Localized argyria: a complication of the repair of inguinal hernia with silver filigree.
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Argyria↗
Biomedical subjects
D W Ellison
Publications and source records attributed to D W Ellison.
Neurocytoma/lipoma (neurolipocytoma) of the cerebellum.
We describe a unique tumour that was removed from the posterior fossa of a woman aged 50 years. It was characterized histologically by bland, oval cells with fibrillary cytoplasm and by small groups of lipocytes. Immunocytochemical studies demonstrated expression of synaptophysin, neuron specific enolase and PGP 9.5, but a few cells also expressed glial fibrillary acidic protein and desmin. The combination of neuroectodermal and mesodermal features in this tumour is discussed in relation to primitive neuroectodermal tumours and neurocytoma.
Cerebellar Neoplasms↗
Ocular melanomas in xeroderma pigmentosum.
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Adult↗
Expression of the p53 protein in a spectrum of astrocytic tumours.
Many human cancers are characterized by mutations of p53, a nuclear phosphoprotein which controls elements of the cell cycle. Turnover of p53 in normal cells is rapid, and the minute quantities of protein that are usually present are not detected by immunocytochemical methods. Mutations of the p53 gene in tumour cells are associated with a slower turnover and subsequent accumulation of the protein in both nucleus and cytoplasm. Genetic abnormalities of the short arm of chromosome 17, which is the site of the p53 gene locus, are a feature of astrocytic tumours. Using a panel of five antibodies to p53 and a standard immunocytochemical method, we found detectable quantities of p53 in the cells of 3/16 diffuse astrocytomas, 8/14 anaplastic astrocytomas, and 24/34 glioblastoma multiforme. Progression of one patient's tumour from a diffuse to an anaplastic astrocytoma was characterized by the accumulation of p53. The more malignant histological features of anaplastic astrocytoma and glioblastoma multiforme appear to be reflected by a greater incidence of p53 accumulation.
Astrocytoma↗
Cellular schwannoma of the vagina.
Schwannomas of the female genital tract are rare, and an example in the vagina has not previously been reported. The case of a 37-year-old woman with a cellular schwannoma of the vagina is described and is accompanied by a review of schwannomas in the female genital tract.
Adult↗
Forecasting the prognosis of a patient with a tumour.
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Astrocytoma↗
Neurochemical characteristics of aluminum-induced neurofibrillary degeneration in rabbits.
Aluminum-induced neurofibrillary degeneration in rabbits is known to affect particular populations of neurons. The neurotransmitter alterations which accompany aluminum neurofibrillary degeneration were examined in order to assess how closely they mimic those of Alzheimer's disease. There was a significant reduction in choline acetyltransferase activity in entorhinal cortex and hippocampus as well as significant reductions in cortical concentrations of serotonin and norepinephrine in the aluminum-treated rabbits. Significant reductions in glutamate, aspartate and taurine were found in frontoparietal and posterior parietal cortex. Concentrations of GABA were unchanged in cerebral cortex. Both substance P and cholecystokinin immunoreactivity were significantly reduced in entorhinal cortex but there were no significant changes in somatostatin, neuropeptide Y and vasoactive intestinal polypeptide. The five neuropeptides were unaffected in striatum, thalamus, cerebellum and brainstem. Neurochemical changes were found in the regions with the most neurofibrillary degeneration while regions with little or no neurofibrillary degeneration were unaffected. The reductions in choline acetyltransferase activity, serotinin and noradrenaline suggest that some neuronal populations preferentially affected in Alzheimer's disease are also affected by aluminum-induced neurofibrillary degeneration; however, the cortical somatostatin deficit which is a feature of Alzheimer's disease is not replicated in the aluminum model.
Aluminum↗
Clinical features and consequences of seizures due to cyclic antidepressant overdose.
