15 research outputs found

    Simulation techniques in an artificial society model

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    Artificial society refers to a generic class of agent-based simulation models used to discover global social structures and collective behavior produced by simple local rules and interaction mechanisms. Artificial society models are applicable in a variety of disciplines, including the modeling of chemical and biological processes, natural phenomena, and complex adaptive systems. We focus on the underlying simulation techniques used in artificial society discrete-event simulation models, including model time evolution and computational performance.;Although for some applications synchronous time evolution is the correct modeling approach, many other applications are better represented using asynchronous time evolution. We claim that asynchronous time evolution can eliminate potential simulation artifacts produced using synchronous time evolution. Using an adaptation of a popular artificial society model, we show that very different output can result based solely on the choice of asynchronous or synchronous time evolution. Based on the event list implementation chosen, the use of discrete-event simulation to incorporate asynchronous time evolution can incur a substantial loss in computational performance. Accordingly, we evaluate select event list implementations within the artificial society simulation model and demonstrate that acceptable performance can be achieved.;In addition to the artificial society model, we show that transforming from a synchronous to an asynchronous system proves beneficial for scheduling resources in a parallel system. We focus on non-FCFS job scheduling policies that permit jobs to backfill, i.e., to move ahead in the queue, given that they do not delay certain previously submitted jobs. Instead of using a single queue of jobs, we propose a simple yet effective backfilling scheduling policy that effectively separates short from long jobs by incorporating multiple queues. By monitoring system performance, our policy adapts its configuration parameters in response to severe changes in the job arrival pattern and/or resource demands. Detailed performance comparisons via simulation using actual parallel workload traces indicate that our proposed policy consistently outperforms traditional backfilling in a variety of contexts

    Epstein-Barr virus, human papillomavirus and mouse mammary tumour virus as multiple viruses in breast cancer

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    Background: The purpose of this investigation is to determine if Epstein Barr virus (EBV), high risk human papillomavirus (HPV), and mouse mammary tumour viruses (MMTV) co-exist in some breast cancers. Materials and Methods: All the specimens were from women residing in Australia. For investigations based on standard PCR, we used fresh frozen DNA extracts from 50 unselected invasive breast cancers. For normal breast specimens, we used DNA extracts from epithelial cells from milk donated by 40 lactating women. For investigations based on in situ PCR we used 27 unselected archival formalin fixed breast cancer specimens and 18 unselected archival formalin fixed normal breast specimens from women who had breast reduction surgery. Thirteen of these fixed breast cancer specimens were ductal carcinoma in situ (dcis) and 14 were predominantly invasive ductal carcinomas (idc). Results: EBV sequences were identified in 68%, high risk HPV sequences in 50%, and MMTV sequences in 78% of DNA extracted from 50 invasive breast cancer specimens. These same viruses were identified in selected normal and breast cancer specimens by in situ PCR. Sequences from more than one viral type were identified in 72% of the same breast cancer specimens. Normal controls showed these viruses were also present in epithelial cells in human milk - EBV (35%), HPV, 20%) and MMTV (32%) of 40 milk samples from normal lactating women, with multiple viruses being identified in 13% of the same milk samples. Conclusions: We conclude that (i) EBV, HPV and MMTV gene sequences are present and co-exist in many human breast cancers, (ii) the presence of these viruses in breast cancer is associated with young age of diagnosis and possibly an increased grade of breast cancer.10 page(s

    Positive EBNA, CD 15 and LMP1 expression in the same invasive ductal carcinoma breast cancer specimen.

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    <p><b>Panel A.</b> Positive EBNA1 expression. <b>Panel B.</b> Positive CD15 expression. <b>Panel C.</b> Positive LMP1 expression. It is not possible to determine whether these cells are Reed Sternberg or granuloma cells.</p

    Variable sequence region of Epstein-Barr viral PCR products compared to the EBV genome (B95-8 strain).

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    <p>EBV, EBV genome; Raji DNA used as a positive control; A1-4 sequences are based on DNA extracts from archival formalin fixed invasive ductal carcinoma (<i>idc</i>) breast cancer specimens; B1-6 sequences are based on DNA extracts from fresh frozen <i>idc</i> breast cancer specimens. M1-2 sequences are from normal breast epithelial cell (milk) DNA extracts. The alignment of sequences demonstrates the high level of nucleotide homology between the EBV genome, the Raji EBV positive control and EBV identified by standard PCR in fixed, fresh <i>idc</i> breast cancer specimens, and normal breast specimens.</p

    HPV and EBV identified by in situ PCR in the same breast cancer cell nuclei – Ductal carcinoma in situ.

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    <p>A.HPV (inner nested primers X 200). B. HPV (outer nested primers X 400). C. HPV (inner nested primers X 400). D. EBV (inner nested primers X 200). E. EBV (outer nested primers X 400). F. EBV (inner nested primers X 400). G. MMTV negative (inner nested primers X 200). H. Negative control (no primers X 200).</p

    EBV, HPV, and MMTV positive and negative according to patient and breast cancer characteristics.

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    <p>These data are based on DNA extracts from 50 fresh frozen invasive breast tumours. There are small variations in the numbers of specimens analysed for each virus because of inadequate outcomes of some analyses based on standard PCR. The p values based on the Chi – square test are for differences in the presence of viruses between grades of breast cancer. The p values are not included for data based on immunohistochemistry because of low numbers.</p><p>These data indicate: (i) patients with HPV, EBV and MMTV positive breast cancer are significantly younger than patients with viral negative breast cancer, (ii) there is a non-significant increase in grade of EBV and MMTV positive breast cancer, (iii) the expression of apoptopic p53 protein is not inhibited in HPV positive breast cancer as it is in HPV positive cervical cancer.</p

    EBV, HPV and MMTV identified in the same ductal carcinoma <i>in situ</i> specimen by <i>in situ</i> PCR.

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    <p>A.EBV positive, B. HPV positive, C. MMTV positive, D. Negative control – no primer, E. Negative control -no Taq. HPV associated koilocytes are present in B.All photographs were taken with a 20X objective and have been cropped. Variations in colour detection can be seen when the <i>in-situ</i> PCR was done at a different time.</p

    Putative Reed Sternberg cells in ductal carcinoma <i>in situ</i> (by immunohistochemistry).

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    <p><b>Panel A.</b> Positive EBNA 1 expression in a putative Reed Sternberg cells. <b>Panel B.</b> Positive CD 15 expression in putative Reed Sternberg cells. It is not possible to determine whether these cells are Reed Sternberg or granuloma cells.</p

    Typical nested PCR amplification for EBV, HPV and MMTV.

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    <p>A. EBV PCR for the second round of amplification of a 209 bp fragment from DNA extracted from 9 breast cancer specimens, B is the no DNA control, Raji DNA as a positive control (+) and M is a size ladder from Puc Hinf1. (12). B. HPV PCR for the second round amplification of a 148 bp fragment from 10 breast DNA extractions. RB is the reagent control,(+ ) is the positive control from Hela DNA containing HPV 18, B1 is a first round no DNA control for the PCR, B2 is a second round no DNA control. C. MMTV PRC for the second round of amplification of a 643 bp fragment from DNA extracted from 8 patient samples. RB is the reagent blank. (+) is the positive control of DNA extracted from mouse tails. B1 is the first round no DNA control, subjected to a second round of PCR. D. Typical <i>b-globin</i> PCR (single amplification) for 6 breast archival specimens showing the integrity of the DNA. + is a positive control from Hela DNA, B is the no DNA control.</p
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