Statistical Parameterized Physics-Based Machine Learning Digital Twin Models for Laser Powder Bed Fusion Process

A digital twin (DT) is a virtual representation of physical process, products and/or systems that requires a high-fidelity computational model for continuous update through the integration of sensor data and user input. In the context of laser powder bed fusion (LPBF) additive manufacturing, a digital twin of the manufacturing process can offer predictions for the produced parts, diagnostics for manufacturing defects, as well as control capabilities. This paper introduces a parameterized physics-based digital twin (PPB-DT) for the statistical predictions of LPBF metal additive manufacturing process. We accomplish this by creating a high-fidelity computational model that accurately represents the melt pool phenomena and subsequently calibrating and validating it through controlled experiments. In PPB-DT, a mechanistic reduced-order method-driven stochastic calibration process is introduced, which enables the statistical predictions of the melt pool geometries and the identification of defects such as lack-of-fusion porosity and surface roughness, specifically for diagnostic applications. Leveraging data derived from this physics-based model and experiments, we have trained a machine learning-based digital twin (PPB-ML-DT) model for predicting, monitoring, and controlling melt pool geometries. These proposed digital twin models can be employed for predictions, control, optimization, and quality assurance within the LPBF process, ultimately expediting product development and certification in LPBF-based metal additive manufacturing.Comment: arXiv admin note: text overlap with arXiv:2208.0290

Series studies of the Potts model. I: The simple cubic Ising model

The finite lattice method of series expansion is generalised to the $q$-state Potts model on the simple cubic lattice. It is found that the computational effort grows exponentially with the square of the number of series terms obtained, unlike two-dimensional lattices where the computational requirements grow exponentially with the number of terms. For the Ising ($q=2$) case we have extended low-temperature series for the partition functions, magnetisation and zero-field susceptibility to $u^{26}$ from $u^{20}$. The high-temperature series for the zero-field partition function is extended from $v^{18}$ to $v^{22}$. Subsequent analysis gives critical exponents in agreement with those from field theory.Comment: submitted to J. Phys. A: Math. Gen. Uses preprint.sty: included. 24 page

Reduced Retinal Function in the Absence of Nav1.6

Background: Mice with a function-blocking mutation in the Scn8a gene that encodes Nav1.6, a voltage-gated sodium channel (VGSC) isoform normally found in several types of retinal neurons, have previously been found to display a profoundly abnormal dark adapted flash electroretinogram. However the retinal function of these mice in light adapted conditions has not been studied. Methodology/Principal Findings: In the present report we reveal that during light adaptation these animals are shown to have electroretinograms with significant decreases in the amplitude of the a- and b-waves. The percent decrease in the a-and b-waves substantially exceeds the acute effect of VGSC block by tetrodotoxin in control littermates. Intravitreal injection of CoCl 2 or CNQX to isolate the a-wave contributions of the photoreceptors in littermates revealed that at high background luminance the cone-isolated component of the a-wave is of the same amplitude as the a-wave of mutants. Conclusions/Significance: Our results indicate that Scn8a mutant mice have reduced function in both rod and the cone retinal pathways. The extent of the reduction in the cone pathway, as quantified using the ERG b-wave, exceeds the reduction seen in control littermates after application of TTX, suggesting that a defect in cone photoreceptors contributes to the reduction. Unless the postreceptoral component of the a-wave is increased in Scn8a mutant mice, the reduction in the b-wave is larger than can be accounted for by reduced photoreceptor function alone. Our data suggests that th

Biomechanics of human fetal hearts with critical aortic stenosis

Critical aortic stenosis (AS) of the fetal heart causes a drastic change in the cardiac biomechanical environment. Consequently, a substantial proportion of such cases will lead to a single-ventricular birth outcome. However, the biomechanics of the disease is not well understood. To address this, we performed Finite Element (FE) modelling of the healthy fetal left ventricle (LV) based on patient-specific 4D ultrasound imaging, and simulated various disease features observed in clinical fetal AS to understand their biomechanical impact. These features included aortic stenosis, mitral regurgitation (MR) and LV hypertrophy, reduced contractility, and increased myocardial stiffness. AS was found to elevate LV pressures and myocardial stresses, and depending on severity, can drastically decrease stroke volume and myocardial strains. These effects are moderated by MR. AS alone did not lead to MR velocities above 3 m/s unless LV hypertrophy was included, suggesting that hypertrophy may be involved in clinical cases with high MR velocities. LV hypertrophy substantially elevated LV pressure, valve flow velocities and stroke volume, while reducing LV contractility resulted in diminished LV pressure, stroke volume and wall strains. Typical extent of hypertrophy during fetal AS in the clinic, however, led to excessive LV pressure and valve velocity in the FE model, suggesting that reduced contractility is typically associated with hypertrophy. Increased LV passive stiffness, which might represent fibroelastosis, was found to have minimal impact on LV pressures, stroke volume, and wall strain. This suggested that fibroelastosis could be a by-product of the disease progression and does not significantly impede cardiac function. Our study demonstrates that FE modelling is a valuable tool for elucidating the biomechanics of congenital heart disease and can calculate parameters which are difficult to measure, such as intraventricular pressure and myocardial stresses

