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  • 1
    Electronic Resource
    Electronic Resource
    An immunohistochemical study of glial and neuronal markers in primary neoplasms of the central nervous system (1986)
    Springer
    Acta neuropathologica 70 (1986), S. 320-326 
    Details
    ISSN: 1432-0533
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Paraffin-embedded tissues from 56 primary neoplasms of the central nervous system and seven cases of non-neoplastic reactive astrocytosis were examined by immunoperoxidase techniques on serial sections using monoclonal antibodies to glial fibrillary acidic protein (GFAP) and the 68 kDa neurofilament subunit and monospecific polyclonal antibodies to α-and γ-enolase. γ-Enolase was present in all neoplasms of neuronal origin, but was also present in anaplastic gliomas (particularly in giant cells), in some well-differentiated astrocytomas and reactive astrocytes. The cells containing γ-enolase in these cases appeared morphologically identical to those containing α-enolase and GFAP in adjacent serial sections. No relationship was found between γ-enolase immunoreactivity and cellular anaplasia in the gliomas studied. Subependymal neoplasms from patients with tuberose sclerosis exhibited evidence of both astrocytic and neuronal differentiation, sometimes in morphologically distinct cell populations, consistent with their suggested origin from a primitive cell line.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00686091
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  • 2
    Electronic Resource
    Electronic Resource
    Neuropathological and neurophysiological effects of interstitial white matter autologous and non-autologous protein containing solutions: Further evidence for a glioma derived permeability factor (1993)
    Springer
    Acta neurochirurgica 120 (1993), S. 164-174 
    Details
    ISSN: 0942-0940
    Keywords: Brain edema ; blood brain barrier ; serum protein ; evoked potential ; glioma ; cerebral blood flow ; permeability factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The feline infusion model of brain edema was used to evaluate the pathophysiological effects of 0.6ml infusions of autologous serum protein (66%), human serum protein (66%), human glioma cyst fluid and a tissue culture medium (TCM) on the structure and function of the forebrain white matter. These infusions increased local white matter water content by between 10.8 and 12.5 ml/100 g brain and were associated with moderate increases in ICP and CSF outflow resistance and a significant decrease in lumped craniospinal compliance. Cortical somatosensory potentials, motor evoked potentials, EEG and local cerebral blood flow (rCBF) at normocapnia were generally unchanged by the various infusions. All infusates except the 66% autologous serum protein infusion impaired rCBF CO2 reactivity. Histologically all infusates caused marked extracellular edema. The autologous serum protein infusion caused no additional histological changes whereas the glioma cyst infusates caused profound endothelial and astrocytic swelling, focal endothelial necrosis, basement membrane disruption, perivascular microglial reaction and pavementation and perivascular migration of polymor-phonuclear leukocytes. Similar but less marked changes were seen after infusion of human serum protein whilst the TCM produced only minimal changes. The intensity and extent of Evans Blue extravasation into the forebrain white matter was greatest with glioma cyst infusates and with all infusions reflected the extent to microvascular changes. These studies show that products derived from gliomas cause additional damage to the blood-brain-barrier than that caused by non-autologous serum proteins. These results add further support for the existence of glioma derived permeability factors (GDPF), but suggest neither serum proteins nor glioma derived compounds in the white matter interstitium significantly influence local electrophysiological function. Some limitations of the infusion edema model when using non-autologous infusions and difficulties quantitating brain dysfunction are emphasised.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02112037
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  • 3
