Biomedical subjects

P J Tutton

Publications and source records attributed to P J Tutton.

At least 55 records · Page 3Linked to original sources

PubMed1977

Neural and endocrine control systems acting on the population kinetics of the intestinal epithelium.

Mechanisms for the control of cell proliferation in those tissues where continuous cell loss is balanced by continuous cell production are still poorly understood. In this paper the factors influencing cell proliferation in the intestinal epithelium are reviewed and it is hypothesised that cell division in the intestinal crypt is regulated by two interacting systems. One of these systems is highly localised, mediated by autonomic nerves and responsive to changes in the rate of cell loss, whereas the other system is generalised throughout the intestine, mediated by hormones and responsive to the nutritional needs of the organism. Experiments to disprove these hypothesis are then suggested.

Animal Nutritional Physiological Phenomena↗

PubMed1976

Adrenergic inhibition of cell proliferation in the buccal epithelium of rat.

Mitotic rates in the basal layer of cells in the buccal epithelium of rat were measured using a stathmokinetic technique. Adrenaline was found to inhibit cell proliferation in this tissue and the effect of adrenaline could be blocked by the beta-adrenergic antagonist propranolol but not by the alpha-adrenergic antagonist phentolamine nor by the specific beta2-adrenergic antagonist butoxamine. Cell proliferation in the buccal mucosa was also inhibited by terbutaline, a synthetic beta2-adrenergic agonist. The effect of terbutaline was not blocked by either butoxamine or by the specific beta1-adrenergic antagonist practolol.

Animals↗

PubMed1976

Cell proliferation in the descending colon of dimethylhydrazine treated rats and in dimethylhydrazine induced adenocarcinomata.

A stathmokinetic technique which has estimable precision has been used to estimate mitotic rates in the crypts of Lieberkühn in the descending colon of normal, and of dimethylhydrazine (DMH)-treated rats, as well as in DMH-induced adenocarcinomata. Estimates of the mean number of proliferating and of non-proliferating cells per crypt of Lieberkühn were also made in normal and in DMH-treated rats. In normal rats, epithelial cell proliferation was found to be relatively slow in the basal one-fifth of the crypts of Lieberkühn and to be most rapid in the second one-fifth of the crypt. In DMH-treated rats the number of cells around the circumference of transversely sectioned crypts was significantly increased, as was the number of proliferating cells present in longitudinally sectioned crypts. The region of relatively slow cell proliferation in the base of the crypts was expanded to occupy the lower two-fifths of the crypt in DMH-treated rats whilst the region of most rapid cell proliferation was displaced upwards to occupy the third one-fifth of the crypt. In DMH-induced adenocarcinomata cell proliferation occurred at a rate similar to that in the relatively quiescent zone at the bases of the colinic crypts in normal animals. However, tumour cell proliferation was substantially slower than that in the second one-fifth of the crypt in normal animals.

Adenocarcinoma↗

PubMed1976

A comparison of cell proliferation in normal and neoplastic intestinal epithelia following either biogenic amine depletion or monoamine oxidase inhibition.

Epithelial cell proliferation was studied in the jejunum and in the colon of normal rats, in the colon of dimethylhydrazine-treated rats and in dimethylhydrazine-induced adenocarcinoma of the colon using a stathmokinetic technique. Estimates of cell proliferation rates in these four tissues were then repeated in animals which had been depleted of biogenic animes by treatment with reserpine and in animals whose monoamine oxidase was inhibited by treatment with nialamide. In amine-depleted animals cell proliferation essentially ceased in all four tissues examined. Inhibition of monoamine oxidase did not significantly influence cell proliferation in nonmalignant tissues but accelerated cell division in colonic tumours.

Adenocarcinoma↗

PubMed1976

The influence of thyroidectomy and of triiodothyronine administration on epithelial cell proliferation in the jejunum of rat.

Mitotic rates in epithelial cells lining the bases of the crypts of Lieberkühn in rat jejunum were measured using a stathmokinetic technique. Two weeks after surgical thyroidectomy the mitotic rate in the jejunal crypt cells was significantly lower than that in control animals. During the four hour period immediately after injection of triiodothyronine into thyroidectomized rats the crypt cell mitotic rate was significantly higher than in control animals.

Animals↗

PubMed1975

Absence of a circadian rhythm in crypt cell mitotic rate following chemical sympathectomy in rats.

The circadian rhythms in both consumption of food by rats and in the mitotic rate in epithelial cells lining the bases of the crypts of Lieberkühn of the proximal jejunum were studied in normal and in chemically sympathectomised rats. In normal rats both food consumption and crypt cell mitotic rat showed a distinct circadian rhythm, both parameters having a peak around 00.00 to 04.00 hours. Following chemical sympathectomy the circadian rhythm in food consumption was essentially unchanged whereas that in the crypt cell mitotic rate was abolished.

Animals↗

PubMed1975

Neural stimulation of mitotic activity in the crypts of lieberkühn in rat jejunum.

The influence of nerve stimulation and sham-stimulation on the mitotic rate in epithelial cells lining the crypts of Lieberkühn in the jejunum of anaesthetized rats was studied. Administration of the anaesthetic and opening the abdominal cavity was without significant effect on the crypt cell mitotic rate. However, externalizing a loop of jejunum and applying sham-stimuli to its mesenteric nerves resulted in a significant decrease in the crypt cell mitotic rate in that loop. Application of electrical stimuli to the mesenteric nerves of another externalized jejunal loop resulted in a significant increase in the mitotic rate in the crypt cells of that segment. Similar acceleration of crypt cell proliferation by electrical stimuli applied to mesenteric nerves was also seen in chemically sympathectomized rats.

Animals↗

PubMed1974