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Biomedical subjects

A Delpech

Publications and source records attributed to A Delpech.

At least 55 records · Page 3Linked to original sources
PubMed1981

[Nervous system tumour proteins. G.F.A. and hyaluronectin (author's transl)].

G.F.A. (gliofibrillary acid protein) and hyaluronectin studied here are two antigens defined by the heteroantibodies which appear in the serum of the immunised animal. G.F.A. is associated with gliofilaments and is considered as an astrocyte marker, either normal or tumoral. Hyaluronectin, is found in the Ranvier nodes and at the periphery of neurones. It is not specific to the nervous system. It is found in all tissues and tumors, and in particular marks the intercellular spaces of gliomas, where it is associated with hyaluronic acid for which it has a great affinity. Serum estimation of these Proteins is being undertaken with the view to a clinical application.

Animals↗
PubMed1980

Brain glycoprotein in tumours of the nervous system.

We studied various tumours of the nervous system by the immunofluorescence technique using an anti-brain specific alpha 2 glycoprotein antiserum (anti-NSA3 antiserum). We found the antigen in 24/27 astrocytomas and 4/4 oligodendrogliomas but in none of the 8 meningiomas tested. There was an identity between the astrocytoma/oligodendroglioma antigen and that of normal brain as shown by the immunoprecipitation technique. By the immunofluorescence technique using inhibition of the antiserum we demonstrated that the tumour antigen is devoid of some specific nervous system determinants present in normal brain.

Antigens, Neoplasm↗
PubMed1979

[Association of brain glycoprotein (NSA 3) with neuronal membranes and with the nodes of Ranvier].

The localisation of brain glycoprotein NSA 3 was studied by means of indirect immunofluorescence on alcohol fixed, paraffin embedded sections of Rat brain. These techniques allowed the localisation of NSA 3 to the membrane of some (about 10%) of the neurons. In the white matter, the patterns were in agreement with the localisation of the Ranvier nodes. The nodes of Ranvier were also stained in peripheral nerves.

Brain Chemistry↗
PubMed1979

An antigen associated with mesenchyme in human tumours that cross-reacts with brain glycoprotein.

Anti-NSA3 antiserum was found to react with many kinds of benign and malignant tumours, as well as foetal skin and intestinal extracts. The corresponding antigens isolated from nervous tissue, benign breast adenoma, and a fibrosarcoma were compared. Immunoprecipitation cannot distinguish between these antigens, and their amino-acid contents were comparable. However, immuno-absorption identified an antigenic determinant that was confined to nervous tissue. Indirect immunofluorescence further confirmed the validity of the concept of a nervous form vs a mesenchymal form of the antigen. Furthermore, immunofluorescence enabled the localization of the antigen found in non-nervous tissue to mesenchyme (mesenchyme-associated antigen: MAA), whether the mesenchymal tissue be normal (foetal organs), tumoral (fibrosarcoma) or reactional (connective-tissue stroma of epithelial tumours).

Amino Acids↗
PubMed1978

[Mesenchyme-associated antigen: a new immunochemical marker of human tumors].

An antiserum raised in Rabbits against brain glycoprotein precipitated an identical antigen in faetal dermis and intestine extracts, and also in non nervous tumors (breast adenocarcinomas and adenofibromas, ovarian cystadenoma, gastric and colonic adenocarcinomas, hepatomas, malignant melanomas, rhabdomvosarcoma, fibrosarcomas). By the indirect immunofluorescence technique, this antigen was always found associated with the mesenchymal proliferation, either malignant (fibrosarcoma) or reactive (fibrous stroma reaction of carcinomas).

Animals↗
PubMed1978

[Disappearance of the gliofibrillar protein (GFA) during the cultivation of glioblastoma cells].

Absence of GFA in established cell lines from glioblastomas promped us to look for this protein from the first replication of malignant cells in vitro and in following subcultrues. Our results show that GFA disappeared during the first twelve replications, often before the fifth replication. No correlation was observed with a morphological transformation of the cells.

Antigens, Neoplasm↗
PubMed1978

Glial fibrillary acidic protein in tumours of the nervous system.

Glial fibrillary acidic protein (GFA) was assayed in nerve-tumour extracts and located in these tumours by indirect immunofluorescence study. We conclude that GFA is a specific marker of both malignant and normal astrocytes. Non-astrocytic tumours (oligodendroglioma, meningioma) do not contain GFA. Tumours with astrocytic differentiation potential (medulloblastoma) may contain GFA. Comparison of microscopic and GFA assays leads us to conclude that GFA concentration is proportional to the amount of malignant astrocytes in the tumour and inversely proportional to the necrotic area of a tumour. Normal tissue GFA and glioblastoma GFA were found to be immunologically identical.

Antigens↗
PubMed1975

[Detection of anti-DNA antibodies by electroimmunodiffusion. Comparison of the results with the study of antinuclear factors by immunofluorescence].

The detection of anti-DNA antibodies was carried out by the electroimmunodiffusion method. The results were compared to those of the immunofluorescent method for anti-nuclear factors. Positive results were obtained with the electroimmunodiffusion method in 86% of the lupus erythematosus cases, 77% of the sero-positive rhumatoid polyarthritis cases and 67% of the scleroderma cases. They are comparable to those obtained by other methods. The electroimmunodiffusion method allowed in 3 out of 54 sera to defect anti-DNA antibodies although no anti-nuclear factor was found.

Antibodies, Antinuclear↗
PubMed1973

Acute renal failure associated with combined gentamicin and cephalothin therapy.

Three patients with normal renal function developed acute renal failure between the ninth and twenty-seventh days of combined gentamicin and cephalothin therapy. The dose of gentamicin (4-6 mg/kg/day) was in the normal range, but that of cephalothin (180 mg/kg/day) was abnormally high. The nephropathy was of the tubular-interstitial type and the clinical picture similar to that seen in acute drug-induced nephropathies. Frusemide was given only after the onset of renal failure. In these three patients the high intravenous doses of cephalothin combined with gentamicin were probably nephrotoxic.

Acute Kidney Injury↗