405 research outputs found

    Electromagnetic shielding properties of LPBF produced Fe2.9wt.%Si alloy

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    Ferromagnetic materials are used in various applications such as rotating electrical machines, wind turbines, electromagnetic shielding, transformers, and electromagnets. Compared to hard magnetic materials, their hysteresis cycles are featured by low values of coercive magnetic field and high permeability. The application of additive manufacturing to ferromagnetic materials is gaining more and more attraction. Indeed, thanks to a wider geometrical freedom, new topological optimized shapes for stator/rotor shapes can be addressed to enhance electric machines performances. However, the properties of the laser powder bed fusion (LPBF) processed alloy compared to conventionally produced counterpart must be still addressed. Accordingly, this paper presents for the first time the use of the LPBF for the manufacturing of Fe2.9wt.%Si electromagnetic shields. The process parameter selection material microstructure and the magnetic shielding factor are characterized

    Characterization of LPBF Produced Fe2.9wt.%Si for Electromagnetic Actuator

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    This study aims to produce Fe2.9wt.%Si ferromagnetic material via laser powder bed fusion (L-PBF) for the realization of electromagnetic actuators (EMA). This study is necessary as there are no documents in scientific literature regarding the manufacturing of Iron-Silicon plungers using the L-PBF additive manufacturing (AM) technique. The microstructure, and magnetic properties were characterized using various techniques. The results indicate that the samples produced via L-PBF process exhibit good magnetic properties (μ = 748, H C= 87.7 [A/m] ) especially after annealing treatment at 1200° C for 1h (μ = 3224, H C= 69.1 [A/m]), making it a promising material for use in electromagnetic actuators

    Spinal Compressive Forces in Adolescent Idiopathic Scoliosis With and Without Carrying Loads: A Musculoskeletal Modeling Study

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    The pathomechanisms of curve progression in adolescent idiopathic scoliosis (AIS) remain poorly understood and biomechanical data are limited. A deeper insight into spinal loading could provide valuable information toward the improvement of current treatment strategies. This work therefore aimed at using subject-specific musculoskeletal full-body models of patients with AIS to predict segmental compressive forces around the curve apex and to investigate how these forces are affected by simulated load carrying. Models were created based on spatially calibrated biplanar radiographic images from 24 patients with mild to moderate AIS and validated by comparing predictions of paravertebral muscle activity with reported values from in vivo studies. Spinal compressive forces were predicted during unloaded upright standing as well as standing with external loads of 10, 15, and 20% of body weight (BW) applied to the scapulae to simulate carrying a backpack in the regular way on the back as well as in front of the body and over the shoulder on the concave and convex sides of the scoliotic curve. The predicted muscle activities around the curve apex were higher on the convex side for the erector spinae (ES) and multifidi (MF) muscles, which was comparable to the EMG-based in vivo measurements from the literature. In terms of spinal loading, the implementation of spinal deformity resulted in a 10% increase of compressive force at the curve apex during unloaded upright standing. Apical compressive forces further increased by 50–62% for a simulated 10% BW load and by 77–94% and 103–128% for 15% and 20% BW loads, respectively. Moreover, load-dependent compressive force increases were the lowest in the regular backpack and the highest in the frontpack and convex conditions, with concave side-carrying forces in between. The predictions indicated increased segmental compressive forces during unloaded upright standing, which could be ascribed to the scoliotic deformation. When carrying loads, compressive forces further increased depending on the carrying mode and the weight of the load. These results can be used as a basis for further studies investigating segmental loading in AIS patients during functional activities. Models can thereby be created using the same approach as proposed in this study

    In Situ Hexavalent Chromium Reduction by Injection of Organic Substrates in the Aquifer

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    Among the innovative technologies for in situ remediation of hexavalent chromium in groundwater, bio-induced reduction is under investigation. In this process the reduction of Cr(VI) is stimulated by a strongly reducing environment, created by the injection of organic substrates that are rapidly degraded by autochthonous heterotrophic microorganisms. Tests were performed at the laboratory scale to investigate the behavior of two different organic substrates from food industry (permeate from cheese whey ultrafiltration and a waste from the brewing process), in terms of dissolved Cr(VI) abatement and kinetics, also as a function of the initial Cr(VI) concentration (5000 or 10000 μg/L). The tests showed that, under proper conditions, very low Cr(VI) concentrations (1.3 g/L) and removal efficiency up to about 100% can be obtained after 36 d incubation

    Multiple sclerosis cortical and WM lesion segmentation at 3T MRI: a deep learning method based on FLAIR and MP2RAGE.

