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  • 1
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  60th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN); 20150826-20150828; Berlin; DOC15dgnnND2 /20150825/
    Publication Date: 2015-08-26
    Keywords: ddc: 610
    Language: English
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  • 2
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN); 20120912-20120915; Erlangen; DOC12dgnnPP4.1 /20120911/
    Publication Date: 2012-09-12
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 3
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  81. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie; 20100512-20100516; Wiesbaden; DOC10hnod626 /20100422/
    Publication Date: 2010-04-23
    Keywords: ddc: 610
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  • 4
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN); 20120912-20120915; Erlangen; DOC12dgnnPP7.4 /20120911/
    Publication Date: 2012-09-12
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 5
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  60th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN); 20150826-20150828; Berlin; DOC15dgnnP6 /20150825/
    Publication Date: 2015-08-26
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 6
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Basal nucleus of Meynert ; Neuronal cytoskeleton ; Tau protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study examines the evolution of Alzheimer’s disease (AD)-related pathology in a subcortical predilection site, the basal nucleus of Meynert (bnM), which is a major source of cortical cholinergic innervation. Brains of 51 autopsy cases were studied using silver techniques and immunostaining for tau-associated neurofibrillary pathology and for amyloid β protein (Aβ) deposits. All cases are classified according to a procedure permitting differentiation of six stages of AD-related neurofibrillary changes in the cerebral cortex. Initial cytoskeletal abnormalities in the bnM are already noted in stage I of cortical neurofibrillary changes. The gradual development of the neurofibrillary pathology in the bnM parallels the progression of the AD-related stages in the cerebral cortex. A variety of morphologically distinguishable cytoskeletal alterations are observed in large nerve cells which predominate in the bnM. Based on these cellular alterations, a sequence of cytoskeletal deterioration is proposed. Initially, the abnormal tau protein is distributed diffusely throughout the cell body and the neuronal processes. Subsequently, it aggregates to form a neurofibrillary tangle, which appears as a spherical somatic inclusion. The cell processes gradually become fragmented. Finally the parent cell dies, leaving behind an extraneuronal “ghost tangle”. With regard to the cortical stages of AD-related ¶neurofibrillary changes, the initial forms of cytoskeletal changes in the bnM predominate in the transentorhinal AD stages (I and II), while “ghost tangles” preferentially occur in the neocortical stages (V and VI). The considerable morphological diversity of cytoskeletal alterations is typical of stages III and IV. These results indicate that individual neurons of the bnM enter the sequence of cytoskeletal deterioration at different times.
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  • 7
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Plaques ; β-Amyloid ; Amyloid precursor protein ; Apolipoprotein E
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Regional differences in senile plaques immunostained by antibodies against β-amyloid A4 (β-A4), amyloid precursor protein 695 (APP) and apolipoprotein E (apo E) were studied in the hippocampus and the entorhinal, temporal and occipital cortices both quantitatively and semiquantitatively with respect to the laminar cortical distribution of the plaques. These patterns were related to the staging of Alzheimer’s disease in regard to the distribution of neurofibrillary tangles [Braak and Braak (1991) Acta Neuropathol 82: 239–259]. In the hippocampus and especially in sector CA 1, no significant differences in the number of plaques visualized by the different antibodies were found. In contrast, there was a striking difference in neocortical regions. Here, significantly higher numbers of plaques positive for β-A4 than that for APP and apo E were present in all stages, except in the stages I and VI, and for apo E in stage II. The highest densities of β-A4-positive plaques were found in the isocortical layers III and V and in the entorhinal pre-α, pre-γ, pri-α and pri-β layers. The preferentially affected area, showing plaques positive for all three antibodies, was the entorhinal-hippocampal circuit with early affection of CA 1, which represents the direct and indirect target of the entorhinal neurons of the upper layers. Therefore, we suggest that plaques with dystrophic neurites, positive for APP, seem to be generated secondarily in afferent areas such as the hippocampus, which is the main afferent target of the entorhinal region. Diffuse plaques, negative for APP and apo E, are virtually absent in the CA 1 and seem to originate independently of afferent neuronal dysfunction, as indicated by neurofibrillary tangles.
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  • 8
    ISSN: 1432-0533
    Keywords: Key words Amyloid β-protein ; Amyloid β-protein precursor ; Astrocytes ; Alzheimer’s disease ; Fleecy amyloid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The deposition of the amyloid β-protein (Aβ) is a pathological hallmark of Alzheimer’s disease (AD). Aβ is a peptide consisting of 39–43 amino acids and is derived by β- and γ-secretase cleavage from the Aβ protein precursor (AβPP). An N-terminal-truncated form of Aβ can occur following α- and γ-secretase cleavage of AβPP. Fleecy amyloid is a recently identified distinct type of Aβ deposits occurring in the internal layers (pri-α, pri-β and pri-γ) of the human entorhinal cortex. Fleecy amyloid consists exclusively of N-terminal-truncated Aβ and is a transient form of Aβ deposits, which disappears in late-stage β-amyloidosis. In this study, the entorhinal cortex of 15 cases with AD-related pathology was used to examine astrocytes in the vicinity of N-terminal-truncated Aβ in fleecy amyloid of the layers pri-α, pri-β, and pri-γ in comparison to astrocytes in the vicinity of full-length Aβ in layers pre-β and pre-γ. Immunohistochemistry was performed with antibodies directed against AβPP, Aβ40, Aβ42, Aβ17–24, Aβ1–17 and Aβ8–17 as well as by double-labeling with antibodies directed against Aβ17–24, Aβ42, and glial fibrillary acid protein (GFAP). A large number of GFAP-positive astrocytes containing N-terminal-truncated Aβ fragments appeared in the vicinity of N-terminal-truncated Aβ, whereas Aβ-containing astrocytes were rarely seen in the vicinity of full-length Aβ. These results suggest that N-terminal-truncated Aβ peptide may be cleared preferentially from the extracellular space by astrocytic uptake and processing. Such an astroglial uptake of N-terminal-truncated Aβ may account for the transient nature of fleecy amyloid and point to the use of N-terminal truncation of Aβ in potential therapeutic strategies aimed at preventing the brain from amassing full-length Aβ deposits.
