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Biomedical subjects

S Fielding

Publications and source records attributed to S Fielding.

At least 37 records · Page 2Linked to original sources
PubMed1988

Initial experience with Tc-99m-HM-PAO in the study of brain tumors.

A preliminary study of the distribution of the 99mTc complex of hexamethylpropylene amine oxime (HM-PAO) in 12 patients with brain neoplasms before, during, and after radiotherapy has been performed. Untreated brain tumors were found to exhibit a range of 99mTc-HM-PAO uptake, varying from areas of markedly increased isotope activity to photopenic areas, when compared to normal brain tissue. A ratio of 99mTc-HM-PAO tumor uptake to contralateral normal tissue uptake was calculated prior to and during radiotherapy. This ratio tended to return towards unity in lesions responding to therapy. A predictable alteration in whole brain 99mTc-HM-PAO uptake during radiotherapy was not demonstrated. Unlike the radiolabeled amines, 99mTc-HM-PAO localizes in primary tumors, probably indicating that its uptake mechanism is independent of non specific amine receptors. 99mTc-HM-PAO may be useful in the study of brain tumor physiology and response to therapy.

Adult↗
PubMed1988

The biodistribution and pharmacokinetics of meta-iodobenzylguanidine in childhood neuroblastoma.

MIBG is generating considerable interest for the treatment of neuroblastoma. This study has investigated the biological variation in handling of the compound in children with neuroblastoma. The biodistribution of the compound has been characterised in children undergoing tracer administrations of 123I and 131I-mIBG. Estimates of hepatic and whole body radiation dose delivery have been made. The results indicate substantial interpatient variation in hepatic dose delivery. This organ may be critical in some patients undergoing targeted radiotherapy with mIBG.

3-Iodobenzylguanidine↗
PubMed1987

The response to DNA damage induced by 4-nitroquinoline-1-oxide or its 3-methyl derivative in xeroderma pigmentosum fibroblasts belonging to different complementation groups: evidence for different epistasis groups involved in the repair of large adducts in human DNA.

The data in this paper show that when the inhibition of growth is measured, xeroderma pigmentosum (XP) complementation groups A, G and D are very sensitive to 4-nitroquinoline-1-oxide (4NQO), whereas only XP groups G and D are very sensitive to 3-methyl-4NQO (3me4NQO). Cells belonging to XP-C group are not particularly sensitive to either agent. Thus there are different epistasis groups for the excision repair of DNA adducts induced by these agents as opposed to the repair of u.v. damage. DNA polymerase alpha is involved in the repair of 4NQO-induced lesions because aphidicolin blocks their repair. XP cells from all the above groups are defective to some extent in this repair. The degree of repair defectiveness follows that seen after u.v., with even the XP-C cell line used having reduced repair (despite the fact that the inhibition of growth by 4NQO in this cell line was not markedly different from normal). Aphidicolin did not induce breaks in the normal or XP cell lines exposed to 3me4NQO, thus the repair of lesions induced by 3me4NQO does not involve DNA polymerase alpha in any of the cell lines. Finally, catalase reduces the alkaline labile lesions induced by 4NQO, but not 3me4NQO, suggesting the latter agent does not induce substantial amounts of DNA damage by the generation of radicals.

4-Nitroquinoline-1-oxide↗
PubMed1984

Pharmacology of nomifensine: a review of animal studies.

Nomifensine has demonstrated efficacy in several animal models that have been found to be predictive of clinical antidepressant activity, and has also been found to have a low potential for both cardiovascular and anticholinergic side effects. A comparison of nomifensine's profile with those of standard antidepressant agents shows this drug to possess clear advantages which may make it an attractive choice for the treatment of endogenous depression.

Acetylcholine↗
PubMed1982

Comparison of the actions of trimethadione and chlordiazepoxide in animal models of anxiety and benzodiazepine receptor binding.

