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Biomedical subjects

J A Ball

Publications and source records attributed to J A Ball.

At least 37 records · Page 2Linked to original sources
PubMed1993

Magnetic resonance imaging in tonic spasms of multiple sclerosis.

Two cases of unilateral tonic spasm are described in which high signal lesions typical of demyelination were identified on magnetic resonance imaging in the contralateral cerebral peduncle. Both cases exhibited subtle upper motoneuron signs on the side of the tonic spasms that were exacerbated immediately following an attack. In one case, functional impairment of contralateral corticospinal pathways was demonstrated by delayed central motor conduction. These cases support the view that tonic spasms in multiple sclerosis are due to lesions within the corticospinal tract.

Adult↗
PubMed1993

Alien hand sign in association with Alzheimer's histopathology.

A 68 year old man is described with an alien left hand, cortical myoclonus, bilateral parietal lobe dysfunction and memory impairment but preserved language skills. The clinical diagnosis was of corticobasal degeneration but at necropsy, four years after the onset of symptoms, the pathology was of Alzheimer's disease together with some scattered chromatolytic pale neurons in the cerebral cortex. The alien hand sign has not previously been described in Alzheimer's dementia and is an illustration of the clinical heterogeneity that may occur in association with Alzheimer histopathology.

Aged↗
PubMed1989

Diazepam binding inhibitor-like immunoreactivity(51-70): distribution in human brain, spinal cord and peripheral tissues.

We have used a specific radioimmunoassay to describe the distribution of diazepam binding inhibitor-like immunoreactivity (DBI-IR(51-70) in human post-mortem tissues. In brain, highest concentrations were found in the cerebellum, amygdala, hippocampus, hypothalamus and substantia nigra. In the spinal cord, DBI-IR(51-70) was evenly distributed. In peripheral tissues, highest concentrations were found in the liver and kidney. Chromatographic analysis revealed several molecular forms of DBI-IR(51-70) the major form being of greater molecular weight and hydrophobicity than the synthetic fragment peptide. In peripheral tissues, but not in the CNS, a small peak of immunoreactivity was indistinguishable from the synthetic peptide. DBI-IR(51-70) is therefore widespread, but tissue processing may be different.

Aged↗
PubMed1988

Increase in diazepam binding inhibitor-like immunoreactivity (51-70) in Huntington's disease.

In Huntington's disease (HD), reduction in striatal GABA is one of the most striking abnormalities and alterations in benzodiazepine receptors, which are allosterically linked to the GABAA receptor, have also been reported. Diazepam binding inhibitor (DBI), recently isolated from rat and human brain, has been proposed as an endogenous ligand at the benzodiazepine receptor. The content of DBI-like immunoreactivity(51-70) (DBI-IR(51-70), has therefore been compared in control postmortem human brains and in HD brains (matched for age, sex and post-mortem delay), using a specific radioimmunoassay. DBI-IR(51-70) was more than 1.5-fold increased in the putamen, caudate, globus pallidus and nucleus accumbens of HD brains compared to the control group (P less than 0.001). Gel filtration chromatography showed similar elution profiles of the peptide in both control and HD extracts, thus providing no evidence for a change in the nature of the peptide itself.

Aged↗
PubMed1988

The effect of cholinergic blockade on the growth hormone response to galanin in humans.

The effect of cholinergic blockade with pirenzepine or atropine on growth hormone (GH) release after galanin administration was investigated in five normal male subjects. The mean peak GH response to an infusion of galanin (40 pmol/kg/min for 40 minutes) was significantly reduced from 17.2 mU/L to 2.9 mU/L (P less than .001) with prior administration of pirenzepine (30 mg IV). When galanin was infused at a higher dose (80 pmol/kg/min), this suppression of release by pirenzepine was partially overcome, with GH rising to a mean peak response of 8.0 mU/L (P less than .05). Repeated administration of atropine (two bolus doses of 0.6 mg IV) also failed to abolish the GH response to this higher dose of galanin in two subjects. It has been proposed that cholinergic pathways control GH release via somatostatin, and this study suggests that galanin may also act by modulating hypothalamic somatostatinergic tone either directly or by facilitating cholinergic transmission.

Adult↗
PubMed1988

Potent and comparable vasodilator actions of A- and B-calcitonin-gene-related peptides on the superficial subcutaneous vasculature of man.

1. Vasoactivity of human A- and B-calcitonin-gene-related peptides was studied in normal subjects, using reflectance plethysmography to measure relative changes in blood flow produced by superficial subcutaneous injections of the peptides. 2. Injection of 10(-11) mol of either peptide caused an immediate 200% increase in local blood flow and prolonged hyperaemia lasting up to 3 h. The hyperaemic response to 10(-13) mol of each peptide was significantly (P less than 0.01) smaller and shorter in duration than that elicited by 10(-11) mol of the same peptide, and 10(-15) mol of both peptides produced no hyperaemia other than that attributable to needle insertion alone. 3. At all three dosages examined, there were no significant differences between A- and B-calcitonin-gene-related peptides in magnitude or time course of the hyperaemic response. 4. Human A- and B-calcitonin-gene-related peptides are therefore potent vasodilators in man, causing comparable dose-related vasodilatation in the superficial tissues.

