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Biomedical subjects

A D Mosnaim

Publications and source records attributed to A D Mosnaim.

At least 37 records · Page 2Linked to original sources
PubMed1989

Blood-brain barrier passage of azidothymidine in rats: effect of insulin.

Azidothymidine (AZT) crosses the blood-brain barrier (BBB) of 6-8 week old Sprague-Dawley male white rats (Oldendorf technique, ipsilateral cerebral hemisphere) with a brain-uptake index (BUI) of 5.4 +/- 0.8 (mean +/- S.D., n = 13, range 4.4-6-6) using 14C-antipyrine as the diffusible standard. Pretreatment of the animals with the higher doses of insulin (0.6 or 1.0, but not 0.1, 0.2, or 0.3 units per rat, 3 or 10 min. before decapitation) resulted in higher values for the BUI of AZT in most individual animals. In the group of rats treated with 1.0 unit of insulin 10 min. before decapitation, a statistically significant increase in the BUI was observed. Some possible clinical applications of this pharmacologic strategy are discussed.

Animals↗
PubMed1988

Studies of the in vitro human plasma degradation of methionine-enkephalin.

1. Incubation of [3H]tyrosine methionine-enkephalin (6 x 10(-9) M final concentration) with human platelet-poor plasma (1:9 ratio to Trizma Base buffer, pH 7.4) results mostly (greater than 95%) in hydrolysis of the tyrosyl-glycine peptide bond. This enzymatic reaction is essentially completed within 90 min, showing a half-life, Km and Vmax of 12.8 +/- 2.5 min, 0.70 +/- 0.01 mM and 17.90 +/- 1.05 mumol/L/min, respectively. These values are comparable to those previously reported for the human plasma degradation of leucine-enkephalin. 2. As expected hydrolysis of the methionine-enkephalin tyrosyl-glycine peptide bond was blocked by the known aminopeptidase inhibitors bestatin and puromycin (IC50 1.2 +/- 0.4 and 4.3 +/- 2.4 microM, respectively) but not by either thiorphan or captopril. 3. Neither the storing (up to 60 days) nor the freezing and thawing (up to ten times during a 60 days periods) significantly changed the above kinetic parameters, showing the stability of the plasma methionine-enkephalin degrading aminopeptidase.

Chromatography, Thin Layer↗
PubMed1988

Administration of butaperazine and plasma methionine-enkephalin levels in schizophrenic and affective disorder patients with tardive dyskinesia.

The levels of plasma methionine-enkephalin in male chronic schizophrenic and affective disorder patients with or without tardive dyskinesia (TD) were in a range similar to those of sex-matched adult control volunteers. Administration of butaperazine resulted in significant changes (increases) of neuropeptide plasma concentration only in the affective disorder with TD subgroup, reaching statistical significance over their own baseline at 8, 10.5, and 24 hours, and at baseline (0 hr), 8-, and 48-hour intervals when compared with the affective disorder patients without TD.

Adolescent↗
PubMed1987

Phenylethylamine metabolism to tyramine by postmortem human brain preparations.

Human brain preparations obtained from either the putamen, thalamus, hippocampus or lateral occipital gyrus p-hydroxylate phenylethylamine to tyramine, a reaction carried out by a microsomal (100,000 xg pellet) membrane bound, NADPH-requiring enzyme. This is a minor metabolic pathway occurring in chronic psychiatric patients, as well as in age-comparable controls.

Aged↗
PubMed1987

Risk factors for tardive dyskinesia according to primary psychiatric diagnosis.

The role of different variables in the development of tardive dyskinesia was examined among patients in two different diagnostic categories. Age and length of hospitalization were associated with development of tardive dyskinesia in the schizophrenic subjects while parkinsonism and alcoholism were related to tardive dyskinesia in the affective disorder patients. Schizophrenic subjects constituted the largest absolute number of tardive dyskinesia patients, but in relative terms they represented the patient population least likely to develop tardive dyskinesia in comparison to affective disorder and organic mental disorder subjects. The clinical implications of these findings are discussed.

Age Factors↗
PubMed1985

Vulnerability to tardive dyskinesia.

