Ultrastructure of Rabbit Pyloric Mucosa Following Ligation of Common Bile Duct / 체질인류학회지

The purpose of this study was to examine the ultrastructural characteristic of the normal pylorus mucosa, and their structural changes induced by the ligation of common bile duct of the male rabbits weighing about 1.5 kg each. Experiment animals were divided into normal, sham operation, and experimental groups. Common bile duct ligation was performed under ether anesthesia and anjmals were sacrificed on the 1st, 3rd, 5th, 7th and 14th day after operation. The mucosal specimen of the pylorus, were fixed and embedded with common method. The sections were cut on a LKB-V ultratome, and observed under a JEM 100CX II electron microscope. The results were as follow : 1. In the early stages (1st, 3rd, 5th day groups) following the ligation, surface mucous cells have the various electron densities and shape of the mucous granules. In the late stages (7th, 14th day groups) following the ligation, many surface mucose cells containing numerous electron dense mucous granules are seen. 2. In the early stage of the ligation of bile duct, secretory function of EC cells was depressed, but in the later stage, the cells showed recovered secretory activity. 3. Secretory function of D cells was depressed on the early groups after the ligation of common bile duct, but they showed recovered secretory activity from the late groups after the ligation of the common bile duct. 4. Secretory function of G cells was activated on the early groups after the ligation of common bile duct, but they showed depressed secretory activity from the late groups after the ligation of the common bile duct. Considering the above findings, common bile duct ligation probably causes the dysfunction of the pyloric surface mucous cells that results in delayed mucous formation and secretion, and recovered mucous secretory function on the late stages. EC cells and G cells, depressed the secretory activities on the early stages and recovered on the late stages of the ligation of common bile duct. But D cells in the pyloric mucosa was activated on the early groups after the ligation of common bile duct ligation, but they was depressed secretory activities on the late groups.

Comparative Study on Serum Gastrin and G-cell in Gastric Antrum of Three Rat Models of Syndrome of Deficiency of Spleen-QI / 中华中医药杂志

Objective: To make comparative study on serum gastrin(SG) and gastrin secretory cell(G-cell) in gastric antrum(GA) of three rat models of syndrome of deficiency of spleen-QI.Methods: Animals were randomly divided into four groups in terms of control group,rhubarb group,double factors group(combination of rhubarb method and swimming exhausting energy method) and triple factors group(combination of rhubarb method,swimming exhausting energy method and starvation method).The indexes such as Serum gastrin and G-cell in gastric antrum(GA) et al were detected.Results: Compared with control group,the variances of above-mentioned indexes in double factors group and triple factors group have statistical significance(P

IMMUNOELECTRON MICROSCOPIC STUDY ON G CELLS AND D CELLS IN ANTRAL MUCOSA OF RAT / 解放军医学杂志

Revised immunoelectron microscopic technique was used to examine G cells and D cells in rat antral mucosa. The number of colloidal gold granules in G and D cells was analysed through quantitative analysis. The results showed that immunological granules of colloidal gold distributed in both G and D cells. Gastrin- or somatostatin-labeled granules were present mainly as lobation-like or island-like congeries. Most of the golden congeries dissociated in the cytoplasm of G or D cells, being in the basement membrane side. A few of the golden congeries located in nucleus. The number of golden granules was 107. 04 ?19. 68 and 83. 36?17. 58 per one G and D cell, respectively.

STUDY ON THE VARIATIONS OF G AND D CELLS IN GASTRIC ANTRUM AFTER H.PYLORI INFECTION / 解放军医学杂志

0 05). However, the gray of G cells were significantly enhanced( ?

The effect of Helicobacter pyiori infecton on the function of antral G cell in patients with active duodenal ulcer and functional dyspepsia / 中华消化杂志

