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Biomedical subjects

G Willems

Publications and source records attributed to G Willems.

At least 109 records · Page 6Linked to original sources

Restoration of colorectal continuity reverses atrophy in human rectal mucosa.

Cell kinetic activity and adaptive response of rectal mucosa from patients with Hartmann's procedure were studied before and after restoration of colorectal continuity. Patients without colostomy and with normal rectal mucosa were used as controls. Autoradiography of in vitro labeled mucosal samples with [3H]thymidine was used. The proliferative activity in the rectal crypts was estimated by measuring labeling and mitotic indices, total DNA of isolated crypts, and total crypt cell numbers. One hundred forty days after creating a proximal end colostomy, labeling index (P less than 0.05), mitotic index (P less than 0.01), DNA content per crypt (P less than 0.05), and number of cells per crypt (P less than 0.05) decreased significantly compared to control values. Restoration of colorectal continuity resulted in a significant increase of the labeling index (P less than 0.05), the mitotic index (P less than 0.01), the DNA content per crypt (P less than 0.05), and the cell number per crypt (P less than 0.05). There were no significant differences between the postclosure values and the controls. These data indicated that excluding the human rectal mucosa from fecal stream determined a mucosal atrophy that could be reversed by restoration of colorectal continuity.

Aged↗

Gastrin stimulates the self-replication rate of enterochromaffinlike cells in the rat stomach. Effects of omeprazole, ranitidine, and gastrin-17 in intact and antrectomized rats.

The enterochromaffinlike cells in the rat stomach are rich in histamine and are thought to be under the influence of gastrin. The effect of sustained endogenous and exogenous hypergastrinemia on the activity and proliferation rate of the enterochromaffinlike cells was studied by determining the histidine decarboxylase activity and histamine concentration and by combining histamine immunocytochemistry and autoradiography after in vivo labeling with [3H]thymidine. The proliferation rate of the stem cells in the oxyntic mucosal progenitor zone was also studied. Exogenous hypergastrinemia was induced by infusion of rat gastrin-17 (60 nmol.kg-1.day-1). Endogenous hypergastrinemia was induced by inhibition of gastric acid secretion with omeprazole (80 mumol.kg-1.day-1) or ranitidine (1200 mumol.kg-1.day-1). The effect of omeprazole was also studied in antrectomized rats. In intact rats, all treatments resulted in elevated plasma gastrin levels and were accompanied by an increase in the histidine decarboxylase activity and the histamine content of the oxyntic mucosa. This resulted in an increase in the enterochromaffinlike cell proliferation rate, leading to enterochromaffinlike cell hyperplasia. The number of labeled stem cells was increased, but this effect was not as pronounced as in the enterochromaffinlike cells. In antrectomized rats, the inhibition of acid secretion by omeprazole did not result in elevated plasma gastrin or in an increase in the activity or number of enterochromaffinlike cells, indicating that omeprazole per se had no effect on these cells. These data support the view that gastrin stimulates the proliferation rate of both enterochromaffinlike cells and stem cells. Gastrin also stimulates the activity of the enterochromaffinlike cells.

Animals↗

Serum gastrin concentration affects the self replication rate of the enterochromaffin like cells in the rat stomach.

The influence of antrectomy and antrum exclusion on the enterochromaffin like cell kinetics in the gastric mucosa of the rat was studied using a combination of histamine immunocytochemistry and autoradiography after in vivo labelling with tritiated thymidine. In all experimental groups, the enterochromaffin like cells were found to incorporate the DNA precursor, thus indicating an ability to divide. The serum gastrin concentration was raised by antrum exclusion and reduced by antrectomy. After antrum exclusion, the enterochromaffin like cell proliferation rate increased as indicated by a doubling of the labelling index and by the resulting enterochromaffin like cell hyperplasia (after six weeks). After antrectomy, the enterochromaffin like cell labelling index decreased to reach 25% of the control value; at this time the enterochromaffin like cell density had not decreased significantly. The observed correlation between the enterochromaffin like cell labelling indices and the serum gastrin concentration supports the hypothesis that enterochromaffin like cell proliferation is influenced by serum gastrin.

