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Biomedical subjects

B D Jones

Publications and source records attributed to B D Jones.

At least 109 records · Page 6Linked to original sources
PubMed1981

Lack of tolerance to long-term neuroleptic treatment in dopamine tuberoinfundibular system.

The plasma prolactin (PRL) levels of 35 chronic schizophrenic patients undergoing long-term maintenance treatment with neuroleptic drugs were measured before and after either neuroleptic withdrawal or a switch to a fixed dose of chlorpromazine 900 mg/day. In both men and women there tended to be a significant correlation between the initial log plasma PRL level while on neuroleptic maintenance treatment and the dosage received converted to chlorpromazine equivalents. Neuroleptic withdrawal in ech of 19 cases was followed by a decline in PRL plasma levels. Switching to chlorpromazine 900 mg/day (16 cases) produced either increases or decreases in PRL plasma levels that were significantly correlated with the change in neuroleptic dosage converted to chlorpromazine equivalents. Thus there was no evidence of tolerance to the PRL-elevating effect of neuroleptics in these patients who had been treated for many years with neuroleptics.

Adult↗
PubMed1980

Neuroleptic-induced supersensitivity psychosis: clinical and pharmacologic characteristics.

Tardive dyskinesia is thought to result from neostriatal dopaminergic receptor supersensitivity induced by chronic treatment with neuroleptics. The authors suggest that dopaminergic supersensitivity also occurs in the mesolimbic region after chronic neuroleptic exposure, resulting in the development of a supersensitivity psychosis. Neuroleptic-induced supersensitivity psychosis is illustrated by data from 10 patients that demonstrate the syndrome's clinical and pharmacologic characteristics. An implication of neuroleptic-induced mesolimbic supersensitivity is that the tenaency toward psychotic relapse in such patients is determined by more than just the normal course of the illness.

Acute Disease↗
PubMed1979

Evidence of brain dopamine deficiency in schizophrenia.

It is proposed that the increased dopamine function suggested by the dopamine hypothesis of schizophrenia is a dopaminergic postsynaptic receptor supersensitivity resulting from a dopamine deficiency. In support of this, three double-blind controlled studies conducted on drugs which alter brain dopaminergic activity in a manner different from that of classic neuroleptics are reported. 1) alpha-methyldopa-neuroleptic interaction proved efficacious for schizophrenic positive symptoms but only on a short-term basis. 2) Rubidium improved negative symptoms rapidly, and in contrast has a late onset of action on positive symptoms of schizophrenia. 3) Tryptophan-benserazide was efficacious in controlling both negative and positive symptoms of schizophrenia (although less so than chlorpromazine). It is concluded that currently accepted modes of pharmacological therapy (classical neuroleptics) are in the short-term controlling the dopamine supersensitivity secondary to a deficiency, but contributing in the long-term to increase the dopamine deficiency, and so exacerbate the supersensitivity. More effective forms of treatment may involve the use of agents which alter dopamine activity without inducing dopamine supersensitivity.

Benserazide↗
PubMed1979

Laryngeal tuberculosis: a case report.

A case of laryngeal tuberculosis, in a 21-year-old female, is presented. The pathophysiology and natural course of the disease are discussed. The incidence of apical tuberculosis and associated laryngeal spread is noted.

Adult↗
PubMed1979

Diagnosis and treatment of peritonitis caused by a larval cestode Mesocestoides spp., in a dog.

Infection of the peritoneal cavity with cestode larvae, presumptively diagnosed as tetrathyridia of the genus Mesocestoides, was found by exploratory celiotomy in a dog with clinical signs consisting of episodic anorexia, vomiting, and depression. Lymphopenia and hypoalbuminemia were associated clinicopathologic abnormalities. Dystrophic calcification and midline duodenal displacement were found on abdominal radiographs. Therapy with mebendazole was instituted after recurrence of the initial episodic clinical signs postoperatively. Daily use of mebendazole for intermittent periods of up to 3 months led to remission of gastrointestinal signs for 30 months. However, 17 months after the initial diagnosis, infection of the vaginal tunic of the testicle with similar cestode larvae necessitated castration and removal of the vaginal tunic to the inguinal ring. Mebendazole therapy was reinstituted and continued for 31/2 months postoperatively. The dog was free of clinical signs of infection during and for the 16 months since this period of treatment.

Animals↗
PubMed1978

Death attributed to ventricular arrhythmia induced by thioridazine in combination with a single Contac C capsule.

Phenothiazines are known to produce electrocardiographic repolarization abnormalities. Thioridazine and mesoridazine appear to induce such changes more frequently than other neuroleptics and are also known to induce fatal ventricular arrhythmia. The woman described in this article died after taking her usual dose of thioridazine, 100 mg/d, in combination with a single capsule of Contac. C, a decongestant-antihistamine containing phenylpropanolamine and chlorpheniramine. Phenylpropanolamine, an ephedrine-like drug, was thought to have favoured the initiation by thioridazine of the ventricular arrhythmia that led to the woman's death. It is therefore suggested that ephedrine-like medications not be given to patients receiving thioridazine.

Adult↗
PubMed1977

Disseminated intravascular coagulation complicating aflatoxicosis in dogs.

An outbreak of chronic liver disease was investigated in a kennel of dogs. Anorexia, depression, polyuria, polydipsia, icterus and a terminal hemorrhagic diathesis were noted in clinically affected dogs. Thrombocytopenia, hypofibrinogenemia, elevated fibrinogen degradation products and prolonged activated partial thrombosplastin times (PTT) and one-stage prothrombin times (PT) were associated with the hemorrhagic crisis. Aflatoxicosis was confirmed by the presence of significant levels of aflatoxicosis was confirmed by the presence of significant levels of aflatoxin B in the commercial dog food being fed. A subacute hepatitis was found on necropsy. Disseminated intravascular coagulation was suspected as the cause of the hemorrhage in these cases and treatment was instituted.

Aflatoxins↗
PubMed1977

Mycotoxins in foods and feeds. Their occurrence and significance.

In 1973, TPI carried out a world-wide survey to ascertain the data available on aflatoxin contamination of food and feedingstuffs (JONES, 1975). Considerable interest was shown in this work which led us to attempt a similar exercise to determine the situation with respect to mycotoxins generally. It was felt that there was a need for this information which was not immediately available. Questionnaires were distributed to as many organizations as possible and the replies evaluated. The data obtained gives only general indications of the current situation, but it is feld that this information will be of use to those concerned with the subject of mycotoxins.

Africa↗