Trimethadione was compared with chlordiazepoxide for anti-anxiety activity in two behavioral tests known to predict the anxiolytic action of drugs. In the drug-discrimination test, male hooded rats were trained to discriminate the anxiogenic action of pentylenetetrazol from saline by responding for food reinforcement on one of two levers after treatment with pentylenetetrazol (1450 mumol/kg) and on the other lever after injection of saline. Pretreatment with either chlordiazepoxide (2.8-33 mumol kg) or trimethadione (559-2236 mumol/kg) prior to the injection of pentylenetetrazol, produced a dose-dependent antagonism of the anxiogenic stimulus. In the other test, male Wistar rats were trained to respond for milk reinforcement in a conflict procedure in which some of the reinforced responses resulted in the delivery of footshock. Treatment of these rats with chlordiazepoxide (17-67 mumol/kg) or trimethadione (1118-2236 mumol/kg) antagonized the footshock-induced suppression of responding. In a receptor binding study, trimethadione failed to inhibit flunitrazepam binding. These data suggest that trimethadione is an effective anxiolytic agent whose action does not directly involve benzodiazepine receptors.

Animals↗
PubMed1979

Antinociceptive activity of clonidine and its potentiation of morphine analgesia.

The activity of clonidine and its interaction with morphine was assessed in the mouse tail flick assay. In this assay, clonidine was found to be 10 times more potent than morphine. Clonidine potentiated morphine antinociceptive activity approximately five-fold and morphine potentiated clonidine activity four-fold. Clonidine's agonstic activity was not reversed by naloxone hydrochloride (10 mg/kg) while the potentiating effect of clonidine by morphine was. Tolerance to the antinociceptive effect of morphine was observed in morphine pellet-implanted mice but no cross tolerance was observed for clonidine. These data indicate that clonidine-induced analgesia is not a result of an interaction at morphine receptors; but rather, common pathway(s) are present which appear to complement the agonistic interaction of each.

Analgesics↗
PubMed1979

Pharmacology of anti-anxiety drugs with special reference to clobazam.

1 In several studies clobazam exhibited a potency which ranges between that of chlordiazepoxide and diazepam. Its anxiolytic and anti-aggression effects are produced by doses usually ranging below those that cause disorders in motor activity. 2 This separation was demonstrable to an even greater degree with the desmethyl metabolite. The activity of the metabolite, however, was weaker than that of the original substance. 3 The advantage of clobazam compared with the 1.4 benzodiazepines lies mainly in the fact that motor activity is influenced only after very high doses, these doses being markedly above those required to induce tranquillizing and anti-agression activities. 4 Clobazam has no marked effect on the cardiovascular system, respiration of excretion.

Aggression↗
PubMed1978

Synthesis of spiro[isobenzofuran-1(3H),4'-piperidines] as potential central nervous system agents. 4. Central nervous system depressants.

The synthesis of 1'-[3-(4-fluorobenzyoyl)propyl]-3-phenylspiro[isobenzofuran-1(3H),4'-piperidine] (2a) and eight halo and methoxy analogues is described. The compounds were generally more potent per os than chlorpromazine in the Sidman avoidance paradigm in rats and less potent than haloperido. 1'-[3-(4-Fluorobenzoyl)propyl]-3-(4-fluorophenyl)spiro[isobenzofuran-1(3H),4'-piperidine] (2e) approached the per os potency of haloperidol in this test and was shown to be active in inhibiting monkey avoidance also. Compound 2e was much less active than haloperidol in antagonizing apomorphine-induced emesis in dogs, apomorphine-induced stereotypy in rats, and amphetamine-induced circling in lesioned rats. This lack of nonselective, dopamine-receptor blocking effects makes 2e attrative as a potential neuroleptic.

Amphetamine↗
PubMed1978

A comparison of clonidine with morphine for antinociceptive and antiwithdrawal actions.

Clonidine was found to possess dose-dependent analgesic and antiwithdrawal activity. In mice, clonidine prolonged the tail flick latency and inhibited phenylquinone-induced writhing. In rats, it inhibited tail withdrawal from hot water and a pain response to pressure application on an inflamed paw. The effective doses of clonidine were different in the different tests employed, but they were always smaller than those of morphine. Naloxone failed to antagonize the analgesic actions of clonidine but effectively antagonized those of morphine. Phenoxybenzamine also did not alter the inhibition of tail flick-induced by clonidine. Clonidine suppressed morphine withdrawal body shakes in a dose-dependent manner as does morphine. This action of clonidine was not reversed by naloxone. In usual laboratory tests, clonidine appears to be an effective analgesic which antagonizes signs of morphine withdrawal.

Analgesics↗