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Biomedical subjects

E Morel

Publications and source records attributed to E Morel.

At least 73 records · Page 4Linked to original sources
PubMed1987

Grossularine-1 and grossularine-2, alpha carbolines from Dendrodoa grossularia, as possible intercalative agents.

Dendrodoine A, grossularines-1 and -2, metabolites isolated from the tunicate Dendrodoa grossularia, have exhibited a cytotoxic activity on L1210 leukemia cells in culture. The inhibition of DNA synthesis induced by grossularines and the plane structure of the alpha-carboline common moiety were in favor of an intercalative process for their mechanism of action. In fact, the results of viscometry, fluorescence quenching and DNA melting experiments clearly indicated the intercalative properties of grossularine-2 explained by its quasi-planar structure and the non-intercalative DNA binding of grossularine-1 explained by the presence of a bulky indole chain at the 2-position of the alpha-carboline ring.

Animals↗
PubMed1987

Protective effect of myasthenic immunoglobulins against the lethal toxicity of alpha bungarotoxin.

Using a radioimmunological method performed in the presence and absence of the acetylcholine agonist decamethonium (DC), it was demonstrated that 98% of myasthenia gravis (MG) patients' sera (positive for anti-acetylcholine receptor (anti-AChR) antibody titres in the conventional assay) contain antibodies that block the binding of alpha bungarotoxin (alpha Bgt) to human AChR. The positive effect of myasthenic immunoglobulins against the alpha Bgt toxicity was revealed by a test devised to investigate the biological significance of these blocking antibodies in vivo in Balb/c mice. IgG from sera containing blocking antibodies, detected either directly or in the presence of DC, protected the mice treated (24 of 25); nevertheless no overt clinical signs of a myasthenic syndrome were observed. Control IgG, from normal human sera or from a systemic lupus erythematosus patient, provided no protection (22 dead out of 26). IgG from MG sera devoid of anti-AChR antibodies (eight out of eight) and IgG from serum containing anti-AChR antibodies but devoid of blocking antibodies offered no defence against alpha Bgt toxicity (13 dead out of 15). The pathological role of blocking antibodies, cell mediated immunity or other mechanisms is discussed.

Animals↗
PubMed1986

[Assay of anti-acetylcholine receptor antibodies in myasthenic syndromes of newborn infants].

Eighteen neonates were investigated for antibodies directed against acetylcholine receptors. No antibody was detected in 3 cases of congenital myasthenic syndrome, whereas positive results (3.5 to 250 nM) were obtained in 7 cases of transitory neonatal myasthenia and in 7 of 8 asymptomatic infants born to myasthenic mothers. The neonatal antibodies are fully cleared within 1 to 6 months (half-life: 9 days to 2 and a half months). The prognostic value of the maternal and infantile antibody titers is limited: maternal titer at the end of pregnancy, though usually higher in the mothers of myasthenic children, do not predict or preclude the occurrence of transitory myasthenia, and there is no clear correlation between the severity and duration of the myasthenia and the initial titer or the level of the child's antibodies. The assay which measures antibodies against acetylcholine receptors is useful in that it confirms the diagnosis of transitory myasthenia and excludes congenital myasthenic syndromes.

Amniotic Fluid↗
PubMed1986

Heterogeneity of antibodies directed against the alpha-bungarotoxin binding site on human acetylcholine receptor and severity of myasthenia gravis.

A rapid and sensitive radioimmunological method is described, using decamethonium (DC), which revealed antibodies which blocked alpha-bungarotoxin (alpha-Bgt) binding to human acetylcholine receptor (AChR) in 98% of myasthenia gravis (MG) patients' sera tested. These sera had anti-AChR antibody titres by the conventional assay. The titre of blocking antibodies (1 to 110 nM) could be measured and was found to produce from 1 to 54% inhibition of alpha-Bgt binding. No relationship was found between these titres and anti-AChR antibody titres. MG sera were divided into 2 major groups on the basis of their blocking effects, with and without DC, but there was no correlation between these and the clinical status, as defined by Osserman's classification. However, no sera from asymptomatic or ocular MG patients had the dual capacities of blocking alpha-Bgt binding, directly and in the presence of DC.

