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L P Thomas

Publications and source records attributed to L P Thomas.

11 recordsLinked to original sources
PubMed1991

Review of the literature and report of a case of a dermoid cyst.

This article presents a large dermoid cyst discovered in the floor of the mouth of a young male patient. The lesion was clinically detected by manual palpation and confirmed by the use of magnetic resonance imaging. Treatment of this case was by surgical removal of the dermoid cyst. The patient recovered without any complications or evidence of re-occurrence of the cyst.

Child↗
PubMed1989

Prostaglandin E2 production by dispersed canine fundic mucosal cells. Contribution of macrophages and endothelial cells as major sources.

Endogenous prostaglandins (PGs) influence resistance of the gastric mucosa to injury, but the source of PGs is unknown. Using radioimmunoassay, we studied PG production by dispersed canine fundic mucosal cells. PGE2 production, stimulated by bradykinin, epidermal growth factor, zymosan, and calcium ionophore, was greater in the small-cell elutriator fraction (SCEF) than in the medium and large cell fractions, which contained mucous, chief, and parietal cells. Linear density gradients of SCEF cells revealed maximal PGE2 production in cells of light density. Mast, endocrine, and endothelial cells did not account for this PGE2 production. Macrophages, identified by uptake of acetylated-LDL, immunoreactivity with antibodies to the human Ia antigen, and phagocytosis of fluorescent latex particles, were enriched in the SCEF and correlated with PGE2 production in the density gradient. Magnetic separation of cells in the SCEF-ingesting iron particles enriched PGE2 production. Fractions enriched in endothelial cells present in intact capillary fragments, but depleted of macrophages, also produced PGE2. Regulation of PGE2 production differed among cell types. Fibroblasts were easily cultured from submucosa, but were not detected in the SCEF. We conclude that macrophages and capillary endothelial cells are major producers of PGE2 in the canine fundic mucosa.

Animals↗
PubMed1984

Release of somatostatinlike immunoreactivity from canine fundic mucosal cells in primary culture.

We have developed a model to allow study of the release of somatostatinlike immunoreactivity (SLI) from gastric mucosal cells. Collagenase-dispersed canine fundic mucosal cells were separated by counterflow elutriation. SLI-containing cells were identified in the fractions with small cells (9-11 microns), and these fractions were plated onto collagen. After 2 days in culture, SLI content of the cells was maintained; SLI-positive cells, detected by peroxidase-antiperoxidase immunohistochemistry, comprised 70 +/- 6% (mean +/- SE, n = 6) of these cultured cells. Release of SLI from these cultures into the medium was determined by radioimmunoassay. Epinephrine, dibutyryl cAMP, and gastrin each stimulated SLI release in a time-dependent manner, with a steady rate of secretion maintained for 120 min of incubation. Both epinephrine and dibutyryl cAMP markedly potentiated the release of SLI stimulated by gastrin but were not themselves mutually potentiating. Upon Sephadex G-50 column chromatography of incubation medium and extracts of cultured cells, SLI eluted primarily in a single peak that cochromatographed with synthetic somatostatin tetradecapeptide. Our data suggest that gastrin and adrenergic stimuli act directly on canine fundic somatostatin cells and that potentiating interactions between secretagogues may be important modulating elements in somatostatin cell secretory function.

Animals↗
PubMed1984

Gastrin receptors on nonparietal cells isolated from canine fundic mucosa.

The cellular localization of gastrin receptors was studied using dispersed canine fundic mucosal cells. In previous studies 125I-[Leu15]gastrin-17 (125I-[Leu15]G-17) binding was found to parietal cells, but gastrin binding was also found in the small-cell elutriator fractions (SCEF). In the present study a density gradient was used to further separate the SCEF and the distribution of 125I-[Leu15]G-17 binding correlated with cellular content of somatostatinlike immunoreactivity (SLI). In contrast, 125I-[Leu15]G-17 binding was inversely correlated with the histamine content of the fractions. 125I-[Leu15]G-17 binding to the SCEF was rapid and reversible. Total binding was 0.29 +/- 0.02 fmol/10(6) cells (mean +/- SE, n = 15); excess unlabeled G-17 inhibited 85% of this binding. G-17, [Leu15]G-17, and 127I-[Leu15]G-17 were equipotent in inhibiting 125I-[Leu15]G-17 binding and stimulating SLI secretion from the SCEF placed in short-term culture, whereas 127I-G-17 had a low potency for both effects. Proglumide, known to inhibit cholecystokinin binding to pancreatic acinar cell receptors, also inhibited 125I-[Leu15]G-17 binding to the SCEF and inhibited G-17 stimulated SLI release. We conclude that in the canine fundic mucosa gastrin interacts with receptor sites on parietal cells and somatostatin cells but probably not on fundic mucosal histamine-containing cells. These receptor sites for gastrin may activate counterbalancing mechanisms regulating the secretion of acid.

