Biomedical subjects
Publications and source records attributed to J C Lawrence.
A portable air purifier significantly reduced mal odour in a small room. If the atmosphere was deliberately contaminated with Serratia marcescens the unit rapidly removed this organism. However, if incorrectly sited, the purifier could disperse organisms into the atmosphere.
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Respiration and sulphate uptake have been measured in guinea-pig skin subjected to heat damage and maintained on a medium containing sodium succinate. Succinate was found to have a protective effect against loss of oxygen uptake, a higher temperature being required for 50% effect than that reported with glucose as substrate. The protective effect did not extend to sulphate incorporation, suggesting that this process is itself heat-labile and that its failure with heat damage is not directly caused by diminution of the energy supply.
An apparatus to produce shallow linear burns is described. The burns contained about the same amount of damaged tissue as a shallow cut. The initiation of healing in cuts and burns on guinea-pig ears was studied using an 3H-thymidine and autoradiographic technique to determine the number of cells in DNA synthesis in epidermis adjacent to the wound. Cuts caused epidermal cells to enter DNA synthesis rapidly; the maximum response was 1 day after injury. Thus response was delayed in burns and the maximum was not seen until at least 3 days after burning. Extracts of normal skin stimulated epidermal DNA synthesis, whereas extracts of burned skin did not. Possible mechanisms affecting the delay in the healing of burns are discussed.
Autoantibodies to the insulin receptor mimic the effects of insulin on glycogen synthase and phosphorylase. The interaction of antibodies with adipocyte cell surface insulin receptors seems sufficient to promote stable changes in the activities of these intracellular enzymes, suggesting that internalization or processing of insulin is not important in the generation of these biological responses.
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An array of epidural electrodes was acutely implanted in locally anesthetized, curarized rats in order to map the surface distribution of rhythmic slow activity (RSA) which appears within the neocortex. Peak amplitudes (of about 122 muV) were centered over the dorsal hippocampus outline. A laminar profile of RSA recorded within the neocortex indicated no shifts in phase relative to a homotopic, epidural electrode. RSA increased slightly in amplitude (mean increase = 53%) at the deepest level or neocortex, but it did not approximate an amplitude peak or null within the neocortex. Multiple-unit activities within the neocortex were not phase-locked to RSA. On the other hand, all of these manifestations of an RSA generator were observed as electrodes passed into the dorsal hippocampus. A unilateral cortical spreading depression (CSD) treatment, which markedly attenuated barbiturate spindles in all subjects (N = 10), usually (N = 7 of 10) had no effect on the neocortically monitored RSA. Dissociations between depressed and non-depressed hemispheres, and between neocortical and hippocampal RSA, were obtained in some subjects during CSD. However, concurrent dissociations were also apparent between recording sites within the hippocampus. It is concluded that the neocortical RSA of rats is passively spread from the underlying hippocampus, and dissociations in neocortical and hippocampal RSA in the rat are secondary to changes in the organization of multiple generators of hippocampal RSA.
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Incubation of fat cells with insulin increased glycogen synthase I activity without changing total synthase activity. This effect of insulin was dependent upon the particular lot of albumin present in the medium and was abolished by incubating cells with trypsin. Half-maximal activation of glycogen synthase was obtained with 8 microunits/ml of insulin, a concentration very similar to that which half-maximally stimulated 3-O-methylglucose uptake. The basal percentage of phosphorylase a activity was not detectably altered by insulin, although it was decreased by incubating cells with 5 mM glucose. Insulin (50 microunits/ml) markedly opposed actions of epinephrine (0.05 to 10 muM) to increase phosphorylase a activity and decrease glycogen synthase I activity, effects which were observed without glucose. Partial activation of glycogen synthase by insulin was seen after 1 min and complete activation after 4 min. Glucose alone produced a transient increase in synthase I activity. When cells were incubated with insulin plus glucose for 4 min, the increase in the percent synthase I activity was much greater than the additive effects of insulin and glucose alone. This potentiation of the effect of insulin on glucogen synthase I activity depended on the time of incubation with glucose and on the concentration of the hexose. If cells were incubated with cytochalasin B before insulin plus glucose, the effect of glucose was abolished. These results suggest that there are at least two mechanisms by which insulin can increase fat cell glycogen synthase I activity. One requires glucose and activation occurs secondary to an increase in glucose transport; where another mechanism(s) is operative even in the absence of glucose.
Two double-blind controlled clinical trials of the effectiveness of prophylactic low dose subcutaneous calcium heparin (dose based on body weight) in the prevention of deep vein thrombosis (DVT) have been completed. The first was concerned with upper abdominal operations in 242 patients over 21 years of age, and the second with 50 patients presenting with a fracture of the neck of the femur. There was no increase in the incidence of bleeding or wound complications in the patients given heparin. In each trial, the incidence of DVT as diagnosed by 125I-labelled fibrinogen was significantly reduced in the treated group. The incidence of DVT in the control groups varied significantly during the period of the trials. The incidence was much higher in the cold half of the year than in the hot months. In the first trial, this variation in incidence was directly correlated with the average temperature and the diurnal variation in temperature in the perioperative period. These results may help to explain the considerable variation in the incidence of postoperative DVT reported from various parts of the world, and also from within Australia.
This review summarises evidence supporting the view that the therapeutic anticoagulant properties of heparin are related to its physiological function in the organism, especially its activation of lipoprotein lipase and lecithinase. The conflicting results obtained from studies of the effect of heparin on platelet function are discussed, together with reasons for these differences of opinion. Finally, a hypothesis which links heparin, heparin-activated enzymes and platelet function is proposed, this hypothesis being complementary to the current views concerning the activation by heparin of the inhibitor of activated factor X.