[Enteropathic amyloidosis: clinical features, place among other forms of amyloidosis].
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Biomedical subjects
Publications and source records attributed to L P Miagkova.
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Mucosal repair in the stomach and duodenum was assessed clinically and morphologically in various ulcer phases in 475 patients with gastroduodenal ulcer. It was found that poorly scarring ulcers are characterized by severe impairment of regeneration with epithelial proliferation prevailing over its differentiation. Participation of immune system, primarily T-cell component, in regeneration regulation is shown. Helicobacter pylori is not involved in repair. Superoxide dismutase activity in red cells and ulcer edges mucosa is prognostically significant indicating the disease phase, completeness of ulcer process.
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Helicobacter pylori (HP) in 41 patients (10 with stomach ulcer and 31 with duodenum ulcer) was found in gastro-biopsies from the stomach antrum before and after the treatment. The following methods to reveal HP were used: Giemsa staining, immunoperoxidase reaction with polyclonal monospecific antibodies against HP, urease rapid test. HP was also revealed in the blood serum by antibodies against HP by means of enzyme immunoassay. Electron microscopy was performed in 5 patients and bacteriologic study in 10 patients. Immunohistochemical method allows one to judge about real HP colonization of the gastric mucosa. Bacterioscopy with Giemsa staining gives good results but they are not true markers of HP presence this being explained by other methods. Serologic enzyme immunoassay gives an idea about the patient contamination, but not about HP eliminations as a result of treatment. Urease-test is adjuvant.
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The description is given of Shwachman syndrome in a male of 17, with a long anamnesis of malabsorption syndrome, granulocytopenia, repeated bronchopneumonia, somatogenic subnanism and hypogonadism. The death resulted from acute cardiovascular insufficiency. Post-mortem examination revealed exocrine pancreas hypoplasia with lipomatosis, Wirsung duct atresia, fibrocholangiocytosis and fat hepatosis, visceral anemia, delay in the maturation of granulocytes in the bone marrow, somatogenic polyglandular endocrinopathy, metabolic myocardium necrosis, calcinosis of the small arteries wall, lymphoid tissue atrophy, focal pneumonia of the upper lobe of the left lung.
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The paper deals with reparative potential of gastric and duodenal mucosa in ulcer in connection with the presence and quantity of Campylobacter pylori (CP) which is found practically in all patients not only with duodenal localization of ulcer but with mediogastric and pyloroantral localization as well. No correlation between the CP presence and CP mucosa colonization on the one hand and the type of reparative processes in the mucosa is found. The presence or the absence of CP as well as the degree of CP mucosal dissemination have no influence on the clinical course of the ulcer. Antiulcer treatment aiming at aggression factors (histamine H2-receptors blockers) and protective factors (enprostil) and lacking antibacterial activity improves the reparative processes but does not influence CP. Thus, CP is not etiological and probably is not a main pathogenetic factor in ulcer development. Its participation in the genesis of ulcer is possibly brought about under conditions of suppression of local protective mechanisms.
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Comparative studies of reparative processes in the gastric mucosa were carried out in 96 experimental mice with acute (immobilization) and chronic (acetic acid applications) gastric ulcerations. The common features in both models of ulcerations were revealed: (1) marked reduction of the regeneratory potentials of the epithelium of the entire gastric mucosa early in the ulcer formation as an expression of a stress-reaction; (2) gradual increase of a proliferation pool more marked at the site of the ulcer formation; (3) a sharp increase in the number of DNA-synthesizing cells in the ulcer edges by the time of its morphological formation; (4) extension of the zone of DNA-synthesizing cells with the progression of proliferative processes in the gastric mucosa. The time course of morphological alterations in the gastric mucosa developing in immobilization stress and acetic acid applications reflects the regularities of the development of both local and general reactions of the compensatory-adaptative nature.
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