Search

Wear and corrosion involve many mechanical and chemical mechanisms, and the combined action of these mechanisms often result in significant mutual reinforcement. Other researchers have studied the interactions of wear and corrosion in a qualitative way for specific wear-corrosion environments. The US Bureau of Mines is interested in presenting the results of wear, corrosion and wear-corrosion tests in a standard format, so that these data can be utilized to develop practical engineering criteria for any tribosystem. To reach this goal, penetration rate equations have been developed to quantify the wear and corrosion processes and wear-corrosion synergism.

A US Bureau of Mines study to quantify synergism between wear and corrosion of white cast iron in an aqueous sulfate environment was conducted using a rotating cylinder-anvil apparatus. A commercial 13.5% Cr white cast iron sample and the individual constituents of a white cast iron were studied to determine the role of each phase in the degradation processes of wear, corrosion and wear-corrosion synergism. These constituent phases consisting of matrix (13%Cr87%Fe), Cr-depleted matrix (5%Cr95%Fe) two M 7 C 3 's and two M 3 C (where MFe,Cr) were fabricated by powder metallurgy. The wearcorrosion studies consisted of four tests: the potentiodynamic polarization tests with and without anvil pressure and wear tests with and without cathodic protection. The force on the anvils was 28 kg and the rotation speed of the approximately 2.5 cm diameter samples was 5.24 (rad s −1 ) with peripheral velocity of 0.0654 m s −1 . Even though corrosion alone was a small percentage of the total degradation, representing as little as 0.1% of the total degradation, the wear-corrosion synergism contribution was significant, accounting for as much as 91% of the total degradation.

Experiments were conducted by US Bureau of Mines researchers with iron-aluminum alloys (5–25wt.%Al) in 1 N H 2 SO 4 to determine the amount of charge required to repassivate their surfaces following scratching with a diamond indenter, to gain a better understanding of how wear and corrosion interact. This understanding is aimed at reducing the corrosion and wear of materials. Solutions saturated with air were used at ambient temperature. Formation of the passive films was studied by measuring the current transient resulting from stepping from the open circuit corrosion potential to the passive region of +1.175 V(NHE). The repassivation kinetics were studied by measuring the current transient caused by scratching a rotating disc electrode with a diamond indenter while holding at the passivation potential. Comparison of the charge density required to form or repair the passive film was made for the potential step and scratching experiments. The amount of charge required to repassivate the film was determined as a function of indenter load, shape, velocity and aluminum content.

Summary Plasma, urine and faeces were assayed for total radioactivity after administration of 14 C-haloperidol (0.6 mg/kg) to rats divided into three groups; intravenous, oral fasting and oral with food. Most urinary and faecal excretion of radioactivity occurred in the first 24 hours; by 5 days 96.5%, 81.5% and 62% of total 14 C had been recovered from both routes for the intravenous, oral fasting and oral with food groups respectively. The fractionation pattern of urine radioactivity for all three groups was similar. Metabolite distribution did not change with time. Approximately 64% of the activity existed as amphoteric or non-ionised polar metabolites and 30% as substances which were benzene extractable from alkaline solution. Unchanged haloperidol was always less than 1% of total urine activity. An increase in peak level and a reduction in time to peak was seen in the plasma data for the oral with food group compared to the oral fasting group. This trend was confirmed and accentuated in a fourth group of rats trained to eat a large meal before drug administration. The apparent stimulatory effect of food on the rate and extent of absorption did not appear to be due to increased gastric emptying but could be related to the fat content in food. It is suggested that the lymphatics may play a part in haloperidol absorption in rats.

Received 22 March 1977 Revised version received 17 May 1977 1. Introduction 2. Methods Garlick et al. [1 ] have described a procedure for estimating protein synthesis rates in experimental animals. Radiolabetled amino acid is infused for a short time, usually 6 h, and serial plasma samples are taken during this period to determine the rate at which a steady state of labelling in the plasma is obtained. After the infusion the animal is sacrificed, the selected tissue excised and the specific radioactivities of the intraceUular free amino acid pool and the protein bound pool determined. Equations were derived to transform these data into estimates of k s , the rate constant for transfer of amino acid from the free intra- cellular pool to the protein bound pool and the procedure has been used in a number of subsequent publications by these workers [2-4]. For optimal reliability of k s estimates, serial tissue biopsies should also be taken during the infusion. While this is difficult with current technology it should become more feasible in the near future. In the meantime, however, the terminal sampling of the tissue compartments provides data which should be utilized to the fullest extent. The equations of Garlick et al. produce k s values which give no indication of their reliability. An alternative treatment is proposed here based on a 3 compartmental model which gives k s together with an estimate of its uncertainty. It is used with data on [14C]tyrosine incorporation in myocardial tissue of dogs.

