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Relevant bibliographies by topics / Soluble complement receptor 1

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Academic literature on the topic 'Soluble complement receptor 1'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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Journal articles on the topic "Soluble complement receptor 1"

1

&NA;. "Myelin protected by soluble recombinant complement receptor 1." Inpharma Weekly &NA;, no. 944 (July 1994): 11. http://dx.doi.org/10.2165/00128413-199409440-00025.

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Luan, Nguyen M., Yuji Teramura, and Hiroo Iwata. "Immobilization of soluble complement receptor 1 on islets." Biomaterials 32, no. 20 (July 2011): 4539–45. http://dx.doi.org/10.1016/j.biomaterials.2011.03.017.

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Chávez-Cartaya, Rafael E., Gilda Pino DeSola, Les Wright, Neville V. Jamieson, and David J. G. White. "REGULATION OF THE COMPLEMENT CASCADE BY SOLUBLE COMPLEMENT RECEPTOR TYPE 1." Transplantation 59, no. 7 (April 1995): 1047–52. http://dx.doi.org/10.1097/00007890-199504150-00023.

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Swift, A. J., T. S. Collins, P. Bugelski, and J. A. Winkelstein. "Soluble human complement receptor type 1 inhibits complement-mediated host defense." Clinical and diagnostic laboratory immunology 1, no. 5 (1994): 585–89. http://dx.doi.org/10.1128/cdli.1.5.585-589.1994.

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Gillinov, A. Marc, Patrick A. DeValeria, Jerry A. Winkelstein, Ian Wilson, William E. Curtis, David Shaw, C. Grace Yeh, et al. "Complement inhibition with soluble complement receptor type 1 in cardiopulmonary bypass." Annals of Thoracic Surgery 55, no. 3 (March 1993): 619–24. http://dx.doi.org/10.1016/0003-4975(93)90264-i.

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Couser, W. G., R. J. Johnson, B. A. Young, C. G. Yeh, C. A. Toth, and A. R. Rudolph. "The effects of soluble recombinant complement receptor 1 on complement-mediated experimental glomerulonephritis." Journal of the American Society of Nephrology 5, no. 11 (May 1995): 1888–94. http://dx.doi.org/10.1681/asn.v5111888.

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Complement is a major mediator of tissue injury in several types of glomerulonephritis. However, no therapeutic agents that inhibit complement activation are available for human use. sCR1 (TP10, BRL 55736) is a recombinant, soluble human complement receptor 1 (CR1) molecule lacking transmembrane and cytoplasmic domains that inhibits C3 and C5 convertase activity by preferentially binding C4b and C3b. To test the efficacy of sCR1 on complement-mediated glomerulonephritis, rats were pretreated with sCR1 (60 mg/kg per day) before and during the induction of three models of complement-dependent glomerulonephritis (concanavalin A and antithymocyte serum models of proliferative glomerulonephritis, passive Heyman nephritis). Daily sCR1 and complement hemolytic activity levels were measured, and renal histology and urine protein excretion were examined. Mean serum sCR1 levels of 100 to 200 micrograms/mL were maintained with a reduction in complement hemolytic activity to less than 15% in most animals. In the antithymocyte serum model, sCR1-treated animals had significant reductions in mesangiolysis, glomerular platelet and macrophage infiltrates, and proteinuria at 48 h. In the concanavalin A model, sCR1 significantly reduced glomerular C3 and fibrin deposits, platelet infiltrates, and proteinuria at 48 h. In passive Heymann nephritis, proteinuria was also significantly reduced (199 +/- 8.5 versus 125 +/- 16 mg/day, P < 0.002) at 5 days. It was concluded that sCR1 significantly reduces both morphologic and functional consequences of several different types of complement-mediated glomerulonephritis and deserves evaluation as a potential therapeutic agent in complement-mediated immune glomerular disease in humans.

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Moulds, JM, and KE Rowe. "Neutralization of Knops system antibodies using soluble complement receptor 1." Transfusion 36, no. 6 (June 1996): 517–20. http://dx.doi.org/10.1046/j.1537-2995.1996.36696269510.x.

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Sadallah, Salima, Christoph Hess, Sylvie Miot, Olivier Spertini, Hans Lutz, and Jürg-Alfred Schifferli. "Elastase and metalloproteinase activities regulate soluble complement receptor 1 release." European Journal of Immunology 29, no. 11 (November 1999): 3754–61. http://dx.doi.org/10.1002/(sici)1521-4141(199911)29:11<3754::aid-immu3754>3.0.co;2-5.

