30 research outputs found

    Compensation of deep drawing tools for springback and tool-deformation

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    Manual tool reworking is one of the most time-consuming stages in the\ud preparation of a deep drawing process. Finite Elements (FE) analyses are now widely\ud applied to test the feasibility of the forming process, and with the increasing accuracy of the\ud results, even the springback of a blank can be predicted. In this paper, the results of an FE\ud analysis are used to carry out tool compensation for both springback and tool/press\ud deformations. Especially when high-strength steels are used, or when large body panels are\ud produced, tool compensation in the digital domain helps to reduce work and save time in the\ud press workshop. A successful compensation depends on accurate and efficient FE-prediction,\ud as well as a flexible and process-oriented compensation algorithm. This paper is divided in\ud two sections. The first section deals with efficient modeling of tool/press deformations, but\ud does not discuss compensation. The second section is focused on springback, but here the\ud focus is on the compensation algorithm instead of the springback phenomenon itself

    Compensating springback in the automotive practice using MASHAL

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    Iterative springback compensation of NUMISHEET benchmark #1

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    Upon unloading after the forming stage, a sheet metal product will spring back due to internal stresses. Springback\ud is a major problem for process-planning engineers. In industrial practise, deformations due to springback are compensated\ud manually, by doing extensive measurements on prototype parts, and altering the tool geometry by hand. This is a time\ud consuming and costly operation. In this paper the application of two compensation algorithms, based on the finite element\ud simulation of the forming process are discussed. The smooth displacement adjustment (SDA) method and the springforward\ud (SF) method have been applied to several industrial products, such as the NUMISHEET 2005 benchmark#1. With the SDA\ud method successful compensations have been carried out. For the SF method some principal problems remain

    Compensating springback in the automotive practice\ud using MASHAL

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    New materials are used in the automotive industry to reduce weight and to improve crash performance. These\ud materials feature a higher ratio of yield stress to elastic modulus leading to increased springback after tool release. The resulting\ud shape deviations and their efficient reduction is of major interest for the automotive industry nowadays. The usual strategies for\ud springback reduction can diminish springback to a certain amount only. In order to reduce the remaining shape deviation a\ud mathematical compensation algorithm is presented. The objective is to obtain the tool geometry such that the part springs back\ud into the right shape after releasing the tools.\ud In practice the process of compensation involves different tasks beginning with CAD construction of the part, planning the\ud drawing method and tool construction, FE-simulation, deep drawing at try-out stage and measurement of the manufactured part.\ud Thus the compensation can not be treated as an isolated task but as a process with various restrictions and requirements of\ud today’s automotive practice. For this reason a software prototype for compensation methods MASHAL – meaning program to\ud maintain accuracy (MASsHALtigkeit) – was developed. The basic idea of compensation with MASHAL is the transfer and\ud application of shape deviations between two different geometries on a third one. The developed algorithm allows for an effective\ud processing of these data, an approximation of springback and shape deviations and for a smooth extrapolation onto the tool\ud geometry.\ud Following topics are addressed: positioning of parts, global compensation and restriction of compensation to local areas,\ud damping of the compensation function in the blank holder domain, simulation and validation of springback and compensation of\ud CAD-data. The complete compensation procedure is illustrated on an industrial part

    Springback Compensation: Fundamental Topics and Practical Application

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    Now that the simulation of deep drawing processes has become more reliable the virtual\ud compensation of the forming tools has become reality. In literature, the Displacement Adjustment (DA)\ud algorithm has proved to be most effective. In this article it is shown how the compensation factor, required for\ud (one-step) DA depends on material, process and geometrical parameters. For this an analytical bar stretchbending\ud model was used. A compensation factor is not required when DA is applied iteratively and the\ud products geometrical accuracy is improved further. This was demonstrated on an industrial part. The\ud compensation varies over the product, leading to a reduction in shape deviation of 90% and more, a result that\ud could not have been achieved with one-step compensatio

    The development of a finite elements based springback compensation tool for sheet metal products

