High-resolution, high sensitivity detectors for molecular imaging with radionuclides: The coded aperture option RID F-8402-2011

Molecular imaging with radionuclides is a very sensitive technique because it allows to obtain images with nanomolar or picomolar concentrations. This has generated a rapid growth of interest in radionuclide imaging of small animals. Indeed radiolabeling of small molecules, antibodies, peptides and probes for gene expression enables molecular imaging in vivo, but only if a suitable imaging system is used. Detecting small tumors in humans is another important application of such techniques. In single gamma imaging, there is always a well known tradeoff between spatial resolution and sensitivity due to unavoidable collimation requirements. Limitation of the sensitivity due to collimation is well known and affects the performance of imaging systems, especially if only radiopharmaceuticals with limited uptake are available. In many cases coded aperture collimation can provide a solution, if the near field artifact effect can be eliminated or limited. At least this is the case for "small volumes" imaging, involving small animals. In this paper 3D-laminography simulations and preliminary measurements with coded aperture collimation are presented. Different masks have been designed for different applications showing the advantages of the technique in terms of sensitivity and spatial resolution. The limitations of the technique are also discussed. (c) 2006 Elsevier B.V. All rights reserved

An interferon-β-resistant and NLRP3 inflammasome–independent subtype of EAE with neuronal damage

Inflammation induced by innate immunity influences the development of T cell-mediated autoimmunity in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). We found that strong activation of innate immunity induced Nod-like receptor protein 3 (NLRP3) inflammasome-independent and interferon-β (IFNβ)-resistant EAE (termed type B EAE), whereas EAE induced by weak activation of innate immunity requires the NLRP3 inflammasome and is sensitive to IFNβ treatment. Instead, an alternative inflammatory mechanism, including membrane-bound lymphotoxin-β receptor (LTβR) and CXC chemokine receptor 2 (CXCR2), is involved in type B EAE development, and type B EAE is ameliorated by antagonizing these receptors. Relative expression of Ltbr and Cxcr2 genes was indeed enhanced in patients with IFNβ-resistant multiple sclerosis. Remission was minimal in type B EAE due to neuronal damages induced by semaphorin 6B upregulation on CD4+ T cells. Our data reveal a new inflammatory mechanism by which an IFNβ-resistant EAE subtype develops