The study of intergranular corrosion in aircraft aluminium alloys using X-ray tomography

Atmospheric corrosion is one of the leading causes of structural damage to aircraft. Of particular importance is pitting and intergranular corrosion, which can develop into fatigue cracks, stress corrosion cracks, or exfoliation. Therefore it is of interest to the Australian Defence Force (ADF) to understand how corrosion ensues in susceptible aircraft aluminium alloys, such as AA2024-T351 and 7050-T7451. However, there are many difficulties in measuring the extent of intergranular corrosion, since it is predominantly hidden below the surface. Traditionally, cross-sectioning has been used to view and measure the depth of attack. In the present work, 2 mmdiameter pin specimens were contaminated with a droplet of 3.5% NaCl and exposed to constant humidity that resulted in intergranular corrosion. X-ray computed tomography was then used to non-destructively assess the depth and volume of corrosion both as a function of time in 97% relative humidity, and as a function of relative humidity after 168 h exposure. Both corrosion depth and volume increased with time, but there was evidence for a limiting depth in AA2024. Depth and volume also increased with relative humidity of the environment, for which the time-of-wetness and oxygen concentration of the droplets were considered the important factors in driving the corrosion process

Atmospheric pitting corrosion of aircraft aluminium alloys

Aircraft aluminium alloys tend to be engineered to maximise their mechanical properties and therefore have an increased susceptibility to localised corrosion. The Australian Defense Force (ADF) have witnessed numerous occurrences of localised corrosion on aluminium alloys that have in some cases reduced structural integrity of the aircraft and in most cases lead to costly repair. The initiation and growth of pitting corrosion on aircraft exposed to atmospheric conditions is not fully understood due to the majority of pervious work concentrating on immersed experiments

Parenteral magnesium sulfate versus amiodarone in the therapy of atrial tachyarhythmias: A prospective randomized study

ObjectiveTo compare the efficacy of parenteral magnesium sulfate vs. amiodarone in the therapy of atrial tachyarrhythmias in critically ill patients.DesignProspective, randomized study.SettingMultidisciplinary intensive care unit (ICU) at a university teaching hospital.PatientsForty-two patients, 21 medical and 21 surgical, of mean (SD) age 67 +/- 15 yrs and mean Acute Physiology and Chronic Health Evaluation II score of 22 +/- 6, with atrial tachyarrhythmias (ventricular response rate of > or = 120 beats/min) sustained for > or = 1 hr.InterventionsAfter correction of the plasma potassium concentration to > or = 4.0 mmol/L, patients were randomly allocated to treatment with either a) magnesium sulfate 0.037 g/kg (37 mg/kg) bolus followed by 0.025 g/kg/hr (25 mg/kg/hr); or b) amiodarone 5 mg/kg bolus and 10 mg/kg/24-hr infusion. Therapeutic plasma magnesium concentration in the magnesium sulfate group was 1.4 to 2.0 mmol/L. Therapeutic end point was conversion to sinus rhythm over 24 hrs.Measurements and main resultsAt study entry (time 0), initial mean ventricular response rate and systolic blood pressure were 151 +/- 16 (SD) beats/min and 127 +/- 30 mm Hg in the magnesium sulfate group vs. 153 +/- 23 beats/min and 123 +/- 23 mm Hg in the amiodarone group, respectively (p = .8 and .65). Plasma magnesium (time 0) was 0.84 +/- 0.20 vs. 1.02 +/- 0.22 mmol/L in the magnesium and amiodarone group, respectively (p = .1). Eight patients had chronic dysrhythmias (magnesium 3, amiodarone 5). Excluding the two patient deaths (amiodarone group, time 0 + 12 to 24 hrs), no significant change in systolic blood pressure subsequently occurred in either group. In the magnesium group, mean plasma magnesium concentrations were 1.48 +/- 0.36, 1.82 +/- 0.41, 2.16 +/- 0.45, and 1.92 +/- 0.49 mmol/L at time 0 + 1, 4, 12 and 24 hrs, respectively. By logistic regression, the probability of conversion to sinus rhythm was significantly better for magnesium than for amiodarone at time 0 + 4 (0.6 vs. 0.44), 12 (0.72 vs. 0.5), and 24 (0.78 vs. 0.5) hrs. In patients not converting to sinus rhythm, a significant decrease in ventricular response rate occurred at time 0 + to 0.5 hrs (mean decrease 19 beats/min, p = .0001), but there was no specific treatment effect between the magnesium and the amiodarone groups; thereafter, there was no significant reduction in ventricular response rate over time in either group.ConclusionsIntravenous magnesium sulfate is superior to amiodarone in the conversion of acute atrial tachyarrhythmias, while initial slowing of ventricular response rate in nonconverters appears equally efficacious with both agents.John L. Moran, John Gallagher, Sandra L. Peake, David N. Cunningham, Mary Salagaras and Phil Leppar

Eukaryotic elongation factor 2 kinase regulates foam cell formation via translation of CD36

Eukaryotic elongation factor 2 kinase (eEF2K) is an atypical protein kinase that controls protein synthesis in cells under stress. Although well studied in cancer, less is known about its roles in chronic inflammatory diseases. Here, we examined its regulation of macrophage cholesterol handling in the context of atherosclerosis. eEF2K mRNA expression and protein activity were upregulated in murine bone marrow-derived macrophages (BMDMs) exposed to oxidized low-density lipoprotein cholesterol (oxLDL). When incubated with oxLDL, BMDMs from eEF2K knockout (Eef2k-/- ) mice formed fewer Oil Red O+ foam cells than Eef2k+/+ BMDMs (12.5% ± 2.3% vs. 32.3% ± 2.0%, p < .01). Treatment with a selective eEF2K inhibitor, JAN-384, also decreased foam cell formation for C57BL/6J BMDMs and human monocyte-derived macrophages. Disabling eEF2K selectively decreased protein expression of the CD36 cholesterol uptake receptor, mediated by a reduction in the proportion of translationally active Cd36 mRNA. Eef2k-/- mice bred onto the Ldlr-/- background developed aortic sinus atherosclerotic plaques that were 30% smaller than Eef2k+/+ -Ldlr-/- mice after 16 weeks of high cholesterol diet (p < .05). Although accompanied by a reduction in plaque CD36+ staining (p < .05) and lower CD36 expression in circulating monocytes (p < .01), this was not associated with reduced lipid content in plaques as measured by oil red O staining. Finally, EEF2K and CD36 mRNA levels were higher in blood mononuclear cells from patients with coronary artery disease and recent myocardial infarction compared to healthy controls without coronary artery disease. These results reveal a new role for eEF2K in translationally regulating CD36 expression and foam cell formation in macrophages. Further studies are required to explore therapeutic targeting of eEF2K in atherosclerosis.Sanuja Fernando, Thalia Salagaras, Nisha Schwarz, Lauren Sandeman, Joanne T. M. Tan, Jianling Xie ... et al