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It has long been recognized that trypanosomes are dependent on an adequate supply of glucose for the maintenance'of their metabolic processes (Yorke, Adams, and Murgatroyd, 1929;Geiger, Kligler, and Comaroff, 1930; von Brand, 1933). Later work has given some indication of the mechanism of the glucose metabolism of various species of the parasite, and the nature of the endpoints formed. Reiner and Smythe (1934) showed that the end-point of glucose metabolism in T. equiperdum was pyruvic acid, and the same group of workers (Reiner, Smythe, and Pedlow, 1936) showed that T. lewisi metabolized glucose more completely to yield formic, acetic and succinic acids, ethyl alcohol and carbon dioxide. Fulton and Stevens (1945) reported that the products of metabolism of T. rhodesiense were succinic, pyruvic, lactic, acetic and formic acids, glycerol, ethyl alcohol, and carbon dioxide.Regarding the respiratory activity of trypanosomes, Christophers and Fulton (1938) showed that oxygen consumption by T. rhodesiense was entirely dependent on the presence of glucose, and that 1 molecule of glucose required 1 molecule of oxygen. They also demonstrated the presence of dehydrogenase systems in trypanosome metabolism, and the absence of inhibition by cyanide. Reiner and Smythe (1934) reported that T. equiperdum produced very little carbon dioxide in the absence of bicarbonate, and that 1.80 molecules of acid (mostly pyruvic) were produced from the metabolism of 1 molecule of glucose. These workers also showed that trypanosomes could metabolize glycerol as well as glucose, but only under aerobic conditions. More recent work by Searle and Reiner (1940Reiner ( , 1941 Chen and Geiling (1946), has any direct evidence of glucose phosphorylation been demonstrated. These workers have shown that lysed trypanosomes will transform glucose to fructose-1,6-diphosphate and triose phosphates, and will oxidize phosphoglyceraldehyde to phosphoglyceric acid.The investigations described in this communication corroborate the findings of other workers regarding the respiratory activity of trypanosomes, and provide further evidence that glycolysis proceeds via the typical chain of phosphorylation reactions. Some preliminary indications are given of the points of attack-by trypanocidal agents, on which there are no previous reports. MATERIALS AND METHODSThe organism was a strain of Trypanosoma evansi isolated from a camel in the Sudan in 1938, and maintained in mice, in which it produces heavy, acute blood infections. Infected blood was-obtained from the exposed hearts of mice killed by placing them in an atmosphere of carbon dioxide.Respiration experiments.-Oxygen consumption was measured in conventional Warburg constant volume respirometers, using 15 ml. flasks maintained at 38' C.A set of twelve respirometers was run in duplicate, triplicate, or quadruplicate groups, according to the number of variants required. Since normal mouse blood showed only a negligible oxygen uptake, whole blood containing the trypanosomes was usually used, diluted with "isot...

Synopsis In the years from to 1995, Adelaide‐based mobile intensive care teams transported 4443 critically ill patients from rural areas in South Australia and adjacent States to tertiary‐level hospitals in Adelaide. The SA Ambulance Service undertook communications, support staffing and deployment of transport. Average radial distances in 819 road missions were 71 km, in 808 helicopter missions 122 km, and in 2777 fixed‐wing aircraft missions 398 km. The largest groups of patients were neonates (23%) and those with trauma (25%). Rural hospitals made 96% of the requests for intensive care transport; 4% came from ambulance or other emergency service crews at accident locations. Emergency surgical or operative obstetrical procedures were performed on 2.7% of patients before transport. One hundred and thirteen patients (2.5%) died during resuscitation or transport, with one death deemed to be preventable.

The anti-acetylcholine potency of a number of anti-Parkinsonism drugs and related phenQthiazine compounds was determined using the isolated guinea-pig ileum. The antagonism was assessed by the difference between the pA2 and pAio values and by log concentration-response curves for acetylcholine in presence and absence of the antagonists. All compounds except chlorpromazine showed some evidence of competitive antagonism to acetylcholine. The anti-tremor potency of the compounds was assessed from suppression of Tremorine-induced tremors in mice. There was a relation between anti-acetyIcholine and anti-Tremorine potency among the antiParkinsonism drugs, but not among the phenothiazine compounds. Some implications of the findings are discussed in relation to the mode of action of anti-Parkinsonism drugs.To explain the effectiveness of atropine in the treatment of Parkinsonism, Feldberg (1945) suggested the possibility of an atropine-acetyicholine antagonism at central synapses. Since then a number of synthetic drugs have been introduced for the treatment of Parkinsonism, all having peripheral and central atropine-like properties. Jenkner & Ward (1953) have suggested that, in experimental lesions producing Parkinsonian-like tremors, the disconnected neurones in the medial reticular formation become hypersensitive to endogenous acetylcholine released from near-by uninvolved cells. If human Parkinsonian tremor results from central hypersensitivity to acetylcholine, then it is reasonable to expect that effective antiParkinsonism drugs would be specific antagonists of acetylcholine.As no comprehensive quantitative assessment of the anti-acetylcholine potency of the anti-Parkinsonism drugs has yet been made, the present work was undertaken to measure anti-acetylcholine activity and its relation to anti-tremor potency in drug-induced tremor in mice. METHODSMeasurement of anti-acetylcholine potency. Estimations of pA2 and pAio values were carried out essentially according to the method of Schild (1947). Pieces of distal ileum were removed from freshly killed guinea-pigs which had been fasted overnight. The organ bath,