Enzyme histochemistry of the normal human gastric mucosa using the technique of the semipermeable membranes and the other methods.
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Biomedical subjects
Publications and source records attributed to M Brozman.
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With the aid of morphological methoda, differences have been described between the active ferritin shock and the ferritin-antiferritin shock in guinea-pigs, which clinically appear as identical. The two processes can be differentiated from each other on the light microscopical level, but with particular clarity on the electron microscopical level. In contrast to the active ferritin shock, the guinea pigs in whom the ferritin-antiferritin shock had been produced showed agglomerates of platelets and ferritin-antiferritin complexes either present free in the dirculation or ingested in macrophages or granulocytes.
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The ultrastructure and certain cytochemical parameters of endocrine cells of the rat gastric mucosa during 168 h of fasting were investigated. To some of the fasting animals peroral food or alcohol was administered before decapitation. The EC (enterochromaffin cells) the ECL (enterochromaffin-like cells), D1 cells, AL (A-like cells) and G cells were identified by means of electron microscopy. Only the EC, ECL, and G cells could be identified by means of light microscopy by an adequate histochemical technique. The ultrastructural picture of the ECL and of the EC cells did not change markedly during the fasting. In the D1 cells there occurred an agglomeration of secretory granules. Some of them disintegrated and disappeared. In the AL cells an agglomeration of granules during the fasting was also observed. Granules engulfed in lysosomes were often found. The participation of lysosomes in the degradation of granules during the fasting was more marked in the AL cells than in the G cells. The participation of lysosomes was questionable in the EC and D1 cells, and in the ECL cells no lysosomes were observed. In contradistinction to the G cells of the non-fasting animals, where more than one half of the gastrin granules were "empty", the G cells during the fasting were filled with agglomerated dense granules and contained lysosomes with fragments of engulfed secretory granules. Following the administration of food (Larsen's diet) 3 h before sacrificing the dissolution of the content of granules with well preserved membranes was observed (emiocytosis did not take place). The administration of food did not lead to changes in the ultrastructural appearance of the EC cells. The peroral administration of alcohol did not lead to any changes in the ultrastructural appearance of the AL and G cells.
The influence of starving on the activity of enzymes of the rat gastric mucosa was investigated by selected histochemical methods. Beside the conventional methods of enzymatic histochemistry the technique of semipermeable membranes was used in the proof of lysosomal enzymes. Dehydrogenases were proved in aqueous and also in gel media with PMS. During the starvation in the parietal cells a marked increase took place in the activity of acid phosphatase, E-600 resistant esterase, less in beta-glucuronidase. High activity of the lysosomal enzymes in macrophages did not change during starvation. Nor did any changes took place in the activity of alkaline phosphatase in the endothelium of the capillaries. The chief cells in the control and starving animals, in contrast to the human gastric mucosa, did not contain any non-specific esterase. Concerning dehydrogenases, parietal cells with a different activity of these enzymes were observed both in starved and control animals. In the rat gastric mucosa starving induced changes in the activity of the enzymes which mark important organelles of the cells. Thus it is possible to consider the observed histochemical changes as a functional manifestation of morphological damage of cellular structures which are affected during starvation.
In the paper we observed histochemically the distribution and activity of 16 enzymes in the normal rat gastric mucosa. The lysosomal enzymes were demonstrated by the method of semipermeable membranes (LOJDA 1972). At the proof of dehydrogenases aqueous and gel media were used. The parietal cells of the gastric mucosa contained a moderate activity of acid phosphatase, E-600 resistant esterase, and only a very slight activity of beta-glucuronidase and N-acetyl-beta-D-glucosaminidase. The macrophages of the interstice contained a high activity of beta-glucruonidase, acid phosphatase, E-600 resistant esterase and a low activity of N-acetyl-beta-D-glucosaminidase. The chief cells of the rat gastric mucosa, in contrast to the human, did not contain nonspecific esterase and also in them acid phosphatase was mostly lacking. The alkaline phosphatase was found only in the endothelium of the capillaries of the gastric mucosa. The parietal cells contained high activities of succinate dehydrogenase, alpha-glycerophosphate dehydrogenase, beta-hydroxybutyrate dehydrogenase, NADH tetrazolium reductase, a lower activity of NADPH tetrazolium reductase, as well as other soluable dehydrogenases. At the examination of dehydrogenases using aqueous as well as gel media with PMS during optimal short incubation periods, we found more and less active forms of parietal cells. The different oxidoreductase capacity of parietal cells in normal rat gastric mucosa can point to their unequal-functional load at the production of hydrochloric acid. The findings obtained are compared with the findings in older papers concerning different experimental animals and with the distribution of enzymes in the human gastric mucosa.
