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A R Cabral

Publications and source records attributed to A R Cabral.

At least 19 recordsLinked to original sources
PubMed2004

Anaerobic biodegradation of an organic by-products leachate by interaction with different mine tailings.

Deinking by-products from paper recycling have been used as cover materials on acid-producing tailings. Due to residual cellulose, anaerobic degradation leads to the production of an organic-rich leachate, which may percolate through the tailings. This study aims at describing the influence of the tailings' characteristics on the attenuation of organic matter in leachate and at discussing the degradation mechanisms. To this end, leachate was mixed with different types of tailings, including three unoxidized tailings with varying acid generation potentials and one tailing in three states of oxidation. Regularly, selected biochemical parameters were analyzed to access the evolution of organic components. The results show that when leachate from deinking by-products was placed in contact with tailings, phase and acid-base balance reactions took place in the beginning. Subsequently, oxidation-reduction reactions dominated the chemistry of the system. The type, the constituents, and the state of oxidation of the mine tailings condition the mechanisms of biodegradation of organic components. Methanogenesis was predominant in the control sample (pure organic leachate) but was absent in all leachate-tailings mixtures. No biodegradation was observed in the liquid phase for oxidized tailings and the organic concentration remained constant for unoxidized tailings, independently of the acid-generation potential. The biodegradation efficiency was optimal when the leachate was in contact with a mixture of oxidized and unoxidized tailings due to sulfate-reduction.

Acids↗
PubMed2004

Heterogeneity of antibodies to beta2-glycoprotein 1 from patients with systemic lupus erythematosus.

We studied antibodies to beta2-glycoprotein 1 (anti-beta2GP1) from 72 patients with systemic lupus erythematosus (SLE) with or without antiphospholipid syndrome (APS) or with or without anticardiolipin antibodies (aCL). Fifteen patients had APS and positive antiphospholipid antibodies [clinical APS(+)/aPL(+)], 12 patients had APS, negative serum IgG and IgM aCL, antiphosphatidylethanolamine, anti-phosphatidylserine and no lupus anticoagulant [clinical APS(+)/ aPL(-)]. A third group included 16 patients without APS but high aCL levels [clinical APS(-)/ aPL(+)]. In a fourth group we studied 29 patients without clinical manifestations of APS or aCL [clinical APS(-)/aPL(-)]. One hundred anticardiolipin and VDRL-negative normal sera were studied as controls. IgG antibodies to cardiolipin proper in a bovine beta2GP-free system, to human beta2GP1 immobilized on cardiolipin or to human beta2GP1 alone were detected in all sera by ELISA using irradiated and nonirradiated plates from two manufacturers. Sera from APS(+)/aPL(+) patients showed IgG binding to CL, CL + beta2GP1 and beta2GP1 in irradiated and nonirradiated plates. APS(+)/ aPL(-) sera had more significant IgG binding to beta2GP1 than normal controls when studied in both irradiated or nonirradiated plates (P = 0.001). This binding was inhibited by solid-phase cardiolipin in a dose-dependent manner. Sera from the APS(-)/aPL(+) subgroup had comparable IgG activity in both the CL and CL + beta2GP1 assays, while no anti-beta2GP1 activity was detected in these sera. Sera from the clinical APS(-)/aPL(-) patients were negative in the three ELISA systems. Antibodies to human beta2GP1 from SLE patients recognize various epitopes. Those from APS(+)/ aPL(+) patients appear to react with an epitope boosted by cardiolipin in addition to another one present in the native protein. In contrast, anti-beta2GP1 from patients with APS(+)/aPL(-) are blocked by cardiolipin, suggesting that their epitope is the phospholipid-binding site.

Adult↗
PubMed2000

The anti-phospholipid antibody syndrome: clinical and serological aspects.

The association of thromboses and/or cytopenias with anti-phospholipid antibodies (aPL), the anti-phospholipid syndrome (APS), is well recognized. The syndrome may be primary or occur within systemic lupus erythematosus (SLE). The notion of the syndrome occurring within SLE is important since patients found to have aPL may be at risk for developing APS manifestations, those who develop some manifestations may be at risk for developing others and, finally, SLE patients with this syndrome may need special treatment. There are subtle differences between the primary and the secondary forms, mostly due to the frequently higher and more persistent autoantibody levels in the primary and the influence of lupus in the secondary. These syndromes may be related to various antigen/antibody systems in which phospholipids participate either directly or through their effect on the proteins that bind them. Similar clinical manifestations also occur in patients who have serum antibodies to such proteins (e.g. beta2-glycoprotein-I) in the absence of phospholipid. Some of these antibodies may even be more important pathogenically than the antibodies against cardiolipin that were originally described. Testing for the latter is, however, still the first choice when suspecting an antiphospholipid syndrome. If this is negative in this situation, a search for the other autoantibodies is indicated.