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    Springback is a major problem in the deep drawing process. When the tools are released after the forming stage, the product springs back due to the action of internal stresses. In many cases the shape deviation is too large and springback compensation is needed: the tools of the deep drawing process are changed so, that the product becomes geometrically accurate after springback. In this paper, two different ways of geometric optimization are presented, the smooth displacement adjustment (SDA) method and the surface controlled overbending (SCO) method. Both methods use results from a finite elements deep drawing simulation for the optimization of the tool shape. The methods are demonstrated on an industrial product. The results are satisfactory, but it is shown that both methods still need to be improved and that the FE simulation needs to become more reliable to allow industrial application

    HIV's evasion of the cellular immune response

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    Despite a strong cytotoxic T-lymphocyte (CTL) response directed against viral antigens, untreated individuals infected with the human immunodeficiency virus (HIV-1) develop AIDS, We have found that primary T cells infected with HIV-1 downregulate surface MHC class I antigens and are resistant to lysis by HLA-A2-restricted CTL clones. In contrast, cells infected with an HIV-1 in which the nef gene is disrupted are sensitive to CTLs in an MHC and peptide-specific manner. In primary T cells HLA-A2 antigens are downmodulated more dramatically than total MHC class I antigens, suggesting that nef selectively downmodulates certain MHC class I antigens. In support of this, studies on ceils expressing individual MHC class I alietes have revealed that nef does not downmodulate HLA-C and HLA-E antigens, This selective downmodulation allows Infected cells to maintain resistance to certain natural killer cells that lyse infected cells expressing low levels of MHC class I antigens. Downmodulation of MHC class I HLA-A2 antigens occurs not only in primary T cells, but also in B and astrocytoma cell lines. No effect of other HIV-1 accessory proteins such as vpu and vpr was observed. Thus Nef is a protein that may promote escape of HIV-1 from immune surveillance.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75570/1/j.1600-065X.1999.tb01283.x.pd

    Single amino acid change in gp41 region of HIV-1 alters bystander apoptosis and CD4 decline in humanized mice

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    <p>Abstract</p> <p>Background</p> <p>The mechanism by which HIV infection leads to a selective depletion of CD4 cells leading to immunodeficiency remains highly debated. Whether the loss of CD4 cells is a direct consequence of virus infection or bystander apoptosis of uninfected cells is also uncertain.</p> <p>Results</p> <p>We have addressed this issue in the humanized mouse model of HIV infection using a HIV variant with a point mutation in the gp41 region of the Env glycoprotein that alters its fusogenic activity. We demonstrate here that a single amino acid change (V38E) altering the cell-to-cell fusion activity of the Env minimizes CD4 loss in humanized mice without altering viral replication. This differential pathogenesis was associated with a lack of bystander apoptosis induction by V38E virus even in the presence of similar levels of infected cells. Interestingly, immune activation was observed with both WT and V38E infection suggesting that the two phenomena are likely not interdependent in the mouse model.</p> <p>Conclusions</p> <p>We conclude that Env fusion activity is one of the determinants of HIV pathogenesis and it may be possible to attenuate HIV by targeting gp41.</p

    Transcriptional Profiling in Pathogenic and Non-Pathogenic SIV Infections Reveals Significant Distinctions in Kinetics and Tissue Compartmentalization

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    Simian immunodeficiency virus (SIV) infection leads to AIDS in experimentally infected macaques, whereas natural reservoir hosts exhibit limited disease and pathology. It is, however, unclear how natural hosts can sustain high viral loads, comparable to those observed in the pathogenic model, without developing severe disease. We performed transcriptional profiling on lymph node, blood, and colon samples from African green monkeys (natural host model) and Asian pigtailed macaques (pathogenic model) to directly compare gene expression patterns during acute pathogenic versus non-pathogenic SIV infection. The majority of gene expression changes that were unique to either model were detected in the lymph nodes at the time of peak viral load. Results suggest a shift toward cellular stress pathways and Th1 profiles during pathogenic infection, with strong and sustained type I and II interferon responses. In contrast, a strong type I interferon response was initially induced during non-pathogenic infection but resolved after peak viral load. The natural host also exhibited controlled Th1 profiles and better preservation of overall cell homeostasis. This study identified gene expression patterns that are specific to disease susceptibility, tissue compartmentalization, and infection duration. These patterns provide a unique view of how host responses differ depending upon lentiviral infection outcome
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