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The administration of a sufficient dose of heterologous antibodies against renal glomeruli in rats produces symptoms of respiratory insufficiency and pulmonary oedema causing death of the animals. Under these experimental conditions the basic pathogenic mechanism appears to be binding of the injected antibodies on the basement membrane structures of pulmonary capillaries resulting in their damage. Such changes are followed by widespread haemorrhagic exsudative changes in the lungs. Localization of the injected antiglomerular antibodies has been studied with the aid of immunohistochemical methods and in addition, by a method using antibodies labelled with radioactive isotopes of iodine, the so-called "paired administration technique". After the administration of a lethal dose of antiglomerular antibodies, they later appeared to be predominantly localized in the lungs. This fact correlates well with the idea of the effect of the antibodies upon pulmonary parenchyma in the present experiment. A remarkable finding was a rather high localization of the injected antibodies in the liver parenchyma which could be explained either by a cross reaction between the antibodies and the antigens of hepatic vascular spaces, or by a shock reaction associated with heart failure and circulatory disturbances.
Observations of Lyell's syndrome in two girls, one 2 and the other 7 years of age, investigated serologically, histologically and by immunofluorescent technique, are reported. In both cases. the disease had been preceded by a prolonged or repeated treatment with acetylsalicylic acid, in the first case in combination with sulphonamides and antibiotics and in the second in combination with mephenytoin. Immunofluorescent staining revealed immunoglobulins in subepidermal blisters and along the dermal vessels. Acetylsalicylic acid has been assumed to have been one of the causative factors of the violent progression of toxic epidermal necrolysis, probably by an antigen-antibody reaction. This has been supported by serologic demonstration of antibodies to acetylsalicylic acid in both cases.
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In this study the influence of fasting on the structures in the human gastric mucosa was followed using selective histoenzymological and electronmicroscopic method. The gastrobioptical material of 7 healthy volunteers was examined after 24 to 240 hour fasting. During fasting an increased acid phosphatase activity in the chief cells of the human fundal mucosa was observed. The activity of the nonspecific esterase (naphtyl esterase) in the chief cells decreased mainly after 240 hour fasting. In the electronmicroscopic examination of the chief cells during fasting a multiplication of lysosomes and narrowing of the granular endoplasmic reticulum was observed. In some chief cells during fasting an agglomeration of zymogen granules was seen while in others only a few granules were observed. In the parietal and other cells of the human gastric glands a steatosis, which attained excessive values, was seen after 72 and 240 hours of fasting. We believe that this steatosis occurred mainly on the strength fasting lipemia with the possible participation of other factors. The changes in the mitochondrial structure of the parietal and other cells of the human gastric mucosa were only slightly pronounced. "The decreased" activity of dehydrogenase in the steatotic parietal cells under a histochemical examination may represent only findings caused by the agglomeration of a large amount of lipid drops in the steatotic cells. After 72 and 240 hours of fasting the parietal cells contained collapsed, underdeveloped intracellular canaliculi and narrowed tubulovesicular profiles probably related to the decreased HCl production. Generally it can be said that the observed morphological changes are the consequences of the decreased function of human gastric mucosa cells during fasting and that these regressive changes are reversible and they are caused by an insufficiency of nutrition.
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Scientific and technological development in morphological disciplines has created an creates unheard of possibilities for scientific research and practical examination of morphological changes and in its consequences has contributed also in a substantial way to a change in fundamental views on the subcellular and supramolecular structural level of the organization of living matter. Despite this pathology is faced with difficulties and has at present many unresolved theoretical and practical problems. Pathology has expanded so much that is differentiation as regard contents and methods is inevitable to preserve its integrity and to promote its integrity with other disciplines in particular biochemistry of tissue changes. The basic types of activity of pathology will remain also in future (histological) biopsy, cytodiagnostics and necropsy whereby it is necessary to use to an increasing extent new methods contributed by the scientific and technological revolution. It must not be forgotten that pathology is not only a specialized but also scientific discipline and important source for all doctors in their therapeutic and preventive and scientific activities.