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Sökning: WFRF:(Brun Arne)

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1.
  • Bjurberg, Maria, et al. (författare)
  • Early changes in 2-deoxy-2-[18F]fluoro-D-glucose metabolism in squamous-cell carcinoma during chemotherapy in vivo and in vitro.
  • 2009
  • Ingår i: Cancer Biotherapy & Radiopharmaceuticals. - : Mary Ann Liebert Inc. - 1557-8852 .- 1084-9785. ; 24:3, s. 327-332
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: The aim of this study was to investigate early changes in uptake of 2-deoxy-2-[(18)F]fluoro-D-glucose (FDG) in vivo and in vitro in a squamous-cell carcinoma (SCC) cell line originating from a human head and neck SCC during cytotoxic therapy with respect to metabolism in tumor cells and in surrounding stromal tissue. MATERIALS AND METHODS: In 60 nude mice with xenografted SCC, 50 animals were treated with cisplatin. Early changes in the tumor FDG uptake following therapy were evaluated sequentially with phosphor imaging. Using this technique, areas with focal hypermetabolism were detected. The cells creating the focal hypermetabolism were then identified histopathologically on the corresponding sections. In addition, early FDG uptake versus the number of viable tumor cells was measured in vitro following cisplatin treatment. RESULTS: An early transient increase in FDG uptake in tumor cells was seen on day 1 in treated tumors, followed by a rapid decrease confirmed by subsequent tumor regression. This metabolic flare was present in all treated tumors but not in the controls. In vitro, an increase in FDG uptake per cell was observed. CONCLUSIONS: Our results provide new insights into the early metabolic changes in squamous-cell carcinomas subjected to cytotoxic therapy and thus contribute to the discussion on the feasibility of early predictive PET studies.
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2.
  • Brun, Eva, et al. (författare)
  • Prognostic value of histopathological response to radiotherapy and microvessel density in oral squamous cell carcinomas
  • 2001
  • Ingår i: Acta Oncologica. - : Informa UK Limited. - 1651-226X .- 0284-186X. ; 40:4, s. 491-496
  • Tidskriftsartikel (refereegranskat)abstract
    • The prognostic value of histopathological response to preoperative radiotherapy (50 Gy) in radically resected oral carcinomas was studied in 39 consecutive patients. Microvessel density (MVD) was evaluated for relation to radioresponse and outcome. Resected tumour tissue was examined histopathologically and response to radiotherapy was scored according to induced morphological changes. Pretreatment biopsies were stained with antibodies to von Willebrand factor to evaluate MVD in hot-spot regions, in stromal tissue and in tumour epithelial tissue. Histopathological response to radiotherapy was highly prognostic of local failures and survival (p = 0.002), though microscopic surgical radicality was obtained. In good responders to preoperative radiotherapy, the 5-year survival rate was 68% compared with 24% in poor responders. In 12 patients with local recurrence after radical surgery, 11 had poor histopathological radiotherapy responses. In univariate analysis, a high MVD score in tumour epithelium was associated with poor clinical outcome but MVD did not correlate with histopathological radiotherapy response.
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3.
  • Larsson, Elna-Marie, et al. (författare)
  • Magnetic resonance imaging and histopathology in dementia, clinically of frontotemporal type
  • 2000
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 11:3, s. 123-134
  • Tidskriftsartikel (refereegranskat)abstract
    • The magnetic resonance imaging (MRI) and computed tomography findings in 28 patients with the clinical diagnosis of frontotemporal dementia (FTD) were compared with the findings in a control group of 76 individuals without dementia or stroke. A pattern of frontal and temporal atrophy with predominantly frontal white matter changes was found in the FTD patients, and this was significantly different from the radiological findings in the control group. Six of the FTD patients have undergone autopsy. Histopathological evaluation showed a primary cortical degenerative disease (frontal lobe degeneration of non-Alzheimer type) in 3 of them, and primary white matter disorder, mainly frontal, of basically ischemic type (selective incomplete white matter infarction) in 3 of them. MRI could be a helpful tool to support the clinical diagnosis FTD, especially in young patients. MRI may also be helpful for the differentiation of a primary neurodegenerative from a mainly ischemic-vascular type of dementia.
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4.
  • Andin, Ulla, et al. (författare)
  • A Clinico-Pathological Study of Heart and Brain Lesions in Vascular Dementia.
  • 2005
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 19:4, s. 222-228
  • Tidskriftsartikel (refereegranskat)abstract
    • All vascular dementia (VaD) cases, neuropathologically verified in a longitudinal prospective dementia project, were classified according to the vascular brain lesion type and related to the dementia type and cardiovascular pathology. From 1976 to 1995, there were 175 VaD cases, 49 of which were pure, without Alzheimer pathology and only one type of cerebrovascular lesion. Furthermore, it was found that 6 cases suffered hypoxic hypoperfusive disease, while 7 were found to have large vessel disease and 36 small vessel disease. In addition to Alzheimer pathology, more than one type of vascular brain pathology was found in the remaining 126 cases. In these cases, diagnosed in accordance with the predominant type of VaD, hypoxic-hypoperfusive lesions were found in 55, large vessel lesions in 50 and small vessel lesions in 110 cases. It should be stressed that 87% of all cases with hypoxic hypoperfusive lesions also had Alzheimer pathology. Cardiovascular and aortic pathologies were more prevalent in small vessel dementia than in the other VaD groups. Clinically diagnosed arterial hypertension was significantly associated with small vessel dementia, but not with hypoxic-hypoperfusive dementia. Cardiovascular symptoms varied considerably in frequency between different dementia groups. VaD is a heterogeneous group regarding lesions caused by different pathophysiological mechanisms and with different combinations of brain pathologies. It is therefore necessary to identify the various types of vascular brain lesions for a correlation with clinical symptoms and for diagnostic purposes in the search for risk factors and therapeutic strategies.
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7.
  • Balbin, Milagros, et al. (författare)
  • A novel mutation in the β-protein coding region of the amyloid β-protein precursor (APP) gene
  • 1992
  • Ingår i: Human Genetics. - 1432-1203. ; 89:5, s. 580-582
  • Tidskriftsartikel (refereegranskat)abstract
    • A novel mutation, a C to T transition at base pair 2124 in exon 17 of the amyloid beta-protein precursor (APP) gene, has been identified by direct sequencing of amplified DNA from two Alzheimer's disease (AD) patients. A simple oligonucleotide-hybridization procedure was developed to allow population studies of this DNA variation. The mutation, which is silent at the protein level, was present in 2 out of 12 investigated AD patients, in 1 out of 60 non-AD patients and in 1 out of 30 healthy individuals. The mutation can be used as a new marker for linkage studies involving the APP gene, although more comprehensive population studies are required to determine the status of the mutation as a possible risk factor for the development of AD.
