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Biomedical subjects

A Caron

Publications and source records attributed to A Caron.

At least 19 recordsLinked to original sources

Cytoplasmic body myopathy: familial cases with accumulation of desmin and dystrophin. An immunohistochemical, immunoelectron microscopic and biochemical study.

Muscle biopsy samples from five patients with cytoplasmic body myopathy (CBM) were investigated by immunohistochemical (antibodies to desmin, actin, dystrophin, spectrin, alpha actinin and utrophin), immunoelectron microscopic (antibodies to desmin, actin and dystrophin) and biochemical (desmin, dystrophin, actin and utrophin western blots) methods. Using immunofluorescence it was shown that the centers of cytoplasmic bodies (CB) were stained by anti-actin, anti-utrophin and three different anti-dystrophin antibodies. The peripheries were labeled by the anti-desmin antibody. Moreover, fibers containing CB showed a markedly increased staining of their entire sarcoplasm with the anti-desmin antibody. Using immunoelectron microscopy it was shown that anti-dystrophin antibodies selectively stained the external limit of the central granular region. Anti-desmin antibody labeled the filamentous halo, and anti-actin antibody stained the central core and the radiating filaments. Biochemical studies showed storage of desmin and dystrophin, both of normal molecular weight. Our results suggest that CBM should be considered along with a wider group of intermediate filament pathologies that include desmin-storage myopathies.

Antibodies

[Pulsed Doppler ultrasonography to measure the vasoactive effects of hemoglobin-dextran 10-benzene-tetracarboxylate, a potential erythrocyte substitute].

The effects of Dextran-Benzene-Tetracarboxylate-Hemoglobin (Dex-BTC-Hb), a chemically-modified hemoglobin-based oxygen carrier, on the vascular tone were compared to those of standard solutions, i.e. the animal's own blood and a 50 milligrams albumin solution, by measuring the carotid blood flow velocity, the mean arterial pressure, the heart rate and respiratory frequency, in anesthetized Hartley guinea pigs after a hemorragic shock. Stroma-free hemoglobin induced 40% hypertension and a 110% rise in blood flow velocity immediately after injection. The velocity was still increased 38%, 3 hours after injection. The calculations of the vascular resistances showed an increase in carotid vascular tone. Dex-BTC-Hb brought about 35% hypertension for two hours with no significant modifications of the vascular tone. These effects are similar to those of the albumin solution. These results indicate that, unlike stroma-free hemoglobin, Dex-BTC-Hb does not significantly affect the vascular tone, probably because of its slight interaction with the factors that regulate vascular tone.

Animals

Tissue expression of the Schistosoma mansoni 28 kDa glutathione S-transferase.

The expression of the Schistosoma mansoni 28 kDa glutathione S-transferase (Sm28) was studied using molecular (PCR, in situ hybridization), and immunocytochemical techniques. The presence of Sm28 was demonstrated in all developmental stages of the parasite except the intra-uterine immature egg. In the parenchyma of male and female adult worms the distribution of Sm28 was limited to a subpopulation of parenchymal cells and to the dorsal tubercles of the male. The tegument, the muscles, the digestive tract, the neural mass, the vitelline glands, and mature gametes were not immunoreactive. Immature germinal cells in both sexes, and the ootype in the female genital system, were found to express Sm28. Deposits of immunoreactive material on host skin following cercarial penetration, exfoliation from the male tubercles, and especially emission of Sm28 from eggs in hepatic granulomas are suspected to be a source of antigen during the parasite infection. The reduction in worm fecundity previously observed in immunization experiments may result from an antibody response directed against Sm28 present in the ootype. There was no cross-reactivity observed, under the experimental conditions used, between the anti-Sm28 sera and either vertebrate or invertebrate host tissue.

Animals

Visual modelling.

The first purpose of this paper is to present a neural net model of the visual cortex of higher vertebrates based on the electrophysiological properties of the ganglion cells. This model takes Hebb's law [1] as the physiological learning rule for synaptic modification. The model consists of 85 x 85 neurons forming a layer similar to the cortex. The neurones are massively connected via weights that are typically adapted. We simulate several input patterns and show that the model reproduces the pattern recognition, contours pictures and moving perception.

Algorithms

Anti-P30 IgA antibodies as prenatal markers of congenital toxoplasma infection.