The charts of 30 patients with seizures caused by cyclic antidepressant toxicity were reviewed to determine the natural history of these seizures and their effect on outcome. Mortality was 10%. Onset of seizures was within 1.5 hours of admission in all but two patients. Both patients with seizures occurring later than 1.5 hours had also ingested ethanol. Antecedent mental status did not predict the occurrence of seizures; 23% of seizures occurred when patients were alert. The majority of patients (25 of 30) had one or two brief (less than 2 minute), self-limited, generalized, tonic/clonic seizures that terminated without anticonvulsant therapy. Six patients had prolonged or repetitive seizures. Most seizures, even when multiple or sustained, had no sequela. However, four patients developed marked cardiovascular deterioration immediately following seizures, with hypotension and ventricular tachycardia or bradyarrhythmias. All four had a QRS duration greater than 200 msec at some time during their hospitalization. It is concluded that most seizures associated with cyclic antidepressant toxicity occur soon after admission, are brief, and terminate without specific anticonvulsant therapy. Even when brief, however, seizures may occasionally lead to abrupt cardiovascular deterioration and death. It is not clear which patients are at risk for severe cardiovascular complications.
Adolescent↗
Somatostatin and neuropeptide Y concentrations in pathologically graded cases of Huntington's disease.
Somatostatin and neuropeptide Y concentrations have previously been reported to be increased in the basal ganglia in Huntington's disease (HD). In the present study we have extended these findings by examining both somatostatin-like immunoreactivity (SLI) and neuropeptide Y-like immunoreactivity (NPYLI) in cases of HD, which were graded according to the severity of pathological degeneration in the striatum. In addition, we surveyed a large number of subcortical nuclei and cortical regions for alterations. Both SLI and NPYLI were significantly increased about threefold in the caudate, putamen, and the nucleus accumbens. Increases in mild and severe grades were similar, which is consistent with a relative but not absolute sparing of striatal aspiny neurons in which somatostatin and neuropeptide Y are colocalized. Significant increases of NPYLI were also found in the external pallidum, subthalamic nucleus, substantia nigra compacta, claustrum, anterior and dorsomedial thalamus, bed nucleus of the stria terminalis, and locus ceruleus. SLI was significantly increased in the external pallidum, red nucleus, and locus ceruleus. Measurements of both neuropeptides were made in 24 regions of the cerebral cortex. Significant increases in both NPYLI and SLI were found in the frontal cortex (Brodmann areas 6, 8, 9, 10, 11, and 45) and temporal cortex (Brodmann area 21), whereas NPYLI was also increased in Brodmann areas 12, 20-22, 25, and 42. Alterations in the cerebral cortex were as pronounced in cases with mild striatal pathological changes as in those with severe striatal pathological changes. These alterations may occur early in HD and could reflect a selective sparing of somatostatin-neuropeptide Y cortical neurons combined with cortical atrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
A detailed examination of substance P in pathologically graded cases of Huntington's disease.
Substance P concentrations have been found to be reduced in the basal ganglia in Huntington's disease (HD). In order to further examine this finding in the present study we measured substance P-like immunoreactivity (SPLI) in cases of HD which had been graded as to the severity of pathological changes in the striatum. Marked significant reductions of SPLI were found in all striatal nuclei which were significantly correlated with the percentage of neuronal loss in the varying pathologic grades. Similar changes were found in the projection sites of striatal substance P neurons, the globus pallidus interna and the substantia nigra. These changes are consistent with a loss of striatal substance P containing projection neurons in HD. Significant reductions in SPLI were also found in the external pallidum, bed nucleus of the stria terminalis and the subthalamic nucleus. Small significant increases in SPLI (20-30%) were found in 3 frontal cortical regions (Brodmann areas 6, 8 and 9). The finding of neurochemical changes in the subthalamic nucleus is of particular interest since lesions in this nucleus are known to result in chorea and therefore might contribute to the chorea which is a cardinal symptom of HD.
Aged↗
Phosphoethanolamine and ethanolamine are decreased in Alzheimer's disease and Huntington's disease.
Measurements of both phosphoethanolamine (PEA) and ethanolamine (EA) were made in postmortem brain samples from patients with Alzheimer's disease (AD) and Huntington's disease (HD) using high-performance liquid chromatography with electrochemical detection. In AD levels of PEA were significantly reduced by 64% in temporal cortex, 48% in frontal cortex and 40% in hippocampus. In HD concentrations of PEA were significantly reduced by 76% in the caudate, 53% in putamen and 48% in the nucleus accumbens. EA concentrations showed similar but smaller reductions in both diseases. Both PEA and EA are involved in phospholipid metabolism and can be released with depolarizing stimuli in some circumstances. Since two diverse neuropathologic processes can result in depleted levels of both amines in their respective regions of pathologic predilection, it is likely that the depletions accompany neuronal death.
