Relevant bibliographies by topics / Antibody avidity

Contents

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

Academic literature on the topic 'Antibody avidity'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Antibody avidity"

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Arifa, Julian Eva, Budiman Bela, Silvia Tri Widyaningtyas, and Jeanne Elvia Christian. "Penggunaan antigen p24, IDR-Gp41 dan ID2-Pol dalam uji aviditas untuk identifikasi kasus baru pada infeksi HIV-1." Jurnal Biotek Medisiana Indonesia 8, no. 1 (December 18, 2019): 1–8. http://dx.doi.org/10.22435/jbmi.v8i1.2578.

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AIDS is a severe immunodeficiency disease caused by HIV. Identification of new HIV infection in a population is required for the evaluation of intervention strategy of HIV-1 transmission. The avidity assay has been promoted for HIV-1 detection. Avidity assay is based on affinity strength of the epitopes of the HIV antigen against its specific corresponding antibodies. The binding of the antigen - the antibody formed in the initial phase of infection is relatively weak and easy to break with chaotropic reagents. In contrary, the antigen-antibody binding formation in long-term infection is stron
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Racine-Brzostek, Sabrina E., Mohsen Karbaschi, Christian Gaebler, P. J. Klasse, Jim Yee, Marina Caskey, He S. Yang, et al. "TOP-Plus Is a Versatile Biosensor Platform for Monitoring SARS-CoV-2 Antibody Durability." Clinical Chemistry 67, no. 9 (April 29, 2021): 1249–58. http://dx.doi.org/10.1093/clinchem/hvab069.

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Abstract Background Low initial severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antibody titers dropping to undetectable levels within months after infection have raised concerns about long-term immunity. Both the antibody levels and the avidity of the antibody–antigen interaction should be examined to understand the quality of the antibody response. Methods A testing-on-a-probe “plus” panel (TOP-Plus) was developed to include a newly developed avidity assay built into the previously described SARS-CoV-2 TOP assays that measured total antibody (TAb), surrogate neutralizing antibod
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Pereira Arias-Bouda, Lenka M., Sjoukje Kuijper, Anouk Van Der Werf, Lan N. Nguyen, Henk M. Jansen, and Arend H. J. Kolk. "Changes in Avidity and Level of Immunoglobulin G Antibodies to Mycobacterium tuberculosis in Sera of Patients Undergoing Treatment for Pulmonary Tuberculosis." Clinical Diagnostic Laboratory Immunology 10, no. 4 (July 2003): 702–9. http://dx.doi.org/10.1128/cdli.10.4.702-709.2003.

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ABSTRACT Much is known about specific antibodies and their titers in patients with tuberculosis. However, little is known about the avidity of these antibodies or whether changes in avidity occur during the progression of the disease or during treatment. The aims of this study were to determine the avidity of antibodies to Mycobacterium tuberculosis in patients with pulmonary tuberculosis, to explore the value of avidity determination for the diagnosis of tuberculosis, and to study changes in levels of antibodies and their avidity during treatment. Antibody avidity was measured by an enzyme-li
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Intner, Sara, Michelle Altrich, and Niraj Patel. "Comparison of Pneumococcal Avidity and Antibody Concentration in Children with Recurrent Infections: A Retrospective Pilot Study." Journal of Immunological Sciences 4, no. 4 (October 10, 2020): 24–30. http://dx.doi.org/10.29245/2578-3009/2020/4.1194.

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Measurement of pneumococcal antibody concentration is a frequently used parameter for functional antibody response to vaccination. Antibody concentration in response to vaccination and strength of antigen-antibody (avidity) interaction are both important measurements of functional antibody response. Both antibody concentration and avidity contribute to immunity against invasive pneumococcal disease. Higher avidity is correlated with increasing bactericidal activity and opsonophagocytosis. On the other hand, patients with lower pneumococcal avidity may be more likely to develop clinically signi
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Tiburcio, Monique Gomes Salles, Laís Anversa, Kelly Aparecida Kanunfre, Antonio Walter Ferreira, Virmondes Rodrigues Júnior, and Luciana de Almeida Silva. "Anti-Leishmania infantum IgG Antibody Avidity in Visceral Leishmaniasis." Clinical and Vaccine Immunology 20, no. 11 (September 4, 2013): 1697–702. http://dx.doi.org/10.1128/cvi.00367-13.

