Biomedical subjects
T Lowry
Publications and source records attributed to T Lowry.
Mastoiditis, lymphoma, and AIDS.
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Neuronal injury in experimental status epilepticus in the rat: role of acidosis.
Systemic and cerebral acidosis accompanies generalized tonic-clonic seizures and status epilepticus. Acidosis during status may be modified by neuromuscular paralysis, intubation and ventilation, or administration of a base, but the effect of acidosis on neuronal injury from status is uncertain. We studied the effect of acidosis, induced by hypercarbic ventilation, on heat-shock protein (HSP72) induction in rat brain as a measure of neuronal injury in experimental status epilepticus. Acidosis was found to attenuate neuronal injury, independent of its anticonvulsant effect.
Epileptic tolerance: prior seizures protect against seizure-induced neuronal injury.
Heat shock proteins (HSPs) are induced by a variety of insults to the nervous system, including seizures, and may be neuroprotective. If this is so, prior induction of HSPs should decrease neuronal damage upon re-exposure to an injurious stimulus. To test this hypothesis in relation to seizures, bicuculline was given to rats in two sessions, separated by 1, 3, 5 or 7 days; seizure activity was recorded, and HSP-like immunoreactivity and neuronal injury (acid-fuchsin staining) were quantified in the CA3c sector of the hippocampus. Prior seizures conferred a time-dependent protective effect against hippocampal injury induced by subsequent seizures, which may represent 'epileptic tolerance', analogous to the previously described phenomenon of 'ischemic tolerance'.
Expression of CD60 on multiple cell lineages in inflammatory synovitis.
BACKGROUND: CD60 is a recently described T cell subset marker that is expressed on the surface of most T lymphocytes in synovial tissue and fluid and on a smaller proportion of peripheral T cells. Activation of T lymphocytes can be triggered through CD60. CD60 is also expressed by neuroectodermally derived cells in thymic epithelium and in skin. EXPERIMENTAL DESIGN: Immunohistologic analysis of CD60 expression in synovium and thymus was performed using formalin-fixed tissue samples. Nonlymphoid cell lines grown from similar tissues were analyzed by flow cytometry. RESULTS: CD60 was readily identified in formalin-fixed, paraffin-embedded tissues. Simultaneous examination of CD60 distribution and cell morphology demonstrated that, in addition to its presence on T cells, CD60 was also expressed by a variety of nonlymphoid cells in synovium, including synovial lining cells, vascular endothelium, and dendritic-appearing cells deep within synovial tissue. Synovial tissue expression of CD60 was similar in rheumatoid arthritis and in other forms of inflammatory arthritis. In addition, it was strongly expressed by giant cells in pigmented villonodular synovitis. Surface expression of CD60 was detected by flow cytometry on cultured synoviocytes and on other CD60+ nonlymphoid cells, thus excluding adsorption of CD60 shed by T cells as a sufficient explanation of the immunohistologic findings. CONCLUSIONS: These results define the T cell-activating CD60 determinant as a broadly distributed Ag within synovial tissue, with a possible functional role in the activation of a variety of cellular populations. CD60 may also be a marker for previously undescribed cell subsets in the synovial compartment, possibly including a cell population of neuroectodermal origin.
Bilateral intranigral NMDA blockade increases status duration and neuronal injury from systemic kainic acid.
Limbic seizures may be under the regulation of the substantia nigra, pars reticulata (SNpr). Using microinjection of the NMDA antagonist AP7, we investigated the role of SNpr in modulating seizures induced by kainic acid. Seizure severity was analyzed electrographically and neural injury assessed by measurement of heat shock protein (HSP) expression and acid fuchsin (AF) staining of vulnerable hippocampal cells. Intranigral injection of AP-7 increased the duration of electrographic seizure discharges and the number of HSP-positive and acid fuchsin stained cells in all hippocampal sectors, suggesting that blockade of the NMDA receptors in SNpr enhanced neural injury.
Experience with ciprofloxacin.
The authors report results of a multicenter study of 65 patients treated with ciprofloxacin. Twenty infections were microbiologically proven; eradication of the pathogen was achieved in 80%.
What happens in spinal cord injury.
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