Relevant bibliographies by topics / Phospholipid antibodies

Academic literature on the topic 'Phospholipid antibodies'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Phospholipid antibodies.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Phospholipid antibodies"

1

Out, HJ, PG de Groot, M. van Vliet, GC de Gast, HK Nieuwenhuis, and RH Derksen. "Antibodies to platelets in patients with anti-phospholipid antibodies." Blood 77, no. 12 (June 15, 1991): 2655–59. http://dx.doi.org/10.1182/blood.v77.12.2655.2655.

Full text
Abstract:
Abstract Binding of anti-phospholipid antibodies to circulating platelets and its consequences on platelet activation and aggregation was investigated in 11 patients with anti-phospholipid antibodies. Seven patients had mild thrombocytopenia. Nine healthy donors served as controls. Binding to platelets was investigated by performing enzyme- linked immunosorbent assays (ELISAs) with phospholipids as antigen on platelet eluates. Platelet activation was measured by flow cytofluorometry using monoclonal antibodies to an activation-specific lysosomal membrane protein. Findings in ELISA were compared with results of a conventional immunofluorescence method to detect platelet autoantibodies. In seven patients antibodies to negatively charged phospholipids were present in platelet eluates. In all thrombocytopenic patients and controls the platelets were not activated and aggregation was not impaired. There was a positive concordance of 50% between the results of immunofluorescence and ELISA. No apparent relation was found between the results of ELISA or immunofluorescence and platelet counts. It is concluded that anti-phospholipid antibodies can bind to circulating platelets. This binding is not associated with measurable aggregation abnormalities nor with platelet activation characterized by exposure of lysosomal membrane proteins. More studies are necessary to determine the exact role of anti-phospholipid antibodies in the pathogenesis of thrombocytopenia and thrombosis.
APA, Harvard, Vancouver, ISO, and other styles
2

Out, HJ, PG de Groot, M. van Vliet, GC de Gast, HK Nieuwenhuis, and RH Derksen. "Antibodies to platelets in patients with anti-phospholipid antibodies." Blood 77, no. 12 (June 15, 1991): 2655–59. http://dx.doi.org/10.1182/blood.v77.12.2655.bloodjournal77122655.

Full text
Abstract:
Binding of anti-phospholipid antibodies to circulating platelets and its consequences on platelet activation and aggregation was investigated in 11 patients with anti-phospholipid antibodies. Seven patients had mild thrombocytopenia. Nine healthy donors served as controls. Binding to platelets was investigated by performing enzyme- linked immunosorbent assays (ELISAs) with phospholipids as antigen on platelet eluates. Platelet activation was measured by flow cytofluorometry using monoclonal antibodies to an activation-specific lysosomal membrane protein. Findings in ELISA were compared with results of a conventional immunofluorescence method to detect platelet autoantibodies. In seven patients antibodies to negatively charged phospholipids were present in platelet eluates. In all thrombocytopenic patients and controls the platelets were not activated and aggregation was not impaired. There was a positive concordance of 50% between the results of immunofluorescence and ELISA. No apparent relation was found between the results of ELISA or immunofluorescence and platelet counts. It is concluded that anti-phospholipid antibodies can bind to circulating platelets. This binding is not associated with measurable aggregation abnormalities nor with platelet activation characterized by exposure of lysosomal membrane proteins. More studies are necessary to determine the exact role of anti-phospholipid antibodies in the pathogenesis of thrombocytopenia and thrombosis.
APA, Harvard, Vancouver, ISO, and other styles
3

Rauch, J., and AS Janoff. "Antibodies against Phospholipids other than Cardiolipin: Potential Roles for Both Phospholipid and Protein." Lupus 5, no. 5 (October 1996): 498–502. http://dx.doi.org/10.1177/096120339600500534.

Full text
Abstract:
Autoantibodies to phospholipids other than cardiolipin have received less attention, to date, than anti-cardiolipin antibodies. This review focuses on these antibodies and potential roles for both phospholipid and protein in their reactivity. We review data in the literature indicating that antibodies to phosphatidylethanolamine and some lupus anticoagulant antibodies recognize phospholipid-binding proteins in association with phospholipid. Kininogens appear to be involved in the binding of antibodies to phosphatidylethanolamine, while phosphatidylserine-binding proteins, such as prothrombin and annexin V, have been implicated in lupus anticoagulant antibody recognition. These proteins bind to phospholipids that normally reside in the inner monolayer of the cell membrane, suggesting that exposure of these lipids is necessary for protein binding and antibody recognition to occur. In contrast, other autoantibodies, in particular those reactive with erythrocytes, appear to be directed at phospholipids that normally occur in the outer membrane leaflet, such as phosphatidylcholine. In summary, there is clearly accumulating evidence that antibodies to phospholipids other than cardiolipin recognize epitopes on phospholipid-binding proteins. It is not clear whether recognition of these epitopes is due to an increase in antigen density or a change in the protein or phospholipid structure, but it is likely that both protein and phospholipid structure play an important role in the in vivo interactions of these antibodies.
APA, Harvard, Vancouver, ISO, and other styles
4

Harris, EN, and SS Pierangeli. "Functional Effects of Anticardiolipin Antibodies." Lupus 5, no. 5 (October 1996): 372–77. http://dx.doi.org/10.1177/096120339600500507.

