Quantifying the efficiency and understanding the mechanism of localised corrosion inhibition using the wire beam electrode

Parameters extracted from the wire beam electrode (WBE) galvanic current maps have been used in conjunction with electrochemical noise patterns to directly quantify the degree of localised corrosion inhibition provided by inhibitors and to understand the mechanism of localised corrosion inhibition. The behaviour of two traditional localised corrosion inhibitors has been assessed by their effects on the maximum anodic current density (imax), total anodic current density (itot), the number of anodic sites (Na) and the localised corrosion intensity index (LCII). Typical experiments are presented to illustrate the application of these parameters in providing useful information on the efficiency and mechanism of localised corrosion inhibition.

cGMP phosphodiesterase inhibition improves the vascular and metabolic actions of insulin in skeletal muscle

There is considerable support for the concept that insulin-mediated increases in microvascular blood flow to muscle impact significantly on muscle glucose uptake. Since the microvascular blood flow increases with insulin have been shown to be nitric oxide-dependent inhibition of cGMP-degrading phosphodiesterases (cGMP PDEs) is predicted to enhance insulin-mediated increases in microvascular perfusion and muscle glucose uptake. Therefore, we studied the effects of the pan-cGMP PDE inhibitor zaprinast on the metabolic and vascular actions of insulin in muscle. Hyperinsulinemic euglycemic clamps (3 mU·min−1·kg−1) were performed in anesthetized rats and changes in microvascular blood flow assessed from rates of 1-methylxanthine metabolism across the muscle bed by capillary xanthine oxidase in response to insulin and zaprinast. We also characterized cGMP PDE isoform expression in muscle by real-time PCR and immunostaining of frozen muscle sections. Zaprinast enhanced insulin-mediated microvascular perfusion by 29% and muscle glucose uptake by 89%, while whole body glucose infusion rate during insulin infusion was increased by 33% at 2 h. PDE2, -9, and -10 were the major isoforms expressed at the mRNA level in muscle, while PDE1B, -9A, -10A, and -11A proteins were expressed in blood vessels. Acute administration of the cGMP PDE inhibitor zaprinast enhances muscle microvascular blood flow and glucose uptake response to insulin. The expression of a number of cGMP PDE isoforms in skeletal muscle suggests that targeting specific cGMP PDE isoforms may provide a promising avenue for development of a novel class of therapeutics for enhancing muscle insulin sensitivity.

Short-interval intracortical inhibition is not affected by varying visual feedback in an isometric task in biceps brachiii muscle

Purpose : To establish if visual feedback and force requirements influence SICI.

Methods : SICI was assessed from 10 healthy adults (5 males and 5 females aged between 21 and 35 years) in three submaximal isometric elbow flexion torque levels [5, 20, and 40% of maximal voluntary contraction (MVC)] and with two tasks differing in terms of visual feedback. Single-pulse and paired-pulse motor-evoked potentials (MEPs), supramaximal M-wave, and background surface electromyogram (sEMG) were recorded from the biceps brachii muscle.

Results : Repeated measures MANOVA was used for statistical analyses. Background sEMG did not differ between tasks (F = 0.4, P = 0.68) nor was task × torque level interaction observed (F = 1.2, P = 0.32), whereas background sEMG increased with increasing torque levels (P = 0.001). SICI did not differ between tasks (F = 0.9, P = 0.43) and no task × torque level interaction was observed (F = 2.3, P = 0.08). However, less SICI was observed at 40% MVC compared to the 5 and 20% MVC torque levels (P = 0.01–0.001).

Conclusion : SICI was not altered by performing the same task with differing visual feedback. However, SICI decreased with increasing submaximal torque providing further evidence that SICI is one mechanism of modulating cortical excitability and plays a role in force gradation.

Carbon dioxide corrosion inhibition : an overview of recent research on new inhibitor development

Since the introduction of inhibitors to the oil and gas industry in the 1940’s, corrosion inhibition has played a key role in carbon dioxide (CO2) corrosion control. Major inhibitor discoveries occurred from the late 1940's to the late 1960's, followed by the refinement of formulations and the development of improved application methods. Over the past two to three decades, although some new derivatives of existing inhibitors such as amide, amine and imidazoline have been reported, there have been few if any discoveries of new CO2 corrosion inhibitors. In recent years, the development of environmentally friendly inhibitors and the inhibition of localised corrosion have become driving forces behind new advances in corrosion inhibitor technology. Recently a rare earth metal organic compound, lanthanum 4-hydroxy cinnamate has been found to be an efficient corrosion inhibitor for mild steel in CO2 containing aqueous media. A resorcinarene acid has been found to provide effective localised corrosion inhibition by promoting a random distribution of insignificant anodic currents. The advent of advanced scanning probe techniques and an electrochemical integrated multi-electrode array have facilitated the discovery of corrosion inhibitors. This paper provides a brief overview of recent progress in this field.

