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Biomedical subjects

F Pinkerton

Publications and source records attributed to F Pinkerton.

9 recordsLinked to original sources
PubMed1989

A neurophysiological study of children with reading, writing and spelling difficulties.

Recordings of early and late auditory evoked potentials and spectral analysis of scalp EEGs of 14 eight- and nine-year-old boys with difficulties in reading, writing and spelling were compared with those of 18 matched controls. The recordings of the poor readers lacked the normal asymmetry of central conduction time and wave amplitude in the early (brainstem) auditory evoked potentials, and late (cortical) evoked potential components were reduced in amplitude. Spontaneous EEG activity was significantly increased in power in all spectral bands, and this activity was less responsive to changes in sensory stimulation. These observations provide evidence for disturbed early and late auditory processing and altered cortical function. Correlations with behavioural measures considered to be indices of reading, writing and spelling ability support the view that the electrophysiological differences in the group of poor readers reflect a disturbance in the mechanisms subserving the acquisition of written language. These differences are consistent with a primary disturbance of selective attention, which may contribute to a less efficient cognitive strategy for the acquisition of reading skills.

Brain↗
PubMed1986

Development of a chemically defined serum- and protein-free medium for growth of human peripheral lymphocytes.

A chemically defined, protein-free medium (designated CFBI 1000, where CFBI = Clayton Foundation Biochemical Institute) that supports human peripheral lymphocyte proliferation has been developed. This medium allows exploration of individual metabolic differences by varying the medium composition as well as providing a base to explore further the mechanisms of lymphocyte activation in a system initially free of added macromolecular species other than mitogen. The peripheral blood lymphocyte is an ideal system for metabolic studies because it is easily obtained, is a primary resting cell that can be activated to proliferate, and presumably reflects both the genetic makeup and biochemical environmental history of the individual at the time the cells were formed. Examination of the role of various factors in lymphocyte activation and subsequent events may be simplified by the utilization of a medium that is protein-free and chemically defined. The CFBI 1000 medium supports the growth response of human peripheral lymphocytes to mitogen as measured by [3H]thymidine incorporation to an extent comparable to other media used widely in assessment of lymphocyte proliferation.

Aphidicolin↗
PubMed1979

Defective regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase in a somatic cell mutant.

A somatic cell mutant of the CHO-K1 cell selected to be resistant to the killing effects of 25-hydroxycholesterol in the absence of cholesterol is shown to be defective in the inhibition of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase activity by 25-hydroxycholesterol, cholesterol, and lipoproteins, thus maintaining the enzyme activity found in cells in the absence of exogenous sterol constitutively. The mutants phenotype is shown to be dominant with respect to the wild type. Actinomycin D and cycloheximide prevent the increase of HMG-CoA reductase activity that occurs in the CHO-K1 cell when cholesterol is removed from medium. Degradation of the enzyme, measured during inhibition of protein synthesis by cycloheximide, occurs at the same rate in the mutant as in the wild type. Kinetic studies indicate that the Km for two substrates, the activation energy, and a break in the Arrhenius plot are the same for HMG-CoA reductase determined in wild type and mutant cells. From these studies it is concluded that the mutant is defective in the regulation of synthesis of HMG-CoA reductase. Of the four processes which determine cellular cholesterol levels: biosynthesis, esterification, efflux, and uptake, only biosynthesis is altered, demonstrating that these processes are not co-ordinately controlled as has been suggested previously.

Animals↗
PubMed1979

Rate limitation of (Na+ + K+)-stimulated adenosinetriphosphatase by membrane acyl chain ordering.

A somatic cell mutant (CR1) of the Chinese hamster ovary cell line (CHO-K1) that is defective in the regulation of cholesterol biosynthesis can be grown under conditions in which plasma membranes from these cells display various cholesterol contents and acyl chain order parameters. The (Na+ + K+)-stimulated adenosinetriphosphatase (ATP phosphohydrolase, EC 3.6.1.3) from these cells was shown to vary in activity by a factor of 10 as the order parameter was varied, and the activity exhibited an exponential dependence on this parameter. Under these conditions the number of Na+,K+-ATPase molecules was shown to remain constant by affinity labeling with [gamma-32P]ATP in the absence of Na+. Control experiments showed that alteration in cholesterol content without change in order parameter did not result in altered enzyme activity. It is concluded that, under our conditions, the rate of catalysis by the Na+,K+-ATPase is determined by the order parameter. These studies suggest a physical mechanism by which variation of membrane lipid composition or other factors that determine membrane lipid acyl chain order parameter can result in variation in membrane enzyme activity.

Acylation↗
PubMed1976

Serinol as an activator of toxin production in attenuated cultures of Helminthosporium sacchari.

Successive transfer in synthetic medium of spores and mycelial fragments from original toxin-producing cultures of Helminthosporium sacchari results in attenuated cultures which do not produce the host-specific toxin helminthosporoside. When attenuated cultures are grown on material obtained from the water wash of sugarcane leaves susceptible to this fungus, the production of heminthosporoside resumes. Compounds that activate toxin production in the fungus are present on the leaf surface and presumably arise via plant metabolism. One activator was identified as a novel free amine, serinol (2-amino-1,3-propanediol). It activates toxin production in attenuated cultures at 1 muM. Several experiments described in this report argue against the selection theory for the attenuation of cultures. The biological significance and some possible mechanisms for the activation of toxin biosynthesis are discussed.

Journal Article↗