coupled to microscale solidification showing the microstructure evolution and solute redistribution. The results highlight the complex interaction of the various physical phenomena and also show the method's potential to disrupt the epitaxial growth defect. The model predictions are supported by preliminary experimental results that demonstrate the dependency of the melt pool depth on magnetic field orientation. The results highlight how a time-dependent field has the potential to provide an independent control mechanism to tailor microstructures

    The association between IgG and IgM antibodies against cardiolipin, β2-glycoprotein I and Domain I of β2-glycoprotein I with disease profile in patients with multiple sclerosis

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    Antiphospholipid antibodies (aPL) occur in patients with multiple sclerosis (MS) with a number of studies reporting elevated levels; their exact prevalence and pathogenic role remain unclear. Epidemiological studies associate MS with an increased risk of deep venous thromboembolism and stroke; overlapping clinical features with APS. Antibodies against the first domain – Domain I (DI) – of β2glycoprotein I (β2GPI), show the most clinical significance and evidence for pathogenicity in the antiphospholipid syndrome (APS), but have not yet been investigated in MS. Serum from a well-defined cohort of 127 MS patients and 92 healthy controls were tested for IgM and IgG antibodies against cardiolipin (CL), β2GPI and DI. Higher frequency of IgM and IgG anti-CL were found in MS patients (18.1% and 21.3%), compared to controls (1.1% in both cases, p < 0.0001). We report that anti-DI antibodies were associated with MS patients, with 6.3% and 7.1% positive for IgM and IgG, respectively, compared to controls, 1.1% (p < 0.05). IgM anti-CL antibodies were elevated in secondary progressive MS and primary progressive MS compared to relapse-remitting MS, (p < 0.005). This study enrolled the largest number of patients with definite MS for studying the association with aPL. Although we confirmed IgM and IgG anti-CL antibodies occur in patients with MS, this is the first study that identified anti-DI antibodies in MS patients. This new finding may prove valuable and future studies are required to evaluate its role as a potential risk factor of thromboembolic phenomena in MS

    Inhaled corticosteroids reduce senescence in endothelial progenitor cells from COPD patients

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    Cellular senescence contributes to the pathophysiology of chronic obstructive pulmonary disease (COPD) and cardiovascular disease. Using endothelial-colony-forming-cells (ECFC), we have demonstrated accelerated senescence in smokers and COPD patients compared to non-smokers. Subgroup analysis suggests that ECFC from COPD patients on inhaledcorticosteroids (ICS) (n=14; 8 on ICS) exhibited significantly reduced senescence (Senescence-associated-beta galactosidase activity, p21CIP1), markers of DNA damage response (DDR) and IFN-γ-inducible-protein-10 compared to COPD patients not on ICS. In vitro studies using human-umbilical-vein-endothelial-cells showed a protective effect of ICS on the DDR, senescence and apoptosis caused by oxidative-stress, suggesting a protective molecular mechanism of action of corticosteroids on endothelium

    Anti-protein C antibodies and acquired protein C resistance in SLE: novel markers for thromboembolic events and disease activity?

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    OBJECTIVES: Risk factors for thromboembolism in SLE are poorly understood. We hypothesized a possible role for protein C, based on its dual activity in inflammation and haemostasis and on the evidence of an association between acquired activated protein C (APC) resistance (APCR) and high-avidity anti-protein C antibodies (anti-PC) with a severe thrombotic phenotype in venous thrombosis APS patients. METHODS: In a cross-sectional study of 156 SLE patients, the presence and avidity of IgG anti-PC was established by in house-ELISA, and APCR to exogenous recombinant human APC (rhAPC) and Protac (which activates endogenous protein C) was assessed by thrombin generation-based assays. Associations with aPL profile, thrombotic history and disease activity (BILAG and SLEDAI-2K) were also established. RESULTS: Anti-PC were detected in 54.5% of patients and APCR in 59%. Anti-PC positivity was associated with APCR to both rhAPC (P <0.0001) and Protac (P =0.0001). High-avidity anti-PC, detected in 26.3% of SLE patients, were associated with APCR in patients with thrombosis only (P <0.05), and with the development of thrombosis over time (range: 0-52 years; P =0.014). High-avidity anti-PC levels correlated with SLEDAI-2K (P =0.033) and total BILAG (P =0.019); SLEDAI-2K correlated inversely with APCR to Protac (P =0.004). CONCLUSION: Anti-PC occur in patients with SLE, independently of aPL profile, and are associated with APCR. High-avidity anti-PC are associated with thrombosis and with active disease and might prove a novel marker to monitor the risk of thrombosis and disease progression in SLE

    The effects of natural, forced and thermoelectric magnetohydrodynamic convection during the solidification of thin sample alloys

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    Using a fully coupled transient 3-dimensional numerical model, the effects of convection on the microstructural evolution of a thin sample of Ga-In25%wt. was predicted. The effects of natural convection, forced convection and thermoelectric magnetohydrodynamics were investigated numerically. A comparison of the numerical results is made to experimental results for natural convection and forced convection. In the case of natural convection, density variations within the liquid cause plumes of solute to be ejected into the bulk. When forced convection is applied observed effects include the suppression of solute plumes, preferential secondary arm growth and an increase in primary arm spacing. These effects were observed both numerically and experimentally. By applying an external magnetic field inter-dendritic flow is generated by thermoelectrically induced Lorentz forces, while bulk flow experiences an electromagnetic damping force. The former causes preferential secondary growth, while the latter slows the formation of solute plumes. This work highlights that the application of external forces can be a valuable tool for tailoring the microstructure and ultimately the macroscopic material properties

    Anti-factor Xa antibodies in patients with antiphospholipid syndrome and their effects upon coagulation assays

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    - Introduction: The aim of this study was to examine the prevalence and functional effects of antibodies directed against Factor (F)Xa and other serine proteases (SP) in patients with antiphospholipid syndrome (APS). - Methods: Serum from patients with APS (n = 59), systemic lupus erythematosus (SLE; n = 106), other autoimmune rheumatic disease (ARD; n = 63) and 40 healthy controls (HC) were tested for IgG activity against thrombin (Thr), FXa, FVIIa, phosphatidylserine (PS)/FXa and antithrombin (AT)-III by enzyme-linked immunosorbent assay (ELISA). Anti-FXa positive IgG were purified to measure their avidity by chaotropic ELISA and functional effects upon clotting time (FXa-ACT) and FXa enzymatic activity (± AT-III). - Results: Anti-FXa IgG were found in patients with SLE (49.1%) and APS (33.9%) (P <0.05) but not in ARD controls and HC. In contrast, anti-Thr and anti-PS/FXa IgG were identified in other ARD and anti-FVIIa IgG were low in all groups. The avidity of APS-IgG to FXa was significantly higher than SLE-IgG (P <0.05). Greatest prolongation of FXa-ACT was observed with APS-IgG and greatest inhibitory effect upon FXa enzymatic activity was found with APS-IgG followed by SLE-IgG compared to HC-IgG. ATIII inhibition of FXa was significantly reduced by APS-IgG compared with HC and SLE (P <0.05) and did not correlate with binding to AT-III. - Conclusion: APS anti-FXa IgG have higher avidity to FXa and greater effects upon the enzymatic and coagulant activity of FXa compared with SLE anti-FXa IgG. Further studies of anti-FXa antibodies in APS, SLE and other non-autoimmune thrombotic disease cohorts are now required to evaluate whether targeting FXa with selective inhibitors in patients bearing anti-FXa antibodies may be an effective treatment strategy
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