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Artykuły w czasopismach na temat "Phospholipid antibodies"
Out, HJ, PG de Groot, M. van Vliet, GC de Gast, HK Nieuwenhuis i RH Derksen. "Antibodies to platelets in patients with anti-phospholipid antibodies". Blood 77, nr 12 (15.06.1991): 2655–59. http://dx.doi.org/10.1182/blood.v77.12.2655.2655.
Pełny tekst źródłaOut, HJ, PG de Groot, M. van Vliet, GC de Gast, HK Nieuwenhuis i RH Derksen. "Antibodies to platelets in patients with anti-phospholipid antibodies". Blood 77, nr 12 (15.06.1991): 2655–59. http://dx.doi.org/10.1182/blood.v77.12.2655.bloodjournal77122655.
Pełny tekst źródłaRauch, J., i AS Janoff. "Antibodies against Phospholipids other than Cardiolipin: Potential Roles for Both Phospholipid and Protein". Lupus 5, nr 5 (październik 1996): 498–502. http://dx.doi.org/10.1177/096120339600500534.
Pełny tekst źródłaHarris, EN, i SS Pierangeli. "Functional Effects of Anticardiolipin Antibodies". Lupus 5, nr 5 (październik 1996): 372–77. http://dx.doi.org/10.1177/096120339600500507.
Pełny tekst źródłaBRIGHTON, Timothy A., Yan-Ping DAI, Philip J. HOGG i Colin N. CHESTERMAN. "Microheterogeneity of beta-2 glycoprotein I: implications for binding to anionic phospholipids". Biochemical Journal 340, nr 1 (10.05.1999): 59–67. http://dx.doi.org/10.1042/bj3400059.
Pełny tekst źródłaHarris, E. N., A. E. Gharavi i G. R. V. Hughes. "Anti-phospholipid Antibodies". Clinics in Rheumatic Diseases 11, nr 3 (grudzień 1985): 591–609. http://dx.doi.org/10.1016/s0307-742x(21)00606-8.
Pełny tekst źródłaTincani, A., L. Andreoli i Y. Shoenfeld. "Anti-phospholipid antibodies". Rheumatology 53, nr 2 (27.11.2013): 201–2. http://dx.doi.org/10.1093/rheumatology/ket394.
Pełny tekst źródłaDeegan, Michael J. "Anti-Phospholipid Antibodies". American Journal of Clinical Pathology 98, nr 4 (1.10.1992): 390–91. http://dx.doi.org/10.1093/ajcp/98.4.390.
Pełny tekst źródłaMackworth-Young, C. G. "Anti phospholipid antibodies". Current Opinion in Immunology 1, nr 4 (styczeń 1988): 747–52. http://dx.doi.org/10.1016/0952-7915(89)90052-6.
Pełny tekst źródłaBanerji, Benoy, i Carl R. Alving. "Antibodies to liposomal phosphatidylserine and phosphatidic acid". Biochemistry and Cell Biology 68, nr 1 (1.01.1990): 96–101. http://dx.doi.org/10.1139/o90-012.
Pełny tekst źródłaRozprawy doktorskie na temat "Phospholipid antibodies"
Kang, Sun-ah. "Apoptotic Cells, Anti-Phospholipid Antibodies, and Anti-Chromatin Antibodies in Autoimmunity". Diss., Temple University Libraries, 2008. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/15651.
Pełny tekst źródłaPh.D.