This study extends a previous study and confirms that the detection of anti-P30 IgA antibodies is very helpful in the diagnosis of acute acquired or congenital toxoplasmosis. Moreover, we demonstrate that an anti-P30 IgA response can be mounted in the fetuses infected by Toxoplasma gondii during their intra-uterine life as early as week 23 of gestation. A double-sandwich ELISA described in our previous work was used to detect anti-P30 IgA antibodies in 1378 human serum samples collected from 551 patients, including 162 fetuses whose mothers had been infected by T. gondii during pregnancy, 46 congenitally infected and 90 uninfected newborns and 253 women suspected of having been infected during pregnancy, including the mothers of fetuses and newborns previously described. Anti-P30 IgA antibodies were detected in all cases of acute toxoplasmosis but in no case of chronic toxoplasmosis: in the majority of cases, the IgA antibody titre fell below cut-off in 3-9 months. Among the 46 congenitally infected newborns, anti-P30 IgA antibodies were detected in sera of 41 infected newborns (38 at birth, two in the first months of life, one in the seventh month of life), while anti-P30 IgM antibodies were detected in only 30 cases at birth and in one case during the first month of life. Among 162 fetuses, anti-P30 IgA response was observed in five infected fetuses, but was not detected in either 152 uninfected fetuses or in five fetuses considered as infected. The absence or presence of anti-P30 IgA antibodies in the fetus is discussed in relation to the date of maternal infection and collection of the fetal blood. It clearly appears from our study that the combined testing of both IgM and IgA in the fetus and the newborn is essential for a more efficient diagnosis of infection.

Acute Disease

IgA antibodies against P30 as markers of congenital and acute toxoplasmosis.

Specific IgA antibodies against P30, a major surface protein of Toxoplasma gondii were sought in 198 serum samples (from 133 patients) by means of a double-sandwich enzyme-linked immunosorbent assay. These antibodies were detected in all cases of acute toxoplasmosis but in no cases of chronic toxoplasmosis nor in seronegative patients. They were not detected in samples from patients with "natural IgM antibodies" or in those containing rheumatoid factor or antinuclear antibodies. Among 26 infants whose mothers were infected during pregnancy, anti-P30 IgA antibodies were exclusively detected in the samples from the 8 infected infants, although anti-P30 IgM antibodies were detected in only 3 of the infected infants. No uninfected infant had IgA, though 5 had IgM at birth. Thus, the detection of IgA anti-P30 antibodies seems a better means than the detection of IgM antibodies of identifying infected infants, which is very important for treatment. In addition, the very early detection of IgA antibodies may be important for the diagnosis of acute toxoplasmosis, especially during pregnancy and perhaps also in patients infected by human immunodeficiency virus.

Acute Disease

[A new ELISA method for the diagnosis of toxoplasmosis. Assay of serum IgM by immunocapture with an anti-Toxoplasma gondii monoclonal antibody].

The diagnosis of acute toxoplasmosis is based exclusively on the detection of IgM anti-Toxoplasma antibodies. The principal of the immunoenzymatic test reported here is the capture of serum IgM antibodies which are detected indirectly by the sequential addition of antigen and a monoclonal antibody directed against the immunodominant epitope at the surface of the tachyzoite. This test combines the sensitivity of enzyme-based assays and the specificity of monoclonal reagents and represents an important contribution to the diagnosis of Toxoplasma gondii infection.

Acute Disease

The solution of an integral equation with its application to human joints.

The fundamental fluid transport mechanisms in a cavity of a joint and the deformation of the bearing surfaces are important for the understanding of the bio-mechanical process involved in the physiology of normal and pathological synovial joints. We present here a study of elasto-rheodynamic lubrication of a self-acting dynamically loaded bearing which employs a porous, elastic material (articular cartilage) and a visco-elastic non-linear lubricant (synovial fluid). The tangible solution of the model is, finally, subjected to the resolution of a non-linear integral equation. Important conclusion is drawn from the results obtained for bearing characteristics which show the self-adjusting nature of human joints.

Biomechanical Phenomena

Inclusions in familial cytoplasmic body myopathy are stained by anti-dystrophin antibodies.

We report here for the first time positive anti-dystrophin labelling of inclusions in three cases belonging to the same family affected by familial cytoplasmic body myopathy (CBM). Inclusions are also stained, as reported previously, by anti-actin antibodies. The anti-desmin reaction was negative in the centre of cytoplasmic bodies (CB) but showed an enhancement of staining in the peripheral part. Abnormal sarcoplasmic staining of fibres with CB was also observed with that antibody. Anti-vimentin antibody labelling was negative. At present, the significance of this labelling by anti-dystrophin antibodies is unknown, but will open new fields for further investigations in an attempt to understand CB pathogenesis.

Actins