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ABSTRACTIgG avidity tests are used to discriminate acute from chronic infections. There are few reports on the IgG avidity profile of patients with visceral leishmaniasis (VL). This study investigated the anti-LeishmaniaIgG avidity in patients with classic VL (n= 10), patients showing clinical cure after treatment (n= 18), and asymptomatic subjects with at least one positiveLeishmaniatest (n= 20). All subjects were from areas in Brazil where VL is endemic. Serum samples were collected from each subject on two different occasions. IgG avidity was evaluated by Western blotting. The proportion of
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Marcipar, Iván S., Marikena G. Risso, Ariel M. Silber, Silvia Revelli, and Alberto J. Marcipar. "Antibody Maturation in Trypanosoma cruzi-Infected Rats." Clinical Diagnostic Laboratory Immunology 8, no. 4 (July 1, 2001): 802–5. http://dx.doi.org/10.1128/cdli.8.4.802-805.2001.

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ABSTRACT The study of antibody avidity changes during infection has improved the understanding of the pathologic processes involved in several infectious diseases. In some infections, like toxoplasmosis, this information is being used for diagnostic purposes. Results of the evolution of antibody avidity for different specific antigens inTrypanosome cruzi-infected rats are presented. A Western blotting technique, combined with avidity analysis to identify antigens that elicit high-avidity antibodies, is suggested. In this system, antibodies showed high avidity values only during the chronic pha
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Alex, Diviya, Tennison Inba Raj Williams, Jaiprasath Sachithanandham, Swaminathan Prasannakumar, John Paul Demosthenes, Veena Vadhini Ramalingam, Punitha John Victor, Priscilla Rupali, Gnanadurai John Fletcher, and Rajesh Kannangai. "Performance of a Modified In-House HIV-1 Avidity Assay among a Cohort of Newly Diagnosed HIV-1 Infected Individuals and the Effect of ART on the Maturation of HIV-1 Specific Antibodies." Current HIV Research 17, no. 2 (September 2, 2019): 134–45. http://dx.doi.org/10.2174/1570162x17666190712125606.

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Background: Viral kinetics impact humoral immune response to HIV; antibody avidity testing helps distinguish recent (<6 months) and long-term HIV infection. This study aims to determine the frequency of recent HIV-1 infection among clients attending ICTC (Integrated Counselling and Testing Centre) using a commercial EIA, to correlate it with a modified in-house avidity assay and to study the impact of ART on anti-HIV-1 antibody maturation. Method: Commercial LAg Avidity EIA was used to detect antibody avidity among 117 treatment naïve HIV-1 infected individuals. A second-generation HIV ELIS
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Yoshida, Márcia, Maria Carmen Arroyo Sanchez, and Maria Aparecida Shikanai-Yasuda. "Increased Immunoglobulin G Anti-Paracoccidioides brasiliensis Serum Antibody Avidity as a Predictor of Favorable Posttherapeutic Evolution in Paracoccidioidomycosis." Clinical and Vaccine Immunology 16, no. 11 (September 2, 2009): 1583–86. http://dx.doi.org/10.1128/cvi.00265-09.

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ABSTRACT Paracoccidioidomycosis is endemic in Latin America, and ca. 80% of all cases occur in Brazil. Little is known about antibody avidity or the evolution of such avidity in the posttherapeutic period for the different clinical presentations of the disease. In the present study, we evaluated 53 patients with paracoccidioidomycosis and calculated the avidity index. Medium- and high-avidity antibodies were found in 79.5% of patients with chronic presentation (n = 39). Among patients with the acute form (n = 14), 57.1% of the antibodies presented low avidity. In the posttherapeutic period, th
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Chan, K. H., K. Sonnenberg, M. Niedrig, S. Y. Lam, C. M. Pang, K. M. Chan, S. K. Ma, W. H. Seto, and J. S. M. Peiris. "Use of Antibody Avidity Assays for Diagnosis of Severe Acute Respiratory Syndrome Coronavirus Infection." Clinical and Vaccine Immunology 14, no. 11 (September 19, 2007): 1433–36. http://dx.doi.org/10.1128/cvi.00056-07.

