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Several studies have suggested that infectious agents may induce the development of abdominal aortic aneurysms and/or accelerate their progression. The aim of this study was to evaluate the presence of the respiratory-transmitted viruses such as influenza A and B and parainfluenza type 1 genomes in bioptic fragments of abdominal aortic aneurysms. Furthermore, the association between viral infection and traditional risk factors for aneurysms was investigated employing multivariate logistic regression models. The genome of parainfluenza 1 was detected in 11 out of 57 patients with abdominal aortic aneurysm, influenza A only in one, whereas none of the specimens analyzed resulted positive for influenza B. After adjustment of age, gender, and clinical diagnosis, being current smokers was associated independently with parainfluenza 1 detection in aneurysms. The identification of parainfluenza 1 in aortic aneurysm biopsies supports previous observations of a possible role of viruses in the lesion development. Smoking, by interfering with the respiratory tract's ability to defend itself and predisposing to upper and lower respiratory tract infections may accelerate the onset and progression of abdominal aortic aneurysms., (Copyright © 2012 Wiley Periodicals, Inc.)

Objective: To concurrently investigate with magnetic resonance (MR) the brain activation and regional brain atrophy in patients with Huntington disease (HD)., Methods: Nine symptomatic HD patients and 11 healthy subjects underwent an MR study including functional MR acquisition during finger tapping of the right hand and high-resolution T1-weighted images. Functional and structural data were analyzed using Statistical Parametric Mapping 2 software., Results: As compared with control subjects, HD patients showed decreased activation in the left caudate nucleus and medial frontal and anterior cingulate gyri and increased activation in the right supplementary motor area and supramarginal gyrus and left intraparietal sulcus. The pattern of atrophy included thinning of the gray matter (GM) in the insula, inferior frontal gyrus, caudate, lentiform nucleus, and thalamus, bilaterally, in the left middle frontal, middle occipital, and middle temporal gyri, and of periventricular, subinsular, right temporal lobe, and left internal capsule white matter. Only the decreased activation in the caudate nucleus correlated topographically with the caudate GM loss., Conclusion: The cortical areas of functional changes do not correspond to those of GM atrophy in patients with HD and are likely to reflect decreased output of the motor basal ganglia-thalamo-cortical circuit and compensatory recruitment of accessory motor pathways.