ABSTRACT
Experiments were performed to demonstrate that adherence of Helicobacter pylori to gastric epithelial cells causes alterations in the cell cytoskeleton. H. pylori intimately attached to cultured human gastric epithelial cells on small cellular projections, while there was no intimate association of H. pylori with cultured human esophageal epithelial cells. Fluorescein-conjugated phalloidin staining of gastric epithelial cells showed that H. pylori adherence stimulated actin polymerization; this stimulation was not observed with esophageal cells. Also, this organism's selectivity for gastric mucosa was supported by rare binding of bacteria to esophageal epithelial cells and gastric fibroblasts.
Subject(s)
Bacterial Adhesion , Gastric Mucosa/microbiology , Helicobacter Infections/pathology , Helicobacter pylori/pathogenicity , Actins/metabolism , Adenocarcinoma/microbiology , Adenocarcinoma/pathology , Cytoskeleton/ultrastructure , Epithelium/microbiology , Esophagus/cytology , Esophagus/microbiology , Fibroblasts/microbiology , Humans , Microscopy, Electron , Stomach Neoplasms/microbiology , Stomach Neoplasms/pathologyABSTRACT
A review of 34 patients was conducted to investigate the causes of hepatic encephalopathy. Hypokalemia, infection, and gastrointestinal tract bleeding were found to be the usual precipitating factors. Women are affected more commonly, and gastrointestinal tract hemorrhage is usually the terminal event.
Subject(s)
Hepatic Encephalopathy/etiology , Adult , Aged , Female , Humans , Liver Cirrhosis, Alcoholic/etiology , Male , Middle Aged , Retrospective StudiesABSTRACT
Dysphagia was observed in two patients receiving combination chemotherapy for metastatic carcinoma of the breast. Results of esophagogram and esophagoscopy were unremarkable. Vincristine, an anticancer drug, was incriminated as the causative agent. Cessation of vincristine therapy resulted in definite improvement. In one patient, inadvertent administration of vincristine caused prompt recurrence of dysphagia, which again disappeared upon discontinuation of the drug. The major toxicity of vincristine is neurologic. The exact mechanism for vincristine-induced dysphagia is unknown, but it does appear to be reversible.
