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Biomedical subjects

M Dumas

Publications and source records attributed to M Dumas.

At least 235 records · Page 13Linked to original sources
PubMed1981

N-Hexane- and methylethylketone-induced polyneuropathy. Abnormal accumulation of glycogen in unmyelinated axons. Report of a case.

This report presents the ultrastructural nerve study of a patient with sensorimotor neuropathy by a shoe glue containing an association of n-hexane and methylethylketone. Giant axons, distended by microfilamentous proliferation typical of such cases of neuropathy, were found in significant amounts. An unusual histological feature of this case was the considerable distension by a marked accumulation of glycogen granules in certain unmyelinated axons. Such a lesion has never been described in neuropathy induced by industrial agents.

Adult↗
PubMed1980

Familial Creutzfeldt-Jakob disease. Autosomal dominance in 14 members over 3 generations.

Discovery oa a second affected branch of a family with transmitted Creutzfeldt-Jakob disease (CJD), originally reported by Buge et al. in 1978, brings the total number of cases to 14 in 3 generations, with at least 20 members of the next young adult generation presently at risk. Complete segregation of the illness to the descendants of these 2 branches, with no skipped generations, and an overall frequency of CJD in affected sibships of 56%, clearly defines a pattern of autosomal dominance. The disease is indifferent to sex, either in terms of affected members (8 males and 6 females) or of lineage (3 fathers and 3 mothers). Acquisition of CJD virus from a point source contamination is unlikely, and case-to-case transmission, if it occurred, would have required an average minimum incubation period of 17 years.

Creutzfeldt-Jakob Syndrome↗
PubMed1980

[Visual complications of mitral leaflet prolapse (author's transl)].

Among ten patients with acute ischemic cerebral accident and mitral leaflet prolapse, two women presented with visual disturbances consistent with embolism in the ophthalmic or posterior cerebral circulation. These observations emphasize the importance of thorough cardiovascular assessment in all patients with acute cerebral or ocular ischemia, and we suggest that echocardiography should be part of routine investigation of such patients.

Adult↗
PubMed1979

Steroids and hypertension. 1--Gas-liquid chromatography and gas chromatography mass spectrometry of 3,15- and 3, 16-dihydroxy-17-oxosteroids.

In order to analyse and quantitate the urinary 16-oxysteroids known or thought to be associated with hypertension, we have established for six 16-oxy-C19 reference steroids the following parameters: elution volume on lipophilic gel columns, gas chromatographic retention data expressed as methylene unit values of trimethylsilyl ether and O-methoxime trimethylsilyl ether derivatives on OV-1 and OV-17 packed columns and on SE-30 capillary column, and mass spectra of these compounds. These reference steroids were: 3 alpha, 16 alpha-dihydroxy-5 alpha-androstan-17-one, 3 alpha, 16 alpha-dihydroxy-5 beta-androstan-17-one, 3 beta, 16 alpha-dihydroxy-5 alpha-androstan-17-one, 3 beta, 16 alpha-dihydroxy-5-androsten-17-one, 3 beta, 16 beta-dihydroxy-5-androsten-17-one, 3 beta, 17 beta-dihydroxy-5-androsten-16-one and 3 alpha, 15 alpha-dihydroxy-5 beta-androstan-17-one. The proposed method was shown to be applicable to the specific analysis of 16-oxy-C19-steroids in biological samples since it achieved the selective isolation of these compounds from other steroids and their quantitative elution in a single fraction. The analysis of the urinary steroids of two patients with arterial hypertension demonstrated an elevated rate of 3 beta, 16 alpha-dihydroxy-5-androsten-17-one.

17-Ketosteroids↗
PubMed1979

Retrograde axonal transport of specific macromolecules as a tool for characterizing nerve terminal membranes.

The uptake of macromolecules by nerve terminals which is followed by retrograde axonal transport seems to occur by two different mechanisms, a specific and a nonspecific one. The nonspecific uptake depends on the presence of macromolecules (e.g., horseradish peroxidase) in the vicinity of the nerve terminals at very high concentrations and is enhanced by neuronal activity. In contrast, the specific uptake and subsequent retrograde axonal transport becomes apparent at much lower concentrations of the appropriate macromolecules, depends on the affinity of these ligands for specific binding sites on the surface of the neuronal membrane, and is independent of neuronal activity. The fact that lectins and some bacterial toxins bind to specific membrane glycoproteins or glycolipids allows conclusions to be drawn regarding qualitative and even quantitative aspects of the composition of the plasma membrane of the nerve terminals. 125I-labelled nerve growth factor (NGF), tetanus toxin, cholera toxin, wheat germ agglutinin (WGA), ricin II, phytohemagglutinin (PHA), and concanavalin A (ConA) were injected into the anterior eye chamber of rats where they were taken up by adrenergic nerve terminals and transported retrogradely to the superior cervical ganglion. The saturation of the uptake-transport found for NGF, WGA, choleragenoid and an atoxic binding-fragment of tetanus toxin indicates that limited numbers of binding sites, which showed also different affinities, are present for each ligand on the membrane of the nerve terminals. Competition experiments showed that the binding sites for the ligands investigated are largely independent. Two different classes of binding sites (high affinity--low capacity and intermediate affinity--intermediate capacity) seem to be involved in the saturable retrograde axonal transport of NGF. In contrast, WGA seems to have only a single class of binding-uptake sites with high capacity and relatively low affinity. Strong evidence for positive cooperativity was obtained for the uptake and subsequent transport of the tetanus toxin fragment.

Animals↗