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Biomedical subjects

W Romen

Publications and source records attributed to W Romen.

At least 73 records · Page 4Linked to original sources
PubMed1978

[The disease pattern of the diffuse, nesidioblastic hyperplasia of the pancreatic islets in newborn and infants (author's transl)].

The course of illness of a male infant who lived for seven months with a diffuse, nesidioblastic hyperplasia of pancreatic islets is described. Before surgical intervention the diagnosis should be ascertained by 1. observation of acetonuria which is always absent after hypoglycemic episodes, 2, the typical constellation of insulin concentration, free fatty acid concentration and beta-hydroxybutyrat during a hypoglycemia (as found by Baker et al. 1976) and/or by simultaneous measuring of glucose-insulin levels under the conditions of fasting as well as of oral leucine, oral glucose and intravenous tolbutamide loading. Therapy with diazoxide should be tried in any case. If all conservative measure fail and relative or absolute hyperinsulinemia is proved, experience shows that an immediate operation is indicated.

Adenoma, Islet Cell↗
PubMed1978

Functional and morphological alterations of the exocrine pancreas in the rat following pretreatment with rifampicin.

Following oral pretreatment with rifampicin over 3 and 9 days, the exocrine pancreatic function was studied in urethane-anaesthetized rats under exocrine stimulation. The volume and electrolyte content, and especially the protein and amylase outputs of the pancreatic secretion showed a virtually dose- and time-dependent decrease. Histologically, there was a corresponding decline of the zymogen granules in the acinar cells. The suggested explanation for the observed disorders of the pancreatic exocrine function is primarily an inhibition of protein synthesis due to rifampicin.

Animals↗
PubMed1977

[The structure of the nucleolus during the inhibition of RNA-and protein synthesis (author's transl)].

In cells treated with antimetabolites to inhibit RNA- and protein synthesis, electron microscopic studies reveal structural alterations of the nucleolus. The morphological appearance of the nucleolus differs depending of the inhibitor used. If transcription is prevented, segregation of nucleolar components is observed. Inhibition of processing of newly synthesized RNA results in a degranulation and an increase in the amount of nucleolar fibrils. A disturbance of the release of nucleolar ribonucleoproteins into the cytoplasm leads to an enlargement and a hypergranulation of the nucleolus. On the other hand interruption of translation of mRNAs has no immediate effect on the appearance of the nucleolar structure. Only after longer treatment of the cells with the translation inhibitor the nucleolus shrinks and becomes degranulated. The use of inhibitors with clearly defined mechanisms of action in a morphological study should make it possible to interpret similar nucleolar alterations seen in cancer cells and virus-infected cells on a molecular biological basis.

Animals↗
PubMed1977

[Comparison of the nuclear alterations induced by actinomysin D and alpha-amantine in hapatocytes of the rat (author's transl)].

Comparing the morphological effects of actinomycin D and alpha amanitine on the rat liver, it can be seen that the nuclear alterations caused by actinomycin (=segregation of the nucleolus and condensation of all the chromatin) occur simultaneously. After treatment with amanitine, the lesions appear in two steps. First of all one sees condensation of only the extranucleolar chromatin and fragmentation of the nucleolus. These two phenomena are related to each other not only chronogically but also causetively. In our opinion the shrinkage of the extranucleolar parts of chromosones results in the individual nucleolus-organizers being removed into different quarters of the nucleoplasm. The fragments themselves must not be altered structurally and functionally, as Kedinger and Simard (1974) have already shown. We always observed changes of the nucleolar fragments 30-90 min after the fragmentation. These changes consisted of the condensation of the intranucleolar chromatin, and the segregation and degranulation of the nucleolus, in the same manner found directly after the actinomycin-poisoning in the whole nucleolus. The delay of the lesions observed on the dispersed nucleolar fragments indicates that is a consequence of the amanitine-poisoning -- probably the result of the disturbed protein synthesis and the inactivation of a hypothetical extranucleolar regulatorgene, which controls nucleolar function.

Amanitins↗
PubMed1977

[Intensive care in rabies. A case report (author's transl)].

A case of human rabies is reported showing a peculiar course in some respects. The lack of a satisfactory history concerning an animal bite 5 months earlier as well as a misleading psychiatric history led to difficulty and delay in reaching a diagnosis. Under intensive care, including mechanical ventilation and cardiac pacing, the disease reached a final stage, which is rarely seen. The clinical course and the pathological findings are described in detail and the etiology and prognosis of the disease are discussed. The latter remains rather hopeless de spite modern intensive care.

Adult↗
PubMed1976

Synthesis of the glomerular basement membrane in the rat kidney. Autoradiographic studies with the light and electron microscope.

To study the origin and the formation of the glomerular basement membrane, autoradiographic investigations with 3H-proline and 3H-leucine have been performed in ultrathin with semithin sections of the glomeruli of 42 male rats. The results of this study indicate that, of the three cell types of the glomerulus, the epithelial cells (=podocytes) synthesize the proline-rich scleroproteins of the glomerular basement membrane. Our autoradiographic studies have yielded no evidence for participation of the endothelial or mesangial cells in the formation of the basement membrane. The mesangial cells appear to be responsible for the synthesis of the mesangial matrix only.

Animals↗
PubMed1976

Defects in granulocyte function in various chromosome abnormalities (Down's-, Edwards'-, Cri-du-chat syndrome).

