Relevant bibliographies by topics / Immunology, Experimental

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Immunology, Experimental'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Immunology, Experimental"

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Embleton, M. J. "Immunology of experimental oncogenesis." Current Opinion in Immunology 1, no. 5 (June 1989): 867–71. http://dx.doi.org/10.1016/0952-7915(89)90062-9.

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Pasqualini, Christiane, Raul Ruggiero, Oscar Bustuoabad, Irene Nepomnaschy, and Isabel Piazzon. "Experimental Onco-Immunology Revisited." Current Cancer Therapy Reviews 1, no. 3 (November 1, 2005): 289–98. http://dx.doi.org/10.2174/157339405774574225.

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Denman, A. "Handbook of Experimental Immunology." Journal of Clinical Pathology 41, no. 1 (January 1, 1988): 118–19. http://dx.doi.org/10.1136/jcp.41.1.118-b.

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Chase, Merrill W. "Immunology and Experimental Dermatology." Annual Review of Immunology 3, no. 1 (April 1985): 1–30. http://dx.doi.org/10.1146/annurev.iy.03.040185.000245.

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Behan, Wilhelmina M. H. "Handbook of experimental immunology." Journal of Neuroimmunology 15, no. 2 (June 1987): 217–18. http://dx.doi.org/10.1016/0165-5728(87)90095-6.

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Emmrich, Frank. "Handbook of experimental immunology." Immunology Today 7, no. 12 (December 1986): 384–85. http://dx.doi.org/10.1016/0167-5699(86)90032-0.

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WEIL, RICHARD. "Transplantation Immunology: Clinical and Experimental." Archives of Surgery 120, no. 12 (December 1, 1985): 1399. http://dx.doi.org/10.1001/archsurg.1985.01390360059016.

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Horwitz, David L. "Immunology of Clinical and Experimental Diabetes." JAMA: The Journal of the American Medical Association 253, no. 8 (February 22, 1985): 1182. http://dx.doi.org/10.1001/jama.1985.03350320108034.

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Roggero, Eduardo, Ana R. Pérez, Oscar A. Bottasso, Hugo O. Besedovsky, and Adriana Del Rey. "Neuroendocrine-immunology of Experimental Chagas' Disease." Annals of the New York Academy of Sciences 1153, no. 1 (February 2009): 264–71. http://dx.doi.org/10.1111/j.1749-6632.2008.03982.x.

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Shortman, Ken. "The experimental foundations of modern immunology." Immunology Today 13, no. 1 (January 1992): 39. http://dx.doi.org/10.1016/0167-5699(92)90206-m.

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Dissertations / Theses on the topic "Immunology, Experimental"

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Andrén, Maria. "The Role of Fc Gamma Receptors in Experimental Arthritis." Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4724.

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Induction of collagen-induced arthritis (CIA), an animal model for human rheumatoid arthritis, is dependent on anti-collagen type II (CII) antibodies. The effector mechanism by which autoantibodies contribute to inflammatory reactions in autoimmune diseases is not well understood. In this thesis I have studied the effector pathways used by IgG anti-CII antibodies to initiate arthritis, namely the IgG Fc receptors (FcγRs) and the complement system. We have found that FcγRIII is crucial for development of CIA, as CII-immunized mice lacking this receptor do not develop arthritis and IgG1 and IgG2b anti-CII antibodies require FcγRIII to trigger arthritis when transferred to naïve mice. The antibody-mediated arthritis was further enhanced in mice deficient in the inhibitory FcγRIIB, indicating that FcγRIIB regulates the activation of FcγRIII. Furthermore, we demonstrate that FcγRIII exist as three distinct haplotypes in mice, FcγRIII:H, FcγRIII:V and FcγRIII:T. Mice expressing the FcγRIII:H haplotype are more susceptible to CIA than mice expressing the FcγRIII:V haplotype, indicating that certain FcγRIII haplotype predisposes for CIA. We also show that the most likely FcγRIII-expressing effector cell in CIA is the macrophage, since FcγRIII-expressing macrophages exclusively can induce arthritis in FcγRIII-deficient mice challenged for CIA.

The complement system was also investigated in development of CIA. We found that this effector pathway is also necessary for onset of arthritis, as CIA was inhibited by treatment with anti-complement factor 5 (C5) antibodies. C5-deficient mice could neither develop CIA unless provided with C5-containing sera.