Aged↗
Subset of neurons characterized by the presence of NADPH-diaphorase in human substantia innominata.
The substantia innominata encompasses an area of the basal forebrain that is ventral to the lenticular nucleus and anterior commissure, medial to the claustrum and external capsule, and lateral to the hypothalamus. The nucleus basalis of Meynert consists primarily of large acetylcholinesterase (AchE)-positive neurons embedded within the substantia innominata. Damage to these neurons may be important in the pathogenesis of cortical dysfunction in Alzheimer's disease. In order to characterize other neuronal elements in the substantia innominata and their relationship to the nucleus basalis, we chose to study a biochemically distinct neuronal subset containing the enzyme nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d). The substantia innominata was blocked from six normal brains obtained postmortem and fixed in neutral-buffered formalin at 4 degrees C for 48 hours. Free-floating 50-micron sections from several levels were stained for NADPH-d or AchE activities. Selected sections were double stained for NADPH-d and AchE. NADPH-d activity was present in a network of pleomorphic neurons that extended through all levels of the substantia innominata and into the striatum and amygdala. NADPH-d neurons were particularly numerous at the level of the anterior commisure and were closely associated with the cholinergic neurons of the nucleus basalis. They were not seen in the ventral pallidum, or the vertical limb of the diagonal band of Broca or in the islands of Calleja. The cell bodies of NADPH-d neurons were quite varied in shape, ranging from ovoid to fusiform, and about half the cells were bipolar. Where neuronal density was high, their dendrites formed an interlacing pattern. NADPH-d-positive fibres were seen coursing through the external capsule, hypothalamus, and amygdala. This novel set of neurons in the substantia innominata may be part of a more extensive network that interacts with the magnocellular basal forebrain system at the level of the nucleus basalis. Whether other neurotransmitters are present within these neurons and whether NADPH-d neurons are involved in Alzheimer's disease remain to be elucidated.
Aged↗
Amino acid neurotransmitters in postmortem human brain analyzed by high performance liquid chromatography with electrochemical detection.
In the present study we have developed a method of measuring putative neurotransmitter amino acids using high performance liquid chromatography (HPLC) with electrochemical detection. The assay had a sensitivity in the low pmol range and sample turnover time was 30 min. The postmortem stability of amino acids was examined in an animal model simulating human autopsy conditions. Aspartate concentrations increased 15% between 4 and 24 h postmortem while gamma-aminobutyric acid (GABA) concentrations rose 35% by 4 h but were stable thereafter. Glutamate and taurine were stable at all time points. The assay has been used to examine concentrations of neurotransmitter amino acids in 15 patients without neurological or psychiatric disease. Results agree well with previous work and knowledge of amino acid neurotransmitter pathways. The current technique provides a reliable method for the study of amino acid transmitter abnormalities in neurological illness.
Aged↗
Amino acid neurotransmitter abnormalities in Huntington's disease and the quinolinic acid animal model of Huntington's disease.
Concentrations of gamma-aminobutyric acid (GABA), glutamate, aspartate, and taurine were measured in postmortem tissue from the brains of patients with Huntington's disease (HD) and in the quinolinic acid (QA) lesioned rat striatum. The aim of the study was to assess further the ability of the QA model of HD to reproduce the neurochemical features of the disease. Nine cortical and 9 subcortical regions were examined from 17 pathologically graded cases of HD and 10 controls. Significant reductions in both GABA and glutamate were found in HD striatum. The reductions were greater in the more severely affected grades of HD, and there was a gradient of amino acid loss across the striatal nuclei (caudate greater than putamen greater than nucleus accumbens) which was consistent with the known pattern of pathological involvement. Taurine and aspartate concentrations showed no significant change. GABA reductions were found in both segments of the globus pallidus (external greater than internal) and both parts of the substantia nigra (reticulata greater than compacta). In advanced cases of HD, there were significant reductions in glutamate in Brodmann cortical areas 3-1-2, 6, 9, and 17, but GABA, aspartate, and taurine were unaltered in the cortex. The QA lesions reproduced the striatal deficits of both GABA and glutamate but, in contrast to HD, there was a decrease in taurine, possibly due to species differences. Chronic QA lesions resulted in a secondary dying back of corticostriatal glutamatergic terminals, but did not produce a change in cortical glutamate concentration. This suggests that reductions in cortical glutamate in HD may reflect a primary loss of glutamatergic neurons. Our findings extend previous observations on amino acid neurotransmitters in HD and, with the exception of taurine, confirm the general applicability of the QA model.