Antiphospholipid antibodies (APAs) are detected in various autoimmune diseases, such as antiphospholipid syndrome (APS) and systemic lupus erythematosus. In addition to their binding to negatively charged phospholipids, APAs often cross-react with other molecules. Their potential biological effects are not fully understood. Apoptotic cells are a potential source of auto-antigens during systemic autoimmunity. Inefficient clearance of apoptotic cells results in the development of autoimmune manifestations and intracellular antigens such as nucleosomes become accessible during apoptosis. We examined a panel of monoclonal APAs generated from NZW/BXSB F1, a strain which spontaneously develops autoimmune symptoms reminiscent of APS. These APAs did not bind to live cells, but reacted strongly with different structures within apoptotic cells. Further analysis with various inhibitors indicated that the binding of APAs to apoptotic cells depends on specific caspase activities and on the modification of auto-antigens by reactive oxygen species (ROS). Therefore, apoptotic cells provide a potential source of APA antigens that may not be limited to phospholipids. Our data also indicate that physical accessibility and apoptosis-specific modification of auto-antigens by caspases or ROS are crucial factors for APA-antigen interactions. Various auto-antibodies such as APAs and anti-chromatin antibodies are pathogenic outcome of chronic autoimmune diseases. Their binding to auto-antigens, presumably exposed on apoptotic cells, elicits subsequent amplification of inflammatory responses, thus worsening disease progression. However, the precise immunological functions of auto-antibodies and the mechanism behind are not fully comprehended yet. We investigated immune responses generated by four different auto-immune complexes (auto-ICs) composed of auto-antibodies and apoptotic cells. In the presence of TLR ligation, the presence of auto-antibodies in auto-ICs amplified immune responses generated by apoptotic cells. In most cases, almost all the auto-ICs tested suppressed IL12, TNFa, while increasing IL10 production from macrophages. Further studies with various anti-Fc?R antibodies implied the essential role of various Fc?Rs in elevation of IL10 by auto-ICs. Studies with Mer-/- macrophages indicated that Mer is also crucial in auto-IC mediated augmentation of IL10 production. However, Mer was dispensable for the suppression of IL12. Taken together, auto-antibodies, by forming immune complexes with apoptotic cells, perform strong immunomodulatory functions. Particular importance is in the role of Fc?Rs and Mer in anti-inflammatory responses generated by auto-ICs. Paradoxical, but indispensible contribution of TLR ligation, especially TLR4, in anti-inflammatory responses generated by auto-ICs suggests that auto-antibodies may work as another layer of defense against endogenous danger signals.
Temple University--Theses
Robinson, Cheryl. "The role of anti-phospholipid antibodies in pregnancy loss /". Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82414.
Pełny tekst źródłaD'Agnillo, Paolo. "Characterization of the reactivity of prothrombin-dependent anti-phospholipid antibodies with apoptotic cells". Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32987.
Pełny tekst źródłaGiannakopoulos, Bill Clinical School St George Hospital Faculty of Medicine UNSW. "Investigations on beta 2-glycoprotein I and antiphospholipid antibodies". Publisher:University of New South Wales. Clinical School - St George Hospital, 2008. http://handle.unsw.edu.au/1959.4/41440.
Pełny tekst źródłaRadway-Bright, Emma-Louise. "The pathogenic potential of the anti-phospholipid antibodies associated with the antiphospholid syndrome and systemic lupus erythematosus". Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270189.
Pełny tekst źródłaGatenby, Paul, Gytis Danta, Roger Tuck, Colin Andrews i Carolyn Hawkins. "Cerebrovascular disease associated with antiphospholipid antibodies: more questions than answers". Master's thesis, BioMed Central, 2006. http://hdl.handle.net/10440/104.
Pełny tekst źródłaPaavola, T. (Timo). "Associations of low HDL cholesterol level and premature coronary heart disease with functionality and phospholipid composition of HDL and with plasma oxLDL antibody levels". Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526223360.
