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Sökning: L773:1750 3639 OR L773:1015 6305

  • Resultat 1-10 av 73
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1.
  • Brunnström, Hans, et al. (författare)
  • A 76-year-old man with cognitive and neurological symptoms
  • 2009
  • Ingår i: Brain Pathology. - : Wiley. - 1750-3639 .- 1015-6305. ; 19:4, s. 4-731
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • A 76-year-old man presented with cognitive symptoms, followed by headache and weakness of the lower limbs and left arm. The clinical course was progressive but fluctuating. On magnetic resonance imaging (MRI), a contrast-enhancing lesion 1 cm in diameter was seen in the left temporal lobe. This lesion became attenuated and a new contrast-enhancing lesion 1 x 2 cm was seen in the left frontal lobe on a subsequent MRI. Following additional tests, treatment with corticosteroids for presumptive neurosarcoidosis was started, however, he soon expired. At autopsy, there was a tumor-like mass in the left frontal lobe. Pathologic evaluation revealed a primary T-cell lymphoma of the central nervous system (CNS). CNS T-cell lymphomas may be difficult to diagnose, even histologically, due to their frequent small cell morphology and lack of significant atypia.
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2.
  • Johansson, Barbro, et al. (författare)
  • Functional recovery after brain infarction: plasticity and neural transplantation
  • 1994
  • Ingår i: Brain Pathology. - : Wiley. - 1750-3639 .- 1015-6305. ; 4:1, s. 85-95
  • Tidskriftsartikel (refereegranskat)abstract
    • In the past, little attention has been given to the role of brain plasticity for the long term functional outcome in experimental stroke although there is substantial evidence for plasticity in other experimental models of neurological disorders. Under clinical conditions, functional improvement occurs in most stroke survivors during the initial months after the ischemic incidence. Recent PET studies in stroke patients, investigated two months or later after stroke, indicate a considerable potential for functional plasticity in the adult human cerebral cortex. Research aimed at the identification of the mechanisms underlying functional recovery should be given high priority, particularly with regard to environmental factors and pharmacological interventions. Pilot experiments of environmental enrichment significantly improved the functional outcome of laboratory animals after brain infarction. Fetal neocortical tissue grafted into the infarcted area in adult rats received afferent fibres from the intact brain and responded to contralateral sensory stimulation with increased metabolic activity, indicating functional integration between neocortical grafts and host afferent systems. However, reciprocal connections from the graft to the host tissue were rare, and it remains to be shown whether grafting will be able to restore the complex cortical organization of the infarcted tissue.
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3.
  • Levy, Efrat, et al. (författare)
  • The role of cystatin C in cerebral amyloid angiopathy and stroke: Cell biology and animal models : cell biology and animal models
  • 2006
  • Ingår i: Brain Pathology. - : Wiley. - 1750-3639 .- 1015-6305. ; 16:1, s. 60-70
  • Tidskriftsartikel (refereegranskat)abstract
    • A variant of the cysteine protease inhibitor, cystatin C, forms amyloid deposited in the cerebral vasculature of patients with hereditary cerebral hemorrhage with amyloidosis, Icelandic type (HCHWA-I), leading to cerebral hemorrhages early in life. However, cystatin C is also implicated in neuronal degenerative diseases in which it does not form the amyloid protein, such as Alzheimer disease (AD). Accumulating data suggest involvement of cystatin C in the pathogenic processes leading to amyloid deposition in cerebral vasculature and most significantly to cerebral hemorrhage in patients with cerebral amyloid angiopathy (CAA). This review focuses on cell culture and animal models used to study the role of cystatin C in these processes.
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4.
  • Alafuzoff, Irina, et al. (författare)
  • Staging of neurofibrillary pathology in Alzheimer's disease : a study of the BrainNet Europe Consortium.
  • 2008
  • Ingår i: Brain Pathology. - : Wiley. - 1015-6305 .- 1750-3639. ; 18:4, s. 484-96
  • Tidskriftsartikel (refereegranskat)abstract
    • It has been recognized that molecular classifications will form the basis for neuropathological diagnostic work in the future. Consequently, in order to reach a diagnosis of Alzheimer's disease (AD), the presence of hyperphosphorylated tau (HP-tau) and beta-amyloid protein in brain tissue must be unequivocal. In addition, the stepwise progression of pathology needs to be assessed. This paper deals exclusively with the regional assessment of AD-related HP-tau pathology. The objective was to provide straightforward instructions to aid in the assessment of AD-related immunohistochemically (IHC) detected HP-tau pathology and to test the concordance of assessments made by 25 independent evaluators. The assessment of progression in 7-microm-thick sections was based on assessment of IHC labeled HP-tau immunoreactive neuropil threads (NTs). Our results indicate that good agreement can be reached when the lesions are substantial, i.e., the lesions have reached isocortical structures (stage V-VI absolute agreement 91%), whereas when only mild subtle lesions were present the agreement was poorer (I-II absolute agreement 50%). Thus, in a research setting when the extent of lesions is mild, it is strongly recommended that the assessment of lesions should be carried out by at least two independent observers.
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7.
  • Brundin, L., et al. (författare)
  • Neural stem cells : A potential source for remyelination in neuroinflammatory disease
  • 2003
  • Ingår i: Brain Pathology. - : Wiley. - 1015-6305 .- 1750-3639. ; 13:3, s. 322-328
  • Tidskriftsartikel (refereegranskat)abstract
    • In multiple sclerosis, the central nervous system is lesioned through invasion of plaque-forming inflammatory cells, primarily contributing to immune attack of myelin and oligodendrocytes. In this report we address the possible activation and differentiation of central nervous system stem cells following such immunological insults in a well-characterized rat model of multiple sclerosis characterised by spinal cord pathology. Dye-labeled central nervous system stem cells, residing within the ependymal layer of the central canal responded to the multiple sclerosis-like conditions by proliferation, while some of the migrating stem cell-derived cells expressed markers typical for oligodendrocytes (04) and astrocytes (glial fibrillary acidic protein, GFAP) in the demyelinated area. Our results indicate that regenerative stem cell activation following immunoactivity is different from that after trauma, exemplified by the slower time course of stem cell proliferation and migration of progeny, in addition to the ability of the stem cell-derived cells to express oligodendrocyte markers. Finally,, deleterious effects of macrophages on the stem cell population were evident and may contribute to the, depletion of the stem cell population in neuroinflammatory disorders.
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9.
  • Gray, F, et al. (författare)
  • Neuropathology of early HIV-1 infection
  • 1996
  • Ingår i: Brain pathology (Zurich, Switzerland). - : Wiley. - 1015-6305 .- 1750-3639. ; 6:1, s. 1-12
  • Tidskriftsartikel (refereegranskat)
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  • Resultat 1-10 av 73

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