Pathophysiological processes in multiple sclerosis: focus on nuclear factor erythroid-2-related factor 2 and emerging pathways

Philipp Arnold,1,* Deb Mojumder,2,* John DeToledo,2 Ralph Lucius,1 Henrik Wilms2 1Institute of Anatomy, Christian-Albrechts-University Kiel, Kiel, Germany; 2Department of Neurology, Texas Tech University Health Science Center, Lubbock, TX, USA *These authors contributed equally to this work Abstract: Multiple sclerosis (MS) is a disease of the central nervous system that is characterized by the demyelination of neuronal axons. Four different patterns of demyelination have been described, showing the heterogeneity in the immunopathologic processes involved in the demyelination. This review will focus on reactive oxygen species (ROS)-related inflammation in MS. Special emphasis will be placed on the nuclear factor erythroid-2-related factor 2 (Nrf2) as it regulates the transcription of ROS-protective genes. In the cytosol, Nrf2 binds to Keap1 (Kelch-like ECH-associated protein 1), and together they are degraded by the 26S proteasome after ubiquitination. If challenged by ROS Nrf2, binding to Keap1 is abrogated, and it translocates into the nucleus. Here it binds to the antioxidant response element and to a small protein termed Maf (musculoaponeurotic fibrosarcoma oncogene homolog). This leads to an enhanced transcription of ROS protective genes and represents the physiological answer against ROS challenge. It has been shown that dimethyl fumarate (DMF) has the same effect and leads to an enhanced transcription of ROS-protective genes. This response is mediated through a reduced binding of Nrf2 to Keap1, thus resulting in a higher level of free Nrf2 in the cytosol. Consequently, more Nrf2 translocates to the nucleus, promoting transcription of its target genes. DMF has been used for the treatment of psoriasis for many years in Germany without the occurrence of major side effects. In psoriasis, DMF reduces ROS-related inflammation in skin. A DMF analog, BG-12, was recently approved for the treatment of relapsing-remitting MS by the European Union and the US Food and Drug Administration. As an oral formulation, it gives patients a convenient and effective alternative to the injectable immune modulators in the long-term treatment of MS. Keywords: MS, fumaric acid ester, RO

Calretinin and calbindin-28 kDa are differentially distributed in amacrine cells as seen in retinal whole-mounts

Double labeling for calretinin (red) and calbindin-28 kDa (green) in the inner nuclear layer shows that labeling for each was present in a distinct set of amacrine cells For the apparent region of overlap (arrowhead) in the overlay of this confocal plane, examination of different z-planes revealed that these were disparate cells located at different depths. Arrows indicate calbindin-28 kDa-immunopositive cells. Scale bar represents 20 µm. Abbreviations: bv is blood vessel.<p><b>Copyright information:</b></p><p>Taken from "Subcellular compartmentalization of two calcium binding proteins, calretinin and calbindin-28 kDa, in ganglion and amacrine cells of the rat retina"</p><p></p><p> 2008;14():1600-1613.</p><p>Published online 31 Aug 2008</p><p>PMCID:PMC2528027.</p><p></p

Comparison of immunofluorescence for the calcium binding proteins, calretinin and calbindin-28 kDa, and voltage-gated sodium channel antibodies in the ganglion cell layer (GCL)/nerve fiber layer (NFL) as seen in retinal whole-mounts

Calcium binding proteins (CBP) in the NFL are extensively colocalized with Pan-NaV. Some Pan-Na stained retinal ganglion cell (RGC) somata were also immunopositive for CBPs (arrowhead) while others were not (double arrows). Initial segments of RGCs, (arrow) some of which can be seen emerging from the RGC somata, were immunopositive for Pan-Na but not colabeled with CBPs. Na1.1-immunopositive (green) RGC nerve fiber bundles in the nerve fiber layer (NFL) were colabeled with CBPs (red), but the axon initial segments (arrow) were not. Na1.2 immunopositive (green) RGC nerve fiber bundles in the NFL were colabeled with CBPs (red) but not the axon initial segments (arrow). Na1.6 immunopositive (green) axon initial segments (arrow) were not colabeled with CBPs (red). Scale bar equals 20 µm. Abbreviations: bv is blood vessel.<p><b>Copyright information:</b></p><p>Taken from "Subcellular compartmentalization of two calcium binding proteins, calretinin and calbindin-28 kDa, in ganglion and amacrine cells of the rat retina"</p><p></p><p> 2008;14():1600-1613.</p><p>Published online 31 Aug 2008</p><p>PMCID:PMC2528027.</p><p></p