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8.
  • Brown, J, et al. (författare)
  • Frontotemporal dementia linked to chromosome 3
  • 2004
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 17:4, s. 274-276
  • Tidskriftsartikel (refereegranskat)abstract
    • A large pedigree with autosomal dominant frontotemporal dementia has been identified. Positional cloning has linked the disease gene to the pericentromeric region of chromosome 3. Clinical, neuropsychological, imaging, pathological and molecular genetic data are presented. The genetic mutation responsible for the disease has not been identified.
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9.
  • Brun, Arne (författare)
  • Alzheimer´s and other neurodegenerative cognitive disorders. : A strategy to find cause and cure
  • 2018
  • Ingår i: Acta Scientiarum Lundensia. - 1651-5013. ; 2018:006, s. 1-11
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this treatise is to sketch out a strategy how to find a cause and cure for cognitive brain disorders and then primarily Alzheimer’s disease (AD) based on recent and little explored research progress. Step one is to find the cause. Recent evolution has supplied the human brain with new astrocytes which regarding their remarkable properties can be expected to harbor the cause of AD and several other cognitive neurodegenerative disorders. Plausible causes have already been proposed and will be accounted for in what follows. A cause proved or made plausible provides a good ground for finding a therapy. We must also be able to diagnose the disorder at an early stage ahead of widespread and severe brain damage for a treatment not to leave behind a crippling condition! This possibility appears now to become a reality since recent research has identified the same changes in the retina as in the brain. They can there be diagnosed with modern ophthalmological techniques and appear long before brain damage produces symptoms during the several decades long silent phase when AD is under way. After arrest of the disorder the neuronal plasticity can be expected to deliver repair, more the earlier the disorder is arrested.
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13.
  • Brun, Arne (författare)
  • Identification and characterization of frontal lobe degeneration - Historical perspective on the development of FTD
  • 2007
  • Ingår i: Alzheimer Disease and Associated Disorders. - 0893-0341. ; 21:4, s. 3-4
  • Tidskriftsartikel (refereegranskat)abstract
    • This is a historical account of the development of the concept frontotemporal dementia, beginning with our discovery in the late 60s of a simple degenerative form. It was named frontal lobe degeneration of non-Alzheimer type to clearly separate it from the then almost totally dominating diagnosis Alzheimer disease. In the absence of immunohistochemical methods for specific disease markers, we had to rely solely on structural features. Later, from the 80s, the successively introduced methods to show glial acidic protein, tau, synaptophysin, ubiquitin, and other markers confirmed our impression of a simple type of degeneration. These methods also added further forms with additional features, and from the 90s genetics has contributed new disease characteristics, all these advances leading up to the present conceptual structure of frontotemporal lobar degeneration.
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14.
  • Brun, Arne (författare)
  • Recent discoveries widen the basis for future research in Alzheimer´s disease.
  • 2016
  • Ingår i: Acta Scientiarum Lundensia. - 1651-5013. ; 2016:002, s. 1-12
  • Forskningsöversikt (övrigt vetenskapligt/konstnärligt)abstract
    • Abstract. Intended as food for thought this revue offers a general orientation on Alzheimer’s disease (AD) with comments on the brain changes and clinical features. But more importantly, it points out recent research findings which may offer new alleys for AD research pertinent to the etiology and pathogenesis of AD and alternatives to the so far rather unfruitful and costly amyloid research trail. This new knowledge thus comes from various fields of research such as epigenetics, pointing to possible environmental etiologic factors. Further exosomes may provide information on the state of the neuronal population for diagnostic purposes and might become useful as carriers of therapeutic substances. The newly disclosed protein complexity of the synapses may harbor a large yet unexplored field for neurochemical research pertinent to the early or likely initial loss of synapses in Alzheimer disease. The finding of a more generalized neuronal gene disturbance in Alzheimer’s disease shifts the focus from age related changes to developmental disturbances and increased neuronal vulnerability. BBB incompetence with a start in the hippocampus has also recently been pointed out and may initiate the degenerative process of Alzheimer’s disease. Finally, recent basic research findings on glial evolution, underscoring the distance between humans and rodents, our prime disease model animal, points to several new unexplored mechanisms, which may be relevant for the understanding of neurodegenerative processes. Also stressed is the need to institute treatment at an early stage of the disease, necessitating research for markers, which will enable a diagnosis way ahead of the widespread damage present at the time of clinical debut.
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15.
  • Brun, Arne, et al. (författare)
  • The Birth and Early Evolution of the Frontotemporal Dementia (FTD) Concept.
  • 2011
  • Ingår i: Journal of Molecular Neuroscience : MN. - : Springer Science and Business Media LLC. - 1559-1166 .- 0895-8696. ; 45, s. 324-329
  • Tidskriftsartikel (refereegranskat)abstract
    • An historical overview of the development of the concept of frontotemporal dementia is presented, regarding the last 30 years, using as a backbone the conferences held on this theme, with a start in 1986 in Lund, Sweden. Since then, a dramatic increase in research activities and publications has rapidly expanded our knowledge in this field, a step necessary for the ultimate goal to find an effective treatment of this devastating disorder.
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  • Capala, Jacek, et al. (författare)
  • Clinical BNCT studies in Sweden
  • 2002
  • Ingår i: Research and development in neutron capture therapy. - : Monduzzi Editore Print. ; , s. 1101-
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)
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19.
  • Ceberg, Crister, et al. (författare)
  • A comparative study on the pharmacokinetics and biodistribution of boronated porphyrin (BOPP) and sulfhydryl boron hydride (BSH) in the RG2 rat glioma model
  • 1995
  • Ingår i: Journal of Neurosurgery. - 0022-3085. ; 83:1, s. 86-92
  • Tidskriftsartikel (refereegranskat)abstract
    • Boron neutron capture therapy is a treatment modality for cancer that depends on the specific uptake of boron by the tumor cells. The infiltrative growth of malignant gliomas requires that boron reach and accumulate in migrating cells outside the margin of the tumor; thus, it is important that the biodistribution of new boron compounds is also studied in the surrounding healthy brain tissue. This study is undertaken in the present work, in which the biodistribution and pharmacokinetics of sulfhydryl boron hydride (BSH) and boronated porphyrin (BOPP) in the RG2 rat glioma model are investigated. This model mimics the characteristics of human glioma with cells migrating into the surrounding brain. The animals were infused intravenously with either BSH (25 micrograms or 175 micrograms of boron per gram of body weight) or BOPP (12 micrograms of boron per gram body weight). For the low dose of BSH, the maximum tumor-boron content was 8 ppm at approximately 9 hours after the infusion with a tumor-to-blood ratio of 0.6. At the higher dose, the corresponding figures were 15 ppm after 12 hours with a tumor-to-blood ratio of 0.5. For BOPP, a tumor-boron concentration of 81 ppm was achieved 24 hours after the infusion and sustained in that range for at least 72 hours. The tumor-to-blood ratio at 24 hours was slightly above 6, but continued to increase as the blood was cleared. These results indicate that both compounds are spread into the normal brain tissue following the same pathways as the migrating tumor cells and in this way can be taken up even in distant tumor cell foci.
