1,053 research outputs found

    A fabrication history based strain-fatigue model for prediction of crack initiation in a radial loading wheel

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    A strain-based fatigue model concerning fabrication history is applied to predict the fatigue life of a commercial car wheel under radial loads. As the prior conditions, the strain fatigue testing is performed on standard specimen of DP590 and FB540 steels at various fabrication states, including raw materials, pre-strain and pre-strain + bake. Furthermore, the strain distribution of car wheel during its rotation under radial loads is simulated via ANSYS. The fatigue properties mainly determined by crack initiation of car wheels at various fabrication states are predicted via local stress–strain method, in which the scale and surface factors are also taken into account. The radial fatigue testing is carried out, and the results are used to validate the present model. The fracture mechanism is analysed using FEI Nova 400 field emission gun scanning electron microscope

    Experimental study of the flow velocity reduction behind fishing net

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    A series of physical model experiments is conducted to investigate the flow velocity reduction downstream from fishing net in current. The plane net is fixed on a steel frame, which is 0.3 m in width and 0.3 m in height, and positioned in the center of the flume normal to the flow direction. In the experiments, the acoustic Doppler velocimeter (ADV) is applied to measure the flow velocity behind the plane net. This paper presents the flow velocity reduction behind the plane net(s) with different solidity, spacing distances between two plane nets and plane net numbers. According to the experimental data, there exists an obvious flow velocity reduction downstream from the\ud plane net and the flow velocity reduction increases with increasing net solidity. For two plane nets with different spacing distances, the average value of flow velocity reduction factor is 0.90 between and 0.83 downstream the two plane nets. As the net number increases from 1 to 4, the minimum flow velocity reduction factor downstream from the\ud plane nets decreases from 0.90 to 0.68. It is found that there is a close relationship between the flow velocity reduction and the above parameters of the plane net. These results should help improve understanding of flow around the net cage

    Directional motion of Gallium-based liquid metal induced by asymmetric chemical surrounding

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    Interfacial, or surface tension, is a significant topic in chemical education. This paper describes the directional motion of gallium-based liquid metal drops, resulting from a difference of interfacial tension across the drop. This demonstration can engage students in discovering the underlying chemical principles. A mechanism for the drop’s directional motion is proposed to provide insight into this intriguing phenomenon. It appears that unbalanced chemical environments cause different physical or chemical processes to occur on each hemisphere of the drop, such as a pH difference, redox reactions, galvanic replacement, or adsorption. As a result, a difference in the interfacial tension across the drop is generated, providing the driving force that acts on the drop. This demonstration can be used to introduce the fundamental principles in chemical reactions, such as redox activity, electrical double-layer formation, and interfacial tension

    Computational Fluid Dynamics Simulations at Micro-Scale Stenosis for Microfluidic Thrombosis Model Characterization

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    Platelet aggregation plays a central role in pathological thrombosis, preventing healthy physiological blood flow within the circulatory system. For decades, it was believed that platelet aggregation was primarily driven by soluble agonists such as thrombin, adenosine diphosphate and thromboxane A2. However, recent experimental findings have unveiled an intriguing but complementary biomechanical mechanism—the shear rate gradients generated from flow disturbance occurring at sites of blood vessel narrowing, otherwise known as stenosis, may rapidly trigger platelet recruitment and subsequent aggregation. In our Nature Materials 2019 paper [1], we employed microfluidic devices which incorporated micro-scale stenoses to elucidate the molecular insights underlying the prothrombotic effect of blood flow disturbance. Nevertheless, the rheological mechanisms associated with this stenotic microfluidic device are poorly characterized. To this end, we developed a computational fluid dynamics (CFD) simulation approach to systematically analyze the hemodynamic influence of bulk flow mechanics and flow medium. Grid sensitivity studies were performed to ensure accurate and reliable results. Interestingly, the peak shear rate was significantly reduced with the device thickness, suggesting that fabrication of microfluidic devices should retain thicknesses greater than 50 µm to avoid unexpected hemodynamic aberration, despite thicker devices raising the cost of materials and processing time of photolithography. Overall, as many groups in the field have designed microfluidic devices to recapitulate the effect of shear rate gradients and investigate platelet aggregation, our numerical simulation study serves as a guideline for rigorous design and fabrication of microfluidic thrombosis models

    Cooperation of the Inducible Nitric Oxide Synthase and Cytochrome P450 1A1 in Mediating Lung Inflammation and Mutagenicity Induced by Diesel Exhaust Particles

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    Diesel exhaust particles (DEPs) have been shown to activate oxidant generation by alveolar macrophages (AMs), alter xenobiotic metabolic pathways, and modify the balance of pro-antiinflammatory cytokines. In this study we investigated the role of nitric oxide (NO) in DEP-mediated and DEP organic extract (DEPE)-mediated inflammatory responses and evaluated the interaction of inducible NO synthase (iNOS) and cytochrome P450 1A1 (CYP1A1). Male Sprague-Dawley rats were intratracheally (IT) instilled with saline, DEPs (35 mg/kg), or DEPEs (equivalent to 35 mg DEP/kg), with or without further treatment with an iNOS inhibitor, aminoguanidine (AG; 100 mg/kg), by intraperitoneal injection 30 min before and 3, 6, and 9 hr after IT exposure. At 1 day postexposure, both DEPs and DEPEs induced iNOS expression and NO production by AMs. AG significantly lowered DEP- and DEPE-induced iNOS activity but not the protein level while attenuating DEPE- but not DEP-mediated pulmonary inflammation, airway damage, and oxidant generation by AMs. DEP or DEPE exposure resulted in elevated secretion of both interleukin (IL)-12 and IL-10 by AMs. AG significantly reduced DEP- and DEPE-activated AMs in IL-12 production. In comparison, AG inhibited IL-10 production by DEPE-exposed AMs but markedly increased its production by DEP-exposed AMs, suggesting that NO differentially regulates the pro- and antiinflammatory cytokine balance in the lung. Both DEPs and DEPEs induced CYP1A1 expression. AG strongly inhibited CYP1A1 activity and lung S9 activity-dependent 2-aminoanthracene mutagenicity. These studies show that NO plays a major role in DEPE-induced lung inflammation and CYP-dependent mutagen activation but a lesser role in particulate-induced inflammatory damage

    A new ghost cell/level set method for moving boundary problems:application to tumor growth

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    In this paper, we present a ghost cell/level set method for the evolution of interfaces whose normal velocity depend upon the solutions of linear and nonlinear quasi-steady reaction-diffusion equations with curvature-dependent boundary conditions. Our technique includes a ghost cell method that accurately discretizes normal derivative jump boundary conditions without smearing jumps in the tangential derivative; a new iterative method for solving linear and nonlinear quasi-steady reaction-diffusion equations; an adaptive discretization to compute the curvature and normal vectors; and a new discrete approximation to the Heaviside function. We present numerical examples that demonstrate better than 1.5-order convergence for problems where traditional ghost cell methods either fail to converge or attain at best sub-linear accuracy. We apply our techniques to a model of tumor growth in complex, heterogeneous tissues that consists of a nonlinear nutrient equation and a pressure equation with geometry-dependent jump boundary conditions. We simulate the growth of glioblastoma (an aggressive brain tumor) into a large, 1 cm square of brain tissue that includes heterogeneous nutrient delivery and varied biomechanical characteristics (white matter, gray matter, cerebrospinal fluid, and bone), and we observe growth morphologies that are highly dependent upon the variations of the tissue characteristics—an effect observed in real tumor growth
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