Animals↗

Factors influencing the implantation of colon cancer cells on the colonic suture line in rats.

An experimental model is proposed to study suture line recurrence. By giving enemas with K12 colon carcinoma cells, derived from a 1,2-dimethylhydrazine-induced colon cancer in male syngeneic BDIX rats, we were able to obtain a suture implantation in about 30% of the control animals. Possible systemic and local factors which might influence this implantation rate could be studied using this model. Only local irrigations of the colon lumen with sodium hypochlorite 0.2% prior to anastomosis produced a significant decrease in implantation rate. Irrigations with chlorhexidine-cetrimide 2.5%, the use of iodized suture material and altering the cellular immune system of the hosts by ciclosporin or excessive surgical stress, had no significant effect on the implantation rate.

Animals↗

Self-replication of enterochromaffin-like cells in the mouse stomach.

The renewal mechanisms for enterochromaffin-like (ECL) cells, the predominating endocrine cell population in the oxyntic mucosa of the stomach, were investigated in the mouse. The ECL cells were selectively demonstrated by immunostaining using histamine antibodies. Under basal conditions, when observed during the night, ECL cells in mitosis could be seen. This observation proved their ability to divide. Autoradiography after a single pulse and after multiple injections of 3H-thymidine made it possible to study some of their cytokinetic characteristics. The observed replication rate of the labeled ECL cells suggested that self-replication is the main mechanism by which the ECL cell population is renewed. The time interval between two successive divisions of labeled ECL cells was estimated to be around 60 days. Since ECL cells proliferate through mitosis, it may be expected that specific mitogenic stimuli might promote the induction of ECL cell hyperplasia and eventually ECL cell tumors (gastric carcinoids).

Animals↗

[Rectal resection with colo-anal anastomosis for ergotamine-induced rectal stenosis].

Anorectal ulcers due to ergotamine suppositories are extremely rare. We report the first case of rectal stenosis following regular abuse of ergotamine suppositories which required rectal resection and coloanal anastomosis, despite stopping the intoxication 1 year previously. The rectal eversion during the perineal procedure allowed a low anastomosis to be performed, on the dentate line. One year later, the functional result was considered to be good, demonstrating the place of coloanal anastomosis in benign rectal pathology.

Adult↗

Aesthetic limits of light-cured composite resins in anterior teeth.

The aesthetic limits of light-cured composite resins in anterior teeth are determined mainly by the size and nature of the lesion and the respective preparation. Also the shortcomings of the restorative material itself are of primary importance. The oral environment and the ageing effects ultimately limit the aesthetic expectations.

Chemical Phenomena↗

[Marginal adaptation of posterior composites. A complex clinical problem].

In this article, the authors deal with the problem of marginal fit for posterior composites, where direct class-II aesthetic restoration is involved. For different materials, they analyse and discuss the influence of their physicochemical properties, the contour of preparations, and composite handling. Three types of clinical cases are described: preparation using the tunneling technique, adhesive preparation, conventional preparation.

Bicuspid↗

Antithrombin III-dependent anti-prothrombinase activity of heparin and heparin fragments.

Heparin and heparin fragments in the molecular mass range 1,700-20,000 Da were examined for their ability to accelerate the antithrombin III (AT III)-dependent inhibition of human factor Xa and the prothrombin converting complex (prothrombinase) during human prothrombin activation. The prothrombinase reaction was modeled by a 3-parameter 2-exponential equation to determine the initial rate of prothrombin activation and the pseudo-first order rate constants of inhibition of prothrombinase and in situ generated thrombin activity. The catalytic specific activities of the heparins increased with increasing molecular size for both the inhibition of prothrombinase and factor Xa. A 10-fold increase over the entire Mr range was found. In contrast to results obtained by others (Ellis, V., Scully, M. F., and Kakkar, V. V. (1986) Biochem. J. 233, 161-165; Barrowcliffe, T. W., Havercroft, S. J., Kemball-Cook, G., and Lindahl, U. (1987) Biochem. J. 243, 31-37), all the heparins showed a 5-fold higher rate of inhibition of factor Xa when compared with the inhibition of prothrombinase, indicating that the factor Va-mediated protection of factor Xa from inhibition by AT III/heparin is independent of the molecular size of the heparin. Our original approach has also revealed a hitherto unrecognized phenomenon, namely, in addition to the accelerating effect of the heparins on the rate of formation of the inactive AT III-factor Xa complex, heparins with Mr greater than 4,500 reduce the initial rate of thrombin generation in the presence of AT III in a concentration-dependent way. We hypothesize that the formation of the dissociable ternary AT III-heparin-factor Xa complex results in a (partial) loss of factor Xa activity towards its natural substrate prothrombin.

