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147 results on '"Gheuens J"'

1. Leaders, pioneers and followers in environmental governance

Author

Joergens, H., Knill, C., Steinebach, Y., Liefferink, J.D., Andersen, M.S., Gheuens, J., Tobin, Paul, Torney, D., Wurzel, R.K.W., Joergens, H., Knill, C., Steinebach, Y., Liefferink, J.D., Andersen, M.S., Gheuens, J., Tobin, Paul, Torney, D., and Wurzel, R.K.W.

Abstract

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Published
2023

5. Early-onset Alzheimer's disease in 2 large Belgian families

Author

Martin, J.J., Gheuens, J., Bruyland, M., Cras, P., Vandenberghe, A., Masters, C.L., Beyreuther, K., Dom, R., Ceuterick, C., Lubke, U., Van Heuverswijn, H., De Winter, G., and Van Broeckhoven, C.

Subjects
Alzheimer's disease -- Genetic aspects, Health, Psychology and mental health
Abstract

The majority of cases of Alzheimer's disease are sporadic. However, there are also numerous examples of families in which Alzheimer's disease is passed from generation to generation. While the sporadic cases of Alzheimer's disease generally begin only at an advanced age, the familial cases are usually of much earlier onset. Some researchers are returning to familial cases of Alzheimer's disease with renewed interest. The authors describe the occurrence of Alzheimer's disease as an inherited trait in two large Belgian families. In both families, the disorder seems to be passed along as an autosomal dominant trait, although mapping of the gene to a particular chromosome has not yet been accomplished for these two families. (Other research has indicated that the gene is on chromosome 21.) A total of 63 affected patients occurred in the two families, and the majority first developed symptoms of Alzheimer's disease in their thirties. While the age of onset of AD for some family members is not known, an onset as early as 26 years was observed and no onset later than age 45 has been documented. The neuropathological examination of autopsy material from the first family revealed the typical neurofibrillary tangles and senile plaques associated with Alzheimer's disease. Since the second family had a greater frequency of myoclonus and pyramidal signs, there was some suggestion that the syndrome might, in fact, be Gerstmann-Straussler-Scheinker syndrome (GSS). However, neuropathological examination of autopsy specimens from this family as well showed the typical changes of Alzheimer's disease and did not show any of the spongiform changes associated with GSS. Numerous studies of Alzheimer's disease have failed to reveal a clear understanding of the underlying genetics; some authors feel that a strong genetic component is masked simply because many people carrying the putative gene do not live long enough to express it. Conversely, studies on identical twins have demonstrated that a single gene is not sufficient to explain the clinical disease. The authors emphasize that familial Alzheimer's disease provides a unique opportunity and urge that if such families are encountered, they be studied in a careful and reliable way and that blood specimens be obtained for subsequent genetic analysis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

23. Demonstration of a novel neurofilament associated antigen with the neurofibrillary pathology of Alzheimer and related diseases

Author

Gheuens, J., Cras, P., Perry, G., Boons, J., C. C., De, Lübke, U., Mercken, M., Tabaton, Massimo, Gambetti, P. L., Vandermeeren, M., Mulvihill, P., Siedlak, S., Van Heuverswijn, H., and Martin, J. J.

Subjects
Brain Diseases, Microscopy, Staining and Labeling, analysis/metabolism, Alzheimer Disease, immunology/pathology, Antigens, analysis/metabolism, Brain Diseases, immunology/pathology, Epitopes, Humans, Immunoblotting, Immunologic Techniques, Intermediate Filaments, immunology, Microscopy, Electron, Neurofibrillary Tangles, immunology/pathology, Phosphorylation, Staining and Labeling, Immunoblotting, Intermediate Filaments, Neurofibrillary Tangles, Electron, immunology, Epitopes, Immunologic Techniques, immunology/pathology, Humans, Antigens, Phosphorylation
Published
1991

32. Earlyonset Alzheimer's disease in 2 large Belgian families

Author

Martin, J. J., Gheuens, J., Bruyland, M., Cras, P., Vandenberghe, A., Masters, C. L., Beyreuther, K., Dom, R., Ceuterick, C., Lübke, U., Van Heuverswijn, H., De Winter, G., and Van Broeckhoven, C.

Abstract

Familial Alzheimer's disease (FAD) is a dominantly inherited condition that may present with an early onset, and myoclonus occurs frequently in the course of the disease. We report clinical and neuropathologic data on 2 large Belgian families with FAD in which we obtained 17 autopsies of the CNS. In family A, each of 11 autopsies had the typical neuropathologic features of Alzheimer's disease (AD), and there were a few cerebellar plaques in the molecular layer. In family B, in addition to the typical characteristics of AD in 6 autopsies, there were numerous amyloid plaques in the cortical cerebellar layers. In both families, we immunostained the amyloid deposits for the A4 protein, and they were negative for prion-associated protein immunoreactivity.

Published
1991

34. Idiotypes and biological activity of murine monoclonal antibodies against the hemagglutinin of measles virus

Author

Gheuens, J, McFarlin, D E, Rammohan, K W, and Bellini, W J

Abstract

Three hybridomas, designated C2, V17, and B2, were produced from BALB/c mice after immunization with measles virus. All three were directed against the virus hemagglutinin (HA). The HA is a structural peptide of the virus and constitutes a major target for the host immune response during measles infection. The monoclonal anti-HA antibodies have biological functions such as (i) measles virus neutralization in vitro, (ii) binding to acutely and persistently infected cells, and (iii) inhibition of HA-mediated Rhesus monkey erythrocyte agglutination. Different idiotypes, designated HAMM-1, HAMM-2, and HAMM-3, were defined on C2, V17, and B2, respectively, by syngeneic anti-idiotype sera against those three monoclonal antibodies. A limited cross-reactivity with the HAMM-1 idiotype was detected in sera from some BALB/c mice immunized with measles virus. The anti-idiotype sera could significantly inhibit the biological functions of the HAMM-1 and HAMM-3 idiotypes bearing monoclonal anti-HA-antibodies. This suggests a possible role for auto-anti-idiotypes in the immune response after infection with measles virus.