Pełny tekst źródłaTiivistelmä Sepelvaltimotauti on ateroskleroosin kliininen ilmenemismuoto. Se on merkittävimpiä kuolleisuuden ja sairastavuuden aiheuttajia niin Suomessa kuin maailmalla. Parhaillakin tunnetuilla hoidoilla sepelvaltimotaudille jää huomattava jäännösriski. Plasman matala HDL-kolesterolitaso (HDL, high-density lipoprotein) on yleinen lipidipoikkeavuus varhaista sepelvaltimotautia sairastavilla ja myös eräs metabolisen oireyhtymän, eli keskivartalolihavuuteen liittyvän ateroskleroosin riskitekijäkasauman, komponentti. Tässä väitöskirjassa tutkittiin matalan HDL-kolesterolitason ja varhaisen sepelvaltimotaudin fenotyyppiä kahdessa pohjoissuomalaisessa sukuaineistossa. Tavoitteena oli löytää uusia biologisia tekijöitä fenotyypin kohonneen sepelvatimotautiriskin taustalta. Ensimmäisen aineiston henkilöiden plasmasta mitattiin vasta-ainetasoja (IgG, IgM, IgA) LDL-hiukkasten (LDL, low-density lipoprotein) kokeellisia hapettuneita epitooppeja (malonidialdehydi-asetaldehydi-modioitu ja kuparilla hapetettu LDL) vastaan. Toisessa aineistossa mitattiin henkilöiden HDL-fraktioiden (kokonais-HDL, HDL2 ja HDL3) kykyä saada aikaan kolesterolin ulosvirtausta kokeellisesta THP-1 vaahtosolumallista. Lisäksi heidän HDL-fraktioidensa (HDL2, HDL3) fosfolipidikoostumus mitattiin nestekromatografi-massaspektrometri-laitteistolla. Vasta-ainetasot eivät liittyneet sepelvaltimotautiin tai HDL-kolesterolitasoon. Sen sijaan kolesterolin ulosvirtaus HDL2-fraktioon oli selkeästi alentunut sepelvaltimotaudissa, mikä liittyi potilaiden pieneen HDL-kolesterolipitoisuuteen. Alentunut ulosvirtaus HDL2-fraktioon liittyikin ensisijaisesti metaboliseen oireyhtymään. HDL-fraktioiden fosfolipidikoostumus erosi terveiden ja sairaiden välillä. Esimerkiksi metabolisessa oireryhtymässä tunnusomaista oli lysofosfatidyylikoliinien ja fosfatidyylikoliinien sisältämän palmitiinihapon, palmitoleiinihapon tai oleiinihapon suurentunut määrä suhteessa niiden sisältämän linoleenihapon määrään. Loppupäätelmä on, että matalan HDL-kolesterolitason ja varhaisen sepelvaltimotaudin fenotyypin HDL-fraktio on sekä toiminnaltaan että koostumukseltaan muuntunut. Erityisesti HDL2-fraktion kyky saada aikaan kolesterolin ulosvirtausta ja näin ollen sen monet toiminnalliset ominaisuudet voivat olla alentuneet. Fenotyypin HDL:n fosfolipidikoostumuksessa on monia tunnusomaisia piirteitä, joita havaittiin sekä HDL2- että HDL3-fraktiossa
Nissinen, A. (Antti). "Humoral immune response to phosphatidylethanol". Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514295232.
Pełny tekst źródłaTiivistelmä Runsas alkoholinkulutus aiheuttaa maailmanlaajuisesti merkittäviä terveydellisiä haittoja. Alkoholin aineenvaihduntatuotteet muuttavat kudoksien rakenteita ja aiheuttavat kudosvaurioita. Fosfatidyylietanoli on alkoholin aineenvaihdunnan tuloksena solukalvoilla syntyvä fosfolipidi, jota on tutkittu kahdenkymmenen vuoden ajan lupaavana alkoholin suurkulutuksen merkkiaineena. Tutkimuksen tavoitteena oli selvittää fosfatidyylietanolin immunisoinnin aiheuttamaa vasta-aineiden muodostumista koe-eläinmallina käytetyissä hiirissä sekä määrittää ihmisten plasmanäytteistä vasta-aineita, jotka sitoutuvat fosfatidyylietanoliin. Tutkimuksessa havaittiin immuunivasteen muodostuminen hiirissä, jotka immunisoitiin ihmisen LDL hiukkasiin liitetyllä fosfatidyylietanolilla. Hiiren monoklonaalisia fosfatidyylietanoliin sitoutuvia IgM-luokan vasta-aineita tuotettiin tutkimuksessa soluviljelyn avulla. Fosfatidyylietanolin aiheuttama vasta-aineiden muodostuminen hiirillä johdatti mittaamaan fosfatidyylietanoliin sitoutuvia vasta-aineita myös ihmisiltä. Tutkimuksessa havaittiin fosfatidyylietanoliin sitoutuvia IgG-, IgA- ja