Of 99 consecutive male patients studied at the North Chicago VA Tardive Dyskinesia Program, 58 had tardive dyskinesia and 41 did not. Factors that were significantly related, singly and in combinations, to tardive dyskinesia were 1) diagnosis of affective disorder with alcoholism and/or drug-induced parkinsonism, and 2) diagnosis of schizophrenia with advanced age (over 50) and/or prolonged hospitalization (over 14 years). A diagnosis of schizophrenia in patients under age 50 with short hospitalizations was not significantly associated with the presence of tardive dyskinesia.

Age Factors↗
PubMed1984

Electroencephalogram in tardive dyskinesia.

The electroencephalogram was studied in affective disorder and schizophrenic patients both with and without tardive dyskinesia. There were no significant differences in electroencephalographic changes among the groups. The majority of electroencephalographic abnormalities appear to be drug induced. Tardive dyskinesia is not associated with specific changes in the electroencephalogram.

Adult↗
PubMed1983

Phenylethylamine in neuropsychiatric disorders.

Phenylethylamine is an endogenous neuroamine conceptualized as the body's natural amphetamine. PEA has been suggested to play a role in the etiology of several neuropsychiatric disorders. Increased PEA turnover in phenylketonuria contributes to the pathophysiology of this condition. Depressed and chronic paranoid schizophrenic patients show decreased and increased PEA urinary excretion, respectively. Parkinsonian patients show decreased urinary PEA excretion. In animals, drugs that relieve or produce depression and parkinson result in increased or decreased brain PEA levels, respectively. PEA has been postulated to play a role in the etiology of migraine headache and aggression.

Affective Disorders, Psychotic↗
PubMed1983

Studies in the mechanism of phenylethylamine uptake by rabbit erythrocytes.

The mechanism of phenylethylamine (PEA) uptake by in vitro rabbit erythrocyte preparations involve both a larger component of passive diffusion and an Na+-dependent facilitated transport system. This is reflected by the fast rate and lack of saturation of PEA erythrocyte uptake, and by the decrease in PEA tissue/medium ratio when the amine was incubated in an Na+-free medium or in the presence of ouabain. Results obtained after the addition of iodoacetamide or by the use of glucose-free medium suggest the Na+-K+ gradient as the driving force responsible for operation of the carrier mechanism. Preliminary results indicate that amphetamine PEA share a similar mechanism for their uptake by rabbit erythrocytes. At the levels normally present in rabbit blood (c. 1 X 10(-8)M), about one-third of the PEA is found in the serum and only a very small portion of it (less than 1%) is present as the "biologically active" non-ionized amine. Most of the remaining phenylethylamine is bound to plasma protein or inside the erythrocytes.

Animals↗
PubMed1983

Cognitive functions in tardive dyskinesia.

Cognitive functions of psychiatric patients with and without tardive dyskinesia were evaluated using the Wechsler Adult Intelligence Scale, Wechsler Memory Scale and Rey Auditory Verbal Learning Test. Schizophrenic patients with and without tardive dyskinesia did not differ in their performance on the administered psychological tests. However, affective disorder patients with tardive dyskinesia showed significantly more impairment on the Wechsler Memory Scale and Rey Auditory Verbal Learning Test than affective disorder patients without tardive dyskinesia. These findings suggest that affective disorder patients who develop tardive dyskinesia may have some predisposing brain damage or that tardive dyskinesia in these patients represents both a motor and a dementing disorder.

Antipsychotic Agents↗
PubMed1983

Plasma and cerebrospinal fluid concentration of phenylacetic acid in humans and monkeys.

A rapid and reliable mass-fragmentographic method for assay of plasma and cerebrospinal fluid (CSF) concentrations of free and conjugated phenylacetic acid (PAA) is described. The method is used to compare plasma and CSF concentrations of PAA in humans and monkeys. Both packed and capillary columns are used. In humans approximately 45% of total plasma PAA is conjugated in contrast to approximately 60% in monkeys. Both free and conjugated PAA concentrations tend to be higher in monkeys than in humans. Plasma mean concentration of total PAA in humans and monkeys are, respectively, 459.1 and 838 ng/ml. Approximately 55 and 25% of total PAA in the CSF are conjugated in humans and monkeys, respectively. Total PAA mean concentrations in human and monkey CSF are 41.6 and 84.2 ng/ml. Because over 90% of total urine PAA in humans is conjugated, it is concluded that over 50% of urine phenylacetylglutamine may be derived from kidney conjugation of free plasma PAA and/or from the kidney's preferential filtration of conjugated PAA as contrasted with free PAA.

Animals↗