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20.
  • Ceberg, Crister, et al. (författare)
  • A stochastic model for subcellular dosimetry in boron neutron capture therapy
  • 1995
  • Ingår i: Physics in Medicine and Biology. - : IOP Publishing. - 1361-6560 .- 0031-9155. ; 40:11, s. 1819-1830
  • Tidskriftsartikel (refereegranskat)abstract
    • The therapeutic effectiveness of boron neutron capture therapy is highly dependent on the microscopic distribution of the administered boron compound. Two boron compounds with different uptake mechanisms in the tumour cells may thus cause effects of different degrees even if the macroscopic boron concentrations in the tumour tissue are the same. This difference is normally expressed quantitatively by the so-called relative local efficiency (RLE). In this work, a stochastic model for the subcellular dosimetry has been developed. This model can be used to calculate the probability for an energy deposition above a certain threshold level in the cell nucleus due to a single neutron capture reaction. If a threshold cell-kill function is assumed, and if the dose is low enough that multiple energy depositions are rare, the model can also be applied to calculations of the survival probability for a cell population. Subcellular boron distributions in rats carrying RG 2 rat gliomas were measured by subcellular fractionation after administration of two different boron compounds: a sulphydryl boron hydride (BSH) and a boronated porphyrin (BOPP). Based on these data, the RLE factors were then calculated for these compounds using the stochastic model.
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21.
  • Ceberg, Crister, et al. (författare)
  • Neutron capture imaging of 10B in tissue specimens
  • 1993
  • Ingår i: Radiotherapy and Oncology. - 1879-0887. ; 26:2, s. 139-146
  • Tidskriftsartikel (refereegranskat)abstract
    • Boron Neutron Capture Therapy (BNCT) is an attractive concept for radiation treatment of malignant tumours. The patients receive a 10B-carrying compound with selective uptake in tumour cells, after which they are irradiated with epithermal neutrons. Theoretically, the tumour cells are killed by the high-LET particles produces in 10B(n, alpha)7Li reactions inside or close to the cell nucleus, while healthy brain cells with no boron uptake will be spared. In practice, a successful BNCT depends on the actual boron-distribution in the tissue, and consequently a new boron-compound aimed for BNCT must undergo detailed bio-distribution studies before clinical trials. In experimental work there is accordingly a great need for methods for quantitative bio-distribution measurements in tissue samples. In this paper we present an improved technique for neutron activated autoradiography providing quantitative boron images of freeze-sectioned tissue specimens from highly malignant rat brain gliomas. Particular attention has been paid to the correlation with the morphology of the specimens and to the altered self-absorption properties due to freeze-drying. A self-absorption correction factor for tumour tissue has been experimentally determined.
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22.
  • Ceberg, Crister, et al. (författare)
  • Performance of sulfhydryl boron hydride in patients with grade III and IV astrocytoma: a basis for boron neutron capture therapy
  • 1995
  • Ingår i: Journal of Neurosurgery. - 0022-3085. ; 83:1, s. 79-85
  • Tidskriftsartikel (refereegranskat)abstract
    • This study investigated the rationale of boron neutron capture therapy (BNCT) for the treatment of Grade III and IV astrocytoma. The European Community joint research program on BNCT plans to use sulfhydryl boron hydride (BSH) in clinical trials. The work presented here, examines the performance of BSH in eight patients with Grade III and IV astrocytoma using a measurement technique which precisely correlates the boron uptake with the histology of the tumor and the peritumoral brain. Astrocytomas are exceptionally heterogeneous and spread migrating tumor cells into the surrounding brain. The patients were infused with 50 mg BSH per kilogram of body weight at 12, 18, 24 or 48 hours before surgery. At the time of operation, specimens were obtained of the tumor, skin, muscle, dura, blood, urine, and, when surgically possible, the brain adjacent to tumor. In three patients the intracellular boron distribution was investigated by subcellular fractionation. The blood clearance was biphasic with half-lives of 0.6 and 8.2 hours. After 3 days, approximately 70% of the dose injected was excreted in the urine. The maximum boron concentration in the tumor was 20 ppm, 12 hours after the infusion. The tumor-to-blood ratios ranged between 0.2 and 1.4, with the highest values after 18 to 24 hours. In the brain specimens the boron concentration never exceeded 1 ppm. This work confirms a selective uptake of boron in the tumor compared to the surrounding brain and that boron, to some extent, is incorporated in the tumor cells.
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23.
  • Eberhardt, Jacob, et al. (författare)
  • Blood-brain barrier permeability and nerve cell damage in rat brain 14 and 28 days after exposure to microwaves from GSM mobile phones.
  • 2008
  • Ingår i: Electromagnetic Biology and Medicine. - : Informa UK Limited. - 1536-8386 .- 1536-8378. ; 27:3, s. 215-229
  • Tidskriftsartikel (refereegranskat)abstract
    • We investigated the effects of global system for mobile communication (GSM) microwave exposure on the permeability of the blood-brain barrier and signs of neuronal damage in rats using a real GSM programmable mobile phone in the 900 MHz band. Ninety-six non-anaesthetized rats were either exposed to microwaves or sham exposed in TEM-cells for 2 h at specific absorption rates of average whole-body Specific Absorption Rates (SAR) of 0.12, 1.2, 12, or 120 mW/kg. The rats were sacrificed after a recovery time of either 14 or 28 d, following exposure and the extravazation of albumin, its uptake into neurons, and occurrence of damaged neurons was assessed. Albumin extravazation and also its uptake into neurons was seen to be enhanced after 14 d (Kruskal Wallis test: p = 0.02 and 0.002, respectively), but not after a 28 d recovery period. The occurrence of dark neurons in the rat brains, on the other hand, was enhanced later, after 28 d (p = 0.02). Furthermore, in the 28-d brain samples, neuronal albumin uptake was significantly correlated to occurrence of damaged neurons (Spearman r = 0.41; p < 0.01).
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  • Grafström, Gustav, et al. (författare)
  • Histopathological examinations of rat brains after long-term exposure to GSM-900 mobile phone radiation.
