Search

The problem of minimising the overall duration of a project subject to constraints on the availability of resources is considered with particular reference to the use of branch and bound methods. A new resource based bound, new dominance rules and an innovatory network breakdown technique which preserves optimality are reported. Computational experience and comparisons with schedules obtained by decision rule methods are given.

This paper presents a practical approach for resource constrained scheduling within a given project duration. The method ensures a stable project plan when activity durations are reduced to achieve this. It handles all four categories of resource (unconstrained, renewable, non-renewable and doubly-constrained resources), and aims to shorten the project duration at minimum cost. Soft constraints and resource availabilities which vary over time are allowed in the method. Computational experience is reported.

Computer Simulation is a well-established technique for modelling complex problems. Australian mining has, until quite recently, relied on more ad hocmethods for planning and operating. This case study describes how a large ore mine was successfully studied using animated computer simulation and points out how this approach can overcome traditional resistance to formal models and how useful results were readily obtained and accepted by management.

This paper describes two complementary studies concerning the maintenance and replacement of heavy haul railway track. Minimum cost policies are derived using decision networks in one case and a group replacement model in the other. The results indicate relatively large cost savings on current practice.

A case study of the application of two O.R. techniques for determining optimal shift sizes for telephone betting operators is described. The first formulation uses linear programming and the second, network flow techniques. The network flow model has a considerable computational speed advantage, but the L.P. model is currently in operation.

The epicyclic differential gear has been known in modern times since 1575 when it appeared as a mechanism in a clock. Artifacts from an ancient shipwreck prove that it was known to the ancient Greeks at least 100 hundred years before Christ. The methods of kinematic analysis by either the relative angular velocity method or the instant center and linear velocity method, as given in the literature, are oriented toward specific solutions rather than general ones; they do not readily allow for parametric trend studies and they require a degree of imagination and intuition which may well be beyond the capabilities of those who are not practitioners of the art. The discussed methodology defines simple and compound epicyclic gears in terms of the overall ratio of a geometrically similar planetary gear. The kinematic analysis is derived in general terms for both the simple and compound epicyclic gear. It is shown that location of the point of zero tangential velocity of the velocity triangle relative to the system datum governs the characteristics of the gearset and whether it will perform as a differential gearset, or as a solar, star, or planetary gear. Simple mathematical relationships are given which define the proportions of the component gears, their speeds (rpm) and directions of rotations, and the resulting power splits. The formulas may be incorporated into simple computer programs oriented toward specific design requirements.

During commissioning of the medical gas system of a new hospital, fourteen connection defects were found; six of these were potentially lethal cross-connections. A major contaminant was also detected throughout the medical gas system.The methods of testing a new medical gas system described in this report highlight the need for up-grading of existing standards.

The usefulness of reductive silver precipitation for the histo chemical localization of assorbic acid in mouse lung has been examined under standard conditions. The estimated stoichiometry of the reaction shows that only one quarter of the silver precipitated in fresh tissue by the silver nitrate reagent was due to ascorbic acid. Although no evidence was found that diffusion of ascorbic acid proceeded more rapidly than reductive silver precipitation in the tissue, diffusion artifacts at the cellular led would seem likely to occur. Thiosulphate was shown to be more effective than ammonia m removing un reacted silver from tissues treated with silver nitrate.

Rat lungs were perfused by recycling Krebs-bicarbonate solution in an apparatus which allowed negative pressure ventilation of the lungs. After addition of either reduced or oxidized ascorbic acid to the perfusion fluid serial samples were taken over 60 min and assayed for both reduced and oxidized ascorbic acid. At the end of perfusion, lungs were assayed for ascorbic acid. The results show that reduced ascorbic acid was taken up by the lung and concentrated in the tissue. No appreciable transport of oxidized ascorbic acid was measured.

