Relevant bibliographies by topics / Perforin

Academic literature on the topic 'Perforin'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Perforin"

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Urrea Moreno, Ramon, Juana Gil, Carmen Rodriguez-Sainz, Elena Cela, Victor LaFay, Brian Oloizia, Andrew B. Herr, Janos Sumegi, Michael B. Jordan, and Kimberly A. Risma. "Functional assessment of perforin C2 domain mutations illustrates the critical role for calcium-dependent lipid binding in perforin cytotoxic function." Blood 113, no. 2 (January 8, 2009): 338–46. http://dx.doi.org/10.1182/blood-2008-08-172924.

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Abstract Perforin-mediated lymphocyte cytotoxicity is critical for pathogen elimination and immune homeostasis. Perforin disruption of target cell membranes is hypothesized to require binding of a calcium-dependent, lipid-inserting, C2 domain. In a family affected by hemophagocytic lymphohistiocytosis, a severe inflammatory disorder caused by perforin deficiency, we identified 2 amino acid substitutions in the perforin C2 domain: T435M, a previously identified mutant with disputed pathogenicity, and Y438C, a novel substitution. Using biophysical modeling, we predicted that the T435M substitution, but not Y438C, would interfere with calcium binding and thus cytotoxic function. The capacity for cytotoxic function was tested after expression of the variant perforins in rat basophilic leukemia cells and murine cytotoxic T lymphocytes. As predicted, cells transduced with perforin-T435M lacked cytotoxicity, but those expressing perforin-Y438C displayed intact cytotoxic function. Using novel antibody-capture and liposome-binding assays, we found that both mutant perforins were secreted; however, only nonmutated and Y438C-substituted perforins were capable of calcium-dependent lipid binding. In addition, we found that perforin-Y438C was capable of mediating cytotoxicity without apparent proteolytic maturation. This study clearly demonstrates the pathogenicity of the T435M mutation and illustrates, for the first time, the critical role of the human perforin C2 domain for calcium-dependent, cytotoxic function.
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Bird, Lucy. "Perforin protection." Nature Reviews Immunology 15, no. 11 (October 16, 2015): 667. http://dx.doi.org/10.1038/nri3926.

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Joag, SV. "Perforin in myocarditis." Biomedicine & Pharmacotherapy 45, no. 2-3 (January 1991): 126. http://dx.doi.org/10.1016/0753-3322(91)90138-j.

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Ahmed, Najwa, Amal Fayyad, Salimeh Mohammadi, Subhi Hamza, and Abdul Al-Faisal. "Purification of perforin and study expression of perforin in leukemia patient." Egyptian Academic Journal of Biological Sciences. C, Physiology and Molecular Biology 5, no. 2 (December 1, 2013): 1–9. http://dx.doi.org/10.21608/eajbsc.2013.16090.

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Kafsack, Björn F. C., and Vern B. Carruthers. "Apicomplexan perforin-like proteins." Communicative & Integrative Biology 3, no. 1 (January 2010): 18–23. http://dx.doi.org/10.4161/cib.3.1.9794.

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Arnaout, Ramy A. "Perforin deficiency: fighting unarmed?" Immunology Today 21, no. 11 (November 2000): 592. http://dx.doi.org/10.1016/s0167-5699(00)01730-8.

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McDiarmid, S. V., D. G. Farmer, J. S. Kuniyoshi, M. Robert, A. Khadavi, A. Shaked, and R. W. Busuttil. "PERFORIN AND GRANZYME B." Transplantation 59, no. 5 (March 1995): 762–66. http://dx.doi.org/10.1097/00007890-199503150-00021.

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Krähenbühl, Olivier, and Jürg Tschopp. "Perforin-induced pore formation." Immunology Today 12, no. 11 (November 1991): 399–402. http://dx.doi.org/10.1016/0167-5699(91)90139-k.

