A further action of sodium cromoglycate [proceedings].
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Biomedical subjects
Publications and source records attributed to D M Jackson.
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Ten Pseudomonas aeruginosa and six Pseudomonas cepacia strains recently isolated from infected patients were tested for susceptibility to the antimicrobial activity of two commercially-available soft contact lens soaking solutions. No strain showed evidence of viability after two hours but survivors were found in both solutions after one-half hour and in one solution after one hour. The solution most effective in inhibiting the Pseudomonas strains contained chlorhexidine and disodium edetate but each solution was effective in reducing heavy inocula of both species within the times recommended by the manufacturers.
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Dopamine (5 to 50 mug) applied bilaterally to the nucleus accumbens of reserpine-nialamide pretreated rats produced a marked dose-dependent rise in coordinated locomotor activity, devoid of stereotypies such as gnawing, rearing and licking seen after dopamine application (50 mug) to the neostriatum. The locomotor activity was completely blocked by pimozide, but not by phenoxybenzamine. The effects of apomorphine or d-noradrenaline was similar to those of dopamine. In contrast, l-noradrenaline produced a "convulsive" syndrome devoid of coordinated locomotor activity, and this convulsive syndrome could be completely blocked by phenoxybenzamine but not by pimozide. Release of endogenous dopamine by d- or l-amphetamine (10 and 50 mug) in the nucleus accumbens produced a rise in coordinated activity, the d-isomer was about 4 times as potent as the l-isomer, and the effect of the d-isomer was blocked completely by alpha-methyltyrosine. Bilateral application of trifluoperazine (2.5 mug) to the nucleus accumbens completely blocked the effect of systemically administered d-amphetamine (1.5 and 3.0 mg/kg), but similar application to the area of the central nucleus of the amygdala or the neostriatum was much less effective. Partial protection of the endogenous dopamine stores against the depleting action of reserpine by local application of metatyramine to the nucleus accumbens resulted in a higher level of basal activity than in control animals. Application of dopamine or noradrenaline to the area of the central nucleus of the amygdala or to the olfactory tubercles did not lead to any consistent changes in locomotor activity. The nucleus accumbens and olfactory tubercles contained most of the dopamine in the limbic forebrain, with noradrenaline more evenly distributed. These data suggest that the nucleus accumbens plays an important role in the locomotor activity in rats.
The effect of local application of dopamine to the nucleus accumbens or corpus striatum on locomotor activity was studied in rats 4 days after withdrawal from a 6 weeks term of penfluridol medication. The bilateral application of dopamine into the nucleus accumbens of penfluridol-treated rats produced a very marked increase in coordinated locomotor activity which was 3-5 times higher than that of rats not treated with penfluridol. This effect of dopamine in both penfluridol-treated and control rats was antagonized by intraperitoneally administered haloperidol. The bilateral application of dopamine into the corpus striatum of penfluridol-treated animals produced a marked stereotyped behavioural syndrome in all rats studied, whereas no signs of stereotyped behaviour were observed in any of the rats not treated with penfluridol. The results indicate that long-term treatment of rats with the dopamine receptor blocking agent penfluridol produces an increase in the sensitivity of the dopamine receptors in the nucleus accumbens and corpus striatum and that the nucleus accumbens may play a role in locomotor activity.
The onset and duration of tolerance to three effects of delta9-tetrahydrocannabinol (delta9-THC) given orally to mice were compared. The effects of delta9-THC studied were: hypothermia, the depression of intestinal motility and the effect on spontaneous locomotor activity. When mice were dosed and tested at 24 hrs intervals it was apparent that tolerance was complete to its hypothermic and locomotor depressant effects after the first doses and to depression of intestinal motility after the fourth dose. Duration of tolerance also differed so that the normal hypothermic response had returned after 12 dose-free days, but not after 5 drug-free days; the effect on locomotor activity had returned within 4 days; and apparent partial tolerance to the depressant effect of an acute challenging dose of delta9-THC on intestinal motility still existed after 19 dose-free days. It is apparent that the time of onset and the duration of tolerance to delta9-THC in mice showed a different pattern in the three parameters studied. It seems unlikely therefore that any one mechanism, such as metabolic tolerance, explains all the results observed and that several mechanisms should be explored to explain the phenomenon of tolerance to delta9-THC.
Asymmetry of the femoral head within the acetabular cup shown in an antero-posterior radiograph of the hip is an indication of dislocation of the prosthesis after a Charnley-Müller procedure. However, this rule does not apply to modifications such as the Aufranc-Turner prosthesis.
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The increased motor activity of reserpine-nialamide pretreated rats given dopamine into the nucleus accumbens was potentiated in a dose-dependent manner by systemically administered caffeine. Similarly, the increase in motor activity seen when the endogenous dopamine was released by intraperitoneally administered amphetamine was potentiated by systemically given caffeine. These effects might be due to an increase in the dopamine-induced accumulation of cyclic AMP in the nucleus accumbens after inhibition of the phosphodiesterase by caffeine.
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Beta-phenylethylamine on injection into mice (100 mg/kg i.p.) produces a marked hyperthermia which is followed by a prolonged hypothermia. The hyperthermic response was studied in this report. The hyperthermic response was inhibited by p-chlorophenylalanine, methysergide, cyproheptadine, alpha-methyl-tyrosine, propranolol, practolol, phenoxybenzamine, phentolamine, haloperidol, pimozide, protriptyline and desipramine. Lysergic acid diethylamide potentiated the response, while p-chloroamphetamine was without effect. While FLA-63 potentiated the response, disulfiram and reserpine were ineffective in preventing the hyperthermia. Nicotinic acid and prostaglandin E1 did not prevent PE induced hyperthermia. It was concluded from these results that PE induced hyperthermia in mice is blocked by agents that reduce the effective concentration of either DA or 5-HT in the central nervous system (by either synthesis inhibitors or receptor blockers). The involvement with catecholaminergic neurons at least was postulated to be a result of PE induced release of DA from DA neurons.
Beta-Phenylethylamine on injection into mice produced both an early and late phase of increased locomotor activity. The early phase produced by 50 mg phenylethylamine/kg was inhibited by pretreatment with phenoxybenzamine, phentolamine, alpha-methyl-tyrosine, diethyldithiocarbamate, pimozide and haloperidol, but not by propranolol, protriptyline and reserpine. The late phase produced by 100 mg phenylethylamine/kg was blocked only by pimozide and haloperidol, both of these in doses at least ten times higher than those required to block the early phase. From these results it was concluded that the increased early phase of locomotor activity was due to the release of dopamine and noradrenaline synthetic pathway, but not intact reserpine sensitive amine stores. In contrast the late phase of locomotor activity was independent of catecholamine stores and appeared to be produced by a direct action by either phenylethylamine or metabolites on dopamine receptors.
The oxygen uptakes by pieces of gut from the porcine roundworm, Ascaris suum, under Po2 10 to 710 torr were from 0.6 to 3.0 mul/mg dry wt/hr (Qo2). Increasing concentrations of tissue, 30 to 90 mg (dry wt/3 ml) decreased Qo2 in air from 1.9 to 1.1 and only technical grade catalase was found to relieve this inhibition. Conversely aerobic fermentation, judged by acid production, was directly proportional to the amount of tissue present: the acids from this fermentation were 2-methyl-butyric (1% of the total), succinic (8%), propionic (40%), and acetic (51%). Glucose did not increase Qo2 but it doubled the incorporation of labeled carbon into protein from glycine-1-14C. Judged by this, protein synthesis proceeded at the same rate under low Po2 (0.01 torr) as under air.
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