Assessment of the nitrosylation process.

Purpose Of Review: To understand the principles and limits of the methodologies used for the measurement of S-nitrosylated proteins.

Recent Findings: Among methods for studying protein S-nitrosylation, chemoluminescence and biotin switch assay have rapidly gained popularity. However, recent findings have attempted to highlight potential pitfalls for these methods.

B-type natriuretic peptides for the diagnosis of congestive heart failure in dyspneic oldest-old patients.

Objectives: To evaluate the accuracy of B-type natriuretic peptide (BNP) and amino-terminal pro-brain natriuretic peptide (NT-proBNP) for the diagnosis of congestive heart failure (CHF) in dyspneic patients aged >or=85 years admitted to the Emergency Department (ED), and to define threshold values in this oldest-old population.

Design And Methods: This study involved 210 oldest-old patients, and 360 patients aged from 65 to 84 years (<85 years), admitted to the ED for dyspnea.

Results: Median BNP and NT-proBNP levels were significantly higher in CHF oldest-old patients (p<0.

Glucose transport in fibroblasts is unaffected by polyamines.

Objective: Wound healing is characterized by a net increase in glucose utilization in wound tissues. The mediators involved in this process remain largely unknown. Because polyamines are known to stimulate d-glucose uptake in brush-border membrane vesicles, we investigated whether or not they stimulated sugar uptake in confluent cultured fibroblasts.

Implication of cytosolic phospholipase A2 (cPLA2) in the regulation of human synoviocyte NADPH oxidase (Nox2) activity.

NADPH oxidase Nox2 is involved in the production of superoxide by rheumatoid synovial cells, constitutively and after pro-inflammatory cytokine treatment. The aims of the study were to evaluate the capacity of these cells to produce the superoxide anion in response to arachidonic acid (AA), and to study the involvement of cytosolic phospholipase A(2) (cPLA(2)) in the cytokine regulation of Nox2. Superoxide production was quantified in synovial cells obtained from six patients with rheumatoid arthritis (RA) and six with osteoarthritis (OA), stimulated with (i) AA, and (ii) PLA(2) inhibitors prior to IL-1beta or TNF-alpha treatment.

Expression and extracellular release of Trx80, the truncated form of thioredoxin, by TNF-alpha- and IL-1beta-stimulated human synoviocytes from patients with rheumatoid arthritis.

Thioredoxin (Trx) plays several important roles, through changes to sulfhydryl reactions and protein interactions, in controlling cellular signalling processes in RA (rheumatoid arthritis). Trx80, the 10 kDa C-terminal truncated form of Trx, is a potent mitogenic cytokine and is involved in the Th1 response. In the present study, we have investigated the ability of synoviocytes from five RA patients to induce Trx80 after ex vivo stimulation by the pro-inflammatory cytokines IL-1beta (interleukin-1beta) and TNF-alpha (tumour necrosis factor-alpha) or by H(2)O(2).

High redox thioredoxin but low thioredoxin reductase activities in the serum of patients with rheumatoid arthritis.

Background: Thioredoxin (Trx)/thioredoxin reductase (TrxR) is a redox-active system induced by oxidative stress. We investigated its status as a function of RA disease activity.

Methods: 64 consecutive RA patients and 27 healthy subjects were enrolled in the study.

Effects of repeated infliximab therapy on serum lipid profile in patients with refractory rheumatoid arthritis.

Background: Patients with rheumatoid arthritis (RA) frequently display an atherogenic lipid profile which has been linked with inflammation. Tumor necrosis factor-alpha (TNF-alpha), a pivotal pro-inflammatory cytokine in RA may be involved in the development of the disturbed lipid metabolism. We investigated whether infliximab, an anti-TNF-alpha therapy, may modify the lipid profile.

Nifedipine protects against overproduction of superoxide anion by monocytes from patients with systemic sclerosis.

We have reported previously that dihydropyridine-type calcium-channel antagonists (DTCCA) such as nifedipine decrease plasma markers of oxidative stress damage in systemic sclerosis (SSc). To clarify the cellular basis of these beneficial effects, we investigated the effects in vivo and in vitro of nifedipine on superoxide anion (O2*-) production by peripheral blood monocytes. We compared 10 healthy controls with 12 patients with SSc, first after interruption of treatment with DTCCA and second after 2 weeks of treatment with nifedipine (60 mg/day).

