Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our aim was to determine whether the development of gap junctions in the human gastric mucosa has any relation to gastric ulcer and gastric carcinoma. Freeze-fracture replicas were prepared from the endoscopic biopsy specimens of 20 patients with gastric ulcer and 7 healthy volunteers. Large fractured areas of lateral cell membranes of surface mucous cells were examined randomly under an electron microscope. 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 the areas of intestinal metaplasia, gap junctions were occasionally seen between absorptive cells of the villi, but not in the lateral membranes of goblet cells. Fresh frozen sections for indirect immunofluorescence were prepared from the endoscopic biopsy specimens of 19 patients with gastric ulcer and 5 patients with gastric cancer. Monoclonal antibody against liver gap junction protein (anti-connexin 32, 6-3G11) was used for the indirect immunofluorescence. On the border of gastric ulcer, fluorescent spots in the surface mucous cells were significantly fewer than in the surface mucous cells of the body and antrum which were distant from the ulcer area in the same patients. In gastric cancer tissue specimens, fluorescent spots were not observed at all.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Freeze-fracture and immunohistochemical studies of gap junctions in human gastric mucosa with special reference to their relationship to gastric ulcer and gastric carcinoma. 767 Jan 61

In this study we investigated the relationship between chronic gastric ulcers and the appearance of connexin 32 or connexin 43. Samples were taken endoscopically and the appearance of connexin 32 or connexin 43 was assessed by Western blotting using anticonnexin 32 or anticonnexin 43 antibodies. Normal gastric mucosa contained both connexin 32 and connexin 43. In contrast, gastric mucosa surrounding a chronic gastric ulcer lesion contained a smaller amount of connexin 32 and connexin 43. We also investigated the relationship between the appearance of connexins and ulcer healing. Antiulcer treatment for chronic gastric ulcer was administered. When ulcer healing was observed, connexins 32 and 43, which decreased at the active ulcer stage, had returned almost to levels observed in normal gastric mucosa. These data clearly indicate that disappearance of both connexin 32 and connexin 43 is closely related to the stage of chronic gastric ulcer lesions.
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PMID:Human chronic gastric ulcer and connexin. 877

This study examined the relationship between healing of acetic acid-induced chronic gastric ulcer and connexin formation. In addition, the effect of anti-ulcer drugs on ulcer healing and the presence of connexin was investigated. In a rat model, acetic acid-induced gastric ulcers were healed without administration of drugs after 14 days. Appearance of an electrophoretic connexin 32 band was observed 7 days after ulcer induction. Administration of cimetidine (3 mg/day) promoted ulcer healing, i.e., ulcers were healed 12 days after ulcer induction, 2 days earlier than the control. The appearance of a connexin 32 band in electrophoresis was observed on the fourth day after ulcer induction. Administration of cimetidine at a higher dose further promoted ulcer healing and the connexin 32 band was more strongly visible. After administration of i.p. 2 nM EGF, acetic acid-induced gastric ulcers were healed 12 days after ulcer induction and the appearance of connexin 32 was observed on the fourth day after induction. These results indicate that connexin 32 is related to the healing of acetic acid-induced gastric ulcers.
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PMID:Relationship between healing of acetic acid-induced chronic gastric ulcer and connexin. 947 36

The patient was a 72-year-old man who had a history of subtotal gastrectomy for gastric ulcer at age of 37 years. He had no familial history of hereditary disorders. In 1980 he noticed mild ataxic gait which exaggerated while he closed eyes. The symptoms increased gradually, and four years later he noticed hypoesthesia of his soles. In 1983 he was admitted to the National Center Hospital for Mental, Nervous and Muscular Disorders for the first time. Neurological examination revealed dysarthria, ataxic gait, disturbance of coordination to a slight degree, and muscle strength of the upper and lower limbs were in normal range. Mild hypoesthesia of pain and temperature sensation, and marked decrease of deep sensation and vibration of the lower extremities were demonstrated. Romberg sign was positive. EMG studies revealed low amplitude of action potential and normal motor nerve conduction velocity. Biopsy of the sural nerve showed marked decrease of both large and small myelinated fibers. In 1998 he was admitted second time for the further examination. Laboratory examination including routine blood examination, blood chemistry including CRP, TPHA, vitamin B1, B2, B12, A, E, K, hexosaminidase A in leucocyte were in normal range. CSF was normal. Genetic studies including SCA 1, 2, 3, 6, DRPLA, CMT1A, CMTX 1 were all negative. MCV of lower limbs was in normal range, though SCV was not evoked in the upper and lower limbs. MRI studies showed mild atrophy of the bilateral lobulus of the cerebellum which was not so much changed in the last 5 years. The clinical symptoms revealed dominant posterior column disturbance, ataxia and sensory neuropathy. These combination was not described in the previous literature, and this case may be a new variant of the spinocerebellar degeneration.
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PMID:[A case with posterior column ataxia associated with cerebellar ataxia and sensory neuropathy]. 1061 59