Prepartum depression; a study of seventy unwed mothers treated with d-amphetamine sulfate and amobarbital. (25/167)

Seventy unwed pregnant patients in states of mild to moderate depression evidenced by one or more symptoms (tenseness, "nervousness," crying spells, listlessness, fatigue, nausea and vomiting, insomnia and overeating), received informal psychotherapy and a sustained-release capsule combining d-amphetamine sulfate and amobarbital.Forty-eight patients had complete or substantial relief of symptoms, 15 had partial relief, seven had slight or no relief. Use of the preparation seemed to make tense, "nervous" patients more communicative and amenable to counseling, but was less effective in listless, easily fatigued patients. Because of its direct mood-alleviating action and its ability to facilitate psychotherapy, the d-amphetamine sulfate-amobarbital combination proved a very effective treatment for mild and moderate depression accompanying pregnancy.  (+info)

Properties of the 3-o-methyl-D-glucose transport system in Acholeplasma laidlawii. (26/167)

Transport of 3-O-methyl-D-glucose (3-O-MG) by Acholeplasma laidlawii cells was studied. The 3-O-MG transport system appeared to be constitutive in cells grown on 3-O-MG and glucose; the transport process depended on the concentration of substrate used and exhibited typical saturation kinetics, with an apparent Km of 4.6 muM. 3-O-MG was transported as a free carbohydrate and was not metabolized further in the cell. Dependence on pH and temperature and the results of efflux and "counterflow" experiments demonstrated the carrier nature of the transport system. 6-Deoxyglucose and glucose competitively inhibited 3-O-MG transport, whereas maltose inhibited in non-competitively. p-Chloromercuribenzoate, p-chloromercuribenzene sulfonate, N-ethylmaleimide, and iodoacetate inhibited transport of 3-O-MG. Cells were able to accumulate 3-O-MG against a concentration gradient. Some electron transfer inhibitors (rotenone and amytal), arsenate, dicyclohexylcarbodiimide, and proton conductors such as 2,4-dinitrophenol, carbonylcyanide, m-chlorophenylhydrazone, pentachlorophenol, and tetrachlorotrifluoromethylbenzimidazole inhibited this process.  (+info)

The effect of drugs on a fixed-ratio performance suppressed by a pre-time-out stimulus. (27/167)

Pecking was reinforced by a fixed-ratio schedule with food, and responses during a red light produced a time out. If the bird did not respond during the red light, the light terminated and the bird could complete the FR schedule of positive reinforcement uninterrupted. The bird stopped responding during the red light sufficiently to avoid most of the possible time outs. In general, the pre-time-out stimulus suppressed responding more when the FR schedule was large than when it was small. The occurrence of the pre-time-out stimulus in the fixed ratio produced FR strain and extreme curvature atypical of normal fixed ratios of this size. Amobarbital, pentobarbital, chlorpromazine, and d-amphetamine injected when the FR performance was strained by the pre-time-out procedure produced marked increases in responding. The drug administration lowered the rate of responding only at larger doses; and then this occurred predominantly just after the injection.  (+info)

Effects of a single experience on subsequent reactions to drugs. (28/167)

The activity of rats in an unfamiliar environment was studied in order to determine how far their reactions to an amphetamine-barbiturate mixture depended on whether or not they had been under the influence of this mixture while exposed to the same environment once before. The environment consisted of a Y-shaped runway, and the activity studied was the number of entries into the arms of the Y during a three-minute trial; the two trials took place three days apart. At the first trial the drug mixture practically doubled activity. At the second trial rats which had been under the influence of the drug mixture at the first trial were again made more active by the drug mixture, but the drug mixture did not increase the activity of rats which had received only saline at the first trial. These results showed that a single brief exposure to an unfamiliar environment can markedly affect subsequent reactions to drugs, and interactions of this kind may have to be taken into account when it is desired to use animals repeatedly in tests of the action of drugs on behaviour. The drug mixture also produced ataxia which was assessed quantitatively by measuring the variability of the "splay" of the rats' footprints; ataxia was unaffected by previous experience.  (+info)

ACTION OF DIHYDROSTREPTOMYCIN AND ANTAGONISM BY CATIONS. (29/167)

Bragg, P. D. (University of British Columbia, Vancouver, Canada) and W. J. Polglase. Action of dihydrostreptomycin and antagonism by cations. J. Bacteriol. 85:590-594. 1963.-A number of antibiotics including dihydrostreptomycin inhibited the induction of beta-galactosidase in Escherichia coli and, except in the case of chloramphenicol, magnesium antagonized the inhibition. Of the antibiotics tested, only dihydrostreptomycin caused formation of pyruvate from the oxidation of glucose. Under similar conditions, inhibitors of terminal respiration (cyanide, azide, amobarbital) also caused formation of pyruvate. Magnesium and the polyamines, putrescine and spermidine, were observed to antagonize dihydrostreptomycin in systems in which the antibiotic showed an inhibitory action.  (+info)

