Oxygen toxicity in the newborn. Necrotizing bronchiolitis in mice exposed to 100 per cent oxygen.
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Biomedical subjects
Publications and source records attributed to S K Ludwin.
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With radioactive chromium, platelet kinetic studies were carried out in four patients with onyalai, a form of thrombocytopenic purpura occurring in the African Negro. Results were compared with those of White patients suffering from idiopathic thrombocytopenic purpura. In the onyalai patients platelet life-span was considerably reduced, and this was associated with a definite rise in radioactivity over the spleen in three of the four cases. In two patients remission was associated with steroid therapy, while in the other two remission followed splenectomy after steroids had failed to raise the platelet count. These findings are similar to those in White patients with idiopathic thrombocytopenic purpura.
It has long been thought that mature oligodendrocytes in the adult mammalian central nervous system (CNS) are post-mitotic and are unable to proliferate in response to injury. The implications of this have been profound, because it has been suggested that this failure of oligodendrocytes to undergo mitosis is perhaps one of the reasons for the failure of the human CNS to undergo remyelination after demyelinating disease. This is in contrast with the normal peripheral nervous system in which there is consistent remyelination, and brisk Schwann cell mitosis. Although it has recently been shown that oligodendrocytes can be regenerated following some specific instances of demyelination, it has long been accepted that unlike mature astrocytes and microglia (macrophages), oligodendrocytes do not proliferate in response to general conditions damaging the nervous system. Here we show that mature oligodendrocytes in adult animals, as well as astrocytes and microglia, are able to respond to damage in the CNS following trauma by incorporating tritiated thymidine into their nuclei.
Perineuronal satellite oligodendrocytes in the mouse have been investigated immunocytochemically using antisera to myelin basic protein and myelin-associated glycoprotein. In the normal animal, during remyelination, and following trauma the staining characteristics of these cells resembled those of other grey and white matter oligodendrocytes. It is concluded that these cells are, in many respects, functionally similar to other oligodendrocytes.
Recovery from rabies was studied in an experimental model. Young adult mice were inoculated in a hindlimb footpad with street rabies virus (fox salivary gland isolate). In a group of 62 mice, 97% developed clinical rabies with paresis of the extremities and spasticity, and 37% recovered with neurological sequelae. There was an acute inflammatory reaction in the brainstem and grey matter of the spinal cord, and degeneration of myelinated axons in the white matter of the cord and in the dorsal roots. Rabies virus antigen was found in the central nervous system of all mice examined between day 5 and 13, and also in trigeminal and dorsal root ganglia. Surviving mice had neutralizing antibodies in serum and brain tissue, and 90% survived an intracerebral challenge with the CVS strain of fixed rabies virus. Spontaneous recovery from rabies encephalomyelitis was demonstrated with evidence of viral replication and pathological changes in the central nervous system.
We report 2 patients with acute symmetrical axonal motor and sensory polyneuropathy associated with vasculitis. The clinical presentation in each case was not that of a mononeuritis multiplex. Serial electrophysiological studies in 1 of the patients documented the development of confluent axonal degeneration involving several motor and sensory territories over the same period of time. In both patients the diagnosis of necrotizing vasculitis was established by peripheral nerve biopsy and recovery followed treatment with prednisone and cyclophosphamide. Biopsy of an involved nerve should be routinely sought in unexplained acute axonal polyneuropathies.