Acoustic emission from particulate-reinforced metal matrix composites

A systematic study of the effect of microstructural parameters on the fracture behaviour of silicon carbide particle reinforced aluminium matrix composites has been carried out. Acoustic emissions have been monitored during tensile testing, giving the size and number of emmissions as a function of strain. This has been shown to be simply related to the rate of void nucleation at the reinforcing phase. Both particle fracture and particle/matrix decohesion mechanisms can be detected. Void nucleation was observed from the onset of plastic deformation and a linear relationship between damage initiation rate and strain was found. The rate of emission increased with reiforcing particle size and volume fraction but was independent of matrix alloy composition and heat treatment. These results show that the failure strain of particulate metal matrix composites is not controlled solely by the onset of void nucleation at the reinforcing phase. Local failure processes in the matrix are shown to promote void coalescence and dominate the ductility. However, suppression of void nucleation at the particles increases the ductility. It is suggested that a critical number of fractured particles is required before failure.     

Compartmental analysis of dopa decarboxylation in living brain from dynamic positron emission tomograms

The trapping of decarboxylation products of radiolabelled dopa analogs in living human brain occurs as a function of the activity of dopa decarboxylase. This enzyme is now understood to regulate, with tyrosine hydroxylase, cerebral dopamine synthesis. Influx into brain of dopa decarboxylase substrates such as 6-[18F]fluorodopa and beta-[11C]dopa measured by positron emission tomography can be analyzed by solution of linear differential equations, assuming irreversible trapping of the decarboxylated products in brain. The isolation of specific physiological steps in the pathway for catecholamine synthesis requires compartmental modelling of the observed dynamic time-activity curves in plasma and in brain. The several approaches to the compartmental modelling of the kinetics of labelled substrates of dopa decarboxylase are now systematically and critically reviewed. Labelled catechols are extensively metabolized by hepatic catechol-O-methyltransferase yielding brain-penetrating metabolites. The assumption of a fixed blood-brain permeability ratio for O-methyl-6-[18F]fluorodopa or O-methyl-beta-[11C]dopa to the parent compounds eliminates several parameters from compartmental models. However, catechol-O-methyltransferase activity within brain remains a possible factor in underestimation of cerebral dopa decarboxylase activity. The O-methylation of labelled catechols is blocked with specific enzyme inhibitors, but dopa decarboxylase substrates derived from m-tyrosine may supplant the catechol tracers. The elimination from brain of decarboxylated tracer metabolites can be neglected without great prejudice to the estimation of dopa decarboxylase activity when tracer circulation is less than 60 minutes. However, elimination of dopamine metabolites from brain occurs at a rate close to that observed previously for metabolites of glucose labelled in the 6-position. This phenomenon can cause systematic underestimation of the rate of dopa decarboxylation in brain. The spillover of radioactivity due to the limited spatial resolution of tomographs also results in underestimation of dopa decarboxylase activity, but correction for partial volume effects is now possible. Estimates of dopa decarboxylase activity in human brain are increased several-fold by this correction. Abnormally low influx of dopa decarboxylase tracers in the basal ganglia is characteristic of Parkinson's disease and other movement disorders. Consistent with postmortem results, the impaired retention of labelled dopa is more pronounced in the putamen than in the caudate nucleus of patients with Parkinson's disease; this heterogeneity persists after correction for spillover. Current in vivo assays of dopa decarboxylase activity fail to discriminate clinically distinct stages in the progression of Parkinson's disease and are, by themselves, insufficient for differential diagnosis of Parkinson's disease and other subcortical movement disorders. However, potential new avenues for therapeutics can be tested by quantifying the rate of metabolism of exogenous dopa in living human brain.     

Electro-erosion of metal surfaces

Craters produced by single electrical discharges in kerosene under conditions similar to Electro-Discharge Machining were formed on the following metals: Al, Cr, Cu, Fe, Mg, Mo, Nb, Ni, Ta, Ti, V, W, and Zn. Anode and cathode crater volumes were measured by a profilometer imaging technique and except for Nb, Mo and Ta, the cathode craters were always found to be larger. An empirical equation was developed to relate the volume of the electro-erosion craters formed to the physical properties of the electrodes. Crater morphology and surface texture were studied using both Scanning and Transmission Electron Microscopy. An Electron Microprobe was used to determine the distribution of cross deposited metal in the case of dissimilar electrodes. Crater volumes and morphologies resulting from single electrical discharges in liquid and dry nitrogen were shown to be radically different from those produced in kerosene.