1,071 research outputs found

    Tearing and Delaminating of a Polymer Laminate

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    The minimum mean monopoly energy of a graph

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    The motivation for the study of the graph energy comes from chemistry, where the research on the so-called total pi - electron energy can be traced back until the 1930s. This graph invariant is very closely connected to a chemical quantity known as the total pi - electron energy of conjugated hydro carbon molecules. In recent times analogous energies are being considered, based on Eigen values of a variety of other graph matrices. In 1978, I.Gutman [1] defined energy mathematically for all graphs. Energy of graphs has many mathematical properties which are being investigated. The ordinary energy of an undirected simple finite graph G is defined as the sum of the absolute values of the Eigen values of its associated matrix. i.e. if mu(1), mu(2), ..., mu(n) are the Eigen values of adjacency matrix A(G), then energy of graph is Sigma(G) = Sigma(n)(i=1) vertical bar mu(i)vertical bar Laura Buggy, Amalia Culiuc, Katelyn Mccall and Duyguyen [9] introduced the more general M-energy or Mean Energy of G is then defined as E-M (G) = Sigma(n)(i=1)vertical bar mu(i) - (mu) over bar vertical bar, where (mu) over bar vertical bar is the average of mu(1), mu(2), ..., mu(n). A subset M subset of V (G), in a graph G (V, E), is called a monopoly set of G if every vertex v is an element of (V - M) has at least d(v)/2 neighbors in M. The minimum cardinality of a monopoly set among all monopoly sets in G is called the monopoly size of G, denoted by mo(G) Ahmed Mohammed Naji and N.D.Soner [7] introduced minimum monopoly energy E-MM [G] of a graph G. In this paper we are introducing the minimum mean monopoly energy, denoted by E-MM(M) (G), of a graph G and computed minimum monopoly energies of some standard graphs. Upper and lower bounds for E-MM(M) (G)are also established.Publisher's Versio

    A Case of Critical Aortic Stenosis Masquerading as Acute Coronary Syndrome

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    Serum cardiac troponins I and T are reliable and highly specific markers of myocardial injury. Studies have shown that at least 20% of patients with severe aortic stenosis have detectable serum troponins. This case report describes a patient who presented as suspected acute coronary syndrome with markedly elevated troponin levels, who was later found to have normal coronaries and critical aortic stenosis. This case highlights the need for comprehensive and accurate physical examination in patients who present with angina. Critical aortic stenosis may cause such severe subendocardial ischemia as to cause marked elevation in cardiac markers and mimic an acute coronary syndrome. Careful physical examination will lead to an earlier use of non invasive techniques, such as echocardiography to confirm the correct diagnosis and the avoidance of inappropriate treatments such as intravenous nitroglycerin and glycoprotein IIb/IIIa inhibitors

    Additively Manufactured Carbon Fiber- Reinforced Thermoplastic Composite Mold Plates For Injection Molding Process

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    Polymer injection molding processes have been used to create high-volume parts quickly and efficiently. Injection molding uses mold plates that are traditionally made of very hard tool steels, such as P20 steel, which is extremely heavy and has very long lead times to build new molds. In this study, composite-based additive manufacturing (CBAM) was used to create mold plates using long-fiber carbon fiber and polyether ether ketone (PEEK). These mold plates were installed in an injection molding machine, and rectangular flat plates were produced using Lustran 348 acrylonitrile butadiene styrene (ABS). Tensile and flexural testing was performed on these parts as well as parts produced using traditional P20 steel mold plates with the same geometry to compare the performance of the different mold plates. The parts produced using the carbon fiber mold plates were within 5% of the tensile strength and 10% of the flexural strength of the traditionally manufactured parts. However, the parts produced using the carbon fiber mold plates required additional cooling time due to the lower conductivity of the carbon fiber composite compared to the P20 steel. This allows additively manufactured composite molds to be a good substitute for conventional molds in low-volume injection molding production

    In vitro and in silico characterization of an antimalarial compound with antitumor activity targeting human DNA topoisomerase IB

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    Human DNA topoisomerase IB controls the topological state of supercoiled DNA through a complex catalytic cycle that consists of cleavage and religation reactions, allowing the progression of fundamental DNA metabolism. The catalytic steps of human DNA topoisomerase IB were analyzed in the presence of a drug, obtained by the open-access drug bank Medicines for Malaria Venture. The experiments indicate that the compound strongly and irreversibly inhibits the cleavage step of the enzyme reaction and reduces the cell viability of three different cancer cell lines. Molecular docking and molecular dynamics simulations suggest that the drug binds to the human DNA topoisomerase IB-DNA complex sitting inside the catalytic site of the enzyme, providing a molecular explanation for the cleavage-inhibition effect. For all these reasons, the aforementioned drug could be a possible lead compound for the development of an efficient anti-tumor molecule targeting human DNA topoisomerase IB

