Soluble Vascular Biomarkers in Rheumatoid Arthritis and Ankylosing Spondylitis: Effects of 1-year Antitumor Necrosis Factor-α Therapy.

Objective: Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) have been associated with cardiovascular disease. The treatment of arthritis by tumor necrosis factor-α (TNF-α) inhibitors may decrease the serum concentrations of vascular biomarkers. We determined circulating levels of oxidized low-density lipoprotein (oxLDL)/β glycoprotein I (β-GPI) complexes, antibodies to 60 kDa heat shock protein (anti-Hsp60), soluble urokinase plasminogen activator receptor (suPAR), and B-type natriuretic peptide (BNP) fragment in sera of RA and AS patients undergoing anti-TNF treatment.

Predictive Value of Oxidized Low-Density Lipoprotein/β-Glycoprotein-I Complexes (oxLDL/βGPI) in Nonautoimmune Atherothrombosis.

Introduction: Lipid oxidation is a definite feature of atherosclerosis, and oxidized low-density lipoprotein (oxLDL) is not only highly immunogenic but toxic to several cell types. Beta-2-glycoprotein-I (βGPI) dampens oxLDL toxicity by forming binary oxLDL/βGPI complexes. We evaluated whether circulating oxLDL/βGPI complexes are associated to atherosclerosis-related events (ARE) and to venous thromboembolism (VTE).

Prognostic value of urinary 11-dehydro-thromboxane B for mortality: A cohort study of stable coronary artery disease patients treated with aspirin.

Aim: There is a variable cardiovascular risk reduction attributable to aspirin because of individual differences in the suppression of thromboxane A and its downstream metabolite 11-dehydro-thromboxane B (11dhTxB ). The aim of this study is to evaluate the optimal cut point of urinary 11dhTxB for the risk of mortality in aspirin-treated coronary artery disease (CAD) patients.

Methods And Results: This was a prospective cohort study including stable CAD patients who visited the Baylor Heart and Vascular Hospital in Dallas or the Texas Heart Hospital Baylor Plano, TX between 2010 and 2013.

Urinary 11-Dehydro-Thromboxane B and Mortality in Patients With Stable Coronary Artery Disease.

Antiplatelet therapy with aspirin has been shown to reduce adverse outcomes in patients with coronary artery disease (CAD). Aspirin irreversibly inhibits platelet cyclooxygenase-1 and attenuates thromboxane A (TXA)-mediated platelet aggregation, but there is variable suppression of cyclooxygenase-1. From a cohort of patients with stable CAD, we performed blinded, detailed chart abstraction, and measured urinary 11-dehydro-thromboxane B (11dhTxB), an inactive metabolite of TxA from frozen samples.

Residual thromboxane activity and oxidative stress: influence on mortality in patients with stable coronary artery disease.

Background: Aspirin use is effective in the prevention of cardiovascular disease; however, not all patients are equally responsive to aspirin. Oxidative stress reflected by F2-isoprostane [8-iso-prostaglandin-F2α (8-IsoPGF2α)] is a potential mechanism of failure of aspirin to adequately inhibit cyclooxygenase-1. The objective was to examine the relation between all-cause mortality and the concentrations of urinary 11-dehydro thromboxane B2 (11dhTxB2) and 8-IsoPGF2α in patients with stable coronary artery disease (CAD).

Differential assay reactivity of immunglobulin A anti-ß glycoprotein I antibodies: implications for the clinical interpretation of antiphospholipid antibody testing.

Objective: The routine measurement of IgA anticardiolipin (aCL) and IgA anti-β glycoprotein I (anti-β GPI) antibodies remain controversial despite several studies demonstrating an association with thromboembolic disease in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). This controversy may be a contributing factor for the current under use of IgA antiphospholipid antibodies. We aimed to investigate the nature of discrepant IgA anti-β GPI reactivity to help define the diagnostic value of IgA antiphospholipid antibodies.

Oxidized Low-Density Lipoprotein-β2-Glycoprotein I Complex But Not Free Oxidized LDL Is Associated With the Presence and Severity of Coronary Artery Disease.

Oxidized low-density lipoprotein (oxLDL) and β2-glycoprotein I (β2GPI) have been identified in human atherosclerotic lesions and when complexed have been implicated as a pro-atherothrombotic antigen. We examined the association of free oxLDL and oxLDL-β2GPI complex in patients with coronary artery disease who underwent elective cardiac catheterization. Serum was collected from patients with suspected coronary artery disease immediately before elective cardiac catheterization who were either treated (n = 385) or not treated (n = 150) with statins and from healthy volunteers (n = 134).