In five infants with autosomal aberrations and diminished resistance to infection (in spite of intact humoral and cellular immune mechanisms) several granulocyte functions (chemotaxis, phagocytosis, intracellular killing and metabolism of killing) were measured. A serum-dependent or a cell-dependent disturbance of phagocytosis of Candida albicans was found in two infants with cat-cry syndrome and one with trisomy 18. In one of these children there was an additional serum dependent defect of the killing of Candida albicans and of Staphylococcus aureus, serum levels of opsonins (IgG, IgM, CH50 and C3) being within normal range. An infant with trisomy 21 showed, in addition to a cellular defect of chemotaxis, a reduced cellular ability of the killing of Staphylococcus aureus and of Escherichia coli in autologous and AB-pool-serum. Phagocytosis of these bacteria remained normal.

Blood Bactericidal Activity↗
PubMed1976

[On the pathogenesis of the glomerulosclerosis ultrastructural and autoradiographic investigations on the rat kidney (author's transl)].

The light- and electron microscopic changes in the glomeruli of the rat's kidney have been investigated in the course of ageing and after subtotal nephrectomy, constriction of the renal vein, and intoxication by N-nitrosomorpholine. In spite of the fact that four different experimental models have been used, identical changes were always found in the glomeruli. Morphologically they consisted of a diffuse thickening of the glomerular basement membrane and of an increase in the mesangial matrix without a proliferation of the glomerular cells. Despite this thickening of the glomerular basement membrane, functionally an increased permeability of the glomerular capillaries for macroproteins could be observed, shown by a moderate proteinuria. For these morphological changes the term "glomerulosclerosis" is suggested; they are interpreted as a non-specific, non-inflammatory reaction of the glomerulus to an impairment caused by a number of varied influences. From the study of the formal pathogenesis of the glomerulosclerosis presented here one can conclude that in the individual experimental models the same result has been achieved in different ways. One possibility in the development of glomerulosclerosis is an increased production of the components of the basement membrane and of the mesangial matrix. This is the pathway which appears to be followed after nephrectomy. Another possibility is a slowing down of the breakdown of both the matrix and the membrane. This seems to be the case in the glomerulosclerosis occuring in the course of ageing, and after hypoxic and toxic changes. It could be accounted for by a functional disturbance of, presumably, the mesangial cells responsible for the breakdown of the basement membrane and of the matrix. On the other hand, one may have to consider a primary alteration of the macromolecules of these structures, as is already known from studies of the, chemically closely related, collagen. The light- and electron microscopic studies of the normal and of the altered glomeruli have led to certain conclusions concerning the origin and the fomation of the glomerular basement membrane and the mesangial matrix. In order to widen the scope of the studies, additional autoradiographic investigations with 3H-proline and 3H-leucine have been performed in ultrathin and semithin sections of the rat's glomeruli. The results of the studies presented here suggest that of the three cell types of the glomerulus the visceral epithelial cells (podocytes, "Deckzellen") may participate on the formation of the glomerular basement membrane, whereas the mesangial cells appear to be responsible for the synthesis of the mesangial matrix.

Aging↗
PubMed1975

Toxic glomerulosclerosis-morphology and pathogenesis. Light and electron microscopic studies fo the glomerular changes in the kidney of rats poisoned by N-nitrosomorpholine.

75 male rats were given toxic dosage of the hepatotoxin N-nitrosomorpholine (NNM) using varied concentrations over varied time intervals. During and after the toxic dosings the kidneys were examined by light and electron microscopy in order to decide, whether the kidneys are also damaged by NNM. Our studies reveal that under the influence of a low concentration of NNM a distinct thickening of the GBM and an increase of the mesangial matrix occurs (changes referred by us as glomerulosclerosis). When a high concentration of NNM was given, toxic lesions of the mesangial and epithelial cells of the glomeruli were found, but a glomerulosclerosis was not observed during the intoxication. After this toxic dose was stopped, however, a progressive glomerulosclerosis did develop, which at first was accompanied by a transient proliferation of the mesangial cells. The glomerular changes found in the course of poisoning with NNM were interpreted as a direct effect of the NNM. From studies of the formal pathogenesis of the glomerulosclerosis presented here one can conclude that the poisoning leads to a decrease in breakdown of the components of the basement membrane and the mesangial matrix, thus causing the widening of the GBM and the augmentation of the mesangial matrix.

Animals↗
PubMed1975

Differences in the incorporation of L- and DL-Amino acids into renal tubular cells. An autoradiographic study.

The cytoplasmic uptake of 3H-L-leucine and 3H-L-proline by hepatocytes and cells of the proximal and distal convoluted and of the collecting tubules of the kidney was compared with that of 3H-DL-leucine and 3H-DL-proline in an autoradiographic study. 34 male white Sprague-Dawley rats were killed 1, 2, 6, and 24 hours after the intraperitoneal injection of these amino acids. The rate of incorporation of 3H-L-leucine in the liver and in the renal tubules, as judged by the number of silver grains counted, was about twice that of 3H-L-proline. In the tubules of the kidney the intensity of labelling progressively declined from the proximal convoluted to the collecting tubules. When the two 3H-DL-amino acids were used, almost identical rates of incorporation were found in the liver as well as in the kidney. The only exception was the pars recta of the proximal tubule: Here there could be found an unusually high uptake of 3H-DL-proline. The values were not only higher than those found for the uptake of 3DL-leucine in this particular segment, but they also surpassed those due to 3H-DL-proline and 3DL-leucine in the other parts of the renal tubules, as well as in the liver. The conspicuously high labelling seen in the pars recta after the injection of 3H-DL-proline suggests that there is present in the cells of this segment a d-amino acid oxidase, which may be relatively specific for D-proline. The possibility is considered that this enzyme may participate in a detoxifying function of the pars recta.

Amino Acids↗