    Creation of 3D Digital Anthropomorphic Phantoms which Model Actual Patient Non-rigid Body Motion as Determined from MRI and Position Tracking Studies of Volunteers

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    Background: Patient motion during emission imaging can create artifacts in the reconstructed emission distributions, which may mislead the diagnosis. For example, in myocardial-perfusion imaging, these artifacts can be mistaken for defects. Various software and hardware approaches have been developed to detect and compensate for motion. There are various ways of testing the effectiveness of motion correction methods applied in emission tomography, including the use of realistic digital anthropomorphic phantoms. Purpose: The purpose of this study was to create 3D digital anthropomorphic phantoms based on MRI data of volunteers undergoing a series of clinically relevant motions. These phantoms with combined position tracking were used to investigate both imaging-data-driven and motion tracking strategies to estimate and correct for patient motion. Methods: MRI scans were obtained of volunteers undergoing a series of clinically relevant movements. During the MRI, the motions were recorded by near-infra-red cameras tracking using external markers on the chest and abdomen. Individual-specific extended cardiac-torso (XCAT) phantoms were created fit to our volunteer MRI imaging data representing pre- and post-motion states. These XCAT phantoms were then used to generate activity and attenuation distributions. Monte Carlo methods will then be performed to simulate SPECT acquisitions, which will be used to evaluate various motion estimation and correction strategies. Results: Three volunteers were scanned in the MRI with concurrent external motion tracking. Each volunteer performed five separate motions including an axial slide, roll, shoulder twist, spine bend, and arm motion. These MRI scans were then manually digitalized into 3D anthropomorphic XCAT phantoms. Activity and attenuation distributions were created for each XCAT phantom, representing fifteen individual-specific motions. Conclusions: Our results will be combined with the external motion tracking data to determine if external motion tracking accurately reflects heart position in patients undergoing cardiac SPECT imaging. This data will also be used to evaluate other motion correction methods in the future

    Immune Regulation of Mammary Fibroblasts and the Impact of Mammographic Density

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    Mammographic density is associated with a 4–6-fold increase in breast cancer risk independent of age and BMI. High mammographic density is characterized by breast tissue with high proportions of stroma comprised of fibroblasts, collagen, and immune cells. This study sought to investigate whether stromal fibroblasts from high mammographic density breast tissue contributes to increased extracellular matrix deposition and pro-tumorigenic signaling. Mammary fibroblasts were isolated from women with high and low mammographic density and exposed to immune factors myeloperoxidase (MPO), eosinophil peroxidase (EPO), transforming growth factor beta 1 (TGFB1) and tumour necrosis factor alpha (TNFA) for 72 h and profiled for expression of cancer-associated fibroblast and extracellular matrix regulation markers. No differences in gene expression profiles or collagen production were observed between fibroblasts with high or low mammographic density, and they did not have a differential response to immune mediators. MPO and EPO significantly increased the production of collagen 1. TGFB and TNFA induced variable changes in gene expression. Fibroblasts cultured in vitro from women with high mammographic density do not appear to be inherently different to those from women with low mammographic density. The function of fibroblasts in mammographic density-associated breast cancer risk is likely to be regulated by immune signals from surrounding cells in the microenvironment.Maddison Archer, Pallave Dasari, David Walsh, Kara L. Britt, Andreas Evdokiou, and Wendy V. Ingma

    Lung Cancer in Pulmonary Fibrosis: Tales of Epithelial Cell Plasticity

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    Lung epithelial cells exhibit a high degree of plasticity. Alterations to lung epithelial cell function are critically involved in several chronic lung diseases such as pulmonary fibrosis. Pulmonary fibrosis is characterized by repetitive injury and subsequent impaired repair of epithelial cells, which leads to aberrant growth factor activation and fibroblast accumulation. Increased proliferation and hyper- and metaplasia of epithelial cells upon injury have also been observed in pulmonary fibrosis; this epithelial cell activation might represent the basis for lung cancer development. Indeed, several studies have provided histopathological evidence of an increased incidence of lung cancer in pulmonary fibrosis. The mechanisms involved in the development of cancer in pulmonary fibrosis, however, remain poorly understood. This review highlights recently uncovered molecular mechanisms shared between lung cancer and fibrosis, which extend the current evidence of a common trait of cancer and fibrosis, as provided by histopathological observations. Copyright (C) 2011 S. Karger AG, Base
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