Full text
Abstract:
The ‘lupus anticoagulant’ phenomenon is the best documented functional effect of antiphospholipid (aPL) antibodies, occurring either by inhibition of the prothrombinase and/or Factor X activation reactions. Understanding the mechanism by which aPL antibodies inhibit phospholipid dependent coagulation reactions may yield important clues about their ‘thrombogenic effects’ in vivo. We conducted a series of studies to determine the specificity, diversity, and mechanism by which aPL antibodies inhibit phospholipid dependent reactions. Results showed that purified immunoglobulins with lupus anticoagulant and anti-cardiolipin activities were absorbed by negatively charged phospholipids and both activities were recovered from the phospholipid-antibody precipitate. Purified aPL antibodies inhibited the prothrombinase reaction in a plasma free system in which β2-glycoprotein 1 (β2-GP1) was absent. Affinity purified aPL antibodies had 25–50 times the inhibitory activity of immunoglobulin preparations. The phospholipid binding proteins, β2-GP1 and placental anticoagulant protein I (PAP I), independently inhibited the prothrombinase reaction, and when these proteins were combined with aPL, inhibition of the prothrombinase reaction was additive. Antibodies of syphilis had no inhibitory effect, partially accounted for by lack of specificity for phosphotidylserine (PS). Although aPL antibodies inhibited the protein C activation reaction, there was no correlation of these activities with inhibition of the prothrombinase reaction. Together, these results show that aPL exert their effects by interaction with negatively charged phospholipids, in particular phosphotidylserine, but lack of correlation between inhibition of the prothrombinase and protein C activation reactions, suggests that the nature of the coagulation protein is also important.
APA, Harvard, Vancouver, ISO, and other styles
5

BRIGHTON, Timothy A., Yan-Ping DAI, Philip J. HOGG, and Colin N. CHESTERMAN. "Microheterogeneity of beta-2 glycoprotein I: implications for binding to anionic phospholipids." Biochemical Journal 340, no. 1 (May 10, 1999): 59–67. http://dx.doi.org/10.1042/bj3400059.

Full text
Abstract:
Considerable interest is currently focused on the interactions of beta-2 glycoprotein I (β2GPI) and anti-phospholipid antibodies with anionic phospholipids in an attempt to understand the association between these antibodies and clinical diseases such as thrombosis. The interactions of β2GPI and anionic phospholipids have only been characterized partially, and the physiological role of this glycoprotein remains uncertain. In this study we have explored in detail the physical and phospholipid-binding characteristics of a number of β2GPI preparations. We have found (i) that perchloric acid-purification methods are damaging to β2GPI during purification, (ii) that the dissociation constants of the various preparations for phosphatidylserine vary between 0.1-2 μM and are considerably weaker than previously reported, (iii) that considerable differences in affinity of the various β2GPI preparations for anionic phospholipids are obtained when comparing anionic phospholipids immobilized to a solid-phase versus phospholipid assembled in unilamellar vesicles, (iv) that the integrity of the fifth domain of β2GPI is important for binding immobilized anionic phospholipid but not especially important in binding vesicular anionic phospholipid, and (v) that β2GPI preparations with differing isoelectric species content bind anionic phospholipids differently, suggesting that varying glycosylation and/or protein polymorphisms impact upon phospholipid binding. These results highlight the importance of assessing the determinants of the interaction of β2GPI with anionic phospholipids assembled in unilamellar vesicles.
APA, Harvard, Vancouver, ISO, and other styles
6

Harris, E. N., A. E. Gharavi, and G. R. V. Hughes. "Anti-phospholipid Antibodies." Clinics in Rheumatic Diseases 11, no. 3 (December 1985): 591–609. http://dx.doi.org/10.1016/s0307-742x(21)00606-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Tincani, A., L. Andreoli, and Y. Shoenfeld. "Anti-phospholipid antibodies." Rheumatology 53, no. 2 (November 27, 2013): 201–2. http://dx.doi.org/10.1093/rheumatology/ket394.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Deegan, Michael J. "Anti-Phospholipid Antibodies." American Journal of Clinical Pathology 98, no. 4 (October 1, 1992): 390–91. http://dx.doi.org/10.1093/ajcp/98.4.390.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Mackworth-Young, C. G. "Anti phospholipid antibodies." Current Opinion in Immunology 1, no. 4 (January 1988): 747–52. http://dx.doi.org/10.1016/0952-7915(89)90052-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Banerji, Benoy, and Carl R. Alving. "Antibodies to liposomal phosphatidylserine and phosphatidic acid." Biochemistry and Cell Biology 68, no. 1 (January 1, 1990): 96–101. http://dx.doi.org/10.1139/o90-012.