Antibodies↗
PubMed1985

[Myasthenia induced by D-penicillamine. Study of immuno-clinical correlations in 23 cases].

Sera from 23 patients with D-penicillamine-induced myasthenia gravis (MG) contained antibodies directed against the human muscle acetylcholine receptor (anti-AChR) in 83% of the cases at the onset of the disease. Twenty-one were patients with rheumatoid arthritis. The anti-AChR antibody titers were comparable to those of sera from ocular MG patients and were related to the presence of clinical signs but not to their severity. The anti-AChR antibodies persisted in autonomous MG (5 cases) and disappeared in the other cases. The same phenomenon occurred for antinuclear antibodies detected in sera from 13 patients at the onset of the disease: anti-ss DNA 9/13, antinuclear 4/13 and anti-histones 7/13. The latter antibodies seem to result from, and follow the D-penicillamine treatment.

Adult↗
PubMed1984

Callus characteristics following intramedullary nailing with stainless steel or epoxy-carbon nails.

Biological mechanical improvements of osteosynthesis make intramedullary nailing an attractive alternative to bone plate fixation. However, little is known about stress shielding induced by intramedullary implantation of a nail. To evaluate the effect of the nail rigidity on bone healing, mid-metatarsal osteotomies were performed in sheep and fixed with either stainless steel or epoxy-carbon composite V-shaped nails. Mechanical and histomorphometric features of the callus were evaluated 4 months postoperatively. No statistical difference between the two groups were demonstrated for either mechanical or microstructural characteristics. The presence of a fibrous membrane filling the bone/nail interface and allowing sliding micromotions of the implants and the much smaller effect of nail rigidity, as compared to bone plate after implantation, were assumed to be the main reason for this uniformity. At this stage of healing, bone characteristics were more related to a nonspecific (vascular) bone remodeling phenomenon than to a stress-shielding effect.

Animals↗
PubMed1984

Neonatal myasthenia gravis. Anti-acetylcholine receptor antibodies in the amniotic fluid.

Neonatal myasthenia gravis (NMG) with mild arthrogryposis was observed at birth in the newborn infant of a myasthenic mother. Anti-acetylcholine receptor (anti-AChR) antibodies were present in the serum of both mother and child, in umbilical cord serum and in the amniotic fluid. The presence of anti-AChR antibodies in the amniotic fluid may be one of the causes of the NMG.

Adult↗
PubMed1984

Evidence for the presence of immunoreactive acetylcholine receptors on human thymus cells.

Triton extracts from thymuses and thymomas from either normal subjects or MG patients specifically bind [125I] alpha-bungarotoxin (alpha Bgt). This binding is saturable (apparent Ks = 5.9 X 10(-9) M) and can be inhibited by cold alpha Bgt, acetylcholine or nicotinic agonists. These results demonstrate the presence on human thymus cells of acetylcholine receptor (ACh.R), 2.8% for normal human thymus in regard of ACh.R concentration in human muscle. Normal human thymic extracts were used as an antigen source in the radioimmunoassay for the detection of anti-ACh.R antibodies in positive MG patients' sera. 72% of these sera were also positive with the thymic antigen. The demonstration of ACh.R in human thymus brings further support to the hypothesis of intrathymic autosensitivity against ACh.R as a major factor in MG pathogenesis.

Antibodies↗
PubMed1984

Anti-AChR antibodies, thymic histology, and T cell subsets in myasthenia gravis.