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Liu, Chau-Ching, Craig M. Walsh, and John Ding-E. Young. "Perforin: structure and function." Immunology Today 16, no. 4 (April 1995): 194–201. http://dx.doi.org/10.1016/0167-5699(95)80121-9.

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Covas, Dimas Tadeu. "Perforin and hematological cancer." Revista Brasileira de Hematologia e Hemoterapia 33, no. 4 (2011): 254–55. http://dx.doi.org/10.5581/1516-8484.20110070.

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Dissertations / Theses on the topic "Perforin"

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Kägi, David. "The role of perforin protein in lymphocyte mediated cytotoxicity /." [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10050.

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Uhl, Dieter. "Einfluss körperlicher Ausdauerbelastung auf Perforin und Granzyme-B-exprimierende Lymphozytenpopulationen." [S.l.] : [s.n.], 2002. http://www.freidok.uni-freiburg.de/volltexte/440.

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Semple, Patricia Lynn. "The role of the cytolytic mediators, granulysin and perforin, in tuberculosis." Doctoral thesis, University of Cape Town, 2008. http://hdl.handle.net/11427/12403.

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Includes bibliographical references (leaves 150-175).
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Protective immunity against mycobacterial infection requires an effective cytolytic response, in addition to an intact Type l (Th1) cytokine pathway. Natural killer (NK) cells and cytolytic T-cells (CTL) are essential components of protective immunity against tuberculosis (TB) and mediate granule-dependent killing of infected cells. Granulysin, an antimicrobial protein, and perforin, a pore-forming molecule, have been found to co-localise in the granules of these two cell types. Granulysin has been shown to be directly cytotoxic to extracellular Mycobacterium tuberculosis (M.tb) and, together with perforin, is cytolytic against intracellular mycobacteria. This project evaluated the role of these two cytolytic mediators in TB.
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Haeryfar, Seyed Mohammad Mansour. "Antiestrogens modulate the perforin/granzyme pathway of natural killer cell-mediated cytolysis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0001/MQ45052.pdf.

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Fraser, Stephanie A. "Regulation of Perforin-mediated lysis by two endogenous grandule proteins, Calreticulin and Chymase I /." abstract and full text PDF (UNR users only), 1999. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:9961145.

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Cartwright, Adam. "Investigating the gasket function and perforin secretion of the natural killer cell immune synapse." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24104.

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Natural Killer (NK) cells interact with other cells through a structured interface, the immune synapse (IS). A balance of signals controls NK cell activity through ligation of activating and inhibitory receptors. If signaling favours activation, NK cells mediate the directed secretion of cytotoxic mediators, such as perforin (PFN). To test whether the IS also functions as a gasket to extracellular molecules, fluorescently labeled nanometer-scale dextrans of varying sizes were co-incubated with effector-target cell-cell conjugates. Quantitative fluorescence microscopy of synapses revealed that dextrans with hydrodynamic diameters ≥32 nm were excluded from activating synapses, whilst smaller dextrans could enter. Size-dependent exclusion required an intact filamentous actin scaffold, but not continuous reorganisation following synapse formation. Time-lapse microscopy further revealed that the synapse assembles in a zipper-like manner, clearing larger dextran from the synapse. In addition, monoclonal antibodies and low-density lipoproteins were also excluded from the IS, whereas smaller domain antibodies could penetrate. NK cells can lyse more than one target in series. Whilst it is known that, among other proteins, PFN is secreted to lyse diseased cells, the amount of PFN secreted by NK cells is currently unknown. To quantify PFN release following stimulation through NKG2D or CD16, NK cells were plated on protein-coated surfaces that could capture PFN. Quantification using fluorescence microscopy revealed that PFN secretion was analogue, varying with increased ligand density. Simulating serial killing, repeated stimulation decreased the amount of PFN secreted with sequential activation. Unexpectedly, CD16 stimulation following serial NKG2D ligation recovered this decrease in secretion, however a similar recovery was not seen under reciprocal conditions. These data show that the activating IS clears and excludes extracellular molecules, including antibodies, in a size-dependent manner. Further, NK cell PFN secretion is an analogue response that varies with both ligand density and the receptors ligated in series.
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Tinangon, Maria M. "Strategies to identify granzyme J /." abstract and full text PDF (UNR users only), 2001. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1404986.