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ABSTRACT An indirect immunofluorescent assay (Euroimmun AG, Luebeck, Germany) was used to investigate the avidity of immunoglobulin G (IgG), IgM, IgA, and total Ig (IgGAM) antibody responses to severe acute respiratory syndrome coronavirus (SARS CoV) infections. Serial serum samples from eight patients collected during the first, third, and ninth months after the onset of infection were evaluated. It was found that low-avidity IgG antibodies were detected in 15/15 (100%), 1/5 (20%), and 0/8 (0%) serum samples collected during the first, third, and ninth months after the onset of symptoms, resp
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Griswold, William R. "A Quantitative Relationship Between Antibody Affinity and Antibody Avidity." Immunological Investigations 16, no. 2 (January 1987): 97–106. http://dx.doi.org/10.3109/08820138709030567.

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Dissertations / Theses on the topic "Antibody avidity"

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Canelle, Quentin. "Real Time Surface Plasmon Resonance Biosensors, a Powerful Technology to Assess Polyclonal Antibody Avidity." Doctoral thesis, Universite Libre de Bruxelles, 2015. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/216754.

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The present research focused on the development of a new methodology to assess the strength of the interaction between vaccine antigens and elicited polyclonal antibodies through SPR biosensors. Quantifying the binding strength of polyclonal antibodies is of first importance to evaluate the quality of the vaccine as well as to increase the scientific knowledge of immune protection mechanisms. To now the development of such tool has been complicated by the non-specific binding caused by high protein abundance in the blood and serum samples but also by the way of interpreting the data resulting
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Newman, Peter Michael Pathology UNSW. "Antibody and Antigen in Heparin-Induced Thrombocytopenia." Awarded by:University of New South Wales. Pathology, 2000. http://handle.unsw.edu.au/1959.4/17485.

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Immune heparin-induced thrombocytopenia (HIT) is a potentially serious complication of heparin therapy and is associated with antibodies directed against a complex of platelet factor 4 (PF4) and heparin. Early diagnosis of HIT is important to reduce morbidity and mortality. I developed an enzyme immunoassay that detects the binding of HIT IgG to PF4-heparin in the fluid phase. This required techniques to purify and biotinylate PF4. The fluid phase assay produces consistently low background and can detect low levels of anti-PF4-heparin. It is suited to testing alternative anticoagulants because
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Meireles, Luciana Regina. "Estudo das Fontes de Infecção da Toxoplasmose Humana em Diferentes localidades do Estado de São Paulo." Universidade de São Paulo, 2001. http://www.teses.usp.br/teses/disponiveis/42/42135/tde-24112004-110833/.

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A toxoplasmose é uma protozoose de alta prevalência no Brasil, causada pelo Toxoplasma gondii, sendo transmitida pela ingestão de alimentos contaminados com oocistos, excretados em fezes de felinos, ou cistos, em carnes cruas ou mal cozidas. A doença é usualmente assintomática, mas em fetos ou pacientes com imunodepressão, pode ser devastadora. Neste trabalho, estudamos a prevalência sorológica da infecção em animais de diferentes regiões do estado de São Paulo, tanto de vida livre, cães (200/ABC) como indicadores ambientais, e gatos (100/São Paulo) como hospedeiros definitivos, e em animais d
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Santana, Silas Silva. "Análise cinética da resposta imune humoral contra a proteína recombinante SAG2A em pacientes com Toxoplasmose aguda." Universidade Federal de Uberlândia, 2011. https://repositorio.ufu.br/handle/123456789/16676.

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Fundação de Amparo a Pesquisa do Estado de Minas Gerais<br>Recombinant proteins from Toxoplasma gondii have been used in several experimental models, as well as for serodiagnosis of human toxoplasmosis, particularly to differentiate acute from chronic phases of the infection. In the present study, we evaluated the kinetics of IgM, IgA, and IgG isotypes, in addition to IgG1 and IgG3 subclasses, by testing sequential serum samples from patients with acute toxoplasmosis. It was carried out immunoassays by using SAG2A recombinant antigen and soluble antigen of Toxoplasma (STAg). The avidity of IgG
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Cilla, Brian. "Comparison of two methods for estimating antibody avidity a thesis submitted in partial fulfillment ... Master of Science in Periodontics ... /." 1989. http://books.google.com/books?id=St89AAAAMAAJ.

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Books on the topic "Antibody avidity"

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Fard, Amir Hossein Mohagheghi. Positivity for and avidity of human herpesviruses IgG antibody determined by ELISA. Manchester: University of Manchester, 1996.

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Bristow, Michelle A. Measurement of antibody avidity for hepatitis B virus. 1996.

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Lyons, Marie. The development of a redioimmunoassay for use in antibody avidity measurements in the diagnosis of human herpesvirus-6 infections. 1995.

