| 1. |
- Kongstad, Poul, et al.
(författare)
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Mechanical compressions and autopsy findings
- 2005
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Ingår i: Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. - 1757-7241. ; 13:2, s. 87-88
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Tidskriftsartikel (refereegranskat)
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| 2. |
- Rebetz, Johan, et al.
(författare)
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Glial Progenitor-Like Phenotype in Low-Grade Glioma and Enhanced CD133-Expression and Neuronal Lineage Differentiation Potential in High-Grade Glioma
- 2008
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Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 10:6, s. 1107-1107
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Tidskriftsartikel (refereegranskat)abstract
- Background: While neurosphere-as well as xenograft tumor-initiating cells have been identified in gliomas, the resemblance between glioma cells and neural stem/progenitor cells as well as the prognostic value of stem/progenitor cell marker expression in glioma are poorly clarified. Methodology/Principal Findings: Viable glioma cells were characterized for surface marker expression along the glial genesis hierarchy. Six low-grade and 17 high-grade glioma specimens were flow-cytometrically analyzed for markers characteristics of stem cells (CD133); glial progenitors (PDGFR alpha, A2B5, O4, and CD44); and late oligodendrocyte progenitors (O1). In parallel, the expression of glial fibrillary acidic protein (GFAP), synaptophysin and neuron-specific enolase (NSE) was immunohistochemically analyzed in fixed tissue specimens. Irrespective of the grade and morphological diagnosis of gliomas, glioma cells concomitantly expressed PDGFRa, A2B5, O4, CD44 and GFAP. In contrast, O1 was weakly expressed in all low-grade and the majority of high-grade glioma specimens analyzed. Co-expression of neuronal markers was observed in all high-grade, but not low-grade, glioma specimens analyzed. The rare CD133 expressing cells in low-grade glioma specimens typically co-expressed vessel endothelial marker CD31. In contrast, distinct CD133 expression profiles in up to 90% of CD45-negative glioma cells were observed in 12 of the 17 high-grade glioma specimens and the majority of these CD133 expressing cells were CD31 negative. The CD133 expression correlates inversely with length of patient survival. Surprisingly, cytogenetic analysis showed that gliomas contained normal and abnormal cell karyotypes with hitherto indistinguishable phenotype. Conclusions/Significance: This study constitutes an important step towards clarification of lineage commitment and differentiation blockage of glioma cells. Our data suggest that glioma cells may resemble expansion of glial lineage progenitor cells with compromised differentiation capacity downstream of A2B5 and O4 expression. The concurrent expression of neuronal markers demonstrates that high-grade glioma cells are endowed with multi-lineage differentiation potential in vivo. Importantly, enhanced CD133 expression marks a poor prognosis in gliomas.
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| 3. |
- Brunnström, Hans, et al.
(författare)
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A 76-year-old man with cognitive and neurological symptoms
- 2009
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Ingår i: Brain Pathology. - : Wiley. - 1750-3639 .- 1015-6305. ; 19:4, s. 4-731
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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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| 4. |
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| 5. |
- Brunnström, Hans, et al.
(författare)
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Cause of death in patients with dementia disorders.
- 2009
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Ingår i: European Journal of Neurology. - : Wiley. - 1351-5101 .- 1468-1331. ; 16, s. 488-492
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Tidskriftsartikel (refereegranskat)abstract
- Background: Investigations on cause of death may provide valuable information about life expectancy and on conditions of terminal dementia care, which perhaps can be ameliorated. Methods: The autopsy reports were studied on all patients (n = 524; 55.3% females; median age 80 years) with a clinically and neuropathologically diagnosed dementia disorder who underwent a complete autopsy at the University Hospital in Lund, Sweden, during 1974-2004. Results: The two most common causes of death were bronchopneumonia (38.4%) and ischaemic heart disease (23.1%), whilst neoplastic diseases were uncommon (3.8%). In a general population of elderly studied for comparison, bronchopneumonia accounted for 2.8%, ischaemic heart disease for 22.0%, and neoplasm for 21.3% of the deaths. Amongst the demented patients, circulatory and respiratory system diseases were the causes of death in 23.2% and 55.5% of the Alzheimer patients, respectively, whilst the corresponding figures were 54.8% and 33.1% for the patients with vascular dementia. Conclusions: In patients with dementia, pneumonia as the immediate cause of death may reflect a terminal stage in which patient care and feeding is difficult to manage well. Knowledge about what actually causes death is of value in the terminal care of patients with dementia disorders.
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| 6. |
- Holm, Ida Elisabeth, et al.
