7,694 research outputs found
Interview with Wilmore Perry
No full textGunnery Sergeant Wilmore Perry was born in Washington, D.C., where he completed high school and a year of business school. Before entering the Corps in 1943, he was employed by the federal government with the Foreign Broadcast Intelligence Agency. He served in Guam and the Mariana Islands and was discharged in 1946, returning to Washington to work for the Foreign Broadcast Intelligence Agency until it was taken over by the Central Intelligence Agency in 1947. He then joined the Post Office, where he worked until he retired in 1978. He lives in Washington, D.C
Axon damage and repair in multiple sclerosis
No full textIt is well known that within long-standing multiple sclerosis (MS) lesions there is axonal loss but whether it is an early or late event has been more difficult to establish. The use of immunocytochemical methods that reveal axonal end-bulbs is a valuable approach to investigating acute axonal injury in human pathological material. The application of these techniques to multiple sclerosis tissue reveals evidence of axonal injury in acute lesions; the distribution of the end-bulbs in acute and active-chronic lesions is associated with regions of maximal density of infiltrating macrophages. Axon injury within the MS lesion will result in both Wallerian degeneration of the axon and also retrograde degeneration of the cell body. The functional consequences of the axon injury will depend upon numbers of axons injured and the topographical organization of the fibres coursing through the lesion. The molecular mechanisms by which the recruited leucocytes damage or transect the axons are not known. However, investigations in the Wld mutant mouse with very slow Wallerian degeneration demonstrate that axon degeneration is not simply a passive disintegration of the axon but has clear parallels with the active processes of programmed cell death. The presence of early axon injury and the consequences of an ever increasing load of neuronal damage has important implications not only for when therapy should be initiated in MS but also the therapeutic target
Stroke: a double-edged sword for cleaving clots?
No full textThe discovery that tissue plasminogen activator can promote neuronal degeneration has uncovered a novel pathway leading to neuronal cell death and raises important issues concerning the use of tissue plasminogen activator as a thrombolytic therapy for stroke
Loss of the tight junction proteins occludin and ZO-1 from cerebral vascular endothelium during neutrophil-induced blood-brain barrier breakdown in vivo.
No full textThe tight junctions found between cerebral vascular endothelial cells form the basis of the blood-brain barrier. Breakdown of the blood-brain barrier is a feature of a variety of CNS pathologies that are characterized by extensive leucocyte recruitment, such as multiple sclerosis and stroke. The molecular mechanisms associated with opening of the blood-brain barrier and leucocyte recruitment in vivo are currently poorly understood. We have used an in vivo rat model to investigate the molecular response of the CNS endothelium to neutrophil adhesion and migration. Injection of interleukin-1 beta into the striatum of juvenile brains results in a neutrophil-dependent increase in vessel permeability at 4 h. Only a subset of blood vessels were associated with neutrophil recruitment. These particular vessels displayed an increase in phosphotyrosine staining, loss of the tight junctional proteins, occludin and zonula occludens-1, and apparent redistribution of the adherens junction protein vinculin. Examination of these vessels under the electron microscope indicated that the cell-cell adhesions in such vessels are morphologically different from normal junctions. This study provides the first direct evidence in vivo that leucocyte recruitment can trigger signal transduction cascades leading to junctional disorganization and blood-brain barrier breakdown. Our results have established an endothelial cell molecular profile associated with leucocyte-induced blood-brain barrier breakdown in vivo, and the relevance of different in vitro cell culture models may now be viewed more objectively
Georgetown College Graduating Class, 1864
No full textPictured, left to right: R. Ross Perry of Washington, D.C.; ? Closs; Thomas Rudd of Kentucky; Cypriani Zegarra of Peru; Edward S. Reilly of Pennsylvania; and James P. McElroy of New York
The evidence for primary axonal loss in multiple sclerosis
No full textINTRODUCTION: At what stage in the pathogenesis of multiple sclerosis (MS) does the damage to axons occur, and why should there be any axon loss at all in what is thought to be principally an axon sparing demyelinating disease? A recently described new technique for investigating axon damage depends for its ability on the immunoreactivity of amiloid precursor protein (APP), which has been shown to be more sensitive than silver stains for detecting damaged axons. DEVELOPMENT: We used APP immunoreactivity as a method to investigate whether axon damage occurs in acute MS lesions. The results of our APP staining showed that the expression of APP in MS lesions is associated with acute MS lesions and the active border of less acute lesions. There was little, if any, APP expression in the chronic lesions. If we accept that the APP staining represents irreversible damage to some axons, the next question is what factors are responsible for mediating damage to axons in MS? Matrix metalloproteinases (MMP) are expressed by macrophages in acute MS lesions and in the active borders of active chronic lesions. The injection of highly-purified MMP into the brain results in demyelination, blood-brain barrier breakdown, and axonal loss. Moreover, the inhibition of the MMP activity reduces the severity of MS-like lesions in experimental models. Thus the properties and distribution of these enzymes make them rational targets for therapeutic intervention. CONCLUSION: Whatever mechanism proves to be responsible for axonal damage in MS, it is clear that this disease should, perhaps, be more appropriately recognized as a primary demyelinating entity with associated primary axonal loss.<br/
The role of axonal pathology in MS disability
No full textIt is well recognized that in end-stage multiple sclerosis (MS) pathology there is axon loss. Since the axons of central nervous system fibre tracts regenerate very poorly (if at all), it is axon loss that is likely to be responsible for the permanent clinical deficits of MS. Thus, the key question is not whether there is axon degeneration in MS, but when it occurs during the course of the disease. If it develops early in the disease, and is not just a consequence of long-standing demyelination, this would suggest that therapies directed at preventing the pathology early in the disease should be implemented. This article reviews the recent evidence that axonal damage does indeed occur early in MS and considers the mechanisms by which an inflammatory response might damage the axons acutely
CINC-1 is an early hepatic acute phase protein induced by focal brain injury that causes leukocyte mobilization and liver injury
No full textColonel and Brevet Brigadier General Alex J. Perry, quartermaster general's office, division of clothing and equipage, to Captain A.H. Heath, 99th Indiana Volunteers, Company A, Indianapolis, Indiana
No full textPerry acknowledges receiving the return of clothing and camp and garrison equipage report made by Heath.Heath, Alfred H.1860s (1860-1869)Washington (D.C.)600ppiCivil War Military FrontDC046This Civil War Military Front collection was funded by LSTA
The blood-brain barrier and the inflammatory response.
No full textThe environment of the brain is controlled by a sophisticated endothelial barrier that prevents the free entry of solutes from the blood. It is commonly assumed that this blood-brain barrier (BBB) also prevents the entry of leukocytes into the central nervous system. However, recent evidence in animal models shows that this is not the case, and leukocytes can cross an intact BBB during health and disease. Indeed, in many neurological diseases, including Alzheimer's disease, prion diseases and AIDS-related dementia, leukocytes enter the brain parenchyma without concomitant BBB breakdown. Current research is concentrating on factors that control the integrity of the BBB and the mechanisms that leukocytes use to enter the brain
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