Fusao Ueda

Electron microscopic study of intercellular junctions in human gastric mucosa with special reference to their relationship to gastric ulcer.

The development of gap junctions in the human gastric mucosa has been examined to see if there is any relation to gastric ulcer. Freeze fracture replicas were prepared from the endoscopic biopsy specimens of 20 patients with gastric ulcer (15 men and five women, aged 49 (13) years) and seven healthy volunteers (four men and three women, aged 41 (19) years). Large fractured areas of lateral cell membranes of surface mucous cells were observed randomly at a direct magnification of 15,000 using electron microscopy. Small gap junctions were observed between gastric surface mucous cells in all healthy volunteers. Gap junctions in the patients with gastric ulcer were significantly fewer than in the healthy volunteers. In addition, gap junctions in patients with recurrent ulcer were significantly fewer than in those with first onset ulcer. There was no obvious relationship between age and the development of gap junctions in patients with gastric ulcer or in healthy volunteers. In areas of intestinal metaplasia, gap junctions were occasionally seen between absorptive cells of the villi, but not in the lateral membranes of goblet cells. These findings suggest that loss of intercellular communication via gap junctions is associated with gastric ulcer formation.

Behavioral and Electroencephalographic Studies of Beagles with an Eck's Fistula: Suitability as a Model of Hepatic Encephalopathy

Behavioral manifestations, electroencephalograms (EEGs) and visually evoked potentials (VEPs) were studied in beagles with Ecks fistula (portacaval shunt [PCS]), an established model of hyperammonemia, to determine whether they developed CNS disorders characteristic of hepatic encephalopathy. After PCS, behavioral changes occurred in the form of listlessness, sluggishness (altered gait, snapping and transient catatonia-like symptoms) and apparent blindness, which appeared in that order and progressed to coma and death in some animals. The EEGs from the frontal cortex showed a gradual decrease in voltage and frequency. Development of snapping and catatonia-like symptoms coincided with the occurrence of high voltage fast waves in the EEGs from the occipital cortex. In comatose Ecks fistula dogs. flattening of the EEGs was recorded from the frontal cortex and a lowered voltage was noted in the EEGs from the occipital cortex. After PCS, the latencies and amplitudes of the components of VEP were increased. The snapping and catatonia-like symptoms were markedly ameliorated by carbamazepine and the coma by flumazenil and thyrotropin-releasing hormone. These findings indicate that Ecks fistula dogs provide a useful model of hepatic encephalopathy.