A portable slurry wear apparatus, developed by the U.S. Bureau of Mines, was used to study slurry erosion in the laboratory and in situ at a gold ore processing plant. The wear cell of the apparatus was identical with an earlier laboratory model. It used an impeller running at tip speeds of less than 22 m s −1 to drive a continuous flow of fresh slurry past 16 specimens. Laboratory experiments run in an aqueous slurry of silica sand showed that ultrahigh molecular weight polyethylene (UHMWPE) wore less than any metal alloy or other polymers evaluated at 8 or 12 m s −1 , and at 16 m s −1 several polymers wore less than two steels. However, in gold ore slurries from an industrial float cell and rod mill, high chromium white cast irons wore less than UHMWPE at 8 and 12 m s −1 ; and in the rod mill slurry at 16 m s −1 the polymers wore no better than the steels. The same trends were observed previously in an industrial slurry containing a lead-zinc sulfide ore. In all cases the wear rate varied roughly as the fourth power of the impeller tip velocity. When particle shape was held constant, the wear rate always increased with particle size. The effect of particle shape was more complex: angular particles were more detrimental to polymers and rounded ones were more detrimental to alloys. Pitting corrosion also removed material from the alloys. For high chromium white cast irons, corrosion and erosion varied with microstructure.

The Shaker locus of Drosophila melanogaster encodes a family of A-type potassium channel subunits. Shaker mutants behave as antimorphs in gene dosage tests. This behaviour is due to the production of truncated A-channel subunits. We propose that they interfere with the function of their normal counterpart by forming multimeric A-channel structures. This hypothesis was tested by constructing transgenic flies carrying a heat-inducible gene encoding a truncated A-type potassium channel subunit together with a normal wild type doses of A-type potassium channel subunits. The altered subunit leads at larval, pupal or adult stages to the transformation of wild type into Shaker flies. The transformed flies exhibited a heat-inducible abnormal leg shaking behaviour and a heat-inducible facilitated neurotransmitter release at larval neuromuscular junctions. By the overexpression of an aberrant A-channel subunit the normal behaviour of transgenic D. melanogaster can be altered in a predictable way.

It is known that narcotic antagonists interact with many cholinergic pathways but less in known about specific mechanisms. Using neonatal rat myoballs to study single channel behaviour of the acetylcholinegated nicotinic receptor, it was found that micromolar concentrations of naltrexone had no effect on channel conductance but caused open channel blockade by increasing the flickering from the open to the closed state in a concentration-dependent manner. At micromolar concentrations of naltrexone, the frequency of channel opening was decreased and bursts were grouped in clusters, whereas at nanomolar levels the frequency of opening was increased. The sequential model for ion-channel blockade cannot explain these effects, and an alternative allosteric mechanism of action is proposed. Narcotic antagonist Naltrexone Nicotinic receptor Electrophysiology Single channel recording Channel activation Channel blockade

The interactions of naltrexone with the nicotinic acetylcholine receptor were studied electrophysiologically using the frog sciatic nerve-sartorius muscle and biochemically using membranes from the electric organ of Torpedo ocellata. At nanomolar concentrations naltrexone increased the peak amplitude of endplate currents with little change in the decay time constant. At micromolar concentrations there was a concentration-dependent depression of endplate current and miniature endplate current amplitudes and decay time constants. Decay time constant depression was enhanced with hyperpolarization. Only marginal curvature was induced in peak endplate current amplitude versus membrane voltage plots by naltrexone. Naltrexone had no effect on single channel conductance but decreased open channel lifetime, according to fluctuation analysis. Naltrexone alone (less than or equal to 3 microM) did not impair binding of [125I]alpha-bungarotoxin to the receptor in a fast pre-equilibration assay, but increased the ability of acetylcholine to displace [125I]alpha-bungarotoxin. The drug displaced the agonist-stimulated binding of [3H]perhydrohistrionicotoxin to the channel site. Biphasic functional changes in neuromuscular transmission can be attributed to an allosteric mechanism with increased agonist binding to the nicotinic receptor at nanomolar concentrations and caused a non-competitive blockade of the ionic channel at micromolar concentrations.