Animals↗
PubMed1984

Gastrin receptors on isolated canine parietal cells.

The receptors in the fundic mucosa that mediate gastrin stimulation of acid secretion have been studied. Synthetic human gastrin-17-I (G17) with a leucine substitution in the 15th position ( [Leu15]-G17) was iodinated by chloramine T; high saturable binding was found to enzyme-dispersed canine fundic mucosal cells. 127I-[Leu15]-G17, but not 127I-G17, retained binding potency and biological activity comparable with uniodinated G17. Fundic mucosal cells were separated by size by using an elutriator rotor, and specific 125I-[Leu-15]-G17 binding in the larger cell fractions was highly correlated with the distribution of parietal cells. There was, however, specific gastrin binding in the small cell fractions, not accounted for by parietal cells. Using sequential elutriation and stepwise density gradients, highly enriched parietal and chief cell fractions were prepared; 125I-[Leu15]-G17 binding correlated positively with the parietal cell (r = 0.98) and negatively with chief cell content (r = -0.96). In fractions enriched to 45-65% parietal cells, specific 125I-[Leu15]-G17 binding was rapid, reaching a steady state at 37 degrees C within 30 min. Dissociation was also rapid, with the rate similar after 100-fold dilution or dilution plus excess pentagastrin. At a tracer concentration from 10 to 30 pM, saturable binding was 7.8 +/- 0.8% per 10(6) cells (mean +/- SE) and binding in the presence of excess pentagastrin accounted for 11% of total binding. G17 and carboxyl terminal octapeptide of cholecystokinin (26-33) were equipotent in displacing tracer binding and in stimulating parietal cell function ( [14C]aminopyrine accumulation), whereas the tetrapeptide of gastrin (14-17) had a much lower potency. Proglumide inhibited gastrin binding and selectively inhibited gastrin stimulation of parietal cell function. Canine parietal cells have specific receptors for gastrin that mediate stimulation of parietal cell function. Gastrin receptors were undetectable on chief cells, and yet present on another smaller mucosal cell(s).

Aminopyrine↗
PubMed1982

Electrical effects of histamine on monolayers formed in culture from enriched canine gastric chief cells.

To develop techniques for studying transport properties and secretory function of selected cell types in the gastric mucosa, separated fractions of dispersed canine fundic mucosal cells were placed in short-term culture to form epithelial monolayers. Cell fractions enriched in either chief, parietal, or mucous cells were prepared by using counterflow centrifugation and were plated on type I collagen. An epithelial monolayer formed by approximately equal to 36 hr. Immunofluorescence with an antipepsinogen I antibody revealed pepsinogen-containing granules in greater than 95% of the cells, regardless of whether the monolayers were formed from the mucous, chief, or parietal cell-enriched fractions. Upon achieving confluency, chief cell monolayers were mounted in Ussing chambers to study their electrical properties. Under basal conditions, monolayers (n = 6) had a spontaneous potential difference (PD) (+/- SEM) of 26 +/- 4 mV (apical surface negative), a short-circuit current (Isc) (+/- SEM) of 16 +/- 2 microA/cm2, and a transepithelial resistance (R) (+/- SEM) of 1,480 +/- 210 omega X cm2. Histamine increased the short-circuit current, an effect blocked by an H2-receptor antagonist. Seventy percent of the spontaneous PD was amiloride sensitive, suggesting sodium absorption accounted for a major component of the PD. These preparative techniques yield highly enriched chief cell monolayers, which maintain morphological and functional cellular differentiation for greater than 48 hr in culture, thus allowing study of oriented functions of a selected cell type. The present studies indicate that an H2 receptor enhances electrogenic ion transport in chief cell monolayers, indicating that histamine can act on fundic mucosal cells other than just parietal cells.

Animals↗