13 research outputs found
Investigation of the possibility of improving spatial resolution in SPECT with the combination of LaBr3:Ce-based detector and 3D-OSEM reconstruction algorithms
This study investigates the potential of improving spatial resolution in SPECT imaging using a combination of LaBr(3):Ce detectors and 3D-OSEM image reconstruction algorithms. Potential spatial resolution improvement was assessed intrinsically and extrinsically using GATE Monte Carlo simulation. Significantly improved MTF of LaBr(3):Ce detectors suggests better resolution performance at all spatial frequencies. In comparison to conventional Nal(Tl) scintillators, a combination of the LaBr(3):Ce crystal and 3D-OSEM incorporating resolution recovery could significantly improve the extrinsic spatial resolution of SPECT images. (C) 2010 Elsevier B.V. All rights reserved
Evaluation of the hepatoprotective, anti-inflammatory, antinociceptive and antiepileptic activities of Chrysanthemum trifurcatum
Species conservation importance index (SCI) for comparing sites’ conservation value at landscape level
Automatic Thalamus Segmentation on Unenhanced 3D T1 Weighted Images: Comparison of Publicly Available Segmentation Methods in a Pediatric Population
Large deletions and point mutations involving the dedicator of cytokinesis 8 (DOCK8) in the autosomal-recessive form of hyper-IgE syndrome
International audienceBackground: The genetic etiologies of the hyper-IgE syndromes are diverse. Approximately 60% to 70% of patients with hyper-IgE syndrome have dominant mutations in STAT3, and a single patient was reported to have a homozygous TYK2 mutation. In the remaining patients with hyper-IgE syndrome, the genetic etiology has not yet been identified. Objectives: We aimed to identify a gene that is mutated or deleted in autosomal recessive hyper-IgE syndrome. Methods: We performed genome-wide single nucleotide polymorphism analysis for 9 patients with autosomal-recessive hyper-IgE syndrome to locate copy number variations and homozygous haplotypes. Homozygosity mapping was performed with 12 patients from 7 additional families. The candidate gene was analyzed by genomic and cDNA sequencing to identify causative alleles in a total of 27 patients with autosomal-recessive hyper-IgE syndrome. Results: Subtelomeric biallelic microdeletions were identified in 5 patients at the terminus of chromosome 9p. In all 5 patients, the deleted interval involved dedicator of cytokinesis 8 (DOCK8), encoding a protein implicated in the regulation of the actin cytoskeleton. Sequencing of patients without large deletions revealed 16 patients from 9 unrelated families with distinct homozygous mutations in DOCK8 causing premature termination, frameshift, splice site disruption, and single exon deletions and microdeletions. DOCK8 deficiency was associated with impaired activation of CD4(+) and CD8(+)T cells. Conclusion: Autosomal-recessive mutations in DOCK8 are responsible for many, although not all, cases of wautosomal-recessive hyper-IgE syndrome. DOCK8 disruption is associated with a phenotype of severe cellular immunodeficiency characterized by susceptibility to viral infections, atopic eczema, defective T-cell activation and T(H)17 cell differentiation, and impaired eosinophil homeostasis and dysregulation of IgE. (J Allergy Clin Immunol 2009;124:1289-302.
Structure and properties of polydiacetylene-containing peptide amphiphile fibres
Contains fulltext :
83167.pdf (publisher's version ) (Open Access)Radboud Universiteit Nijmegen, 10 februari 2011Promotor : Hest, J.C.M. van
Co-promotor : Lowik, D.W.P.M.184 p