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Biomedical subjects

F S VOGEL

Publications and source records attributed to F S VOGEL.

At least 19 recordsLinked to original sources
PubMed1962

Concentric lamination of glial processes in oligodendrogliomas.

Tissues were obtained by open biopsy of a series of human intracranial neoplasms, fixed in Veronal-buffered osmium tetroxide, and embedded in Vestopal-W. In two instances in which specimens were obtained from oligodendrogliomas in regions where the tumor had infiltrated but not entirely destroyed cortical tissues, glial processes were found to be arranged in a highly organized laminar fashion. This feature was not observed in two additional oligodendrogliomas nor in other types of intracerebral neoplasms. Three types of laminar structures were recognized: (a) perikaryal sheaths composed of several layers of overlapping or concentrically orientated glial processes, (b) layers of longitudinally orientated glial processes along the outer aspect of myelinated axons, and (c) small laminated figures composed of several concentrically disposed glial processes. Spirally constituted lamellar systems were not demonstrated. These findings indicate that under certain circumstances glial cells have the capacity to form sheaths and sheath-like structures by concentric lamination of several processes, rather than by spiraling of a single process.

Brain Neoplasms↗
PubMed1961

Morphologic alterations produced by copper in neural tissues with consideration of the role of the metal in the pathogenesis of Wilson's disease.

The injection into the cerebrospinal fluid of cats of 52 to 208 gamma of copper in the form of an albumin complex or as cupric sulfate, was followed by small elevations in the content of metal in the neural tissues, but regularly and promptly produced persistent quadriplegia and conspicuous histologic changes. Smaller amounts of copper caused less, or no, neurologic manifestations or histologic alterations. The earliest lesions were essentially unaccompanied by inflammation and were initially characterized by hydropic swelling of the myelin sheaths. They progressed rapidly to focal necrosis of all parenchymal components with marked degeneration of myelin and axis cylinders in the peripheral margins of the spinal cord, brain stem, mid-brain, and cerebrum. These histologic changes did not occur in neural tissues incubated in vitro in solutions of the copper-albumin complex. They did not appear in animals injected intraventricularly with ferric sulfate or saccharated iron. Considered together, the findings make it clear that copper in concentrations comparable to those present in the neural tissues of patients with Wilson's disease has the property of profoundly altering neural function and causing conspicuous morphologic alterations.

Animals↗
PubMed1956

Demyelinization induced in the brains of monkeys by means of fast neutrons; pathogenesis of the lesion and comparison with the lesions of multiple sclerosis and Schilder's disease.

Demyelinization was regularly conspicuous in the white matter of the rostral portions of the brains of 6 monkeys sacrificed 14 to 22 months after exposure of the ocular regions to 850 r.e.p. of 14 mev. neutron radiation and it was not present in the brain of a monkey 2 months after radiation under identical conditions; or in those of 5 non-radiated animals serving as controls. In early lesions, the individual myelin sheaths were varicose and fragmented, while the neurons, axons, and glial cells remained normal in appearance. With the passage of time, the degeneration of myelin became more marked and in later stages was accompanied by a degeneration of the axis cylinders, a proliferation of astrocytes and microglia, and minor cytological changes in the oligodendroglia, the whole process occurring essentially without inflammation or notable changes in the cerebral or meningeal blood vessels. The findings show that neutron radiation has the property of destroying myelin in the living animal and inducing changes that are notably similar in their pathogenesis to those that characterize disseminated encephalomyelitis in human beings.

Animals↗
PubMed1953

Studies on the pathogenesis of kernicterus, with special reference to the nature of kernicteric pigment and its deposition under natural and experimental conditions.

Kernicteric pigment was extracted by means of chloroform from the brains of 3 infants. Solutions of it gave a positive diazo reaction, and, as determined electrophotometrically, gave maximum absorption of light having a wavelength of 425 mmicro, being identical in these properties with chloroform solutions of crystalline mesobilirubin. Experimental kernicterus was regularly induced by injecting crystalline mesobilirubin intracerebrally in newborn kittens, the pigment staining the cerebral tissues a bright canary-yellow and being deposited abundantly in the nerve cells, as microscopic examinations showed, although these latter were otherwise intact. Bilirubin, likewise injected intracerebrally in newborn kittens, had no such effects. The possibility is discussed that the blood-brain barrier is altered in some infants with hyperbilirubinemia in such a way that bilirubin crosses it and is then reduced within the brain to mesobilirubin thus giving rise to the cerebral pigmentation of kernicterus. The fact that the pigment itself does not seem to damage the neurons, as the present studies show, makes it necessary to seek some other cause for the neuronal damage that is sometimes seen, in association with the pigmentation, in the naturally occurring disease.

Bilirubin↗