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Biomedical subjects

S R Bloom

Publications and source records attributed to S R Bloom.

At least 919 records · Page 51Linked to original sources
PubMed1983

Gut hormone secreting tumours.

Gut peptide secreting tumours originate most commonly from the pancreatic Islets of Langerhans. Tumours at a variety of other sites have also been shown to synthesize and release these peptides, reflecting the wide distribution of the peptide secreting cells of the diffuse neuroendocrine system. Tumours such as the glucagonomas, insulinomas, VIPomas and gastrinomas are associated with characteristic clinical syndromes resulting from the effects of the peptide they secrete. The majority of the islet cell tumours in fact secrete a number of different peptides and many of these are present in several molecular forms, some of which may not be biologically active. This may explain the lack of clinical sequelae in association with tumours such as the somatostatinomas. The clinical features, methods of diagnosis, localisation and treatment of these tumours will be discussed.

Adenoma, Islet Cell↗
PubMed1983

Localization of S-100 protein in Müller cells of the retina--1. Light microscopical immunocytochemistry.

S-100 is an acidic brain protein previously found to be present in glial cells of the brain and the nervous system of gut and respiratory tract. Immunocytochemistry at the light microscopical level localized immunoreactivity for S-100 in the Müller cells in the retina of rat, guinea pig, and Chinese hamster. The Müller cells represent the main glial component of the retina, with a structural role in the support and insulation of neurons and sensory elements. The use of S-100 protein as an immunocytochemical marker of Müller cells may be useful in the study of pathologic conditions of the retina where glial cell proliferation could reflect the index of neuronal injury.

Animals↗
PubMed1983

Gut hormones in disease.

The anatomical basis of gastrointestinal neuroendocrinology is formed by mucosal endocrine cells and the mainly intrinsic enteric nerves. The endocrine cells contain electron-dense secretory granules which are characteristic of each peptide being produced by the separate cell types. The peptides produced by these neuroendocrine elements act in a tripartite manner; via the blood stream, locally or as neurotransmitters. Investigation of the actions of these peptides necessitates development of new physiological approaches. Furthermore, the interplay, whether agonistic or antagonistic, between the elements and hormones must be taken into account. Technological developments have provided new means for the investigation of the diffuse neuroendocrine system of the gut. This system can now be visualised in its entirety using the simple marker, neuron-specific enolase (NSE). Advances in the chemical characterisation of peptides have enabled the subsequent raising of antibodies to various specific fragments of hormones and prohormones. In addition, new immunocytochemical methods, in particular the use of gold particulate markers, enables us now to visualise the intracellular events of peptide biosynthesis. It is evident that more regulatory peptides are being discovered and application of new immunological probes, eg monoclonal antibodies, will reveal the total extent of the diffuse neuroendocrine system and its possible abnormalities in disease states, thereby opening new vistas in clinical endocrinology.

Autonomic Nervous System↗
PubMed1983

Neural regulation of pancreatic polypeptide release.

To clarify the nervous system's role in the regulation of pancreatic polypeptide (PP) release, extrinsic innervation to the in situ pancreas was eliminated in five dogs. Before and 2 weeks after denervation, PP was measured during insulin hypoglycemia and ingestion of a protein meal. Exogenous insulin caused a similar marked hypoglycemia in both control and denervated dogs. Hypoglycemia caused a significant increase in plasma PP in control dogs from a baseline of 42 +/- 8 pg/ml to 86 +/- 18 pg/ml at 20 minutes (P less than 0.01). In denervated dogs plasma PP did not increase with hypoglycemia, and levels were significantly less than in the control animals at 30 and 60 minutes (P less than 0.05). With a protein meal, PP increased in the control animals from 53 +/- 12 to 116 +/- 16 pg/ml at 10 minutes (P less than 0.05), 164 +/- 22 pg/ml at 20 minutes (P less than 0.05), and 193 +/- 20 pg/ml at 60 minutes (P less than 0.01). Denervation markedly blunted this response, and PP increased only from 53 +/- 6 to 64 +/- 4 pg/ml at 10 minutes, to 83 +/- 12 pg/ml at 20 minutes, and to 91 +/- 8 pg/ml at 60 minutes. PP became significantly elevated above baseline in denervated dogs only at 60 minutes (P less than 0.05), and PP was significantly lower than in the control group at 10, 20, and 60 minutes after the meal (P less than 0.05). Immunostaining for insulin, glucagon, somatostatin, and PP showed no difference in the number and distribution of these endocrine cells in predenervation and postdenervation specimens. Adrenergic and cholinergic nerves were seen in all control specimens but, except for a few adrenergic fibers, were not seen in denervated animals. Peptidergic nerves that contained vasoactive intestinal polypeptide (VIP) were seen in all areas of the pancreas before and after denervation. This study confirms that the initial rise in PP with a protein meal is governed by vagal cholinergic pathways. Later postprandial PP secretion is controlled by an interplay between these cholinergic pathways and other uncertain influences such as hormonal or substrate changes. The pancreas has a rich intrinsic peptidergic system of VIP-containing nerves.

Animals↗
PubMed1983

Evidence for a humoral mechanism after small intestinal resection. Exclusion of gastrin but not enteroglucagon.

