Search PubMed⌕ Search

Biomedical subjects

F J Seil

Publications and source records attributed to F J Seil.

At least 91 records · Page 5Linked to original sources
PubMed1976

Neuroelectric blocking factors in multiple sclerosis and normal human sera.

Serum samples from 13 multiple sclerosis (MS) patients and ten normal human serum samples were applied to cerebral neocortex cultures and evaluated for their ability to block evoked electric activity. A high proportion of sera positive for neuroelectric blocking factors was found in both groups, and there was no substantial difference between serum samples from MS patients and those from normal human volunteers. Some of the neuroelectric blocking factors were thermolabile, others were thermostable, and still others may have been complement-dependent. It is concluded that the ability to block evoked electric responses in tissue cultures is a nonspecific serum property, and that it is not specifically related to the pathogenesis of demyelinating disease.

Adult↗
PubMed1975

Myelination inhibiting and neuroelectric blocking factors in experimental allergic encephalomyelitis.

Sensitization of Lewis rats with whole central nervous system tissue or with purified myelin induced both experimental allergic encephalomyelitis (EAE) and a serum factor which inhibited myelin formation in vitro. Sensitization with the encephalitogenic factor, myelin basic protein, induced EAE, but not the myelination inhibition factor. Sensitization with cerebroside induced neither EAE nor myelination inhibition factor. The serums from control animals without EAE as well as from animals sensitized with all of the above antigens blocked evoked electrical responses in vitro.

Animals↗
PubMed1975

Neural antigens and induction of myelination inhibition factor.

Rabbits were sensitized or immunized with a variety of central nervous system antigens, including bovine spinal cord, bovine, monkey, human, guinea pig, rabbit and rat S myelin basic proteins, and a polypeptide derived from guinea pig basic protein. The animals were observed for development of experimental allergic encephalomyelitis, and their sera were collected at varying intervals after inoculation and evaluated for presence of precipitating anti-basic protein antibody and for their ability to inhibit myelin formation in cerebellar tissue cultures. The resulting complete dissociation between development of experimental allergic encephalomyelitis, the presence of anti-basic protein antibody and the occurrence of myelination inhibition factor suggests that myelination inhibition factor is not involved in the pathogenesis of experimental allergic encephalomyelitis, and argues against a role for anti-basic protein antibody as an antimyelin factor in vitro.

Animals↗
PubMed1972

Multiple sclerosis. Current etiological concepts.

An animal model for acute multiple sclerosis (ms) is experimental allergic encephalomyelitis (eae). eae is produced by intradermal injection of a protein component of central nervous system (cns) myelin. Ultrastructural studies of eae and of a peripheral nerve analog, experimental allergic neuritis (ean), have revealed an orderly sequence of cellular events leading to the destruction and removal of myelin with sparing of axons (primary demyelination). Acute ms has not been studied electron microscopically, but the ultrastructural similarities between ean and a case of acute Landry-Guillain-Barré syndrome, a primary demyelinating disease of the peripheral nervous system, suggest that a similar sequence of events might be found in acute ms. While the pathological findings support a cellmediated or delayed hypersensitivity response, there is also evidence for the pathogenetic role of circulating antibodies. Among such evidence is included the finding that sera from animals with eae and humans with acute ms rapidly produce a reversible block of complex (polysynaptic) electrical activity when applied to cns tissue cultures, which suggests a possible mechanism for transient symptoms in ms. Epidemiological and other studies link ms with a viral cause, although no direct evidence that ms is caused by a virus exists. Viral and immunological mechanisms are not mutually exclusive in considering pathogenetic possibilities for ms, for it can be postulated that a viral infection of the central nervous system acts as a triggering agent for a series of immune responses, including production of a bioelectric blocking antibody and demyelination mediated by sensitized cells, the combination of which ultimately produces the total clinical picture of ms.

Animals↗
PubMed1970

Cerebellar granule cells in vitro. A light and electron microscope study.

The behavior of granule cells in mature cerebellar cultures derived from newborn mice was studied by light and electron microscopy. Many granule cells remained in the explants as an external granular layer. These cells were differentiated, as evidenced by formation of bundles of parallel fibers and by development of synapses between granule cell axons and Purkinje cell branchlet spines, and between Golgi cell axons and granule cell dendrites. Although the over-all architecture of the cerebellar explants after 18-33 days in vitro was similar to that of the newborn mouse, the evident differentiation of the granule cells suggested that interneuronal relationships resemble those of the mature cerebellum in vivo.

Animals↗
PubMedDate not supplied

Biphasic electrophysiological effects of phenytoin on neural tissue cultures.

Cerebellar and cerebral neocortical explants were exposed to concentrations of phenytoin (DPH) ranging from 2 to 22.5 micrograms/ml of buffered balanced salt solution while extracellular electrical activity was recorded. DPH applied to cerebellar cultures produced a biphasic effect on cortical spontaneous activity, with an initial excitatory phase followed by more sustained suppression. The duration of each of these phases was dose dependent. A similar biphasic effect of DPH on stimulus-elicited responses in cultures of cerebral neocortex was noted. An enhancement of the amplitudes of these responses and prolonged oscillatory afterdischarges were early consequences of DPH application. After variable intervals up to 1/2 hour later, there was a prolonged attenuation of these responses. The initial excitatory effect of DPH demonstrated upon direct application to neurons in culture raises the possibility that intravenous DPH may not be the most appropriate drug for the rapid treatment of status epilepticus in man.

Animals↗
PubMedDate not supplied

Neuromuscular responses to pyridostigmine bromide in organotypic spinal cord-muscle culture.

Pyridostigmine bromide (PB) promotes and then silences cholinergic muscle activity, and disrupts the junctional regions of muscle fibers and associated nerve terminals, in organotypic mouse spinal cord-muscle cultures continuously treated with low concentrations of the drug for up to 14 days. Spontaneous muscle activity is restored within 1 week of drug removal.

Animals↗