| 1. |
- Bjurberg, Maria, et al.
(författare)
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Early changes in 2-deoxy-2-[18F]fluoro-D-glucose metabolism in squamous-cell carcinoma during chemotherapy in vivo and in vitro.
- 2009
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Ingår i: Cancer Biotherapy & Radiopharmaceuticals. - : Mary Ann Liebert Inc. - 1557-8852 .- 1084-9785. ; 24:3, s. 327-332
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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)
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Prognostic value of histopathological response to radiotherapy and microvessel density in oral squamous cell carcinomas
- 2001
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Ingår i: Acta Oncologica. - : Informa UK Limited. - 1651-226X .- 0284-186X. ; 40:4, s. 491-496
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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)
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Magnetic resonance imaging and histopathology in dementia, clinically of frontotemporal type
- 2000
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Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 11:3, s. 123-134
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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)
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A Clinico-Pathological Study of Heart and Brain Lesions in Vascular Dementia.
- 2005
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Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 19:4, s. 222-228
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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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| 5. |
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| 6. |
- Brown, J, et al.
(författare)
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Frontotemporal dementia linked to chromosome 3
- 2004
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Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 17:4, s. 274-276
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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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| 7. |
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| 8. |
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| 9. |
- Brun, Arne
(författare)
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Identification and characterization of frontal lobe degeneration - Historical perspective on the development of FTD
- 2007
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Ingår i: Alzheimer Disease and Associated Disorders. - 0893-0341. ; 21:4, s. 3-4
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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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| 10. |
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| 11. |
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| 12. |
- Capala, Jacek, et al.
(författare)
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Clinical BNCT studies in Sweden
- 2002
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Ingår i: Research and development in neutron capture therapy. - : Monduzzi Editore Print. ; , s. 1101-
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 13. |
- Ceberg, Crister, et al.
(författare)
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A comparative study on the pharmacokinetics and biodistribution of boronated porphyrin (BOPP) and sulfhydryl boron hydride (BSH) in the RG2 rat glioma model
- 1995
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Ingår i: Journal of Neurosurgery. - 0022-3085. ; 83:1, s. 86-92
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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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| 14. |
- Ceberg, Crister, et al.
(författare)
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A stochastic model for subcellular dosimetry in boron neutron capture therapy
- 1995
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Ingår i: Physics in Medicine and Biology. - : IOP Publishing. - 1361-6560 .- 0031-9155. ; 40:11, s. 1819-1830
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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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| 15. |
- Ceberg, Crister, et al.
(författare)
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Performance of sulfhydryl boron hydride in patients with grade III and IV astrocytoma: a basis for boron neutron capture therapy
- 1995
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Ingår i: Journal of Neurosurgery. - 0022-3085. ; 83:1, s. 79-85
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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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| 16. |
- Eberhardt, Jacob, et al.
(författare)
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Blood-brain barrier permeability and nerve cell damage in rat brain 14 and 28 days after exposure to microwaves from GSM mobile phones.
- 2008
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Ingår i: Electromagnetic Biology and Medicine. - : Informa UK Limited. - 1536-8386 .- 1536-8378. ; 27:3, s. 215-229
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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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| 17. |
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| 18. |
- Grafström, Gustav, et al.
(författare)
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Histopathological examinations of rat brains after long-term exposure to GSM-900 mobile phone radiation.
- 2008
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Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230. ; 77, s. 257-263
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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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| 19. |
- Gustafson, Lars, et al.
(författare)
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A 50-year perspective of a family with chromosome 14-linked Alzheimer’s disease
- 1998
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Ingår i: Human Genetics. - : Springer Science and Business Media LLC. - 1432-1203 .- 0340-6717. ; 102:3, s. 253-257
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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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| 20. |
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| 21. |
- Gydesen, S, et al.
(författare)
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Chromosome 3 linked frontotemporal dementia (FTD-3)
- 2002
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Ingår i: Neurology. - 1526-632X. ; 59:10, s. 1585-1594
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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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| 22. |
- H-Stenstam, B., et al.
(författare)
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Neuropathological postmortem evaluation of BNCT for GBM
- 2007
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Ingår i: Acta Neurologica Scandinavica. - : Hindawi Limited. - 1600-0404 .- 0001-6314. ; 116:3, s. 169-176
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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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| 23. |
- Källén, Kristina, et al.
