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P Cras

Publications and source records attributed to P Cras.

At least 55 records · Page 3Linked to original sources
PubMed1998

Determination of growth fraction and cell density to evaluate the potential growth of human oligodendroglial and astrocytic tumours.

UNLABELLED: The object of this work was PURPOSE: to develop a methodology that enables net tumour growth, a balance between actual tumour growth and tumour cell loss, to be approximately evaluated. METHODS: The methodology proposed relies on detecting the growth fraction immunohistochemically by means of MIB-1 antibody labelling combined with cell density determination, carried out on 5-microm-thick Feulgen-stained histological sections with computer-assisted microscopy. The series investigated included 25 oligodendrogliomas (OLG-II), 9 anaplastic oligodendrogliomas (OLG-III). 13 astrocytomas (AST), 14 anaplastic astrocytomas (ANA) and 8 mixed oligoastrocytomas (OLG-AST). RESULTS: The results show that the biological characteristics of some cases were in total accordance with their histopathological diagnoses. This was the case for the "weakly proliferating weakly dense" OLG-II and AST-II tumours, and for the "highly proliferating highly dense" OLG-III and AST-III ones. In contrast, the biological characteristics of some cases seemed to contradict the histopathological case labels. This was the case for the "highly proliferating highly dense" OLG-II and AST-II tumours, the biological aggressiveness of which would be undervalued on the basis of the morphology-based grading system alone, and also for the "weakly proliferating weakly dense" OLG-III and AST-III tumours, the aggressiveness of which would be overvalued. CONCLUSIONS: Combining the determinations of the MIB-1 and the cell density variables appears to be satisfactory in terms of the cell kinetic characterization of glial tumours as a complement to the prognostic information given by a morphology-based grading system alone.

Adult↗
PubMed1998

Characterization of astroglial versus oligodendroglial phenotypes in glioblastomas by means of quantitative morphonuclear variables generated by computer-assisted microscopy.

The current WHO classification places glioblastomas in the astrocytoma category. However, whether or not glioblastomas also show oligodendroglial differentiation remains a matter of controversy. This study investigates, at the morphonuclear level, the hypothesis that some glioblastomas (GBMs) may also represent the ultimate level of malignancy in the oligodendroglial lineage. Using a series of 164 GBMs, we sought to ascertain whether any of these GBMs exhibited phenotypical characteristics that were more closely related to oligodendroglial lineages than astrocytic lineages. Phenotypical features were quantitatively determined by means of the computer-assisted microscope analysis of Feulgen-stained nuclei, a process that made it possible to quantitatively describe the patterns of the cell nuclei (and, more specifically, of their chromatin) through 16 variables, and the distribution of the nuclear DNA content (DNA ploidy) through 8 variables. The phenotypical characteristics typical of astrocytic and oligodendroglial tumors were analyzed by means of Discriminant Analysis, a statistical multivariate analysis, performed on a series of 65 astrocytic and oligodendroglial tumors. This series consisted of 14 WHO grade II and 19 grade III astrocytomas and 24 WHO grade II and 8 grade III oligodendrogliomas. This multivariate analysis enabled an accurate model to be produced that distinguished between astrocytomas and oligodendrogliomas on the basis of 5 cytometry-generated variables. This model was used to characterize the phenotype of each of the 164 glioblastomas. The results show that of these 164 glioblastomas, 6 (about 3.5%) displayed phenotypes that were very similar to oligodendrogliomas, and 141 displayed phenotypes that were very similar to astrocytomas. The phenotypes of the 17 remaining GBMs were too ambiguous to be categorized as having a pure astrocytic or oligodendroglial lineage.

Adolescent↗
PubMed1998

Drug-induced spongiform leucoencephalopathy, a case report with review of the literature.

A nineteen year-old girl developed rhabdomyolysis and central pyrexia after the ingestion of multiple drugs: amphetamines, benzodiazepines, methadone, ethanol, and cocaine. On admission, the patient was deeply comatose and during the hospitalisation asymmetrical spastic quadriparesis was noted. Brain biopsy was diagnostic of spongiform leucoencephalopathy. A review of the literature concerning drug-induced spongiform encephalopathy revealed a large amount of heroin-induced cases. The role of cocaine, however, is less well described. After prolonged hospitalisation, our patient improved clinically and radiologically and could be transferred to a rehabilitation center.