Inorganic phosphate (Pi) accumulates extremely rapidly in ischaemic heart muscle and intracellular binding of this metabolite may account for the precipitous loss of function seen at the onset of severe ischaemia. We have used31P-NMR spectroscopy to measure the free cytosolic [Pi] and chemical assay techniques to measure total tissue Pi at 0, 1, 2, 3, 5, and 12 min of complete global ischaemia in the isolated isovolumic rat heart. At zero time, the Pi assayed chemically was 30.77±5.52 µmol/g dry wt (mean±SD, n=7) whilst Pi assayed by NMR was 3.39±1.21 µmol/g dry wt (n=15). Thus, 27.38 µmol/g dry wt of Pi was bound at a cytosolic [Pi] of 0.82 mM. After 12 min of ischaemia, 49.88 µmol/g dry wt of Pi was bound at a cytosolic [Pi] of 4.11 mM. When all data were fitted, using a non-linear, least squares fit (p<0.05), to the binding isotherm: Bound Pi=B'max. [Pi]/(K'd+[Pi]), the apparent binding parameters K'd and B'max were estimated to be 1.1±0.6 mM and 64.0±10.2 µmol/g dry wt respectively. During the first minute of global ischaemia when the rate-pressure product had decreased by 79% of its pre-ischaemic value, bound Pi had increased by 58% and free cytosolic [Pi] by 162%. When functional and metabolite changes were expressed as a fraction of the total change which occurred during the 12-min ischaemic period, bound Pi had the profile most similar to the rate-pressure product. Both the amount of bound Pi and free cytosolic [Pi] correlated with loss of contractile function as the ischaemic period progressed. The results snow that during ischaemia, Pi is bound progressively as free cytosolic [Pi] is increased as the result of high energy phosphate hydrolysis. While these results are consistent with the possibility that Pi binding may contribute to ischaemic contractile failure, no molecular explanation for the possible effect of bound Pi on contraction has been propsed.

Vitamin E is an endogenous antioxidant and is known to afford protection against lipid peroxidation. If lipid peroxidation was an important factor in the pathogenesis of reoxygenation injury in heart, then both the extent of lipid peroxidation and cell injury would be expected to be exacerbated in vitamin E-deficient hearts. To study reoxygenation injury in the present experiments, rat hearts were perfused in the Langendorff mode with a modified Krebs-Henseleit buffer under anoxic conditions for 60 min before resuming normoxic perfusion for 20 min. Creatine phosphokinase (CPK) activity and malonyldialdehyde (MDA), a product of lipid peroxidation, were assayed in the perfusate effluent from hearts during reoxygenation injury. Also, myocardial MDA and vitamin E contents were measured in extracts of freeze-clamped heart tissue obtained immediately before and 2 min after reoxygenation. Experiments were performed on hearts from groups of weanling rats fed either a vitamin E-deficient or vitamin E-supplemented diet (50 I.U. vitamin E/kg) for 5 to 6 weeks. After 5 weeks, the myocardial vitamin-E content was 103.8±5.3 (n=5) and 11.5±1.6 (n=4) ng/mg protein (mean±SEM) in the vitamin E-supplemented and vitamin E-deficient groups respectively. Perfused hearts from both dietary groups showed a peak of enzyme release 2 to 3 min after the reintroduction of oxygen, and enzyme release from vitamin E-deficient hearts was two-fold greater than enzyme release from vitamin E-supplemented hearts. MDA was not detected in the effluent perfusate of either group of hearts (<0.24 nmol MDA/min/g wet wt) and the myocardial MDA content was not altered by diet or reoxygenation. There was no evidence that myocardial vitamin E was consumed during reoxygenation. In conclusion, vitamin E was found to afford significant protection against reoxygenation injury and this is consistent with the involvement of free radicals in the injury process. However, MDA was not detectable in the coronary effluent or heart tissue during the first 20 min of reoxygenation injury, even in vitamin E-deficient hearts, suggesting that it is a relatively unimportant event in the early pathogenesis of reoxygenation injury.

Changes in 5′-nucleotidase activity were calculated on the basis of alterations in ATP, ADP, phosphocreatine, Pi, Mg2+, IMP and AMP, determined by using 31P n.m.r. spectroscopy and h.p.l.c., during isoprenaline infusion, graded hypoxia and graded underperfusion in isolated rat heart. Calculated activity changes were compared with the total efflux of purines (adenosine + inosine + hypoxanthine) in order to assess the involvement of various 5′-nucleotidases in formation of adenosine. Purine efflux exhibited an exponential relation with cytosolic [AMP] during isoprenaline infusion and hypoxia (r = 0.92 and 0.95 respectively), supporting allosteric activation of 5′-nucleotidase under these conditions. Purine efflux displayed a linear relation with cytosolic [AMP] during graded ischaemia (r = 0.96), supporting substrate regulation in the ischaemic heart. The calculated activities of membrane-bound ecto-5′-nucleotidase were similar to the observed relations between purine efflux and cytosolic [AMP] in all hearts. The calculated activities of the ATP-activated cytosolic and lysosomal enzymes and of the ATP-inhibited cytosolic 5′-nucleotidase could not explain the observed release of purines under the conditions examined. These results indicate that the kinetic characteristics of the membrane-bound ecto-enzyme are consistent with an important role in the formation of extracellular adenosine, whereas the characteristics of the other 5′-nucleotidases are inconsistent with roles in adenosine formation under the conditions of the present study.

The problem of creating an activity-on-arrow network diagram from activity precedence data is considered. An heuristic is described which is incorporated into a computer program that can tackle problems of a practical size. Some computational experience is reported.