Intraarticular masses can be classified as noninfectious synovial proliferative processes (lipoma arborescens, synovial osteochondromatosis, pigmented villonodular synovitis, rheumatoid arthritis), infectious granulomatous diseases (tuberculous arthritis, coccidioidomycosis arthritis), deposition diseases (gout, amyloid arthropathy), vascular malformations (synovial hemangioma, arteriovenous malformations), malignancies (synovial chondrosarcoma, synovial sarcoma, synovial metastases), and miscellaneous (cyclops lesion). Knowledge of articular anatomy aids the radiologist in localizing masses to the joint space. Some joints have complex anatomy with contiguous or adjacent bursae, recesses, and tendinous connections from which masses may originate or into which masses may extend. Many of the diseases causing intraarticular masses have specific imaging characteristics, especially on magnetic resonance images, and knowledge of these characteristics will allow for a more confident diagnosis.
Spontaneous dissection of the superior mesenteric artery (SMA) is a rare occurrence, especially when not associated with aortic dissection [1]. Currently, only 28 cases appear to have been reported. Due to the scarcity of cases in the literature, the natural history of isolated, spontaneous SMA dissection is unclear. CT has been reported to be useful for the initial diagnosis of SMA dissection [2-5]. We present two recent cases of spontaneous SMA dissection in which enhanced spiral CT was instrumental in following the disease process and guiding clinical decision making.
Amyloidosis is a disease complex caused by the extracellular deposition of an insoluble protein called amyloid. Amyloid arthropathy results from localized amyloid deposition in and around the joints. This article discusses the types of amyloidosis associated with amyloid arthropathy and presents their characteristic imaging findings.
Both transgenic mouse and cell culture models of familial amyotrophic lateral sclerosis (FALS) support a gain-of-function effect for the mutations in copper-zinc superoxide dismutase (CuZnSOD) associated with FALS, but the nature of the function gained remains incompletely characterized. We previously reported an enhanced peroxidase activity for FALS-associated CuZnSOD mutants. Because one of the targets of such activity is CuZnSOD itself, we examined peroxide-mediated inactivation of wild-type and mutant CuZnSODs, and found that the mutants are more readily inactivated. Inactivation of the mutants was associated with fragmentation, which did not occur in the wild-type enzyme under these conditions. Furthermore, the reduction of the FALS-associated mutants by ascorbate was enhanced markedly when compared to the wild-type enzyme. The visible spectra of the mutants showed a consistent blue shift of the peak at 680 nm in the wild-type enzyme, suggesting an alteration in copper-site geometry. These results extend previous studies demonstrating enhanced peroxidase activity in the mutants, and suggest that the toxic function that leads to motor neuron degeneration may result from a loss of specificity of the redox reactions catalyzed by CuZnSOD.
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