Adult↗
PubMed1998

Differential diagnosis in dementia.

Dementia is characterised by progressive memory loss, associated with agnosia, aphasia, dyscalculia, apraxia, and deficits in executive functioning. Alzheimer disease is the most frequent cause of dementia, with vascular dementia, diffuse Lewy body disease, and other etiologies being important differential diagnoses. A strategy and diagnostic hierarchy for diagnosis in dementia is proposed. Diagnostic criteria for Alzheimer disease, diffuse Lewy body disease, and vascular dementia are discussed.

Alzheimer Disease↗
PubMed1998

Creutzfeldt-Jakob disease and blood transfusion.

Experimental data suggest that blood components from patients with CJD may carry infectivity. However, most of the studies have been made on the classic form of CJD. Further studies are needed to discern whether infectivity levels in blood from patients with the nvCJD differ from those with the classic form. Possibility of transmission of CJD by blood or blood products can not be excluded and therefore adequate surveillance should be implemented. People who have been exposed to contaminated blood should be followed, while recommendations are being adapted according to new scientific data on infectivity.

Creutzfeldt-Jakob Syndrome↗
PubMed1998

Cervical myelopathy due to rheumatoid arthritis. Case report and review of the literature.

We present the case report of a 62 year-old female suffering from destructive rheumatoid arthritis (RA) for more than 20 years. She had complaints of progressive gait impairment and numbness in hands and feet. Neurological examination showed an unstable gait and pyramidal tract signs. Anterior atlantoaxial subluxation with pannus formation and cervical myelopathy were demonstrated using conventional X-ray studies and MRI. She was conservatively treated with a soft collar. Treatment with methotrexate and an intensive gait revalidation program were started. RA commonly involves the cervical spine, usually in advanced systemic disease after a mean delay of 16 years. Subluxations of the cervical spine are found in 43 to 86%, 50% of these patients are asymptomatic. The reported rate of neurological impairment due to cervical instability ranges from 7 to 58%. The three most common lesions resulting from cervical RA are atlantoaxial subluxation (50 to 70%), subaxial subluxation (15 to 25%) and cranial settling (20%). It is important to differentiate between cranial settling and atlantoaxial instability, as the latter may have a more benign history with less than 20% showing progressive instability. Cranial settling progresses in 35 to 50% of patients. The commonest presenting features of rheumatoid cervical myelopathy are isolated sensory symptoms. Most patients were found to have multiple neurological deficits once the myelopathy was diagnosed. A mean delay of 31 weeks between the first symptom and the diagnosis of the myelopathy is reported. The sensory symptoms are often misinterpreted as being due to entrapment neuropathy or rheumatoid peripheral neuropathy. Radiographic analysis indicates that the posterior atlantoodontoid interval (< or = 14 mm) is an important parameter that shows excellent correlation with the severity of paralysis.

Aged↗
PubMed1997

Quantitative chromatin pattern description in Feulgen-stained nuclei as a diagnostic tool to characterize the oligodendroglial and astroglial components in mixed oligo-astrocytomas.

The oligoastrocytoma, as a mixed glioma, represents a nosologic dilemma with respect to precisely defining the oligodendroglial and astroglial phenotypes that constitute the neoplastic cell lineages of these tumors. In this study, cell image analysis with Feulgen-stained nuclei was used to distinguish between oligodendroglial and astrocytic phenotypes in oligodendrogliomas and astrocytomas and then applied to mixed oligoastrocytomas. Quantitative features with respect to chromatin pattern (30 variables) and DNA ploidy (8 variables) were evaluated on Feulgen-stained nuclei in a series of 71 gliomas using computer-assisted microscopy. These included 32 oligodendrogliomas (OLG group: 24 grade II and 8 grade III tumors according to the WHO classification), 32 astrocytomas (AST group: 13 grade II and 19 grade III tumors), and 7 oligoastrocytomas (OLGAST group). Initially, image analysis with multivariate statistical analyses (Discriminant Analysis) could identify each glial tumor group. Highly significant statistical differences were obtained distinguishing the morphonuclear features of oligodendrogliomas from those of astrocytomas, regardless of their histological grade. When compared with the 7 mixed oligoastrocytomas under study, 5 exhibited DNA ploidy and chromatin pattern characteristics similar to grade II oligodendrogliomas, I to grade III oligodendrogliomas, and I to grade II astrocytomas. Using multifactorial statistical analyses (Discriminant Analysis combined with Principal Component Analysis). It was possible to quantify the proportion of "typical" glial cell phenotypes that compose grade II and III oligodendrogliomas and grade II and III astrocytomas in each mixed glioma. Cytometric image analysis may be an important adjunct to routine histopathology for the reproducible identification of neoplasms containing a mixture of oligodendroglial and astrocytic phenotypes.