Antithrombin III↗

Recurrent pancreatitis secondary to hypercalcemia following vitamin D poisoning.

A 66-year-old patient had been admitted four times for recurrent episodes of acute pancreatitis. At each time, elevated serum calcium levels, between 13.5-14.5 mg/dl, were found. Surgical drainage of necrotic pancreatic tissue had to be done on one occasion. Extensive investigations failed to disclose any conventional hypercalcemic disease. At his latest admission, the serum calcium level was 13.4 mg/dl, and the serum amylase level was 440 IU/L (N, less than 85). This time, the serum 25-OH vitamin D levels were investigated using radioimmunology and proved to be raised to 330 micrograms/L (normal, 16-74 micrograms/L). Specific questioning of the patient revealed that he had been taking regularly excessive quantities of vitamin supplements as a self medication. After stopping vitamin intake, his serum amylase levels returned to normal, and he had no more episodes of pancreatitis. This case illustrates vitamin D intoxication as a cause of recurrent pancreatitis. Measuring serum 25-OH vitamin D levels is advocated in pancreatitis associated with hypercalcemia of unclear origin.

Acute Disease↗

Proliferation of enterochromaffinlike cells in omeprazole-treated hypergastrinemic rats.

The effect of high doses of omeprazole on the proliferation of the histamine-storing endocrine cells in the oxyntic mucosa, the so-called enterochromaffinlike (ECL) cells, was studied in the rat stomach by combining immunocytochemical staining for histamine with autoradiography after in vivo labeling with [3H]thymidine. Under basal conditions the ECL cells divided very slowly. A progressive increase in the ECL cell labeling index was observed from the second day of omeprazole treatment. The ECL cell density increased progressively from the ninth day of treatment. The plasma gastrin levels were doubled and the labeling index of the cells in the progenitor cell zone was significantly increased. Our data indicate that the omeprazole-evoked ECL cell hyperplasia is a result of accelerated self-replication. The positive correlation between the plasma gastrin concentration and the ECL cell labeling index is compatible with a causal relationship between circulating gastrin levels and increased ECL cell density.

Animals↗

Peroperative ultrasonography in the diagnosis of splenic vein thrombosis.

A case of recurrent bleeding from gastric varices due to isolated splenic vein thrombosis is reported. There was no evidence of pancreatic, retroperitoneal or infectious disease. The final diagnosis was made by intraoperative ultrasonography during an emergency laparotomy for massive bleeding from a ruptured gastric vein. Splenectomy is the treatment of choice in this case. The patient was cured after splenectomy.

Adult↗

Inhibition of factor IXa and factor Xa by antithrombin III/heparin during factor X activation.