  • 2008
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230. ; 77, s. 257-263
  • Tidskriftsartikel (refereegranskat)abstract
    • In order to mimic the real life situation, with often life-long exposure to the electromagnetic fields emitted by mobile phones, we have investigated in a rat model the effects of repeated exposures under a long period to Global System for Mobile Communication-900MHz (GSM-900) radiation. Out of a total of 56 rats, 32 were exposed once weekly in a 2-h period, for totally 55 weeks, at different average whole-body specific absorption rates (SAR) (of in average 0.6 and 60mW/kg at the initiation of the experimental period). The animals were exposed in a transverse electromagnetic transmission line chamber (TEM-cell) to radiation emitted by a GSM-900 test phone. Sixteen animals were sham exposed and eight animals were cage controls, which never left the animal house. After behavioural tests, 5-7 weeks after the last exposure, the brains were evaluated for histopathological alterations such as albumin extravasation, dark neurons, lipofuscin aggregation and signs of cytoskeletal and neuritic neuronal changes of the type seen in human ageing. In this study, no significant alteration of any these histopathological parameters was found, when comparing the GSM exposed animals to the sham exposed controls.
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27.
  • Gustafson, Lars, et al. (författare)
  • A 50-year perspective of a family with chromosome 14-linked Alzheimer’s disease
  • 1998
  • Ingår i: Human Genetics. - : Springer Science and Business Media LLC. - 1432-1203 .- 0340-6717. ; 102:3, s. 253-257
  • Tidskriftsartikel (refereegranskat)abstract
    • A Swedish family with two generations suffering from presenile dementia with an unusually severe Alzheimer encephalopathy was first reported in 1946. The hypothesis that the disease was inherited through a dominant gene is strongly supported by the follow-up 50years later of three additional generations and molecular genetic findings of a novel presenilin-1 gene mutation in the family. The pedigree contains six cases with well-documented dementia in four consecutive generations. The Alzheimer encephalopathy was unusually severe in the three cases studied post-mortem, with a pronounced involvement of the central grey structures, such as the claustrum, the nuclei around the third ventricle, the central thalamic nuclei and the brain stem. There were no vascular lesions and little amyloid angiopathy. All six affected cases showed the typical temporoparietal symptom pattern and other core symptoms of Alzheimer’s disease, such as logoclonia, myoclonic twitchings and major motor seizures. Other predominant features were psychomotor slowness, increased muscular tension, a stiff stooped gait and a rapid loss of weight. The symptom pattern is convincingly explained by the consistent and severe involvement of cortical and central grey structures and is probably linked to the presenilin-1 gene mutation.
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  • Gustafson, Lars, et al. (författare)
  • A factor analytic approach to symptom patterns in dementia.
  • 2010
  • Ingår i: International Journal of Alzheimer's Disease. - : Hindawi Limited. - 2090-0252 .- 2090-8024.
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous publications have shown a high diagnostic sensitivity and specificity of three short clinical rating scales for Alzheimer's disease (AD), frontotemporal dementia (FTD), and vascular dementia (VaD) validated against neuropathological (NP) diagnoses. In this study, the aim was to perform an exploratory factor analysis of the items in these clinical rating scales. The study included 190 patients with postmortem diagnoses of AD (n = 74), VaD (n = 33), mixed AD/VaD (n = 31), or FTD (n = 52). The factor analysis produced three strong factors. Factor 1 contained items describing cerebrovascular disease, similar to the Hachinski Ischemic Score. Factor 2 enclosed major clinical characteristics of FTD, and factor 3 showed a striking similarity to the AD scale. A fourth symptom cluster was described by perception and expression of emotions. The factor analyses strongly support the construct validity of the diagnostic rating scales.
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  • Gustafson, Lars, et al. (författare)
  • The accuracy of short clinical rating scales in neuropathologically diagnosed dementia.
  • 2010
  • Ingår i: The American journal of geriatric psychiatry. - 1064-7481 .- 1545-7214. ; 18:9, s. 810-820
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The overall aim was to evaluate to what extent the diagnosis of dementia subtypes, obtained by three clinical rating scales, concurred with postmortem neuropathologic (NP) diagnosis of Alzheimer disease (AD), frontotemporal dementia (FTD), vascular dementia (VaD) and mixed AD/VaD. Design: A prospective longitudinal clinical work-up with postmortem NP examination. Participants: Two hundred nine patients with dementia referred for clinical evaluation and follow-up. Methods: The diagnostic scores in a set of three short clinical rating scales for AD, FTD, and VaD were evaluated against NP diagnoses. Results: The sensitivity and specificity of the AD scale were 0.80 and 0.87, respectively, of the FTD scale 0.93 and 0.92, respectively, and of the Hachinski Ischemic Score (HIS, VaD diagnosis) 0.69 and 0.92, respectively. Cases with mixed AD/VaD generally presented a combination of high AD and ischemic scores. A preferred cutoff score of six was identified for both the AD and FTD scales. Conclusions: All three clinical rating scales showed a high sensitivity and specificity, in close agreement with final NP diagnosis-for the HIS a moderate sensitivity. These scales may thus be considered good diagnostic tools and are recommended for clinical and research center settings.
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31.
  • Gydesen, S, et al. (författare)
  • Chromosome 3 linked frontotemporal dementia (FTD-3)
  • 2002
  • Ingår i: Neurology. - 1526-632X. ; 59:10, s. 1585-1594
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The authors have identified and studied a large kindred in which frontotemporal dementia (FTD) is inherited as an autosomal dominant trait. The trait has been mapped to the pericentromeric region of chromosome 3. Methods: The authors report on the clinical, neuroimaging, neuropsychological, and pathologic features in this unique pedigree collected during 17 years of study. Results: Twenty-two individuals in three generations have been affected; the age at onset varies between 46 and 65 years. The disease presents with a predominantly frontal lobe syndrome but there is also evidence for temporal and dominant parietal lobe dysfunction. Late in the illness individuals develop a florid motor syndrome with pyramidal and extrapyramidal features. Structural imaging reveals generalized cerebral atrophy; H-2 O-15-PET scanning in two individuals relatively early and late in the disease shows a striking global reduction in cerebral blood flow affecting all lobes. On macroscopic pathologic examination, there is generalized cerebral atrophy affecting the frontal lobes preferentially. Microscopically, there is neuronal loss and gliosis without specific histopathologic features. Conclusions: FTD-3 shares clinical and pathologic features with other forms of FTD and fulfills international consensus criteria for FTD. There is involvement of the parietal lobes clinically, radiologically, and pathologically in FTD-3 in contrast to some forms of FTD. This more diffuse involvement of the cerebral cortex leads to a distinctive, global pattern of reduced blood flow on PET scanning.