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Bradley, Michael Joseph. "Role of CD44, Fas Ligand, and Perforin in the Cytotoxicity Mediated by Natural Killer Cells." Thesis, Virginia Tech, 1997. http://hdl.handle.net/10919/36792.

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Two important mechanisms of lymphocyte-mediated cytotoxicity, one perforin based and the other Fas ligand (FasL) based, have been characterized recently. It has also been shown that CD44, an adhesion molecule, can participate in signaling cytotoxic activity of cytotoxic T lymphocytes (CTLs). In the current study we tested the hypothesis that activation of natural killer (NK) or lymphokine activated killer (LAK) cells induces the expression of FasL, perforin, and CD44 which together contribute towards increased cytolytic activity. To this effect, we used wild-type mice, perforin-knockout mice, and mice lacking a functional FasL. We observed that both interleukin-2 (IL-2) and Poly I:C triggered NK/LAK cells to lyse targets through the perforin- and FasL- pathways. In addition, Fas+ tumor targets were more susceptible to lysis by poly I:C and IL-2 activated NK/LAK cells when compared to Fas- targets. Furthermore, Fas- tumor cells injected subcutaneously into syngeneic mice could grow and induce tumors, whereas, Fas+ tumors were rejected. IL-2 treatment increased the CD44 expression on NK cells, which was responsible for the lysis of endothelial cells through its ligand, hyaluronate. Upregulation of perforin and FasL in activated NK/LAK cells may explain why such cells can kill a wide variety of tumor cells efficiently. On the other hand, activated NK/LAK cells express increase increased levels of CD44 and use this molecule to mediate cytotoxicity of endothelial cells, which may account for the vascular leak seen during IL-2 therapy.
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Rafatpanah, Baygi Houshang. "Immunogenetic analysis of patients with HTLV-I infection : associations with HLA, cytokine and perforin gene polymorphisms." Thesis, University of Manchester, 2003. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488453.

