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Biomedical subjects

L C Cork

Publications and source records attributed to L C Cork.

At least 109 records · Page 6Linked to original sources
PubMed1980

Biochemical characterization of the virus causing leukoencephalitis and arthritis in goats.

Goat leukoencephalitis-arthritis virus (GLV) has the density of a retrovirus in sucrose and contains an endogenous RNA-dependent DNA polymerase (reverse transcriptase). The virion reverse transcriptase utilizes the synthetic RNA template poly(rA). (dT)12 but not the synthetic DNA template poly(dA). (dT)12. A high mol. wt. RNA similar in size to visna virus RNA was isolated from 3H-uridine-labelled virions. The major structural protein of GLV has the same mol. wt. as that of visna virus. From these data the GLV appears to be a retrovirus.

Animal Diseases↗
PubMed1980

Exocytosis of residual bodies in a lysosomal storage disease.

Scanning and transmission electron-microscopic study of the livers of 2 kittens suffering from GM2 gangliosidosis revealed discontinuities in the plasma membrane of hepatocytes and Kupffer cells, indicating an attempt by the cells to free themselves of excess lysosomal residues by means of exocytosis. Inclusions morphologically similar to those seen in the hepatocytes were observed in the perisinusoidal space. Openings were seen on all surfaces of the hepatocytes. Such extrusion of lysosomal residues is an example of a mechanism rarely observed in viable metazoan cells.

Animals↗
PubMed1980

The pathogenesis of viral leukoencephalomyelitis-arthritis of goats. I. Persistent viral infection with progressive pathologic changes.

The pathogenesis of viral leukoencephalomyelitis of goats was studied in newborn and adult goats using purified, concentrated leukoencephalitis virus. The disease could be transmitted using purified leukoencephalitis virus or tissue suspensions from a goat experimentally infected with leukoencephalitis virus. As early as 1 week following inoculation, goats developed lesions in the brain, joint, and lung. Lesions persisted 8 to 21 months, were not age-dependent, and were inflammatory in character. In the brain they were accompanied by demyelination. Virus could be isolated from experimental goats by cocultivation of peripheral blood leukocytes and by explantation of tissues beginning a week after inoculation and throughout the life of the goat. These studies confirm that leukoencephalitis virus is the etiologic agent of leukoencephalitis-arthritis of goats and produces a persistent infection characterized by demyelinating encephalitis, progressive arthritis, and interstitial pneumonia.

Age Factors↗
PubMed1979

Hereditary spinal muscular atrophy in Brittany Spaniels: clinical manifestations.

A progressive neurologic disease was identified in a family of closely related Britanny Spaniel dogs. The disease developed in dogs less than 1 year old and characteristically resulted in paraspinal and proximal pelvic limb muscular atrophy. Neurologic examination, electrodiagnostic testing, and histologic studies indicated that the disease results from motor horn cell degeneration. A colony of affected dogs was established, and breeding studies incriminated an inherited basis for the disease.

Animals↗
PubMed1979

Hereditary canine spinal muscular atrophy.

Hereditary canine spinal muscular atrophy is a newly recognized motor neuron disease occurring in Brittany Spaniels. The clinical manifestations, pattern of inheritance, electrodiagnostic findings, and muscle biopsies have features in common with human spinal muscular atrophy. Neuropathological examination discloses some loss of motor neurons in the spinal cord and brainstem. Many of the surviving motor neurons have neurofibrillary swellings in proximal axons, an abnormality similar to that which occurs early in the course of human amyotrophic lateral sclerosis. These axonal swellings are filled with maloriented skeins of neurofilaments. Since the proteins comprising neurofilaments are carried by slow axonal transport, their accumulation within axons suggest that the swellings may result from impaired slow transport, a hypothesis that can be tested in affected Brittany Spaniels. Hereditary canine spinal muscular atrophy is a new genetic, clinical, and pathological entity, and, at present, it appears to be the best currently available animal model of motor neuron disease.

Animals↗
PubMed1978

The pathology of feline GM2 gangliosidosis.

