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  • 1
  • 2
    ISSN: 0277-9536
    Keywords: adaptation (psychological) ; bereavement ; female ; grief ; health
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Gerbil ; Ischemia ; Hsp70 ; Stress proteins ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Induction of the 70-kDa heat shock protein, hsp70, has been demonstrated in brain following experimental stroke. In the present study, hsp70 was localized in gerbil brain at intervals after transient ischemia using a monoclonal antibody specific for stress-inducible forms of hsp70-related proteins. Induced immunoreactivity was found only in neurons, primarily in hippocampus, striatum, entorhinal cortex and some neocortical regions. Notably hsp70 accumulation was minimal in hippocampal CA1 neurons which die after brief ischemic episodes, but was most pronounced in dentate granule cells and CA3 neurons which are spared. The peak of CA3 immunoreactivity occurred at 48-h recirculation, at the onset of CA1 neuron loss at 2–4 days, demonstrating that hsp70 induction is also a component of this delayed hippocampal pathophysiology rather than a direct response to the metabolic disruption of the initial ischemic episode. These results suggest that hsp70 immunocytochemistry may serve as a marker for neuronal circuitry involved in proposed excitotoxic mechanisms after ischemia and other stresses. Control animals showed immunoreactivity in ependymal cells lining the ventricles, indicating a role for hsp70 in normal functioning of these specialized cells.
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  • 4
    ISSN: 1432-0533
    Keywords: Experimental allergic encephalomyelitis ; Peripheral nervous system (PNS) ; Ia-Antigen ; T-Lymphocytes ; Immunoelectron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The distribution of T cells and Ia-antigen in peripheral nervous system (PNS) lesions of experimental allergic encephalomyelitis was studied by light- and electron-microscopic immunocytochemical techniques. Sprague Dawley rats, sensitized with guinea pig spinal cord tissue, developed a biphasic disease with acute inflammatory and chronic inflammatory demyelinating lesions in the PNS. In both the acute non-demyelinating and the chronic demyelinating disease inflammatory infiltrates were composed of T cells and Ia-positive monocytes/macrophages. Dependent upon the stage of the disease a variable percentage of T-lymphocytes carried the Ox 8 antigen (suppressor/cytotoxic cells). In demyelinating lesions no evidence for an interaction of T cells with myelin or Schwann cells was observed, thus arguing against a direct T-cell cytotoxicity in demyelination. The whole sequence of myelin destruction and digestion was performed by W3/13−, Ia+ mononuclear cells with ultrastructural features of monocytes/ macrophages. In contrast to the acute inflammatory stage of the disease, high titers of anti-myelin antibodies were present in sera of affected animals sampled during the chronic inflammatory demyelinating stage. The sera from the latter animals also showed pronounced in vivo demyelinating activity when transferred into the cerebrospinal fluid (CSF) of normal recipient rats. It is thus suggested that demyelination in this model is induced by a co-operation of cell-mediated and humoral immune mechanisms. We did not find evidence for Ia-antigen expression on local elements of the PNS (Schwann cells, axons, or endothelial cells).
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  • 5
    ISSN: 1432-0533
    Keywords: Ia antigen ; Central nervous system ; Experimental allergic encephalitis ; Immunohistochemistry ; Electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ia antigen, encoded within the major histocompatibility complex, plays an important role in the activation of T lymphocytes. Since experimental allergic encephalitis is an essentially T cell-mediated disease, Ia antigen in the central nervous system (CNS) may be pathogenetically relevant. The occurrence of Ia antigen in the CNS of normal rats and of rats with experimental allergic encephalitis was studied by light and electron microscope immunocytochemistry using the monoclonal anti-Ia antibodies Ox 4 and Ox 6. In normal, unsensitized animals a distict population of stellate cells in the meninges and some perivascular mononuclear cells in the nervous tissue carried Ia antigen. In rats with experimental allergic encephalitis a dramatic increase of Ia-positive cells was found. In addition to the positive cells found in normal animals, monocytes, macrophages and many lymphocytes in the meningeal perivascular and parenchymal inflammatory infiltrates as well as “activated microglia” stained for Ia antigen. We did not find evidence for Ia expression on endothelial cells, astrocytes or other components of the CNS in either normal or diseased rats.
