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Biomedical subjects

A J Cooper

Publications and source records attributed to A J Cooper.

At least 235 records · Page 13Linked to original sources
PubMed1980

13N,15N isotope and kinetic evidence against hyponitrite as an intermediate in dentrification.

13N- and 15N-labeling experiments were carried out with Paracoccus denitrificans, grown anaerobically on nitrate, to determine whether hyponitrite might be an obligatory intermediate in denitrification and a precursor of nitrous oxide. From experiments designed to trap [13N]- or [15N,15N]hyponitrite by dilution into authentic hyponitrite it was calculated that the intracellular concentration of a presumptive hyponitrite pool must be less than 0.4 mM. In order for a pool of this size to turn over rapidly enough to handle the flux of nitrogen during dentrifucation, the spontaneous rate of hyponitrite dehydration must be enhanced by a factor of several thousand through enzyme catalysis. Cell extracts failed to catalyze this reaction under a variety of conditions. It is concluded that hyponitrite cannot be an intermediate in dentrification. In addition, the assimilation of inorganic nitrogen was studied in P. denitrificans using 13N as tracer. At low concentrations (less than 10(-8) M) of labeled nitrate and nitrite 5 to 10% of the label was assimilated into non-volatile metabolites and 90 to 95% was reduced to N2. Similarly, with 15 mM [13N]nitrate, 5% of the label went into metabolites and 95% to N2. High pressure liquid chromatography analysis of the labeled metabolites indicated that the major pathway for assimilation of inorganic nitrogen in P. denitrificans under these conditions is through ammonia incorporation via the aspartase reaction.

Amino Acids↗
PubMed1980

The applicability of freeze-thaw Percoll gradients to whole-cell isopycnic fractionations: preliminary results.

The freeze-thaw method of gradient generation, using Percoll as the density medium, is shown to be adaptable for the isopycnic sedimentation of live whole cells. Methods of controlling gradient profiles are examined with preliminary evidence showing that three types of cells brought to isopycnic equilibrium in these gradients and recovered from them retain satisfactory levels of several vital functions.

Animals↗
PubMed1980

Glutathione and ascorbate during ischemia and postischemic reperfusion in rat brain.

Thirty minutes of total cerebral ischemia (decapitation) decreased total glutathione (GSH + GSSG) by 7% but had no detectable effect on the concentration of oxidized glutathione (GSSG), reduced ascorbate, or total ascorbate, In a model of reversible, bilateral hemispheric ischemia (four-vessel occlusion) no changes in glutathione or ascorbate were detected after 30 min of ischemia. During 24 h of reperfusion following such an insult no detectable change in total ascorbate, reduced ascorbate, or oxidized glutathione was noted: however, total brain glutathione declined by 25%. The findings are discussed in relation to the hypothesis that the deleterious effects of ischemia are due to an increase in free radical production which in turn leads to increased lipid peroxidation.

Animals↗
PubMed1980

A placebo controlled evaluation of L-tryptophan in depression in the elderly.

Two groups of unmatched patients attached to a Geriatric Hospital suffering from mild to moderate depression considered suitable for drug therapy were randomly allocated either 6 grams L-tryptophan daily or a similar dose of identical placebo for six weeks on a double-blind basis. Ratings (HRS and a 7 point global evaluation) were made pretrial and fortnightly up to and including six weeks. Both groups steadily improved, but there was no statistical difference between the L-tryptophan patients and those receiving placebo. Therefore, it would appear that L-tryptophan is not an effective anti-depressant.

Aged↗
PubMed1980

A placebo-controlled study of pyritinol ('Encephabol') in dementia.

A double-blind, placebo-controlled trial was carried out on 40 patients suffering from moderately advanced dementia. The patients were allocated randomly either pyritinol (800 mg daily) or identical placebo for 3 months. Assessments using a modified Crichton Geriatric Behavioural Rating Scale were made pre-treatment and monthly up to 3 months, and then at follow-up at 6 months. Patients on pyritinol showed significantly higher levels of improvement than did those on placebo. Laboratory tests conducted throughout remained within normal limits for both groups.

Aged↗
PubMed1979

The metabolic fate of 13N-labeled ammonia in rat brain.