    Electronic Resource
    Electronic Resource
    Nitric oxide synthase is expressed in experimental malignant glioma and influences tumour blood flow (1996)
    Springer
    Acta neurochirurgica 138 (1996), S. 870-876 
    Details
    ISSN: 0942-0940
    Keywords: Nitric oxide ; glioma ; cerebral blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The distribution and function of nitric oxide synthase (NOS) was studied in the rodent C6 implantation glioma model. Using a histochemical stain for NADPH diaphorase, which colocalises with NOS, morphological studies revealed non homogenous staining of the constituent tumour cells and the neoplastic endothelium. Immunocytochemical staining for macrophages (ED1, ED2) showed dense positivity at the tumour brain interface with more patchy positivity within the tumour mass. This finding suggests that both macrophages, which are known to produce large amounts of NO, and the C6 cells contribute to the NADPH diaphorase positivity. Administration of the NOS inhibitor Ng-nitro-L-argine methyl ester (L-NAME) significantly reduced both tumour (40%) and contralateral local cerebral blood flow (20%) compared to control animals. These findings demonstrate that (i) NOS is present in experimental malignant glioma; (ii) NO mediated mechanisms contribute to tumour blood vessel dilatation and blood flow regulation; and (iii) using this model there is a significant differential sensitivity of the tumour and brain parenchymal vascular beds to a NOS inhibitor. Further investigations are required to determine the potential therapeutic and biological relevance of these findings and the relative contributions of tumour cells, neoplastic endothelium and reactive macrophages to NO mechanisms in gliomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01411266
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  • 4
    Electronic Resource
    Electronic Resource
    Identification and Characterisation of 5-Hydroxytryptamine3 Recognition Sites in Human Brain Tissue (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: [3H]Zacopride displayed regional saturable specific binding to homogenates of human brain tissues, as defined by the inclusion of BRL43694 [endo-N-(9-methyl-9-azabicyclo[3.3.1]non-3-yl)-l-methylindazole-3-carboxamide] in the incubation media. Scatchard analysis of the saturation data obtained from amygdaloid and hippocampal tissues identified the binding as being of high affinity and to a homogeneous population of binding sites (KD= 2.64 ± 0.75 and 2.93 ± 0.41 nmol/L and Bmax= 55 ± 7 and 44 ± 9 fmol/ mg of protein in the amygdala and hippocampus, respectively). 5-Hydroxytryptamine3 (5-HT3) receptor agonists and antagonists competed for the [3H]zacopride binding site, competing with up to 40% of total binding with a similar rank order of affinity in both tissues; agents acting on various other neurotransmitter receptors failed to inhibit binding. Kinetic data revealed a fast association that was fully reversible (k+1= 6.61 × 105 and 7.65 × 105/mol/L/s and k-1= 3.68 × 10−3 and 3.45 × 10−3/s in the amygdala and hippocampus, respectively). It is concluded that [3H]zacopride selectively labels with high affinity 5-HT3 recognition sites in human amygdala and hippocampus and, if these binding domains represent 5-HT3 receptors, may provide the opportunity for 5-HT3 receptor antagonists to modify 5-HT function in the human brain
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09244.x
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  • 5
    Electronic Resource
    Electronic Resource
    Neuroleptic malignant syndrome in the intensive therapy unit (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Anaesthesia 45 (1990), S. 0 
    Details
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A case of the neuroleptic malignant syndrome occurred in a 40-year-old male after administration of chlorpromazine while on an Intensive Therapy Unit. Treatment with dantrolene sodium was successful, and a muscle biopsy was examined in the recovery phase of the illness. The importance of this condition and the difficulties in establishing a diagnosis at an early stage in patients on an Intensive Therapy Unit are discussed, along with implications for treatment .