Full text
Abstract:
Polyclonal antisera to phosphatidylserine or phosphatidic acid were induced in rabbits by injecting liposomes containing phosphatidylserine or phosphatidic acid and lipid A. Adsorption of antisera with liposomes containing different phospholipids revealed that some degree of reactivity with one or more phospholipids other than the immunizing phospholipid was often observed. However, cross-reactivity with other phospholipids was not a universal phenomenon, and one antiserum to phosphatidylserine failed to cross-react (i.e., was not adsorbed) with liposomes containing other phospholipids. All of the antisera were inhibited by soluble phosphorylated haptens (e.g., phosphocholine but not choline), but one of the antisera to phosphatidylserine was inhibited both by phosphoserine and by serine alone. Liposomal membrane composition influenced the activity of antiserum to phosphatidylserine. Regardless of whether unsaturated (beef brain) or saturated (dimyristoyl) phosphatidylserine was used in the immunizing liposomes, the antisera reacted more vigorously with liposomes containing unsaturated than saturated phosphatidylserine. We conclude that liposomes containing lipid A can serve as vehicles for stimulating polyclonal antisera to phosphatidylserine and phosphatidic acid. Although cross-reactivity with certain other phospholipids can be observed, sera from selected animals apparently can exhibit a high degree of specific activity to the immunizing phospholipid antigen.Key words: liposomes, antibodies, phospholipids, phosphatidylserine, phosphatidic acid.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Phospholipid antibodies"

1

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.

Full text
Abstract:
Microbiology and Immunology
Ph.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
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
Abstract:
Recurrent pregnancy loss is associated with anti-phospholipid antibodies (aPL), in particular in women with anti-phospholipid syndrome. aPL are a large family of autoantibodies, directed against phospholipids and phospholipid-binding proteins (e.g., prothrombin and beta2-glycoprotein I). Although the association between aPL and recurrent pregnancy loss is well documented, little is known about which aPL subset is responsible. To address this, we characterized a panel of six murine monoclonal aPL, which were subsequently administered to pregnant mice via passive transfer. While both anti-beta2GPI antibodies evaluated caused significant increase in fetal resorption, the effects of anti-PT antibodies varied from no effect to increased pregnancy loss. Similarly, neither lupus anticoagulant activity nor murine cross-reactivity predetermined aPL pathogenicity. We conclude that there is no obvious common reactivity between the aPL capable of increasing pregnancy loss, suggesting that a combination of reactivities, rather than one aPL specificity in particular, may lead to aPL-mediated pregnancy loss.
APA, Harvard, Vancouver, ISO, and other styles
3

D'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.

Full text
Abstract:
Anti-phospholipid antibodies (aPL) occur in patients with the anti-phospholipid syndrome, and are directed against various combinations of phospholipids and phospholipid-binding proteins (e.g., beta2-glycoprotein I and prothrombin). Lupus anticoagulants (LA), a subset of aPL, exhibit anticoagulant properties in vitro, but are strikingly procoagulant in vivo. We have previously demonstrated that some aPL bind specifically to apoptotic, but not viable, thymocytes in the presence of beta2-glycoprotein 1. Here, we demonstrate that prothrombin binds selectively to the surface of apoptotic Jurkat cells, and supports the binding of LA-positive murine monoclonal antibodies (mAb) and patient-derived IgG to apoptotic cells. Despite similar LA activity and reactivity with apoptotic cells, the mAb differed in affinity and specificity. One mAb was highly reactive with prothrombin alone, while the other required anionic phospholipid for elevated binding. These results demonstrate that aPL recognize multiple epitopes on apoptotic cells, suggesting that apoptotic antigens contribute to the induction and/or perpetuation of aPL.
APA, Harvard, Vancouver, ISO, and other styles
4

Giannakopoulos, 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.

Full text
Abstract:
An outline of the work contained in this thesis is presented. The first chapter is a critical review of the literature pertaining to the pathophysiological mechanisms operational with regards to the antiphospholipid syndrome (APS). The syndrome is characterised by venous and arterial thrombosis, and recurrent fetal loss, in association with the persistent presence of antibodies targeting the main autoantigen beta 2-glycoprotein I (β2GPI). The second chapter reviews the literature delineating the diverse physiological functions of β2GPI, and then relates them to its role in our current understanding of the pathophysiology of APS. The third chapter presents a critical review of the evidence base for the diagnosis and management of APS. The fourth chapter describes the interaction between β2GPI and the glycoprotein Ib alpha (GPIbα) subunit of the platelet receptor GPIb-IX-V. GPIbα is an important platelet adhesion receptor, which mediates multiple additional functions on the platelet surface, including binding coagulation factor XI (FXI). The implication of the interaction between β2GPI and GPIbα on platelet activation and the release of thromboxane in the presence of anti-β2GPI antibodies is explored, as well as the intracellular pathways via which this activation occurs. The relevance of these findings to understanding APS pathogenesis, in particular thrombosis, is discussed. The fifth chapter delineates the interaction between the fifth domain of β2GPI and FXI and its activated form factor XIa (FXIa). The ability of FXIa to cleave β2GPI between lysine (Lys) 317 and threonine (Thr) 318, and modulate its function is reported. The sixth chapter describes the ability of β2GPI to inhibit FXIa autoproteolytic hydrolysis at the specific FXIa residues arginine (Arg) 507, Arg532 and Lys539. This interaction with β2GPI stabilizes FXIa activity over time, and leads to enhanced FXIa mediated fibrin formation. This is a novel physiological function of β2GPI with important implications. Recent epidemiological studies by others have emphasized the critical role of FXIa in pathological thrombus propagation. The seventh chapter defines the relevance of the FXIa residues Arg507, Arg532 and Lys539 to FXIa mediated inactivation by the main FXIa inhibitor Protease Nexin 2 (PN2), and by Antithrombin III (ATIII). Insights into future directions for research are presented and discussed within each individual chapter.
APA, Harvard, Vancouver, ISO, and other styles
5