Published
1981
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38. Value of glial fibrillary acidic protein determination in amniotic fluid for prenatal diagnosis of neural tube defects.

Author

Van Regemorter, Nicole, Gheuens, J, Noppe, M, Vamos, Elie, Seller, M J, Lowenthal, Armand, Van Regemorter, Nicole, Gheuens, J, Noppe, M, Vamos, Elie, Seller, M J, and Lowenthal, Armand

Abstract

Glial fibrillary acidic protein (GFAp), an intracellular protein specific to astrocytes of the central nervous system, was determined by 2-site immunoradiometric assay in amniotic fluid from 78 pregnancies with a normal, and 100 with an abnormal outcome. GFAp was not detectable in any of the normal pregnancies, but there were measurable, and so raised, levels in 23 out of 25 cases of anencephaly and 4 out of 7 cases of spina bifida, which therefore allowed prenatal diagnosis. GFAp was also increased in 4 of 6 cases of fetal intrauterine death, but not in other congenital malformations associated with elevated alphafetoprotein levels or abnormal acetylcholinesterase banding pattern, such as exomphalos, other gastrointestinal malformations or renal abnormalities. GFAp is therefore specific for diagnosing open neural tube defects. The determination of GFAp in amniotic fluid was slightly less efficient overall than AFP for the prenatal diagnosis of neural tube defects, but can be a useful ancillary test and has the advantage of specificity., Journal Article, Research Support, Non-U.S. Gov't, SCOPUS: ar.j, info:eu-repo/semantics/published

Published
1987

39. Genetic linkage studies suggest that Alzheimer's disease is not a single homogeneous disorder

Author

Peter St George-Hyslop, Haines, J. L., Farrer, L. A., Polinsky, R., Broeckhoven, C., Goate, A., Mclachlan, D. R. C., Orr, H., Bruni, A. C., Sorbi, S., Rainero, I., Foncin, J. -F, Pollen, D., Cantu, J. -M, Tupler, R., Voskresenskaya, N., Mayeux, R., Growdon, J., Fried, V. A., Myers, R. H., Nee, L., Backhovens, H., Martin, J. -J, Rossor, M., Owen, M. J., Mullan, M., Percy, M. E., Karlinsky, H., Rich, S., Heston, L., Montesi, M., Mortilla, M., Nacmias, N., Gusella, J. F., Hardy, J. A., Abe, K., Amaducci, L., Bergamini, L., Bruyland, M., Cappa, S., Connor, L., Winter, G., Drachman, D., Feldman, R. G., Fracarro, M., Franco, M. E., Frommelt, P., Gavrilova, S. I., Gei, G., Gheuens, J., Haynes, A., Henry, J., James, L., James, M. F., O Donnell, B., Piacentini, S., Pinessi, L., Roques, P., Ruiz, C., Swearer, J., Tanzi, R. E., Vandenberghe, A., Vartanian, M., Vaula, G., Watkins, P. C., and Williamson, R.

40. LINKAGE ANALYSIS IN ALZHEIMERS-DISEASE

Author

Christine Van Broeckhoven, Backhovens, H., Raeymaekers, P., Stinissen, P., Vancamp, G., Vanhul, W., Wehnert, A., Dewinter, G., Gheuens, J., and Vandenberghe, A.

42. Scientific Meeting of the Flemish Society of Neurology-Psychiatry held in Aalst, May 9th 1987

Author

Lenders, M.B., primary, de Wit, P., additional, Castelein, P., additional, Schuddinck, L., additional, Vanhooren, G., additional, Dehaene, I., additional, van Zandijcke, M., additional, Marchau, M., additional, De Bleecker, J., additional, de Reuck, J., additional, Vingerhoets, G., additional, Thiery, E., additional, van Calenbergh, F., additional, Dom, R., additional, Goffin, J., additional, Plets, C., additional, van den Bergh, R., additional, de Koninck, J., additional, Ceusters, W., additional, van Ooteghem, Ph., additional, Vakaet, A., additional, Claeys, G., additional, Verschraegen, J., additional, van Orshoven, M., additional, van Orshoven, F., additional, Gouban, P., additional, Carton, H., additional, Taelman, H., additional, Druyts-Voets, E., additional, De Smyter, J., additional, Picssesn, F., additional, Meyer, B., additional, van den Bergh, V., additional, Hoogenraad, T.U., additional, Triau, E., additional, Malfroid, M., additional, Baro, F., additional, Mercelis, R., additional, de Jonghe, P., additional, Gheuens, J., additional, and Martin, J.J., additional

Published
1987
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49. Absence of genetic linkage of CharcotMarieTooth disease HMSN Ia with chromosome 1 gene markers

Author

Raeymaekers, P., De Jonghe, P., Backhovens, H., Wehnert, A., De Winter, G., Swerts, L., Gheuens, J., Martin, J.-J., Vandenberghe, A., and Van Broeckhoven, C.

Abstract

We previously reported a large Charcot-Marie-Tooth family not linked to the Duffy blood group marker, supporting the existence of genetic heterogeneity in this neuropathy. In order to investigate the possibility of another disease locus on chromosome 1, we analyzed this family further, using DNA polymorphisms of 6 genes. Absence of linkage makes a second disease locus on chromosome 1 unlikely.

Published
1989

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