An 11-week-old and a 6-month-old kitten with feline GM2 gangliosidosis and deficiency in both A and B isoenzymes of beta-D-N-acetyl hexosaminidase were studied by light transmission (TEM), and scanning electron microscopy (SEM). Neurons throughout the nervous system contained cytoplasmic, membrane-bound inclusions which were PAS-positive at the fine structure level these inclusions were composed of membranous arrays in whorls, vesicles, or multilaminated stacks. Fusion of the bounding membranes of adjacent inclusions resulted in large inclusion-containing vacuoles. Hepatocytes and Kupffer cells contained inclusions slightly different from those in the central nervous system. SEM of cryofractured liver demonstrated their coalescence to form larger composite vacuoles. Vacuoles with inclusions were also seen in pancreatic acinar cells, endothelial cells, vascular smooth muscle, fibroblasts, myocardial cells, renal interstitial cells, corneal stromal cells, and R-E cells of bone marrow and spleen. The specific granules of eosinophils were swollen and took on bizarre forms. Pathologic manifestations of feline GM2 gangliosidosis differ from those seen in feline GM1 gangliosidosis but closely resemble those of Sandhoff disease in humans.

Animals↗
PubMed1977

GM2 ganglioside lysosomal storage disease in cats with beta-hexosaminidase deficiency.

Two kitteens with progressive neurologic disease had increased concentrations of GM2 ganglioside in their cerebral cortex. Examination under the light microscope revealed cytoplasmic vacuolation of neurons and hepatocytes. Transmission and scanning electron microscopy demosntrated cytoplasmic inclusions encompassed by membranes in various central nervous system cell types and in hepatocytes. Beta-D-N-acetyl-hexosaminidase activity was reduced to about 1.0 percent of normal in brain, liver, and cultured skin fibroblasts of the diseased kittens; both major electrophoretic forms, A and B, of the enzyme were deficient. In fibroblasts from the parents of the diseased kittens, this enzyme activity was intermediate between that of affected and normal cats, suggesting an autosomal recessive mode of inheritance of the enzyme defect. Histopahtological and ultrastructural lesions, glycolipid storage, enzyme defect, and pattern of inheritance are similar to those of human GM2 gangliosidosis type 2.

Animals↗
PubMed1977

Neurofibrillary accumulation in the zebra (Equus burchelli).

Two young zebra siblings from consecutive pregnancies suffered from neurological disease, characterized by ventral deviation of the neck and tetraparesis which progressed to tetraplegia within a few weeks. On histological examination widespread neuronal degeneration was observed in the ventral horns of the spinal cord and in the lower brain stem. Ultrastructurally the neuronal degeneration was characterized by accumulation of neurofibrillary material resembling neurofilaments. The findings are compared to other diseases with neurofibrillary accumulation in man and animals.

Animals↗
PubMed1976

Differential diagnosis of viral leukoencephalomyelitis of goats.

In clinical evaluation of 13 kid goats with viral leukoencephalomyelitis, diseases goats were found to be usually 2 to 4 months old, afebrile, and with unaltered mental status. The most frequent neurologic signs were posterior paresis and ataxia. Pleocytosis and lymphopenia were consistent antemortem laboratory findings. Absence of other abnormal laboratory and radiographic changes were also typical of the disease. Confirmation of the diagnosis can be obtained only be thorough histologic examination of the brain and spinal cord.

Animals↗
PubMed1975

Ultrastructural features of viral leukoencephalomyelitis of goats.

Ultrastructural studies were made of the central nervous system of three goats during the early stages of viral leukoencephalomyelitis of goats and of one goat 3 years after onset of the disease. In both early and late lesions, the following features were recognized: loss of myelin from normal axons, separation of the myelin sheath from the axon by cell processes, pronounced astrocytosis with numerous cell processes packed with heavy fibrils, paucity of oligodendrocytes, normal capillaries, and normal cellular elements in the adjacent gray matter. Early lesions also had many cells of the lymphoid series infiltrating perivascular spaces, within lesions, and, particularly, along axons undergoing demyelination. Although viral particles were extensively sought, only one suspect structure, with a tubular nucleocapsid-like configuration, was seen. Individual tubules of this particle measured 22 nm. in diameter. The ultrastructural features of demyelination in viral leukoencephalomyelitis of goats were compared with those described for demyelination that occurs in multiple sclerosis, experimental allergic encephalomyelitis, canine distemper encephalomyelitis, and that produced by diphtheria toxin.

Animals↗
PubMedDate not supplied

Age differences in recognition memory of the rhesus monkey (Macaca mulatta).

