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Biomedical subjects

M Hutton

Publications and source records attributed to M Hutton.

132 records · Page 8Linked to original sources
PubMed1979

Quantitative effect of oral feeding on gastrointestinal myoelectric activity in the conscious dog.

Gastrointestinal myoelectric activity was recorded in seven studies in five dogs during two hours of fasting immediately followed by feeding and subsequent recording for four hours. In four studies serial plasma samples were taken for radioimmunoassay of insulin and gastrin. In all animals there was a significant reduction (P less than 0.01) in gastric basic electrical rhythm (BER) frequency on feeding which was sustained throughout the postprandial period. There was no change in the duodenal BER. Feeding induced a significant (P less than 0.01) increase in overall jejunal and ileal (but not duodenal) spike activity. Ileal (but not jejunal) spike activity again increased significantly (P less than 0.05) after the first two post-prandial hours. The changes in serum gastrin or in serum insulin did not appear to account for most of the observed changes in myoelectric activity, suggesting that other humoral and/or neural factors mediate the response to food.

Animals↗
PubMed1978

Factors influencing lactation performance in rural Gambian mothers.

Breast-milk consumption has been measured in a rural African community in which breast-feeding on demand is universally practised until the baby is 18 mos old. The mother's long-term capacity for breast-milk production is determined by the end of the second month of lactation, yield being closely correlated with the infant's birth-weight. Other factors significantly influencing output were parity, month of lactation, baby's weight-for-age, season, and maternal diet. Daily milk consumption was limited primarily by the amount delivered per feed, not the frequency of feeding.

Body Weight↗
PubMed1978

Quantitative comparison of the effects of cholecystokinin, secretin, and pentagastrin on gastrointestinal myoelectric activity in the conscious fasted dog.

The effects on gastrointestinal myoelectric activity of infused pentagastrin, cholecystokinin (CCK), and secretin at physiological doses were studied in live dogs with implanted serosal electrodes during 56 six-hour studies. Pentagastrin dose-dependently increased gastric and duodenal slow-wave frequencies; secretin and CCK did not. Pentagastrin and CCK diminished the incidence of fasting migrating myoelectric complexes (MMCs), but MMCs were abolished only in the proximal small intestine. Pentagastrin infusion was not reflected in an increased number of spikes, whereas CCK induced a dose-dependent increase in jejunal spike activity. Secretin dose-dependently decreased duodenal and jejunal spike incidence without a marked effect on MMC incidence. Analysis of patterns of spike activity showed significant dose-dependent changes with all three peptides. The different effects of pentagastrin and CCK on spike activity in these studies may have been a consequence of pentagastrin-stimulated gastric acid secretion. None of the three peptides produced a pattern of myoelectric activity which closely resembled that seen on feeding; since, unlike food, all three peptides had little or no effect on the distal small intestine, it seems unlikely that combinations of these peptides are responsible for the change induced by food. The failure of these peptides to abolish fasting patterns in the distal intestine suggests a possible mechanism for some types of post-vagotomy dysfunction.

Action Potentials↗
PubMedDate not supplied

Phenotypic correlations in FTDP-17.

Frontotemporal dementias with parkinsonism linked to chromosome 17 (FTDP-17) are hereditary tauopathies affecting at least 50 known kindred worldwide. Most kindred present with severe behavioral or psychiatric manifestations progressing to dementia, while some kindred first manifest a parkinsonian-plus syndrome. Nine missense mutations, one deletion mutation, and two transition mutations not altering the encoded amino acid, have been described in or near the microtubule-binding domains within exons 9, 10, 12, and 13. In addition, five different intronic mutations have been reported in the 5' splice-site of the alternatively spliced exon 10. Missense mutations affecting constitutively expressed exons affect all six major tau isoforms and result in neurofibrillary tangles similar to those present in secondary tauopathies, such as Alzheimer's disease. In contrast, mutations that affect the alternatively spliced exon 10 or its 5' splice regulatory region alter the ratio of the tau isoforms incorporated into the tangles and result in filamentous inclusions resembling those seen in the primary tauopathies, such as progressive supranuclear palsy, corticobasal degeneration, and Pick's disease. The severity and heterogeneity of the clinicomorphologic phenotype may, in part, reflect the diversity in the primary molecular mechanisms of disease in FTDP-17.

Brain↗