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Biomedical subjects

R Lesch

Publications and source records attributed to R Lesch.

At least 37 records · Page 2Linked to original sources
PubMed1978

[Liver disease in homozygous alpha1-antitrypsin deficiency (author's transl)].

Among twelve patients with homozygous alpha1-antitrypsin deficiency (Pi-type Z), five cases of infantile liver disease were diagnosed. The course of the disease was extremely variable; only one patient died of liver cirrhosis at the age of fourteen. In four cases the clinical, biochemical and histological (2 cases) findings became normal over a follow-up period of one to fifteen years. The results of these observations demonstrate that in alpha1-antitrypsin deficiency even when associated with proven liver disease the prognosis need not be unfavorable.

Adolescent↗
PubMed1978

Adaptive changes of rat liver cells induced by repeated intraperitoneal injections of d-galactosamine. III-Light- and electron-microscopic investigations of hepatocellular cytoplasmic changes.

In rats hepatocellular cytoplasmic changes after daily repeated D-galactosamine (GalN) intoxication--i.e. subacute GalN intoxication--were studied by light and electron microscopy. The number of GalN injections--and thus the days of survival--was between one and 30. The rats were killed six hours after the last GalN injection. Less degenerative changes were found after repeated GalN injections. An increased formation of atypical dense bodies (ADB), a temporary pronounced lipid accumulation and changes of the rough and smooth endoplasmic reticulum were prominent features of subacute GalN intoxication. The implications with respect to a modified GalN action in subacute GalN intoxication are discussed with special reference to biochemical data obtained in the same experimental model (Schuchhardt et al., 1977).

Adaptation, Physiological↗
PubMed1978

Effect on vitamin A on the development of galactosamine-induced hepatitis in rats.

In order to elucidate the role of lysosomes in experimental hepatitis caused by D-galactosamine in rats the activities of cathepsin A and D and acid carboxypeptidase were measured. Enzyme activities were assayed in liver homogenate, lysosomal supernatant fraction and lysosomal sediment fraction. Lysosomal enriched fractions were prepared according to De Duve. Vitamin A in high doses aggravates the morphological alterations observed in galactosamine treated rats. At the same time the labilization of lysosomes increases substantially. This effect was induced by doses of retinyl-palmitate that normally caused only an activation of Kupffer cells and no significant liberation of lysosomal peptidehydrolases. The activities of cathepsin A and D increased 2-fold in liver homogenate after combined treatment with galactosamine and vitamin A, whereas the activity of acid carboxypeptidase decreased markedly.

Animals↗
PubMed1978

[Intrafocal BCG therapy of metastasizing malignant melanoma].

Therapeutical possibilities and side effects of intrafocal BCG-vaccination into metastases of malignant melanomas are discussed. Only in one of our three cases, this special method of unspecific immunstimulation induced a remarkable regression of tumor size. The second patient showed a partial remission and in the third there was no effect at all. Besides local irritation with ulceration we observed severe generalized side effects in all patients. A granulomatous hepatitis, which represents the most severe complication of this therapeutical method, occurred in one case. Its successful treatment with tuberculostatic agents favors the assumption of an infectious genesis.

Adult↗
PubMed1977

Adaptive changes of the rat liver cells induced by repeated intraperitoneal injections of d-galactosamine. II. Light and electron microscopic investigations of hepatocellular nucleolar alterations.

The effects of repeated d-galactosamine (GalN) administration - i.e. subacute GalN intoxication - on rat liver cell nucleoli were examined. After an initial intraperitoneal injection of 375 mg GalN/kg body weight the rats were treated with 250 mg GalN/kg body weight daily at intervals between 24 h and 30 days. The rats were sacrificed six h after the last injection by decapitation. Specimens of liver were studied by light and electron microscopy. According to the nucleolar size three stages were to be distinguished. Stage I: decreased nucleolar size after one injection, stage II: increased and maximal nucleolar size after two to five injections, stage III: slightly increased relatively stable nucleolar size after six and more injections. Fine structural observations suggest a nucleolar hyperfunction in subacute GalN intoxication as well as a minor disturbance of the transcription and the transfer of the nucleolar RNA.

Adaptation, Biological↗
PubMed1976

The appearance and degradation of specific hepatocellular cytoplasmic inclusion bodies in rat liver due to D-galactosamine. I. The relation between the amount of liver glycogen and the appearance of the atypical dense bodies in the liver cell.

One of the most sensitive and specific signs of the galactosamine effect upon the rat liver cell is the appearance of PAS-positive and diastase-resistant granules within the cytoplasm of hepatocytes. Light-microscopic, histochemical, biochemical, and electron-microscopic findings reveal that the appearance of these ADB (= atypical dense bodies) depends upon a working glycogen metabolism at the time of GalN treatment. The ADB are composed of particles resembling, due to shape and size, ribosomes and beta particles of glycogen. Most of them are surrounded by the rER, but they are never enclosed by a limiting membrane. Due to sequential changes they can be generally classified into three types; the early, the intermediate, and the late type. In seven experiments it can be shown, that the appearance of the ADB depends upon the time and dosage after GalN treatment. They occur even if an additional treatment with galactose or uridine prevents the liver from the features of a hepatitis, as also shown in the livers of newborn animals up to 3 weeks of age. The histochemical response against various glucosidases, hexosaminidases, pronase, and RNAse as well as against various fixatives indicates that ADB are composed of, at least, two different constituents, the former RNAse-sensitive and visible with routine light-microscopic staining procedures, the latter RNA-resistant, PAS-positive, and invisible after staining with H & E or toluidine blue. The latter is diastase-resistant, suggesting that this portion of ADB does not represent the usual glycoproteins but some abnormal metabolite of glycogen. The ADB can be detected with maximal accumulation in the cytoplasm of hepatocytes at that time when the glycogen content determined in the liver homogenate by biochemical methods is greatly reduced.

Animals↗
PubMed1976

Investigations on d-galactosamine hepatitis after pretreatment with alpha-hexachlorocyclohexane.

D-Galactosamine hepatitis cannot be induced in rapidly replicating liver tissue at various times after induction of proliferation. Proliferation was induced by administration of alpha-hexachlorocyclohexane. The morphological features of galactosamine hepatitis do not appear or are very mild. The onset of DNA synthesis is delayed to about 12 hrs as also shown in partially hepatectomized rats.

Alcohol Oxidoreductases↗