(författare)
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Evaluation of malignancy in ring enhancing brain lesions on CT by thallium-201 SPECT
- 1997
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Ingår i: Journal of Neurology, Neurosurgery and Psychiatry. - 1468-330X. ; 63:5, s. 569-574
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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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| 24. |
- Källén, Kristina, et al.
(författare)
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Preoperative grading of glioma malignancy with thallium-201 single-photon emission CT: comparison with conventional CT
- 1996
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Ingår i: AJNR. - 1936-959X. ; 17:5, s. 925-932
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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.
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| 25. |
- Liu, X, et al.
(författare)
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Synapse density related to cerebral blood flow and symptomatology in frontal lobe degeneration and Alzheimer's disease
- 1999
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Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 10:Suppl 1, s. 64-70
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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.
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| 26. |
- Londos, Elisabet, et al.
(författare)
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Clinical Lewy body dementia and the impact of vascular components
- 2000
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Ingår i: International Journal of Geriatric Psychiatry. - 1099-1166. ; 15:1, s. 40-49
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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.
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| 27. |
- Londos, Elisabet, et al.
(författare)
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Contributions of other brain pathologies in dementia with lewy bodies.
- 2002
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Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 13:3, s. 130-148
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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
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| 28. |
- Londos, Elisabet, et al.
(författare)
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Neuropathological correlates to clinically defined dementia with Lewy bodies
- 2001
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Ingår i: International Journal of Geriatric Psychiatry. - : Wiley. - 1099-1166 .- 0885-6230. ; 16:7, s. 667-679
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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.
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| 29. |
- Londos, Elisabet, et al.
(författare)
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Regional cerebral blood flow and EEG in clinically diagnosed dementia with Lewy bodies and Alzheimer's disease.
- 2003
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Ingår i: Archives of Gerontology and Geriatrics. - 1872-6976. ; 36:3, s. 231-245
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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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| 30. |
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| 31. |
- Nittby, Henrietta, et al.
(författare)
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Cognitive impairment in rats after long-term exposure to GSM-900 mobile phone radiation
- 2008
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Ingår i: Bioelectromagnetics. - : Wiley. - 0197-8462 .- 1521-186X. ; 29:3, s. 219-232
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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).
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| 32. |
- Nittby, Henrietta, et al.
(författare)
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Increased blood-brain barrier permeability in mammalian brain 7 days after exposure to the radiation from a GSM-900 mobile phone.
- 2009
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Ingår i: Pathophysiology. - : Elsevier BV. - 1873-149X .- 0928-4680.
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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.
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| 33. |
- Nittby, Henrietta, et al.
(författare)
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Radiofrequency and extremely low-frequency electromagnetic field effects on the blood-brain barrier.
- 2008
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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.
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| 34. |
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| 35. |
- Persson, Bertil R, et al.
(författare)
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Blood-brain barrier permeability in rats exposed to electromagnetic fields used in wireless communication
- 1997
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Ingår i: Wireless Networks. - 1022-0038. ; 3, s. 455-461
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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).
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| 36. |
- Persson, Bertil R.R., et al.
(författare)
-
Effects of microwaves from GSM mobile phones on the blood-brain barrier and neurons in rat brain
- 2005
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Ingår i: PIERS 2005 - Progress in Electromagnetics Research Symposium, Proceedings. - 1933077077 - 9781933077079 ; , s. 638-641
-
Konferensbidrag (refereegranskat)abstract
- Our group has since 1988 studied the effects of different intensities and modulations of 915MHz RF in a rat model where the exposure takes place in a TEM-cell during various time periods and post exposure recovery times. The power fed into TEM-cells was 0.125, 1.25, 12.5 or 125mW corresponding to whole body SAR (determined experimentally): 0.2, 2, 20 or 200mW/kg. The rats were awake and not restrained during exposure and after the recovery period the animals were anaesthetized and sacrificed by perfusion-fixation with 4% formaldehyde. Paraffin embedded 5 μm. thick brain slices were stained for albumin by applying albumin antibodies (Dakopatts), by which albumin is revealed as brownish discolorations. Dark neurons were revealed by staining for RNA/DNA with cresyl violet. In series of more than 1800 Fisher rats, we have proven that sub thermal power levels from both pulse-modulated and continuous RF fields - including those from real GSM mobile phones - have the potency to significantly open the BBB for the animals' own albumin (but not fibrinogen) to pass out into the brain and to accumulate in the neurons and glial cells surrounding the capillaries. Albumin extravasations are most prominent at the lower SAR values. This dose-response behaviour suggests some kind of energy or electromagnetic field strength windowing effect. A linear dose-response relationship for dark neurons was found at 50 days after exposure, with most prominent occurrence at SAR 200mW/kg.
