Entity

Time filter

Source Type


Pankowska E.,Institute of the Mother and Child | Blazik M.,Institute of the Mother and Child | Groele L.,Medical University of Warsaw
Diabetes Technology and Therapeutics | Year: 2012

Background: Our study examines the hypothesis that in addition to sugar starch-type diet, a fat-protein meal elevates postprandial glycemia as well, and it should be included in calculated prandial insulin dose accordingly. The goal was to determine the impact of the inclusion of fat-protein nutrients in the general algorithm for the mealtime insulin dose calculator on 6-h postprandial glycemia. Subjects and Methods: Of 26 screened type 1 diabetes patients using an insulin pump, 24 were randomly assigned to an experimental Group A and to a control Group B. Group A received dual-wave insulin boluses for their pizza dinner, consisting of 45g/180kcal of carbohydrates and 400kcal from fat-protein where the insulin dose was calculated using the following algorithm: n Carbohydrate Units×ICR+n Fat-Protein Units×ICR/6h (standard+extended insulin boluses), where ICR represents the insulin-to-carbohydrate ratio. For the control Group B, the algorithm used was n Carbohydrate Units×ICR. The glucose, C-peptide, and glucagon concentrations were evaluated before the meal and at 30, 60, 120, 240, and 360min postprandial. Results: There were no statistically significant differences involving patients' metabolic control, C-peptide, glucagon secretion, or duration of diabetes between Group A and B. In Group A the significant glucose increment occurred at 120-360min, with its maximum at 240min: 60.2 versus -3.0mg/dL (P=0.04), respectively. There were no significant differences in glucagon and C-peptide concentrations postprandial. Conclusions: A mixed meal effectively elevates postprandial glycemia after 4-6h. Dual-wave insulin bolus, in which insulin is calculated for both the carbohydrates and fat proteins, is effective in controlling postprandial glycemia. © Copyright 2012, Mary Ann Liebert, Inc. 2012. Source


Hochstenbach R.,University Utrecht | Nowakowska B.,Institute of the Mother and Child | Ummels A.,University Utrecht | Kutkowska-Kazmierczak A.,Institute of the Mother and Child | And 5 more authors.
Molecular Syndromology | Year: 2015

We present 2 cases with multiple de novo supernumerary marker chromosomes (sSMCs), each derived from a different chromosome. In a prenatal case, we found mosaicism for an sSMC(4), sSMC(6), sSMC(9), sSMC(14) and sSMC(22), while a postnatal case had an sSMC(4), sSMC(8) and an sSMC(11). SNP-marker segregation indicated that the sSMC(4) resulted from a maternal meiosis II error in the prenatal case. Segregation of short tandem repeat markers on the sSMC(8) was consistent with a maternal meiosis I error in the postnatal case. In the latter, a boy with developmental/psychomotor delay, autism, hyperactivity, speech delay, and hypotonia, the sSMC(8) was present at the highest frequency in blood. By comparison to other patients with a corresponding duplication, a minimal region of overlap for the phenotype was identified, with CHRNB3 and CHRNA6 as dosage-sensitive candidate genes. These genes encode subunits of nicotinic acetylcholine receptors (nAChRs). We propose that overproduction of these subunits leads to perturbed component stoichiometries with dominant negative effects on the function of nAChRs, as was shown by others in vitro. With the limitation that in each case only one sSMC could be studied, our findings demonstrate that different meiotic errors lead to multiple sSMCs. We relate our findings to age-related aneuploidy in female meiosis and propose that predivision sister-chromatid separation during meiosis I or II, or both, may generate multiple sSMCs. © 2015 S. Karger AG, Basel. Source

Discover hidden collaborations