Analysis and Optimization of Dimensional Accuracy and Porosity of High Impact Polystyrene Material Printed by FDM Process: PSO,JAYA, Rao,and Bald Eagle Search Algorithms

High impact polystyrene (HIPS) material is widely used for low-strength structural applications. To ensure proper function, dimensional accuracy and porosity are at the forefront of industrial relevance. The dimensional accuracy cylindricity error (CE) and porosity of printed parts are influenced mainly by the control variables (layer thickness, shell thickness, infill density, print speed of the fused deposition modeling (FDM) process). In this study, a central composite design (CCD) matrix was used to perform experiments and analyze the complete insight information of the process (control variables influence on CE and porosity of FDM parts). Shell thickness for CE and infill density for porosity were identified as the most significant factors. Layer thickness interaction with shell thickness, infill density (except for CE), and print speed were found to be significant for both outputs. The interaction factors, i.e., shell thickness and infill density, were insignificant (negligible effect) for both outputs. The models developed produced a better fit for regression with an R² equal to 94.56% for CE, and 99.10% for porosity, respectively. Four algorithms (bald eagle search optimization (BES), particle swarm optimization (PSO), RAO-3, and JAYA) were applied to determine optimal FDM conditions while examining six case studies (sets of weights assigned for porosity and CE) focused on minimizing both CE and porosity. BES and RAO-3 algorithms determined optimal conditions (layer thickness: 0.22 mm; shell thickness: 2 mm; infill density: 100%; print speed: 30 mm/s) at a reduced computation time equal to 0.007 s, differing from JAYA and PSO, which resulted in an experimental CE of 0.1215 mm and 2.5% of porosity in printed parts. Consequently, BES and RAO-3 algorithms are efficient tools for the optimization of FDM parts.     

The Additive Manufacturing of Aluminum Matrix Nano Al2O3 Composites Produced via Friction Stir Deposition Using Different Initial Material Conditions

The current work investigates the viability of utilizing a friction stir deposition (FSD) technique to fabricate continuous multilayer high-performance, metal-based nanoceramic composites. For this purpose, AA2011/nano Al₂O₃ composites were successfully produced using AA2011 as a matrix in two temper conditions (i.e., AA2011-T6 and AA2011-O). The deposition of matrices without nano Al₂O₃ addition was also friction stir deposited for comparison purposes. The deposition process parameters were an 800 rpm rod rotation speed and a 5 mm/min feed rate. Relative density and mechanical properties (i.e., hardness, compressive strength, and wear resistance) were evaluated on the base materials, deposited matrices, and produced composites. The microstructural features of the base materials and the friction stir deposited materials were investigated using an optical microscope (OM) and a scanning electron microscope (SEM) equipped with an EDS analysis system. The worn surface was also examined using SEM. The suggested technique with the applied parameters succeeded in producing defect-free deposited continuous multilayer AA2011-T6/nano Al₂O₃ and AA2011-O/nano Al₂O₃ composites, revealing well-bonded layers, grain refined microstructures, and homogeneously distributed Al₂O₃ particles. The deposited composites showed higher hardness, compressive strengths, and wear resistance than the deposited AA2011 matrices at the two temper conditions. Using the AA2011-T6 temper condition as a matrix, the produced composite showed the highest wear resistance among all the deposited and base materials.     

Exacerbation of apoptosis of cortical neurons following traumatic brain injury in par-4 transgenic mice

Traumatic brain injury (TBI) is a significant clinical problem, yet few effective strategies for treating it have emerged. People that sustain and survive a TBI are left with significant cognitive, behavioral, and communicative disabilities. Apoptotic neuronal death occurs following TBI. Prostate apoptosis response-4 (Par-4) is a death domain-containing protein initially characterized as a critical regulator of apoptosis in prostate cancer cells. We have recently generated and characterized Par-4 transgenic mice in which the expression of the par-4 transgene was limited to cells of neuronal lineage. We now provide evidence that, in cortical neurons from these mice, Par-4 drastically increases apoptotic neuronal death in both in vitro and in vivo models of TBI. In vitro experiments were performed in 7-day-old primary cultures of cortical neurons using a previously published, scratch-induced mechanical trauma model. Neurons that overexpress Par-4 showed not only a significant decrease in overall neuron survival after TBI compared to wild-type cells, but also exhibited a sharper decrease in mitochondrial transmembrane potential, a higher degree of free radical accumulation, and earlier activation of caspase-3 than wild-type cells did. In vivo experiments were performed utilizing a weight drop TBI model. A significantly increased volume of cortical injury and exacerbated activation of caspase-3 were observed in Par-4 transgenic mice when compared to those in wild-type mice. These data suggests that aberrant Par-4 expression exacerbates neuronal cell death following TBI by altering mitochondrial function, enhancing oxidative damage, and execution of apoptosis via caspase activation.     

Acute and hyperacute humoral rejection in kidney allograft recipients treated with anti-human thymocyte antibodies

Equine and rabbit antihuman thymocyte globulins (ATGs) have been used in renal transplantation for prevention and treatment of acute rejection. We now report that hyperacute and acute antibody-mediated rejection of renal allografts occurred in three newly transplanted patients who received ATG for induction therapy. Antibody studies performed using complement-dependent cytotoxicity, flow cytometry, enzyme-linked immunosorbent assay, and Luminex yielded negative results for antilymphocytic and antiendothelial cell antibodies in the pretransplant sera obtained from these patients. ATG treatment was initiated at the time of transplantation. One of the patients experienced hyperacute rejection and required transplant nephrectomy within 24 h of transplantation. The other two patients developed acute antibody-mediated rejection within 14 days after transplantation. None of the patients developed antihuman leukocyte antigen antibodies when humoral rejection occurred. However, xenoantibodies that strongly bound to human lymphocytes and, importantly, to activated endothelial cells, were identified in the sera obtained at the time of humoral rejection. Hence, our results strongly implicate ATG in the induction of antibody-mediated rejection of kidney allografts. Flow cytometry testing of ATG reactivity to endothelial cells may be useful in identifying and discarding the ATG lots containing xenoantibodies that can bind to activated endothelial cells of the transplant.     

Acrylonitrile Potentiates Noise-Induced Hearing Loss in Rat

Acrylonitrile, one of the 50 most commonly produced industrial chemicals, has recently been identified as a promoter of noise-induced hearing loss (NIHL). This agent has the potential to produce oxidative stress through multiple pathways. We hypothesize that acrylonitrile potentiates NIHL as a consequence of oxidative stress. The objectives of this study were to characterize acrylonitrile exposure conditions that promote permanent NIHL in rats and determine the ability of this nitrile to produce auditory dysfunction by itself. Additionally, we sought to determine whether a spin-trap agent that can form adducts with ROS would protect against the effects of acrylonitrile. Acrylonitrile administration produced significant elevation in NIHL detected as a loss in compound action potential sensitivity. The effect was particularly robust for high-frequency tones and particularly when acrylonitrile and noise were given on repeated occasions. Acrylonitrile by itself did not disrupt threshold sensitivity. Administration of the spin-trap agent phenyl-N-tert-butylnitrone (PBN), given to rats prior to acrylonitrile and noise, did block the elevation of NIHL by acrylonitrile. However, PBN at the dose and time interval given was ineffective in protecting auditory function in subjects exposed to noise alone. The results suggest that oxidative stress may play a role in the promotion of NIHL by acrylonitrile.