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32.
  • H-Stenstam, B., et al. (författare)
  • Neuropathological postmortem evaluation of BNCT for GBM
  • 2007
  • Ingår i: Acta Neurologica Scandinavica. - : Hindawi Limited. - 1600-0404 .- 0001-6314. ; 116:3, s. 169-176
  • Tidskriftsartikel (refereegranskat)abstract
    • Background - Thirty patients with glioblastoma multiforme (GBM) were treated by boron neutron capture therapy (BNCT) at the Studsvik facility in Sweden, in a clinical trial exploring a procedure in which 900 mg p-boronophenylalanine (BPA) per kilo body weight was infused in 6 h. Objective - The present study was designed to assess tumor efficacy and radiation damage to the brain for the seven patients in the Studsvik trial that were available for postmortem neuropathological examination. Method - Whole brain slices containing the initial tumor site and other regions showing pathological changes were chosen for microscopy and selected areas were studied by immunological methods. Results - Local control of GBM was observed in all cases. Conclusive evidence for radiation induced brain damage was not found. Conclusion - Using a novel procedure for BPA infusion, BNCT achieves local control of GBM for minimum tumor doses as low as 15 wGy, allowing treatment with very low concomitant doses to surrounding healthy tissues.
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  • Källén, Kristina, et al. (författare)
  • Evaluation of malignancy in ring enhancing brain lesions on CT by thallium-201 SPECT
  • 1997
  • Ingår i: Journal of Neurology, Neurosurgery and Psychiatry. - 1468-330X. ; 63:5, s. 569-574
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To investigate patients with cystic enhancing lesions on CT and to determine whether thallium-201 (201Tl) SPECT adds to further preoperative information in differential diagnosis between gliomas and abscesses. METHODS: Twenty one patients with cystic ring enhancing CT findings were studied and uptake indices were compared with CT enhancement volumes, histopathology, and survival times. RESULTS: Fourteen high grade gliomas, three low grade gliomas, and four abscesses were found. Uptake was higher in the highly malignant glioma group (median thallium index (TI)=2.1), than in the low grade glioma group (median TI=1.4) or among the abscesses (median TI=1.6). Overlapping indices were found between high and low malignant cystic gliomas as well as between either one of the glioma groups and the infectious lesions, and there were no significant differences between groups. There was a level at the value 2, where TI > or = 2 correlated with tumour diagnosis. One low grade tumour had an extremely high index and a very high enhancement volume. Indices correlated significantly with CT enhancement volumes (P=0.005). There was no significant correlation between Tl indices and patient survival times among the high grade gliomas. One patient with a highly malignant tumour but low Tl uptake < 2, had a survival > five years. CONCLUSIONS: It is concluded that high 201Tl uptake in enhancing cystic lesions is an indicator of highly malignant glioma. However, the differentiation between the high malignant gliomas and abscesses or low malignant gliomas by 201TL SPECT is only partial with an overlap between these groups.
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34.
  • Källén, Kristina, et al. (författare)
  • Preoperative grading of glioma malignancy with thallium-201 single-photon emission CT: comparison with conventional CT
  • 1996
  • Ingår i: AJNR. - 1936-959X. ; 17:5, s. 925-932
  • Tidskriftsartikel (refereegranskat)abstract
    • PURPOSE: To compare thallium-201 single-photon emission CT with conventional CT in grading the malignancy of gliomas and to determine the reliability of each in tumor assessment. METHODS: We studied 37 patients who had gliomas (31 high grade and 6 low grade) and compared the CT findings with the thallium-201 index, which we defined as tumor uptake relative to the uptake in the contralateral hemisphere. RESULTS: Among the high-grade gliomas, we observed a significant correlation between breakdown volume of the blood-brain barrier and thallium-201 uptake. However, 8 of the high-grade gliomas had low thallium-201 uptake, in the same range as the low-grade gliomas. Of these, 2 were nonenhancing and the other 6 showed ring enhancement on CT scans. Analysis of variance showed no significant difference in thallium-201 indexes between low-grade gliomas and highly malignant (grade II-III) gliomas. Accuracy of thallium-201 imaging was lower (78%) than that of CT (84%) in identifying high-grade gliomas. CONCLUSIONS: Damage to the blood-brain barrier is a prerequisite for uptake of thallium-201 in gliomas. Tumors with central necrotic areas and moderate ring enhancement tend to be underestimated when evaluated by means of thallium-201 scintigraphy. The results indicate a need for caution when interpreting findings on images obtained with thallium-201 single-photon emission CT in preoperative evaluation of brain tumors.
  •  
35.
  • Liu, X, et al. (författare)
  • Synapse density related to cerebral blood flow and symptomatology in frontal lobe degeneration and Alzheimer's disease
  • 1999
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 10:Suppl 1, s. 64-70
  • Tidskriftsartikel (refereegranskat)abstract
    • In order to evaluate the functional significance of synaptic pathology, synaptic density was quantitated and related to clinical symptomatology and regional cerebral blood flow (rCBF) in 8 patients with frontal lobe degeneration of non-Alzheimer type (FLD) and 19 patients with Alzheimer's disease (AD). Synaptic density was measured in all layers of prefrontal and parietal cortex. The clinical picture of FLD was dominated by a frontal lobe syndrome with changes in personality and behavior, while AD was dominated by temporoparietal symptoms. This parallels the finding of frontal rCBF reductions in FLD patients and temporoparietal reductions in AD patients. Synaptic density was significantly decreased in both FLD and AD, with a regional severity which closely correlated with that of the degeneration, symptomatology and rCBF deficit. The results suggest that synaptic pathology is a likely cause of clinical symptoms and regional metabolic decrement in dementia.
  •  
36.
  • Ljunggren, Kaj, et al. (författare)
  • Beta camera low activity tumor imaging
  • 1993
  • Ingår i: Acta Oncologica. - : Informa UK Limited. - 1651-226X .- 0284-186X. ; 32:7-8, s. 869-872
  • Tidskriftsartikel (refereegranskat)abstract
    • A new technique, the beta camera, to complement film autoradiography, with fast quantitative imaging of beta particle-emitting radionuclides has been developed. It consists of a thin plastic scintillator and a light-sensitive microchannel plate detector. The thin tissue sample is mounted on the scintillator. Our first system had a high background and a moderate spatial resolution of 900 microns. We now report an improved system with a photomultiplier tube mounted on the scintillator of the microchannel plate detector. Only events registered by both detectors are accepted. A fast coincidence unit processes the signals, and if a time overlap exists, an event is generated in the beta camera. In the coincidence mode, images with low activity distribution of 201Tl (count rate 1 s-1) in 50 microns-thick slices of a human glioma tumor could be recorded with a spatial resolution of 500 microns.
