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U N Riede

Publications and source records attributed to U N Riede.

At least 55 records · Page 3Linked to original sources

Quantitative topography of organelles in the liver. A combined histochemical and morphometric analysis.

After seven days of feeding fructose the liver of Wistar rats showed enormous accumulations of glycogen, which completely altered the original pattern of distribution of organelles. A quantitative morphological method was used to analyze these changes. The cytoplasm was mapped into arbitrary "distance classes" corresponding to concentric rings beginning at the outer nuclear membrane. This allowed the density of organelles in a given zone to be estimated. In cells filled with glycogen as a result of the fructose feeding, the following rearrangements were found: in the intermediate zone of both cellular poles (i.e., bile canalicular pole and sinusoidal pole) the mitochondria disappeared, being replaced by glycogen. The endoplasmic reticulum was accumulated in the perinuclear zone of both cellular poles, as in control animals, but was reduced throughout the rest of cytoplasm. It showed a peripheral density maximum at the biliary canalicular pole, in contrast to the cells of control animals. These changes in the distribution of the organelles and cellular "compartments" correspond to histochemical findings and demonstrate an adaptive reaction in the liver parenchyma to fructose ingestion, the organelles arranging themselves in cytoplasmic regions which still show a metabolic activity.

Animals↗

A contribution to the pathogenesis of cholesteatoma. A histochemical and ultrastructural study.

In a histochemical and ultrastructural study the pathogenesis of cholesteatoma ostitis is analysed on human tissue. In the subepithelial layer there is evidence of an inflammatory reaction leading to proliferation of granulation tissue with bony invasion. Bony destruction is initiated by osteocytic osteolysis. In the case of cholesteatoma there is a combined action of extraosseous and osseous lysosomal enzymes. The pathological changes of the fibrillar elements suggest that the self-perpetuation of degeneration is maintained by a disturbance of fibrillogenesis. The causal pathogenesis of cholesteatoma formation is discussed as a function of a disturbance between cellular activity, extracellular matrix, and cellular surface.

Cholesteatoma↗

[Pathology and pathophysiology of circulatory shock with respect to shock lung (author's transl)].

The circulatory and acute generalized failure of the circulation, in particular of the lesser peripheral circulation, and may possibly but not necessarily be accompanied by a decrease in blood pressure and damage to the tissue due to a lack of oxygen. The main question concerning the causal pathogenesis of shock is still unsettled, but an interaction between a lack of oxygen as well as of other factors, like endotoxin, complements and vasoactive amines, and the presence of a microthrombosis must be held responsible for the appearance of this condition. In modern intensive medicine the lung must be considered as the preferential area for the manifestation of shock. The clinical picture of shock lung may be described as acute respiratory deficiency accompanied by an impaired diffusion of oxygen, an increase in dead-space ventilation together with an increased shunt volume and intensified respiratory activity. The pathology of shock lung shows two phases and has its onset in exudative alveolitis followed by alveolar fibrosis which can be hardly be controlled by therapy. The early phase of shock lung manifesting itself by exudative alveolitis is decisive with regard to diagnosis and further therapeutic measurements. If the condition can be brought under control at this stage there is a chance that the patient may survive.

Disseminated Intravascular Coagulation↗

[Measurements of tibio-femoral contact area after experimental partial and subtotal meniscectomie (author's transl)].

By means of section material, 24 partial and 58 subtotal meniscectomies were performed and the loss of tibio-femoral contact was evaluated by the Touchier-method planimetrically. In cases of partial resection this loss was 12% only, where as in subtotal resection 46%, where by the remaining contact zones lay in the central-, anyway meniscusfree area. The diagram of the chondral splitting lines showed a maximum of compression here, consecutively the remaining contact zone is reduced to the in earlier times most affected cartilage areas. The result correlates to the appearance of chondromalacies of the central tibial plateau in our own section cases and of postoperative osteoarthritis after subtotal meniscectomies in literature. Subtotal meniscectomies lead to incongruence and increased pressure. a pseudo-regeneration seems not to compensate the meniscus function sufficiently. A result for the clinic one should, when possible, resect menisci only partially.

Adolescent↗

[Experimental patello-femoral contactprint measurements. 2. Report: sagittal osteotomy of the patella according to Morscher (author's transl)].