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Human T lymphotropic virus type (HTLV-I) is associated with HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) and adult T-cell leukaemia (ATL). Fewer than 2% of HTLV-I-infected individuals develop HAM/TSP. The different outcome of HTLV-I infection may be explained by the existence of viral agents, genetic background or even environmental factors. In the initial part of this study we determined if there was a correlation between cytokine gene polymorphisms, mainly Thl and Th2, in Iranian patients with HAM/TSP, asymptomatic HTLV-I carriers and healthy controls. It was shown that polymorphisms in the TNF-alpha gene promoter at position -308, in TGF-beta1 gene at codons 10_and 25, in IL-10 at positions -1082, -819, -592, in IFN-gamma at position +874, in IL-13 at position +2043 and in IL-4 at position -590 correlates with differential production of these cytokines in vitro. There was a significant difference between HAM/TSP patients and healthy controls in the distribution of IL-10 promoter polymorphisms at position -819 and -592 (p=0.01) and HTLV-I carriers and healthy controls (p=0.02). The frequency of the IL-10 low producer haplotype (ATA) was significantly associated with HAM/TSP compared with healthy controls (p=0.01) and HTLV-I carriers with healthy controls (p=0.02). These data suggest that IL-10 -819 and -592 polymorphisms are associated with HTLV-I infection. However, how this influences HAM/TSP patients and HTLV-I carriers remain unknown. In contrast, we failed to detect any differences in the frequencies of other cytokines between any of the three groups. In this part, we also analysed the influence of HLA class II DRB1 alleles and class I HLA-A2, A-30, CW8 and B54 alleles in all three groups. The frequency of the HLA-DRB1*01 allele was significantly increased in HAM/TSP patients compared with carriers (p=0.03). In contrast, the distribution of HLA-DRB1*014 was higher in HTLV-I carriers compared to HAM/TSP patients (p=0.03). There was also a significant difference in the frequency of HLA-CW8 between HAM/TSP patients and healthy controls (p=0.01). HLA typing suggests that HLA-DRB1*01 and HLA-CW8 are relative risk factors for development to HAM/TSP, whereas possession of the HLA-DRB1*014 allele decreases the risk of HAM/TSP. In this case, the role of other genetic backgrounds should be taken into account. The second part of this study was to define GM-CSF polymorphisms and to seek association between GM-CSF polymorphism and HTLV-I infection. The 5'-flanking region, promoter, exon 1 and 2 and 3'UTR of GM-CSF was screened for detection of polymorphism by SSCP and sequencing. Three novel polymorphisms were found in the 5'-flanking region of GM-CSF at positions -677*A/C, -1440*A/G and -1916*T/C, relative to the translation start site. Mitogenic stimulation of PBMCs from healthy controls showed no correlation between GM-CSF gene polymorphisms and protein level. However, a gel shift assay demonstrated that the -611*A allele binds the transcriptional factor TEF-2 better than the -677*C allele. The frequencies of GM-CSF polymorphisms were the same in all of the HTLV-I groups and controls. In the third part of our study, we screened the promoter and first intron of the perforin gene, as a key factor in elimination of viral-infected cells, to determine novel polymorphisms. A novel polymorphism at position +418 relative to the transcription start site was detected. Results from flow cytometry and Western blotting in non stimulated and stimulated PBMCs showed no association between perforin gene polymorphism and perforin expression. The frequency of the +418*C allele in HAM/TSP patients was significantly increased compared with healthy controls (p=0.015). There was also a difference in the distribution of +418*C allele between HAM/TSP patients and HTLV-I carriers, but this did not reach significant levels (p=0.09). This result suggests that the +418*C allele acts as genetic risk factor for development of HAM/TSP.
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Woodsworth, Daniel. "Characterizing the granzyme-perforin pathway and its utility as a cell-to-cell delivery system for cellular therapeutics." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/62073.

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Alongside small molecules and biologics, cell-based therapies are emerging as a third class of medical therapy. Additional sensors, actuators and control circuits would greatly expand the range of function and application of cellular therapeutics. To this end, a cell-to-cell delivery module has been developed by investigating and re-engineering the granzyme-perforin pathway of cytotoxic lymphocytes. A computational biophysical model of this process was developed and implemented using a spatial stochastic simulation algorithm, which indicated that hindered diffusion in the immune synapse is critical to ensure reliable granzyme internalization and that large amounts of granzyme escape the synapse, but should not have toxic effects due to rapid spatiotemporal dilution. Additionally, these results indicated that passive diffusion is sufficient for granzyme entry into the target cell, which motivated efforts to use granzyme as a molecular chaperone to transfer exogenous payloads from effector to target cells. Using a fluorescent protein payload, the subcellular localization of several granzyme B derived chaperones was characterized using fluorescence microscopy, and then their capacity to transfer the payload to target cells was evaluated in co-culture experiments. The results indicated that the motifs in granzyme B that are required for lytic granule loading are only functional and contiguous in the folded protein. Additionally, these experiments demonstrated that full length granzyme B is a suitable chaperone for delivering protein payloads to target cells via the granzyme-perforin pathway. Attempts were then made to use this system to deliver potent orthogonal toxins to apoptosis and lymphocyte resistant tumor cells. A range of granzyme B toxin fusion proteins were constructed, all of which retained toxic activity to varying degrees. To render target cells resistant to lymphocyte attack both small molecule and protein based inhibitors of apoptosis were tested in several cell lines, which delayed cell death, but did not stop it. Using effector target dose response curves, a moderate increase in target cell death was observed in cells targeted by lymphocytes expressing granzyme toxin fusion proteins, as compared to wild type lymphocytes, but the biological significance of this effect is uncertain. Approaches to improve this granzyme-perforin mediated delivery system and its therapeutic utility are discussed and explored.
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Books on the topic "Perforin"

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Meerzon, Yana. Performing Exile, Performing Self. London: Palgrave Macmillan UK, 2012. http://dx.doi.org/10.1057/9780230371910.

