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Relevant bibliographies by topics / Tumour necrosis; Cancer

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Academic literature on the topic 'Tumour necrosis; Cancer'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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Journal articles on the topic "Tumour necrosis; Cancer"

1

Balkwill, Frances. "Tumour necrosis factor and cancer." Nature Reviews Cancer 9, no. 5 (April 3, 2009): 361–71. http://dx.doi.org/10.1038/nrc2628.

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Waters, John P., Jordan S. Pober, and John R. Bradley. "Tumour necrosis factor and cancer." Journal of Pathology 230, no. 3 (June 7, 2013): 241–48. http://dx.doi.org/10.1002/path.4188.

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Balkwill, Frances R. "Tumour necrosis factor and cancer." Progress in Growth Factor Research 4, no. 2 (January 1992): 121–37. http://dx.doi.org/10.1016/0955-2235(92)90027-f.

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Szlosarek, Peter, Kellie A. Charles, and Frances R. Balkwill. "Tumour necrosis factor-α as a tumour promoter." European Journal of Cancer 42, no. 6 (April 2006): 745–50. http://dx.doi.org/10.1016/j.ejca.2006.01.012.

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Selby, P. J., S. Hobbs, C. Viner, E. Jackson, I. E. Smith, and T. J. Mcelwain. "ENDOGENOUS TUMOUR NECROSIS FACTOR IN CANCER PATIENTS." Lancet 331, no. 8583 (February 1988): 483. http://dx.doi.org/10.1016/s0140-6736(88)91286-x.

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Lui, Philip C. W., Yuen Shan Fan, Guiyan Xu, C. Y. Ngai, Kwok Pui Fung, Gary M. K. Tse, Alex M. C. Yu, and Jian Yi Li. "Apoptotic and necrotic effects of tumour necrosis factor-alpha potentiated with hyperthermia on L929 and tumour necrosis factor-alpha-resistant L929." International Journal of Hyperthermia 26, no. 6 (August 13, 2010): 556–64. http://dx.doi.org/10.3109/02656736.2010.486777.

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Aderka, Dan, Shimshon Fisher, Yoram Levo, Helmut Holtmann, Talia Hahn, and David Wallach. "CACHECTIN/TUMOUR-NECROSIS-FACTOR PRODUCTION BY CANCER PATIENTS." Lancet 326, no. 8465 (November 1985): 1190. http://dx.doi.org/10.1016/s0140-6736(85)92713-8.

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&NA;. "Recent advances in tumour necrosis factor in cancer." Inpharma Weekly &NA;, no. 770 (January 1991): 22–23. http://dx.doi.org/10.2165/00128413-199107700-00065.

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Trentin, L., R. Zambello, P. Bulian, A. Cerutti, C. Enthammer, M. Cassatella, D. Nitti, M. Lise, C. Agostini, and G. Semenzato. "Tumour-infiltrating lymphocytes bear the 75 kDa tumour necrosis factor receptor." British Journal of Cancer 71, no. 2 (February 1995): 240–45. http://dx.doi.org/10.1038/bjc.1995.50.

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Wigmore, S. J., D. N. Redhead, B. N. J. Thomson, E. J. Currie, R. W. Parks, K. K. Madhavan, and O. J. Garden. "Postchemoembolisation syndrome – tumour necrosis or hepatocyte injury?" British Journal of Cancer 89, no. 8 (October 2003): 1423–27. http://dx.doi.org/10.1038/sj.bjc.6601329.

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Dissertations / Theses on the topic "Tumour necrosis; Cancer"

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Naylor, Michael Stuart. "Tumour necrosis factor and ovarian cancer." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332896.

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Sampson, Louise E. "Investigations into the mechanism of action of tumour necrosis factor." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304660.

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Sagoo, Jasbir K. "Towards nuclear magnetic resonance studies of human tumour necrosis factor - alpha." Thesis, University of Nottingham, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335697.

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Leek, Russell D. "The role of tumour associated macrophages in breast cancer angiogenesis." Thesis, Oxford Brookes University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302449.

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Kahmann, Jan D. "Structural and functional studies on the link module from human TSG-6." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302067.

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Bossard, Maud. "The role of epithelial cell-derived tumour necrosis Factor Alpha in pancreatic carcinogenesis." Thesis, Queen Mary, University of London, 2012. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8563.