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Cheung, Alfred K., Charles J. Parker, and Mary Hohnholt. "Soluble complement receptor type 1 inhibits complement activation induced by hemodialysis membranes in vitro." Kidney International 46, no. 6 (December 1994): 1680–87. http://dx.doi.org/10.1038/ki.1994.468.

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Lehmann, Thorsten G., Thomas A. Koeppel, Michael Kirschfink, Martha-Maria Gebhard, Christian Herfarth, Gerd Otto, and Stefan Post. "COMPLEMENT INHIBITION BY SOLUBLE COMPLEMENT RECEPTOR TYPE 1 IMPROVES MICROCIRCULATION AFTER RAT LIVER TRANSPLANTATION1,2." Transplantation 66, no. 6 (September 1998): 717–22. http://dx.doi.org/10.1097/00007890-199809270-00005.

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Dissertations / Theses on the topic "Soluble complement receptor 1"

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LUAN, NGUYEN MINH. "PROTECTION OF ISLETS OF LANGERHANS FROM COMPLEMENT MEDIATED CYTOTOXICITY." 京都大学 (Kyoto University), 2011. http://hdl.handle.net/2433/151986.

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Pierre, Andrew F. "The effect of complement inhibition with soluble complement receptor 1 (sCR1) on pig allo-transplant lung function." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ29290.pdf.

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Crehan, H. "Complement receptor 1 in microglia : implications for Alzheimer's disease." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1425685/.

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Recent genome wide association studies in Alzheimer’s disease have highlighted the importance of the complement cascade in the pathogenesis of Alzheimer’s disease. However, the cellular and molecular roles of these complement proteins are not fully understood. Microglia express complement receptors and the activation of specific receptors may increase Aβ clearance and reduce/prevent neurodegeneration. The work presented in this thesis was aimed at investigating the contribution of Complement receptor 1 (CR1), the second most significant hit in GWAS studies, on microglia to neuronal damage. To explore the consequences of blocking CR1 to microglial-neuronal interactions, primary rat microglia were treated with a CR1 functional blocking antibody together with microglial activators for 24 h. It was found that microglia displaying an activated phenotype demonstrated an increase in CR1 expression. Activation of microglial CR1 was found to be detrimental to neurons and this correlated with an increase in microglial intracellular superoxide generation, nitric oxide (NO) production, tumor necrosis factor-α (TNFα) and interleukin-1 β (IL-1β) secretion. Amyloid-β 1-42 (Aβ1-42)-treated microglia displayed an increased ability to phagocytose dextran beads following antibody blockade of CR1 but a decreased capacity to phagocytose fluorescent-tagged Aβ1-42. CR1 immunoreactivity was investigated by immunohistochemistry in AD and control human post-mortem brain tissue. A higher level of CR1 immunoreactivity was found in areas of high Aβ plaque burden in AD brain tissue. A difference in CR1 expression on red blood cells between individuals was measured by flow cytometry. Together, these results indicate that microglial CR1 plays a role in the neuronal death observed in AD and investigating this further may provide a possible strategy to control neurotoxicity in the AD brain.

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Masilamani, Madhan. "Immunological investigation of human complement receptor type II (CR2/CD21) : serum soluble CD21 in health and disease /." Konstanz, 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=967076668.

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Imrie, Heather. "Studies on the reduction in expression of erythrocyte complement receptor 1." Thesis, University of Nottingham, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363932.

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Clark, Nicola Suzanne. "Structural and functional studies on SCR domains from human complement receptor 1." Thesis, University of Southampton, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242559.

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McKeeman, G. C. "The measurement of circulation soluble vascular endothelial growth factor receptor-1 (sFlt-1)." Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273085.

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Murase, Takatoshi. "Identification of soluble forms of lectin-like oxidized LDL receptor-1." Kyoto University, 2004. http://hdl.handle.net/2433/148276.

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Mitsuoka, Hirokazu. "Interleukin 18 stimulates release of soluble lectin-like oxidized LDL receptor-1(sLOX-1)." Kyoto University, 2008. http://hdl.handle.net/2433/124235.

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Etheridge, W. "Production of soluble recombinant complement receptor (CR1) antigens to detect or inhibit antibodies to Knops (KN) blood group system antigens." Thesis, University of the West of England, Bristol, 2015. http://eprints.uwe.ac.uk/26375/.

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The purpose of this study was to produce a reagent to use in investigation of antibodies directed against the Knops blood group system antigens. A novel reagent based on sr-proteins was produced and used in a new test to inhibit these antibodies. Current investigation of patients with alloantibodies directed against Knops blood group system antigens can be a difficult, time-consuming process and the provision of blood for transfusion of these patients can often be delayed. This is because these antibodies are hard to identify and the most commonly found anti-Knops antibodies react with most reagent or donor cells that they are tested with because the corresponding Knops antigens are found at high frequency in most populations. The presence of Knops related antibodies can mask underlying antibodies that are clinically significant. The Knops antigens are carried on Complement Receptor 1 (CR1) located on the red blood cell membrane. Two DNA constructs encoding different parts of CR1 termed long homologous repeat (LHR) C and D were used to transfect human embryonic kidney (HEK293) cells. The cells were grown in different culture systems. Cell culture supernatant containing soluble recombinant (sr)-LHRC or sr-LHR-D was harvested and purified by affinity gel chromatography. The production and purification processes were optimised in terms of protein yield and cost. The resulting purified sr-LHR-C and sr-LHR-D proteins were used to create a novel reagent containing both proteins. This reagent was used in a new inhibition test based on an indirect antiglobulin technique using commercial gel cards. Using the reagent all examples of previously identified Knops antibodies were inhibited. In addition once these antibodies had been inhibited, underlying antibodies were then detected and identified in some samples. For the first time Knops specific antibodies can be detected and identified using one unique test. Any underlying clinically significant antibodies will be rapidly identified if present due to inhibition of the KN antibodies. Introduction of the inhibition test into nine NHSBT patient testing laboratories will reduce the time taken for investigation of these patients and make provision of blood for patients a safer, faster process.

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Books on the topic "Soluble complement receptor 1"

1

Pierre, Andrew F. The effect of complement inhibition with soluble complement receptor 1 (sCR1) on pig allo-transplant lung function. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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2

Oran, Alp Eren. Definging sites of interaction in the A-chain of C3 for factor H, membrane cofactor protein (MCP), and complement receptor 1 (CR1). Ottawa: National Library of Canada, 1997.

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3

Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.

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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.

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Complement Receptor Type 1(Cr1) on Human Erythrocytes: Functional Studies With Particular Reference to the Interaction With Complement Opsonized Immune Complexes. Univ Pr of Southern Denmark, 1992.

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Book chapters on the topic "Soluble complement receptor 1"

1

Pruitt, Scott K., William M. Baldwin, R. Randall Bollinger, Henry C. March, and Fred Sanfillippo. "Soluble Complement Receptor and Hyperacute Rejection." In Vascular Endothelium, 3–10. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0355-8_1.

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Marsh, H. C., and U. S. Ryan. "Therapeutic Effect of Soluble Complement Receptor Type 1 in Xenotransplantation." In Xenotransplantation, 437–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60572-7_33.

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Nishiura, Hiroshi. "The Alternative C5a Receptor Function." In Complement Therapeutics, 111–21. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4118-2_7.

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Ross, G. D. "Complement Receptor Type 1." In Membrane Defenses Against Attack by Complement and Perforins, 31–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77014-2_3.

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Tolnay, Mate, and George C. Tsokos. "Regulation of Complement Receptor Gene Expression." In The Complement System, 61–73. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/1-4020-8056-5_4.

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Qidwai, Tabish. "Human Complement Receptor 1 Polymorphisms." In Exploration of Host Genetic Factors associated with Malaria, 113–22. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4761-8_10.

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Nielsen, Gitte Krogh, and Thomas Vorup-Jensen. "Detection of Soluble CR3 (CD11b/CD18) by Time-Resolved Immunofluorometry." In The Complement System, 355–64. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-724-2_30.

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Donius, Luke R., and John H. Weis. "Quantification of Complement Receptor 2 Calcium Signaling Enhancement Using Flow Cytometry." In The Complement System, 311–17. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-724-2_25.

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Fearon, D. T., and J. M. Ahearn. "Complement Receptor Type 1 (C3b/C4b Receptor; CD35) and Complement Receptor Type 2 (C3d/Epstein-Barr Virus Receptor; CD21)." In Current Topics in Microbiology and Immunology, 83–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74977-3_5.

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Lord, Jenny, and Kevin Morgan. "Complement Component (3b/4b) Receptor 1 (CR1)." In Genetic Variants in Alzheimer's Disease, 77–101. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7309-1_5.

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Conference papers on the topic "Soluble complement receptor 1"

1

Krasnoshtanova, Alla, and Alesya Yudina. "PRODUCTION OF ANTIBODIES FROM POULTRY YOLK (IgY) AND INVESTIGATION OF THEIR IMMUNOCHEMICAL PROPERTIES." In GEOLINKS Conference Proceedings. Saima Consult Ltd, 2021. http://dx.doi.org/10.32008/geolinks2021/b1/v3/17.

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"A particularly important aspect of immunology is to develop non-invasive methods of obtaining antibodies which could be a great alternative to traditional ones that based on the harmful procedure of isolation of immunoglobulins from animal blood sera. That’s why the extraction of antibodies from poultry egg yolks (IgY) is the most promising. Due to the fact of variation of IgY structural features that determine the definite immunochemical properties, yolk antibodies in comparison with mammalian immunoglobulins (IgG) does not interact with rheumatoid factor (Rf), contribute to the activation of the complement system, bind to the Fc-receptor (FcR), and also has weak cross-reactivity, which confirms the possibility of their widespread use in medicine and food. Also the presence of phylogenetic distance between chickens and mammalians guarantees immune response against conservative mammalian protein molecules which is highly important for the creation of new generation test systems. The aim of this work is to develop a selective method of producing high-purity immunoglobulin Y preparations from the yolk of chicken eggs. There were adopted selective conditions of isolation of IgY under spontaneous thawing procedure at the room temperature of firstly frozen yolk solution in a sodium-phosphate buffer mixed with water (pH 5.0) in a ratio of 1:6, which leads to receiving a water-soluble fraction further precipitated with the sodium chloride at a concentration of 10% of the solution mass and subsequently concentrated using ultrafiltration with membrane UAM-10, that allows achieving the content of IgY not less than 95% per dry substance in immunoglobulin fraction. It is possible to produce a protein fraction with a protein content of at least 9 g/l. The purity of the immunoglobulin fraction was verified using polyacrylamide gel electrophoresis. The presence of a light chain in the IgY solution was proved to be a low-molecular compound using the method of gel-filtration-chromatography. The immunological activity of IgY was studied with respect to bovine serum albumin (BSA) as an antigen. The enzymatic resistance of IgY against proteolytic enzymes was tested in area of the gastrointestinal tract."

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Lin, C., C. Ho, M. Yao, S. Hsu, and C. Yu. "sTREM-1 (Soluble Triggering Receptor Expressed on Myeloid Cells-1) as Marker Indicating Infection in Patients with Neutropenic Fever." 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.a4704.

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Testa, Nathan, Laura Bartle, Olga Ab, Judy Cheng, Gillian Payne, Robert J. Lutz, Ben Wolf, and Christina Carrigan. "Abstract 3503: A method for quantifying soluble folate receptor 1 in IMGN853 0401 clinical trial patients." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3503.

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Makey, K., SG Patterson, J. Robinson, M. Loftin, DE Waddell, L. Miele, E. Chinchar, et al. "P3-08-03: Exercise Increases Soluble Vascular Endothelial Growth Factor Receptor-1 (sFlt-1) in the Circulation of Adult Women." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p3-08-03.

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Ji, Yu bin, Chen feng Ji, and Yong cui Min. "Effect of Asparagus polysaccharide on the number and activity of erythrocyte complement receptor 1(CD35) of S180 mice." In 2009 ICME International Conference on Complex Medical Engineering - CME 2009. IEEE, 2009. http://dx.doi.org/10.1109/iccme.2009.4906583.

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Ji, Yu bin, Chen feng Ji, and Yong cui Min. "Effect of Asparagus polysaccharide on the number and activity of erythrocyte complement receptor 1(CD35) of S180 mice." In Education (ITIME). IEEE, 2009. http://dx.doi.org/10.1109/itime.2009.5236266.

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Ji, Chenfeng, Yubin Ji, Yongcui Min, and Xuejun Chen. "Effect of Asparagus Polysaccharide on the Number and Activity of Erythrocyte Complement Receptor 1(CD35) of S180 Mice." In 2009 3rd International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2009. http://dx.doi.org/10.1109/icbbe.2009.5162685.

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Ji, Yu bin, Chen feng Ji, and Yong cui Min. "Effect of Asparagus Polysaccharide on the Number and Activity of Erythrocyte Complement Receptor 1(CD35) of S180 Mice." In 2009 2nd International Conference on Biomedical Engineering and Informatics. IEEE, 2009. http://dx.doi.org/10.1109/bmei.2009.5305665.

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Jeremic, I., N. Stojanovic, Z. Stanojevic, B. Jovanovic, J. Tosic, S. Vidicevic, and A. Isakovic. "AB0582 Soluble triggering receptor expressed on myeloid cells-1 (STREM-1) and adrenomedulin are elevated in patients with systemic lupus erythematosus." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6570.

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Mitchell, Dianne, Eileen G. Pobre, Aaron W. Mulivor, Asya V. Grinberg, Roselyne Castonguay, Travis E. Monnell, Nicolas Solban, et al. "Abstract B5: ACE‐041, a soluble activin receptor‐like kinase‐1 fusion protein, is a novel antiangiogenic agent." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b5.

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