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J Goudemand

Publications and source records attributed to J Goudemand.

At least 109 records · Page 6Linked to original sources
PubMed1981

[Histocompatibility antigens in early and late onset childhood psychoses].

Childhood psychoses could have a genetic etiology, but early and late onset psychoses have to be separated. Genetic factors are certainly implicated in the development of late onset psychoses and appear to overlap with those of adult schizophrenia. Evidence implicating genetics in early onset psychoses is likely, as twin studies have supported this hypothesis. HLA system is a particularly suitable genetic marker. We report the results of an investigation on HLA A and B antigens we have performed on 57 psychotics (30 early onset psychotics, 27 late onset psychotics). No genetic association appears in the whole population, as well as in the early and late onset psychosis series. These results have to be compared with Golse's et al. (1977, 1980), Stebbs and Magenis' (1980) and adult schizophrenia data. Further researches with population and family pedigree are required with other major histocompatibility complex markers.

Adolescent↗
PubMed1980

Erythrocyte glyoxalase I and esterase D polymorphisms in four French populations.

The genetic polymorphism of two new erythrocyte markers GLO I (EC 4.4.1.5) and esterase D (EC 3.1.1.1) has been investigated in four French populations: Basques and Toulouse groups (southwest area), Lille and Strasbourg (northern and eastern part of the territory). The distribution of GLO I and EsD alleles within these communities has shown some significant differences. Basques samples are characterized by the highest frequency of EsD1 gene (0.911) and the lower rate of GLO1 (0.364). The observed data are compared with other results previously reported in France and in Western European populations.

Electrophoresis, Starch Gel↗
PubMed1980

[Detection of platelet autoantibodies. Comparison of an antiglobulin consumption assay with a radioactive direct Coombs test (author's transl)].

131 patients (124 with idiopathic thrombocytopenic purpura) have been investigated for platelet autoantibodies with an antiglobulin consumption assay (ACA) and a direct Coombs test (DCT) using 125I-antiglobulin. The two assays have been simultaneously performed on 165 platelet-suspensions. The results of ACA (expressed as normal or abnormal amounts of platelet bound IgG or PBlgG) and those of DCT (expressed as positive or negative) were concordant in 128 out of 165 cases (77.6 per cent). In 37 of 165 cases (22.4 per cent) the DCT was negative while PBgG was found to be slightly elevated with ACA. There was a significant correlation (r = 0.44) between PBlgG levels and radioactivity index calculated in DCT. The relationship between these data was graphically expressed as a curve constructed on semilog paper meaning that PBlgG levels corresponding to high radioactivity index were more uncertain than those corresponding to lower index. The quantitative expression of DCT would be improved by refering the results to a standard curve and not only to normal platelets. In the case, results of DCT would be probably equivalent to those of ACA.

Autoantibodies↗
PubMed1979

[Monoclonal myelomatous IgA with antilipoprotein antibody activity of Ra specificity (author's transl)].

Investigations performed in a patient with myeloma, hyperlipidemia, and xanthomatosis demonstrated the antilipoprotein activity of the monoclonal IgA directed against an antigenic site--called Ra.--different from those previously described. A complex IgA beta-lipoprotein has been firstly characterized. After isolation and purification of the IgA, it has been shown that the association between IgA and lipoprotein was immunologically mediated. The antibody is an IgA lambda bound via its Fab portion and in fixed combining ratio to an antigenic determinant shared only by LDL and VLDL of humans and some other mammalians to the exclusion of any other serum proteins. The results obtained with passive hemagglutination and inhibition of hemagglutination suggest that the antigenic site Ra. is not located on apoprotein B (major proteic moiety of LDL and VLDL), since the antigenic determinants of apolipoproteins are different in humans and in animals and since IgA Ra. fails to react with apolipoprotein B obtained by delipidation of LDL. On the other hand, the lack of reaction between IgA Ra. and HDL suggests that the antigenic determinant is not only present on the lipid hapten such as in the case of PG and AS determinants which are located on VLDL, LDL, and HDL from humans and animals. So the antigenic determinant revealed by IgA Ra. seems to be different from those previously described.