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Book chapters on the topic "Antibody avidity"

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Bruderer, U., E. Fürer, S. J. Cryz, and A. B. Lang. "The Role of Human Monoclonal Antibody Specificity and Avidity in the Protection Against Gram-negative Bacteria." In Immunotherapeutic Prospects of Infectious Diseases, 373–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-76120-1_50.

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Dakshinamurti, Krishnamurti, and Edward S. Rector. "[12] Monoclonal antibody to biotin." In Avidin-Biotin Technology, 111–19. Elsevier, 1990. http://dx.doi.org/10.1016/0076-6879(90)84266-j.

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KOSTULAS, V., T. OLSSON, and H. LINK. "Detection of Oligoclonal IgG in Unconcentrated Cerebrospinal Fluid by Agarose Isoelectric Focusing and Double Antibody Avidin–Biotin-Peroxidase." In Protides of the Biological Fluids, 171–74. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-08-031739-7.50044-6.

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Shively, John E., Christoph Wagener, and Brian R. Clark. "[43] Solution-phase RIA and solid-phase EIA using avidin-biotin systems for analysis of monoclonal antibody epitopes and affinity constants." In Immunochemical Techniques Part I: Hybridoma Technology and Monoclonal Antibodies, 459–72. Elsevier, 1986. http://dx.doi.org/10.1016/0076-6879(86)21045-9.

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"from CD99 high expressors but membranes from CD99 low expressors required exposure of 5 minutes before the 32 kD band was apparent [50]. Unfortunately, these tests gave no information about the Xga protein because the position of the Xga band was masked by the antibody light chain which became labelled. However, a 32 kD band was seen in the Xga-immunoprecipitate from Xg(a+) but not from Xg(a-) cells [50]. It has not yet been proved that this is the CD99 protein because this band was not stained by immunoblotting Xga-immunoprecipitates with 12E7. The luciferin-enhanced luminescent proceedure to detect the avidin-biotin label is very much more sensitive than immunoblotting. Our results support the theory that Xga and CD99 may be associated in the membrane. Cloning of the XG gene will increase our understanding of this relationship. The important blood group genes have been cloned but two big problems remain, regulation on antigen expression and the function of blood group polymorphisms. Rare phenotypes should still be studied because they will contribute to unravelling the mechanisms responsible for the polymorphisms. The wealth of serological information which continues to increase includes many examples of variable expression of red cell antigens. Some antigens do not show the same variation on other cells suggesting that some modes of regulation may be limited to red cells. Association of blood group antigens with proteins of known function and identification of red cell antigens on cells other than red cells will contibute to understanding the functions of the blood group polymorphisms. REFERENCES 1. P.L. Mollison, C.P. Engelfreit and M. Contreras, Blood Transfusion in Clinical Medicine. Blackwell Scientfic Publications, Oxford (1993). 2. M. Lewis (Chairman) et al, Vox Sang., 61_, 158-160 (1991). 3. G.L. Daniels, J.J. Moulds (chairman) et al, Vox Sang., 65, 77-80 (1993). 4. A.C. Petty, J. Immunol. Meth., 161. 91-95 (1993). 5. J. M. Moulds, in Immunobiology of Transfusion Medicine. G. Garratty ed. Marcel Dekker. Inc., New York, (1994) pp. 273-297. 6. J.M. Moulds, M.W. Nickells, J.J. Moulds, M.C. Brown and J.P. Atkinson, J. Exp. Med., 173, 1159-1163 (1991). 7. N. Rao, D.J. Ferguson, S-F. Lee and M.J. Telen, J. Immun., 146, 3502-3507 (1991). 8. A.C. Petty, (abs) Transfusion Medicine 3 Suppl 1, 84 (1993). 9. J.M. Moulds, J.J. Moulds, M. Brown and J.P. Atkinson, Vox Sang. 62, 230-235 (1992)." In Transfusion Immunology and Medicine, 198. CRC Press, 1995. http://dx.doi.org/10.1201/9781482273441-16.