Adult↗
PubMed1997

Prolonged and atypical course in some cases of subacute sclerosing panencephalitis.

Subacute sclerosing panencephalitis (SSPE) is a persistent viral infection of the central nervous system due to a defective measles virus. Beginning with progressive cognitive malfunctioning, myoclonus and other less specific neurologic signs and symptoms, it usually evolves to a vegetative, decorticated state and death. Disease course and characteristics can be highly variable. Since the widespread measles vaccination in the Western countries started in the late seventies and early eighties, the incidence of SSPE has dropped significantly. Also adult onset is more frequently seen which changes the field of differential diagnosis. In this article 3 atypical cases of SSPE are described with peculiarities such as adult onset, pronounced extrapyramidal involvement, remission and prolonged disease course. Common features of the disease are emphasized to enable accurate diagnosis which is based on clinical features, presence of high titers of serum and cerebrospinal fluid (CSE) measles antibodies, MRI and EEG.

Adolescent↗
PubMed1997

MR of the brain in Sjögren-Larsson syndrome.

Cerebral MR was performed in three patients with Sjögren-Larsson syndrome. In each case, a 1.5-T system was used, and the patient was under general anesthesia. The MR findings included confluent hyperintense white matter lesions in the periventricular and deep white matter of the centrum semiovale, with sparing of the subcortical U fibers. The topography of the white matter abnormalities correlated well with the clinical signs and symptoms.

Adult↗
PubMed1997

Autoradiographic mapping of 5-HT1B- and 5-HT1D receptors in human brain using [3H]alniditan, a new radioligand.

[3H]alniditan, a new potent non-indole serotonin 5-HT1B/1D agonist, was used as a radioligand to characterize 5-HT1B and 5-HT1D receptor (previously termed 5-HT1D beta and 5-HT1D alpha) in various regions of the human brain. Quantitative receptor autoradiography was applied for high anatomical resolution and sensitivity. Highest densities of 5-HT1B/1D receptors were found in the substantia nigra and in the globus pallidus. High to moderate densities were measured in the caudate nucleus, putamen, nucleus accumbens, central gray and hippocampal formation. Very low densities were detected in various cortical regions. In the cerebellum no [3H]alniditan binding was detected. Selective 5-HT1B receptor labeling was achieved using [3H]alniditan in the presence of 300 nM of ketanserin (sufficient to block 5-HT1D receptor labeling). The identity of the 5-HT1B binding sites under these conditions was corroborated by the pIC50 of sumatriptan, which corresponded to its affinity for cloned human 5-HT1B receptors expressed in cells. Surprisingly, the distribution of selective 5-HT1B receptor labeling was completely identical to the distribution of labeling of 5-HT1B + 5-HT1D receptors. The present data indicate that [3H]alniditan is a suitable radioligand for measuring 5-HT1B/1D receptor in the human brain and that the 5-HT1B binding sites are predominant in the presently investigated regions of the human brain.

Animals↗
PubMed1996

Beta-amyloid precursor protein and early-onset Alzheimer's disease.

One of the major pathological hallmarks of Alzheimer's disease is the deposition in the brain parenchyma and cerebral blood vessel walls of amyloid beta-protein, a 4kDa proteolytic product of the longer beta-amyloid precursor protein (APP). Six different single base mutations in the APP gene have been reported causing early-onset Alzheimer's disease (age at onset < or = 65 years) or related amyloidosis in a small number of families. Cell transfection experiments using wild-type and mutant APP cDNA indicated that APP mutations result in the production of more or longer, aggregation prone, A beta peptides.

Alzheimer Disease↗
PubMed1996

Increased writing activity in neurological conditions: a review and clinical study.

