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Biomedical subjects

H Gregory

Publications and source records attributed to H Gregory.

At least 55 records · Page 3Linked to original sources
PubMed1986

Urinary excretion of epidermal growth factor in the newborn.

Urinary epidermal growth factor (EGF) excretion was studied serially in 36 newborn infants, from 26 to 40 weeks gestation, from birth to three months of age. All infants excreted EGF from birth. Excretion was significantly higher in term infants than in preterm infants at birth; in term infants excretion rose steadily in early infancy and there was a similar but delayed rise in EGF excretion by preterm infants. Urinary EGF excretion appears to be related to age from conception and birth does not influence it. There was no correlation between urinary EGF excretion and the rapid maturation of the lungs and skin which occurs in preterm infants in the early neonatal period.

Aging↗
PubMed1986

Urogastrone-epidermal growth factor concentrations in prostatic fluid of normal individuals and patients with benign prostatic hypertrophy.

High concentrations (272 +/- 33 ng/ml) of urogastrone-epidermal growth factor were measured in prostatic fluid from normal males by a specific radioimmunoassay. Significantly lower concentrations (155 +/- 24 ng/ml) were observed in the prostatic fluid of patients with benign prostatic hypertrophy than in the age-matched normal controls (2P less than 0.01). The growth factor content of seminal fluid was accounted for by the contribution of prostatic fluid. Immunochemical studies failed to show evidence of synthesis within the gland nor could high affinity receptors for the protein be demonstrated in membrane preparations of the gland.

Chromatography, Gel↗
PubMed1986

Inhibition of acid formation by epidermal growth factor in the isolated rabbit gastric glands.

The effects of epidermal growth factor (EGF) on basal and stimulated (with histamine, dibutyryl cyclic AMP, and high concentrations of K+) acid formation have been studied in isolated glands from the rabbit gastric mucosa. The changes in the accumulation of [14C]aminopyrine [14C]AP have been used as an indirect measurement of acid production in the glands. Unstimulated gastric glands accumulated [14C]AP indicating the existence of basal acid production in these glands, and EGF caused a small but significant reduction in basal [14C]AP uptake. A similar reduction of basal [14C]AP uptake was observed after exposure to omeprazole but not after ranitidine or prostaglandin E2 (PGE2). Histamine, dibutyryl cyclic AMP and K+ caused a strong and dose-dependent stimulation of acid formation by the glands. EGF, like omeprazole, reduced dose-dependently the [14C]AP accumulation stimulated by both histamine and dibutyryl cyclic AMP, while ranitidine and PGE2 reduced histamine- but not dibutyryl-cyclic-AMP-stimulated accumulation of [14C]AP. In the absence of other external stimuli, an increased K+ concentration enhanced [14C]AP accumulation to levels similar to those produced by histamine and this effect was not changed by EGF, ranitidine or PGE2 but was inhibited by omeprazole. We conclude that EGF interferes with the final steps of acid production between cyclic nucleotides and proton pump of the parietal cells.

Aminopyrine↗
PubMed1986

Acceleration of wound healing by recombinant human urogastrone (epidermal growth factor).

Urogastrone, a human peptide growth factor that is closely related by its amino acid sequence to mouse epidermal growth factor, has been prepared by recombinant DNA techniques. The powerful mitogenic activity of urogastrone led us to evaluate its potential as an aid to wound healing. We have used the repair reaction that follows transection of the Achilles tendon in the rat to evaluate the action of urogastrone in this model. Twice-daily injections of recombinant urogastrone (20 micrograms/kg) close to the site of the wound led to more rapid increases in the dry weight of the repair lesion and its collagen and DNA contents compared with those in saline-injected controls (5 days). At 15 and 30 days after surgery the urogastrone-treated lesion continued to show enhanced dry weights and collagen contents, whereas the DNA content declined to that of saline-treated lesions. When urogastrone treatment was stopped after 15 days, the repair lesions examined at 30 days were little different from those in animals untreated throughout. Our results provide encouragement for an eventual clinical assessment of recombinant urogastrone in humans as an aid to wound healing provided that satisfactory answers are found to several outstanding questions.