The recommended treatment method for chondropathy from Morscher 1978 using a sagittal patellaosteotomy was tested experimentally with contact area measurements with the erasing method on 11 corpse knees of the types II, II/III and III. Measurements were made in the bending region up to 90 degrees, and in isolated positions up to 140 degrees. The measurements showed a clear decrease in the contact area of the medial side of the lateral facet, and occassional displacement of contact whereby loses on the paramedial segment were compensated for by early loading on the border segment. Thus unphysiological loading of the medial facet occurred, from which chondromalasys could develop. Only three patellas had an increased contact area during inflexions up to 90 degrees, and then only because the central cartilage area, which usually undergoes the greatest loses, was already incongruent. Since during a complete knee bending the retropatella cartilage has almost 100% contact and that due to the medial cartilage ridge a considerably smaller incongruence is present as can be expected from the bone crosssection of the patella, we cannot expect any contact increase through an osteotomy.

Biomechanical Phenomena↗

[Morphometric analysis of the proximal tibial cartilage tissue (author's transl)].

We analysed the tibial cartilage of 5 juvenile and 10 adult non-degenerative knees for morphometric criteria. Determination of cellular and nuclear total volume per unit cartilage volume,, number of cells and nuclei per unit cartilage volumen and cellular and nuclear single volumen of chondrocytes in the superficial and basal cartilage layer was done in relation to their being covered by meniscus. We found cells and nuclei and their total volumen in the superficial layer constantly smaller, number of chondrocytes and nuclei constantly higher than in the basal layer. This was clearly seen in the meniscus-covered part of cartilage, less marked in the central non-covered part. In adults the central cells are superficially hypertrophic and gain few individual and total volume in the basal layer. These superficial central cells are on a high level of metabolism, synthesising much intercellular substance, but they prostrate in basal direction. The aging chondrocyte is maximal adapted to the strain and uncapable to react to further load.

Adolescent↗

[Cholesteatoma, oto- and tympanosclerosis: their general mechanism of tissue destruction (author's transl)].

The connective tissue contains extracellular enzymes for the turnover of the ground substance. If this enzyme system gets out of control there is development of a complex metabolic disturbance of all tissue components. The lysosomal dysfunction is the basis of the general mechanism of tissue destruction in cholesteatoma, oto- and tympanosclerosis. This process seems most enhanced in cholesteatoma. Emphasis is placed on the role of extracellular lysosomes (= matrix vesicles).

Cholesteatoma↗

The concept of homology in quantitative organelle pathology. Application of symbolic logic to glycogenosis type I in the liver.

The process of quantification has led pathology into an objective and abstract direction to which it is unaccustomed. The introduction of the concept of homology in pathology by Doerr has proven to be very fruitful, since it has helped to clarify otherwise poorly understood relationships. As shown in the foregoing paper, the success of the homology concept applies also to quantitative organelle pathology. Homologies have demonstrated relationships within the ergastoplasmic - mitochondrial - peroxisomal system which are apparent only with the help of symbolic logic. These homologies permit inferences, shown here with the example of glycogenosis type I, regarding the adaptive potential of the cell and the degree of cellular damage. In addition, these homologies, which are described in terms of formal logic, may serve as a model for human pathologic anatomy.

Glycogen Storage Disease Type I↗

A contribution to the pathogenesis of otosclerosis.

In a histochemical and electron microscopical study the pathogenesis of otosclerosis was investigated. The morphological changes in the extra- and intracellular space indicated a complex metabolic disturbance of all tissue components. The observed chondrocytic chondrolysis stressed the role of the cartilage remnants in the otic capsule as an etiological factor. There was morphological evidence of a superimposed enzymatic defect.

Cartilage↗

Reaction patterns of cell organelles in vitamin B6 deficiency. Ultrastructural-morphometric analysis of the liver parenchymal cell.

Under the influence of seven weeks of vitamin B6-free nutrition, the hepatocyte single volume is diminished in the face of an unchanged nuclear single volume, posing the question of whether there is proportional atrophy of all cell organelles or single organelle atrophy with counter-regulatory hyperplasia in other cellular compartments. The nucleoli hypertrophy, as the result of segregation and protein synthesis inhibition. The rough endoplasmic reticulum experiences hypoplasia, but the ultrastructural-morphometric analysis does not determine which metabolic steps are attacked. By contrast one observes hyperplasia in the smooth endoplasmic reticulum, which may be regarded as a counter-regulatory mechanism to the choking of protein synthesis. As with the rough endoplasmic reticulum, the mitochondria also show hypoplasia. This is due to the dependency of the mitochondria upon the endoplasmic protein synthesis. The disturbed functional output of the endoplasmic reticulum is seen in the reduced number of orthoperoxisomes as well. The Golgi apparatus experiences hypoplasia as a result of B6 hypovitaminosis, and this must be considered in the context of fatty change in the liver.

Animals↗