Inaugurating a Dutch Napoleon? Conservative criticism of the 1815 constitution of the United Kingdom of The Netherlands

International audienc

Changes in thyroid hormone state in children receiving chemotherapy

Objective The concentrations of thyroid function determinants may change during severe illness. Our goal was to quantify their changes in children with cancer during chemotherapy, and to correlate them to clinical condition and type of drugs. Design During a 3-month period all patients admitted for chemotherapy to the paediatric oncology ward were evaluated for inclusion. Patients with brain tumours, neuroblastoma (cranio)spinal irradiation and use of dexamethasone before the first blood sample were excluded. Measurements Plasma concentrations of T4, T3, rT3, thyroxine-binding globulin (TBG), thyroglobulin (Tg), TSH, IGF-1, cortisol, PRL and physical well-being by means of questionnaires were measured before and during chemotherapy. Results In 19 children, 46 courses of chemotherapy and 123 plasma samples were analysed. During chemotherapy, mean concentrations of TSH, T3, Tg and cortisol decreased to 53, 67, 69 and 15% of the baseline value, respectively. Mean plasma rT3 increased to 217% of baseline. In 87% of all courses, one or more thyroid parameter(s) was aberrant. Furthermore, in 23 samples (19%) from 10 patients (53%), the concentration of IGF-1 was below the reference value (adjusted for sex and age). Small changes were seen in scores for clinical condition but none was related to a change in thyroid function determinant. Most changes in thyroid hormones could be attributed to using dexamethasone. Conclusions These results demonstrate that, in children, thyroid hormone state changes significantly during chemotherapy, apparently not related to physical well-being but to the drugs administered. Future investigations should focus on the impact for patient care and possibilities of (preventive) interventio

Optosensoric based on amorphous and porous silicon

Stiebig H, Thonissen M, Kruger M, et al. Optosensoric based on amorphous and porous silicon. tm - Technisches Messen. 1997;64(4):136-142.Amorphous silicon (a-Si:H) and porous silicon (PS) allow the realization of novel optoelectronic devices based on silicon. Both in common is the low cost fabrication process and the integration possibility with silicon technology. Whereas the optoelectronic properties of a-Si:H can be adjusted by the process gas of the plasma enhanced chemical vapour deposition (PECVD) process, the refractive index of PS can be varied by the etching parameters. Amorphous silicon multi-layers optimized with regard to the bandgap and mu tau-(carrier mobility x lifetime) product can be used as color detectors. Changing the applied voltage of the sensor leads to a shift of the maximum of the response front blue, green to red. In this way, a single detector generates sequentially a RGB-signal without the need of optical filters. Three color detectors employed as two terminal devices are based on pin or nipin layer structures. They exhibit a good linearity and a dynamic range of more than 90 dB. The refractive index of PS depends strongly on ifs porosity and microstructure. These quantities can easily be controlled by the anodization current density applied during the formation process. Stacks of layers with different refractive indices can be formed by modulating the anodization current density. These effects allow the realization of passive optical components like interference filters, rugate filters, antireflectance coatings, waveguides, and diffraction gratings

Non-Syndromic Cleft Lip with or without Cleft Palate: Genome-Wide Association Study in Europeans Identifies a Suggestive Risk Locus at 16p12.1 and Supports SH3PXD2A as a Clefting Susceptibility Gene

Contains fulltext : 215284.pdf (publisher's version ) (Open Access)Non-syndromic cleft lip with or without cleft palate (nsCL/P) ranks among the most common human congenital malformations, and has a multifactorial background in which both exogenous and genetic risk factors act in concert. The present report describes a genome-wide association study (GWAS) involving a total of 285 nsCL/P patients and 1212 controls from the Netherlands and Belgium. Twenty of the 40 previously reported nsC/LP susceptibility loci were replicated, which underlined the validity of this sample. SNV-based analysis of the data identified an as yet unreported suggestive locus at chromosome 16p12.1 (p-value of the lead SNV: 4.17 x 10(-7)). This association was replicated in two of three patient/control replication series (Central European and Yemeni). Gene analysis of the GWAS data prioritized SH3PXD2A at chromosome 10q24.33 as a candidate gene for nsCL/P. To date, support for this gene as a cleft gene has been restricted to data from zebrafish and a knockout mouse model. The present GWAS was the first to implicate SH3PXD2A in non-syndromic cleft formation in humans. In summary, although performed in a relatively small sample, the present GWAS generated novel insights into nsCL/P etiology

Non-Syndromic Cleft Lip with or without Cleft Palate:Genome-Wide Association Study in Europeans Identifies a Suggestive Risk Locus at 16p12.1 and Supports SH3PXD2A as a Clefting Susceptibility Gene

Non-syndromic cleft lip with or without cleft palate (nsCL/P) ranks among the most common human congenital malformations, and has a multifactorial background in which both exogenous and genetic risk factors act in concert. The present report describes a genome-wide association study (GWAS) involving a total of 285 nsCL/P patients and 1212 controls from the Netherlands and Belgium. Twenty of the 40 previously reported nsC/LP susceptibility loci were replicated, which underlined the validity of this sample. SNV-based analysis of the data identified an as yet unreported suggestive locus at chromosome 16p12.1 (p-value of the lead SNV: 4.17 × 10−7). This association was replicated in two of three patient/control replication series (Central European and Yemeni). Gene analysis of the GWAS data prioritized SH3PXD2A at chromosome 10q24.33 as a candidate gene for nsCL/P. To date, support for this gene as a cleft gene has been restricted to data from zebrafish and a knockout mouse model. The present GWAS was the first to implicate SH3PXD2A in non-syndromic cleft formation in humans. In summary, although performed in a relatively small sample, the present GWAS generated novel insights into nsCL/P etiology

Novel IRF6 Mutations Detected in Orofacial Cleft Patients by Targeted Massively Parallel Sequencing

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Novel mutations in LRP6 highlight the role of WNT signaling in tooth agenesis

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