Increased writing activity in a 70 year old, right handed man presenting with a history of alcohol misuse and maturity onset diabetes is reported. Brain CT disclosed corticosubcortical atrophy and 99mTc-HMPAO SPECT disclosed severe bilateral frontal hypoperfusion more prominent on the right. The patient's neuropsychological symptomatology consisted of severe (verbal) aspontaneity, intermittent utilisation behaviour, and pronounced increased writing activity, which mainly consisted of a perseverative, micrographic written reproduction of visually or verbally perceived language fragments. Several neurological causes of increased writing activity and the equivocal terminology met in the medical literature are reviewed. A distinction between hypergraphia and automatic writing behaviour is proposed. It is concluded that our patient's increased writing activity may be characterised as automatic writing behaviour.

Aged↗
PubMed1996

Parinaud's syndrome in a patient with multifocal glioma.

We describe the clinical and neuroradiological findings in a 63-year-old man with Parinaud's syndrome. Magnetic resonance (MR) imaging showed a mass lesion within the quadrigeminal plate. Additional MR findings included a right frontoparietal subcortical lesion as well as periventricular white matter edema due to acute deterioration of hydrocephalus. On MR, the diagnosis of multifocal glioma was proposed. Neuropathological examination after resection of the supratentorial lesion revealed an oligodendroglioma, grade II.

Brain Neoplasms↗
PubMed1995

Extracellular neurofibrillary tangles reflect neuronal loss and provide further evidence of extensive protein cross-linking in Alzheimer disease.

In this report we quantitatively assess the numbers of intracellular and extracellular neurofibrillary tangles (NFT) in the brains of a series of individuals with Alzheimer's disease and of controls and correlate these with neuronal loss. Our data indicate that in some cases, NFT are not removed from the brain throughout the disease process. This finding, together with our previous demonstration of carbonyl-related modifications in NFT, provides additional evidence that the protein constituents of NFT are resistant to proteolytic removal, possibly as a result of extensive cross-links. Additionally, correlation between the number of NFT and neuronal loss indicates that there are at least two distinct mechanisms responsible for neuronal death in Alzheimer's disease that are directly and indirectly related to the presence of neurofibrillary pathology.

Aged↗
PubMed1995

Postmortem MRI of the brain with neuropathological correlation.

We prospectively correlated in vitro MRI of the brain with the neuropathological findings in patients with suspected intracranial disease. In vitro MRI was performed on 91 consecutive formalin-fixed whole-brain specimens. In 60 cases, the images were correlated with the neuropathological findings (number of lesions, lesion boundaries, spread of oedema and type of lesions). As compared with neuropathology, MRI showed an equal number of lesions in 50 cases, more in 5, and less in 5 specimens, resulting in a sensitivity of 83.3%. The extent of perilesional oedema was better seen on in vitro MRI than on gross pathology. Microscopic extent of glial tumours was underestimated on both T2-weighted images and macroscopic examination. Neuropathology remains the reference study, since on in vitro MRI primary brain tumours, metastatic deposits and non-neoplastic space-occupying lesions cannot be differentiated. However, in our study MRI had a specificity of 76.6%. MRI of postmortem specimens is sensitive to focal brain lesions, and can focus the attention of the neuropathologist to abnormal regions.

Adolescent↗
PubMed1995

Molecular genetic analysis of familial early-onset Alzheimer's disease linked to chromosome 14q24.3.

Genetic linkage studies have indicated that chromosome 14q24.3 harbours a major locus for early-onset (onset age <65 years) Alzheimer's disease (AD3). Positional cloning efforts have identified a novel gene S182 or presenilin 1 as the AD3 gene. We have mapped S182 in the AD3 candidate region between D14S277 and D14S284 defined by genetic linkage studies in the two chromosome 14 linked, early-onset AD families AD/A and AD/B. We have shown that S182 is expressed in lymphoblasts and have determined the complete cDNA in both brain and lymphoblasts by RT-PCR sequencing. S182 is alternatively spliced in both brain and lymphoblasts within a putative phosphorylation site located 5' in the coding region. We identified two novel mutations, Ile143Thr and Gly384la located in, respectively, the second transmembrane domain and in the sixth hydrophilic loop of the putative transmembrane structure of S182. As families AD/A and AD/B have very similar AD phenotype our observation of two mutations in functionally different domains suggest that onset age and severity of AD may not be very helpful predictors of the location of putative S182 mutations.

Age of Onset↗