Achilles Tendon↗
PubMed1985

Urogastrone-epidermal growth factor is trophic to the intestinal epithelium of parenterally fed rats.

The weight of the stomach, small intestine and colon and the mucosal crypt cell production rate of these tissues were significantly decreased after 10 days on an isocaloric TPN diet when compared to orally fed controls. Continuous infusion of recombinant beta urogastrone, at a dose below that needed to inhibit gastric acid secretion, largely prevented this decrease in crypt cell production rate and gastrointestinal tissue weights.

Animals↗
PubMed1985

The causative agent in atrial receptor diuresis in the dog is a low molecular weight, lipophilic and weakly acidic substance.

Stimulation of atrial receptors by distension of a balloon in the left atrium of anaesthetized dogs results in a reflex diuresis mediated by a humoral agent of unknown identity. In previous investigations, a substance was recovered in a low molecular weight fraction from Bio-Gel P-2 (100-1800 daltons) and shown to be related to the reflex diuresis. In this investigation, the active Bio-Gel P-2 fraction was partitioned with ethyl acetate at pH 11.0, with subsequent partition of the aqueous phase with ethyl acetate at pH 7.4; the activity of the humoral agent was soluble in ethyl acetate at pH 7.4. These investigations suggest that the humoral agent is a low molecular weight, lipophilic and weakly acidic substance. The substance is not antidiuretic hormone (ADH) as vasopressin is insoluble in ethyl acetate at pH 7.4.

Acetates↗
PubMed1985

In vivo aspects of urogastrone-epidermal growth factor.

Recent evidence indicates that human urogastrone-epidermal growth factor originates in submandibular and Brunner's glands and that serum levels are low (less than 1 ng ml-1). It occurs in many secreted fluids to a much greater extent and many tissues are thus exposed to concentrations greater than 100 ng ml-1. Rapid actions in vivo of URO-EGF include the ability to inhibit gastric acid secretion at low doses (250 ng kg h-1 in humans) and to provide cytoprotective effects against ulcerogenic agents (250 ng kg h-1 in cats). More prolonged exposure of tissues shows increases in parameters related to wound healing, beneficial effects upon ulceration and also the ability to accelerate crypt cell production rate along the gastrointestinal tract. Synthetic material has been prepared with an identical structure to the natural URO-EGF thus enabling detailed studies of the biological effects to be pursued.

Animals↗
PubMed1984

Effects of epidermal growth factor on gastrointestinal secretions.

Epidermal growth factor (EGF) has been reported to stimulate epithelial cell proliferation and to inhibit gastric H+ secretion, but no details of the latter effect have been studied. This paper reports the effects of EGF on gastric and pancreatic secretions induced by various stimulants in vivo on conscious dogs and in vitro on isolated rabbit gastric glands. EGF was found to be an effective inhibitor of H+ secretion induced from the fully innervated and vagally denervated portions of the stomach stimulated by secretagogues activating receptors of the parietal cells (pentagastrin, histamine, and urecholine) and by natural stimulants such as sham or ordinary feeding. It appears to act directly on the parietal cells, as the inhibitory effect in vivo was not accompanied by any change in postprandial serum gastrin level. In addition, EGF was found to suppress H+ formation in the isolated gastric glands, both under resting conditions and after stimulation with histamine, carbachol, or dibutyryl cAMP. EGF failed to affect pancreatic response to exogenous hormones (secretin and cholecystokinin) but reduced postprandial secretion probably because of inhibition of H+ secretion from the subsequent reduction in duodenal acid loads. We conclude that EGF is a potent, specific, and direct inhibitor of H+ secretion from the parietal cells and that it does not affect alkaline gastroduodenal or pancreatic secretion.

Animals↗
PubMed1982

Trophic action of epidermal growth factor on the pancreas and gastroduodenal mucosa in rats.