Antiphospholipid Syndrome↗
PubMed1999

Serum anti-beta2-glycoprotein-I and anticardiolipin antibodies during thrombosis in systemic lupus erythematosus patients.

PURPOSE: Antibodies to beta2-glycoprotein-I are more strongly associated with clinical antiphospholipid syndrome than are anticardiolipin antibodies. We previously found a decrease in anticardiolipin antibodies at the time of thrombosis in 6 patients with systemic lupus erythematosus (SLE). We therefore sought to determine the prevalence and levels of antibodies to beta2-glycoprotein-I and to cardiolipin before, during, and after thrombosis in patients with SLE, and to compare them with patients who did not have thrombosis. METHODS: We studied 24 patients with SLE who had at least one episode of thrombosis and 102 patients with SLE without thrombosis. Serum anticardiolipin antibodies were measured by conventional enzyme-linked immunosorbent assay (ELISA) using newborn calf serum as the blocking agent. Serum anti-beta2-glycoprotein-I antibodies were measured by ELISA on nonirradiated plates, using purified human beta2-glycoprotein-I without phospholipid. RESULTS: All patients with thrombosis had anti-beta2-glycoprotein-I antibodies, compared with only 17% of controls (P <0.0001). We observed a significant decrease in serum anti-beta2-glycoprotein-I levels at the time of thrombosis, as compared with previous and subsequent samples. The prevalence and levels of IgG and IgM anticardiolipin antibodies were similar in patients with and without thrombosis. A decrease in IgG or IgM anticardiolipin titers occurred during thrombosis in 6 patients. Anticoagulant, corticosteroid, and immunosuppressive treatments did not appear to affect anti-beta2-glycoprotein-I levels at the time of thrombosis. CONCLUSION: Anti-beta2-glycoprotein-I antibodies are strongly associated with thrombosis in patients with SLE. The decrease of anti-beta2-glycoprotein-I levels at the time of thrombosis may indicate a pathogenic role. This antibody may also be a marker of predisposition for thrombosis in these patients.

Adolescent↗
PubMed1998

Hidden anti-phospholipid antibodies in normal human sera circulate as immune complexes whose antigen can be removed by heat, acid, hypermolar buffers or phospholipase treatments.

Heat treatment of normal human serum reveals otherwise masked anti-cardiolipin antibodies (aCL). We studied the mechanism of masking and the nature of the inhibitor of these aCL IgG. Other forms of treatment, besides heating for 30 min at 56 degrees C, can also unmask hidden aCL IgG. These include acid pH, hypermolar buffers and phospholipase digestion. When unmasked, these aCL recognize other anionic and zwitterionic phospholipids, but do not react with DNA, cell antigens or IgG. Using thin layer chromatography we demonstrate that the heat-labile inhibitor(s) of these aCL are phosphatidylserine, phosphatidylethanolamine, phosphatidylglycerol and phosphatidylcholine. These antibodies are not beta2-glycoprotein-I dependent and actually compete with this protein for phospholipid binding. The hidden antibodies are comprised of two populations of IgG autoantibodies: one reactive with cardiolipin, phosphatidylserine, phosphatidylinositol, phosphatidylglycerol, phosphatidylethanolamine and sphingomyelin, and the other reactive almost exclusively with phosphatidylcholine and phosphorylcholine on enzyme-linked immunosorbent assay plates or when exposed by bromelain on the erythrocyte surface. Our data suggest that hidden aCL are natural oligoreactive IgG anti-phospholipid autoantibodies that circulate masked by their antigen.

Antibodies, Antiphospholipid↗
PubMed1998

Autoantibodies in systemic lupus erythematosus.

Cationic germ line gene-encoded anti-DNA antibodies appear to cause inflammatory lesions via deposition and in situ formation of immune complexes, but also perhaps through apoptosis of glomerular mesangial cells. Somatic mutation is not critical for the expression of the electrical net charge of anti-DNA. In one transgenic mouse model, the nephrogenicity of anti-DNA was dependent on the expression of interleukin alpha by epidermal cells. Anti-P autoantibodies are present in the serum of healthy children but are masked by IgG antibodies. Some anti-P antibodies appear to be a subset of antilymphocyte autoantibodies. It was confirmed that anti-Ro/SS-A antibodies react with structurally unrelated conformational epitopes. The combined results of immunofluorescence and enzyme-linked immunosorbent assay in the detection of antineutrophil cytoplasmic antibody has a 99.5% specificity for vasculitis among patients with connective tissue diseases. Antinucleosome antibodies are highly prevalent in patients with systemic lupus erythematosus and show an inverse correlation with nucleosome plasma levels. Transfected T-cell receptor alpha chains specific for nucleosomal autoepitopes from a Th clone that accelerates lupus nephritis, recognized the nucleosomal epitopes presented by antigen presenting cell-bearing 1-A molecules, as well as human DR molecules, via the classical major histocompatibility complex class II groove. IgG antibodies against (beta 2 -glycoprotein (GP)-1 are significantly associated with thrombosis in patients with antiphospholipid syndrome, with a specificity and sensitivity that ranges from 85% to 98% and 32% to 54%, respectively. The lupus anticoagulant activity, or the lack of it, of anti-beta 2-glycoprotein-1 appears to reside on the epitope specificity. Beta 2-glycoprotein-1 binds to apoptotic cells; in turn, anti-beta 2-glycoprotein-1 facilitate apoptotic cell clearance by macrophages. The recently described anti-A2/RA33 autoantibody appears to recognize an epitope capable of distinguishing patients with lupus or with rheumatoid arthritis from those with mixed connective tissue disease.