Lack of association of eNOS (G894T) and p22phox NADPH oxidase subunit (C242T) polymorphisms with systemic sclerosis in a cohort of French Caucasian patients.

Objective: To assess the influence of endothelial nitric oxide synthase (eNOS) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase polymorphisms on the susceptibility of patients to and clinical expression of systemic sclerosis (SSc).

Methods: Seventy-seven French Caucasian patients with SSc were studied. Patients and ethnically matched controls (n=49) were genotyped, by restriction enzyme digestion of polymerase chain reaction (PCR) products, for G894T polymorphism in exon 7 of the eNOS gene and for C242T polymorphism of the gene encoding the p22(phox) NADPH oxidase subunit.

Nifedipine decreases sVCAM-1 concentrations and oxidative stress in systemic sclerosis but does not affect the concentrations of vascular endothelial growth factor or its soluble receptor 1.

Microvascular injury, oxidative stress, and impaired angiogenesis are prominent features of systemic sclerosis (SSc). We compared serum markers of these phenomena at baseline and after treatment with nifedipine in SSc patients. Forty successive SSc patients were compared with 20 matched healthy subjects.

Acute and sustained effects of dihydropyridine-type calcium channel antagonists on oxidative stress in systemic sclerosis.

Purpose: To evaluate the potential antioxidant properties of dihydropyridine calcium channel antagonists in systemic sclerosis.

Methods: Forty-two patients with systemic sclerosis were included (mean [+/- SD] age, 54 +/- 12 years; mean disease duration, 8 +/- 7 years). Plasma markers of oxidative stress (carbonyl residues, advanced oxidation protein products, malondialdehyde, nitrosothiols, and total thiol groups) were determined 72 hours after the discontinuation of usual dihydropyridine treatment (with either nifedipine or nicardipine), shortly after reinitiation of treatment, and 9 to 12 months later (long-term treatment) in 19 of the patients.

Increased pasma S-nitrosothiol concentrations predict cardiovascular outcomes among patients with end-stage renal disease: a prospective study.

The plasma concentrations of S-nitrosothiols, which are circulating nitric oxide metabolites with potential biologic activity, are increased among patients undergoing chronic hemodialysis (HD). However, the ability of S-nitrosothiols to release nitric oxide at physiologically relevant sites may be reduced among HD patients, because of impaired availability and/or activity of factors involved in S-nitrosothiol breakdown. The resultant lack of S-nitrosothiol bioavailability could contribute to the high cardiovascular risk for such patients.

Correlation of serum collagen I carboxyterminal telopeptide concentrations with cutaneous and pulmonary involvement in systemic sclerosis.

Objective: Systemic sclerosis (SSc) is characterized by fibrosis involving the skin and various internal organs. Type I collagen (Col I) is the most abundant extracellular matrix protein deposited in cutaneous involvement. We investigated Col I biochemical markers in patients with SSc.

Increased plasma S-nitrosothiol levels in chronic haemodialysis patients.

Background: An impairment of nitric oxide (NO) bioavailability and/or metabolism may contribute to the excessive incidence of atherosclerotic complications observed in haemodialysis (HD) patients. Recent evidence indicates that NO metabolism involves a family of NO-related molecules that have not yet been explored in such patients. The aim of our study was to determine the plasma levels of S-nitrosothiol and nitrotyrosine in chronic HD patients, and to evaluate potential factors influencing their levels.

Inhibition of inducible NO synthase by TH2 cytokines and TGF beta in rheumatoid arthritic synoviocytes: effects on nitrosothiol production.

The aim of this study was to compare the effects on NO production of IL-4, IL-10, and IL-13 with those of TGF-beta. RA synovial cells were stimulated for 24 h with IL-1 beta (1 ng/ml), TNF-alpha (500 pg/ml), IFN-gamma (10(-4)IU/ml) alone or in combination. Nitrite was determined by the Griess reaction, S-nitrosothiols by fluorescence, and inducible NO synthase (iNOS) by immunofluorescence and fluorescence activated cell sorter analysis (FACS).