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| 37. |
- Risberg, Jarl, et al.
(författare)
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Posterior cingulate cortex in familiar Alzheimer’s disease: A clinicopathological and brain imaging study
- 2003
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Ingår i: Journal of the International Neuropsychological Society. - 1355-6177. ; 9, s. 174-174
-
Konferensbidrag (refereegranskat)abstract
- The degenerative process in Alzheimer´s disease (AD) follows a temporal and topographic pattern of early and accentuated involvement of temporal limbic, parietal and posterior cingulate cortices. We have studied a pedigree with four generations suffering from early onset AD linked to a presenilin-1 gene mutation. This family now contains 7 AD cases, neuropathologically confirmed in four cases of three generations. In all four cases the degeneration was most pronounced in the temporoparietal cortex, but also engaged central grey structures such as the claustrum, central thalamic and brain stem nuclei. There was a consistent and severe degeneration in posterior cingulate cortex in contrast to a compara¬tively spared anterior cingulum. Regional cerebral blood flow (rCBF) was studied repeated¬ly with 133-xenon inhalation and SPECT methods. The rCBF measurements showed the typical cortical pathology of AD with bilateral decreases in temporoparietal and posterior cingulate cortices, accentuating over time and spreading anteriorly. There was a very good correspondence between clinical, neuroimaging and neuropathological features. Our findings indicate that posterior cingulum is a major locus for functional and structural vulnerability in both familial and sporadic forms of AD, something that might be used for diagnostic purposes together with possible posterior cingulate symptomatology.
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| 38. |
- Salford, Leif, et al.
(författare)
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Brain tumour development in rats exposed to electromagnetic fields used in wireless cellular communication
- 1997
-
Ingår i: Wireless Networks. - 1022-0038. ; 3, s. 463-468
-
Tidskriftsartikel (refereegranskat)abstract
- It has been suggested that electromagnetic fields (EMF) act as promoters late in the carcinogenesis process. To date, however, there is no convincing laboratory evidence that EMFs cause tumour promotion at non-thermal exposure levels. Therefore the effects of exposure to electromagnetic fields were investigated in a rat brain glioma model. Some of the exposures correspond to electromagnetic fields used in wireless communication. Microwaves at 915 MHz were used both as continuous waves (1 W), and pulse-modulated at 4, 8, 16 and 217 Hz in 0.57 ms pulses and 50 Hz in 6.67 ms pulses (2 W per pulse). Fischer 344 rats of both sexes were used in the experiments. By stereotaxic technique rat glioma cells (RG2 and N32) were injected into the head of the right caudate nucleus in 154 pairs of rats, 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. Exposed animals were kept unanaesthetized in well-ventilated TEM cells producing 915 MHz continuous or modulated microwaves. Their matched controls were kept in identical TEM cells without EMF exposure. All brains were examined histopathologically and the tumour size was estimated as the volume of an ellipsoid. Our study of 154 matched pairs of rats does not show any significant difference in tumour size between animals exposed to 915 MHz, and those not exposed. Thus our results do not support that even an extensive 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 after about 16 days.
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| 39. |
- Salford, Leif G., et al.
