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U Pfeifer

Publications and source records attributed to U Pfeifer.

At least 109 records · Page 6Linked to original sources
PubMed1980

A morphometric study on growth of bile canaliculi after partial hepatectomy.

19-33 h after partial hepatectomy there is a time-dependent increase of the bile canalicular luminal volume, of the total length of bile canaliculi, and of their non-microvillous, smooth surface, when measured per unit volume of lobular parenchyma. On average the luminal volume fraction is increased by a factor of 2.8, the length per volume by a factor of 1.4, and the density of smooth surface by a factor of 2.0, when compared with sham-operated controls. On the other hand, the volume and surface density of bile canalicular microvilli are only slightly increased after partial hepatectomy. These findings are interpreted as indicating disproportional growth of bile canaliculi which is due predominantly to the formation of new, at first non-microvillous, membrane.

Animals↗
PubMed1980

Experimental non-A, non-B hepatitis: four types of cytoplasmic alteration in hepatocytes of infected chimpanzees.

On the occasion of an outbreak of non-A, non-B hepatitis in a plasmapheresis centre (81 cases, incubation period: 3--6 weeks) a pool of 12 plasma samples was obtained in the early phase of increasing transaminases. Two chimpanzees were inoculated, each receiving 12 ml of the pooled plasma. After an incubation period of 10--12 weeks a mild non-A, non-B hepatitis developed. Serum transaminases were slightly elevated. Needle biopsies, taken fortnightly, showed a slight activation of Kupffer cells (6--8 weeks), single cell necroses, and infiltration of the portal tracts (10--13 weeks). Electron microscopically four types of cytoplasmic change, were found in hepatocytes and assumed to be specific for the infection, Type I: Sponge-like inclusion (6 weeks after inoculation) composed of a dense matrix and irregularly arranged membranes. Type II: Attaching curved membranes (8 weeks), developing by close apposition of two cisternae of smooth endoplasmic reticulum. Type III: Cylindrical complexes (10 weeks), already described in literature. Type IV: Microtubular aggregates, usually neighbouring type III structures. The findings suggest 1) that the agent of the present infection is, at least in part, identical with that of the long incubation type of experimental non-A, non-B hepatitis, and 2) that ultrastructural alterations may precede manifest hepatitis.

Animals↗
PubMed1979

Inhibited autophagic degradation of cytoplasm during compensatory growth of liver cells after partial hepatectomy.

The livers from 56 sham-operated and 56 partially hepatectomized male albino rats killed 4--81 h after operation were investigated by electron microscopic morphometry. Following partial hepatectomy, the principal changes in volume fractions in the hepatocellular cytoplasm were: decrease of glycogen and, to a lesser extent, of mitochondria together with considerable increase of fat droplets. The volume fraction of microbodies (= peroxisomes) showed no significant difference between control and regenerating liver. By evaluating large test fields of about 40,000 micrometers 2 sectioned cytoplasm per animal it could be demonstrated that the volume fraction and the numerical density of autophagic vacuoles (AV's) were significantly reduced after partial hepatectomy. The extent of this reduction depended on the postoperative time interval. AV's were reduced by 75% at day 0 (4--17 h p.o.), by 98% at day I (19--33 h p-o.), by 75% at day II (43--57 h p.o.), and still by 50% at day III (67--81 h p.o.). The different types of AV's, defined on the basis of the different cytoplasmic components enclosed, were reduced to similar extent during the respective time periods. The reduction of AV's seems to be specific for the regenerating organ since no significant differences in the volume fraction of AV's could be found in the proximal tubular cells of the kidney of partially hepatectomized animals when compared with those of sham-operated controls. The inhibition of intracellular autophagic degradation in regenerating liver has its biochemical equivalent, i.e. inhibited protein catabolism, and is interpreted as an important and adequate mechanism in effecting the shift from the physiological steady state between anabolism and catabolism to the positive balance which is required for the compensatory growth of the liver after partial hepatectomy.

Animals↗
PubMed1979

Shedding of peripheral cytoplasm - a mechanism of liver cell atrophy in human amyloidosis.

A liver biopsy specimen from a case of primary amyloidosis was investigated by electron microscopy. The cytoplasmic periphery of the hepatocytes showed degenerativechanges which are interpreted as indicating shedding of peripheral parts of the cytoplasm. Two main variants of this process could be discerned: 1) Protrusion and sequestration of hernia-like blebs of cytoplasm, and 2) shedding of vesicles derived from degenerated endoplasmic reticulum. In the latter case transient defects of the plasma membrane seem to be relevance. Endoplasmic reticulum and cytoplasmic ground substance appeared to be shed preferentially, whereas mitochondria are retained within the cell. As a consequence the fractional volume of the mitochondria in the cytoplasm of atrophic cells is markedly increased. Shedding of peripheral cytoplasm, therefore, seems to be an effective mechanism enabeling the cell to adapt the mass and the composition of its cytoplasm to an unfavourable environment.

Amyloidosis↗
PubMed1978

[Familial liver cirrhosis in pseudohypoparathyroidism in young children (author's transl)].

Two sisters whose mother had pseudo-pseudohypoparathyroidism, simultaneously developed in infancy pseudohypoparathyroidism with severe liver damage leading to cirrhosis and characterised by "ectoplasmic vacuoles", as well as severe anaemia and thrombocytopenia. As any known metabolic or inflammatory liver disease could largely be excluded, a common genetic defect is assumed as the cause of the combined disorder in calcium and hepatic metabolism.

Anemia↗
PubMed1978

Inhibition by insulin of the formation of autophagic vacuoles in rat liver. A morphometric approach to the kinetics of intracellular degradation by autophagy.