Antibodies, Neoplasm↗
PubMed1979

[Detection of platelet antibodies in idiopathic thrombocytopenic purpura (author's transl)].

The amount of IgG present on the surface of platelets (platelet-bound IgG, or PBIgG) was measured using a quantitative antiglobulin consumption assay developed by Dixon et al. (1975). Normal platelets or platelets from patients with thrombocytopenia due to a decreased production had less than 10 X 10(-15) g of IgG/platelet. Studied were 364 blood samples drawn from 196 patients; 173 patients had idiopathic thrombocytopenic purpura; 65 (93 %) of 70 in the acute phase of their disease had elevated PBIgG (values up to 100 times greater than the normal); 98 (76.5 %) of 128 blood samples from patients during a chronic phase had abnormally high PBIgG but the levels of IgG were generally lower than those observed in the acute phase; 75 (75 %) of 100 samples from patients in remission did not have pathologically increased PBIgG. Usually when the platelet count improved (after prednisone therapy or after splenectomy), PBIgG decreased. The PBIgG determination was not useful for predicting the response to prednisone therapy or the further evolution of the disease, except when PGIgG remained elevated after high-dose prednisone therapy; this generally implied a poor prognosis. PBIgG have also been found elevated in other diseases such as lupus erythematosus and in one case of chronic lymphocytic leukemia. This assay may be of a great clinical interest, especially for the diagnosis of ITP.

Antibodies↗
PubMed1978

[Investigation of circulating immune complexes in some diseases associated with a platelets hyperdestruction process (author's transl)].

A possible relationship between the presence of circulating immune complexes (CIC) and the platelet-bound IgG levels was investigated in 38 patients with some diseases associated with a no drug-related platelets hyperdestruction process of which 33 had idiopathic thrombopenic purpura (ITP). By using the 125I-C1q binding test, these CIC were only detected in 4 of the 42 tested sera. No correlation was noticed between the percentage of C1q binding and the platelet IgG levels evaluated by the quantitative hemolysis inhibition test. These results do not allow to consider the involvement of CIC in the thrombocytopenia genesis observed in these diseases.

Adolescent↗
PubMed1977

[HLA antigen and Willebrand's disease (author's transl)].

The frequency of HLA antigens was determined in 28 unrelated patients with Willebrand's disease and in 326 healthy controls. There was no significant difference between the two groups for any of the HLA antigens tested. Segregation analysis processed among the families of 26 of these patients didn't allow us to find any disorder of the HLA antigens distribution in the patient's group: transmission of the disease and transmission of the HLA haplotypes appear to be independant in 25 of 26 families studied. There is no linkage and no association between the Willebrand's disease genes and the HLA system genes.

HLA Antigens↗
PubMed1977

HLA antigens and atopic dermatitis.

The frequency of HLA antigens was determined in 27 unrelated children and 44 of their parents, compared to 326 healthy controls. HLA-BW35 frequency is significantly increased in the patients (37 instead of 11.6%; Pc less than 0.01) and in the parents (34 instead of 11.6%; Pc less than 0.05). However HLA segregation was not disturbed in 23 families with 33 patients and 24 healthy siblings. These data confirm the hereditary character of atopy but does not allow the exclusion of the hypothesis of a linkage between a HLA-B gene and an Ir gene conditioning abnormal humoral response to several allergens.

Asthma↗
PubMed1976

[Attempt to treat a case of chronic familial granulomatous disease by allogenic bone marrow transplantation].

A bone marrow graft was performed in a 3 1/2 year old boy suffering from chronic granulomatous disease. Donor-recipient matching was complete in the ABO, HL-A and M.L.C. systems. The number of injected cells amounted to 5.4 X 10(9) (3.6 X 10(8) cells/kg body weight). The immunosuppression regimen consisted of cyclophosphamide and A.L.S. before the graft, and methotrexate after it. Neither graft versus host reaction, nor secondary infection developed. The take of the graft was monitored by the Gm allotypes. Rejection, however, occurred after 2 months.

Adolescent↗