Aging is accompanied by a gradual decline in memory in both humans and nonhuman primates. To determine whether the impairment in nonhuman primates extends to recognition memory, which is a sensitive index of the integrity of the limbic system, we trained rhesus monkeys of four different age groups (3-6, 14-17, 20-24, and 25-29 years of age) on a delayed nonmatching-to-sample task with trial-unique objects. After the animals had learned the task, which required recognition of single objects presented ten seconds earlier, memory demands were increased by gradually lengthening delay intervals (to 120 seconds) and list lengths (to ten objects). With increasing age, only marginal impairments in learning the basic task were observed. However, clear age-related differences did emerge when either delays or list lengths were increased, with the oldest group of monkeys demonstrating the greatest impairments. The decline in visual recognition ability in aging monkeys parallels the decline in memory observed with advancing age in humans.

Aging↗
PubMedDate not supplied

Loss of NMDA, but not GABA-A, binding in the brains of aged rats and monkeys.

In this quantitative neurochemical study we investigated age-related changes in the GABAergic, glutamatergic, and cholinergic neurotransmitter systems in rats and rhesus monkeys. Sixteen young (5 months) and 20 aged (24 months) rats and seven "young" (4-9 years), six "adult" (20-25 years), and five "aged" (29-34 years) monkeys were studied. NMDA-displaceable 1-[3H]glutamate binding was significantly decreased in many neocortical and subcortical regions examined in aged rats and monkeys. The level of choline acetyltransferase (ChAT) activity and [3H]muscimol binding were unchanged in aged animals.

Aging↗
PubMedDate not supplied

Aged monkeys exhibit behavioral deficits indicative of widespread cerebral dysfunction.

To determine whether the decline of behavioral abilities with aging in monkeys is selective or widespread, we examined 18 monkeys ranging from 3 to 34 years of age on a wide variety of tests with the ultimate goal of correlating behavioral deficits with age-related changes in the brain. In our initial study we found impaired visual recognition ability in the aged monkeys (43). In the present study, we assessed the same animals on tests of spatial memory, visual habit formation, visuospatial orientation, visually guided reaching, motor skill learning, and reaction time, these categories having been chosen to test the integrity of different cerebral systems. There were three major findings. First, age-related impairments were observed in nearly all test categories, though often not on easy versions of the tests, suggesting that the deficits observed were in the specific abilities measured and not an artifact of lowered motivation or other general disability. Second, the behavioral decline began in the late teens for certain spatial abilities but did not affect other abilities until the late 20's, suggesting that although the cerebral dysfunction eventually becomes widespread, the cerebral systems underlying spatial abilities are compromised by aging earlier than others. Finally, the finding of correlations between scores of aged animals primarily within test categories as opposed to across categories suggests that different animals have different patterns of cerebral involvement.

Aging↗
PubMedDate not supplied

Neurotransmitters in neocortex of aged rhesus monkeys.

The effects of aging on levels of neurotransmitters were determined in two regions of the cerebral cortex in rhesus monkeys (Macaca mulatta). Choline acetyltransferase (ChAT) activity as well as somatostatin, neuropeptide Y, and substance P immunoreactivities were analyzed in the right caudal cingulate gyrus and in the left and right inferior occipital poles in five age groups: 4-6 years; 8-11 years; 20-25 years; 26-29 years; and 31-34 years. Neuroactive amino acids and markers for monoamine transmitters were analyzed only in the youngest (4-6 years) and oldest (31-34 years) animals. Across the five age groups studied. ChAT activity as well as somatostatin and neuropeptide Y immunoreactivities were significantly decreased bilaterally in occipital poles of the 31- to 34-year-old group. There were no significant age-related differences in substance P immunoreactivity. In 4-6-year-old vs. 31-34-year-old monkeys, levels of amino acid neurotransmitters were unchanged. However, there were significant reductions in norepinephrine, serotonin and its metabolites, kynurenine, and 4-hydroxyphenyllactic acid in occipital poles of the 31- to 34-year-old monkeys. No significant neurochemical changes were detected in the cingulate cortex. These findings demonstrate that aged nonhuman primates show reductions in cortical markers for a variety of neurotransmitters, including acetylcholine, somatostatin, neuropeptide Y, norepinephrine, and serotonin but that these changes do not occur uniformly in the neocortex.

Aging↗