(författare)
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Non-thermal effects of EMF upon the mammalian brain : The Lund experience
- 2007
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Ingår i: The Environmentalist. - : Springer Science and Business Media LLC. - 0251-1088 .- 1573-2991. ; 27:4, s. 493-500
-
Tidskriftsartikel (refereegranskat)abstract
- The environment in which biology exists has dramatically changed during the last decades. Life was formed during billions of years, exposed to, and shaped by the original physical forces such as gravitation, cosmic irradiation and the terrestrial magnetism. The existing organisms are created to function in harmony with these forces. However, in the late 19th century mankind introduced the use of electricity and during the very last decades, microwaves of the modern communication society spread around the world. Today one third of the world's population is owner of the microwave-producing mobile phones. The question is: to what extent are living organisms affected by these ubiquitous radio frequency fields? Since 1988 our group has studied the effects upon the mammalian blood-brain barrier (BBB) by non-thermal radio frequency electromagnetic fields (RF-EMF). These have been revealed to cause significantly increased leakage of albumin through the BBB of exposed rats as compared to non-exposed animals-in a total series of about two thousand animals. One remarkable observation is the fact that the lowest energy levels give rise to the most pronounced albumin leakage. If mobile communication, even at extremely low energy levels, causes the users' own albumin to leak out through the BBB, also other unwanted and toxic molecules in the blood, may leak into the brain tissue and concentrate in and damage the neurons and glial cells of the brain. In later studies we have shown that a 2-h exposure to GSM 915 MHz at non-thermal levels, gives rise to significant neuronal damage, seen 28 and 50 days after the exposure. In our continued research, the non-thermal effects (histology, memory functions) of long-term exposure for 13 months are studied as well as the effects of short term GSM 1,800 MHz upon gene expression. Most of our findings support that living organisms are affected by the non-thermal radio frequency fields. Studies from other laboratories in some cases find effects, while in other cases effects are not seen. Our conclusion is that all researchers involved in this field have the obligation to intensify this research in order to reduce, or avoid, the possible negative effects of the man made microwaves!
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| 40. |
- Salford, Leif, et al.
(författare)
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Nerve cell damage in mammalian brain after exposure to microwaves from GSM mobile phones.
- 2003
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Ingår i: Environmental Health Perspectives. - 1552-9924. ; 111:7, s. 881-883
-
Tidskriftsartikel (refereegranskat)abstract
- The possible risks of radio-frequency electromagnetic fields for the human body is a growing concern for our society. We have previously shown that weak pulsed microwaves give rise to a significant leakage of albumin through the blood-brain barrier. In this study we investigated whether a pathologic leakage across the blood-brain barrier might be combined with damage to the neurons. Three groups each of eight rats were exposed for 2 hr to Global System for Mobile Communications (GSM) mobile phone electromagnetic fields of different strengths. We found highly significant (p < 0.002) evidence for neuronal damage in the cortex, hippocampus, and basal ganglia in the brains of exposed rats. Key words: blood-brain barrier, central nervous system, microwaves, mobile phones, neuronal damage, rats.
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| 41. |
- Salford, Leif, et al.
(författare)
-
The mammalian brain in the electromagnetic fields designed by man with special reference to blood-brain barrier function, neuronal damage and possible physical mechanisms
- 2008
-
Ingår i: PROGRESS OF THEORETICAL PHYSICS SUPPLEMENT. - 0375-9687. ; :173, s. 283-309
-
Konferensbidrag (refereegranskat)abstract
- Life oil earth was formed during billions of years, exposed to, and shaped by the original physical forces such as gravitation, cosmic irradiation, atmospheric electric fields and the terrestrial magnetism. The Schumann resonances at 7.4 Hz are all example of oscillations possibly important for life.(1)) The existing organisms are created to function in harmony with these forces. However, in the late 19th century mankind introduced the use of electricity, in the early 20th century long-wave radio and in the 1940-ies short-wave radio. High frequency RF was introduced in the 50-ies as FM and television and during the very last decades, microwaves of the modern communication society spread around the world. Today, however, one third of the world's population is owner of the microwave-producing mobile phones and an even larger number is exposed to the cordless RF emitting systems. To what; extent are all living organisms affected by these, almost everywhere present radio frequency fields? And what will be the effects of many years of continuing exposure? Since 1989 Our group has studied the effects upon the mammalian blood-brain barrier (BBB) in rats by non-thermal radio frequency electromagnetic fields (RF-EMF). These have been shown to cause significantly increased leak-age of the rats' own blood albumin through the BBB of exposed rats, at energy levels of 1W/kg and below, as compared to non-exposed animals in a total series of about two thousand animals.