Respirometric characterization of aerobic sulfide, thiosulfate and elemental sulfur oxidation by S-oxidizing biomass.

Respirometry was used to reveal the mechanisms involved in aerobic biological sulfide oxidation and to characterize the kinetics and stoichiometry of a microbial culture obtained from a desulfurizing biotrickling filter. Physical-chemical processes such as stripping and chemical oxidation of hydrogen sulfide were characterized since they contributed significantly to the conversions observed in respirometric tests. Mass transfer coefficient for hydrogen sulfide and the kinetic parameters for chemical oxidation of sulfide with oxygen were estimated.

Proatherogenic oxidized low-density lipoprotein/β2-glycoprotein I complexes in arterial and venous disease.

OxLDL/β2GPI complexes have been implicated in the initiation and progression of atherosclerosis and associated with disease severity and adverse outcomes. We investigate the significance of anti-oxLDL/β2GPI antibodies and oxLDL/β2GPI complexes in patients with arterial and idiopathic venous disease. A cohort of 61 arterial disease patients, 32 idiopathic venous disease patients, and 53 healthy controls was studied.

Aerobic desulfurization of biogas by acidic biotrickling filtration in a randomly packed reactor.

Biotrickling filters for biogas desulfurization still must prove their stability and robustness in the long run under extreme conditions. Long-term desulfurization of high loads of H2S under acidic pH was studied in a lab-scale aerobic biotrickling filter packed with metallic Pall rings. Reference operating conditions at steady-state corresponded to an empty bed residence time (EBRT) of 130s, H2S loading rate of 52gS-H2Sm(-3)h(-1) and pH 2.

Platelet thromboxane (11-dehydro-Thromboxane B2) and aspirin response in patients with diabetes and coronary artery disease.

Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation. The effect of ASA ingestion on thromboxane generation was evaluated in patients with diabetes (DM) and cardiovascular disease. Thromboxane inhibition was assessed by measuring the urinary excretion of 11-dehydro-thromboxane B2 (11dhTxB2), a stable metabolite of thromboxane A2.

Is atherosclerosis an autoimmune disease?

Immunologic research into pathogenic mechanisms operating in autoimmune-mediated atherosclerosis initially focused on adaptive immunity. Current interest is directed to more basic inflammatory mechanisms. Chronic inflammation (innate immunity-associated) may trigger initial events that can lead to atherosclerotic cardiovascular disease.

β2-glycoprotein I and oxidative inflammation in early atherogenesis: a progression from innate to adaptive immunity?

The innate immune system represents the first line of host defense against a wide variety of pathogens and endogenous danger signals. It relies on trans-membrane signaling and cytoplasmic receptors (danger sensors) to trigger early inflammatory responses. As with the adaptive immunity, an innate immune response can cause tissue injury, chronic inflammation and disease.

Aspirin insensitive thromboxane generation is associated with oxidative stress in type 2 diabetes mellitus.

Introduction: Aspirin (ASA) irreversibly inhibits platelet cyclooxygenase-1 (COX-1) leading to decreased thromboxane-mediated platelet activation. The effect of ASA ingestion on platelet activation, thromboxane generation, oxidative stress and anti-oxidant biomarkers was studied in type 2 diabetes mellitus (DM).

Material And Methods: Baseline and post-ASA samples (100/325 mg x 7 days) were obtained from 75 DM patients and 86 healthy controls for urinary 11-dehydro-thromboxane B2 (11 dhTxB2), 8-iso-prostaglandin-F2α (8-isoPGF2α) and serum sP-Selectin, nitrite (NO(2)(-)), nitrate (NO(3)(-)) and paraoxonase 1 (PON1) activity.

Antiphospholipid antibodies and antiphospholipid syndrome: role in portal vein thrombosis in patients with and without liver cirrhosis.

Unlabelled: The antiphospholipid syndrome (APS) has been associated with portal vein thrombosis (PVT). This study explored the contribution of antiphospholipid antibodies (aPL) to PVT in cirrhotic and noncirrhotic patients.

Patients And Methods: A total of 50 patients with liver cirrhosis and PVT, 50 patients with liver cirrhosis without PVT, 50 consecutive PVT without liver cirrhosis, and 50 controls.

Oxidized-LDL/beta(2)-glycoprotein I complexes are associated with disease severity and increased risk for adverse outcomes in patients with acute coronary syndromes.