Taken together, the work presented in this thesis indicates that FcγRs and the complement system are crucial for the induction of experimental arthritis. These findings are important for understanding the mechanisms behind rheumatoid arthritis and blocking of these effector pathways may in the future be used as treatment of rheumatoid arthritis.

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Riley, E. M. "The immunology of experimental Echinoccus granulosus infection in mice." Thesis, University of Liverpool, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332701.

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Sunnemark, Dan. "Immunopathogenesis of experimental Chagas' disease /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980520sunn.

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Boström, Müssener Åsa. "Cytokine regulation in rodents with experimental arthritis /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-2862-2.

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Anthony, L. S. D. "Cellular resistance in experimental murine tularemia." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75429.

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A murine model of host resistance to infection with Francisella tularensis, live vaccine strain, has been established. This facultative intracellular bacterium causes in mice an acute infection which lasts for approximately 12 days. Resistance to infection is associated with the appearance in the spleens of cells with the ability to transfer anti-tularemic resistance to naive mice, a response which is maximal 7 days following infection. Depletion of B cells does not compromise the ability of immune cells to transfer resistance. Treatment of mice with immune serum prior to infection leads to an increased hepatic and decreased splenic growth of Francisella. This effect is attributable to a serum-induced shift in the organ uptake of Francisella from the spleen to the liver. Acquired anti-tularemic resistance is critically dependent upon T lymphocytes, as evidenced by the inability of T lymphocyte-depleted immune cells to transfer resistance, and by the increased susceptibility to infection in mice treated with the T cell immunosuppressant, cyclosporin A. The passive transfer of resistance is mediated mainly by T cells bearing the L3T4 marker, but Lyt 2$ sp{+}$ cells may also play a minor role. Macrophages are essential to the control of Francisella infection, since inhibition of the functional activity of this cell population by silica injection leads to a decrease in the ability of mice to contain bacterial growth. The interactions between T cells and macrophages leading to the expression of anti-tularemic immunity are restricted by the product of the I-A region of the H-2 complex. Resistance to tularemia is influenced by the genetic background of the host. Among inbred mouse strains, several levels of resistance to infection are evident. Genetic analysis of resistance/susceptibility to tularemia in F$ sb1$ and F$ sb2$ hybrid mice, and in recombinant inbred strains of mice derived from resistant and susceptible progenitor strains, indicated that the inheritance pat
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Diab, Asim Eltayeb. "Experimental bacterial meningitis : studies on immunopathogenesis and immunoregulation /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3008-2.

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Kinyanjui, Margaret. "Targeting Th2 transcription factors in experimental asthma." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18717.