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  • 6
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Brain edema ; Cerebral microcirculation ; Hypoperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Three transient episodes of 5 min ischemia spaced at 1-h intervals were produced in Mongolian gerbils by bilateral carotid artery occlusion with an implanted vascular occlusion device. The interval of 1 h was chosen to allow for the development of postischemic hypoperfusion between the ischemic episodes. Three minutes and 1 h after each ischemic episode, and 6 and 24 h after the third occlusion, Evan's blue (EB) was injected intravenously to trace circulating blood, and the number of perfused capillaries was determined in various brain regions by fluorescence microscopy. Brain edema was evaluated by measuring specific gravity in tissue samples taken from adjacent areas. Repetitive ischemia caused progressively increasing brain edema and a progressive reduction of the number of perfused capillaries. Immediately after each ischemic episode, transient recruitment of capillaries occurred, thus excluding noreflow as a main pathogenetic factor of microcirculatory disturbances. The pattern of microcirculation 6 and 24 h after the last occlusion revealed a redistribution of circulating blood, characterized by a reduction in the number of EB-filled capillaries associated with a noticeable dilatation of the larger vascular channels. Our studies suggest a close interrelationship between post-ischemic microcirculatory hypoperfusion and the development of brain edema, the degree and extent of which progresses with the repetition of ischemic episodes when they are carried out during the periods of hypoperfusion.
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  • 7
    ISSN: 0014-5793
    Keywords: Cell growth ; Deuterium-depleted water ; Hydrogen isotope discrimination ; Isotope effect ; Na^+H^+ antiport system
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1459
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei einem 61jährigen Mann setzte rund 48 Jahre nach zunächst komplikationslosem Sturz von einem Baum ein durch 3 Jahre progredientes Spinalsyndrom ein, das sich über leichte spastische Hemiparese links mit homolateraler Vibrationsstörung zu einem kompletten Querschnittssyndrom in C 3 entwickelte. Bei Kopfbewegungen bestanden blitzartig einschießende Schmerzen in den Beinen. Zwei Stürze waren von kurzen Episoden mit Quadruplegie, Atemstörung und Dysarthrie nach Art der „drop attacks“ begleitet. Wenige Wochen ante exitum wurde radiologisch eine pseudarthrotisch geheilte Luxationsfraktur des Dens epistrophei mit inkomplettem myelographischem Stop in Höhe des zweiten HWK aufgedeckt. Extensionsversuche waren von akuten Atemstörungen begleitet, doch bestand als unmittelbare Todesursache eine Pulmonalembolie. Autoptisch lag eine Densfraktur mit Pseudoarthrose und Ventralluxation des Atlas sowie Einengung des Sagittaldurchmessers des Wirbelkanals und ventraler Stufenbildung vor, die von einer mächtigen dorsalen Duraschwarte und Querabplattung der drei obersten Halssegmente begleitet war. Das Rückenmark bot eine „konische“ Läsion von C 1 bis C 3/4 mit Maximum im mittleren Drittel von C 3 und linksseitiger Betonung der Gewebsschäden. Histologisch lagen subtotale Querschnittsnekrose mit mesodermal-gliöser Organisation in C 3 sowie umschriebene Entmarkungs- und Narbenareale im linken Seiten- und Hinterseitenstrang samt Teilen des homolateralen Grau neben Rand- und Arealentmarkung im rechten Seitenstrang sowie symmetrische Hinterstrangschädigung oral und caudal der Querschnittsläsion vor. Als älteste Läsion imponierte eine kleine granulomartige Narbe in C 1. Die mit verzögertem Abbau einhergehende subtotale Gewebsnekrose zeigt relative Verschonung medioventraler Vorderhornabschnitte sowie einer subpialen Markrandzone. Sie läßt sich topisch keinem arteriellen Versorgungsgebiet des spinalen Längs- und Querschnitts zuordnen. Über den oralen Halssegmenten bestand eine linksseitig betonte hyperplastische Arachnopathie mit Hinterwurzelschädigung. Die Spinalgefäße boten außer reaktiver Läsion intramedullärer Zweige im Narbenbereich altersentsprechende Wandveränderungen ohne Verschluß; eine Kompression der A. vertebralis war autoptisch nicht faßbar. Absteigende Pyramidenseitenstrangdegeneration beiderseits im übrigen Rückenmark Die Beobachtung entspricht dem seltenen Bild einer „progressiven Spätmyelopathie nach Luxationsfraktur des Dens epistrophei“, deren Klinik und Radiologie sowie das morphologische Substrat der Wirbel- und Rückenmarksveränderungen unter Berücksichtigung des Schrifttums erörtert und anderen chronischen Myelopathienformen spinaler Genese gegenübergestellt werden. Pathogenetisch sind komplexe mechanische und dynamische Noxen neben vasozirkulatorischen Faktoren, besonders chronischen venösen Abflußstörungen, zu diskutieren. Abschließend werden therapeutische Probleme gestreift.