Electron microscopic morphometry has demonstrated a rapid decrease in the fractional volume of autophagic vacuoles (AV) in hepatocytes of adult male rats after the intraperitoneal administration of insulin (5 U/kg of body weight). Except for a significant decrease in glycogen to about one-half its initial value, no major changes in the composition of the remaining cytoplasm, or in the average volume of the single hepatocyte, were seen. The decrease found in the AVs is attributed to an inhibition of the formation of new AVs-probably the morphologic counterpart of the well-known anticatabolic effects of insulin. The decay of the fractional volume of the AVs appeared to follow first-order kinetics. Thus, the termination of the "life" of an AV by destruction of its contents may not depend directly on the "age" of the AV. The average half-life of the AVs amounted to approximately 9 min. Similar values were found for the different types of AVs, except for those containing glycogen. The half-life of these AVs was approximately 18 min. From the half-life values and from the "segregated fractions" at time zero, which were different for the different cytoplasmic components, rates of removal from the cytoplasm by autophagy were calculated. Expressed as "percent per day", the following rates were found: whole cytoplasm, 2.3; mitochondria, 3.9; microbodies, 8.9; and glycogen, 1.1. The results indicate that autophagy, to some extent, is selective and plays an important, but not an exclusive, role in intracellular turnover.

Animals↗
PubMed1977

A morphometric study of the inhibition of autophagic degradation during restorative growth of liver cells in rats re-fed after starvation.

In the parenchymal cells of the liver of adult male rats re-fed on the evening of the fifth day after a period of absolute starvation, a nearly complete absence of autophagic vacuoles (AV) has been found by the morphometric determination of the fractional cytoplasmic volume of AV. The mean value for that parameter increased only gradually during periods of re-feeding. The value was found to be in the range of the control values only on, or after, the fifth day of re-feeding. As in previous experiments, in the control animals the number of AV was again found to be dependent on a circadian rhythm with maxima during the light, and minima during the dark, periods. This rhythm reappeared in the period of re-feeding without a shift in phase. In the controls as well as in the re-fed animals the "segregated fraction" was highest for microbodies, intermediate for mitochondria and glycogen, but rather low for the remaining components of the cytoplasm. It is suggested that the long term inhibition of cellular autophagy, found in the present study, plays an important role in the restorative cellular growth of the liver during the recovery from the atrophy induced by starvation.

Animals↗
PubMed1977

Inhibition by insulin of the physiological autophagic breakdown of cell organelles.

By using electron microscopic morphometry it was found that the fractional volume of autophagic vacuoles in the cytoplasm of liver cells decreased rapidly after administering 5 units insulin per kg body weight to otherwise untreated rats. From the decay which appears to follow first order kinetics a half-life of 9 min was found for the compartment of autophagic vacuoles. The rates of autophagic breakdown calculated were different for the different cytoplasmic components, indicating that selecting mechanisms are involved in the process of segregation which is the first step in autophagy.

Animals↗
PubMed1976

[Diurnal rhythm of lysosomal organelle decomposition in liver, kidney and pancreas].

The amount of autophagic vacuoles which, under certain presumptions, can be used as a measure of the intensity of cellular autophagy shows clear cut diurnal changes in untreated rats. Liver parenchymal cells, epithelial cells of proximal convoluted tubules of the kidney, and acinar cells of the exocrine pancreas were investigated. The rhythm is synchronous for these three cell types. The "maximum" was found during the light period, the "minimum" during the dark period. The quantitative findings are in keeping with the assumption that cellular organelles are destroyed exclusively by cellular autophagy. Different turnover rates of mitochondrial and peroxisomal constituents, as determined in biochemical experiments, are paralleled by different relative frequencies to which mitochondria and peroxisomes occur in autophagic vacuoles. In liver cells the physiological rhythm can be influenced by alteration of feeding conditions. It is inverted when a single daily meal is fed in the first half of the light period. In early starvation the level of the diurnal "maximum" of cellular autophagy continues for the first hours of the dark period until a slow decline takes place. Cellular autophagy is completely stopped for several days when rats are refed after starvation for 5 days.

Animals↗
PubMed1975

Stimulation of cellular autophagy by parathyroid hormone and cyclic adenosine 3',5': monophosphate in isolated tubular fragments from the rat's kidney cortex.

Tubular fragments isolated from the cortex of the rat's kidney were qualitatively and quantitatively investigated with the electron microscope. The tubules frequently burst open and became "inverted" in such a way that the rarefied brush border now formed the outer circumference. By morphometry a decrease of the average cell volume in the proximal tubular fragments was ascertained. This was mostly caused by a loss of cytoplasmic ground substance, endoplasmic reticulum and ribosomes. Cytoplasmic herniations of the basal surface, filled with free ribosomes, suggested a partial shedding of the protein synthesizing apparatus. The number of autophagic vacuoles (AV) per unit area of cytoplasm was determined in proximal tubular fragments. After isolation alone, without further incubation, the number of AV was as low as the number found in an earlier study in proximal tubular cells in situ during the diurnal minimum. After control incubation the number of AV increased to about the mean value of the AV found in cells in situ during the whole diurnal cycle. By comparison with the control incubation the number of AV increased by a factor of 1.6 to 1.7, if cyclic adenosine 3',5': monophosphate (cyclic AMP) or parathyroid hormone (PTH) were added to the incubation-medium; it now reached about the number of AV found in situ during the diurnal maximum. The increase in the number of AV paralleled that of the production of ammonia and glucose from endogenous sources under the influence of cyclic AMP and PTH. This suggests that the breakdown of cytoplasmic components by cellular autophagy could be functionally related to gluconeogenesis. A quantitative comparison between the measured production of ammonia and glucose indicates, however, that in the system of isolated tubular fragments there may exist other mechanisms of degradation, and of the provision of substrates for gluconeogenesis, than cellular autophagy only.

Animals↗