1. Epidermal growth factor (EGF) infused subcutaneously in a dose of 10 micrograms/kg . h but not 1 microgram/kg . h inhibited spontaneous gastric acid and pepsin secretion, whereas when given intragastrically in a dose of 10 micrograms/kg . h it failed to affect this secretion. 2. EGF injected intraperitoneally at 8 h intervals for 24 h significantly stimulated DNA synthesis in the gastroduodenal mucosa and the pancreas, whereas when administered intragastrically it stimulated DNA synthesis only in the gastroduodenal mucosa but not in the pancreas. 3. Chronic parenteral administration of EGF significantly increased the DNA and RNA contents of the gastroduodenal mucosa and the pancreas. 4. This study demonstrates that parenteral EGF is a potent inhibitor of gastric secretion and trophic agent for the gastroduodenal mucosa and pancreas, and that the gastric inhibitory and trophic effects of EGF are the results of two separate mechanisms.

Animals↗
PubMed1982

Effect of urogastrone on gastric secretion and serum gastrin concentration in patients with duodenal ulceration.

A one-hour infusion of 0.25 micrograms/kg urogastrone administered to seven patients with duodenal ulceration resulted in significant reduction of basal acid secretion (p less than 0.05) but was without significant effect on basal pepsin and intrinsic factor secretion or on serum gastrin concentration. In another group of five patients with duodenal ulceration a one-hour infusion of urogastrone was given on five successive days. On day 1 and 5 urogastrone was administered after establishing a plateau response to intravenous pentagastrin 1.2 micrograms/kg/h. A mean reduction of 65% in acid output during the urogastrtone infusion was seen on day 1 and this was maintained during the next hour. On day 5 the pentagastrin-stimulated acid output was less than on day 1 and a further significant decrease was noted after urogastrone. Pepsin and intrinsic factor output were also significantly inhibited. There was no change in fasting serum gastrin or urogastrone concentration.

Adult↗
PubMed1981

Regulation of gonadotropin secretion in the anterior pituitary.

Studies on the regulation of gonadotropin secretion in dissociated pituitary cell cultures are described. Initial studies employing a ferritin-labelled analogue of gonadotropin hormone releasing hormone (GnRH) to localize its receptor sites on the gonadotropin cell surface that while these receptor sites initially have a random monodisperse distribution, binding of the ligand causes coarse aggregation and internalization of the GnRH receptor. These events are not due to the multivalency of the ligand and probably reflect redistributive events in vivo. By using an octapeptide analogue GnRH that binds to the GnRH receptor but lacks gonadotropin releasing activity in conjunction with sequence-specific antisera it is shown that antibodies that bind the octapeptide can induce the octapeptide to release gonadotropin. These data suggest that receptor aggregation is important in GnRH stimulation. Finally immunocytochemical studies are described in which golg-protein-A-antibody complexes are used to identify gonadotropins on ultrathin frozen sections of porcine pituitary cells. These studies indicate that in porcine gonadotropin cells the majority of the secretory granules contain both luteinizing hormone and follicle-stimulating hormone.

Animals↗
PubMed1981

Role of mucosal prostaglandins and DNA synthesis in gastric cytoprotection by luminal epidermal growth factor.

This study compares the effect of epidermal growth factor and prostaglandins (PGE2 or PGI2), applied topically to gastric mucosa, on gastric secretion and formation of ASA-induced gastric ulcerations in rats. Epidermal growth factor given topically in non-antisecretory doses prevented dose-dependently the formation of ASA-induced ulcers without affecting prostaglandin generation but with a significant rise in DNA synthesis in the oxyntic mucosa. The anti-ulcer effect of topical prostaglandins was also accompanied by an increase in DNA synthesis. This study indicates that topical epidermal growth factor, like PGE2 or PGI2, is cytoprotective and that this cytoprotection is not mediated by the inhibition of gastric secretion or prostaglandin formation but related to the increase in DNA synthesis in oxyntic mucosa.

Animals↗
PubMed1981

Early events following the binding of epidermal growth factor to surface receptors on ovarian granulosa cells.

Receptors for epidermal growth factor (EGF) have been localized on the surface of ovarian granulosa cells using a colloidal gold avidin complex in conjunction with biotinylated EGF. On cells incubated at low temperature the receptors are predominantly monodisperse and have a random distribution. When cells are warmed to 37 degrees C the receptors aggregate into clusters.

Animals↗