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Antigen specific CD4+ T cells adoptively transfer airway inflammation comprised mainly of lymphocytes and eosinophils. The ability of these transferred T cells to induce inflammation is dependent on the cytokines they express particularly Th2 cytokines. In order to better understand the mechanism by which adoptively transferred T cells induce airway inflammation, we chose to modulate the expression (GATA-3) and activity (STAT-6) of two key regulators of Th2 cytokine production. To modify expression of GATA-3, we used a bicistronic retroviral vector encoding GATA-3 and enhanced green fluorescent protein (EGFP). As a control, we used a retrovector encoding EGFP alone. By coupling in vitro antigen stimulation with retroviral transduction we generated antigen specific CD4+ T cells expressing EGFP alone or GATA-3 and EGFP. When transferred into naïve recipients that were subsequently challenged, these transduced CD4+ T cells induced lung inflammatory responses with an increase in both CD4+ lymphocytes and eosinophils. This antigen specific inflammatory response was enhanced in animals receiving T cells overexpressing GATA-3. Analysis of the infiltrating cells also revealed that the EGFP+ T cells were present in the lung following antigen challenge, comprising only a small fraction of the CD4+ T cells recruited to the lung during the antigen response. Thus, GATA-3 amplifies antigen-specific inflammatory responses in the airways by augmenting the ability of antigen specific T cells to recruit inflammatory cells to the lung following antigen challenge. To modify the activity of STAT-6 we used chimeric cell penetrating peptides containing a poly-arginine protein transduction domain (PTD) coupled to a sequence predicted to bind and inhibit STAT-6 activity (SIP-1). Using fluorescein-tagged SIP-1, we demonstrate that the poly-arginine PTD efficiently translocates to the cytoplasm within an hour. In vitro, antigen-induced IL-4 production was inhibited in SIP-1-treated spleno
Les cellules CD4+ T à antigènes spécifiques transfèrent par adoption l'inflammation pulmonaire constituées principalement de lymphocytes et d'éosinophiles. L'habileté de celles-ci à transférer des cellules T pour induire l'inflammation est dépendante de leur expression de cytokines Th2. De manière à mieux comprendre le mécanisme par lequel les cellules T transmises par adoption induisent l'inflammation pulmonaire, nous avons choisi de moduler l'expression de GATA-3) ou l'activité de (STAT-6) des deux régulateurs-clés de production de cytokine Th2. Afin de modifier l'expression de GATA-3 dans les cellules T destinées au transfert par adoption, nous avons utilisé un rétrovirus recombinant concentré avec une filtration par centrifugeuse. Ce procédé a dramatiquement augmenté leurs titres et ainsi leur habileté à transduire les cellules CD4+ T en culture primaire. Nous avons utilisé un rétrovirus recombinant qui encode la GATA-3 et / ou la protéine fluorescente verte (EGFP). En couplant in vitro la stimulation d'antigènes avec la transduction par vecteur viral, nous avons généré des cellules CD4+ T à antigènes spécifiques exprimant de l'EGFP seul ou bien de la GATA-3 et de l'EGFP. Lorsque transféré dans un rat qui avait subséquemment été provoqué avec des antigènes, ces cellules CD4+ T induisent une réaction aux inflammations pulmonaires avec une augmentation des lymphocytes et éosinophiles. Cette réaction inflammatoire fut accrue chez les animaux recevant les cellules T surexprimant la GATA-3. L'analyse des cellules infiltrantes a aussi révélé que bien que les cellules EGFP+ étaient présentes dans les poumons suivant la provocation par antigènes, elles étaient constituées seulement d'une petite fraction de cellules CD4+ T recrutées dans les poumons. Ainsi, la GATA-3 amplifie la réaction inflammatoire des poumons induite par antigènes en augmentant l'habileté des cellules T à antigènes spécifiques à recruter
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Zou, Li-Ping. "Immunoregulation and immunotherapy in experimental autoimmune neuritis /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3918-7/.

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Renno, Toufic. "Cytokine expression and regulation in experimental allergic encephalomyelitis." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41754.

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Experimental allergic encephalomyelitis (EAE) is an autoimmune disease characterized by leukocytic infiltration of the central nervous system (CNS) and demyelination and remission/relapse. It is induced by CD4$ sp{+}$ T cells. We used reverse transcriptase/polymerase chain reaction to analyse T cell and cytokine gene expression in the CNS of SJL/J mice with myelin basic protein-induced EAE. Undetectable in normal CNS and cerebrospinal fluid, the expression of CD3, IL-2, IFN-$ gamma$, and TNF$ alpha$ increased in EAE, correlating with disease severity, then dropped to background levels during remission. IL-2 and IFN-$ gamma$ were produced by CD4$ sp{+}$ CD45RB$ sp{ rm low}$ T cells isolated from LN and CNS. In contrast, TNF$ alpha$ was predominately made by macrophages and microglia in the CNS. Purified microglia from normal CNS were induced to express TNF$ alpha$ by activated TH1 supernatant, suggesting that TNF$ alpha$ expression by cells in the CNS could be regulated by cytokines from infiltrating T cells. IL-4 was not detectable in total CNS or in isolated CD4$ sp{+}$ CD45RB$ sp{ rm low}$ cells from the CNS, but was readily amplified from CD4$ sp{+}$ CD45RB$ sp{ rm low}$ LN T cells. This suggests an enrichment of TH1 cells in autoimmune CNS.
To determine the effect of IFN-$ gamma$ expression in the CNS, we produced transgenic mice using an IFN-$ gamma$ cDNA downstream of an MBP promoter. Expression of the transgene was CNS-specific. MHC class I was induced in the CNS of transgenic mice. Transgenic animals that were backcrossed up to 5 generations with SJL/J did not develop spontaneous pathology. However, when they were immunized with MBP in adjuvant, the penetrance of EAE was greater, symptoms were more severe, and the duration of the first episode significantly longer than in non-transgenic littermates, suggesting a role for IFN-$ gamma$ in the amplification and perpetuation of EAE.
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Remington, Leah. "Glial cell and leukocyte response to experimental demyelination." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98776.