Adolescent↗
PubMed1988

Effect of nivazol in Nelson's syndrome.

We report the use of nivazol in a patient with Nelson's syndrome. Nivazol was highly effective in reducing ACTH secretion but, contrary to reports of its use in other primates, in our patient nivazol did have systemic glucocorticoid effects.

Adrenocorticotropic Hormone↗
PubMed1988

Galanin abolishes the inhibitory effect of cholinergic blockade on growth hormone-releasing hormone-induced secretion of growth hormone in man.

In five healthy normal male volunteers, pretreatment with the cholinergic muscarinic antagonist pirenzepine (30 mg i.v.) almost abolished the growth hormone (GH) response to a maximal dose (120 micrograms i.v.) of growth hormone-releasing hormone (GHRH) (GH response at 40 min 5.6 + 1.3 mU/l with GHRH and pirenzepine vs 40.8 +/- 5.3 mU/l with GHRH alone, P less than 0.02). Concomitant i.v. infusion of galanin (40 pmol/kg/min) with pirenzepine not only restored but significantly potentiated the GH response to GHRH (GH at 40 min 72.2 +/- 10.5 mU/l, P less than 0.001 vs GHRH and pirenzepine, P less than 0.02 vs GHRH alone). Previous studies have proposed that cholinergic pathways control GH release via somatostatin and this study suggests that galanin may act by modulating hypothalamic somatostatinergic tone either directly or, possibly, by facilitating cholinergic neurotransmission.

Adult↗
PubMed1987

Neuromedin N: presence and chromatographic characterization in the rat.

The distribution of neuromedin N and its structurally related peptide, neurotensin, was investigated in the rat and found to be remarkably similar with highest concentrations in the ileum. However, neuromedin N but not neurotensin was found in the kidney. Chromatographic analysis of immunoreactive neuromedin N demonstrated a single peak of immunoreactivity which was distinguishable from the single peak of immunoreactive neurotensin. Neuromedin N is likely to be a naturally occurring peptide and is distinct from neurotensin in rat peripheral tissues.

Animals↗
PubMed1986

Octadecaneuropeptide, benzodiazepine ligand, -like immunoreactivity in rat central nervous system, plasma and peripheral tissues.

Using a specific radioimmunoassay we have investigated the distribution of octadecaneuropeptide (a putative endogenous ligand at the benzodiazepine receptor)-like immunoreactivity (ODN-IR) in rat brain and peripheral tissues. Highest concentrations in brain were found in the hypothalamus, cerebellum and substantia nigra. Significant concentrations of ODN-IR were found in all peripheral tissues studied and in plasma. Chromatographic analysis revealed several molecular forms; one major form, indistinguishable from the synthetic peptide, was found predominantly in peripheral tissues and in plasma, while another major form, of higher molecular weight, was found in brain, peripheral tissues and plasma. Although ODN-IR was present in the synaptosomal fraction, concentrations in the microsomal fraction were higher than for other neuropeptides studied.

Animals↗
PubMed1986

Effective and lasting growth-hormone suppression in active acromegaly with oral administration of somatostatin analogue SMS 201-995.

Oral administration of the long-acting somatostatin analogue, SMS 201-995 (Sandoz), was assessed in five patients with active acromegaly, four of whom had not responded to pituitary irradiation. Doses of 4-8 mg three times daily lowered mean 24 h growth-hormone concentrations by over 50% in every case, with suppression to below 10 mU/l for several hours after the morning dose. Despite effective suppression of serum insulin levels, deterioration in glucose tolerance was very slight, and the drug had no side-effects. Orally administered SMS 201-995 avoids the need for multiple daily injections and is potentially valuable in the medical treatment of acromegaly.

Acromegaly↗
PubMed1982

Microscopic colitis-a cause of chronic watery diarrhoea.

Six patients with severe watery diarrhoea were found to have microscopic total colitis. None had any abnormality detectable by conventional tests used to diagnose inflammatory bowel disease-namely, barium radiology and endoscopy. The diagnosis could only be made by microscopic examination of biopsy specimens from the apparently normal colon. Anaemia, raised erythrocyte sedimentation rate, hypokalaemia, and hypoalbuminaemia were common findings. Small-bowel function was normal in all, though three patients had jejunal lesions of uncertain relevance but seemingly unrelated to the diarrhoea. The five patients given anti-inflammatory drugs showed a satisfactory response with improvement of the diarrhoea and colonic inflammation and return to normal of the abnormal laboratory findings. Microscopic colitis is responsible for a proportion of cases of intractable diarrhoea of obscure origin and rectal and colonic biopsies sould be undertaken in such cases.

Adult↗