  •  
37.
  • Londos, Elisabet, et al. (författare)
  • Clinical Lewy body dementia and the impact of vascular components
  • 2000
  • Ingår i: International Journal of Geriatric Psychiatry. - 1099-1166. ; 15:1, s. 40-49
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To study the prevalence of patients fulfilling the clinical consensus criteria for dementia with Lewy bodies (DLB) in a dementia population followed up with postmortem examination. To compare the clinical and neuropathological findings in the clinical Lewy body dementia (LBD) group with findings in a clinically defined group with Alzheimer's disease (AD). DESIGN: Medical records from 200 patients were studied retrospectively. Clinical consensus criteria for DLB and clinical criteria for other dementias were applied. SETTING: The majority of the cases were examined and cared for in psychogeriatric and psychiatric departments. PATIENTS: The patients, who died between 1985 and 1994, were part of a longitudinal dementia project. Each case was neuropathologically examined. Main outcome measures Prevalence of clinical signs and neuropathology was compared between the clinical groups. RESULTS: Forty-eight (24%) patients fulfilled the clinical criteria for DLB while 45 (22%) fulfilled the clinical criteria for Alzheimer's disease. The clinical LBD group had a higher Hachinski score compared to the clinical AD group. They also showed a tendency towards a 'frontal profile' with disinhibition, confusion, personality change and vocally disruptive behaviour. More than 80% of the AD and LBD groups respectively exhibited Alzheimer pathology. The LBD group had frontal white matter pathology and degeneration of the substantia nigra more often than the clinical AD group. Both LBD and AD groups showed a progressive and marked increase in severity of dementia and decrease in ADL capacity according to an evaluation based on the Berger scale and Katz index. The condition of the LBD group was significantly worse earlier in dementia. CONCLUSION: The results of this study indicate that patients fulfilling the clinical criteria for DLB also exhibit clinical features of possible vascular origin and a frontal profile. Subcortical vascular pathology, nigral degeneration and AD pathology in this group could partly explain the clinical features used to define DLB.
  •  
38.
  • Londos, Elisabet, et al. (författare)
  • Contributions of other brain pathologies in dementia with lewy bodies.
  • 2002
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 13:3, s. 130-148
  • Tidskriftsartikel (refereegranskat)abstract
    • The clinical picture with its pathological correlate was analysed in 16 patients fulfilling consensus criteria for dementia with Lewy bodies (DLB). The cases were part of a larger cohort (n = 200) of patients within a prospective longitudinal study of dementing disorders. Six cases exhibited not only Lewy bodies (LBs) but also other brain pathologies such as Alzheimer changes, multiple infarcts or complete and incomplete white matter infarcts. Degeneration of the nucleus basalis of Meynert and substantia nigra was also seen. The 10 cases without LBs all had Alzheimer changes. In 7 cases, these changes were combined with mainly incomplete frontal white matter infarcts. However, the degeneration of brain stem nuclei was less pronounced in these cases. Symptoms such as fluctuations in cognition, falls and episodic confusion appeared in association with arterial hypotension, which developed during the course of dementia in almost all the 16 cases. The majority of the cases were treated with neuroleptics and other potentially hypotensive medication. This study shows that multiple and different pathological features may contribute to a clinical symptom constellation as in DLB. The case study approach reveals the complexity of the clinico-pathological relationships in dementia that might otherwise be lost in the analysis of larger group data. Copyright 2002 S. Karger AG, Basel
  •  
39.
  • Londos, Elisabet, et al. (författare)
  • Neuropathological correlates to clinically defined dementia with Lewy bodies
  • 2001
  • Ingår i: International Journal of Geriatric Psychiatry. - : Wiley. - 1099-1166 .- 0885-6230. ; 16:7, s. 667-679
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: To analyse the neuropathological changes behind clinically defined dementia with Lewy bodies (clinDLB) compared with clinically diagnosed Alzheimer's disease (clinAD). METHODS: The prevalence of neuropathological findings in 48 clinDLB and 45 clinAD cases was compared. Sixteen clinDLB and 10 clinAD cases were reassessed with alpha-synuclein staining for Lewy bodies (LB). RESULTS: Alzheimer pathology was found in 81% of the clinDLB and 93% of the clinAD cases. The clinDLB group had a higher prevalence of frontal white matter pathology, mostly of ischemic type, and a more severe degeneration of the substantia nigra compared with the clinAD group. In hematoxylin-eosin staining, LBs were identified in seven (15%) of the clinDLB and in four (9%) of the clinAD group. In alpha-synuclein staining, 38% of the clinDLB and 40% of the clinAD cases exhibited LBs. The cases without LBs, in the clinDLB group, had AD pathology in combination with frontal white matter disease. Vascular pathology of significant degree was prevalent in more than 40% of all the cases with verified LBs regardless of clinical diagnosis. CONCLUSION: Consecutive dementia cases, fulfilling the clinical consensus criteria for DLB, may exhibit combinations of neuropathological changes which in themselves can explain the clinical picture of DLB even when LBs are absent.
  •  
40.
  • Londos, Elisabet, et al. (författare)
  • Regional cerebral blood flow and EEG in clinically diagnosed dementia with Lewy bodies and Alzheimer's disease.
  • 2003
  • Ingår i: Archives of Gerontology and Geriatrics. - 1872-6976. ; 36:3, s. 231-245
  • Tidskriftsartikel (refereegranskat)abstract
    • This study was undertaken in order to compare regional cerebral blood now (rCBF) and EEG findings of patients with clinically diagnosed dementia with Lewy bodies (clinDLB) and Alzheimer’s disease (clinAD). Furthermore, within the clinDLB group to compare cases with and without neuropathologically verified Lewy bodies (LBs). When we studied 200 dementia cases in a prospective longitudinal dementia study, 48 had clinDLB and 45 clinAD in retrospective analyses. EEG information was analysed in 34 clinDLB and 28 clinAD patients and cerebral blood flow, measured with the Xe 133 inhalation method, in 26 clinDLB and 25 clinAD. There were no differences in EEG between the clinDLB and clinAD groups or between the cases with and without LBs. The rCBF patterns in the clinDLB and clinAD groups showed similar reductions in the temporoparietal areas. The rCBF in cases with LBs showed heterogeneous pathology. The imaging results in clinDLB and clinAD were strikingly similar. The EEG and rCBF could not differentiate between cases with or without LB. The study illustrates the lack of specific changes of EEG and rCBF in cases with LB pathology.
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41.
  •  
42.