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To understand why remyelination fails in diseases such as multiple sclerosis (MS), I studied the cells and molecules involved in remyelination. I examined the cellular response to cuprizone-induced demyelination in C57B1/6 female mice. In response to the toxin cuprizone, microglia, macrophages, T cells and oligodendrocyte precursor cells (OPCs), accumulated in the corpus callosum. I have identified a novel population of CD11c-expressing microglia with potent antigen presenting capacity, which localized to the demyelinated corpus callosum following cuprizone treatment. A broad panel of chemokines were upregulated as early as 1 week following cuprizone treatment. Administration of one of them, an oligodendrocyte precursor cell growth factor, CXCL1, via adenoviral gene delivery to the CNS, did not affect OPC dynamics in the demyelinated corpus callosum. Insight into cells and molecules produced during demyelination/remyelination will be of use in designing new therapies for MS.
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Books on the topic "Immunology, Experimental"

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R, Clark William. The experimental foundations of modern immunology. 4th ed. New York: Wiley, 1991.

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The experimental foundations of modern immunology. 3rd ed. New York: Wiley, 1986.

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Experimental liver transplantation. Boca Raton, Fla: CRC Press, 1988.

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Clark, William R. The experimental foundations of modern immunology. 4th ed. New York: Wiley, 1991.

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Perelson, Alan S., and Gérard Weisbuch, eds. Theoretical and Experimental Insights into Immunology. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76977-1.

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Molina-París, Carmen, and Grant Lythe, eds. Mathematical, Computational and Experimental T Cell Immunology. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57204-4.

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Hisashi, Narimatsu, Hase Sumihiro, Suzuki Akemi, Ito Yukishige, Kawasaki Toshisuke, and SpringerLink (Online service), eds. Experimental Glycoscience: Glycobiology. Tokyo: Springer Japan, 2008.

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Experimental and applied immunotherapy. New York: Humana Press, 2011.

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NATO Advanced Research Workshop on Fundamental and ExperimentalAspects of Autoimmunity (1993 Acquafredda di Maratea, Italy). Autoimmunity: Experimental aspects. Berlin: Springer-Verlag in cooperation with NATO Scientific Affairs Division, 1994.

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NATO Advanced Study Institute on New Experimental Modalities in the Control of Neoplasia (1985 Maratea, Italy). New experimental modalities in the control of neoplasia. New York: Plenum Press, 1986.

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Book chapters on the topic "Immunology, Experimental"

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Jain, Parag, Ravindra Pandey, and Shiv Shankar Shukla. "Experimental Models for Inflammation." In SpringerBriefs in Immunology, 135–41. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2163-0_5.

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Kumar, Awanish. "Experimental Models for Leishmaniasis." In SpringerBriefs in Immunology, 69–73. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8869-9_7.

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Spaner, David, and Angela Bahlo. "B Lymphocytes in Cancer Immunology." In Experimental and Applied Immunotherapy, 37–57. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-980-2_2.

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Adams, Andrew B., William H. Kitchens, and Kenneth A. Newell. "Experimental models in discovery and translational studies." In Transplant Immunology, 316–36. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781119072997.ch16.

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Fox, G. J., and D. Menzies. "Epidemiology of Tuberculosis Immunology." In Advances in Experimental Medicine and Biology, 1–32. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6111-1_1.

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Parney, Ian F. "Basic Concepts in Glioma Immunology." In Advances in Experimental Medicine and Biology, 42–52. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3146-6_4.

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Li, Qian, and Qiang Liu. "Noncoding RNAs in Cancer Immunology." In Advances in Experimental Medicine and Biology, 243–64. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-1498-7_9.

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La Torre, Daria, and Åke Lernmark. "Immunology of β-Cell Destruction." In Advances in Experimental Medicine and Biology, 537–83. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3271-3_24.

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Yoshimura, Yukinori, and Animesh Barua. "Female Reproductive System and Immunology." In Advances in Experimental Medicine and Biology, 33–57. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3975-1_3.

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Collins, Fraser L., Jonathan D. Schepper, Naiomy Deliz Rios-Arce, Michael D. Steury, Ho Jun Kang, Heather Mallin, Daniel Schoenherr, et al. "Immunology of Gut-Bone Signaling." In Advances in Experimental Medicine and Biology, 59–94. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-66653-2_5.

