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Biomedical subjects

K D Barron

Publications and source records attributed to K D Barron.

At least 73 records · Page 4Linked to original sources

Marchiafava-Bignami disease.

Marchiafava-Bignami disease was diagnosed postmortem in a 39-year-old man who drank excessive amounts of white port wine. This is the fifth report of the disease in a native North-American with no Italian ancestry. The lesion involved the corpus callosum and hippocampal commissure but spared the anterior commissure, middle cerebellar peduncles, optic chiasm, and centrum semiovale. Wernicke-Korsakoff encephalopathy and pellagroid neuronal changes were also present.

Adult↗

Quantitative cytochemistry of RNA in axotomized feline rubral neurons.

One-sided lateral funiculotomy at the C-2 segment induced axon reaction in the contralateral red nucleus of adult cats. Two to 60 days postoperatively the animals were sacrificed and the mesencephalon was fixed in ethanol-acetic acid, 3:1. Ten micrometer paraffin sections including both red nuclei were stained for RNA with azure B after incubation in DNAse. Cytophotometric measurements of RNA content of neurons from the caudal 600-1000 micrometer of each red nucleus were made with a Zeiss Cytoscan system using an automatic scanning stage. In contrast to the heightened RNA synthesis that has been reported for axotomized peripheral (extrinsic) neurons, the axotomized central (intrinsic) neurons of the red nucleus showed no evidence of accumulation of cytoplasmic or nucleolar RNA. Rather depletion of cellular RNA occurred. Further indication of the regressive nature of rubral axon reaction derived from morphometric measurements that showed cytoplasmic, nuclear and nucleolar atrophy of the neurons of the red nucleus contralateral to operation with the exception of a possible transient cytoplasmic enlargement 9 days postoperatively. From the cytophotometric and morphometric data here reported we are led to suggest that the frequently observed failure of axonal repair in mammalian CNS results from the innately regressive nature of the axon reaction of many mammalian central neurons.

Afferent Pathways↗

Quantitative relationships of the fourth complement component in human cerebrospinal fluid.

A technique for the measurement of cerebrospinal fluid C4 concentration in unconcentrated specimens has been developed with the methods of electroimmunodiffusion and immunofixation. The method has proved to be reproducible and requires only microliter volumes of undiluted cerebrospinal fluid (CSF). The mean value for CSF C4 concentrations in 16 neurologically normal individuals was 325 +/- 32 mug/100 ml. A positive correlation between CSF C4 concentration and the concentration of CSF albumin and total protein was observed. The positive correlation between the concentrations of CSF C4 and albumin was, however, more clearly defined than the relationship of CSF C4 to total CSF protein.

Albumins↗

Incorporation of tritiated leucine by axotomized rubral neurons.

Fourteen kittens, 7--10 weeks of age, were injected with [3H]leucine 0.5--24 h before sacrifice 1--30 days after unilateral high cervical rubrospinal tractotomy. Histoautoradiographs of the red nuclei were prepared and counterstained with thionin. Axon reaction, evident histologically 24 h after surgery, was manifested by central chromatolysis or diffuse cytoplasmic chromophobia. Partial reversion toward a normal cytologic appearance was apparent 10--30 days postoperatively. Nucleolar and nuclear shrinkage and cytoplasmic atrophy were conspicuous accompaniments of axon reaction in rubral neurons. Expressed per cell the radioactivity of axotomized rubral nerve cells was consistently less than controls in animals surviving operation from 5 to 30 days. The data indicate that axon reaction in red nucleus is regressive in character and early associated with diminished protein synthesis. The frequently regressive nature of axon reaction in intrinsic neurons, such as those of red nucleus, probably is important in accounting for failure of regeneration of many mammalian CNS fiber tracts after injury.

Animals↗

Hemiplegic amyotrophy. Muscle and motor point biopsy study.

Thirty hemiplegic patients had simple muscle atrophy with reduced mean muscle cross sectional areas (predominantly type II fiber atrophy) and complex, multiple, or enlarged subneural apparatuses, many of which resembled subhuman endplates. Ultrastructural observations in a few patients revealed nonspecific responses of damage to sarcolemma and myofibrils. There was no correlation between structural changes and alteration of tone, sensory impairment, or site of lesion. We propose that hemiplegic amyotrophy results from a combination of disuse, loss of central "trophic" influence, and transsynaptic degeneration.

Hemiplegia↗

Ultrastructure of axonal reaction in red nucleus of cat.

Described here are ultrastructural changes in neurons of feline red nucleus exhibiting axon reaction after unilateral rubropsinal tratotomy at the C-2 level and surviving 2 to 65 days. Ultrastructural alterations included neurofilamentous hyperplasia; proliferation of smooth ER; temporary disappearance of organized granular ER with partial substitution by haphazardly arranged, broad cisternal profiles; loss of rosette ribosomes and occurrence of single ribonucleoprotein granules or an intercisternal amorphous density; increased numbers of subsurface cisterns and allied structures, often disposed in stacks; vesiculation and vacuolation of Golgi cisternae; prevalence of autophagic bodies derived in part from Golgi complexes; probable mitochondrial hyperplasia and various qualitative changes in these organelles; an increase in lipofuscin. Dendritic changes paralleled those of perikarya save that proliferation of subsurface cisterns and autophagic bodies was absent. Abnormalities of myelinated axons and boutons occurred and may have originated from retrograde degeneration of cortical neurons induced by lateral funiculotomy. Some perikarya were devoid of axosomatic boutons. Ultrastructural changes varied with the length of postoperative survival and were, at least partly, reversible. Chromatolysis was detectable light microscopically before ultrastructural abnormality appeared. The bearing of transneuronal mechanisms on axon reaction of central neurons and the protective effect of section of axons beyond the site of origin of collaterals are discussed.

Animals↗

Ultrastructural changes in dendrites of central neurons during axon reaction.

Retrograde atrophy of rat thalamus is marked by the appearance of profound alterations in dendrites. Concurrently, similar changes occur in parent cell somata. Electron-dense and abnormally electron-lucent dendritic profiles appear and are removed over different time courses. The morphologic features of the abnormal dendrites are detailed. Electron-dense and electron-lucent dendritic profiles are not observed in cat red nucleus after rubrospinal tractotomy. Rather, neurofilamentous hyperplasia and proliferation of smooth endoplasmic reticulum appear in affected dendrites and are identical to changes observable at the same time in the reacting parent nerve cells. The literature is reviewed and discussion is developed on the similarities of perikaryal and dendritic changes that occur in axon reaction and transneuronal degeneration.

Animals↗

Enzyme activity of human central nervous system myelin.

Following ultracentrifugation in sucrose and hypotonic exposure ('osmotic shock'), myelin fractions were prepared from homogenates of human centrum ovale obtained post-mortem. Non-specific esterase (NsE), succinic dehydrogenase and acid phosphatase activities were determined. One isolation procedure utilized aqueous sucrose solutions only. Other preparative technics involved addition of phosphate buffer (pH 6.6 or 8.0) or varying concentrations of calcium or magnesium ions to preparative media. The NsE activity of myelin increased greatly when electrolytes were included in these preparative solutions. Morphologic homogeneity and protein and lipid contents of myelin were similar whatever the isolation procedure.

Acid Phosphatase↗