IgM-luokan vasta-aineita alkoholin suurkuluttajilla, alkoholihaimatulehdusta sairastavilla ja verrokkihenkilöillä. Vasta-aineiden pitoisuudet olivat alkoholia runsaasti käyttävillä koehenkilöillä merkitsevästi pienemmät kuin verrokkiryhmällä. Matalat IgA-vasta-ainepitoisuudet osoittautuivat aineistossa paremmaksi alkoholin suurkulutuksen osoittajiksi kuin eräät tavanomaisesti käytetyt alkoholinkäytön merkkiaineet. Plasman fosfatidyylietanoli-vasta-aineiden ja alkoholin aineenvaihdunnan seurauksena syntyvien malondialdehydi-asetaldehydi-addukteihin sitoutuvien vasta-aineiden määrän välillä havaittiin merkitsevä yhteys, jota ei havaittu rasvojen hapettumisen seurauksena syntyvien fosfokoliini-vasta-aineiden ja fosfatidyylietanoli-vasta-aineiden välillä. Tutkimus osoittaa, että hiirillä voidaan aikaansaada vasta-ainevälitteinen immuunivaste, kun ne rokotetaan ihmisen LDL-hiukkaseen liitetyllä fosfatidyylietanolilla. Fosfatidyylietanoliin spesifisesti sitoutuvien monoklonaalisten vasta-aineiden tuottaminen voi tulevaisuudessa johtaa immunologisen diagnostisen määritysmenetelmän kehittämiseen. Fosfatidyylietanoliin sitoutuvien plasman vasta-aineiden havaitseminen viittaa siihen, että fosfatidyylietanoli on vasta-ainevälitteisen immuunivasteen kohde myös ihmisillä
Bouvier, Sylvie. "Nouveaux acteurs moléculaires de la dysfonction vasculo-placentaire". Thesis, Montpellier 1, 2014. http://www.theses.fr/2014MON13505.
Pełny tekst źródłaVascular risk increases during pregnancy, contributing to maternal and foetal morbidity and mortality, and potentially justifying primary and secondary preventive measures. Our work evaluates the impact of some determinants and the contribution of new molecular actors implicated in placental vascular dysfunction. The ultimate aim is to optimize management and to develop new therapeutic strategies. We studied the placental vascular complications associated with known biological markers: the factor V Leiden or prothrombin polymorphisms, and conventional markers of the antiphospholipid antibody syndrome (APS). Women with previous recurrent abortions carrying polymorphisms of either factor V or factor II, or with APS (treated with heparin and low-dose aspirin), had an increased risk of foetal loss during subsequent pregnancies. Women with a previous foetal loss carrying these biological markers, treated according to recommendations during a new pregnancy (heparin for the polymorphisms, heparin plus low-dose aspirin for APS) had a lower risk of foetal loss, but an excess of late complications was observed in the APS group despite prophylaxis. We evaluated the contribution of new markers of placental vascular dysfunction. The placental alkaline phosphatase enzyme (PLAP) is synthesized and expressed by syncytiotrophoblastic cells. We found that the Ile89Leu polymorphism of the PLAP gene provides protection against implantation failure and primary miscarriage and induces increased PLAP activity. We also studied (genetics, plasma determinations, in vitro fertilisation) an angiogenic factor (patent application underway), which we showed to be associated with idiopathic implantation failure and miscarriage. These findings suggest that these molecular actors are potentially useful for the diagnosis of placenta-mediated pregnancy complications and may be relevant biomarkers of embryo implantation and/or placental development. They may indicate new targets for relevant therapeutic strategies, potentially overcoming the limitations of the currently available treatments
Ju, Cheng, i 鄭儒. "The study of human parvovirus B19 infection and anti-phospholipid antibodies". Thesis, 2016. http://ndltd.ncl.edu.tw/handle/51656287136227222383.