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Activating mutations of the kras proto-oncogene are found in more than 90% of human pancreatic ductal adenocarcinoma (PDAC) and can result in increased activity of the NF-κB pathway, leading to constitutive production of proinflammatory cytokines such as TNF-α. Pancreatic cancer progression occurs through a series of pre-invasive lesions, pancreatic intraepithelial neoplasias (PanIN lesions), which progress into invasive carcinoma. The aim of this thesis is to understand the autocrine role of TNF-α produced by premalignant epithelial cells in pancreatic tumour progression. This cytokine has already been shown to be involved in the progression of cancer. The major hypothesis therefore tested was that TNF-α secreted by pre-malignant epithelial cells promotes the early stages of pancreatic carcinogenesis by sustaining an inflamed microenvironment. In the spontaneous kras+/LSL-G12D; pdx1-cre mouse model of pancreatic cancer, concomitant genetic deletion of the TNF-α/IKK2 pathway substantially delayed pancreatic cancer progression and resulted in downregulation of the classical Notch target genes hes1 and hey1. Cell lines from the different PanIN bearing mice were established and used to dissect the cooperation between TNF-α/IKK2 and Notch signalling during PanIN progression. Optimal expression of Notch target genes was induced upon TNF-α stimulation of the canonical NF-κB signalling pathway, in cooperation with basal Notch signals. Mechanistically, TNF-α stimulation resulted in phosphorylation of histone H3 at the hes1 promoter and this signal was lost upon ikk2 genetic deletion. HES1 suppressed the expression of pparg, which encodes for the anti-inflammatory nuclear receptor PPAR-γ. Thus, crosstalk between TNF-α/IKK2 and Notch sustained an intrinsic inflammatory profile of the transformed cells. The treatment of PanIN bearing mice with rosiglitazone, a PPAR-γ agonist, also delayed PanIN progression. A malignant cell-autonomous, low-grade inflammatory process was shown to operate from the very early stages of kras-driven pancreatic carcinogenesis, which may cooperate with the Notch signalling pathway to promote pancreatic cancer progression.

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Fielding, David Ivor Keith. "Effects of interstitial laser photoagulation and photodynamic therapy on lung parenchyma." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264699.

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Chambers, George. "A study of the production of the selected cytokines interleukin 1, interleukin 6, and tumour necrosis factor by certain tumours and tumour cell lines." Thesis, University of Glasgow, 1996. http://theses.gla.ac.uk/4041/.

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An investigation was carried out to examine the production of the inflammatory cytokines IL1, IL1, IL6, TNF, and TNF in two tumour cell lines, the MCF-7 breast cell line and the T-24 bladder cell line, and in samples of breast, bladder, lung and ovarian tumours. Two methods were used to investigate cytokine production. These were the polymerase chain reaction method (PCR) to examine cytokine mRNA production and immuno-staining of frozen or paraffin-embedded tissue sections to demonstrate the presence of the cytokine polypeptide directly. In the PCR experiments, the most frequently found cytokine was IL6, followed by IL1. Only a few tumours of any type displayed TNF, and even fewer produced TNF. In the immunostaining experiments performed on frozen sections, IL1 and IL6 proteins were detected in sections of tumours which gave positive results with PCR. Cell phenotyping indicated that the IL1 and IL6 were probably being synthesised by the tumour cells themselves although there was lymphocyte infiltration in every section examined. In the immuno-histology study performed on the paraffin-embedded sections, a new collection of tumours was used. These tumours were not subjected to parallel PCR due to size of tumour samples being too small. The results obtained from these experiments conflicted with the results observed in the PCR study. IL1 was detected in all of the breast tumours used for immuno-histology but in none of the breast tumours in the PCR experiments. While the conflict could not definately be resolved, it was thought that the results of the immuno-histology experiments were more accurate as they detected expression of cytokine protein on a cellular scale. The immuno-histology experiments demonstrated that some tumour cells produced IL1 in breast and bladder carcinomas, and some produced IL6 in breast and lung carcinomas.

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Pusztai, Lajos. "Regulation of the growth of human breast cancer by tumour necrosis factor-alpha." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333180.

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Mohamed, Ahmed A. A. "Cross-talk between kinases and proteases in tumour necrosis factor-#alpha# receptor subtype-induced apoptosis." Thesis, University of Aberdeen, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274797.

