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12 results on '"Reeser, H."'

2. Efficacy and Safety of Oxandrolone in Growth Hormone-Treated Girls with Turner Syndrome

Author

Menke, Leonie A., Sas, Theo C. J., de Muinck Keizer-Schrama, Sabine M. P. F., Zandwijken, Gladys R. J., de Ridder, Maria A. J., Odink, Roelof J., Jansen, Maarten, Delemarre-van de Waal, Henriëtte A., Stokvis-Brantsma, Wilhelmina H., Waelkens, Johan J., Westerlaken, Ciska, Reeser, H. Maarten, van Trotsenburg, A. S. Paul, Gevers, Evelien F., van Buuren, Stef, DeJonckere, Philippe H., Hokken-Koelega, Anita C. S., Otten, Barto J., and Wit, Jan M.

Published
2010

9. Does the Risk of Childhood Diabetes Mellitus Require Revision of the Guideline Values for Nitrate in Drinking Water?

Author

van Maanen, Jan M.S., Albering, Harma J., de Kok, Theo M.C.M., van Breda, Simone G.J., Curfs, Danielle M.J., Vermeer, Ingrid T.M., Ambergen, Anton W., Wolffenbuttel, Bruce H.R., Kleinjans, Jos C.S., and Reeser, H. Maarten

Abstract

In recent years, several studies have addressed a possible relationship between nitrate exposure and childhood type 1 insulin-dependent diabetes mellitus. The present ecologic study describes a possible relation between the [...]

Published
2000

10. GAD65 antigen therapy in recently diagnosed type 1 diabetes mellitus

Author

Ludvigsson, Johnny, Krisky, David, Casas, Rosaura, Battelino, Tadej, Castaño, Luis, Greening, James, Kordonouri, Olga, Otonkoski, Timo, Pozzilli, Paolo, Robert, Jean-Jacques, Veeze, Henk J., Palmer, Jerry, Samuelsson, Ulf, Elding Larsson, Helena, Åman, Jan, Kärdell, Gunilla, Neiderud, Jan, Lundström, Göran, Albinsson, Eva, Carlsson, Annelie, Nordvall, Maria, Fors, Hans, Arvidsson, Carl-Göran, Edvardson, Stig, Hanås, Ragnar, Larsson, Karin, Rathsman, Björn, Forsgren, Henrik, Desaix, Helena, Forsander, Gun, Nilsson, Nils-Östen, Åkesson, Carl-Göran, Keskinen, Päivi, Veijola, Riitta, Talvitie, Timo, Raile, Klemens, Kapellen, Thomas, Burger, Walter, Neu, Andreas, Engelsberger, Ilse, Heidtmann, Bettina, Bechtold, Suzanne, Leslie, David, Chiarelli, Francesco, Cicognani, Alesandro, Chiumello, Giuseppe, Cerutti, Franco, Zuccotti, Gian Vincenzo, Gomez Gila, Ana, Rica, Itxaso, Barrio, Raquel, Clemente, Maria, López Garcia, Maria José, Rodriguez, Mercedes, Gonzalez, Isabel, Lopez, Juan Pedro, Oyarzabal, Mirentxu, Reeser, H M, Nuboer, Roos, Stouthart, Pauline, Bratina, Natasa, Bratanic, Nina, de Kerdanet, Marc, Weill, Jacques, Ser, Nicole, Barat, Pascal, Bertrand, Anne Marie, Carel, Jean-Claude, Reynaud, Rachel, Coutant, Regis, Baron, Sabine, Ludvigsson, Johnny, Krisky, David, Casas, Rosaura, Battelino, Tadej, Castaño, Luis, Greening, James, Kordonouri, Olga, Otonkoski, Timo, Pozzilli, Paolo, Robert, Jean-Jacques, Veeze, Henk J., Palmer, Jerry, Samuelsson, Ulf, Elding Larsson, Helena, Åman, Jan, Kärdell, Gunilla, Neiderud, Jan, Lundström, Göran, Albinsson, Eva, Carlsson, Annelie, Nordvall, Maria, Fors, Hans, Arvidsson, Carl-Göran, Edvardson, Stig, Hanås, Ragnar, Larsson, Karin, Rathsman, Björn, Forsgren, Henrik, Desaix, Helena, Forsander, Gun, Nilsson, Nils-Östen, Åkesson, Carl-Göran, Keskinen, Päivi, Veijola, Riitta, Talvitie, Timo, Raile, Klemens, Kapellen, Thomas, Burger, Walter, Neu, Andreas, Engelsberger, Ilse, Heidtmann, Bettina, Bechtold, Suzanne, Leslie, David, Chiarelli, Francesco, Cicognani, Alesandro, Chiumello, Giuseppe, Cerutti, Franco, Zuccotti, Gian Vincenzo, Gomez Gila, Ana, Rica, Itxaso, Barrio, Raquel, Clemente, Maria, López Garcia, Maria José, Rodriguez, Mercedes, Gonzalez, Isabel, Lopez, Juan Pedro, Oyarzabal, Mirentxu, Reeser, H M, Nuboer, Roos, Stouthart, Pauline, Bratina, Natasa, Bratanic, Nina, de Kerdanet, Marc, Weill, Jacques, Ser, Nicole, Barat, Pascal, Bertrand, Anne Marie, Carel, Jean-Claude, Reynaud, Rachel, Coutant, Regis, and Baron, Sabine

