A study of RUNX3, E-cadherin and ß-catenin in CagA-positive Helicobacter pylori associated chronic gastritis in Saudi patients.

OBJECTIVE: H. pylori is the most important risk factor for gastric carcinoma. CagA-positive H. pylori is associated with an increased risk for gastric cancer compared with negative strains. RUNX3 is a tumor suppressor gene, which is related to the genesis of gastric cancer. ß-catenin is integrated with E-cadherin in the cell membrane, and aberrant expression of the complex was reported in gastric carcinoma. Aim of this paper is to determine of the relation between RUNX3, E-cadherin and ß-catenin in chronic gastritis associated with cagA-positive H. pylori infection. PATIENTS AND METHODS: Retrospective study was done on formalin fixed paraffin embedded gastric biopsies blocks of 90 patients diagnosed as H. pylori associated chronic gastritis. H. pylori was detected using modified Giemsa stain. Nested PCR was used for detection of cagA, reverse transcription-PCR for detection of RUNX3 and immunohistochemistry for detection of E-cadherin and ß-catenin. RESULTS: Fifty percent of cases were found to be cagA positive. CagA was significantly associated with the intensity of mononuclear inflammation, the intensity of neutrophilic inflammation, the degree of mucosal atrophy and loss of RUNX3 but not with the density of H. pylori, intestinal metaplasia, E-cadherin or ß-catenin. There was significant relation between loss of RUNX3 and increasing density of H. pylori, intensity of neutrophilic inflammation, mucosal atrophy and intestinal metaplasia. RUNX3 was found to be significantly correlated with E-cadherin but not with ß-catenin. E-cadherin showed decreased expression in 36.7% of biopsies while, ß-catenin was decreased in 33% of biopsies. CONCLUSIONS: Loss of RUNX3, E-cadherin and ß-catenin was considered early events in the cascade of gastric carcinoma development. Loss of RUNX3 but neither E-cadherin nor ß-catenin was related to cagA positive H. pylori strains.

Histological evaluation of the role of atypical antipsychotic drugs in inducing non-alcoholic fatty liver disease in adult male albino rats (light and electron microscopic study).

Many of atypical antipsychotic drugs are associated with adverse metabolic effects, including fatty infiltration of the liver. This study aimed at studying the histological evaluation of the role of atypical antipsychotic drugs (olanzapine and aripiprazole) in adult male albino rats. Sixty adult male albino rats were divided equally into three groups. Group I served as a control while groups II and III were treated with olanzapine and aripiprazole consecutively. Sections of the liver were examined by light and electron microscopy. A highly significant increase in the weight of rats in olanzapine- and aripiprazole- treated groups in comparison to the control group was noticed. On the other hand, there was a highly significant increase in body weight of the olanzapine group in comparison to aripiprazole. Olanzapine- and aripiprazole-treated rats showed highly significantly increased fatty infiltration of liver (steatosis) compared with the control group. However, the aripiprazole-treated group showed less steatosis compared with olanzapine. The mean non-alcoholic steatohepatitis scoring and fibrosis of the olanzapine group were highly significantly increased compared to the aripiprazole group. Ultrastructurally, liver from the olanzapine group showed large fat droplets in perinuclear region, between cisternae of the rough endoplasmic reticulum, and in the space of Disse. Large-sized mitochondria and myelin figures were seen. Although histopathological changes of the liver in the form of non-alcoholic fatty liver disease were more prominent in the olanzapine group, they were also evident in the aripiprazole group.