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Biomedical subjects

A Bischoff

Publications and source records attributed to A Bischoff.

At least 127 records · Page 7Linked to original sources
PubMed1980

Myelin and glial membrane structures in the optic nerve of normal and jimpy mouse. A freeze-etching study.

In order to investigate the myelin and the glial cell membranes in the optic nerve of the mutant mouse "Jimpy," the method of freeze-etching was applied. The compact myelin lamellae and the first two glial membranes of the mutant, as compared to the normal mouse, show several abnormalities: absence of intramembraneous particles on the P-face, myelin lamellae separated by cytoplasmic layers, vesicular protrusions forming irregular invaginations, and elevations and tight junctions with a discontinuous, zigzag course. Some of these characteristics were found in the membrane of the oligodendroglia cell of the pathological animal, as well. The astrocytic membranes of both normal and Jimpy mice contain two types of gap junctions. The occurrence of one type seems to be increased in the mutant. Freeze-fractured internodal regions of the axolemma are not significantly different from those of normal animals.

Animals↗
PubMed1979

Recurrent familial neuropathy with liability to pressure palsies: reports of two cases and ultrastructural nerve study.

Electrophysiological, histological and ultrastructural studies on two patients (one family) with familial neuropathy and a liability to pressure palsies are reported. There was slowing of nerve conduction velocities and increase of distal latencies of clinically affected and clinically non-affected nerves. These alterations were confirmed by biopsy of the sural nerive which had the characterized signs of the disease. Pathogenetically there seems to be an endogeneous metabolic defect of the Schwann cell to synthetize a normal myelin sheath, which is responsible for the particular susceptibility to mechanical damage.

Adolescent↗
PubMed1979

Morphological observations in the nervous system of prenatal mucopolysaccharidosis II (M. Hunter).

Light and electron microscopic finding in the nervous system of a 23-week-old fetus are reported, in which MPS II was diagnosed prenatally. The degrees of myelination and neuronal differentiation were similar as in a normal fetus of the same age. A storage of mucopolysaccharides in typical vacuolar inclusion bodies was present throughout the peripheral and central nervous system, mainly in cells of mesenchymal origin. "Zebra" bodies and granulo-membranous bodies, which are thought to represent secondard ganglioside accumulation were only found in the well developed neurons of the spinal cord and spinal ganglia, but not in the poorly developed neurons of the cerebellar and cerebral cortex. Mucopolysaccharide storage in endothelial cells of cerebral bood vessels precedes the appearance of lipid storgae in cerebral neurons.

Brain↗
PubMed1979

Neuropathy, amyloidosis, and monoclonal gammopathy.

Three cases of neuropathy with monoclonal gammopathy and amyloid deposits in peripheral nerves are described. They appeared to present a benign gammopathy because of the duration of the neuropathy in the absence of any clinical or biological sign of myeloma or macroglobulinaemia. The pathological abnormality found in the sural nerves of the three patients was characterised by a marked loss of myelinated and unmyelinated nerve fibres because of active axonal degeneration with Wallerian degeneration. The most striking feature in all three cases was the finding of deposits identified as an accumulation of microfibrils.

Aged↗
PubMed1979

Diabetic encephalopathy. Does it exist?

A case of a diabetic aged 65 years with an insidious progressive cerebral disorder with ataxia, tremor, general rigidity and mental deterioration is reported. Pathological examination revealed multiple small infarcts in the pons, the basal ganglia and medulla oblongata, corresponding to the lacunar state. The parenchymal lesions were associated with changes in the small arteries consistent with diabetic angiopathy. Since the patient was normotensive, the pathogenetic role of hemodynamic abnormalities in relation with diabetes is suggested.

Aged↗
PubMed1978

[Kidney preservation by hypothermic storage in Collins and Sacks solutions: the influence of 0-30 min of warm ischemia on the available preservation period (author's transl)].

123 kidneys of mongrel dogs were stored under hypothermic conditions in Collins or Sacks solutions for 12 up to 72 h and then transplanted. Before preservation the kidneys were subdued to 0-30 min warm ischemia. Kidney function after transplantation was measured by PAH-and inulin-clearances. Successful 24 h preservation was likewise possible with Collins and Sacks solutions if there was not any warm ischemia. Kidney function was reduced by the length of preservation, according to the formula; y = 166.02 . e-0,125x (y = PAH-clearance and x = preservation time). With both solutions the most attainable preservation time after 15 min warm ischemia was only 12 h, longer preservation time or ischemic periods were not tolerable. However, the function of the ischemically damaged organ was significantly better preserved by Sacks solution in comparison with Collins solution-although the preservation period could not be extended by this solution. Therefore, as far as human kidney preservation is concerned, Collins solution should be replaced by Sacks solution.

