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Biomedical subjects

G Willems

Publications and source records attributed to G Willems.

At least 163 records · Page 9Linked to original sources
PubMed1977

Colonic mucosal atrophy induced by a liquid elemental diet in rats.

The weight, the total crypt cell population, and the proliferation parameters of the colon were estimated in rats during a 4-week administration of a liquid elemental diet (Vivonex standard). Both mitotic and DNA synthesis activity were decreased (P less than 0.01) in the colonic mucosa during the administration of the diet. The weight of the colon was electively decreased (P less than 0.01) from the first week of the treatment. After four weeks, a 75% decrease in the cell population of mucosal glands was observed. This showed that considerable atrophy of the colonic mucosa occurred under the effect of feeding the elemental diet. This atrophy was probably mediated by a reduction in the proliferative activity of the stem cells in the mucosal glands.

Animal Nutritional Physiological Phenomena↗
PubMed1977

Relationship of the gastrin response to the amount of food ingested in normal subjects.

The serum gastrin response to three different amounts of a same meal was studied in 8 normal subjects. The peak gastrin response was similar for the three meals, but the integarated gastrin response was larger with the largest meals. Comparison of the response to the two largest meals indicates that in a given subject the gastrin response is similar when test on different occasions. A good correlation was found between individual fasting concentrations of gastrin and peak gastrin levels after feeding but not between basal gastrin and integrated gastrin response. This could indicate that in normal subjects the first two parameters are primarily related to the same control mechanisms (possibly the G cell mass), while the integrated gastrin response reflects the effectiveness of the feedback mechanisms controlling gastrin release.

Food↗
PubMed1976

Direct method for estimating the total gastrin cell number in the stomach of rats.

An original and simple method for counting the total G cell number in the stomach of small rodents is described. Staining the G cells with the peroxidase-antibody technique and counterstaining the nucleus make it possible to correct the nuclear overestimation. Counting directly the total number of G cells in sections from the entire stomach avoids errors due to tissue retraction and to unprecise delineation of the antro-fundic limit.

Animals↗
PubMed1976

Population kinetics of antral gastrin cells in the mouse.

The proliferation of antral gastrin cells has been studied in adult mice by combining their immunoperoxidase identification on semithin Epon sections with radioautography after single or multiple injections of [3H]thymidine. After a single injection, nuclear uptake of [3H]thymidine was observed in 0.25% of the well-differentiated gastrin cells. Ten days after six successive injections of the precursor, the labeling index reached 4.5%. This indicated that the renewal of the gastrin cell population was very slow. The turnover time was roughly estimated at 2 to 4 months. Analysis of the labeling index curves obtained during and after the administration of [3H]thymidine confirmed that the majority of the gastrin cells were renewed through replication of other gastrin cells. However, differentiation of a fraction of this gastrin cell population from "other" cells in the antrum could not be excluded.

Animals↗
PubMed1975

Cell proliferation and atrophic gastritis in explanted canine gastric mucosa.

We produced experimental atrophic gastritis in 7 mongrel dogs by explanting a full-thickness wedge of vascularized mucosa from the gastric greater curvature onto the abdominal wall. Autoradiography of mucosal specimens was done after the iv injection of triated thymidine. The labeling index, S-phase duration, and cell cycle time were measured in normal and explanted fundic mucosa. The spatial distribution histograms of the labeled cells showed an enlarged are of proliferation. As in human atrophic gastritis, proliferation was shifted toward the mucosal surface. Significantly higher labeling indices were observed in the atrophic mucosa. Shortening of the S-phase duration and the cell cycle time was indicated by the curves of the labeled mitoses. Proliferative activity was significantly accelerated in this experimental model of atrophic gastritis.

Animals↗
PubMed1975

Radioautographic and quantitative studies on parietal and peptic cell kinetics in the mouse. A selective effect of gastrin on parietal cell proliferation.

Gastrin was given to mice subcutaneously at 8-hr intervals for 20 days. Control animals received only saline injections. With use of [3H]thymidine and radioautography, a significant increase in the production of new parietal cells (P less than 0.01) was observed in the gastrin-treated group. Increases in fundic progenitor cell DNA synthesis and shortened maturation time of the latter were demonstrated. Both could explain the observed changes in parietal cell kinetics. The quantitative estimation of parietal cell population after the administration of gastrin showed an increase in average parietal cell count per unit (P less than 0.01) and in total parietal cell number (P less than 0.05). This was consistent with the observed acceleration in the rate of parietal cell production under influence of gastrin. In contrast, no radioautographic difference in the proliferative activity of the peptic cells was observed between the gastrin-treated and the control mice. Moreover, at the end of the experiment, no changes in average peptic cell count per unit area, or in total peptic cell number, occurred under the effect of gastrin. The observation that peptic cells are renewed in a different way, independently from fundic progenitor cells and from parietal cells, was consistent with their peculiar lack in proliferative response to the hormone.

Animals↗