Radway-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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Gatenby, Paul, Gytis Danta, Roger Tuck, Colin Andrews, and Carolyn Hawkins. "Cerebrovascular disease associated with antiphospholipid antibodies: more questions than answers." Master's thesis, BioMed Central, 2006. http://hdl.handle.net/10440/104.

Full text
Abstract:
Neurological syndromes occur in a significant number of patients with antiphospholipid antibodies. The optimal management for these patients however remains uncertain. Our study is a descriptive analysis looking retrospectively at 45 patients who presented to the principal tertiary referral centre in the Australian Capital Territory, with either cerebral arterial or venous thrombosis for which there was no obvious cause for their presentation when initially reviewed. The diagnosis was based on the clinical findings made by one of three neurologists attached to our centre. Radiological findings and the presence of either IgM or IgG anticardiolipin antibodies, IgG anti-beta-2 glycoprotein 1 antibodies or a lupus anticoagulant were then documented. In this group of patients three subgroups were identified: 1. Individuals that fulfilled the Sapporo Classification Criteria 2. Individuals with transiently positive antiphospholipid antibodies and 3. Individuals with persistently low positive antiphospholipid antibodies. The most interesting of these three groups are those individuals with transiently positive antiphospholipid antibodies. A potential cause for presentation was identified in only one patient of this group with documented infective endocarditis and bacteraemia. Comparison with the other two groups suggested that there was little in terms of clinical presentation, radiological findings or intercurrent risk factors for thrombotic disease to distinguish between them. With disappearance of antiphospholipid antibodies, the individuals within this group have not had further thrombotic events. Our observations emphasise the problems that continue to exist in relation to the occurrence of cerebrovascular disease in the context of antiphospholipid antibodies and the optimal management of these stratified groups. Our findings also raise an as yet unanswered question as to the signficance of these transiently positive antiphospholipid antibodies. In the absence of significant intercurrent risk factors our findings would suggest that in the group we describe that they are likely to be of clinical significance.
APA, Harvard, Vancouver, ISO, and other styles
7

Paavola, 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.

Full text
Abstract:
Abstract Coronary heart disease (CHD) is a clinical manifestation of atherosclerosis. It is a major cause of mortality and morbidity both in Finland and globally. Even after the best known treatments a significant residual risk of CHD remains. A low plasma HDL cholesterol level (HDL, high-density lipoprotein) is a common lipid abnormality in patients affected by premature CHD and also a component of the metabolic syndrome, a cluster of risk factors for atherosclerosis associated with central obesity. In this study, a phenotype of low HDL cholesterol level and premature CHD was investigated in two Northern Finnish family populations. The aim was to find new biological factors accounting for the elevated CHD risk in the phenotype. In the subjects of family population I, plasma levels of antibodies (IgG, IgM, IgA) against experimental epitopes (malondialdehyde-acetaldehyde-modified, copper-oxidized) of oxidized LDL (low-density lipoprotein) particles were measured. In the subjects of family population II, capacity of HDL fractions (total HDL, HDL2 and HDL3) to accept cholesterol from a THP-1 experimental foam cell model was assayed (cholesterol efflux). In addition, a phospholipid composition of their HDL fractions (HDL2 and HDL3) was measured using liquid chromatography-mass spectrometry. The antibody levels were not related to CHD or to HDL cholesterol level. Instead, the cholesterol efflux to HDL2 fraction was clearly impaired in CHD, which was associated with the low HDL cholesterol level of the patients. The impaired cholesterol efflux to HDL2 fraction was primarily in conjunction with the metabolic syndrome. The phospholipid composition of HDL fractions was different between the affected and the non-affected subjects. As an example, characteristic of the metabolic syndrome were elevated contents of palmitic, palmitoleic or oleic acids relative to linoleic acid in lysophosphatidylcholines and phosphatidylcholines. In conclusion, the HDL fraction is both functionally and compositionally modified in the phenotype of low HDL cholesterol level and premature CHD. Especially the cholesterol efflux capacity of the HDL2 fraction and thus its many functional properties may be impaired. There are many characteristic features in the phospholipid composition of the HDL in the phenotype which were detected in HDL2 and HDL3 fractions
Tiivistelmä 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
APA, Harvard, Vancouver, ISO, and other styles
8

Nissinen, A. (Antti). "Humoral immune response to phosphatidylethanol." Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514295232.