Animals↗
PubMed1978

Filaments in astrocytes and axons of mice optic nerve. A freeze-etching study.

Fixed and nonfixed tissues from optic nerves of 20-day-old mice were examined with the electron microscope using the freeze-etching method. In this study the filaments of fibrious astrocytes are compared with those of axons. Both the astrocytic perikaron and the processes show a characteristic aspect in view of the arrangement and density of filaments. The most reliable criterion to distinguish them from nonmyelinated axons is the presence of areas with packed filaments. Furthermore, we demonstrated morphometrically that the filaments of axons and astrocytes from prefixed specimens had a statistically significant (p less than 0.001) smaller diameter (9.5 +/- 0.3 nm) than those from nonprefixed ones (10.5 +/- 0.3 nm). The diameters of filaments in axons and astrocytes are identical in fixed as well as in nonfixed material. The fine structure of filaments displays in addition to a helical form also a certain periodicity.

Animals↗
PubMed1978

[Preservation of kidneys with ischemic injury using hypothermic storage and mechanical prolonged perfusion].

Dog kidneys were flushed and stored in Collins (n = 30) and Sacks (n = 32) solution under hypothermia. These results were compared with those gained by mechanical perfusion (n = 21). Before preservation, the kidneys were subjected to 15 - 60 min of warm ischemia then stored for 12 - 24 h. It was concluded that 12-h preservation time after 15-min ischemic injury was the limit of hypothermic storage preservation. Sacks' solution gave better results than Collins' solution as regards the immediate function after transplantation. In contrast, mechanical perfusion was well tolerated for 24-h preservation time after a warm ischemia of 30 min. In case of warm ischemic damage, mechanical perfusion should be preferred to hypothermic storage.

Animals↗
PubMed1977

Generalized giant axonal neuropathy: a filament-forming disease of neuronal, endothelial, glial, and schwann cells in a patient without kinky hair.

The process of Giant Axonal Neuropathy (GAN) is not restricted to the peripheral nerves, but also involves the central nervous system. In a 25 year old man with normal hair, abundant axon swellings and spheroids were observed in the spinal cord, brain system, and cerebral cortex. The findings in the sural nerve have already been published by Boltshauser et al. (1977). Accumulations of filaments in the axons and in the perineural cells were accompanied by Rosenthal fibres. The ultrastructural pattern of GAN differs clearly from that of Neuroaxonal Dystrophies.

Adult↗
PubMed1977

Peripheral nerve changes in thiamine deficiency and starvation. An electron microscopic study.

Electron microscopic investigations on sciatic and plantar nerves of thiamine deficient and starved rats show a distally pronounced axonal degeneration. The changes are present in starved and thiamine deficient animals, but the deficient animals are more severely affected. The earliest alterations consist of an increase of mitochondria and a proliferation of vesicular elements of the endoplasmic reticulum. They are followed by loop formations of the axon membrane, clustering and disintegration of neurotubules and neurofilaments, axonal shrinkage and finally myelin disruption. The distal accentuation of the early changes indicates a dying-back mechanism of axonal degeneration.

Animals↗
PubMed1977

Polyneuropathy in hypothyroidism. Clinical and nerve biopsy study of 4 cases.

Clinical and sural nerve biopsy findings are described in four hypothyroid patients with manifestations of a diffuse peripheral neuropathy. Clinical examination revealed distal sensory inpairment, complaints of burning and lancinating extremity pains, ataxia and a decrease of deep tendon reflexes with total ankle jerk loss. In one patient, signs of the peripheral neuropathy comprised the leading symptomatology of the underlying metabolic disorder. Light and electron microscopic investigations of the sural nerve biopsies revealed a marked reduction of myelinated fibers, affecting mainly the large myelinated axons. The histograms showed a pathological unimodal spectrum of myelinated fiber diameters. Dystrophic and degenerative changes in axons of all fiber classes and the presence of clusters of thinly myelinated small fibers suggest that neuroaxonal degeneration and incomplete regeneration may represent the major pathogenetic mechanism of the neuropathy in these hypothyroid patients.

Aged↗
PubMed1977

[Gentamicin neurotoxicity (polyneuropathy--encephalopathy)].

An investigation has been conducted into clinical signs and concomitant ultrastructural alterations in the peripheral nerves of 4 patients who developed polyneuropathy and, in part, encephalopathy following gentamicin therapy. The ultrastructural analysis of the nerve biopsy afforded evidence of an induced lysosomal abnormality comparable to the changes observed in gentamicin nephrotoxicity. As in nephrotoxicity, the neurotoxic effect seems to be reversible.

Aged↗