MUTUAL POTENTIATION OF AMPHETAMINE AND AMYLOBARBITONE MEASURED BY ACTIVITY IN RATS. (30/167)

Dose/response relations have been analysed for the actions of amphetamine-barbiturate mixtures on exploratory activity and ataxia in rats. Amphetamine sulphate and amylobarbitone sodium were studied separately and together (in a constant ratio of 1:20) in doses which ranged from those producing no effect to those which incapacitated the animals. Dexamphetamine and amylobarbitone were similarly studied in a ratio of 1:6.5; this corresponds to the ratio of a commercial preparation, Drinamyl. The results showed that mixtures could stimulate exploratory activity and their maximal effects were much greater than the effects produced by any dose of the separate drugs. The maximal effect with the first dose-ratio included conspicuous ataxia, but the maximal effect with the second ratio did not. Further experiments in which the dose of one drug was held constant and that of the other was varied showed that maximal effects on activity could be obtained with mixtures of dexamphetamine and amylobarbitone. Equivalent effects could be obtained both with relatively small and with relatively large amounts of the two drugs, in varying ratios; some constituent doses of the individual drugs were found to be optimal; whether the mixture effect was accompanied by ataxia depended largely on the constituent amount of barbiturate. For practical purposes mixtures producing maximal effects on activity with the smallest amounts of both drugs and not accompanied by ataxia might be most desirable, and these can be approximately read off from an isobol plotted from the results. It was concluded that the marked stimulant effects of the amphetamine-barbiturate mixtures on activity of rats could be regarded as due to true potentiation.  (+info)

KORSAKOFF'S SYNDROME ASSOCIATED WITH ADRENAL VIRILISM. (31/167)

Korsakoff's syndrome of obscure etiology was observed in a 34-year-old single woman with an 11-year history of hirsutism and mood swings, and previous hospitalizations for mania three years ago and depression 11 years ago.Recently the virilism had intensified with increased muscularity and coarsening of facial features. The 24-hour urinary 17-ketosteroids ranged between 14.4 mg. and 21.5 mg. and were suppressed by dexamethasone. The 17-hydroxycorticosteroid excretion was normal. These and other findings suggested a diagnosis of adrenal virilism due to adrenocortical hyperplasia. In the absence of other discernible causes it appeared that the adrenal pathology was responsible for the Korsakoff's syndrome. Both conditions responded well to glucocorticoid therapy although low doses were necessary to avoid mania.It is speculated that the encephalopathy was due to an associated adrenal insufficiency. Although hypoadrenalism is accepted as a complication of only the infant form of adrenal virilism, it is noteworthy that this patient had pathological pigmentation of her skin.  (+info)

FLAVINE ADENINE DINUCLEOTIDE-LINKED MALIC DEHYDROGENASE FROM ACETOBACTER XYLINUM. (32/167)

Benziman, Moshe (The Hebrew University of Jerusalem, Jerusalem, Israel), and Y. Galanter. Flavine adenine dinucleotide-linked malic dehydrogenase from Acetobacter xylinum. J. Bacteriol. 88:1010-1018. 1964.-The properties of the pyridine nucleotide-nonlinked malic dehydrogenase of Acetobacter xylinum were investigated in the supernatant fluid obtained by high-speed centrifugation of sonic extracts. Ferricyanide, phenazine methosulfate, and to a lesser extent dichlorophenolindophenol were active as oxidants for malate oxidation. After acid ammonium sulfate precipitation, the enzyme lost its malate-oxidizing activity. The enzyme was reactivated by low concentrations of flavine adenine dinucleotide (FAD) but not by flavine mononucleotide (FMN) or riboflavine. Atabrine inhibited the enzyme, and the inhibition was relieved by FAD but not by FMN or riboflavine. Malate-oxidizing activity was inhibited by hematin. The inhibition was prevented by imidazole or globin. o-Phenanthroline, 8-hydroxy quinoline, alpha,alpha'-dipyridyl, and p-chloromercuribenzoate inhibited malate oxidation. Amytal markedly inhibited oxidation of malate in the presence of oxygen, phenazine methosulfate, or dichlorophenolindophenol, but not in the presence of ferricyanide. The results suggest that the malic dehydrogenase of A. xylinum is a FAD enzyme, which contains an ironbinding site essential for its activity. Nonheme iron and sulfhydro groups are possibly involved in enzyme activity. The malic dehydrogenase is functionally linked to the cytochrome chain.  (+info)