We investigated the kinetics of the inhibitory action of antithrombin III and antithrombin III plus heparin during the activation of factor X by factor IXa. Generation and inactivation curves were fitted to a three-parameter two-exponentional model to determine the pseudo first-order rate constants of inhibition of factor IXa and factor Xa by antithrombin III/heparin. In the absence of heparin, the second-order rate constant of inhibition of factor Xa generated by factor IXa was 2.5-fold lower than the rate constant of inhibition of exogenous factor Xa. It appeared that phospholipid-bound factor X protected factor Xa from inactivation by antithrombin III. It is, as yet, unclear whether an active site or a nonactive site interaction between factor Xa and factor X at the phospholipid surface is involved. The inactivation of factor IXa by antithrombin III was found to be very slow and was not affected by phospholipid, calcium, and/or factor X. With unfractionated heparin above 40 ng/ml and antithrombin III at 200 nM, the apparent second-order rate constant of inhibition of exogenous and generated factor Xa were the same. Thus, in this case phospholipid-bound factor X did not protect factor Xa from inhibition. In the presence of synthetic pentasaccharide heparin, however, phospholipid-bound factor X reduced the rate constant about 5-fold. Pentasaccharide had no effect on the factor IXa/antithrombin III reaction. Unfractionated heparin (1 micrograms/ml) stimulated the antithrombin III-dependent inhibition of factor IXa during factor X activation 400-fold. In the absence of reaction components this stimulated was 65-fold. We established that calcium stimulated the heparin-dependent inhibition of factor IXa.

Algorithms↗

Stimulating effect of pentagastrin on cancer cell proliferation kinetics in chemically induced colon cancer in rats.

Pharmacological doses of pentagastrin or gastrin are known to stimulate cell proliferation in normal colonic epithelium but the growth-promoting effect of gastrin on colon carcinoma is still controversial. In this study morphological parameters were measured to study the effect of pentagastrin (240 micrograms/kg) on the cell proliferation kinetics in experimental tumours. Colon cancer was produced in rats by weekly injections (20 mg/kg b.wt.) of 1.2-dimethylhydrazine for 24 weeks. Tritiated thymidine was given after administration of pentagastrin or the control solution to the animals. 75% of the animals from the pentagastrin group and 66% of the controls had at least one colon cancer. Autoradiographs of the colonic tumors were performed and the percentage of labeled cells in the cancer cell population was determined after counting 4000 to 16,000 cancer cells per tumor. The labeling index for cancer cells in the pentagastrin-treated group (21.49 +/- 1.76%) was higher (P less than 0.01) than in the control group (14.76 +/- 0.66%). In a second study vincristine sulphate (1 mg/kg) was given to the animals 20 h after administering pentagastrin or the control solution. The percentage of arrested metaphases in the tumours was determined after counting 10,000 to 24,000 cancer cells per histological section. Pentagastrin increased (P less than 0.01) the mean metaphase index by 108% (4.9 +/- 0.44% vs 2.35 +/- 0.32%). These data indicate that cell cycle manipulation of colon cancer is possible with hormonal peptides.

1,2-Dimethylhydrazine↗

Influence of stress on epithelial cell proliferation in the gut mucosa of rats.

Wistar rats were stressed by immobilization in a cold environment during either 2 or 12 h. The animals were killed 1 h after intraperitoneal injection of 3H-thymidine and autoradiography was used. The proliferative parameters were estimated in the mucosa of the stomach after the 2-hour stress period. After the 12-hour stress period, labeling and mitotic indices were measured in the gastric mucosa as well as in the antrum, duodenum, ileum, colon and epidermis. The stress period of 2 h did not induce significant changes of the proliferative parameters in the mucosa of the stomach whereas cell proliferation was significantly inhibited in all examined tissues, including the skin, after the 12-hour stress period. Gastric hemorrhagic lesions were observed only in the oxyntic part of the stomach and occurred as early as 2 h after stress despite there was no change in the proliferative parameters at this time. The lesions became more obvious after the 12-hour stress period. Our observations indicate that inhibition of cell renewal by stress is not the mechanism by which stress erosions develop in the digestive mucosa.

Animals↗

Aortocolic fistula caused by an ingested chicken bone.

Primary aortocolic fistulas are a rare but lethal complication of aortic or iliac aneurysms. A case of fistula between a nonaneurysmal aortic bifurcation and sigmoid colon caused by an ingested chicken bone is presented. This cause of rectal bleeding, which has never been described, might have been suspected after careful examination of abdominal x-ray films. Surgical management included removal of the foreign body and primary repair of the colonic and aortic rent and appeared to be adequate.

Aged↗