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Hofmann, Bettina. Performing Ethnicity, Performing Gender. New York; London: Routledge, 2016. | Series: Routledge: Routledge, 2016. http://dx.doi.org/10.4324/9781315544977.

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Tʻalchʻum, Tongyang ŭi chŏntʻonggŭk, Sŏyang ŭi sirhŏmgŭk. Sŏul Tʻŭkpyŏlsi: Yŏnʾgŭk kwa Inʾgan, 2002.

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1936-, Jonas Joan, ed. Perform. New York: Thames & Hudson, 2005.

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Hoffmann, Jens. Perform. New York: Thames & Hudson, 2005.

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David, Allen. Performing Chekhov. London: Taylor & Francis Inc, 2004.

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Eddershaw, Margaret. Performing Brecht. New York: Routledge, 1996.

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Spilsbury, Richard. Performing live. Chicago, Illinois: Capstone Raintree, 2015.

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Performing arts. Washington, D.C: National Education Association, 1989.

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Fadlu-Deen, Kitty. Performing arts. Freetown: People's Education Association of Sierra Leone, 1995.

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Book chapters on the topic "Perforin"

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Gooch, Jan W. "Perforin." In Encyclopedic Dictionary of Polymers, 913. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14450.

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Mehlhorn, Heinz. "Perforin-Like Proteins." In Encyclopedia of Parasitology, 2128. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4807.

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Mehlhorn, Heinz. "Perforin-Like Proteins." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4807-1.

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Naneh, Omar, Tadej Avčin, and Apolonija Bedina Zavec. "Perforin and Human Diseases." In MACPF/CDC Proteins - Agents of Defence, Attack and Invasion, 221–39. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8881-6_11.

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Podack, E. R., K. J. Olsen, D. M. Lowrey, and M. Lichtenheld. "Structure and Function of Perforin." In Current Topics in Microbiology and Immunology, 11–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73911-8_2.

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Podack, E. R. "Perforin: Structure, Function, and Regulation." In Membrane Defenses Against Attack by Complement and Perforins, 175–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77014-2_11.

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Lin, M. T., D. R. Hinton, and S. A. Stohlman. "Mechanisms of Viral Clearance in Perforin-Deficient Mice." In Advances in Experimental Medicine and Biology, 431–36. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5331-1_54.

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Podack, E. R. "Perforin, Killer Cells and Gene Transfer Immunotherapy for Cancer." In Pathways for Cytolysis, 121–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79414-8_7.

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Eto, Nozomu, Seiji Kurokui, Shinichi Ikeda, Kintaro Sone, Akinori Hirashima, Yoshinori Fujimura, Sosuke Tanino, Hirofumi Tachibana, Masahide Yasuda, and Chau-Ching Liu. "Putative Protection Mechanism of CTL from Killing by Their Own Perforin." In Animal Cell Technology: Basic & Applied Aspects, 371–77. Dordrecht: Springer Netherlands, 2002. http://dx.doi.org/10.1007/978-94-017-0728-2_65.

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Takayama, Hajime. "Properties of Cytotoxicity Mediated by CD4+, Perforin-Negative T-Lymphocyte Clones." In Cytotoxic Cells: Recognition, Effector Function, Generation, and Methods, 190–95. Boston, MA: Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4684-6814-4_17.

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Conference papers on the topic "Perforin"

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Samara, Katerina D., Eirini Neofytou, Nikolaos Tzanakis, Alexandros D. Karatzanis, Dimitra Papandrinopoulou, Nikolaos Siafakas, and Eleni G. Tzortzaki. "Perforin Expression In COPD Patients With Microsatellite DNA Instability." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3879.

