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Biomedical subjects

J Flament-Durand

Publications and source records attributed to J Flament-Durand.

At least 37 records · Page 2Linked to original sources
PubMed1990

Argyrophilic breast carcinoma, single metastasis to the pituitary gland.

Five years ago, a 44 year-old woman presented with an apparently localized cancer of the right breast, initially treated by surgery, adjuvant chemotherapy and radiotherapy. After a 4 year disease-free interval, she developed bi-temporal hemianopsy, due to a suprasellar tumor causing compression of the optic chiasma. The tumor was resected by the transsphenoidal route and histological examination revealed neuroendocrine characteristics described as "argyrophilic breast carcinoma". The exceptional association of this peculiar histology for breast cancer with a rare pattern of recurrence (single pituitary metastasis) is worthwhile reporting.

Adult↗
PubMed1989

Gd-DTPA-enhanced MR imaging of spinal tumors.

Forty-eight Gd-DTPA-enhanced MR examinations of the spine were performed in 40 patients referred for MR because of clinically suspected spinal tumor or for further evaluation of an expanded cord. The study group consisted of 32 patients with spinal tumors (seven ependymomas; seven astrocytomas; four hemangioblastomas; two arteriovenous malformations; two unidentified intramedullary neoplasms; four meningiomas; and single cases of metastatic breast carcinoma, cavernous hemangioma with associated hematomyelia, neurinoma, angiolipoma, drop metastasis from medulloblastoma, and epidermoid with diastematomyelia). In the remaining eight patients, other diagnoses were established: thoracic disk herniation (two patients), lumbosacral meningocele (one), syringomyelia secondary to arachnoiditis (four), and expanded cord secondary to gliotic tissue (one). All but two diagnoses were proved histologically by biopsy, surgery, or autopsy; in the two patients with arteriovenous malformations, the definitive diagnosis was made by spinal angiography. Contrast enhancement occurred in 30 of the 32 spinal tumors, and Gd-DTPA-enhanced T1-weighted images proved helpful in defining and outlining intra- and extramedullary spinal neoplasms. All ependymomas and astrocytomas (including low-grade astrocytomas) enhanced. In meningiomas, an immediate and uniform contrast uptake was demonstrated. Additional advantages of Gd-DTPA MR include the differentiation of solid tumor components vs syrinx or cyst or pseudotumoral areas of cord expansion, and the differentiation of residual or recurrent tumor from scar tissue in postoperative patients. Our results suggest that IV-injected Gd-DTPA improves MR sensitivity and specificity in the evaluation of spinal lesions.

Astrocytoma↗
PubMed1989

Accumulation of smooth endoplasmic reticulum in Alzheimer's disease: new morphological evidence of axoplasmic flow disturbances.

Numerous enlarged neurites and presynaptic terminals containing tubulovesicular profiles of smooth endoplasmic reticulum (SER) were observed in frontal biopsies from six patients with Alzheimer's disease. These accumulations of SER probably reflect disturbances of axoplasmic flows. In addition, curvilinear tubular inclusions similar to those characteristic of Farber's disease were found in one patient. Finally, accumulation of glycogen within neurites and enlarged mitochondria were observed in all patients.

Alzheimer Disease↗
PubMed1988

Immunocytochemical detection of GABAergic nerve cells in the human temporal cortex using a direct gamma-aminobutyric acid antiserum.

Recently, an immunocytochemical method using glutaraldehyde fixation and an antiserum developed against a GABA--glutaraldehyde--protein conjugate has permitted direct visualization of GABAergic structures in the brains of perfused animals. This paper reports a successful use of this technique on human temporal cortex fixed by immersion. The cerebral tissue was obtained from patients operated for focal epilepsy. GABA-positive somata, fibres and terminals are observed in all layers of the temporal cortex. Terminals are particularly abundant in the superficial portion of layer I and in layers II, III and IV. Dense plexuses of fibres are located in layers II, III, IV and VI and in the underlying white matter. Somata are found in all cortical layers and in the underlying white matter; they are round, oval, fusiform or triangular and exhibit a multipolar, bitufted or bipolar dendritic pattern. This technique for the visualization of GABAergic structures in the human brain may allow a better understanding of the pathogeny of epilepsy in which the GABAergic transmission has been implicated.

Humans↗
PubMed1988

Both adult and juvenile tau microtubule-associated proteins are axon specific in the developing and adult rat cerebellum.

Several antibodies directed against the heterogeneous microtubule-associated protein group tau have been used to determine the immunocytochemical localization of these proteins in the developing rat cerebellum. Immunoblot analysis of brain extracts showed that both monoclonal and polyclonal anti-tau antibodies revealed not only the adult tau proteins (50,000-70,000 mol. wt) but also the immature (48,000 mol. wt) tau form. Immunocytochemical studies showed that, whatever the stage of development, anti-tau antibodies stained several types of axonal fibres. The Purkinje cell bodies and their dendrites were never significantly labelled. This means that immature tau is, as adult tau, localized essentially in axons. Axonal labelling seems to follow the cerebellar developmental pattern. For instance, the climbing fibres which reach the cerebellum during the embryonic life were stained soon after birth by the anti-tau antibodies. In contrast, the parallel fibres, that begin to develop perinatally, do not express tau at early (5 days) postnatal stages; a clear labelling of the deeper parallel fibres (which are more mature than the superficial ones) was seen at day 10 after birth in the vicinity of the developing dendrites of the Purkinje cells. This suggests that (1) the appearance of tau immunoreactivity reflects a certain stage of maturity of the parallel fibre; (2) both immature and mature tau microtubule-associated proteins seem to be axon specific in the developing rat cerebellum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Amyloid scrapie plaques in mice, and Alzheimer senile plaques, share common antigens with tau, a microtubule-associated protein.