It is generally agreed that the adaptive response in the residual bowel after major intestinal resection is dependent on luminal nutrition and pancreaticobiliary secretions. Recent evidence, however, suggests that humoral mechanisms, e.g., gastrin or enteroglucagon, may also play a part in this process. A 75% proximal small bowel exclusion was performed in 16 male Wistar rats and the excluded bowel was fashioned into a Thiry-Vella fistula. Half of the animals were allowed food ad libitum, while the rest were fed intravenously. The animals were killed at 12 days, and plasma, gastrin, and enteroglucagon were measured, while cell proliferation was determined by measuring the crypt cell production rate employing a stathmokinetic method using vincristine and crypt microdissection. In addition to these animals, 16 rats had a jejunal transection only, with half of these animals nourished intravenously, while the remainder were allowed food ad libitum. In the Thiry-Vella rats, plasma enteroglucagon was greater with oral feeding (566 +/- 59 pmol/L) than with intravenous feeding (120 +/- 452 pmol/L) (p less than 0.01), but gastrin levels did not differ in the two groups. In the ileum in continuity, crypt cell production rate per hour was greater in the orally fed animals (52 +/- 8) compared with the intravenously fed group (18 +/- 5) (p less than 0.001). In the excluded fistula, crypt cell production rate per hour was reduced by 23.8 +/- 2 in orally fed rats, but this was greater than in the intravenously fed group (16 +/- 1.5) (p less than 0.01). Both orally and intravenously fed transected rats had significantly lower plasma hormone levels, and reduced crypt cell production rate compared with the respective Thiry-Vella groups. This study suggests a distinct role for a humoral agent responsible for the proliferative changes seen after small bowel resection, and in this respect enteroglucagon appears more relevant than gastrin.

Adaptation, Physiological↗
PubMed1983

Adult cystic fibrosis: postprandial response of gut regulatory peptides.

Responses of 11 gastrointestinal regulatory peptides to a standard test meal were assessed in 10 adult patients with cystic fibrosis. The basal plasma neurotensin was significantly elevated in patients with cystic fibrosis, being 31.5 +/- 6.1 pmol/L compared with a control value of 10.3 +/- 1.5 pmol/L (p less than 0.005). Plasma neurotensin remained elevated throughout the test period. Basal plasma enteroglucagon was similarly elevated, the patients with fibrocystic disease having levels of 51.3 +/- 4.6 pmol/L compared to controls with levels of 33.2 +/- 6.7 pmol/L (p less than 0.02). There was, however, no significant difference in postprandial levels of plasma enteroglucagon. Postprandial motilin was significantly elevated in the patients with cystic fibrosis; this elevation is in contrast with previous findings in children. Release of gastric inhibitory polypeptide was impaired, while release of cholecystokinin showed no significant difference in control values, although there was a tendency for delay. There was no significant postprandial rise of pancreatic polypeptide in the patients, whose levels were grossly lower than controls. Insulin showed a delayed response. No significant differences were observed between patients and controls in levels of gastrin, pancreatic glucagon, somatostatin, or vasoactive intestinal peptide. The elevation of plasma neurotensin and enteroglucagon in the basal state may reflect an adaptive response and may be part of the improved digestive function in adults compared with children with fibrocystic disease.

Adult↗
PubMed1983

Familial chylomicronemia due to a circulating inhibitor of lipoprotein lipase activity.

A mother and her son who have lipoprotein phenotype I are described. They differed from subjects with lipoprotein lipase deficiency in that lipoprotein lipase was present in adipose tissue respectively at 30- and 2-fold the levels seen in normal subjects, and from subjects with apoprotein C-II deficiency in that apoprotein C-II was present in their plasma. They appeared to have an inhibitor to lipoprotein lipase activity in their whole plasma that inhibited that activity eluted from adipose tissue with heparin and that activity present in postheparin plasma of normals. The inhibitor was non-dialyzable, heat-stable, sensitive to repeated freezing and thawing, and appeared to be present in the non-lipoprotein fraction of plasma. The presence of chylomicronemia and the plasma inhibitor in the mother and her son, and possibly in her father and grandson, argues against this being inherited as an autosomal recessive abnormality, as are lipoprotein lipase deficiency and apoprotein C-II deficiency.

Adipose Tissue↗
PubMed1983

The effect of a synthetic enkephalin analogue on postprandial gastrointestinal and pancreatic hormone secretion.

The effect of the synthetic enkephalin analogue Sandoz FK33-824 (DAMME) on gastric emptying and the postprandial secretion of upper gastrointestinal and pancreatic hormones was investigated in six healthy subjects. Gastric emptying was delayed as was the postprandial rise in glucose. There was significant blunting of insulin and gastric inhibitory polypeptide secretion, with complete abolition of the normal postprandial increases in pancreatic polypeptide and motilin. The secretion of gastrin was prolonged. These results demonstrate that pharmacological doses of opiate peptides inhibit gastric emptying and may have direct and indirect effects on gastrointestinal and pancreatic hormone secretion.

Adult↗
PubMed1982

Decreased plasma motilin concentrations in pregnancy.

Plasma motilin concentrations were measured in 37 women during the second and third trimester of pregnancy and one week after delivery. The mean plasma motilin concentrations, both fasting and after a glucose load and a mixed meal, were significantly (p less than 0.001) reduced during pregnancy, returning to the normal range one week post partum. Pregnancy appears to have a profound inhibitory effect on plasma motilin, and this may in part be responsible for the gastrointestinal hypomotility associated with pregnancy.

Female↗