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Biomedical subjects

E Mönch

Publications and source records attributed to E Mönch.

At least 37 records · Page 2Linked to original sources
PubMed1983

Liver pathology in transient neonatal hyperammonemia.

Ultrastructural investigations have been performed on two cases of transient neonatal hyperammonaemia (TNH). This newly recognized metabolic disorder is chiefly characterized by severe hyperammonaemia in the postnatal period, a comatous state, absence of abnormal organic aciduria, normal activity of urea cycle enzymes and, usually, complete recovery. The aetiology is presently unknown. Electron microscopy uncovered rather congruent alterations of hepatocyte structure, with a wide spectrum of mitochondrial lesions, an increase of autophagous bodies with organelle remnants, and changes in the excretory apparatus. Thus, in contrast to some of the hereditary disorders of the urea cycle, no specific structural changes could be found in TNH. This finding is in line with the observation of normal activities of main urea enzymes in these cases, and indicates that a different biochemical system may be pathogenetically involved in TNH.

Ammonia↗
PubMed1983

[Thin layer chromatographic test for the indirect and direct detection of the enzyme defect in histidinemia].

A thin layer chromatographic method for the direct and indirect detection of the enzyme defect in histidineemia is described. Histidin and urocanic acid are analyzed in 0,2-1 mg stratum corneum for specific screening. 5-10 mg skin biopsy material is needed for the direct measurement of the enzyme activity. This simple metabolic test is convenient even in normal hospital laboratories.

Amino Acid Metabolism, Inborn Errors↗
PubMed1979

Hypotonic unmasking of erythrocyte receptor sites.

The study reports on plasmalemmal perturbation of erythrocytes under osmotic stress. In comparison with isotonic human erythrocytes a 10 minutes incubation in 150 mosm sodium cacodylate pH 7.4 at 20 degrees C results in an increase of the anti AH P binding rate by a factor of two. 0.1 M N-acetyl galactosamine inhibits the binding of anti-AH P of both isotonic and hypotonic red cells. Contrary to isotonic mouse erythrocytes the agglutination with peritoneal murine leukocytes of hypotonic red cells is greatly enhanced provided the erythrocytes have been incubated in autologous serum. The findings are considered evidence of the unmasking of binding sites due to nonspecific rearrangement of membrane constituents.

Acetylgalactosamine↗
PubMed1978

[Increased epidemic incidence of hepatitis B in a district hospital].

It is reported on an epidemic of hepatitis B of 29 patients in a district hospital. Due to diagnostic errors in importation and a more frequent appearance of diseases of hepatitis B in the surgical department and the 2nd medical department, in which above all diabetics are treated, took place. The average age of the patients was 55 years. In all patients the clinical course was to be regarded as severe. 4 of 29 patients died. In all patients the hepatitis B disease showed a pronounced jaundice with high transaminases, particularly the SGOT and LAP were clearly increased. Also the duration of the presence was longer than in hepatitis A as well as the transition into chronic hepatitis was more frequent. By diagnostic information of the physicians and the other medical staff as well as improved measures of desinfection the epidemic could be restricted.

Adolescent↗
PubMed1978

Glutaraldehyde mediated echinocyte/discocyte transformation is Ca2+ dependent.

Echinocytes, which were produced from freshly banked blood by repeated washes in phosphate buffered saline, undergo a transformation to the discoid shape within less than 30 seconds of incubation in isotonic 0.05% glutaraldehyde pH 7.4. This echinocyte/discocyte transformation is not associated with a change of cell volume or critical hemolysis volume although a slight decrease of cellular deformability and a 4-8 fold increase of K+ efflux within 1 hour after glutaraldehyde incubation provide evidence of the fixative's attack on the cell membrane. Trypsination prior to the incubation in isotonic glutaraldehyde could not inhibit the shape change. Hypertonic glutaraldehyde solutions partially prevent the E/D transformation with regard to both the osmolarity of the medium and the permeability of the cell membrane. The glutaraldehyde stimulated transformation is entirely inhibited in the presence of a chelating agent the efficiency of which is overcome by addition of a more-than-equivalent amount of Ca2+. The mutual action of either agent is discussed, however, the mechanism of the phenomenon remains unclear.

Aldehydes↗