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Conference papers on the topic "Immunology, Experimental"

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Wenthe, Jessica, Emma Eriksson, Ann-Charlotte Hellström, and Angelica Loskog. "Abstract B07: Immunostimulatory gene therapy enhances PD-1 blockade antibody therapy in experimental lung cancer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-b07.

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Svensson, Emma, Rafael Moreno, Ioanna Milenova, Lisa Christiansson, Ramon Alemany, and Angelica Loskog. "Abstract A25: Immunotherapy using LOAd700 armed with CD40 ligand controls experimental pancreatic cancer and activates immune responses." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-a25.

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McMurray, Diane, Ben Harrison, Katie Ertelt, Richard Walsh, Lindsay Wurst, Steven Leonardo, Nadine Ottoson, et al. "Abstract A08: Distribution, cutoff, and functional significance of a potential biomarker for Imprime PGG, an experimental cancer immunotherapeutic, in a healthy subject population." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-a08.

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Tan, Joanne BL, Ada Chen, Manmohan Leleti, Annette Becker, Erick Lindsey, Jaroslaw Kalisiak, Jay P. Powers, Steve Young, Ulrike Schindler, and Juan C. Jaen. "Abstract B46: Small-molecule inhibitors of ecto-nucleotidase CD73 promote activation of human CD8+ T cells and have profound effects on tumor growth and immune parameters in experimental tumor models." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-b46.

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Newman, Robert G., Eckhard R. Podack, and Robert B. Levy. "Abstract A32: Combining early heat shock protein vaccination with directed IL-2 leads to effective and persistent antitumor immunity in recipients of experimental autologous hematopoietic cell transplantation." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a32.

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Galich, N. E., and M. V. Filatov. "Laser fluorescence fluctuation excesses in molecular immunology experiments." In SPIE Proceedings, edited by Alexander I. Melker and Teodor Breczko. SPIE, 2006. http://dx.doi.org/10.1117/12.726756.

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David, Regis A., and Brian D. Jensen. "Modeling DNA Motion Under Electrostatic Repulsion Within a Living Cell." In ASME 2009 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/detc2009-87413.

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We are developing a new technique, called nanoinjection, to insert foreign DNA into a living cell. Such DNA transfection is commonly used to create transgenic organisms vital to the study of genetics, immunology, and many other biological sciences. In nanoinjection, DNA, which has a net negative charge, is electrostatically attracted to a micromachined lance. The lance then pierces the cell membranes, and the voltage on the lance is reversed, repelling the DNA into the cell. This paper presents a mathematical model to predict the motion (trajectory) of DNA particles within a cell in the presence of the electric field developed by the lance and the substrate. The model is used to predict the scattering of DNA through the cell due to electrostatic repulsion. We are currently preparing experiments which will be used to validate the model.
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Roncaglioni, M. C., A. Falanga, A. P. Bolognese Dalessandro, B. Casali, and M. B. Donti. "ENZYMATIC AND IMMUNOLOGIC CHARACTERIZATION OF A CYSTEINE PROTEINASE PROCOAGULANT IN SEVERAL MURINE METASTASIZING TUMO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643663.

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Involvement of the hemostatic systemin tumor metastasis growth has been repeatedly suggested and several tumor-associated procoagulants have been described. We have studied here the procoagulant activity (PCA) of tissue extracts from 4 murine metastasizing tumors: Lewis Lung Carcinoma (3LL), B16 melanoma (B16), JW sarcoma (JWS) and the M4 variant of the mFS6 fibrosarcoma (M4). The experiments were designed to identify cancer procoagulant (CP) a FVII independent FX activating cysteine proteinase or tissue factor (TF) in these tumors. Tissue extracts from 3LL, B16 and JWS initiated coagulation both in the presence and absence of FVII (FVII independent activity ranging from 70% to 86% of the total activity). The PCA of the same tumors was significantly decreased (p < 0.01) by cysteine proteinase inhibitors (1 mM iodoacetamide (IA) and 0.1 mM HgCl2 ) and the inhibitionby HgCl2 was reversed by -SH group activators (di-thiatreital, KCN, IiDTA). In addition these samples were able of directly activating pure bovineFX in a two stage clotting assay. The PCA of M4 extract was dependent on FVII,was not significantly affected by IA and HgCl2 and was inhibited by concanavalin A, a known TF inhibitor. An Ouchterlony double immunodiffusion study showed immunological cross-reactivity of 3LL, B16 and JWS to a polyclonal antibody to purified CP (from rabbit V2 carcinoma; obtained from S.G. Gordon, Denver, USA). No cross-reactivity was present between this antibody and M4. This study shows that the PCA of M4 is TF, whereas the procoagulant(s) of 3LL, B16 and JWS are enzymatically and immunologically indistinguishable from CP.
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Dintenfass, L. "AGGREGATES OF RED BLOOD CELLS, AND AGGREGATES OF PLATELETS UNDER ZERO GRAVITY: EXPERIMENT ON NASA SPACE SHUTTLE "DISCOVERY" STS 51-C, JANUARY l985." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644538.