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    The presence of cortical lesions in multiple sclerosis patients has emerged as an important biomarker of the disease. They appear in the earliest stages of the illness and have been shown to correlate with the severity of clinical symptoms. However, cortical lesions are hardly visible in conventional magnetic resonance imaging (MRI) at 3T, and thus their automated detection has been so far little explored. In this study, we propose a fully-convolutional deep learning approach, based on the 3D U-Net, for the automated segmentation of cortical and white matter lesions at 3T. For this purpose, we consider a clinically plausible MRI setting consisting of two MRI contrasts only: one conventional T2-weighted sequence (FLAIR), and one specialized T1-weighted sequence (MP2RAGE). We include 90 patients from two different centers with a total of 728 and 3856 gray and white matter lesions, respectively. We show that two reference methods developed for white matter lesion segmentation are inadequate to detect small cortical lesions, whereas our proposed framework is able to achieve a detection rate of 76% for both cortical and white matter lesions with a false positive rate of 29% in comparison to manual segmentation. Further results suggest that our framework generalizes well for both types of lesion in subjects acquired in two hospitals with different scanners

    Dysfunctional d-aspartate metabolism in BTBR mouse model of idiopathic autism.

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    Background: Autism spectrum disorders (ASD) comprise a heterogeneous group of neurodevelopmental conditions characterized by impairment in social interaction, deviance in communication, and repetitive behaviors. Dysfunctional ionotropic NMDA and AMPA receptors, and metabotropic glutamate receptor 5 activity at excitatory synapses has been recently linked to multiple forms of ASD. Despite emerging evidence showing that d-aspartate and d-serine are important neuromodulators of glutamatergic transmission, no systematic investigation on the occurrence of these D-amino acids in preclinical ASD models has been carried out. Methods: Through HPLC and qPCR analyses we investigated d-aspartate and d-serine metabolism in the brain and serum of four ASD mouse models. These include BTBR mice, an idiopathic model of ASD, and Cntnap2-/-, Shank3-/-, and 16p11.2+/- mice, three established genetic mouse lines recapitulating high confidence ASD-associated mutations. Results: Biochemical and gene expression mapping in Cntnap2-/-, Shank3-/-, and 16p11.2+/- failed to find gross cerebral and serum alterations in d-aspartate and d-serine metabolism. Conversely, we found a striking and stereoselective increased d-aspartate content in the prefrontal cortex, hippocampus and serum of inbred BTBR mice. Consistent with biochemical assessments, in the same brain areas we also found a robust reduction in mRNA levels of d-aspartate oxidase, encoding the enzyme responsible for d-aspartate catabolism. Conclusions: Our results demonstrated the presence of disrupted d-aspartate metabolism in a widely used animal model of idiopathic ASD. General significance: Overall, this work calls for a deeper investigation of D-amino acids in the etiopathology of ASD and related developmental disorders

    Dysfunctional dopaminergic neurotransmission in asocial BTBR mice

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    Autism spectrum disorders (ASD) are neurodevelopmental conditions characterized by pronounced social and communication deficits and stereotyped behaviours. Recent psychosocial and neuroimaging studies have highlighted reward-processing deficits and reduced dopamine (DA) mesolimbic circuit reactivity in ASD patients. However, the neurobiological and molecular determinants of these deficits remain undetermined. Mouse models recapitulating ASD-like phenotypes could help generate hypotheses about the origin and neurophysiological underpinnings of clinically relevant traits. Here we used functional magnetic resonance imaging (fMRI), behavioural and molecular readouts to probe dopamine neurotransmission responsivity in BTBR T+ Itpr3tf/J mice (BTBR), an inbred mouse line widely used to model ASD-like symptoms owing to its robust social and communication deficits, and high level of repetitive stereotyped behaviours. C57BL/6J (B6) mice were used as normosocial reference comparators. DA reuptake inhibition with GBR 12909 produced significant striatal DA release in both strains, but failed to elicit fMRI activation in widespread forebrain areas of BTBR mice, including mesolimbic reward and striatal terminals. In addition, BTBR mice exhibited no appreciable motor responses to GBR 12909. DA D1 receptor-dependent behavioural and signalling responses were found to be unaltered in BTBR mice, whereas dramatic reductions in pre- and postsynaptic DA D2 and adenosine A2A receptor function was observed in these animals. Overall these results document profoundly compromised DA D2-mediated neurotransmission in BTBR mice, a finding that is likely to have a role in the distinctive social and behavioural deficits exhibited by these mice. Our results call for a deeper investigation of the role of dopaminergic dysfunction in mouse lines exhibiting ASD-like phenotypes, and possibly in ASD patient populations
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