  • Maeder, Philippe P, et al. (författare)
  • Colloid cysts of the third ventricle: correlation of MR and CT findings with histology and chemical analysis
  • 1990
  • Ingår i: AJNR. - 1936-959X. ; 155:1, s. 135-141
  • Tidskriftsartikel (refereegranskat)abstract
    • Eight patients with colloid cysts of the third ventricle were examined with CT and MR. In six, surgical resection was performed and the material was subjected to histologic evaluation; the concentrations of trace elements were determined by particle-induced X-ray emission. Stereotaxic aspiration was performed in two. The investigation showed that colloid cysts are often iso- or hypodense relative to brain on CT (5/8), but sometimes have a center of increased density. Increased density did not correlate with increased concentration of calcium or other metals but did not correlate with high cholesterol content. Colloid cysts appear more heterogeneous on MR (6/8) than on CT (3/8), despite a homogeneous appearance at histology. High signal on short TR/TE sequences is correlated with a high cholesterol content. A marked shortening of the T2 relaxation time is often noticed in the central part of the cyst. Analysis of trace elements showed that this phenomenon is not related to the presence of metals with paramagnetic effects. Our analysis of the contents of colloid cysts does not support the theory that differing metallic concentrations are responsible for differences in MR signal intensity or CT density. We did find that increased CT density and high MR signal correlated with high cholesterol content.
  •  
43.
  • Nielsen, Henrietta, et al. (författare)
  • NG2 cells, a new trail for Alzheimer's disease mechanisms?
  • 2013
  • Ingår i: Acta Neuropathologica Communications. - : Springer Science and Business Media LLC. - 2051-5960. ; 1:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Neuron Glial 2 (NG2) cells are glial cells known to serve as oligodendrocyte progenitors as well as modulators of the neuronal network. Altered NG2 cell morphology and up-regulation as well as increased shedding of the proteoglycan NG2 expressed on the cell surface have been described in rodent models of brain injury. Here we describe alterations in the human NG2 cell population in response to pathological changes characteristic of Alzheimer's disease (AD).
  •  
44.
  • Nittby, Henrietta, et al. (författare)
  • Cognitive impairment in rats after long-term exposure to GSM-900 mobile phone radiation
  • 2008
  • Ingår i: Bioelectromagnetics. - : Wiley. - 0197-8462 .- 1521-186X. ; 29:3, s. 219-232
  • Tidskriftsartikel (refereegranskat)abstract
    • Considering the frequent use of mobile phones, we have directed attention to possible implications on cognitive functions. In this study we investigated in a rat model the long-term effects of protracted exposure to Global System for Mobile Communication-900 MHz (GSM-900) radiation. Out of a total of 56 rats, 32 were exposed for 2 h each week for 55 weeks to radio-frequency electromagnetic radiation at different SAR levels (0.6 and 60 mW/kg at the initiation of the experimental period) emitted by a (GSM-900) test phone. Sixteen animals were sham exposed and eight animals were cage controls, which never left the animal house. After this protracted exposure, GSM-900 exposed rats were compared to sham exposed controls. Effects on exploratory behaviour were evaluated in the open-field test, in which no difference was seen. Effects on cognitive functions were evaluated in the episodic-like memory test. In our study, GSM exposed rats had impaired memory for objects and their temporal order of presentation, compared to sham exposed controls (P = 0.02). Detecting the place in which an object was presented was not affected by GSM exposure. Our results suggest significantly reduced memory functions in rats after GSM microwave exposure (P = 0.02).
  •  
45.
  • Nittby, Henrietta, et al. (författare)
  • Increased blood-brain barrier permeability in mammalian brain 7 days after exposure to the radiation from a GSM-900 mobile phone.
  • 2009
  • Ingår i: Pathophysiology. - : Elsevier BV. - 1873-149X .- 0928-4680.
  • Tidskriftsartikel (refereegranskat)abstract
    • Microwaves were for the first time produced by humans in 1886 when radio waves were broadcasted and received. Until then microwaves had only existed as a part of the cosmic background radiation since the birth of universe. By the following utilization of microwaves in telegraph communication, radars, television and above all, in the modern mobile phone technology, mankind is today exposed to microwaves at a level up to 10(20) times the original background radiation since the birth of universe. Our group has earlier shown that the electromagnetic radiation emitted by mobile phones alters the permeability of the blood-brain barrier (BBB), resulting in albumin extravasation immediately and 14 days after 2h of exposure. In the background section of this report, we present a thorough review of the literature on the demonstrated effects (or lack of effects) of microwave exposure upon the BBB. Furthermore, we have continued our own studies by investigating the effects of GSM mobile phone radiation upon the blood-brain barrier permeability of rats 7 days after one occasion of 2h of exposure. Forty-eight rats were exposed in TEM-cells for 2h at non-thermal specific absorption rates (SARs) of 0mW/kg, 0.12mW/kg, 1.2mW/kg, 12mW/kg and 120mW/kg. Albumin extravasation over the BBB, neuronal albumin uptake and neuronal damage were assessed. Albumin extravasation was enhanced in the mobile phone exposed rats as compared to sham controls after this 7-day recovery period (Fisher's exact probability test, p=0.04 and Kruskal-Wallis, p=0.012), at the SAR-value of 12mW/kg (Mann-Whitney, p=0.007) and with a trend of increased albumin extravasation also at the SAR-values of 0.12mW/kg and 120mW/kg. There was a low, but significant correlation between the exposure level (SAR-value) and occurrence of focal albumin extravasation (r(s)=0.33; p=0.04). The present findings are in agreement with our earlier studies where we have seen increased BBB permeability immediately and 14 days after exposure. We here discuss the present findings as well as the previous results of altered BBB permeability from our and other laboratories.
  •  
46.
  • Nittby, Henrietta, et al. (författare)
  • Nonthermal GSM RF and ELF EMF effects upon rat BBB permeability
  • 2011
  • Ingår i: The Environmentalist. - : Springer Science and Business Media LLC. - 0251-1088 .- 1573-2991. ; 31:2, s. 140-148
  • Tidskriftsartikel (refereegranskat)abstract
    • Since the late 1980s, our group has examined the effects of radiofrequency electromagnetic fields (RF-EMF), including pulse-modulated waves of the type emitted by mobile phones, upon the blood-brain barrier. In more than 2,000 rats, we have repeatedly demonstrated a passage of the rats' own albumin from the blood through the brain capillaries into the surrounding brain parenchyma at SAR values down to 0.1mW/kg. In most of these experiments, the animals were exposed in TEM-cells, ventilated by an external electrical fan at 50 Hz. In the present study, we examined whether the extremely low frequency (ELF) magnetic fields from the fan (50 Hz, 0.3-1.5 μT) might add to the RF effect. Sixty-four rats were divided into 4 groups: RF only, ELF only and RF + ELF exposure plus a sham group. The GSM-900 MHz RF exposure was at the very low, nonthermal, average whole-body SAR level 0.4 mW/kg. Demonstration of the normally occurring albumin extravasation in the basal hypothalamus is our inbuilt control proving that the staining is reliable. Two full series of staining of the whole material gave negative results for hypothalamus. Not until we changed to avidin, biotin, and antibodies from a third supplier, we received an acceptable staining. Twenty-five percent of the RF animals had a pathological albumin leakage, while the ELF and RF + ELF groups with three and two pathological findings, respectively, were not significantly different from the control group. We conclude that the use of external fans has had no major influence upon the result.
