[Recurrent synovial chondromatosis of the tarsometatarsal joint. Case report and review of literature].

Primary synovial chondromatosis is a rare and usually monoarticular metaplasia of the synovia. It may recur, but the tendency to malignant transformation is very low. The radiological and histopathological differentiation from low grade chondrosarcoma can be difficult.

Credentialing and privileging of advanced practice nurses.

Credentialing and privileging are increasingly common administrative processes that advanced practice nurses must complete. With the intention of assuring the public of safe health care provided by qualified personnel, several federal and state organizations have developed criteria that licensed practitioners must meet. Managed care organizations are also creating credentialing and privileging guidelines for practitioners who are applying to their provider panels.

Phosphorylation of tau, Abeta-formation, and apoptosis after in vivo inhibition of PP-1 and PP-2A.

Chronic inhibition of protein phosphatases 1 and 2A in vivo was induced by infusion of okadaic acid into lateral ventricles of rat brain for up to 4 months. Cytoskeletal pathology, alterations of the amyloid precursor protein, and apoptotic cell death induced by this treatment followed a certain sequence and spatial distribution. Changes in the expression, phosphorylation, and subcellular distribution of neurofilament proteins and tau, as well as first signs of apoptotic cell death, occurred already after about 2 weeks.

Paired helical filament-like phosphorylation of tau, deposition of beta/A4-amyloid and memory impairment in rat induced by chronic inhibition of phosphatase 1 and 2A.

Alzheimer's disease is histopathologically characterized by neurofibrillary tangles, formed by the abnormally high phosphorylated tau protein, and senile plaques which largely consist of the beta/A4-amyloid peptide. Metabolism of the amyloid precursor protein and its processing into beta/A4-amyloid is regulated by protein phosphorylation. Thus, an imbalance between protein phosphorylation and dephosphorylation might be crucial for the development of the molecular hallmarks of Alzheimer's disease.