Pełny tekst źródła中山醫學大學
生化微生物免疫研究所
104
Human parvovirus B19 (B19) is classified as Parvoviridae family and known causing disease in humans. The virus capsid is composed of two structural proteins, VP1 and VP2, which are identical except for 227 amino acids at the amino-terminal end of the VP1-protein, the so-called VP1-unique region (VP1u). B19-VP1u proteins have secretary phospholipase A2 (sPLA2) activity, which is essential for viral infectivity and as the region to neutralize the immune response (VP1u-IgG). Previous studies show B19-VP1u induces the production of anti-phospholipid antibody. To further understand the pathogenesis of B19- VP1u, we used different region of B19-VP1u recombinant proteins to analysis. The results indicated that (1) VP1u region of 61-227a.a. has higher sPLA2 activity; (2) 82-227a.a. region has higher association with anti-phospholipid antibody; (3) Passive immunization mice which injecting 31-227a.a. and 61-227a.a. antibodies may cause thrombocytopenia and aPTT prolong; (4) Passive immunization mice which injecting 21-227a.a and 51-227a.a antibodies may activate the macrophages migration; (5)The different VP1u region can stimulate CD8+/CD4+/Th17/Treg/NK/B cells expression. All together, we firstly demonstrated the region of B19-VP1u in B19 infection and the pathogenesis of anti-phospholipid antibodies in vivo.
Książki na temat "Phospholipid antibodies"
Nigel, Harris E., red. Phospholipid-binding antibodies. Boca Raton: CRC Press, 1991.
Znajdź pełny tekst źródłaImmunophysiology of antiphospholipid antibodies. Austin: R.G. Landes, 1994.
Znajdź pełny tekst źródłaAsherson, Ronald A., Graham R. V. Hughes, E. Nigel Harris i Thomas Exner. Phospholipid-Binding Antibodies. Taylor & Francis Group, 2020.
Znajdź pełny tekst źródłaAsherson, Ronald A., Graham R. V. Hughes, E. Nigel Harris i Thomas Exner. Phospholipid-Binding Antibodies. Taylor & Francis Group, 2020.
Znajdź pełny tekst źródłaPhospholipid-Binding Antibodies. Taylor & Francis Group, 2019.
Znajdź pełny tekst źródłaHarris, E. Nigel, Thomas Exner, Graham R. V. Hughes i Ronald A. Asherson. Phospholipid-Binding Antibodies. Redaktorzy E. Nigel Harris, Thomas Exner, Graham R. V. Hughes i Ronald A. Asherson. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129.
Pełny tekst źródłaAsherson, Ronald A., Graham R. V. Hughes, E. Nigel Harris i Thomas Exner. Phospholipid-Binding Antibodies. Taylor & Francis Group, 2020.
Znajdź pełny tekst źródłaAsherson, Ronald A., Graham R. V. Hughes, E. Nigel Harris i Thomas Exner. Phospholipid-Binding Antibodies. Taylor & Francis Group, 2020.
Znajdź pełny tekst źródłaKhamashta, Munther A., Graham R. V. Hughes i Guillermo Ruiz-Irastorza. Anti-phospholipid antibody syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0120.
Pełny tekst źródłaKhamashta, Munther A., Graham R. V. Hughes i Guillermo Ruiz-Irastorza. Anti-phospholipid antibody syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0120_update_001.
Pełny tekst źródłaCzęści książek na temat "Phospholipid antibodies"
Harris, E. N. "Clinical and immunological significance of anti-phospholipid antibodies". W Early Pregnancy Loss, 43–60. London: Springer London, 1988. http://dx.doi.org/10.1007/978-1-4471-1658-5_6.
Pełny tekst źródłaMiesbach, W., J. Vogt, D. Peez, Th Vigh, B. Bühler, G. Ashmelash i I. Scharrer. "Factor V Inhibitor and Anti-Phospholipid Antibodies after Treatment with Ciprofloxacin". W 32nd Hemophilia Symposium Hamburg 2001, 123–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-18150-4_16.
Pełny tekst źródłaDiener, W., R. Klein, K. Kast, U. Danneberg, M. Mohrmann, P. A. Berg, S. A. Dambinova i R. Korinthenberg. "Increased Incidence of CNS- and Phospholipid Antibodies in Epileptic Syndromes of Childhood". W Neurochemistry, 281–86. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_46.
