Biomedical subjects
Publications and source records attributed to W E Ballinger.
A case of acute nontraumatic rhabdomyolysis in a heroin addict is described. In addition to respiratory failure, the patient's course was complicated by life-threatening arrhythmias and electrocardiographic changes compatible with primary cardiac involvement. This case suggests that rhabdomyolysis may involve cardiac muscle on rare occasions.
We hypothesize that chronic alcohol abuse results in a loss of neurons and their associated synaptic receptors. This encephalopathy may be a precursor of brain atrophy and end-stage dementia. Autopsies were performed on normal brains of 27 alcoholics (mean age 62.5) and 30 nonalcoholic matched controls (mean age 64.4) free of other brain and liver diseases. None had recently received benzodiazepine medications. Gross brain atrophy was slight and equal in both groups. Benzodiazepine receptor densities and affinities in homogenates of frontal cortex were determined using [3H]flunitrazepam. Bmax specific binding was reduced by 20% in alcoholics compared with nonalcoholic controls of comparable age and with similar death-autopsy time intervals. The affinity was slightly less in the alcoholics. Wet tissue brain protein concentrations and their yields of 50,000-g pellet proteins were similar. Aging, death-autopsy time intervals, pneumonia and chronic obstructive pulmonary disease (diseases usually associated with hypoxia) had no significant effect on brain proteins, receptor densities, or affinities. We conclude that chronic alcoholism is associated with a loss of benzodiazepine receptor densities. Alcohol abuse may affect the results of post-mortem neurochemical investigations of other diseases.
Thiamine deficiency (Wernicke-Korsakoff's disease) may not be the only mechanism whereby chronic alcohol abuse affects the brain and not all alcohol-related changes may be evident morphologically. The purpose of this study was to determine if alcohol abuse affects muscarinic cholinergic and benzodiazepine receptors in the hippocampus of histologically normal brains obtained at autopsy in a general hospital population. Because patients were excluded who had significant brain atrophy and/or dementia severe enough to require institutionalization, the reported findings are presumed to be early changes in the development of an alcohol encephalopathy. In addition, patients were excluded from this study if they had clinical brain diseases (including Wernicke's disease), died in coma, had liver disease, or received medications that could potentially alter receptor binding. The reported changes in receptor binding were therefore presumed to be related to alcohol abuse per se and not an alcohol-associated condition. We found that muscarinic cholinergic synaptic receptor density determined with 3[H] quinuclidinyl benzilate was decreased by 30% in homogenates of the hippocampus of 25 alcohol abusers compared with 25 matched nonalcoholic controls. Similarly, densities of benzodiazepine receptors determined with 3[H] flunitrazepam were also decreased by approximately 30% in alcohol abusers. The affinities of both receptor types were not affected by alcohol abuse. Age and death-autopsy time interval had no significant effects on either wet tissue protein concentrations, yields of protein after centrifugation, or receptor binding. The contributions of age and time interval were each less than 2% of the total variance of protein concentrations and receptor binding.(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this investigation was to test the hypothesis that chronic exposure to alcohol may accelerate Alzheimer's disease (AD), either by independently adding receptor losses or by accelerating the AD disease process itself. Muscarinic [3H]quinuclidinyl benzilate and benzodiazepine [3H]-flunitrazepam receptor binding in homogenates of human autopsy brains were determined in four nonalcoholic and seven alcoholic AD brains and in histologically normal brains from 20 alcoholics and 20 nonalcoholics. Muscarinic binding was decreased in alcoholic AD compared with nonalcoholic AD in the parahippocampal region of frontal cortex, premotor temporal cortex, and amygdala, but not in the hippocampus. Benzodiazepine receptors were lost from the temporal cortex and amygdala, but the difference in the amygdala was not statistically significant. Plaque counts considered a marker of the severity of AD were not increased in the brains of alcoholics compared with nonalcoholics. Larger receptor losses in some alcoholic AD were associated with low plaque counts. Since all of these patients were severely demented, it is tentatively suggested that the receptor losses resulting from alcoholism may have contributed to the dementia in these AD patients.
A 65-year-old white woman developed progressive visuospatial abnormalities over an eight-year course, secondary to Alzheimer's disease with amyloid angiopathy. Imaging studies demonstrated focal atrophy of the parietal and occipital lobes without hemorrhage. This patient manifested simultagnosia without ocular dysmetria or optic ataxia; hence, a true Balint's syndrome was not present. Her visual acuities and fields have remained stable status post-occipital lobe biopsy.
Recovery and analysis of ancient tissue and bone of human origin has long been extensively investigated. Only recently, however, has it been technically possible to recover genetic material from ancient human and animal samples. As both previous studies involved dried tissue, it is important to determine whether other conditions may also preserve ancient tissue and genetic material. We describe here an analysis of preserved human bone and soft matter discovered in 1984-85 buried in a small swampy pond in central Florida. The recovered skeletal material represented a minimum of 40 individuals of both sexes and various ages. Corrected radiocarbon dates directly from bone and from peat matrix gave consistent ages in the range of 7,790 to 8,290 yr before present (BP). Nine individuals with intracranial soft matter were recovered and, in five of these, material recognizable as preserved or replaced brain tissue was present. Further analysis demonstrated gross anatomical features, remnant cellular structure and human DNA. As this find appears to be the oldest-known example of preserved human cell structure and DNA, it represents a significant resource for both anthropological and genetic studies.
Reports of melanotic nerve sheath tumors of Schwann cell origin are rare, only three having been found in the literature. Two new cases of spinal intradural melanotic nerve sheath tumors are reported and the literature is reviewed. Controversy has arisen in regard to the origin of melanin within these tumors. Electron microscopic study of one of our cases indicates that the Schwann cell is capable of producing melanin. The available evidence suggests that ultrastructural identification of the cell type in these pigmented tumors is essential in plotting the therapy and prognosis of patients with melanotic nerve sheath tumors.