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The aim of experiment "ARC" on the space shuttle "Discovery STS 51-C, was to define effect of zero gravity on kinetics and morphology of aggregation of red cells in blood obtained from patients suffering from ischaemic heart disease, colon cancer, insulin-dependent diabetes, hyperlipidaemia, IgG and IgM papa-proteins. Space-rated automated slit-capillary photo-viscometer contained a motorized infusion pump capable of handling eight different blood samples. Two cameras and a microscope allowed micro and macrophotography, and total of 500 photographs was obtained in space; and equivalent number on the ground, in the Kennedy Space Center, where a duplicate ground photo-viscometer was present. Identical blood samples have been used in the ground experiments. The slit had a gap of 12.5 microns (micrometers). Blood was anticoagulated with EDTA and adjusted to haematocrit of 0.30 using native plasma. Samples were kept at -5°C prior to the experiment, and at 25°C during experiment; duration of experiment was 91/2 hours. The same computer program was used in both instruments. Photography was carried out at set intervals up to six minutes from the moment of stasis. There was a drastic difference between aggregation on the ground and at zero gravity. Blood from patients was greatly sludged on the ground, but normal rouleaux were formed under zero gravity. Also, aggregates uikder zero g were much smaller. However, red cell shape was not changed. Blood samples from normal donors, which showed normal rouleaux on the ground, exhibited random swarm pattern under zero gravity. Platelets, which tended to aggregate on the ground, and tended to accummulate at the slit entrance, remained monodisperse under zero gravity and no pseudopodia have been noted; under zero g platelet moved through the slit. Subject to future confirmation, it is suggested that zero gravity affects cell-to-cell interaction, and probably causes a modification of the cell membrane. If this is true, a new vista opens in the studies of immunology and oncology under zero gravity.
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Coller, B. S., and J. Jesty. "ANTI-THROMBINneo IgG IN AN ASYMPTOMATIC PATIENT WITH A BENIGN MONOCLONAL GAMMOPATHY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644344.

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A 68 year old male hospitalized for cardiac disease was found to have an elevated prothrombin time (18.5/12.4 s) and aPTT (59.6/25.9s). He had no history of excessive bleeding or bruising. Subsequent evaluation revealed: thrombin time >500/34.1 s; fibrinogen 260 mg/dl functional and 522 mg/dl immunologic; reptilase 25.6/18.1 s; thrombin-induced platelet release of ATP (patient=0 and control=14.6 nmoles/109 platelets at 0.5 U/ml); AT-III 89% functional and 36.5 mg/dl immunologic; and prothrombin 167%. Mixing experiments showed the presence of an inhibitor of the thrombin time, and purification of IgG by protein A affinity chromatography showed the inhibitor of fibrin formation to reside in the IgG fraction. When coupled to Affi-gel 10, patient IgG (but not control IgG) removed purified thrombin from solution; the same gel did not remove prothrombin. The patient's IgG did not inhibit thrombin’s cleavage of a chromogenic substrate (Chromozym TH). Studies on the patient's serum revealed: IgG 2,360 mg/dl, IgA 371 mg/dl, and IgM 107 mg/dl. Serum protein electrophoresis and immunoelectrophoresis showed a monoclonal IgG lambda protein with probably normal amounts of normal IgG. Other parameters (hematocrit, albumin, calcium, bone marrow histology, bone X-rays) indicated that the patient has a benign monoclonal gammopathy, not multiple myeloma. We conclude that our patient is producing an IgG inhibitor that reacts with a neo-antigen produced by the cleavage of prothrombin to thrombin; the IgG can prevent the interaction of thrombin with fibrinogen and the thrombin receptor on platelets, but not small synthetic substrates. We suspect that his monoclonal IgG is the inhibitor and find it remarkable that he has no increase in bleeding.
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