No abstract

To the authors' knowledge, these are the first cases of intraneural ganglia demonstrated to have a connection to the hip joint. This finding at a rare site provides further evidence for the unifying articular (synovial) theory for the formation of intraneural ganglia and reveals a shared mechanism for their propagation. Furthermore, understanding the pathogenesis of these lesions provides insight into their successful treatment and their recurrence.

Schwann cells are crucially important for peripheral nerve regeneration. These cells synthesize several factors that are supposed to enhance axonal regeneration when injured. Platelet-derived growth factor (PDGF) B-chain and its beta-receptor are expressed in Schwann cells in both normal peripheral nerves and culture. To elucidate the role of PDGF-B in peripheral nerve regeneration, we investigated its expression in cut or crush-injured rat sciatic nerves for up to 28 days. Northern blotting identified substantial increase of PDGF B-chain transcripts in injured nerves. Immunohistochemistry demonstrated that protein products of the transcripts were augmented at the distal tip of swollen axons in proximal nerve segments and in regenerating axons. Soon after both types of injury, considerable amounts of PDGF-B accumulated in numerous Schwann cells in distal segments of both models. With restoration of the axon-Schwann cell relationship in the crush model, levels of PDGF-B tended to decrease, eventually returning to normal. In the cut model in which the relationship cannot be restored, the PDGF-B was depleted to a very low level. The spatiotemporal correlation between PDGF-B and cell proliferation was very close throughout the study. These results differed strikingly from those of our previous study of rat optic nerve transection, in which PDGF-B was expressed only in a few recruited macrophages and glial cells. Augmented PDGF-B expression after sciatic nerve injury might contribute to peripheral nerve regeneration because PDGF-B is a mitogen and survival factor for Schwann cells and because it has trophic activity on neurons.

A 71-year-old man was found to have chronic lymphocytic leukemia (CLL) and diffuse large cell lymphoma (DLC) simultaneously and was diagnosed as Richter's syndrome. The CLL had mu lambda surface immunoglobulin (sIg) whereas the DLC had mu kappa sIg. However, the immunoglobulin (Ig) gene rearrangement and surface marker analysis demonstrated that both CLL and DLC had identical rearrangement patterns of the Ig heavy chain (IgH) and identical surface markers CD5+, CD19+, and CD20+. These facts imply that in this case the two malignancies are of single clonal origin initially, and that different sIg of CLL and DLC do not, therefore, necessarily indicate the biclonality of these malignancies. The origin of DLC in Richter's syndrome remains controversial. This case suggests difficulty in concluding the biclonality of these malignancies. For a conclusion on clonality to be definitive, there is a need for cloning and nucleotide sequencing of rearranged Ig genes in more patients with Richter's syndrome.

Schwann cells are crucially important for peripheral nerve regeneration. These cells synthesize several factors that are supposed to enhance axonal regeneration when injured. Platelet-derived growth factor (PDGF) B-chain and its beta-receptor are expressed in Schwann cells in both normal peripheral nerves and culture. To elucidate the role of PDGF-B in peripheral nerve regeneration, we investigated its expression in cut or crush-injured rat sciatic nerves for up to 28 days. Northern blotting identified substantial increase of PDGF B-chain transcripts in injured nerves. Immunohistochemistry demonstrated that protein products of the transcripts were augmented at the distal tip of swollen axons in proximal nerve segments and in regenerating axons. Soon after both types of injury, considerable amounts of PDGF-B accumulated in numerous Schwann cells in distal segments of both models. With restoration of the axon-Schwann cell relationship in the crush model, levels of PDGF-B tended to decrease, eventually returning to normal. In the cut model in which the relationship cannot be restored, the PDGF-B was depleted to a very low level. The spatiotemporal correlation between PDGF-B and cell proliferation was very close throughout the study. These results differed strikingly from those of our previous study of rat optic nerve transection, in which PDGF-B was expressed only in a few recruited macrophages and glial cells. Augmented PDGF-B expression after sciatic nerve injury might contribute to peripheral nerve regeneration because PDGF-B is a mitogen and survival factor for Schwann cells and because it has trophic activity on neurons.