Animals↗
PubMed1997

Autoantibodies in systemic lupus erythematosus.

Research on pathogenic and nonpathogenic anti-DNA antibodies has shown that the charge and affinity for double-stranded DNA may not be adequate predictors of their pathogenicity. In turn, anti-DNA-induced renal damage could be caused by differences in fine specificities. Penetration of anti-double-stranded DNA monoclonal antibodies into live cells appears to require DNA or a DNA-like membrane receptor. Anti-U1 ribonucleoproteins penetrate live cells and induce apoptosis. HLA-DRB1*1501 or HLA-DRB1*1503, DQA1*0102, and DQB1*0602 haplotypes were increased in patients with systemic lupus erythematosus with anti-ribosomal protein P (anti-P) antibodies, particularly in whites, blacks, and Mexican-Americans. Anti-Ro/Sjögren's syndrome antigen A antibodies had a strong predictive diagnostic value for systemic lupus erythematosus among patients positive for antinuclear antibodies and negative for double-stranded DNA but had no utility among those positive for both antinuclear antibodies and anti-DNA antibodies. True antiphospholipid murine monoclonal antibodies display an unusual number of cationic residues in the H-chain CD3 region, whereas anti-beta 2-glycoprotein-I monoclonal antibodies lack them. The association of IgG anti-beta 2-glycoprotein-I with a history of thrombosis in systemic lupus erythematosus has been largely confirmed. Apoptotic thymocytes bind antiphospholipid antibodies in a beta 2-glycoprotein-I-dependent manner and may constitute a source of immunogen in autoimmune disease.

Animals↗
PubMed1997

Thinner abusers.

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Duplicate Publications as Topic↗
PubMed1997

The antiphospholipid/cofactor syndromes. II. A variant in patients with systemic lupus erythematosus with antibodies to beta 2-glycoprotein I but no antibodies detectable in standard antiphospholipid assays.

OBJECTIVE: After the initial description of the anticardiolipin syndrome inpatients with systemic lupus erythematosus (SLE), it became clear that phospholipids other than cardiolipin could also be involved, that there could also be a primary syndrome, and that protein cofactors participate in in vitro reactivity of the autoantibodies. We describe 5 patients with SLE with clinical manifestations of antiphospholipid syndrome (APS) but persistently negative antiphospholipid antibodies (aPL). In all their tested sera we found antibodies to phospholipid-free beta 2-glycoprotein I (a beta 2-GPI). METHODS: We studied 5 patients with SLE with at least 2 clinical manifestations of APS with no serum aPL detected in routine assays. IgG and IgM a beta 2-GPI were studied by ELISA and by Western blot. We also tested for antibodies to phosphatidylcholine, phosphatidylethanolamine, and phosphatidylserine by ELISA. We studied 54 normal sera as controls. RESULTS: Four patients had livedo reticularis, 2 had thrombocytopenia, 2 had hemolytic anemia, and one each had recurrent venous thromboses, repeated fetal loss, pulmonary arterial hypertension, and transverse myelitis. No patient had serum aPL, but all had high titers of IgG a beta 2-GPI (p < 0.001 vs controls). Reactivity found in ELISA was confirmed by Western blot. CONCLUSION: We describe a variant of APS in patients with SLE with negative aPL but serum antibodies to beta 2-GPI.

Adult↗
PubMed1996

The antiphospholipid/cofactor syndromes: a primary variant with antibodies to beta 2-glycoprotein-I but no antibodies detectable in standard antiphospholipid assays.