Full text
Abstract:
Abstract Heavy alcohol consumption places a substantial burden on health all over the world. Metabolites of alcohol evoke alterations that lead to tissue damage in many organs. Phosphatidylethanol (PEth) is a unique phospholipid formed in the cellular membranes during the metabolism of ethanol after alcohol consumption. PEth has attracted special attention as it is postulated to be a reliable marker of long term heavy alcohol consumption. The aims of present study were to investigate the immunogenicity of phosphatidylethanol in mice and to analyze the plasma antibodies binding to phosphatidylethanol in humans. In this study a clear immune response was generated in mice immunized with PEth in human low density lipoprotein (LDL) carrier. Mouse monoclonal IgM antibodies binding specifically to phosphoethyl head group of PEth were generated using hybridoma technology. Since PEth was shown to be immunogenic in mice, plasma was analyzed for the presence of antibodies also in humans. PEth-specific antibodies of IgG, IgA and IgM isotypes in plasma were detected in heavy drinkers of alcohol with or without pancreatitis as well as in the controls. The plasma levels of the antibodies binding to PEth were significantly lower in the study subjects with heavy alcohol use and in this present study sample the low IgA levels to PEth were better indicators of heavy alcohol consumption as compared to the some of the traditional markers of heavy alcohol use. The antibody levels to PEth associated significantly to plasma antibodies binding to malondialdehyde-acetaldehyde adducts that are known to be formed during alcohol metabolism but not to antibodies binding to phosphocholine which is generated by lipid oxidation in humans. In conclusion, this study demonstrates that phosphatidylethanol is immunogenic in mice when using carriers such as human LDL in the immunization process. The binding of the monoclonal antibodies specifically to the PEth head group suggests that it would be feasible to develop a diagnostic immunoassay to PEth. The presence of antibodies binding to PEth in plasma indicates that PEth may be a target of humoral immunity in humans
Tiivistelmä 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
APA, Harvard, Vancouver, ISO, and other styles
9

Bouvier, Sylvie. "Nouveaux acteurs moléculaires de la dysfonction vasculo-placentaire." Thesis, Montpellier 1, 2014. http://www.theses.fr/2014MON13505.

Full text
Abstract:
La grossesse est une période de majoration du risque vasculaire, participant à une morbi-mortalité maternelle et fœtale pouvant justifier des mesures de prévention primaire et secondaire. Notre travail évalue l'impact de certains déterminants et l'apport de nouveaux acteurs moléculaires impliqués dans la dysfonction vasculo-placentaire. Le but ultime étant d'optimiser les prises en charge et de développer de nouvelles stratégies thérapeutiques. Nous avons étudié les complications vasculaires placentaires associées à des marqueurs biologiques connus : mutation du facteur V Leiden, mutation du gène de la prothrombine et marqueurs conventionnels du syndrome des anticorps anti-phospholipides (SAPL). Nos résultats montrent que les femmes à antécédents de fausses couches précoces répétitives et porteuses, soit du polymorphisme du facteur V, soit du polymorphisme du facteur II, soit d'un SAPL (traité par héparine et aspirine faible dose), ont un risque élevé de fausse couche tardive lors d'une nouvelle grossesse. Les femmes à antécédent de fausse couche tardive et porteuses des mêmes particularités biologiques, traitées pendant leur grossesse selon les recommandations (héparine pour l'anomalie du facteur V ou II, héparine plus aspirine faible dose pour le SAPL), ont un risque diminué de récidive de perte fœtale tardive mais demeurent, dans le groupe SAPL, fréquemment exposées aux complications tardives de la grossesse malgré la prophylaxie antithrombotique. Nous avons évalué l'apport de nouveaux marqueurs de la dysfonction vasculaire placentaire. Nous montrons que le polymorphisme Ile89Leu du gène de la phosphatase alcaline placentaire (PLAP), enzyme exprimée par les cellules du syncytiotrophoblaste -polymorphisme associé à une augmentation de l'activité PLAP-, exerce un effet protecteur sur l'échec d'implantation et la survenue d'une fausse couche primaire. Un facteur angiogénique (brevet en cours) a également été étudié (génétique, dosage plasmatique, fécondation in vitro) et nous montrons une association de ce marqueur avec les échecs d'implantation et les fausses couches idiopathiques. L'ensemble de ces travaux suggère que ces nouveaux marqueurs moléculaires pourraient contribuer au diagnostic des complications vasculaires de la grossesse et fournir des biomarqueurs d'implantation embryonnaire et/ou de développement placentaire. Ils pourraient suggérer de nouvelles cibles et stratégies thérapeutiques, répondant aux limites des traitements disponibles
Vascular 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
APA, Harvard, Vancouver, ISO, and other styles
10

Ju, Cheng, and 鄭儒. "The study of human parvovirus B19 infection and anti-phospholipid antibodies." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/51656287136227222383.