The relationship between the titers of antibody against acetylcholine receptor (AChR) and T helper/suppressor balance (assessed by the OKT4/OKT8 ratio) were investigated in 74 patients with myasthenia gravis (MG). All patients with elevated AChR antibody titers (greater than 100 nM) had hyperplastic thymuses, while most patients with low or negative antibody titers (less than 1 nM) had involuted thymuses. All patients with thymoma had positive, though not very high, antibody titers. No correlation was found between anti-AChR antibody levels and OKT4/OKT8 ratios except for patients with thymoma. Thus, it appears that AChR antibody titers are more closely related to thymic pathology than to peripheral T cell imbalance. These results are consistent with the hypothesis giving a central role to thymic lymphocytes in the AChR antibody production, either as antibody producer B cells or helper T cells.

Acetylcholine↗
PubMed1984

[Heterogeneity of antibodies blocking the binding of bungarotoxin to the acetylcholine receptor in myasthenia].

Inhibitory effect of myasthenic patients antibodies on alpha-bungarotoxin binding to the human acetylcholine receptor has been demonstrated by radioimmunoassay. By using decamethonium, an acetylcholine agonist, we have shown the existence of two antibody sub-groups reacting with the toxin-binding site: one sub-group is represented by antibodies which block the binding directly, the other by antibodies that inhibit the binding, only in the presence of decamethonium.

Antibodies↗
PubMed1983

Monoclonal antibodies against the human acetylcholine receptor.

Monoclonal cell lines synthesizing antibodies against partially purified acetylcholine receptor from human muscle (H.AChR) were produced. Eleven clones secreted antibodies against H.AChR. Four were obtained in ascitic form. Two of them have been exhaustively studied. Specificity and affinity for H.AChR were demonstrated. Cross-reactivity with mouse AChR was shown but not with torpedo or porcine AChR at the same concentration. Purified IgG injected intravenously provoked an obvious muscular weakness. Inhibition experiments on myasthenia gravis sera binding have demonstrated that monoclonal antibody specificity is directed against an antigenic determinant shared by human and mouse AChR.

Animals↗
PubMed1983

Cytotoxicity of cyclodepsipeptides on murine lymphocytes and on L 1210 leukemia cells.

By in vitro experiments we have demonstrated an important cytotoxic effect of destruxins A, A2, B, B1 and E on L 1210 leukemia cells. This cytotoxic effect was measured by DNA synthesis. The cytotoxic effect on normal mouse spleen lymphocytes was also evaluated. For the most cytotoxic compound, destruxin E, 16 mg/kg was found to be the minimal dose necessary to kill all mice.

Animals↗
PubMed1982

[Assay of acetylcholine receptor antibodies in myasthenia gravis. A study of 329 sera (author's transl)].

Antibodies directed against acetylcholine receptors were investigated in 329 sera by a radioimmunological technique using human muscle. Eighty-six per cent of patients with generalized myasthenia gave positive results. The percentage of positivity reached 90% when a receptor lipid extract was used. Fifty-six per cent of 25 sera from patients with ocular myasthenia were positive. Conversely, no antibody was detected in controls (other neurological diseases, normal subjects), except for two lupus patients. In addition to its diagnostic value, the assay of antibodies to acetylcholine receptors proved useful in the follow-up of myasthenic patients (notably neonates) treated by thymectomy, immunodepressants and plasmapheresis.

Adolescent↗
PubMed1982

A lipid-associated acetylcholine receptor as an antigen in diagnosis of myasthenia gravis.

Antibodies to the acetylcholine receptor are detected in over 85% of myasthenic patients' sera when acetylcholine receptors extracted from human muscle are used as the antigen. As recent data have shown the importance of the lipid environment for receptor function, we have used a lipid-associated acetylcholine receptor as the antigen for antibody determination. This fraction was shown to discriminate better between normal human sera and sera from myasthenic patients with low antibody titres. Among 12 sera from myasthenic patients in which antibodies were undetectable with the delipidated receptor as the antigen, seven were positive with the lipid-associated receptor. This lipid-associated fraction could be used beneficially for research and clinical investigation.

Acetylcholine↗