Oxidized low-density lipoprotein (oxLDL)/beta(2)-glycoprotein I (beta2GPI) complexes have been implicated in atherogenesis. oxLDL/beta2GPI complexes were measured in 339 patients with suspected acute coronary syndromes. Approximately 68% had angiographically documented coronary artery disease (CAD) and significantly higher mean + or - SD levels of oxLDL/beta2GPI (3.

Autoimmunity, infectious immunity, and atherosclerosis.

Introduction: Vascular inflammation is common in certain systemic autoimmune diseases and contributes to the oxidation of low-density lipoprotein (oxLDL) and oxLDL/beta2-glycoprotein I (beta2GPI) complex formation. These complexes have been implicated as proatherogenic autoantigens that participate in the development of atherosclerotic disease.

Discussion: We have demonstrated that the in vitro macrophage uptake of oxLDL/beta2GPI complexes increases in the presence of IgG anti-beta2GPI antibodies and that IgG immune complexes containing oxLDL/beta2GPI upregulate the expression of both scavenger and Fcgamma receptors to activate beta2GPI specific T cells.

Newer antiphospholipid antibodies predict adverse outcomes in patients with acute coronary syndrome.

Antiphospholipid antibodies (aPLs) have been implicated in atherogenesis. We studied 344 patients with acute coronary syndromes; approximately 40% were aPL+ in 1 or more tests and 60% aPL-. In 215 patients, coronary artery disease (CAD) was angiographically documented, with 43.

The immunology of atherothrombosis in the antiphospholipid syndrome: antigen presentation and lipid intracellular accumulation.

The antiphospholipid syndrome (APS), characterized by elevated serum levels of antiphospholipid antibodies (aPL) and thromboembolic complications, is a common cause of acquired hypercoagulability. The plasma protein beta2-glycoprotein I (beta2GPI) is the most clinically relevant antigenic target for aPL. Recent experimental evidence from our laboratory substantiated the concept that IgG anti-beta2GPI immune complexes containing oxidized LDL (oxLDL) not only facilitated the intracellular accumulation of oxLDL in macrophages but also allowed the presentation of beta2GPI epitopes to pathogenic autoreactive T cells.

Atherosclerosis in autoimmune diseases.

Lipid peroxidation occurs frequently in patients with systemic autoimmune diseases and contributes to autoimmune vascular inflammation. Oxidized low-density lipoprotein (oxLDL) interacts with beta2-glycoprotein I (beta2GPI), forming oxLDL/beta2GPI complexes. Circulating oxLDL/beta2GPI complexes and autoantibodies to these complexes have been demonstrated in patients with systemic lupus erythematosus and antiphospholipid syndrome.

Immunogenic oxidized low-density lipoprotein/beta2-glycoprotein I complexes in the diagnostic management of atherosclerosis.

Oxidized low-density lipoprotein (oxLDL) promotes atherosclerosis through a complex interaction of inflammatory and immunologic factors that lead to macrophage lipid uptake and foam cell formation. OxLDL interacts with beta2-glycoprotein I (beta2GPI) forming oxLDL/beta2GPI complexes. These complexes may be formed in the arterial intima during atherogenesis and released into the circulation.

Preventing autoimmune and infection triggered atherosclerosis for an enduring healthful lifestyle.

Atherosclerosis is a chronic inflammatory disease of the arteries associated with various risk factors that promote lipid abnormalities (i.e., dyslipidemia), development and progression of atherosclerotic lesions, plaque rupture, and vascular thrombosis.

Atherogenic antiphospholipid antibodies in antiphospholipid syndrome.

Macrophage uptake of oxidized LDL (oxLDL) plays a critical role in early stages of atherosclerosis. We previously reported that oxLDL forms stable complexes with beta2-glycoprotein I (beta2GPI), and that these complexes were frequently present in the sera of patients with systemic lupus erythematosus (SLE) and/or antiphospholipid syndrome (APS). oxLDL/beta2GPI complexes were shown to be antigenic targets for autoantibodies present in APS.

Antiphospholipid antibodies in patients with coronary artery disease: new cardiac risk factors?

Antiphospholipid antibodies (aPL) have been implicated in the pathogenesis of coronary artery disease (CAD). We evaluated the presence of aPL in patients with chest pain/acute coronary syndromes (ACS) to determine if aPL were associated with the presence and severity of CAD, adverse outcomes, and other coronary risk factors. Patients with chest pain/ACS were evaluated for aPL prior to diagnostic and therapeutic investigations.