(författare)
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A reassessment of the neuropathology of frontotemporal dementia linked to chromosome 3
- 2007
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Ingår i: Journal of Neuropathology and Experimental Neurology. - 1554-6578. ; 66:10, s. 884-891
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Tidskriftsartikel (refereegranskat)abstract
- A large Danish family has previously been reported in which autosomal dominant frontotemporal dementia (FTD) is genetically linked to chromosome 3 (FTD-3). A mutation was recently identified in the CHMP2B gene that is probably responsible for causing disease in this family. Because of its neuropathologic findings, FTD-3 was originally categorized as a subtype of frontotemporal lobar degeneration, termed "dementia lacking distinctive histopathology." We now report a reevaluation of the neuropathologic changes in this family. Postmortem material from 4 affected family members was available for examination. Gross examination revealed generalized cortical atrophy that was most severe in frontal and temporal cortices. Microscopy showed loss of cortical neurons. microvacuolation of layer 11, mild gliosis, and demyelination of the deep white matter. Results of immunohistochemical staining for alpha-synuclein, prion protein, neurofilament, and tau protein were unremarkable. Variable numbers of small, round, ubiquitin-positive cytoplasmic inclusions were present in the dentate granule layer of the hippocampus in all 4 cases. Rare ubiquitin-positive inclusions were also found in frontal and temporal cortical neurons. These inclusions were also positive for p62 but not for TDP-43. The finding of ubiquitin- and p62-positive, TDP-43-neaative cytoplasmic inclusions in the hippocampus and neocortex suggests reclassification of the neuropathology of FTD-3 as a unique subtype of frontotemporal lobar degeneration with ubiquitin-positive inclusions that are TDP-43 -negative.
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| 7. |
- Karlsson, Christine, et al.
(författare)
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Genetic intratumour heterogeneity in high-grade brain tumours is associated with telomere-dependent mitotic instability.
- 2007
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Ingår i: Neuropathology & Applied Neurobiology. - : Wiley. - 1365-2990 .- 0305-1846. ; 33:4, s. 440-454
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Tidskriftsartikel (refereegranskat)abstract
- Glioblastoma multiforme (GBM) and other high-grade brain tumours are typically characterized by complex chromosome abnormalities and extensive intratumour cytogenetic heterogeneity. The mechanisms behind this diversity have been little explored. In this study, we analysed the pattern of chromosome segregation at mitosis in 20 brain tumours. We found an abnormal segregation of chromatids at mitosis through anaphase bridging (10-25% of anaphase cells) in all 10 GBMs. Anaphase bridging was also found in two medulloblastomas (7-15%), one anaplastic astrocytoma (17%) and one oligodendroglioma (6%). These tumours showed a relatively high degree of cytogenetic complexity and heterogeneity. In contrast, cell division abnormalities were not found in low-grade brain tumours with less complex karyotypes, including two pilocytic astrocytomas and two ependymomas. Further analysis of two GBMs by fluorescence in situ hybridization with telomeric repeat probes revealed excessive shortening of TTAGGG repeats, indicating dysfunctional protection of chromosome ends. In xenografts established from these GBMs, there was a gradual reduction in cytogenetic heterogeneity through successive passages as the proportion of abnormally short telomeres was reduced and the frequency of anaphase bridges decreased from >25% to 0. However, bridging could be reintroduced in late-passage xenograft cells by pharmacological induction of telomere shortening, using a small-molecule telomerase inhibitor. Telomere-dependent abnormal segregation of chromosomes at mitosis is thus a common phenomenon in high-grade brain tumours and may be one important factor behind cytogenetic intratumour diversity in GBM.
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| 8. |
- Li, Jia-Yi, et al.
(författare)
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Lewy bodies in grafted neurons in subjects with Parkinson's disease suggest host-to-graft disease propagation.
- 2008
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Ingår i: Nature Medicine. - : Springer Science and Business Media LLC. - 1546-170X .- 1078-8956. ; 14, s. 501-503
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Tidskriftsartikel (refereegranskat)abstract
- Two subjects with Parkinson's disease who had long-term survival of transplanted fetal mesencephalic dopaminergic neurons (11-16 years) developed alpha-synuclein-positive Lewy bodies in grafted neurons. Our observation has key implications for understanding Parkinson's pathogenesis by providing the first evidence, to our knowledge, that the disease can propagate from host to graft cells. However, available data suggest that the majority of grafted cells are functionally unimpaired after a decade, and recipients can still experience long-term symptomatic relief.
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| 9. |
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| 10. |
- Persson, Annette, et al.
(författare)
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Different assessments of immunohistochemically stained Ki-67 and hTERT in glioblastoma multiforme yield variable results: a study with reference to survival prognosis.
- 2008
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Ingår i: Clinical Neuropathology. - 0722-5091. ; 27:4, s. 224-233
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To investigate a marker of tumor proliferation, Ki-67, and telomerase expression in glioblastoma multiforme and to compare the results of different mainly quantitative assessments, in relation to age and survival rates. METHODS: Immunohistochemical stainings of Ki-67 and hTERT were evaluated in 39 formaldehyde-fixed, paraffin-embedded surgical samples of glioblastoma multiforme diagnosed during 2004, comprising all specimens with sufficient amount of vital tissue sent to the Department of Pathology during this year. Ki-67 counting and hTERT evaluation was assessed on whole tumor sections and on selected areas within each section. Age and length of survival were analyzed in relation to these parameters. RESULTS: We found that different methods of evaluating the stained sections yielded different results regarding Ki-67, but less marked differences for hTERT. With Ki-67 counting on whole sections (non-selected areas), we found a statistically significant correlation with length of survival. There was no corresponding information in the hTERT assessment. We could also confirm a significant inverse correlation between age and length of survival, as previously published. CONCLUSION: Our data demonstrate that different methods of Ki-67 evaluation may give markedly dissimilar results. The significant correlation found between survival and one but not with two other methods of Ki-67 assessment, implicate the value of standardized quantification methods. Our data indicate a possible prognostic use of immunohistochemical Ki-67 proliferation index in glioblastoma multiforme.
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