Rare earth cinnamates and their corrosion inhibition mechanisms for AS1020 steel

Speciation of the inhibitors lanthanum 2-hydroxy cinnamate and lanthanum 3-hydroxy cinnamate in solution has been evaluated and compared to the speciation of lanthanum 4-hydroxy cinnamate. The results have been correlated with corrosion inhibition efficiency for AS1020 steel in an aqueous chloride solution using a combination of analytical tools such as nuclear magnetic resonance (NMR) spectroscopy, electrospray mass spectrometry (ESMS), potentiodynamic polarisation.

Inhibition of corrosion on AA2024-T3 by rare earths & mercaptoacetate

The use of the aluminium alloy AA2024-T3 has long been associated with a strong vulnerability to localised corrosion. Dealloying and pitting corrosion can occur on and around intermetallic particles when exposed to aggressive environments such as sodium chloride electrolytes. Specific combinations of rare earths and organic compounds have demonstrated strong synergistic inhibition on the AA2024-T3 alloy. This work has focused on rare earths and organic compounds containing thiol functional groups. It is believed that the sulphur in the thiol group can form protective films over the surface of copper-rich intermetallic particles due to the affinity between copper and sulphur. Previous studies with the multiwell tests have identified that solutions containing sodium mercaptoacetate provided strong inhibition at pH 3 and 6. This work presents the initial findings from the polarisation tests and constant immersion corrosion experiments in the presence of sodium mercaptoacetate.

Localized corrosion and inhibition studies using the wire beam electrode in conjunction with the electrochemical noise analysis and the scanning reference electrode techniques

Several new technical developments have been made based on the combined use of the wire beam electrode (WBE), electrochemical noise analysis (ENA) and the scanning reference electrode technique (SRET). These have included: (i) The WBE-R n method- the combined use of the WBE and the noise resistance (Rn) to map the rates and patterns of uniform or localized corrosion; (ii) The WBE-Noise Signatures method- the combined use of the WBE and the noise signature to detect the origination and propagation of localized corrosion; and (iii) The WBE-SRET method- the combined use of the WBE and SRET to investigate localized corrosion from both the metallic and electrolyte phases of a corroding metal surface. This paper presents a brief review on these novel methods and their applications for detecting general and localized corrosion, for mapping the rates of corrosion, and for studying corrosion inhibitors.

A corrosion inhibition study of steel grinding balls in an oxygen and alkaline environment

The corrosion of steel grinding balls is a major recurrent cost for mill operators concerned with the production gold. Subsequently, the use of corrosion inhibitors in production fluids, which is typically at pH >9, is an attractive and economical option. This study reports on the corrosion wear of steel grinding balls under alkaline/oxygen conditions and in presence of cyanide. A fundamental study on the influence of several inorganic-based inhibitors (i.e., nitrite, chromate, silicate, hexametaphosphate) on the corrosion rate of carbon steel was undertaken. Subsequently, the corrosion performances of various inhibitors were evaluated in stirred vessels. Corrosion rates were determined via mass loss and electrochemical methods (i.e., linear polarisation, Tafel). It was observed that inhibitors based upon chromate provide superior protection under the conditions investigated in this study. In lime treated, high chloride waters, chromate gave over 80% protection at levels of 10 100 ppm with no evidence of pitting.

Xanthine oxidase inhibition attenuates skeletal muscle signaling following acute exercise but does not impair mitochondrial adaptations to endurance training.

The aim of this research was to examine the impact of the xanthine oxidase (XO) inhibitor allopurinol on the skeletal muscle activation of cell signaling kinases' and adaptations to mitochondrial proteins and antioxidant enzymes following acute endurance exercise and endurance training. Male Sprague-Dawley rats performed either acute exercise (60 min of treadmill running, 27 m/min, 5% incline) or 6 wk of endurance training (5 days/wk) while receiving allopurinol or vehicle. Allopurinol treatment reduced XO activity to 5% of the basal levels (P < 0.05), with skeletal muscle uric acid levels being almost undetectable. Following acute exercise, skeletal muscle oxidized glutathione (GSSG) significantly increased in allopurinol- and vehicle-treated groups despite XO activity and uric acid levels being unaltered by acute exercise (P < 0.05). This suggests that the source of ROS was not from XO. Surprisingly, muscle GSSG levels were significantly increased following allopurinol treatment. Following acute exercise, allopurinol treatment prevented the increase in p38 MAPK and ERK phosphorylation and attenuated the increase in mitochondrial transcription factor A (mtTFA) mRNA (P < 0.05) but had no effect on the increase in peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), nuclear respiratory factor-2, GLUT4, or superoxide dismutase mRNA. Allopurinol also had no impact on the endurance training-induced increases in PGC-1α, mtTFA, and mitochondrial proteins including cytochrome c, citrate synthase, and β-hydroxyacyl-CoA dehydrogenase. In conclusion, although allopurinol inhibits cell signaling pathways in response to acute exercise, the inhibitory effects of allopurinol appear unrelated to exercise-induced ROS production by XO. Allopurinol also has little effect on increases in mitochondrial proteins following endurance training.