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"designation will be used for the 12E7 antigen. CD99 was first detected by 12E7, a monoclonal antibody made in response to a T-cell line, and was initially thought to be a ‘thymus-leukaemia’ marker antigen [41]. Many similar antibodies were made which reacted with different epitopes of the same molecule [see 42]. Independently, CD99 was identified as E2, a T-cell adhesion molecule, and as a marker antigen for Ewing’s tumours [see 40]. CD99 is expressed on many tissues including red cells. By somatic cell hybridization and biochemical studies, Goodfellow and his colleagues have shown that MIC2, the structural locus encoding the 12E7 antigen, is located on the short arm of the X chromosome and on the short arm of the Y chromosome within the pairing regions [43]. MIC2 has been cloned [44]. XG is X-borne. On red cells, CD99 expression is a quantitative polymorphism [45]. Family studies proved that this polymorphism is also caused by regulator genes on X and Y chromosomes. XG appears to be the regulator on the X [46]. There is variation in CD99 expression on cells other than red cells. In a recent publication, CD99 was found on all haemopoeitic cells but was variably expressed during leucocyte differentiation [40]. Use of different monoclonal antibodies and variability of expression during maturation offered an explanation for the previous apparently contradictory findings by different laboratories. Both Xga and CD99 are sialoglycoproteins [47,48,49]. These glycoproteins differ in Mr and in their sialic acid content [49]. Immunostaining of separated membrane components with 12E7 and similar antibodies had demonstated that the MIC2 gene product was a 30-32 kD protein. 12E7 also bound to an intracellular band of 28 kD which was found in mouse cell lines in addition to human cell lines, platelets, lymphocytes and red cells but it was not encoded by the MIC2 gene [47]. Immunoblotting assays have shown that Xga was associated with two diffuse bands of 22-25 kD and 26.5-29 kD [49]. These findings supported the evidence that Xga and CD99 were products of different structural loci. However, XG appears to regulate CD99 expression on red cells and Latron and colleagues found that purified CD99 protein inhibited binding of 12E7 and of anti-Xga to red cells [48]. We have studied the immunochemical relationship of Xga and CD99 [50]. One approach was immunoprecipitation of membrane components from biotin labelled cells. Bands are detected by chemiluminescence via peroxidase-conjugated avidin. The 32 kD protein of CD99 was visualised by this technique and the quantitative polymorphism was also demonstrated since the 32 kD band is seen on X-ray film after 2 minutes in membranes." In Transfusion Immunology and Medicine, 197. CRC Press, 1995. http://dx.doi.org/10.1201/9781482273441-15.

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Conference papers on the topic "Antibody avidity"

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Friess, Thomas, Stefanie Lechner, Esther Abraham, Ann-Marie Broeske, Sabine Bader, Andreas Roller, Meher Majety, et al. "Abstract 952: Induction of avidity-driven hyperclustering of DR5 by a new FAP-DR5 bispecific antibody (RG7386) leads to strong anti-tumor efficacy." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-952.

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Deak, Laura Laura Codarri, Stefan Seeber, Mario Perro, Patrick Weber, Laura Lauener, Standford Chen, Sonja Offner, et al. "Abstract 2270: RG7769 (PD1-TIM3), a novel heterodimeric avidity-driven T cell specific PD-1/TIM-3 bispecific antibody lacking Fc-mediated effector functions for dual checkpoint inhibition to reactivate dysfunctional T cells." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2270.

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Narang, Upvan, George P. Anderson, Keeley D. King, Heidi S. Liss, and Frances S. Ligler. "Enhanced biosensor performance using an avidin-biotin bridge for antibody immobilization." In BiOS '97, Part of Photonics West, edited by Richard B. Thompson. SPIE, 1997. http://dx.doi.org/10.1117/12.273534.

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Meyers, K. M., K. J. Wardrop, C. M. Helmick, and F. P. White. "PRESENCE OF VWF IN VASCULAR ENDOTHELIUM BUT NOT PLATELETS FROM CONTROL DOGS AND VIIIR:AG-DEFICIENT DOGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644501.

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Blood vessels from control and VIIIR:AG-deficient dogs (plasma VIIIR:AG was &lt;5% of control) were surgically removed, cryosectioned, airdried and processed for immunohistochemical detection of VWF using a monoclonal antibody against human VWF, a polyclonal antibody against human VWF, and a polyclonal antibody against canine VWF. All antibodies were monospecific for canine VWF. The secondary antibody was conjugated to fluorescein or rhodamine. A biotin-avidin system was also used. Each antibody detected VIIIR:AG in veins, venules, and arterioles from control and VIIIR:AG-deficient dogs. Immun
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Risberg, B., G. K. Hansson, E. Eriksson, and B. Wiman. "IMMUNOHISTOCHEMICAL LOCALIZATION OF PLASMINOGEN ACTIVATOR INHIBITOR (PAI) IN TISSUE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644443.

