Biomedical subjects

J S Hsieh

Publications and source records attributed to J S Hsieh.

58 records · Page 4Linked to original sources

PubMedDate not supplied

The role of epidermal growth factor in gastric epithelial proliferation in portal hypertensive rats exposed to stress.

BACKGROUND/AIMS: This study was designed to determine whether epidermal growth factor may have a role in the stomach of portal hypertensive rats after exposure to water immersion and restraint stress. METHODOLOGY: Rats with portal hypertension (portal vein partial ligation) were studied to determine the proliferative response of the gastric epithelium to epidermal growth factor (EGF) during stress. The portal hypertensive rats received EGF (0, 10, 25, 50, and 100 microg/kg/day) subcutaneously for 7 days before water immersion restraint stress. Each rat was subjected to water immersion restraint stress for 6 hours, at the end of which the stomachs were excised to evaluate gross and microscopic mucosal damage, and gastric epithelial proliferation using proliferating cell nuclear antigen (PCNA) immunoreactivity. RESULTS: The gross and microscopic mucosal damage were significantly greater in control or low dose EGF-pretreated (10 or 25 microg/kg/day) rats than in high dose EGF-pretreated (50 or 100 microg/kg/day) rats (p<0.01). These changes were accompanied by parallel alterations in the PCNA labeling index. The PCNA labeling index between high dose EGF-pretreated and control or low dose EGF-pretreated rats differed significantly (p<0.01). CONCLUSIONS: This study clearly indicates that the influence of EGF on the proliferative response of the portal hypertensive (PHT) gastric epithelium to stress in rats was dose-dependent, suggesting an important role for EGF in the protection of PHT gastric mucosa from stress injury.

Animals↗

PubMedDate not supplied

Mutations of p53 gene in gastric carcinoma in Taiwan.

BACKGROUND: p53 gene mutation and p53 protein accumulation is the most common event in human cancers. The present study was conducted to investigate the occurrence of p53 mutations in patients with gastric carcinoma in Taiwan. MATERIALS AND METHODS: Tumor samples from 36 patients with primary gastric carcinoma undergoing radical gastrectomy were evaluated. The mutational status of the p53 (exons 5 to 8) was screened by polymerase chain reaction/single strand conformation polymorphism (PCR-SSCP) analysis followed by direct sequencing. These results were compared with p53 protein expression as assessed by immunohistochemical staining. RESULTS: Of all 36 gastric carcinomas, mutations of the p53 gene were found in 7 cases (19.4%). These results from direct sequencing indicated that mutations consisted of five missence mutations, one silent mutation and one mutation within the splice donor site of intron 5. Mutations were found at codon 145 in exon 5 (1 case), intron 5 (1 case), codon 248 in exon 7 (1 case), codon 251 in exon 7 (2 cases), codon 285 in exon 8 (1 case) and codon 287 in exon 8 (1 case). The mutation hot spot at codon 251 in gastric cancer has not been observed previously. Over-expression of p53 oncoprotein was observed in 10 patients (27.8%) immunohistochemically. CONCLUSIONS: p53 gene mutation might contribute to the pathogenesis of human gastric carcinoma. However, the suggestion awaits further investigation for confirmation.

Adenocarcinoma↗

PubMedDate not supplied

The effect of portal hypertension on expression of gastric mucin mRNA in rats.

BACKGROUND/AIMS: Gastric mucin, a principal component of gastric mucus, is thought to play an important role in protecting gastric mucosa and maintaining the homeostasis of the gastric mucosa. Our previous studies have demonstrated that the contents of gastric mucin were decreased in rats with portal hypertension. Thus, the purpose of this present study was designed to confirm the effect of portal hypertension on the expression of gastric mucin mRNA and to localize gastric mucin mRNA production site in rats. METHODOLOGY: Portal hypertension was induced experimentally by partial ligation of the portal vein in Wistar rats. The severity of gastric mucosal lesions was evaluated macroscopically by a gross ulcer index. We simultaneously measured the levels of mRNA in the gastric tissues of control and portal hypertension rats by reverse transcription-polymerase chain reaction, Southern blot hybridization, and in situ hybridization. RESULTS: The damage to gastric mucosa was found to be prominently greater in the portal hypertension rats compared to the control (P < 0.01). The expression of mucin mRNA was significantly reduced in portal hypertension rats compared to the control using the reverse transcription-polymerase chain reaction and Southern blot hybridization (both P < 0.01). In situ hybridization showed that mucin mRNA was localized primarily in the gastric submucosa and mucosa, particularly in the surface mucous and the gland mucous cells. CONCLUSIONS: Our results reveal that portal hypertension would cause a decrease in mucin mRNA, and it would be helpful in understanding the mechanism of gastric mucosal mucin alteration in portal hypertension and the pathogenesis of portal hypertension gastropathy. Furthermore, it may provide the strategy in the prevention and therapy of portal hypertension gastropathy.

Animals↗

PubMedDate not supplied

The effect of portal hypertension on transforming growth factor-alpha and epidermal growth factor receptor in the gastric mucosa of rats.

The aim of this study was to evaluate the expression of transforming growth factor-alpha (TGF-alpha) and epidermal growth factor receptor (EGFR) immunohistochemically in gastric mucosa of portal hypertensive (PHT) and sham-operated rats. PHT was induced experimentally by partial ligation of the portal vein (PVL) in 12 male Wistar rats; another group of 12 rats (control) received sham operations. The severity of macroscopic gastric mucosal lesions and immunoreactivity of TGF-alpha and EGFR were evaluated 14 days following the above procedure. The damage to gross gastric mucosa was found to be significantly greater in the PVL group than the control group (p<0.01). Additionally, the TGF-alpha and EGFR immunoreactivities were significantly more intense in the PVL groups compared to the control (P<0.05). The TGF-alpha and EGFR immunoreactive cells were more prominent around injured mucosa. From these findings, we suggest that locally produced TGF-alpha and EGFR may play an important role in the gastric mucosal repair following PHT to rats.

Animals↗