13N-labeled ammonia was used to study the cerebral uptake and metabolism of ammonia in conscious rats. After infusion of physiological concentrations of [13N]ammonia for 10 min via one internal carotid artery, the relative specific activities of glutamate, glutamine (alpha-amino), and glutamine (amide) in brain were approximately 1:5:400, respectively. The data are consistent with the concept that ammonia, entering the brain from the blood, is metabolized in a small pool of glutamate that is both rapidly turning over and distinct from a larger tissue glutamate pool (Berl, S., Takagaki, G., Clarke, D.D., and Waelsch, H. (1962) J. Biol. Chem. 237, 2562-2569). Analysis of 13N-metabolites, after infusion of [13N]ammonia into one lateral cerebral ventricle, indicated that ammonia entering the brain from the cerebrospinal fluid is also metabolized in a small glutamate pool. Pretreatment of rats with methionine sulfoximine led to a decrease in the label present in brain glutamine (amide) following carotid artery infusion of [13N]ammonia. On the other hand, 13N activity in brain glutamate was greater than that in the alpha-amino group of glutamine, i.e. following methionine sulfoximine treatment the expected precursor-product relationship was observed, indicating that the two pools of glutamate in the brain were no longer metabolically distinct. The amount of label recovered in the right cerebral hemisphere, 5 s after a rapid bolus injection of [13N]ammonia via the right common carotid artery, was found to be independent of ammonia concentration within the bolus over a 1000-fold range. This finding indicates that ammonia enters the brain from the blood largely by diffusion. In normal rats that were killed by a freeze-blowing technique 5 s after injection of an [13N]ammonia bolus, approximately 60% of the label recovered in brain had already been incorporated into glutamine, indicating that the t1/2 for conversion of ammonia to glutamine in the small pool is in the range of 1 to 3 s or less. The data emphasize the importance of the small pool glutamine synthetase as a metabolic trap for the detoxification of blood-borne and endogenously produced brain ammonia. The possibility that the astrocytes represent the anatomical site of the small pool is considered.

Ammonia↗
PubMed1979

Tryptophan antidepressant 'physiological sedative': fact or fancy?

Some recent publications relating to the allegedly antidepressive and sedative effects of L-tryptophan the precursor of 5-HT have been reviewed. The evidence to date suggests that the amino acid is as effective as standard tricyclic drugs in alleviating the symptoms of depression, especially those cases presenting with mainly psychomotor retardation, and is synergistic with MAOIs. L-Tryptophan would also appear to be a 'physiological sedative'. This action, however, appears to be related to the time of administration and at present has only been demonstrated at night. when endogenous levels of 5-HT are at their peak. In terms of practical therapeutics L-tryptophan would appear to have greater potential as an 'antidepressant' than as a 'sedative'.

Affective Symptoms↗
PubMed1979

Effects of neonatal bulbectomy on later discrimination learning in mice.

The olfactory bulbs of mice were lesioned at 24 h of age and their performance in learning a black-white discrimination task was compared with undernourished mice that grew from birth at the same rate as the bulbectomised animals. The mice were tested at 90 days of age and their behaviour in a Y-maze was compared with that of control operated and unoperated samples. The performance of the bulbectomised mice spent more time at the choicepoint and frequently failed to run the maze. The error rate reduction shown by the bulbectomised mice was similar to that of the controls and is accounted for in terms of a reduced frequency of entry and reversals into the maze arms. The results are discussed in relation to the size of the lesions and factors affecting the neurogenesis of the olfactory brain early in life.

Animals↗
PubMed1978

Cyclic forms of the alpha-keto acid analogs of arginine, citrulline, homoarginine, and homocitrulline.

The alpha-keto acid analogs of arginine and citrulline (and of their next higher homologs, homoarginine and homocitrulline) were prepared enzymatically and shown to exist in equilibrium with cyclic forms which predominate in solution and in the solid state. The cyclic forms of the alpha-keto acid analogs of arginine and homoarginine have the structures pyrrolidine-1-amidino-2-hydroxy-2-carboxylic acid and piperidine-1-amidino-2-hydroxy-2-carboxylic acid, respectively. The cyclic forms of the alpha-keto acid analogs of citrulline and homocitrulline have the structures pyrrolidine-1-carbamyl-2-hydroxy-2-carboxylic acid and piperidine-1-carbamyl-2-carboxylic acid, respectively. The latter compound can undergo further cyclization and dehydration to form additional products, whose structures (2H, 5H, 7H-imidazo[1,5-a]pyridine-1,3-dione and 2H, 5H, 7H, 9H-9-hydroxy-imidazo[1,5-a]pyridine-1,3-dione) were deduced. The alpha-keto acids investigated here, which may be formed reversibly by enzymatic transamination of the corresponding amino acids, may be formed in vivo especially in the presence of metabolic abnormalities associated with inborn enzymatic defects.

Arginine↗