ObjectiveTo investigate the effect of Helicobacter pylori (H. pylori) infection on the func-tion of antral G cell in patients with active duodenal ulcer (DU) and functional dyspepsia (FD). Methods According to the status of H. pylori, 77 patients with active DU were randomly divided into three groups:group A, 51 cases whom H. pylori successfully eradicated (male 37 and female 14, with mean age of 35.2± 12.6); group B, 12 cases remained H. pylori positive after eradication therapy (male 9 and female 3, 34.5± 10.3) and group C, 14 H. pylori-negative patients (male 9 and female 5, 37.5 ± 11.8). Twenty-five H.pylori-eradicated FD patients served as controls (male 15 and female 10, 38.1 ± 12.6). Before and one month after therapy gastroendoscopy was performed and antral mucosa specimens were taken to detect the number of G cell (immunohistochemistry) and the expression of gastrin gene (RT-PCR with addition of α-32p-dATP).The plasma gastrin concentrations were also measurece by RIA. ResultsUlcer healed in all DU patients after the therapy. There was no significantly difference in G cell number among the four groups. Before therapy ex-pression levels of gastrin gene were significantly higher in all DU patients (group A 424.5 ± 151.6, group B 435.1 ± 113.8, group C 368.0 ± 184.3) than in FD patients (group D 215.8 ± 94.9 Bq, P ＜ 0.01 ). How-ever, there was not different between those in H. pylori-positive and H. pylori-negative DU patients ( P ＞0.05). Gastrin concentrations and its gene expression levels in DU patients tended to decrease after therapy but the difference was not significant no matter H. pylori was eradicated or not. However in FD patients (group D) they were decreased after H. pylori eradication (P < 0.05). Although gastrin levels in FD were similar to that in DU patients before the therapy, it was significantly decreased in FD than in DU after H. py-lori eradication (P<0.001). There was a positive relationships between plasma gastrin concentrations and its gene expression level in antral mucosa ( P < 0.05). ConclusionH. pylori infection does not affect antral G cell number but stimulates gastrin gene expression and gastrin release, which decreases after H. pylori eradica-tion. So, it can conclude that H. pylori infection and ulcer per se may affect the function of antral G cells.

Relationship of CagA to serum gastrin concentrations and antral G, D cell densities in Helicobacter pylori infection

The purpose of this study was to investigate whether the densities of antral gastrin and somatostatin-immunoreactive cells in Helicobacter pylori (H. pylori) infection were related to the bacterial expression of cytotoxin-associated gene A (CagA). 32 patients who had underwent diagnostic esophagogastroduodenoscopy were studied. On the histologic examination all patients had antral gastritis. We divided the subjects into three groups. Group I consisted of 6 patients who had chronic superficial gastritis, group II, 9 patients who had H. pylori-associated gastritis but with no expression of CagA, and group III, 17 patients who had H. pylori-associated gastritis with the expression of CagA. In group I and II, serum gastrin levels, and antral G cell and D-cell were measured. In group III, serum gastrin levels, and antral G cell and D-cell were measured, before and after the eradication of H. pylori. The results were as follows. Firstly, serum gastrin concentrations were significantly higher in the patients with H. pylori infection than in the negative controls. Nextly, there was no correlation between the changes in antral G or D-cell density and H. pylori infection. Thirdly, group III had a significant increase in serum gastrin concentrations and a significant decrease in antral D-cell density than group I. Forthly, eradication of H. pylori in group III showed a significantly increased antral D-cell density. Our results suggest that hypergastrinemia in H. pylori-associated gastritis is relevant to the presence of CagA, and the possible mechanism of hypergastrinemia may be related to antral D-cell deficiency, which is caused by H. pylori infection with the expression of CagA.

HISTOGENESIS OF THE HUMAN STOMACH / 解剖学报

In this article we collected 2 embryos and 69 fetuses between 7 and 30 weeks of gestational age and 3 neonates to study the development of the human stomach by histological, histochemical and immunogold-siver methods. In 7-week embryo, the superficial layer of gastric mucosa was stratified columnar epithelium, containing a large amount of glycogen. In 9-week fetus, simple columnar epithelium, gastric pits and glandular buds were observed. At this stage a few parietal cells could be identified at the bottom of the glands. The pyloric glands contained parietal cells as fundic glands. At 13-14 week the muscularis mucosa appeared and the wall of stomach formed definitively as the adult. A few argyrophil cells in antrum and fundus were found at 12-week fetus. They scattered in the surface epithelium and concentrated in the lower portion of the glands. The argyrophil cells were round, pyramidal or spindle in shape. More argyrophil ceils were found in the antrum from 14-week on. At 18-week, the argyrophil cells were most numerous. Some cells possessed processes extending to the basement membrane or parietal cells. Between 15-30 weeks various shaped EC cells in fundus were found, with some open-type endocrine cells. G cells in antrum were mostly rounded and often in groups at 13,16 and 21 week. Developing G cells were observed under EM.

IMMUNOHISTOCHEMICAL STUDY ON G AND D CELLS IN PANCREATIC ISLETS OF RAT DURING EXPERIMENTAL GASTRIC ULCER / 解剖学报

Objective Studies on the changes of gastrin and SS immunoreactive cells in pancreatic islets during experimental gastric ulcer. Methods The immunohistochemical ABC technique was used. Results The gastrin immunoreactive cells were located in most of the pancreatic islet. The mumber of G cells in experimental gastric ulcer group were higher than that of control group on the 4th and 10th day after operation.The D cells raised on the 10th day.Conclusion The present work provides the evidence that the G and D cells of pancreatic islets might be involed in the self-healing process of the experimental gastric ulcer by endocrine or paracrine regulation.