Full text
Abstract:
碩士
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.
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Phospholipid antibodies"

1

Nigel, Harris E., ed. Phospholipid-binding antibodies. Boca Raton: CRC Press, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Immunophysiology of antiphospholipid antibodies. Austin: R.G. Landes, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Asherson, Ronald A., Graham R. V. Hughes, E. Nigel Harris, and Thomas Exner. Phospholipid-Binding Antibodies. Taylor & Francis Group, 2020.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Asherson, Ronald A., Graham R. V. Hughes, E. Nigel Harris, and Thomas Exner. Phospholipid-Binding Antibodies. Taylor & Francis Group, 2020.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Phospholipid-Binding Antibodies. Taylor & Francis Group, 2019.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Harris, E. Nigel, Thomas Exner, Graham R. V. Hughes, and Ronald A. Asherson. Phospholipid-Binding Antibodies. Edited by E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, and Ronald A. Asherson. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Asherson, Ronald A., Graham R. V. Hughes, E. Nigel Harris, and Thomas Exner. Phospholipid-Binding Antibodies. Taylor & Francis Group, 2020.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Asherson, Ronald A., Graham R. V. Hughes, E. Nigel Harris, and Thomas Exner. Phospholipid-Binding Antibodies. Taylor & Francis Group, 2020.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Khamashta, Munther A., Graham R. V. Hughes, and Guillermo Ruiz-Irastorza. Anti-phospholipid antibody syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0120.

Full text
Abstract:
The anti-phospholipid syndrome (APS) described almost 30 years ago, is now recognized as a major cause of deep vein thrombosis, stroke, and heart attacks in young people (<45 years of age). It is also the commonest treatable cause of recurrent miscarriages and a major cause of late fetal death. Other clinical manifestations are cardiac valvular disease, livedo reticularis, renal thrombotic microangiopathy, thrombocytopenia, haemolytic anaemia, epilepsy, and cognitive impairment. The presence of anti-phospholipid antibodies (aPL) has been closely related to the development of thrombosis and complications in pregnancy. However, not all patients with aPL will develop the clinical features. Lupus anticoagulant is generally thought to be more strongly associated with the risk of clinical manifestations of APS than anticardiolipin and anti ?2-glycoprotein I antibodies. The exact pathogenic mechanisms leading to thrombosis and/or pregnancy morbidity are poorly understood. Therapy of thrombosis is based on long-term oral anti-coagulation and patients with arterial events should be treated aggressively. Obstetric care is based on combined medical-obstetric high-risk management and treatment with aspirin and heparin.
APA, Harvard, Vancouver, ISO, and other styles
10

Khamashta, Munther A., Graham R. V. Hughes, and Guillermo Ruiz-Irastorza. Anti-phospholipid antibody syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0120_update_001.

Full text
Abstract:
The anti-phospholipid syndrome (APS) described almost 30 years ago, is now recognized as a major cause of deep vein thrombosis, stroke, and heart attacks in young people (<45 years of age). It is also the commonest treatable cause of recurrent miscarriages and a major cause of late fetal death. Other clinical manifestations are cardiac valvular disease, livedo reticularis, renal thrombotic microangiopathy, thrombocytopenia, haemolytic anaemia, epilepsy, and cognitive impairment. The presence of anti-phospholipid antibodies (aPL) has been closely related to the development of thrombosis and complications in pregnancy. However, not all patients with aPL will develop the clinical features. Lupus anticoagulant is generally thought to be more strongly associated with the risk of clinical manifestations of APS than anticardiolipin and anti ?2-glycoprotein I antibodies. The exact pathogenic mechanisms leading to thrombosis and/or pregnancy morbidity are poorly understood. Therapy of thrombosis is based on long-term oral anti-coagulation and patients with arterial events should be treated aggressively. Obstetric care is based on combined medical-obstetric high-risk management and treatment with aspirin and heparin.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Phospholipid antibodies"

1

Harris, E. N. "Clinical and immunological significance of anti-phospholipid antibodies." In Early Pregnancy Loss, 43–60. London: Springer London, 1988. http://dx.doi.org/10.1007/978-1-4471-1658-5_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Miesbach, W., J. Vogt, D. Peez, Th Vigh, B. Bühler, G. Ashmelash, and I. Scharrer. "Factor V Inhibitor and Anti-Phospholipid Antibodies after Treatment with Ciprofloxacin." In 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Diener, W., R. Klein, K. Kast, U. Danneberg, M. Mohrmann, P. A. Berg, S. A. Dambinova, and R. Korinthenberg. "Increased Incidence of CNS- and Phospholipid Antibodies in Epileptic Syndromes of Childhood." In Neurochemistry, 281–86. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_46.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Exner, Thomas, and Douglas Triplett. "Lupus Anticoagulants: Characteristics, Methods of Laboratory Detection and Some Clinical Associations." In Phospholipid-Binding Antibodies, 141–58. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Exner, Thomas, and David Green. "Acquired Circulating Anticoagulants Other than Lupus Anticoagulants." In Phospholipid-Binding Antibodies, 159–74. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Harris, E. N., A. E. Gharavi, and G. R. V. Hughes. "The Anti-Cardiolipin Assay." In Phospholipid-Binding Antibodies, 175–87. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