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Samara, Katerina D., Athanasia Proklou, Eirini Neofytou, Evangelia Stamataki, Eleni Tzortzaki, and Nikolaos Siafakas. "Sputum Perforin Expression In Obstructive Airways Diseases: COPD And Asthma." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1310.

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Proklou, Athanasia, Eirini Neofytou, Sophia Schiza, Vasilios Tzilas, Charis Armeftis, Nikolaos Siafakas, and Eleni G. Tzortzaki. "Serum And Sputum Perforin Expression In Persistent Asthma: Preliminary Results." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5616.

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Barczyk, A., E. Sozanska, and W. Pierzchala. "Increased Expression of Granzyme B, but Not Perforin in CD8+ Cells in Sarcoidosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3185.

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Morcos, M., V. R. Stolberg, M. E. Bates, M. R. Kady, L. McCloskey, J. L. Curtis, and C. M. Freeman. "Perforin Inhibition Blocks NK-Mediated In Vitro Killing of Human Lung Epithelial Cells in COPD." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4546.

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Chen, X., and H. Zeng. "SAT0077 Clinical features and perforin A91V gene analysis in SO-JIA children with macrophage activation syndrome." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.1989.

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Asai, Kazuhisa, Nahoko Shiratsuchi-Nakagawa, Gakuya Tamagaki, Tetsuya Watanabe, Yumiko Imahashi, Yukikazu Ichimaru, Yoshihiro Tochino, Hiroshi Kamoi, Hiroshi Kanazawa, and Kazuto Hirata. "Soluble Perforin, A Marker Of CD8+ T Lymphocyte Activation In Epithelial Lining Fluid In COPD Patients." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4545.

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Xia, Leiming, Yang Xia, Quanning Chen, Yi Wang, Yangyi Bao, Steven K. Lundy Lundy, Fu Dai, Alfred E. Chang, and Qiao Li. "Abstract 1621: Adoptively transferred B cells directly kill tumor cells via the CXCR4/CXCL12 & perforin pathways." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1621.

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Wei, P., and H. Zeng. "AB0264 The perforin A91V gene and clinical features analysis in chinese SO-JIA cases with macrophage activation syndrome." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2061.

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Freeman, CM, FJ Martinez, T. Polak, MK Han, SW Chensue, HS Murphy, DA Arenberg, C. Meldrum, C. Getty, and JL Curtis. "Engagement of TLR3 on CD8+ T Cells from COPD Patients Increases In Vitro Production of IFNγ, TNFα, and Perforin." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3950.

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Reports on the topic "Perforin"

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Fogel, Robert. High Performing Asian Economies. Cambridge, MA: National Bureau of Economic Research, September 2004. http://dx.doi.org/10.3386/w10752.

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2

GONCHAROVA, OKSANA. ELECTRONIC METHODICAL MANUAL "METHODICAL INSTRUCTIONS FOR PERFORMING LABORATORY CLASSES ON THE DISCIPLINE "ENVIRONMENTAL SAFETY" FOR STUDENTS OF THE SPECIALTY 20.02.02 "PROTECTION IN EMERGENCY SITUATIONS" OF SECONDARY VOCATIONAL EDUCATION INSTITUTIONS". SIB-Expertise, July 2021. http://dx.doi.org/10.12731/er0475.12072021.

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ELECTRONIC METHODICAL MANUAL "METHODICAL INSTRUCTIONS FOR PERFORMING LABORATORY CLASSES ON THE DISCIPLINE "ENVIRONMENTAL SAFETY" FOR STUDENTS OF THE SPECIALTY 20.02.02 "PROTECTION IN EMERGENCY SITUATIONS" OF SECONDARY VOCATIONAL EDUCATION INSTITUTIONS. The purpose of the guidelines is to ensure a clear organization of laboratory classes in the discipline, to create an opportunity for students who were absent from the laboratory class to independently perform the work, issue a report and protect the work in a timely manner.
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3

Ryder, Ann Marie. Performing Work at Sandia (FY18 Revision). Office of Scientific and Technical Information (OSTI), March 2018. http://dx.doi.org/10.2172/1528817.