(2)-6)) One remarkable observation is the fact that the lowest energy levels, with whole-body average power densities below 10mW/kg, give rise to the most pronounced albumin leakage. If mobile communication, even at extremely low energy levels, causes the users' own albumin to leak out through the BBB, also other unwanted and toxic molecules in the blood, may leak into the brain tissue and concentrate in and damage the neurons and glial cells of the brain. In later studies we have shown that a 2-h exposure to GSM 915 MHz, at non-thermal SAB-values of 0.2, 2 and 200 mW/kg, gives rise to significant neuronal damage, seen not only 50 days after the exposure 7) but also after 28 days but not after 14 days. Albumin extravasations and uptake into neurons was enhanced after 14 clays, but not after 28.(8)) in our continued research, also the non-thermal effects oil tissue structure and memory function of long-term exposure for 13 months are studied.(9)) We have also performed microarray analysis of brains from rats exposed to short term GSM both at 1,800 MHz and at 900MHz and have found significant effects upon gene expression of membrane associated genes as compared to control animals.(10),11)) Most of our findings support that living organisms are affected by the non-thermal radio frequency fields. Some other Studies agree while others find no effects. The mechanisms by which the EMFs may alter BBB permeability are not Well Understood. At low field strengths, the effects on body temperature are negligible and thus heating effects are not involved. A change in the physicochemical characteristics of membranes has been suggested as a cause.(12)) We have performed experiments to verify a quantum mechanical model for interaction with protein-bound ions. Our results show that controlled frequency and amplitude of ELF EM fields upon spinach plasma vesicles can steer transport over the membrane.(13)) This may be a first proof of a resonance phenomenon where appropriate levels of frequency and amplitude in the right combination have the potency to communicate with the biology of membranes and transport systems. Our study has prompted Lis to elaborate on magnetic resonance models; the Ion Cyclotron Resonance (ICR) model and the Ion Parametric Resonance (IPR) Model in an attempt to explain the occurrence of resonance frequencies. This is extensively described here under the heading: Mechanisms behind the effects of electromagnetical fields upon biology. We also bring forward the concept of solitons being active in membranes and DNA/RNA-transcription as a, possible mean to understand and prove the biological effects of EMF. The Nishinomiya-Yukawa International and Interdisciplinary Symposium 2007 raised the question: What is Life? An obvious and simple answer could be: It is DNA! The DNA strand can be looked upon as an antenna resonating in the microwave band 6GHz with its harmonics and subharmonics.(14)-18)) If this holds true, the dramatic situation might exist, that all living organisms have a receptor for the newly constructed and world-wide man-made microvaves, leading to a direct effect upon the function of DNA - in concordance with our experimental findings! Our generation invented the microwave emitters. We now have in imperative obligation to further investigate the links between EMF and biology in order to prevent possible detrimental effects of the microwaves.
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| 42. |
- Sjöholm, H, et al.
(författare)
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Necrosis of malignant gliomas after intratumoral injection of 201Tl in vivo in the rat
- 1995
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Ingår i: Anti-Cancer Drugs. - 0959-4973. ; 6:1, s. 109-114
-
Tidskriftsartikel (refereegranskat)abstract
- Fourteen adult Fischer 344 rats were inoculated in vivo unilaterally in the caudate nucleus in the brain with malignant RG 2 glioma cells. By 3 weeks a tumor with a diameter of 3-6 mm normally develops. Ten animals which survived the repeated periods of anesthesia and thallium (Tl) injections (intratumorally three times of 201Tl, 15-23 days after inoculation) showed a prolonged retention of radioactivity at the site of injection with no uptake in other organs except for the kidneys. Singular circumscribed necroses were found post-mortem at the site of injection, comprising malignant glioma tumor tissue, which in six animals was absent, in three animals was markedly reduced in size compared with controls and in one animal had the expected size. In four animals metastases were found in distant locations in the brain; in three of these cases there was a retention of radioactivity in the tumor. The selective necrotizing effect on the tumor cells is interpreted as mainly due to emission of Auger electrons from intracellularly accumulated 201Tl, giving rise to very high energy deposition in the vicinity of the cell nucleus. The results should also have implications for the treatment of human malignant gliomas.
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| 43. |
- Skibinski, G, et al.
(författare)
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Mutations in the endosomal ESCRTIII-complex subunit CHMP2B in frontotemporal dementia
- 2005
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 37:8, s. 806-808
-
Tidskriftsartikel (refereegranskat)abstract
- We have previously reported a large Danish pedigree with autosomal dominant frontotemporal dementia (FTD) linked to chromosome 3 (FTD3). Here we identify a mutation in CHMP2B, encoding a component of the endosomal ESCRTIII complex, and show that it results in aberrant mRNA splicing in tissue samples from affected members of this family. We also describe an additional missense mutation in an unrelated individual with FTD. Aberration in the endosomal ESCRTIII complex may result in FTD and neurodegenerative disease.
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