Performance comparison of two dual-head coincidence cameras of the first and latest generation.

This study compares the performance and image quality of two gamma camera based PET systems of the first and latest generation. We investigated two dual head coincidence gamma cameras (PRISM 2000XP and AXIS, manufactured in 1997 and 2001 by Picker/Philips) predominantly in accordance with the NEMA NU2-1994 and NU2-2001 protocols. All performance parameters except for spatial resolution and image quality were determined after measuring a standard cylinder over several half-life periods. Scatter and random fractions were evaluated with the sinogram technique. In order to determine spatial resolution and image quality we used phantoms as described in the NEMA NU2-2001 protocol. The efficiency of the new system was found to be increased. True count rate at activity levels used in clinical conditions is improved and scatter fraction is decreased substantially. Accordingly, improved spatial resolution and image quality were observed with the new system. Altogether, the AXIS represents a further approach to the performance of dedicated positron emission tomographs.

Antigen localization within the splenic marginal zone restores humoral immune response and IgG class switch in complement C4-deficient mice.

Defects of early complement components (C1, C4 and C2) are associated with the development of systemic lupus erythematosus (SLE). The availability of complement knockout mice has increased our knowledge on the role of complement in the regulation of adaptive immunity. An impaired removal of apoptotic bodies, a disturbed clearance of IgG immune complexes (ICs) and an insufficient B-cell regulation via complement receptors CD21/CD35 have been discussed as explanations for the induction of autoimmunity; however, a unifying hypothesis for the loss of B-cell tolerance in the absence of C1 or C4 is still lacking. Using IgM-containing ICs, we observed a significant accumulation of antigen within the splenic marginal zone (MZ) of C4-deficient mice but not in C3-deficient or complement receptors CD21/CD35-deficient mice. The targeting of antigen toward the MZ restored adaptive immunity (antibody response and class switch) in C4-deficient animals. A new explanation for the association of SLE and complement C4 deficiency would be that in the absence of C4, natural antibodies (IgM type) localize more self-antigen toward the MZ so that the auto-antibody response is increased and autoimmune disease ensues. As such, an inadequate localization of self-antigens might be responsible for the annulment of peripheral B-cell tolerance in the absence of C4.