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  • 9
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aims : To study the immunohistochemical and histological features of 158 gastrointestinal stromal tumours (GISTs), consisting of 137 tumours with mutations in c-kit and platelet-derived growth factor receptor-alpha (PDGFRα) genes and 21 wt-GISTs. Additionally, we evaluated the localization of PDGFRα in the normal intestine. PDGFRα gene mutations were recently described in a subset of GISTs and it has been hypothesized that PDGFRα-mutated tumours represent a distinctive entity among GISTs.Results : PDGFRα was expressed in ganglion bodies of the myenteric plexus and in Schwann cells but not in interstitial cells of Cajal. In contrast to other GISTs, tumours with PDGFRα mutations had an epithelioid phenotype and multinuclear giant cells. Kit was down-regulated in PDGFRα-mutated GISTs and PDGFRα expression was decreased in c-kit mutated tumours. Dot-like staining of Kit and PDGFRα was associated very frequently with mutation within the respective gene.Conclusions : Features of PDGFRα-mutated GISTs are multinuclear giant cells and dot-like staining for PDGFRα. In contrast, c-kit-mutated GISTs display a spindle cell phenotype and Kit-dots on immunohistochemistry. Our findings not only help to distinguish distinctive entities of GISTs using histological and immunhistochemical features, but also indicate that Kit and PDGFRα are differentially regulated in a subset of GISTs.
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  • 10
    ISSN: 1432-1963
    Keywords: Schlüsselwörter Rezidivgliome ; WHO-Klassifikation ; Statische DNA-Zytometrie ; Proliferationsindex ; Rezidivfreies Intervall ; Key words Recurrent gliomas ; WHO-classification ; DNA-cytophotometry ; Proliferation index ; Recurrence-free interval
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary DNA-cytophotometry is one of the methods that may contribute to a more precise evaluation of the biological behaviour of tumours in addition to the WHO-classification. In this study 121 tumour specimens of 50 patients suffering from gliomas with one or up to three recurrencies were investigated. In all cases the histological type and WHO-grade and the Ki-67/MIB1 labeling index were determined. DNA cytophotometry was performed after single cell preparation on Feulgen-stained preparations, and the following parameters were calculated: stemline ploidy, 5c-exceeding rate, and 2c-deviation index. Statistical evaluation revealed a highly significant correlation between recurrence-free interval and WHO-grade only. The DNA parameters, however, furnished additional information about increasing genetic instability in the majority of the recurrencies independently of changes in the WHO-grade. They thus seem to be useful as additional parameters for the determination of glioma progression.
    Notes: Zusammenfassung Eine genaue Bestimmung der biologischen Wertigkeit glialer Tumoren erfordert über die WHO-Klassifikation hinaus die Entwicklung und den Einsatz von Spezialmethoden, wozu auch die DNA-Zytophotometrie gehört. In der vorliegenden Studie wurden an insgesamt 121 histopathologisch klassifizierten Proben von Gliomen bei 50 Patienten mit mindestens 1 und bis zu 3 Rezidiven eine Reihe von DNA-Parametern (Stammlinienploidie, 5c-exceeding rate, 2c-deviation index) nach Zellvereinzelung und Feulgen-Reaktion mittels statischer Feulgen-DNA-Zytometrie bestimmt. Daneben wurde die Proliferationsaktivität (immunhistochemischer Ki-67/MIB-1-labeling index) morphometrisch ermittelt. Diese Parameter wurden mit den WHO-Graden und der Länge der rezidivfreien Intervalle statistisch verglichen. In den Rezidiven sowohl mit ansteigendem als auch mit gleichbleibendem WHO-Grad fand sich eine statistisch signifikante Zunahme des 2c DI, der 5c ER und des Ki-67/MIB-1 LI. Dabei ergab sich eine hochsignifikante Korrelation zwischen den WHO-Graden und der Länge der rezidivfreien Intervalle p〈0,00001). Eine statistisch signifikante Korrelation zwischen den DNA- bzw. Proliferationsparametern ließ sich zur Länge des rezidivfreien Intervalls nicht, zum WHO-Grad nur im Falle der ersten Rezidive für die DNA-Parameter herstellen. Die Ergebnisse bestätigen die hohe prognostische Relevanz des WHO-Grades. Die Bestimmung der DNA-Parameter liefert insbesondere bei gleichbleibendem WHO-Grad zusätzliche Informationen über die zunehmende genetische Instabilität des Tumors, welche wie die zunehmende Proliferationsaktivität für die weitere Tumorprogression von Bedeutung ist.
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