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Firstly, we demonstrated that caspase-dependent cell death was enhanced by the over-expression of the type II TNF receptor (TNFR2). HeLa cells, which naturally express high levels of type I TNF receptor (TNFR1) and low levels of TNFR2, were engineered to stably over-express TNFR2. This combined with the use of genetically-engineered mutated TNFs that preferentially activate TNFR1 or TNFR2, we showed that both receptors can induce cell death, although this process occurred predominantly through TNFR1. TNF-induced cell death was inhibited by the stable expression of cytokine response modifier A (CrmA), a potent inhibitor of receptor proximal caspases. By isolating early apoptotic cells, we were able to identify differential activation profiles of members of the mitogen-activated protein kinase (MAPK) family during TNF-induced apoptosis. In dying HeLa-TNFR2 cells, there was increased activation of c-Jun NH₂-terminal kinase (JNK) while the activation levels of p38 MAPK and p42/44 MAPK remained unchanged. The use of peptidergic caspase inhibitors demonstrated that caspase-dependent modulation of JNK but not p38 MAPK or p42/44 MAPK takes place, and as such may provide a mechanism which accounts for the differences observed in MAPK activity during TNF-induced cell death. Through expression of a dominant negative upstream activator of JNK (SEK-1-AL) and a pharmacological inhibitor of JNK activity, we were able to determine the role of JNK activation in TNF receptor-mediated apoptosis. These findings clearly demonstrate that through cross-talk, TNF receptors, are able to further modulate the tightly regulate cellular consequences of TNF treatment and that JNK is a TNF-induced kinase that may play a role in the cytokine’s apoptotic cellular signalling.

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Books on the topic "Tumour necrosis; Cancer"

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service), SpringerLink (Online, ed. Death receptors and cognate ligands in cancer. Heidelberg: Springer, 2009.

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Dworkin, Chaim R. The use of growth factors in cancer therapy. [Bethesda, Md.?]: U.S. DHHS, PHS, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1993.

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Kalthoff, Holger. Death Receptors and Cognate Ligands in Cancer. Springer, 2012.

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Death Receptors in Cancer Therapy (Cancer Drug Discovery and Development). Humana Press, 2004.

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Book chapters on the topic "Tumour necrosis; Cancer"

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Bast, R. C., J. Wiener, S. Kassim, S. Wu, C. M. Boyer, K. De Sombre, J. A. Hurteau, G. Rodriguez, G. B. Mills, and A. Berchuck. "Cell growth regulation in ovarian cancer: tyrosine kinases, tyrosine phosphatases and tumour necrosis factor-α." In Ovarian Cancer 3, 109–13. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4757-0136-4_11.

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Chu, Wen-Ming. "Tumor Necrosis Factor." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_6040-8.

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Chu, Wen-Ming. "Tumor Necrosis Factor." In Encyclopedia of Cancer, 4679–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_6040.

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Zimmermann, Arthur. "Necrobiology of Liver Cancer: Necrosis and Necroptosis." In Tumors and Tumor-Like Lesions of the Hepatobiliary Tract, 1–8. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26587-2_178-1.

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Zimmermann, Arthur. "Necrobiology of Liver Cancer: Necrosis and Necroptosis." In Tumors and Tumor-Like Lesions of the Hepatobiliary Tract, 3263–70. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26956-6_178.

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De Witte, Mark, David J. Shealy, Marian T. Nakada, and G. Mark Anderson. "Tumor Necrosis Factor and Cancer." In Cytokines in the Genesis and Treatment of Cancer, 71–89. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-455-1_4.

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Palladino, Michael A., and Arthur J. Ammann. "Tumor Necrosis Factors Alpha and Beta." In Leukolysins and Cancer, 235–44. Totowa, NJ: Humana Press, 1988. http://dx.doi.org/10.1007/978-1-4612-4586-5_13.

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Ammann, Arthur J., and Michael A. Palladino. "Biologic Effects of Tumor Necrosis Factors Alpha and Beta." In Leukolysins and Cancer, 303–11. Totowa, NJ: Humana Press, 1988. http://dx.doi.org/10.1007/978-1-4612-4586-5_16.

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Lopez, J. J. Bosco, M. Escobar, P. Gallurt, P. Rodriguez, A. Lorenzo, A. Morán, A. Senra, and J. Millán. "Tumor necrosis factor alpha: its relationship with clinical data." In Cancer Treatment An Update, 765–69. Paris: Springer Paris, 1994. http://dx.doi.org/10.1007/978-2-8178-0765-2_162.

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Crescimanno, M., N. Borsellino, V. Leonardi, L. Rausa, and N. D’Alessandro. "Effects of Tumor Necrosis Factor-Alpha on Growth and Doxorubicin Sensitivity of Multidrug Resistant Tumor Cell Lines." In Cancer Therapy, 201–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84613-7_16.