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4

Amela, R., R. Badia, S. Böhm, R. Tosi, C. Soriano, and R. Rossi. D4.2 Profiling report of the partner’s tools, complete with performance suggestions. Scipedia, 2021. http://dx.doi.org/10.23967/exaqute.2021.2.023.

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This deliverable focuses on the proling activities developed in the project with the partner's applications. To perform this proling activities, a couple of benchmarks were dened in collaboration with WP5. The rst benchmark is an embarrassingly parallel benchmark that performs a read and then multiple writes of the same object, with the objective of stressing the memory and storage systems and evaluate the overhead when these reads and writes are performed in parallel. A second benchmark is dened based on the Continuation Multi Level Monte Carlo (C-MLMC) algorithm. While this algorithm is normally executed using multiple levels, for the proling and performance analysis objectives, the execution of a single level was enough since the forthcoming levels have similar performance characteristics. Additionally, while the simulation tasks can be executed as parallel (multi-threaded tasks), in the benchmark, single threaded tasks were executed to increase the number of simulations to be scheduled and stress the scheduling engines. A set of experiments based on these two benchmarks have been executed in the MareNostrum 4 supercomputer and using PyCOMPSs as underlying programming model and dynamic scheduler of the tasks involved in the executions. While the rst benchmark was executed several times in a single iteration, the second benchmark was executed in an iterative manner, with cycles of 1) Execution and trace generation; 2) Performance analysis; 3) Improvements. This had enabled to perform several improvements in the benchmark and in the scheduler of PyCOMPSs. The initial iterations focused on the C-MLMC structure itself, performing re-factors of the code to remove ne grain and sequential tasks and merging them in larger granularity tasks. The next iterations focused on improving the PyCOMPSs scheduler, removing existent bottlenecks and increasing its performance by making the scheduler a multithreaded engine. While the results can still be improved, we are satised with the results since the granularity of the simulations run in this evaluation step are much ner than the one that will be used for the real scenarios. The deliverable nishes with some recommendations that should be followed along the project in order to obtain good performance in the execution of the project codes.
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Ahle, L. E. Performing Neutron Cross-Section Measurements at RIA. Office of Scientific and Technical Information (OSTI), May 2003. http://dx.doi.org/10.2172/15004541.

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Wilkerson, A. M., T. C. Abell, and E. Perrin T. LED Lighting in a Performing Arts Center. Office of Scientific and Technical Information (OSTI), July 2015. http://dx.doi.org/10.2172/1220538.

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Miller, N. J., S. M. Kaye, P. M. Coleman, A. M. Wilkerson, T. E. Perrin, and G. P. Sullivan. LED Lighting in a Performing Arts Building. Office of Scientific and Technical Information (OSTI), July 2014. http://dx.doi.org/10.2172/1221092.

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Ackerman, Glenn H., Monica J. Giovachino, Carla E. Tighe, and R. D. Trunkey. Performing Industrial Base Analyses. Volume 1: Methodology. Fort Belvoir, VA: Defense Technical Information Center, August 1995. http://dx.doi.org/10.21236/ada362377.

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9

Ozdil, Taner R., James Richards, Ryan Brown, Justin Earl, and Dylan Stewart. AT&T Performing Arts Center: Sammons Park. Landscape Architecture Foundation, 2014. http://dx.doi.org/10.31353/cs0790.

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10

Bailey, K. M. Internal dosimetry performing dose assessments via bioassay measurements. Office of Scientific and Technical Information (OSTI), May 1993. http://dx.doi.org/10.2172/10105266.

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