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Biomedical subjects

D R Averill

Publications and source records attributed to D R Averill.

10 recordsLinked to original sources
PubMed1979

Brain carbohydrate metabolism during experimental Haemophilus influenzae meningitis.

Five-day-old infant rats which acquire Haemophilus influenzae b bacteremia and meningitis after intranasal inoculation have a transient depression in weight gain (2 days), but then continue to grow at the same rate as strain U--11 inoculated controls. Brain lactate, glucose, and glycogen concentrations increase during the first 5 days of disease in infected animals. The increase in brain glycogen can be accounted for by an influx of glycogen containing polymorphonuclear leukocytes. The increased concentrations of glucose and lactate were found not to be due to a change in brain weight to dry weight ratio or the volume of entrapped blood. The mean cerebrospinal fluid (CSF) glucose concentration was higher in animals with meningitis (2.7 mM) in comparison to U-11 inoculated controls (1.8 mM). This increase in brain and CSF glucose concentration appeared secondary to an increased brain uptake of hexoses as manifested by an increased [3H]mannitol uptake. Brain lactate accumulation was not explicable from the data available. There was no evidence of cerebral cortical cellular damage because in vitro oxygen uptake and lactate production were equivalent in control and meningitic animals. The ability of the infant rat brain to maintain cerebral adenosine triphosphate (ATP) content in menigitis and the failure of CSF glucose concentration to decrease might be a reflection of the importance of alternative oxidative substrate (e.g., beta-hydroxybutyrate) to the cerebral metabolism of the developing rat brain.

Adenosine Triphosphate↗
PubMed1978

Thiamine deficiency encephalopathy in a specific-pathogen-free cat colony.

Thiamine deficiency encephalopathy occurred in a specific-pathogen-free cat colony where the diet consisted exclusively of commercially canned diet. This product was described by the manufacturer as a complete diet for cats. The clinical diagnosis was confirmed by the demonstration of bilaterally symmetrical hemorrhage and microvascular fibrinoid necrosis in the brain and low erythrocyte transketolase levels. Treatment of clinically ill cats with vitamin B complex was followed by recovery within 24 hours.

Animals↗
PubMed1977

Neonatal endotoxin encephalopathy.

Telencephalic white matter of the neonatal kitten frequently contained diffuse astrogliosis or focal necrosis (sometimes including the thalamus and the caudate) following a single intraperitoneal injection of Escherichia coli lipopolysaccharide. No evidence for a disseminated intravascular coagulopathy was found. Telencephalic lesions in neonatal monkey and rabbit were also hemorrhagic. Enhanced karyorrhexis of glial nuclei was presented in the telencephalic white matter of the neonatal rat. In the kitten, a delay in the generation of macrophages and hypertrophic astrocytes occurs following transient neonatal endotoxemia. Marked weight loss and temperature fluctuation are prominent systemic effects. Large hemispheric cavitary lesions are not accompanied by obvious neurological deficits in the kitten.

Animals↗
PubMed1977

Molecular basis of reovirus virulence: role of the S1 gene.

A genetic approach has been used to define the molecular basis for the different patterns of virulence and central nervous system cell tropism exhibited by reovirus types 1 and 3. Intracerebral inoculation of reovirus type 3 into newborn mice causes a necrotizing encephalitis (without ependymal damage) that is uniformly fatal. Animal inoculated with reovirus type 1 generally survive and may develop epedymal cell damage (without neuronal necrosis) and hydrocephalus. Using recombinant clones derived from crosses between reovirus types 1 and 3, we have been able to determine that the S1 genome segment is responsible for the differing cell tropism of reovirus serotypes and is the major determinant of neurovirulence. The type 1 S1 genome segment is responsible for ependymal damage with subsequent hydrocephalus; the type 3 S1 genome segment is responsible for neuronal necrosis and neurovirulence. We postulate that these differences are due to the specific interaction of the sigma1 outer capsid polypeptide (the protein coded for by the S1 genome segment) with receptors on the surface of either ependymal cells or neuronal cells.

Animals↗
PubMed1977

Inherited necrotizing myelopathy of Afghan hounds.

Eleven examples of a naturally occurring, adolescent-onset spinal cord necrosis in Afghan Hounds were studied. Unusual and characteristic spinal cord lesions were necrosis and small vessel proliferation in the dorsal and ventro-medial spinal cord white matter extending from caudal cervical segments to cranial lumbar segments. Spinal cord gray matter and dorsal and ventral roots were preserved. Four dogs had histologically similar lesions in the superior olivary nucleus. The cause of these lesions was not determined by histopathologic or ultrastructural examination. Chi-square analysis of pooled sibships indicates a simple autosomal recessive mode of inheritance.

Animals↗
PubMed1976

Hereditary cerebellar cortical and extrapyramidal nuclear abiotrophy in Kerry Blue Terriers.

Ten Kerry Blue terriers from a kennel in New York and 3 from a kennel in California developed clinical signs of a progressive cerebellar disorder, with its onset between 9 and 16 weeks of age. In 9 sequential necropsies, progressive cerebellar cortical degeneration, with loss of Purkinje's cells, was demonstrated. As the disease progressed, there was bilateral symmetric degeneration of the olivary nuclei followed by degeneration of the substantia nigra and caudate nucleus, bilaterally. The California and New York dogs were related, and an autosomal recessive inheritance was proposed for the disease.

Animals↗