McNeil, H. Patrick, Steven A. Krilis, and Colin N. Chesterman. "Arterial Thrombosis—Diagnosis and Management." In Phospholipid-Binding Antibodies, 191–203. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Stormorken, Helge. "Spontaneous (Unexplained) Thrombosis: The Inherited Basis for the Thrombohemorrhagic Balance." In Phospholipid-Binding Antibodies, 205–17. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-16.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Derksen, R. H. W. M., P. Hasselaar, and Ph G. de Groot. "The Pathogenetic Role of Anti-Phospholipid Antibodies in Thrombosis." In Phospholipid-Binding Antibodies, 219–30. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-17.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Carreras, Luis O., and Jos Vermylen. "Anti-Phospholipid Antibodies and Impairment of Prostacyclin Synthesis by the Endothelium." In Phospholipid-Binding Antibodies, 231–45. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-18.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Phospholipid antibodies"

1

Triplett, D. A., J. T. Brant, K. Musgrave, and C. A. Orr. "RELATIONSHIP BETWEEN LUPUS ANTICOAGULANTS AND ANTIBODIES TO PHOSPHOLIPID." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643657.

Full text
Abstract:
The relationship of lupus anticoagulants (LA's) to antibodies (IgG and IgM) to cardiolipin (CL), phosphatidylserine (PS), phosphatidylinositol (PI) and phosphatidic acid (PA), detected by an enzyme linked immunoassay, was examined in a series of 100 patients with well characterized LA's. 73% of patients demonstrated antibodies to one or more phospholipids; 62% were positive for CL, 57% were positive for PS, 57% were positive for PI, and 51% were positive for PA. Of the samples with antibodies to phospholipid, 32% had IgG type antibody only, 16% had IgMonly, and 52% had both IgG and IgM antibodies. Of the 100 patients,19% had a history of thrombosis, 8% had ahistory of spontaneous abortion, and 6% had a history of seizure disorder. These complications occurred in the presence (61%) and absence (39%) of detectable phospholipid antibodies. Drug-related LA's were observed in 34 patients; of these 74% were positivefor antiphospholipid antibodies and 24% hada history of thrombosis.The distribution of antibody types with drug-related LA's was similarto the overall group, with 40% IgG only, 8%IgM only and 52% both IgG and IgM These findings indicate that IgG and IgM antibodies to phospholipid are not observed in all patients with lupus anticoagulants, that thrombosis does occur in this population in the absence of detectable antibodies to phospholipid and that drug-related LA's are associated with thrombosis. Furthermore, there appeared to be little relationship between the degree of prolongation of the aPTT and the titer of anti-phospholipid antibody.
APA, Harvard, Vancouver, ISO, and other styles
2

Cucnik, Sasa. "SP0176 PATHOGENIC ANTIBODIES IN PHOSPHOLIPID SYNDROM." In 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Dhir, V., A. Gawalkar, J. Ahluwalia, A. Bahl, S. Sharma, A. Sharma, and S. Jain. "AB0635 Anti-phospholipid antibodies in lupus myocarditis." 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.3672.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Li, C., L. Zhu, Z. Wang, Y. Sun, R. Mu, and Z. Li. "AB0559 The prevalence of non-criteria anti-phospholipid antibodies in anti-phospholipid syndrome." 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.6750.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Brien, W., G. Denome, and B. O’Keefe. "THE PREVELANCE OF ANTIPHOSPHOLIPID ANTIBODIES, BY ELISA TECHNIQUE, IN PATIENTS WITH THE LUPUS ANTICOAGULANT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644234.

Full text
Abstract:
Patients with the Lupus Anticoagulant and/or anticardiolipin antibodies have been reported to be at increased risk of thrombosis and miscarriages. It has been proposed that the lupus anticoagulant is an antiphospholipid antibody.We evaluated 16 patients with the lupus anticoagulant for the presence of antiphospholipid antibodies. The lupus anticoagulant was documented by the presence of an abnormal APTT, abnormal mixing studies, positive tissue thromboplastin inhibition test and positive platelet neutralization test.Plasma from each patient was assessed for the presence of anticardiolipin, antiphosphatidylserine and antiphosphatidyl-glycerol antibodies by ELISAtechniques. As a control, a neutral phospholipid phosphatidylethanolamine was used. A positive result was established when a delta value of lipid minus control was greater than 3SD compared to a normal population (20 pt.).Using three different patient dilutions, positive results were obtained in 10/16 pt. for anticardiolipin, 11/16 pt. for antiphosphatidylserine and 5/16 pt. for antiphosphatidyl-glycerol antibodies. Three patients were negative for all lipids. If a neutral phospholipid was not used and a delta volume not obtained, 15/16 patients would have had positive results.Our results suggest 1) Not all patients with the Lupus Anticoagulant have antiphosphilipid antibodies by ELISA technique. In evaluating patients with thrombosis and/or miscarriages, both tests should be performed.2) Anticardiolipin antibodies are not present in all patients and with a panel of other negatively charged phospholipids more positive results are obtained. 3) A neutral lipid should be used as a control for non-specific binding of antibody and delta values obtained to see if the results obtained is truly against the negatively charged lipid.
APA, Harvard, Vancouver, ISO, and other styles
6