  •  
47.
  • Nittby, Henrietta, et al. (författare)
  • Radiofrequency and extremely low-frequency electromagnetic field effects on the blood-brain barrier.
  • 2008
  • Ingår i: Electromagnetic Biology and Medicine. - : Informa UK Limited. - 1536-8386 .- 1536-8378. ; 27:2, s. 103-126
  • Tidskriftsartikel (refereegranskat)abstract
    • During the last century, mankind has introduced electricity and during the very last decades, the microwaves of the modern communication society have spread a totally new entity--the radiofrequency fields--around the world. How does this affect biology on Earth? The mammalian brain is protected by the blood-brain barrier, which prevents harmful substances from reaching the brain tissue. There is evidence that exposure to electromagnetic fields at non thermal levels disrupts this barrier. In this review, the scientific findings in this field are presented. The result is a complex picture, where some studies show effects on the blood-brain barrier, whereas others do not. Possible mechanisms for the interactions between electromagnetic fields and the living organisms are discussed. Demonstrated effects on the blood-brain barrier, as well as a series of other effects upon biology, have caused societal anxiety. Continued research is needed to come to an understanding of how these possible effects can be neutralized, or at least reduced. Furthermore, it should be kept in mind that proven effects on biology also should have positive potentials, e.g., for medical use.
  •  
48.
  •  
49.
  • Persson, Bertil R, et al. (författare)
  • Blood-brain barrier permeability in rats exposed to electromagnetic fields used in wireless communication
  • 1997
  • Ingår i: Wireless Networks. - 1022-0038. ; 3, s. 455-461
  • Tidskriftsartikel (refereegranskat)abstract
    • iological effects of radio frequency electromagnetic fields (EMF) on the blood-brain barrier (BBB) have been studied in Fischer 344 rats of both sexes. The rats were not anaesthetised during the exposure. All animals were sacrificed by perfusion–fixation of the brains under chloralhydrate anaesthesia after the exposure. The brains were perfused with saline for 3–4 minutes, and thereafter perfusion fixed with 4% formaldehyde for 5–6 minutes. Whole coronal sections of the brains were dehydrated and embedded in paraffin and sectioned at 5 m. Albumin and fibrinogen were demonstrated immunohistochemically and classified as normal versus pathological leakage. In the present investigation we exposed male and female Fischer 344 rats in a Transverse Electromagnetic Transmission line chamber to microwaves of 915 MHz as continuous wave (CW) and pulse-modulated with different pulse power and at various time intervals. The CW-pulse power varied from 0.001 W to 10 W and the exposure time from 2 min to 960 min. In each experiment we exposed 4–6 rats with 2–4 controls randomly placed in excited and non-excited TEM-cells respectively. We have in total investigated 630 exposed rats at various modulation frequencies and 372 controls. The frequency of pathological rats is significantly increased (p < 0:0001) from 62=372 (ratio: 0:170:02) for control rats to 244=630 (ratio: 0:390:03) in all exposed rats. Grouping the exposed animals according to the level of specific absorbed energy (J/kg) give significant difference in all levels above 1.5 J/kg. The exposure was 915 MHz microwaves either pulse modulated (PW) at 217 Hz with 0.57 ms pulse width, at 50 Hz with 6.6 ms pulse width or continuous wave (CW). The frequency of pathological rats (0:17) among controls in the various groups is not significantly different. The frequency of pathological rats was 170=481 (0:350:03) among rats exposed to pulse modulated (PW) and 74=149 (0:500:07) among rats exposed to continuous wave exposure (CW). These results are both highly significantly different to their corresponding controls (p < 0:0001) and the frequency of pathological rats after exposure to pulsed radiation (PW) is significantly less (p < 0:002) than after exposure to continuous radiation (CW).
  •  
50.
  • Persson, Bertil R, et al. (författare)
  • Brain tumour growth in rats exposed to electromagnetic fields used in wireless cellular communication
  • 2014
  • Ingår i: Acta Scientiarum Lundensia. - 1651-5013. ; 2014:001, s. 1-23
  • Tidskriftsartikel (refereegranskat)abstract
    • In 1996 there was no convincing laboratory evidence that EMFs used in wireless communication could cause tumour promotion at non-thermal exposure levels. Therefore we then performed a study of the effects from exposure to such electromagnetic fields in the rat brain glioma model we were using in our research for brain tumour therapy. By stereotaxic technique rat glioma cells (RG2 or N32) were injected into the head of the right caudate nucleus in 154 pairs of Fischer 344 rats in both exposed and matched controls. Starting on day 5 after inoculation, the animals were exposed for 7 hours a day, 5 days a week during 2 - 3 weeks. Rats of both sexes were exposed to electromagnetic fields in the microwaves frequency range 915 MHz both as continuous waves (1 W), and as pulse-modulated at 4, 8, 16 and 217 Hz in 0.57 ms long pulses and 50 Hz in 6.67 ms pulses, all with a maximum power amplitude of 2 W per pulse. The animals were kept un-anaesthetized in well-ventilated TEM cells during 7 hours a day for 5 days a week for 2-3 weeks. Their matched controls were kept in identical TEM cells without EMF exposure. At the end of the exposure period the rat brains were examined histopathologically. The tumour size was measured with a calliper and the volume estimated as an ellipsoid. Our study of the 154 matched pairs of rats did not show any significant difference in tumour volume between animals exposed to 915 MHz microwaves, and those not exposed. Thus our results did not support that daily exposure to EMF promotes tumour growth when given from the fifth day after the start of tumour growth in the rat brain until the sacrifice of the animal 16 days later. In the present review our results published 1997 have been re-evaluated in terms of SAR dependence of tumour volume observed ratio (exposed / control). We thus surprisingly found that the shape of tumour volume-OR versus SAR response was of bath-tube pattern, similar to that found in our parallel studies of albumin leakage through the blood-brain barrier. Since the SAR varies between most other animal studies reviewed and human epidemiological studies this SAR dependence might explain the controversy in rendering the results.
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