9 research outputs found

    Ultra High Strength Steels for Roll Formed Automotive Body in White

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    One of the more recent steel developments is the quenching and partitioning process, first proposed by Speer et al. in 2003 on developing 3rd generation advanced high-strength steel (AHSS). The quenching and partitioning (Q&P) process set a new way of producing martensitic steels with enhanced austenite levels, realised through controlled thermal treatments. The main objective of the so-called 3rd generation steels was to realise comparable properties to the 2nd generation but without high alloying additions. Generally, Q&P steels have remained within lab-scale environments, with only a small number of Q&P steels produced industrially. Q&P steels are produced either by a one-step or two-step process, and the re-heating mechanism for the two-step adds additional complexities when heat treating the material industrially. The Q&P steels developed and tested throughout this thesis have been designed to achieve the desired microstructural evolution whilst fitting in with Tata’s continuous annealing processing line (CAPL) capabilities. The CALPHAD approach using a combination of thermodynamics, kinetics, and phase transformation theory with software packages ThermoCalc and JMatPro has been successfully deployed to find novel Q&P steels. The research undertaken throughout this thesis has led to two novel Q&P steels, which can be produced on CAPL without making any infrastructure changes to the line. The two novel Q&P steels show an apparent reduction in hardness mismatch, illustrated visually and numerically after nano-indentation experiments. The properties realised after Q&P heat treatments on the C-Mn-Si alloy with 0.2 Wt.% C and the C-Mn-Si alloy with the small Cr addition is superior to the commercially available QP980/1180 steels by BaoSteel. Both novel alloys had comparable levels of elongation and hole expansion ratio to QP1180 but are substantially stronger with a > 320MPa increase in tensile stress. The heat treatment is also less complex as there is no requirement to heat the steel back up after quenching due to one-step quenching and partitioning being employed on the novel alloys

    Genome co-amplification upregulates a mitotic gene network activity that predicts outcome and response to mitotic protein inhibitors in breast cancer.

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    BACKGROUND: High mitotic activity is associated with the genesis and progression of many cancers. Small molecule inhibitors of mitotic apparatus proteins are now being developed and evaluated clinically as anticancer agents. With clinical trials of several of these experimental compounds underway, it is important to understand the molecular mechanisms that determine high mitotic activity, identify tumor subtypes that carry molecular aberrations that confer high mitotic activity, and to develop molecular markers that distinguish which tumors will be most responsive to mitotic apparatus inhibitors. METHODS: We identified a coordinately regulated mitotic apparatus network by analyzing gene expression profiles for 53 malignant and non-malignant human breast cancer cell lines and two separate primary breast tumor datasets. We defined the mitotic network activity index (MNAI) as the sum of the transcriptional levels of the 54 coordinately regulated mitotic apparatus genes. The effect of those genes on cell growth was evaluated by small interfering RNA (siRNA). RESULTS: High MNAI was enriched in basal-like breast tumors and was associated with reduced survival duration and preferential sensitivity to inhibitors of the mitotic apparatus proteins, polo-like kinase, centromere associated protein E and aurora kinase designated GSK462364, GSK923295 and GSK1070916, respectively. Co-amplification of regions of chromosomes 8q24, 10p15-p12, 12p13, and 17q24-q25 was associated with the transcriptional upregulation of this network of 54 mitotic apparatus genes, and we identify transcription factors that localize to these regions and putatively regulate mitotic activity. Knockdown of the mitotic network by siRNA identified 22 genes that might be considered as additional therapeutic targets for this clinically relevant patient subgroup. CONCLUSIONS: We define a molecular signature which may guide therapeutic approaches for tumors with high mitotic network activity

    Additional file 1: Tables S1, Tables S2, Tables S3 and Tables S4. of Genome co-amplification upregulates a mitotic gene network activity that predicts outcome and response to mitotic protein inhibitors in breast cancer

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    Table S1. List of genes that are significantly correlated with either PLK1, CENPE or AURKB in breast cancer cell lines and used for constructing gene network. Table S2. Gene ontology (GO) analysis of genes significantly correlated with PLK1, CENPE or AURKB in human breast cancer cell lines. Table S3. Mitotic network gene list. Table S4. Pearson coefficients for correlation (and significance) between cell line responses across 53 breast cell lines derived from tumor and normal tissues. The number of lines used to establish the correlation is listed below each correlation in parentheses. (DOC 282 kb