Harris, EN, G. Wasley, and GRV Hughes. "DISTINCTION BETWEEN ANTI CARDIOLIPIN (aCL) ANTIBODIES IN SYPHLIS AND THE "ANTI PHOSPHOLIPID SYNDROME"." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643658.

Full text
Abstract:
Patients both with syphilis and with the Anti-Phospholipid Syndrome (APS) produce antibodies that bind cardiolipin (CL). However, thrombosis, fetal loss, and thrombocytopenia, as well as lupus anticoagulant (LA) activity occur in APS but not syphilis patients. Differences between aCL antibodies produced in these 2 disorders have been suggested but not proven. We report a newly devised ELI9A assay using carbon coated VDRL (C-VDRL) as antigen, as well as a variety of other ELISA assays with various phospholipids as antigens, to study sera from 20 syphilis and 10 APS patients. Inhibition experiments were alSo performed to support findings with the ELISA assays. Syphilis sera bound both CL and C-VDRL coated plates, but binding to C-VDRL was always greater. APS sera bound CL but not C-VDRL plates. When plates were coated with low concentrations of negatively charged PLs, syphilis sera bound CL almost exclusively but APS sera bound negatively charged phospholipids (PLs) as well as they did CL. Inhibition experiments confirmed the high avidity of syphilis sera for CL, particularly when presented as the VDRL antigen; but APS sera bound negatively charged PLs as avidly as CL. Neither syphilis nor APS sera bound zwitterionic phospholipids. These findings may be important in that CL is limited primarily to mitochondrial membranes, but negatively charged PLs are widely distributed in cell membranes of the body. Hence, autoimmune sera which binds negatively charged PLs as well as CL may affect cell function more readily than syphilis sera which is limited primarily to CL binding. Too, negatively charged PLs (but not CL) are present in PL mixtures used in the LA test, hence APS (but not syphilis) plasma would more likely show LA activity. The genetic origins of these 2 groups of antibodies may also be different although they bind related antigens.
APA, Harvard, Vancouver, ISO, and other styles
7

Chighizola, C. B., F. Pregnolato, M. G. Raimondo, C. Comerio, C. Sobrino Grande, L. Trespidi, M. O. Borghi, et al. "FRI0349 Low titer anti-phospholipid antibodies convey an increased obstetric risk." 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.5887.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Pengo, V., M. J. Heine, P. Thiagarajan, and s. s. Shapiro. "A GENERAL MECHANISM FOR LUPUS ANTICOAGULANTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643660.

Full text
Abstract:
Although- a number of observations have implied that lupus anticoagulants have immunologic specificity towards anionic. phospholipids, thereby prolonging phospholipid-dependent coagulation tests, this assumption has been directly demonstrated in only one patient with a monoclonal IgM paraprotein. We have tested the generality of this hypothesis directly by isolating five IgG lupus anticoagulants from patients with lupus-like syndromes and/or thrombosis. IgG lupus anticoagulant fractions were isolated free of other plasma proteins and free of contaminating phospholipid by adsorption to and elution from cardiolipin-cholesterol-dicetylphosphate liposomes , followed by chromatography on protein A-Sepharose. Cardiolipin liposomes, but not phosphatidylcholine liposomes, were capable of removing all, or nearly all, lupus anticoagulant activity from patient plasma. Anticardiolipin and lupus anticoagulant activity were both present in acidic fractions on isoelectric focusing. F(ab’)2 fragments retained lupus anti coagulant activity and bound to cardiolipin in an ELISA assay. The affinity-purified IgG preparations reacted with cardiolipin, phosphatidyl serine , phosphatidylinositol and phosphatidic acid, but not with phosphatidylcholine or phosphatidyl ethanol amine, and inhibited calcium-dependent binding of prothrombin and of factor X to phosphatidy1serine-coated surfaces. These data demonstrate a general mechanism for the action of lupus anticoagulants: antibodies that have immunologic specificity towards anionic phospholipids, thereby blocking the calcium-mediated binding of vitamin K-dependent coagulation factors to coagulation-active phospholipid surfaces.
APA, Harvard, Vancouver, ISO, and other styles
9

Ince, A., A. Roumany, U. Daud, PH Pepmueller, and TL Moore. "FRI0172 Long-term follow-up of paediatric patients with positive anti-phospholipid antibodies." In 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Day, Cameron, and Paul Neilsen. "Abstract 4601: Phospholipid and enzyme antibodies for the evaluation of novel cancer biomarkers." In 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Phospholipid antibodies' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography