The effect of cooling the motor cortex of a rhesus monkey upon visually controlled movement and associated motor potentials [proceedings].
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Biomedical subjects
Publications and source records attributed to J F Stein.
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The volume of an isolated tracheal segment and of the intrathoracic airways (intrathoracic portion of anatomical dead space) were measured during independent changes in ventilation minute volume and alveolar PCO2 and PO2, in order to assess the separate effects of chemoreceptor and mechanoreceptor signals upon airway calibre. The results were highly dependent upon initial airway tone, initial airway constriction favouring dilator responses and vice versa. Increasing alveolar PCO2 caused reflex airway constriction if ventilation was held constant. The magnitude of this response was reduced if ventilation was maintained at a high level and increased if it was held at a low level. Increasing ventilation caused reflex airway dilatation even if end tidal PCO2 was held constant. The size of the dilatation was reduced at high PCO2s and increased at low PCO2s. The interactions of the chemoreceptor and mechanoreceptor signals and of the effect of initial airway tone put a limit on airway dilatation during hyperventilation and particularly during hypercapnic hyperventilation. These mechanisms also limit the airway constriction following reductions in ventilation. They are consistent with the existence of an airway control system which adjusts airway calibre to minimise the work of breathing.
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Mathematicians, control engineers and information technologists are beginning to take a greater interest in neuroscience. They are perhaps starting to realize that they may be able to learn a few tricks from nature with which to improve their machines. At the same time there is a good chance that neuroscientists will benefit from their input of fresh ideas and techniques with which to attack the problems of understanding neural processing. One area of the brain which seems particularly promising in these respects is the cerebellum.
Family and twin studies consistently demonstrate a significant role for genetic factors in the aetiology of the reading disorder dyslexia. However, dyslexia is complex at both the genetic and phenotypic levels, and currently the nature of the core deficit or deficits remains uncertain. Traditional approaches for mapping disease genes, originally developed for single-gene disorders, have limited success when there is not a simple relationship between genotype and phenotype. Recent advances in high-throughput genotyping technology and quantitative statistical methods have made a new approach to identifying genes involved in complex disorders possible. The method involves assessing the genetic similarity of many sibling pairs along the lengths of all their chromosomes and attempting to correlate this similarity with that of their phenotypic scores. We are adopting this approach in an ongoing genome-wide search for genes involved in dyslexia susceptibility, and have already successfully applied the method by replicating results from previous studies suggesting that a quantitative trait locus at 6p21.3 influences reading disability.
It has been proposed that developmental dyslexia may be associated with relative deficiencies in certain highly unsaturated fatty acids (HUFA). In children with attention-deficit/hyperactivity disorder, minor physical signs of fatty acid deficiency have been shown to correlate with blood biochemical measures of HUFA deficiency. These clinical signs of fatty acid deficiency were therefore examined in 97 dyslexic children in relation to reading and related skills, and possible sex differences were explored. Children with high fatty acid deficiency ratings showed poorer reading (P<0.02) and lower general ability (P<0.04) than children with few such clinical signs. Within males (n=72) these relationships were stronger, and fatty acid deficiency signs were also associated with poorer spelling and auditory working memory (P<0.05, P<0.005 respectively). Within females (n=25) no associations were significant. These results support the hypothesis that fatty acid deficiency may contribute to the severity of dyslexic problems, although sex differences merit further investigation.