Amino Acids↗
The effect of neuropeptide Y on striatal catecholamines.
Neuropeptide Y and peptide YY were injected into rat striatum and their effects on dopamine, serotonin and their metabolites were examined at 1 h. Neuropeptide Y induced a dose-dependent increase in dopamine turnover in the ipsilateral striatum with no effect on serotonin turnover. When neuropeptide Y was coinjected with somatostatin there was an additive effect in increasing dopamine turnover. There was no alteration in striatal concentrations of gamma-aminobutyric acid, glutamate, or aspartate with either neuropeptide Y or somatostatin injections. These results suggest that neuropeptide Y may play a role with somatostatin in regulating striatal dopaminergic transmission.
3,4-Dihydroxyphenylacetic Acid↗
An examination of neuropeptide Y postmortem stability in an animal model simulating human autopsy conditions.
A rabbit antiserum to neuropeptide Y (NPY) was used to develop a radioimmunoassay for measuring NPY in brain tissue. By high-performance liquid chromatography, two peaks of immunoreactivity were detected in human postmortem cortex. A minor peak was seen at the void volume, while the majority of immunoreactivity comigrated with synthetic NPY standards. Using the Spokes-Koch rat model simulating human autopsy conditions, it was shown that cortical, hippocampal and striatal concentrations of NPY-like immunoreactivity are stable for up to 24 h.
Animals↗
A postmortem study of amino acid neurotransmitters in Alzheimer's disease.
Concentrations of putative neurotransmitter amino acids were measured in postmortem brains from 10 patients with Alzheimer's disease and 10 controls. Glutamate, aspartate, taurine, gamma-aminobutyric acid (GABA), and alanine levels were examined in 9 cortical regions, hippocampus, thalamus, and basal ganglia using high-performance liquid chromatography with electrochemical detection. There were no significant alterations in aspartate, taurine, or alanine levels in any of the regions examined. Widespread significant reductions in cortical GABA concentrations were observed in the Alzheimer's brains, with the largest decreases in the temporal lobe. Overall values for glutamate concentrations in temporal and frontal cortices showed a significant 12% reduction in Alzheimer's brains, but the only individual cortical region showing a significant reduction in glutamate was the inferior temporal gyrus. These results suggest that gamma-aminobutyric acidergic neurons in Alzheimer's cerebral cortex may be selectively vulnerable to the disease process.
Aged↗
Studies on the role of alpha 2-adrenoceptors in the control of synaptosomal [3H]5-hydroxytryptamine release: effects of antidepressant drugs.
The sensitivity of alpha 2-adrenoceptors on 5-hydroxytryptamine (5-HT) nerve endings obtained from rat cerebral cortex was investigated following treatment with the antidepressant drugs desipramine (10 mg/kg/day for 21-28 days) or clorgyline (1 mg/kg/day for 21-28 days). [3H]5-HT (100 nM) was used to load cortical synaptosomes (P2) after experiments with uptake inhibitors confirmed that this concentration of amine ensured exclusive uptake into 5-HT nerve terminals. The sensitivity of K+-stimulated release of [3H]5-HT to alpha 2-adrenoceptor occupancy was assessed in a superfusion system by means of the dose-dependent inhibition of [3H]5-HT release by clonidine. This is blocked by yohimbine (1 microM), which, when administered alone, enhances release, suggesting that endogenous catecholamines released from other synaptosomes act on these alpha 2-heteroreceptors. The effect of addition of citalopram (1 microM) to superfusates suggests that some reuptake of [3H]5-HT occurs during superfusion. Of the tritium released into superfusates during "background" and K+-stimulated release, 17 and 90%, respectively is [3H]5-HT. The attenuation of K+-stimulated release by clonidine is apparently diminished by the chronic clorgyline regimen but not by desipramine. However, clorgyline elevates catecholamine levels, and this might increase endogenous noradrenaline (NA) efflux, which by competition with clonidine could appear to alter alpha 2-adrenoceptor sensitivity. This possibility was investigated by depleting NA with the neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4). These studies showed that the apparent effect of chronic clorgyline on alpha 2-adrenoceptor sensitivity to clonidine was due to competition with increased levels of endogenous NA.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