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Conference papers on the topic "Tumour necrosis; Cancer"

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Morrow, ES, F. Gujam, Z. Mohammed, DC McMillan, PG Horgan, AK Roseweir, and J. Edwards. "Abstract P2-08-23: A combined score of tumour budding and tumour necrosis has prognostic value for cancer specific survival in both ER positive and ER negative primary operable breast cancer." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p2-08-23.

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Kang, K., SR Lee, X. Piao, HS Byun, SR Lee, M. Won, KA Park, and GM Hur. "PO-063 Triterpenoids isolated from natural product regulates TNF(tumour necrosis factor)-mediated RIP(receptor-interacting serine/threonine-protein kinase)1-dependent apoptosis." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.107.

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Primak, Svetlana V., Yuan Le, Kevin J. Glaser, Carol A. Reynold, Jinping Lai, Lewis R. Roberts, Philip J. Rossman, Joel P. Felmlee, and Richard L. Ehman. "Magnetic Resonance Elastography Assessment of Focused Ultrasound Surgery in Cancer Models: A Pilot Study." In ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-16010.

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MRI guided focused ultrasound (FUS) has been shown to create thermal lesions where tissue stiffness changes significantly. To assess the correlation between tissue stiffness change and tissue ablation, a pilot animal based study was conducted to treat LNCaP tumors in vivo and Hep3B tumors immediately post mortem. MR elastography was used to analyze tissue stiffness before and after ablation. Treated tissue was excised immediately after each experiment and processed by routine histological analysis. Four prostate cancer tumors and four liver cancer tumors showed, on average, a threefold increase in stiffness due to FUS thermal treatment. Histology showed complete (100%) coagulation necrosis in these cases. These data suggest that MRE may be an effective means to assess tissue ablation.

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Han, Bumsoo, Matthew D. Egberg, Pung-Pung Haung, David J. Swanlund, and John C. Bischof. "Cryoinjury Enhancement of Breast Cancer Cells by Use of a Molecular Adjuvant (TNF-alpha)." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61593.

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Cryoinjury of human breast cancer cells (MCF7) in engineered tissue equivalents and the enhancement of the cryoinjury by use of a molecular adjuvant (tumor necrosis factor alpha, TNF-α) was studied. Tissue equivalents (TEs) were constructed by seeding MCF7 cells in collagen solutions at the concentration of 100,000 cells/ml. After cultured in vitro for 2 days, the TEs were exposed with 100ng/ml TNF-α and cultured for 24 hours, and then underwent a single freeze-thaw cycle by a cryosurgery simulator. With the concentration and duration of TNF-α treatment studied, no apoptotic or necrotic cell death was observed by the administration of TNF-α only. After a freeze/thaw, MCF7 cells within the frozen region of the TEs were significantly injured immediately (i.e. ≤ 20% survival), but gradually repopulated and reached approximately 80% survival in Day3 without TNF-α pre-treatment. MCF7 with TNF-α pre-treatment showed the slight enhancement of immediate injury in the frozen region (i.e. ≤ 10% survival), and the repopulation was significantly inhibited so the viability remained below 40% even in Day 3. These results imply that TNF-α can be a potent adjuvant for cryosurgery.

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Zhang, Aili, Xipeng Mi, and Lisa X. Xu. "Study of Thermally Targeted Nano-Particle Drug Delivery for Tumor Therapy." In ASME 2008 First International Conference on Micro/Nanoscale Heat Transfer. ASMEDC, 2008. http://dx.doi.org/10.1115/mnht2008-52383.

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The efficacy of cancer chemotherapeutics could be greatly enhanced by thermally targeted nanoparticle liposome drug delivery system. The tumor microvasculature response to hyperthermia and its permeability to the nano-liposomes were studied using the 4T1 mouse model and confocal fluorescence microscopy. Based on the experimental results, a new theoretical model was developed to describe the distributions of both the liposomal and free drug released as liposomes broke in tumor for treatment evaluation. In this model, the tumor was divided into two regions: peripheral and central. The drug effect on the tumor cell apoptosis and necrosis was considered. Upon the experimental validation, the model was used to simulate drug distribution in the tumor under either the hyperthermic or the alternate freezing and heating condition. Results showed that hyperthermia alone only enhanced drug accumulation in the tumor periphery and therefore more serious tumor damage induced in the region. But the tumor cells in the central region were hardly damaged due to the lack of drug diffusion. The alternate freezing and heating was proposed to aid the nanoliposomal drug delivery, and better results were found.