    Notes: Summary Clinico-pathological report on a 61 year-old man who in absence of primary complications 48 years after a fall from a tree developed a slowly progressive spinal syndrome over a period of three years. First symptoms were slight spastic hemiparesis on the left and vibratory dysesthesia, finally resulting in a spastic quadriplegia and complete loss of sensations at the level of C 3. Head movements were accompanied by lancinating pains in the legs. At two occasions when he had fallen accidentally, flaccid quadriplegia, respiratory distress and dysarthria resembling “drop attacks” occurred. X-ray examinations disclosed a luxation fracture of the odontoid process with pseudarthrosis and an incomplete stop at the level of the axis on myelography. Attempted extensions were followed by acute respiratory distress. Death, however, occurred from pulmonary embolism. Autopsy revealed an old non-united fracture of the odontoid process with pseudarthrosis and ventral luxation of the atlas resulting in a narrowing of the a—p diameter of the cervical canal and formation of a ventral step accompanied by a thick dorsal dural scar and deformation of the three uppermost cervical segments. The spinal cord revealed a “conic” lesion at C 1 — C 3 to 4 with greatest extent at C 3 involving chiefly the left side. Histologically, there was subtotal transverse necrosis with glio-mesodermal organization at C 3 and circumscribed demyelinated areas and glial scars in the left lateral and dorsolateral tracts including parts of the homolateral gray matter. In addition, there was marginal demyelination of the right lateral tracts and symmetric damage of the dorsal tracts orally and caudally to the transverse lesion. The oldest lesion was suspected to be a small granuloma-like scar at C 1. The medioventral parts of the anterior horns and of a small subpial marginal zone were relatively well preserved inspite of the subtotal necrosis and subsequent protracted degradation. There was no topical coincidence of the lesions with any transverse or longitudinal regions of vascular supply of the spinal cord. There was hyperplastic arachnopathy with damage to the dorsal roots at the upper cervical level. The spinal vessels merely showed reactive lesions of intramedullary branches in the damaged areas. Alterations of other parts of the spinal cord corresponded to the age of the patient. There was no compression of the vertebral arteries to be verifiable by autopsy. The observations are consistent with the rare syndrome of “progressive myelopathy of late onset following luxation fracture of the odontoid process”. The clinical and radiological features as well as the morphological substrate of the lesion of the spine and spinal cord are critically discussed with respect to the literature and are compared with other chronic myelopathies of spinal origin. Pathogenetically, complex mechanical and dynamic noxae besides vasocirculatory factors, especially disorders of venous drainage, are discussed. Finally some therapeutic problems are considered.
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  • 9
    ISSN: 1432-1459
    Keywords: Angioencephalopathy ; Centrencephalic lesion ; Angiodysgenetic necrotizing encephalopathy ; Foix-Alajouanine disease ; Dementia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A previously healthy 58-year-old man developed neurological illness with progressive dementia, hallucinations, central motor and vegetative impairment which led to death in 14 weeks. Autopsy revealed lesions in a symmetrical centrencephalic distribution. Inner cerebral veins and arteries were surrounded by extravasation of plasma and perivascular haemorrhage and were thickened by fibrous scarring and muscle fibre proliferation. Necrotized blood vessels were also found. The parenchyma was damaged by incomplete to complete necrosis. The age and sex of the patient, the progressive clinical course, the increase of cerebrospinal fluid protein, and the histopathology of the lesion show some similarities to angiodysgenetic necrotizing encephalopa thy and spinal Foix-Alajouanine disease.
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  • 10
    ISSN: 1432-2196
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Immunopathological studies on multiple sclerosis (MS) brain clearly indicate that a T cell-mediated immune response is the driving force in the induction of the lesions. This T cell-mediated response alone, however, is not sufficient to explain the widespread and selective destruction of myelin sheaths. According to present evidence, it is likely that antibodies directed against surface components of myelin sheaths are at least one factor involved in the demyelinating process. The patterns of inflammation, demyelination and oligodendrocyte destruction, however, suggest that the pathogenesis of the lesions may be fundamentally different in individual MS patients and that autoimmunity may not be the sole cause. In the case of autoimmune reactions various different proteins of the nervous system may become targets and it appears unlikely, that myelin basic protein is a major candidate for a pathogenetic role in MS.
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