Leptomeningeal melanocytosis in an adult male without large congenital nevi: a rare and atypical case of neurocutaneous melanosis.

Leptomeningeal melanocytosis is a primary melanocytic lesion of the central nervous system that is characterized by diffuse melanocytic infiltration of the leptomeninges. It is seen almost exclusively in children with large congenital nevi and together the findings form a dermatologic syndrome known as neurocutaneous melanosis. We report a rare and atypical case of a 31-year-old adult male with no evident congenital melanocytic lesions who presented with neurologic symptoms and was found to have leptomeningeal melanocytosis. The brain biopsy demonstrated a conspicuous but benign-appearing melanocytic infiltrate that was discordant with the severity of the patient's symptoms. Ultimately, the patient was suspected to represent a case of former fruste neurocutaneous melanosis. Herein the relevant clinical and histopathologic features are discussed along with a brief review of the literature.

Chordoid meningioma of the third ventricle: a case report and review of the literature.

Chordoid meningioma is a rare variant of meningioma with histologic features that mimic chordoma and other chordoid neoplasms. This tumor is important to recognize, as there is a well-documented propensity for local recurrence and aggressive behavior. Most cases occur around the cerebral convexities, in locations that are similar to classical forms of meningioma. Intraventricular forms of chordoid meningioma are rare, with most reported cases arising in the lateral ventricles. We present a case of a chordoid meningioma that presented in the third ventricle of a 63-year-old female. This represents only the second documented case of a third ventricular chordoid meningioma and the first case in an adult. The distinction from other chordoid neoplasms can be challenging, particularly chordoid gliomas, which classically occur in this location. Herein, we compare and contrast chordoid meningioma with chordoid glioma and provide a review of the relevant literature.

Loss of chromosome 13 in a case of soft tissue perineurioma.

Soft tissue perineuriomas are rare mesenchymal tumors that are derived from perineurial cells of the peripheral nerve sheath. Although the histological and immunohistochemical features of soft tissue perineuriomas are well described, little is known regarding the cytogenetic abnormalities in these tumors. Herein, we describe a case of a large (12.2 cm) soft tissue perineurioma that arose in the thigh of a 26-year-old Caucasian female. Histologically, the tumor was composed of a diffuse to fascicular arrangement of spindle cells with bland, elongated nuclei with long, thin, tapering cytoplasmic processes. The immunohistochemical profile was consistent with a perineurial cell origin with expression of epithelial membrane antigen, vimentin, and collagen type IV. Cytogenetic evaluation revealed loss of chromosome 13 as the sole abnormality in the majority of examined cells. In contrast to previous reports, we were unable to demonstrate deletion or structural abnormalities of chromosome 22 by either fluorescence in situ hybridization (FISH) or metaphase cytogenetics. This is the first report of loss of chromosome 13 in soft tissue perineurioma. Although never described in this group of neoplasms, loss of chromosome 13 has been identified in a large number of other soft tissue tumors, particularly sarcomas and malignant peripheral nerve sheath tumors. Herein, we discuss this case and provide a review of the literature.

Drunken-cell footprints: nuclease treatment of ethanol-permeabilized bacteria reveals an initiation-like nucleoprotein complex in stationary phase replication origins.

The nucleoprotein complex formed on oriC, the Escherichia coli replication origin, is dynamic. During the cell cycle, high levels of the initiator DnaA and a bending protein, IHF, bind to oriC at the time of initiation of DNA replication, while binding of Fis, another bending protein, is reduced. In order to probe the structure of nucleoprotein complexes at oriC in more detail, we have developed an in situ footprinting method, termed drunken-cell footprinting, that allows enzymatic DNA modifying reagents access to intracellular nucleoprotein complexes in E.coli, after a brief exposure to ethanol. With this method, we observed in situ binding of Fis to oriC in exponentially growing cells, and binding of IHF to oriC in stationary cells, using DNase I and Bst NI endonuclease, respectively. Increased binding of DnaA to oriC in stationary phase was also noted. Because binding of DnaA and IHF results in unwinding of oriC in vitro, P1 endonuclease was used to probe for intracellular unwinding of oriC. P1 cleavage sites, localized within the 13mer unwinding region of oriC ', were dramatically enhanced in stationary phase on wild-type origins, but not on mutant versions of oriC unable to unwind. These observations suggest that most oriC copies become unwound during stationary phase, forming an initiation-like nucleoprotein complex.