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Rivas, MA, M. Tkach, CJ Proietti, C. Rosemblit, W. Beguelin, V. Sundblad, MC Díaz Flaqué, EH Charreau, PV Elizalde, and R. Schillaci. "Tumor necrosis factor transactivates ErbB2 in breast cancer cells." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-4056.

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Pandey, Ajit K., Isaac Chang, Matthew R. Myers, and Rupak K. Banerjee. "Finite Element Analysis of Radio-Frequency Ablation in a Reconstructed Realistic Hepatic Geometry." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32046.

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Radio-frequency (RF) ablation is a minimally invasive procedure that has the potential for widespread use in hepatic cancer therapy. In the procedure, RF current is applied to the tissue, resulting in the conversion of electrical to heat energy and thus, a rise in temperature, with the goal of eventual tumor necrosis. Potential complications from the procedure include insufficient heating of large tumors, resulting in tumor recursion, as well as excessive thermal damage to healthy tissue. Mathematical models are valuable in predicting the temperature rise within the organ during RF ablation, thereby enhancing the success rate of the procedure. Eventually, models can be used to guide ablation procedures, by predicting the optimal set of operational parameters e.g., catheter probe geometry and placement, given patient-specific information. The present study focuses on the analysis of temperature rise within a reconstructed model of a realistic three-dimensional (3D) section of a porcine liver during RF ablation. This study calculates the effect of blood flow through arteries as well as perfusion through the liver on the time-dependent temperature distribution near the RF ablation probe (Figure 1). For a time duration of 30 min of an ablation procedure, a temperature of about 80°C could be achieved over a diameter of about 4 cm with the present RF probe. As an initial step, the present study includes isotropic hepatic tissue and blood properties.

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Kitadai, Yasuhiko, Yi Luo, Hitoshi Ohmori, Kiyomu Fujii, Tomonori Sasahira, Yoshitomo Chihara, and Hiroki Kuniyasu. "Abstract 2365: Cancer cell necrosis induces tumor growth by releasing HMGB1." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2365.

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Kalra, Jessica, Jennifer Baker, Alastair Kyle, Andrew Minchinton, and Marcel Bally. "Abstract B54: Location of tumor burden influences tumor and vascular architecture, necrosis, and nanoparticle delivery." In Abstracts: AACR Special Conference: Advances in Breast Cancer; October 17-20, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.advbc15-b54.

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Boies, Adam, Pingyan Lei, Jeff Roberts, and Steven Girshick. "Gas-Phase Production of Multifunctional Composite Nanoparticles by Photoinduced Chemical Vapor Deposition." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13181.

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Nano-scale materials and devices allow for unique interactions that are not possible at larger scales. Magnetic particles below a critical size (∼10 nm) demonstrate distinctive behavior known as superparamagnetism, where particles do not exhibit any net magnetic force outside the presence of an external magnetic field. However, within an alternating magnetic field, as in a magnetic resonance imaging (MRI) machine, superparamagnetic particles give off heat as a result of Brownian and Nee´lian relaxation. Heat produced by the shifting pole orientation can raise the temperature of the tissue sufficient to cause cell death through necrosis or apoptosis [1]. Additionally, combinations of electrically conductive and insulating materials within a single nanoparticle give rise to surface plasmon resonance. The resonance of the plasmon absorption can be tuned based on the relative thicknesses of the two layers. These particles can be used to thermally ablate cancer cells if the resonance is tuned to absorb light from an infrared laser. The penetrating ability of the nanoparticles combined with their capacity to kill cells make them excellent candidates for treatment of conditions such as brain tumors and prostate cancer.

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Reports on the topic "Tumour necrosis; Cancer"

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Behbakht, Kian. Modulators of Response to Tumor Necrosis-Related Apoptosis-Inducing Ligand (TRAIL) Therapy in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2008. http://dx.doi.org/10.21236/ada486929.

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Behbakht, Kian. Modulators of Response to Tumor Necrosis-Related Apoptosis-Inducing Ligand (TRAIL) Therapy in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada508266.

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Behbakht, Kian. Modulators of Response to Tumor Necrosis-Factor-Related Apoptosis Inducing Ligand (TRAIL) Therapy in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2010. http://dx.doi.org/10.21236/ada532993.

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