Immunolabelling was performed on brain sections of scrapie-infected mice with antibodies against tau, a microtubule-associated protein, and against the paired helical filaments of Alzheimer's disease. Both kinds of antibodies have been shown previously to label paired helical filaments in neurons and in abnormal neurites associated with the senile plaques of Alzheimer's disease. Amyloid plaques in murine scrapie were labelled by both antisera. The structural substrate for the immunolabelling was probably the dystrophic neurites in the periphery of the plaques, leaving the amyloid core unstained. These results emphasize that similar mechanisms are likely to be involved in the pathogenesis of plaques in both diseases.

Alzheimer Disease↗
PubMed1987

Quantitative assessment of the density of neurofibrillary tangles and senile plaques in senile dementia of the Alzheimer type. Comparison of immunocytochemistry with a specific antibody and Bodian's protargol method.

Counts of neurofibrillary tangles and senile plaques were performed in two adjacent sections from the temporal lobe in 14 women aged over 75 years at death. The mental status of these cases had been prospectively assessed by the test score of Blessed, Tomlinson and Roth. They were either intellectually normal or had senile dementia of the Alzheimer type of various degrees of severity. The first section was silver-impregnated according to Bodian's method; the second one was immunolabeled with an antiserum raised against neurofibrillary tangles. Densities of neurofibrillary tangles and senile plaques evaluated by the two techniques were highly correlated but their means of differences and limits of agreement were large. The correlation with the clinical data was similar for the two methods. Both techniques can thus be used with the same accuracy in correlative studies but their results are not interchangeable without caution.

Aged↗
PubMed1987

Treatment of intracranial mycotic aneurysm: surgery or not. A case report.

Mycotic intracranial aneurysms are of infectious origin and, even nowadays, their treatment remains controversial with advocates for either surgical or medical treatment. We present the case of a 58-year-old patient who was admitted to the hospital with a left hemiparesis due to a large right parietal haematoma. An angiogram demonstrated a small vascular malformation localized on a distal parietal branch of the right Sylvian artery. The patient was operated on and recovered well. Nevertheless, a control angiogram demonstrated the disappearance of the previous malformation but showed a new saccular aneurysm localized on the right rolandic artery. At the same time the patient became septic and the diagnosis of endocarditis complicated by mycotic aneurysm was confirmed. The patient was then medically treated with antibiotics for two months and several angiograms showed the progressive disappearance of this aneurysm. Different treatments of intracranial mycotic aneurysms are finally reviewed and a therapeutic approach is discussed.

Aneurysm, Infected↗
PubMed1987

Reversible capsulo-tegmental locked-in state as first manifestation of multiple sclerosis.

An 18-year-old girl developed a reversible locked-in state with bilateral ptosis and almost complete ophthalmoplegia. She later presented with a relapsing and remitting course suggestive of multiple sclerosis. Autopsy findings demonstrated bilateral capsular and tegmental demyelinating lesions. In addition to this unusual aetiology, this is the first report with pathological evidence of a locked-in syndrome due to lesions outside the ventral brainstem.

Adolescent↗
PubMed1987

Neurofibrillary tangles and the neuronal cytoskeleton.

Antibodies to neurofilaments and the microtubule-associated protein, tau, have been used with anti-paired helical filament (PHF) serum to study Alzheimer neurofibrillary tangles. Tangles and their constituent PHF contain epitopes derived from or cross-reactive with both neurofilaments and tau proteins. These same structures are labelled with anti-PHF antibodies. A component of the anti-PHF serum is against tau proteins. We conclude that PHF are at least in part derived from an abnormal neuronal cytoskeleton.

Alzheimer Disease↗
PubMed1986

Lethal osteopetrosis with multiple fractures in utero.

Severe osteopetrosis was diagnosed in utero in two successive pregnancies resulting from an intermarriage. Hydrocephaly and skeletal hyperdensity were detected at 18 weeks of gestation, and fractures at 24 weeks. We report on extensive ultrasound, radiological, and pathological findings, including those on brain and bone. The markedly reduced number of osteoclasts observed in these sibs and the very early fetal involvement suggest that this form of osteopetrosis might represent a new entity: autosomal recessive lethal osteopetrosis.

Adult↗
PubMed1986

Alzheimer's paired helical filaments share epitopes with neurofilament side arms.

A panel of monoclonal antibodies to neurofilaments have been investigated with regard to the location of their respective epitopes on neurofilament polypeptides and their ability to label the neurofibrillary tangles and paired helical filaments (PHF) which are characteristic of Alzheimer's disease. All of the neurofilament monoclonal antibodies that label tangles and PHF are directed against epitopes in the side arm domains of the two larger neurofilament polypeptides, NF-H and NF-M, and do not recognise the alpha-helical rod domains of these proteins. Immuno-electron microscopy demonstrates that the neurofilament antibodies label the constituent PHF per se and do not simply stain neurofilaments that might be admixed with PHF. These neurofilament epitopes are differentially retained by PHF, following isolation. Thus, antibody labelling of PHF is not simply due to the presence of normal neurofilament polypeptides. We propose that in tangle-bearing neurons, neurofilaments are degraded by proteases and that it is fragments of the side arms which contribute to the composition of PHF.

Alzheimer Disease↗