Pełny tekst źródłaExner, Thomas, i Douglas Triplett. "Lupus Anticoagulants: Characteristics, Methods of Laboratory Detection and Some Clinical Associations". W Phospholipid-Binding Antibodies, 141–58. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-11.
Pełny tekst źródłaExner, Thomas, i David Green. "Acquired Circulating Anticoagulants Other than Lupus Anticoagulants". W Phospholipid-Binding Antibodies, 159–74. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-12.
Pełny tekst źródłaHarris, E. N., A. E. Gharavi i G. R. V. Hughes. "The Anti-Cardiolipin Assay". W Phospholipid-Binding Antibodies, 175–87. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-13.
Pełny tekst źródłaMcNeil, H. Patrick, Steven A. Krilis i Colin N. Chesterman. "Arterial Thrombosis—Diagnosis and Management". W Phospholipid-Binding Antibodies, 191–203. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-15.
Pełny tekst źródłaStormorken, Helge. "Spontaneous (Unexplained) Thrombosis: The Inherited Basis for the Thrombohemorrhagic Balance". W Phospholipid-Binding Antibodies, 205–17. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-16.
Pełny tekst źródłaDerksen, R. H. W. M., P. Hasselaar i Ph G. de Groot. "The Pathogenetic Role of Anti-Phospholipid Antibodies in Thrombosis". W Phospholipid-Binding Antibodies, 219–30. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-17.
Pełny tekst źródłaCarreras, Luis O., i Jos Vermylen. "Anti-Phospholipid Antibodies and Impairment of Prostacyclin Synthesis by the Endothelium". W Phospholipid-Binding Antibodies, 231–45. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-18.
Pełny tekst źródłaStreszczenia konferencji na temat "Phospholipid antibodies"
Triplett, D. A., J. T. Brant, K. Musgrave i C. A. Orr. "RELATIONSHIP BETWEEN LUPUS ANTICOAGULANTS AND ANTIBODIES TO PHOSPHOLIPID". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643657.
Pełny tekst źródłaCucnik, Sasa. "SP0176 PATHOGENIC ANTIBODIES IN PHOSPHOLIPID SYNDROM". W Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8453.
Pełny tekst źródłaDhir, V., A. Gawalkar, J. Ahluwalia, A. Bahl, S. Sharma, A. Sharma i S. Jain. "AB0635 Anti-phospholipid antibodies in lupus myocarditis". W 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.3672.
Pełny tekst źródłaLi, C., L. Zhu, Z. Wang, Y. Sun, R. Mu i Z. Li. "AB0559 The prevalence of non-criteria anti-phospholipid antibodies in anti-phospholipid syndrome". W 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.6750.
Pełny tekst źródłaBrien, W., G. Denome i B. O’Keefe. "THE PREVELANCE OF ANTIPHOSPHOLIPID ANTIBODIES, BY ELISA TECHNIQUE, IN PATIENTS WITH THE LUPUS ANTICOAGULANT". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644234.
Pełny tekst źródłaHarris, EN, G. Wasley i GRV Hughes. "DISTINCTION BETWEEN ANTI CARDIOLIPIN (aCL) ANTIBODIES IN SYPHLIS AND THE "ANTI PHOSPHOLIPID SYNDROME"". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643658.
Pełny tekst źródłaChighizola, C. B., F. Pregnolato, M. G. Raimondo, C. Comerio, C. Sobrino Grande, L. Trespidi, M. O. Borghi i in. "FRI0349 Low titer anti-phospholipid antibodies convey an increased obstetric risk". W 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.5887.
Pełny tekst źródłaPengo, V., M. J. Heine, P. Thiagarajan i s. s. Shapiro. "A GENERAL MECHANISM FOR LUPUS ANTICOAGULANTS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643660.
Pełny tekst źródłaInce, A., A. Roumany, U. Daud, PH Pepmueller i TL Moore. "FRI0172 Long-term follow-up of paediatric patients with positive anti-phospholipid antibodies". W Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.241.
Pełny tekst źródłaDay, Cameron, i Paul Neilsen. "Abstract 4601: Phospholipid and enzyme antibodies for the evaluation of novel cancer biomarkers". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4601.
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