The presence of intracellular aggregates that contain Cu/Zn superoxide dismutase (SOD1) in spinal cord motor neurons is a pathological hallmark of amyotrophic lateral sclerosis (ALS). Although SOD1 is abundant in all cells, its half-life in motor neurons far exceeds that in any other cell type. On the basis of the premise that the long half-life of the protein increases the potential for oxidative damage, we investigated the effects of oxidation on misfolding/aggregation of SOD1 and ALS-associated SOD1 mutants. Zinc-deficient wild-type SOD1 and SOD1 mutants were extremely prone to form visible aggregates upon oxidation as compared with wild-type holo-protein. Oxidation of select histidine residues that bind metals in the active site mediates SOD1 aggregation. Our results provide a plausible model to explain the accumulation of SOD1 aggregates in motor neurons affected in ALS. ALS1 is a fatal neuromuscular disease that presents as weakness, spasticity, and muscle atrophy. The disease is caused by selective degeneration of motor neurons in the brain, brainstem, and spinal cord. Although ALS presents mostly as a sporadic disease, a familial form of ALS is seen in ϳ10% of cases. Twenty percent of familial ALS (FALS) cases are caused by point mutations in the SOD1 gene. More than 90 distinct amino acid mutations spread throughout the sequence of this 153-residue protein have been identified (1). The finding that many FALS-associated SOD1 mutants possess full specific enzyme activity (2) suggests that the disease is not caused by loss of normal dismutase activity. Further support for this idea has come from transgenic mice studies. Transgenic mice that harbor FALS-associated SOD1 mutations develop ALS-like symptoms despite having greater than normal levels of SOD1 activity, including the normal complement of endogenous mouse SOD1 enzyme (3). Furthermore, SOD1 knockout mice do not develop ALS-like symptoms. Thus, it has been proposed that mutations in SOD1 cause FALS by a gain, rather than a loss, of function (reviewed in Ref.

In soccer players with pubalgia, adductor dysfunction is a more frequent MRI finding than osteitis pubis. The findings of this study suggest that both entities are mechanically related and that osteitis pubis and adductor dysfunction frequently coexist but, because adductor dysfunction is commonly identified in the absence of osteitis, that adductor dysfunction most likely precedes the development of osteitis pubis in soccer players. The presence of edema on fat-suppressed images of the symphysis is a strong predictor of abnormality at this site in soccer players when compared with age- and sex-matched control subjects.

The secondary cleft sign demonstrated at MR imaging is a marker of groin injury in athletes presenting with groin pain.

The results of this study indicate that fixation with TightRope provides a more accurate method of syndesmotic stabilization compared with screw fixation. Syndesmotic malreduction is the most important independent predictor of clinical outcomes; therefore, care should be taken to reduce the syndesmosis accurately.

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