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2044.1990.tb14740.x
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  • 6
    Electronic Resource
    Electronic Resource
    Variant Creutzfeldt–Jakob disease: risk of transmission by blood and blood products (2004)
    Oxford, UK : Blackwell Publishing Ltd
    Haemophilia 10 (2004), S. 0 
    Details
    ISSN: 1365-2516
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary.  Variant Creutzfeldt–Jakob disease (CJD) is a novel acquired human prion disease apparently resulting from exposure to the bovine spongiform encephalopathy (BSE) agent. Variant CJD differs from other human prion diseases in that the disease-associated form of the prion protein and infectivity are readily detectable in lymphoid tissues throughout the body. Lymphoid tissues and lymphocytes are implicated in the peripheral pathogenesis of prion diseases (where infectivity may be detected during the preclinical phase of the illness), giving rise to concerns that blood and blood products may also contain infectious particles, representing a possible source of iatrogenic spread of variant CJD. This concern has been reinforced following the experimental transmission of BSE in a sheep model by transfusion of blood and buffy coat from animals in the preclinical phase of the illness, and the recent identification of a UK case of variant CJD in a patient who had received packed red blood cells that had been donated by an individual who subsequently died from variant CJD. Studies in animal models suggest that most prion infectivity in blood may be cell-associated, with lower levels in the plasma, and there is evidence to suggest that any infectivity present may be reduced during the process of plasma fractionation. However, the possibility that plasma or blood products could transmit the disease cannot be excluded. Further studies are required to develop more sensitive means to detect disease-associated prion protein in blood; such techniques could be employed for screening purposes to reduce exposure to contaminated products and to assist with risk management in potentially exposed individuals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2516.2004.00982.x
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  • 7
    Electronic Resource
    Electronic Resource
    Laboratory diagnosis of variant Creutzfeldt–Jakob disease (2000)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Histopathology 37 (2000), S. 0 
    Details
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The neuropathological and biochemical features of 33 cases of variant Creutzfeldt–Jakob disease (vCJD) diagnosed up to the end of 1998 are analysed in relation to the 646 cases of suspected CJD referred to the CJD Surveillance Unit laboratory from 1990 to 1998. Morphological studies of the central nervous system, lymphoid tissues and other organs were accompanied by immunocytochemistry; Western blot analysis of PrPRES was performed on frozen brain tissue. The findings were analysed in relation to clinical and genetic data. The pathology of vCJD showed morphological and immunocytochemical characteristics distinct from other cases of CJD. PrP accumulation was widespread in lymphoid tissues in vCJD, but was not identified in other non-neural tissues. PrPRES accumulation in vCJD brain tissue showed a uniform glycotype pattern distinct from sporadic CJD. All analysed cases of vCJD were methionine homozygotes at codon 129 of the PrP gene.  No evidence currently exists to suggest that cases of CJD diagnosed in individuals who are MV or VV at codon 129 of the PrP gene represent ‘human bovine spongiform encaphalopathy (BSE)’. Continued surveillance is required to further investigate this possibility, with the need to investigate autopsy tissues from suspected cases by histological and biochemical techniques.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2559.2000.00946.x
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  • 8
    Electronic Resource
    Electronic Resource
    Transmissions to mice indicate that ‘new variant’ CJD is caused by the BSE agent (1997)
    [s.l.] : Macmillan Magazines Ltd.
    Nature 389 (1997), S. 498-501 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] There are many strains of the agents that cause transmissible spongiform encephalopathies (TSEs) or ‘prion’ diseases. These strains are distinguishable by their disease characteristics in experimentally infected animals, in particular the incubation periods and neuropathology they ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/39057
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  • 9
    Electronic Resource
    Electronic Resource
    Pharmacological comparison of the sigma recognition site labelled by [3H]haloperidol in human and rat cerebellum (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 345 (1992), S. 197-202 
    Details
    ISSN: 1432-1912
    Keywords: Sigma recognition sites ; Human cerebellum ; Rat cerebellum ; [3H]haloperidol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The radioligand binding characteristics of [3H]haloperidol (in the presence of spiperone, 25 nmolL−1) were investigated in rat and human cerebellar membranes. In both rat and human cerebellar membrane preparations saturation studies with [3H]haloperidol (non-specific binding defined by pentazocine, 10 μmolL−1) demonstrated high affinity saturable specific binding to a homogenous population of binding sites (rat, Bmax 6693 ± 1242 fmol mg−1 protein, pKD 8.33 ± 0.08; human, Bmax 2550 ± 437 fmol mg−1 protein, pKD 8.59 ± 0.11; mean ± SEM, n = 3–6). Competition studies employing a wide range of structurally diverse competing compounds displayed that the [3H]haloperidol binding site was pharmacologically similar in both preparations and comparable to sigma recognition sites previously identified in various tissues originating from different species. In addition, with reference to the potential subtypes of sigma recognition sites, the labelling of these sites by low nanomolar concentrations of [3H]haloperidol provides evidence that they belong to the sigma-1 recognition site subtype. The present findings suggest that the pharmacology of the rat and human cerebellar sigma recognition site are directly comparable and provides further supporting evidence towards the use of [3H]haloperidol radioligand binding studies in the rat to detect sigma receptor ligands with potential therapeutic activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00165736
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