BACKGROUND: Most systemic lupus erythematosus (SLE) patients with two or more clinical manifestations of the antiphospholipid syndrome (APS) and negative antiphospholipid antibodies (aPL) have antibodies to beta 2-glycoprotein-I (a beta 2 GP-I). Herein we describe a similar set of circumstances, but in patients without evidence of SLE. PATIENTS AND METHODS: We studied 6 patients with recurrent venous and/or arterial thromboses without aPL as detected by routine assays nor clinical or serological evidence of other autoimmune disease. Immunoglobin (Ig) G and IgM antibodies to bovine and human phospholipid-free beta 2 GP-I were studied by Western blot test and by enzyme-linked immunosorbent assay (ELISA) utilizing radiated and nonirradiated plates. We also tested antibodies to cardiolipin, phosphatidylserine, and phosphatidylethanolamine by ELISA. As controls, 54 normal sera were studied. RESULTS: All 6 patients had recurrent arterial and/or venous thromboses. Three also had thrombocytopenia, 1 had livedo reticularis, and 2 had valvular heart disease. None of the patients had aPL, but all had serum IgG reactivity against human and bovine beta 2 GP-I (P < 0.001 versus controls for both). Titers of anti-bovine beta 2 GP-I were higher when studied in irradiated plates but were also higher than normal in nonirradiated plates (P < 0.001). These antibodies did not recognize human or bovine beta 2 GP-I bound to cardiolipin in solid phase. We confirmed by Western blot that these autoantibodies recognize human beta 2 GP-I. We found no IgM a beta 2 GP-I. CONCLUSIONS: We describe a primary condition akin to the antiphospholipid syndrome with negative aPL, but with serum IgG antibodies to human and bovine beta 2 GP-I. These antibodies recognize beta 2 GP-I epitopes that are not accessible when beta 2 GP-I is bound to cardiolipin.

Adult↗
PubMed1996

Autoantibodies in systemic lupus erythematosus.

Lupus anti-DNA may have higher homology with germline than those from normal subjects. However, in NZB/NZW mice, bacterial DNA is more antigenic than mammal DNA, which could indicate an antigen-driven origin. High-affinity antibodies to double-stranded DNA cross-react with small nuclear ribonucleoprotein and ribosomal P proteins. These cross-reactive anti-DNA may penetrate live cells. Antibodies to ribosomal P proteins are associated with neuropsychiatric, renal, and hepatic lupus involvement. IgG antibodies to (H2A-H2B)-DNA complexes antedate procainamide-induced lupus. Autoantibodies to some La/Ro peptides in a mother indicates that her children may develop neonatal lupus and determine who will have congenital heart block. Perinuclear antineutrophil cytoplasmic antibodies are present in 25% of systemic lupus erythematosus patients without correlation with anti-DNA or disease activity. Different antiphospholipid antibodies require different protein cofactors for reactivity. Those to anionic phospholipids require beta 2-glycoprotein I, whereas anti-phosphatidylethanolamine antibodies require kininogen or its binding protein. Antibodies to phospholipid-free beta 2-glycoprotein I are associated more strongly with clinical antiphospholipid syndrome than are antiphospholipid antibodies.

Animals↗
PubMed1996

The concept and classification of antiphospholipid/cofactor syndromes.

In 1990, three groups simultaneously reported that putative IgG antibodies to anionic phospholipids were either not directed to phospholipids or at least required beta 2-glycoprotein-I (beta 2-GP-I) for reactivity in vitro. During the same year, our group described a patient with "idiopathic' hemolytic anemia with serum and erythrocyte-bound IgM antibodies to phosphatidylcholine later found to be independent of beta 2-GP-I for antigen recognition. Lately, the field has been expanded considerably with: (1) the description of other potential antigens such as prothrombin for some lupus anticoagulants, (2) the finding of crossreactivity between some antiphospholipid antibodies (aPL) with thrombomodulin, (3) the presence of serum antibodies to beta 2-GP-I (anti-beta 2-GP-I) in patients with SLE and thromboses, (4) the findings that the clinical manifestations of APS in SLE patients associate more strongly with anti-beta 2-GP-I than with aPL, (5) our finding of a group of SLE patients with the clinical manifestations of APS, with negative serum aPL, but with positive anti-beta 2-GP-I, (6) the description of a group of patients with the clinical manifestations of APS, without serum aPL, without serological nor clinical evidence of any autoimmune disease, but with IgG anti-beta 2-GP-I, and (7) the observation that serum anti-phosphatidylethanolamine antibodies detected in some patients with APS require kininogen (alone or complexed with the kininogen-binding protein), prekallikrein and/or factor XI for in vitro reactivity. Thus, there are antibodies that may be considered true aPL; other "aPL' require a protein cofactor for their detection in vitro, at least in the case of beta 2-GP-I it would appear that their epitope is present on the protein proper not on the phospholipid, hence these are pseudo aPL, and a third group of related anti-cofactor autoantibodies that are directed to the protein in the absence of phospholipid. Clearly, the term "antiphospholipid syndrome' has become obsolete. We propose the term "Antiphospholipid/Cofactor Syndromes' to cull the various syndromes.

Antiphospholipid Syndrome↗