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The origin of tissue plasminogen activator inhibitor (PAI) has not been fully elucidated. Platelets are rich in PAI and endothelial cells (EC) in culture produce the inhibitor (PAI 1), which seems to be a major secretory protein. Another inhibitor (PAI 2) has been demonstrated in the placenta. In the present study we localized PAI 1 in various human tissues using a polyclonal antibody against human PAI 1 and fluorescence technique. Tissue sections were incubated with a polyclonal rabbit-anti-human PAI antibody in various dilutions followed by incubation with biotinylated goat-anti-rabbit IgG a
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Mathew, Trupthi, Punarvasu Joshi, Shalini Prasad, Michael Goryll, Andreas Spanias, and Trevor J. Thornton. "Silicon Based Pore Systems for Emerging Biosensor Applications." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-11707.

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Recent research in the domain of single molecule biosensors aims at using silicon pore systems for the electrical detection of charged entities. Detection is achieved through resistive pulse measurements also known as Coulter counting. This work demonstrates the use of silicon based cylindrical micropores which can be used to detect biomolecules with high selectivity and robustness. The micropores used in the experiment were patterned using semiconductor processing techniques to have a final diameter of 5μm and a length of 30μm on a siliconsubstrate. The probes used in the study were silica be
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Tomaslni, B. R., and D. F. Mosher. "PREFERENTIAL RECOGNITION OF VITRONECTIN (S-PR0TEIN) BY A MONOCLONAL ANTIBODY UPON INTERACTION WITH THROMBIN, ANTITHROMBIN AND GLYCOSAMINOGLYCANS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643634.

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V1tronect1n/S-Prote1n (VN/SP) is a glycoprotein present at a concentration of 200-400 ug/ml 1n plasma and serum. It has been shown to promote cel 1-substratum adhesion and to act as an Inhibitor of the membrane attack complex of complement and of the inactivation of thrombin by antithrombin III in the presence of low levels of heparin. We have previously shown that VN/SP binds more avidly to heparln-agarose and to a monoclonal antibody (MaVN/SP)-Sepharose column when present 1n serum rather than 1n plasma. In order to examine the possibility of a serum-induced conformational change, we utilize
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Hirai, K., K. Yasunaga, and R. Ryo. "STUDIES ON PLATELET ANTIGENS AGAINST SERA FROM PATIENTS WITH ITP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644583.

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Chronic idiopathic thrombocytopenic purpura (ITP) is a clinical syndrome characterized by destruction of platelets by antiplatelet antiboodies. The precise pathogenic mechanism of platelet destruction in ITP is not known, although many investigators have reported that platelet-associated IgG (PAIgG) is increased in this desease. We have evaluated PAIgG in 66 patients with ITP by a competitive solidphase microenzyme immunoassay and investigated its specificity aganist antiplatelet antibody in 24 patients with ITP by Western blotting. PAIgG values were elevated in most ITP patients with platelet
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Rodríguez, José A., Héctor E. López-Valdes, Gustavo F. Helguera, Sokuntheavy So, Rosendo Luria-Pérez, Tracy R. Daniels, Andrew C. Charles, and Manuel L. Penichet. "Abstract 4456: Molecular events required for the induction of lethal iron deprivation in malignant hematopoietic cells via an antibody-avidin fusion protein specific for human transferrin receptor 1." 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.am10-4456.

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Grøndahl-HANSEN, J., N. Agerlin, L. S. Nielsen, and K. Danø. "SENSITIVE AND SPECIFIC ENZYME-LINKED IMMUNOSORBENT ASSAY FOR UROKINASE-TYPE PLASMINOGEN ACTIVATOR IN HUMAN PLASMA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644425.

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An enzyme-linked immunosorbent assay (ELISA) was developed for the measurement of human urokinase-type plasminogen activator (u-PA) in plasma and serum. Microtiter plates were coated with a monoclonal antibody and incubated with standard or sample. Bound u-PA was quantitated with polyclonal antibodies conjugated with biotin, followed by avidin-peroxidase. The assay was 10-fold as sensitive as other previously reported ELISAs, the detection limit being approximately 1 pg of u-PA in a volume of 100 μl with a linear dose-response up to 15 pg of u-PA. The assay detected active u-PA and its inactiv
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