Abstract

BACKGROUND: The 65-kD isoform of glutamic acid decarboxylase (GAD65) is a major autoantigen in type 1 diabetes. We hypothesized that alum-formulated GAD65 (GAD-alum) can preserve beta-cell function in patients with recent-onset type 1 diabetes. METHODS: We studied 334 patients, 10 to 20 years of age, with type 1 diabetes, fasting C-peptide levels of more than 0.3 ng per milliliter (0.1 nmol per liter), and detectable serum GAD65 autoantibodies. Within 3 months after diagnosis, patients were randomly assigned to receive one of three study treatments: four doses of GAD-alum, two doses of GAD-alum followed by two doses of placebo, or four doses of placebo. The primary outcome was the change in the stimulated serum C-peptide level (after a mixed-meal tolerance test) between the baseline visit and the 15-month visit. Secondary outcomes included the glycated hemoglobin level, mean daily insulin dose, rate of hypoglycemia, and fasting and maximum stimulated C-peptide levels. RESULTS: The stimulated C-peptide level declined to a similar degree in all study groups, and the primary outcome at 15 months did not differ significantly between the combined active-drug groups and the placebo group (P=0.10). The use of GAD-alum as compared with placebo did not affect the insulin dose, glycated hemoglobin level, or hypoglycemia rate. Adverse events were infrequent and mild in the three groups, with no significant differences. CONCLUSIONS: Treatment with GAD-alum did not significantly reduce the loss of stimulated C peptide or improve clinical outcomes over a 15-month period., Funding Agencies|Diamyd Medical||Swedish Child Diabetes Foundation (Barndiabetesfonden)

Published
2012
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11. Yearly stepwise increments of the growth hormone dose results in a better growth response after four years in girls with Turner syndrome. Dutch Working Group on Growth Hormone.

Author

van Teunenbroek, A, primary, de Muinck Keizer-Schrama, S M, additional, Stijnen, T, additional, Jansen, M, additional, Otten, B J, additional, Delemarre-van de Waal, H A, additional, Vulsma, T, additional, Wit, J M, additional, Rouwé, C W, additional, Reeser, H M, additional, Gosen, J J, additional, Rongen-Westerlaken, C, additional, and Drop, S L, additional

Published
1996
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12. Extending the phenotype of recurrent rearrangements of 16p11.2: deletions in mentally retarded patients without autism and in normal individuals.

Author

Bijlsma EK, Gijsbers AC, Schuurs-Hoeijmakers JH, van Haeringen A, Fransen van de Putte DE, Anderlid BM, Lundin J, Lapunzina P, Pérez Jurado LA, Delle Chiaie B, Loeys B, Menten B, Oostra A, Verhelst H, Amor DJ, Bruno DL, van Essen AJ, Hordijk R, Sikkema-Raddatz B, Verbruggen KT, Jongmans MC, Pfundt R, Reeser HM, Breuning MH, and Ruivenkamp CA

Subjects
Abnormalities, Multiple, Adolescent, Adult, Child, Child, Preschool, Comparative Genomic Hybridization, DNA Mutational Analysis, Family Health, Female, Genetic Testing, Humans, Infant, Learning Disabilities, Male, Speech Disorders, Young Adult, Autistic Disorder genetics, Chromosome Deletion, Chromosomes, Human, Pair 16, Intellectual Disability genetics
Abstract

Array CGH (comparative genomic hybridization) screening of large patient cohorts with mental retardation and/or multiple congenital anomalies (MR/MCA) has led to the identification of a number of new microdeletion and microduplication syndromes. Recently, a recurrent copy number variant (CNV) at chromosome 16p11.2 was reported to occur in up to 1% of autistic patients in three large autism studies. In the screening of 4284 patients with MR/MCA with various array platforms, we detected 22 individuals (14 index patients and 8 family members) with deletions in 16p11.2, which are genomically identical to those identified in the autism studies. Though some patients shared a facial resemblance and a tendency to overweight, there was no evidence for a recognizable phenotype. Autism was not the presenting feature in our series. The assembled evidence indicates that recurrent 16p11.2 deletions are associated with variable clinical outcome, most likely arising from haploinsufficiency of one or more genes. The phenotypical spectrum ranges from MR and/or MCA, autism, learning and speech problems, to a normal phenotype.

Published
2009
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