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Biomedical subjects

M Sandler

Publications and source records attributed to M Sandler.

At least 163 records · Page 9Linked to original sources
PubMed1983

New endogenous benzodiazepine receptor ligand in human urine: identity with endogenous monoamine oxidase inhibitor?

Normal human urine contains both monoamine oxidase-inhibiting and benzodiazepine receptor-binding material. Each was extracted into ethyl acetate at pH 1 and subjected to high performance liquid chromatography: they ran similarly, showing three major peaks. The correlation coefficient between the pattern of MAO inhibition and inhibition of 3H-flunitrazepam binding to benzodiazepine receptors in the second half of the elution process was 0.78 (p less than 0.001): most UV-absorbing material present was eluted earlier in the run. These results are compatible with, although they do not prove, the hypothesis that the endogenous MAO inhibitor, previously shown to be increased in stress, is also an endogenous inhibitor of 3H-flunitrazepam binding to the benzodiazepine receptor. This material is different from other putative endogenous ligands: it migrates more rapidly than the potent but artefactual beta-carboline-3-carboxylic acid ethyl ester previously isolated from human urine; nor can the effect we have identified derive from harmane, inosine, hypoxanthine or nicotinamide which fail to extract into ethyl acetate at pH 1.

Adult↗
PubMed1983

Primary hyperparathyroidism and osteoporosis. A case report.

A case of osteoporosis secondary to primary hyperparathyroidism is reported. A 55-year-old woman presented with a history of persistent lumbar backache for 3 years; numerous radiographs taken during this period had shown 'osteoporosis in keeping with age'. Referral to the Endocrine Clinic to evaluate the osteoporosis resulted in baseline investigations which revealed a raised serum calcium level, further investigation of which led to the diagnosis of primary hyperparathyroidism. Recent studies have shown that, over the past two decades, diffuse undermineralization of the bones (osteopenia) is the most common radiological feature in primary hyperparathyroidism.

Female↗
PubMed1983

Phenylethylamine and phenylacetic acid in CSF of schizophrenics and healthy controls.

Phenylethylamine (PEA) is an endogenous substance with amphetamine-like stimulant properties. On the basis of this ability an abnormal brain PEA metabolism has been proposed as an etiological factor in some forms of schizophrenia. In the present study 28 schizophrenic patients and 15 healthy controls were investigated. No significant difference from control values was found in PEA concentration in cerebrospinal fluid (CSF) of either untreated of neuroleptic-treated schizophrenics. However, 2 schizophrenics with highest BPRS scores had extremely high PES concentrations. Free phenylacetic acid (PAA), the major metabolite of PEA, was significantly decreased in ummedicated but not in drug-treated schizophrenics. Because of the assumed neuromodulatory properties of PEA, it is suggested that lowered PAA concentrations and the tendency for PEA to be elevated may imply that altered central neurotransmission occurs in certain forms of schizophrenia.

Adult↗
PubMed1983

Output of endogenous monoamine oxidase inhibitor in rats: effect of ethanol, tryptamine and tryptophan.

Contrary to prediction, loading rats with tryptamine, tryptophan or methanol failed to produce any rise in endogenous monoamine oxidase inhibitor output, whilst ethanol administration resulted in a significantly decreased excretion. These findings, which provide no support for the hypothesis that the inhibitor is a beta-carboline, may shed some light on the tranquilizing effect of ethanol in man.

Animals↗
PubMed1983

Platelet phenolsulphotransferase activity in Parkinson's disease.

Mean platelet phenolsulphotransferase activity was significantly increased in L-dopa-treated parkinsonian patients compared with controls. The degree of rise was associated with dose of and duration of treatment with L-dopa and may thus represent an adaptive increase to circulating dopamine. Alternatively, the increase may reflect changes supervening with duration of illness.

Age Factors↗
PubMed1983

Human platelet phenolsulphotransferase M and P: substrate specificities and correlation with in vivo sulphoconjugation of paracetamol and salicylamide.

Human platelet phenolsulphotransferase exists in two functional forms. M and P. In this study the substrate specificity of the two forms has been further delineated by correlating activities in different individuals with various substrates. m-Tyramine, noradrenaline, adrenaline, 5-hydroxytryptamine, p-hydroxyamphetamine, isoprenaline, salbutamol and l-naphthol were all specific substrates for the M form of the enzyme. Paracetamol, a mixed substrate, was predominantly metabolized by the M form. Salicylamide at 5 microM was a substrate for the P form but became and M substrate at higher concentration. Phenol itself, a specific substrate for phenolsulphotransferase P at 10 microM, also became an M substrate at 1 mM concentration. These substrate specificities were confirmed with the selective inhibitor, dichloronitrophenol. In this study, we measured phenolsulphotransferase activity in platelets from 13 individuals selected on the basis of their wide variation in ability to sulphoconjugate paracetamol and salicylamide in vivo. There was no significant relationship between the in vivo pattern with either drug and the activity of platelet phenolsulphotransferase assayed with paracetamol or salicylamide respectively.

Acetaminophen↗
PubMed1983

Tyramine-induced noradrenaline release from rat brain slices: prevention by (-)-deprenyl.

Clorgyline (1 and 10 microM) and (+)-deprenyl (10 microM) both significantly potentiated the tyramine (100 microM)-induced release of [3H]-noradrenaline from rat cerebral cortex slices. (-)-Deprenyl (50 microM) significantly reduced it, while lower concentrations had no effect on noradrenaline release. However, in combination, 1 microM (-)-deprenyl blocked the release-facilitating action of 1 microM clorgyline, and 10 microM (-)-deprenyl that of 10 microM (+)-deprenyl. Low concentrations of (+)- and (-)-deprenyl (1 and 10 microM), both selectively inhibited phenylethylamine oxidation by monoamine oxidase B. Higher concentrations of (-)-deprenyl (20 and 50 microM) also inhibited 5-hydroxytryptamine oxidation by monoamine oxidase A. Clorgyline (1 and 10 microM) inhibited both enzymes. Thus, the effects of these drugs on noradrenaline-release cannot be explained solely in terms of irreversible inhibition of monoamine oxidase A and B, and other possible mechanisms are discussed. If the brain-slice model faithfully mirrors the sequence of events manifesting peripherally as the tyramine hypertensive response ('cheese effect'), then it is possible that low doses of (-)-deprenyl, administered with antidepressant monoamine oxidase inhibitors, can prevent this adverse reaction.

Animals↗
PubMed1983

Pressor sensitivity to tyramine in patients with headache: relationship to platelet monoamine oxidase and to dietary provocation.

The pressor responses to oral and intravenous tyramine were not different from controls in migrainous patients with or without a history of attacks triggered by foods. However, patients who reported a dietary trigger were more likely to develop headache after tyramine administration than those without such a dietary history. Pressor responses to intravenous tyramine in patients with cluster headache were indistinguishable from controls. A group of five males with platelet monoamine oxidase activity one standard deviation or more below that of male controls required less intravenous tyramine to raise blood pressure by 30 mm Hg than males with monoamine oxidase levels within one standard deviation of the controls. This finding suggests that platelet monoamine oxidase activity to some extent reflects that of total body monoamine oxidase A plus B.

Administration, Oral↗