We have previously identified mouse DDA3 as a p53-inducible gene. To explore the functional role of DDA3, we screened a mouse brain cDNA library by the yeast two-hybrid assay, and identified the microtubule plus-end binding protein EB3 as a DDA3-interacting protein.Binding of DDA3 to EB3 was verified by glutathione S-transferase (GST) pull-down assay and subcellular colocalization; co-immunoprecipitation further indicated that interaction of these two proteins within cells required intact microtubules. Domains of DDA3-EB3 interaction were mapped by GST pull-down assay to amino acids 118-241 and 242-329 of DDA3 and the N-and C-termini of EB3. Immunofluorescence analysis revealed colocalization of DDA3 with microtubules in various cell phases, and regions encompassing aa 118-241 and 242-329 contained microtubule-interacting and bundling activities. In vitro microtubule-binding assay showed that DDA3 and EB3 associated directly with microtubules, and cooperated with each other for microtubule binding. In addition, DDA3 bound to the EB3 interacting partner adenomatous polyposis coli 2 (APC2), a homolog of the tumor suppressor APC, which is a component of the b-catenin destruction complex. Ectopic expression of DDA3 and EB3 enhanced b-catenin-dependent transactivation and cyclin D1 production, whereas knockdown of endogenous DDA3 or EB3 inhibited b-catenin-mediated transactivation and the ability of cells to form colonies. Together, our results identify DDA3 as a novel microtubule-associated protein that binds to EB3, and implicate DDA3 and EB3 in the b-catenin-mediated growth signaling.

An endoscopic technique for removal of thalamic hematoma with the aid of stereotactic guidance, which allows precise targeting of the lesion, is reported.

OBJECT The objective of this study was to compare the incidence of degeneration and need for subsequent fusion surgery between patients who were treated nonsurgically and patients treated with fusion after a diagnosis of thoracic-or lumbar-level fracture without degenerative disease. METHODS The authors performed a retrospective study of Orthopedic United Healthcare patients diagnosed with thoracic or lumbar fracture. Patients were filtered into thoracic and lumbar fracture groups using diagnostic codes and then assigned to one of 2 treatment subgroups (fusion surgery or no surgery) on the basis of procedural codes. Disc degeneration and follow-up surgery were recorded. Chi-square statistical analysis was used. RESULTS Of 3699 patients diagnosed with a thoracic fracture, 117 (3.2%) underwent thoracic fusion and 3215 (86.9%) were treated nonsurgically. Within 3 years, 147 (4.6%) patients from the nonsurgical subgroup and fewer than 11 (0.9%–8.5%) from the fusion subgroup were diagnosed with thoracic disc degeneration. From the nonsurgical subgroup, 11 (0.3%) patients underwent a thoracic surgery related to disc degeneration compared with zero from the fusion group (p > 0.05). Of 5016 patients diagnosed with lumbar fracture, 150 (3.0%) underwent fusion and 4371 (87.1%) had no surgery. Within 3 years, 503 patients (11.5%) from the nonsurgical subgroup and 35 (23.3%) from the fusion subgroup were diagnosed with lumbar disc degeneration (p < 0.05). From the nonsurgical subgroup, 42 (1.0%) went on to have surgery related to disc degeneration, compared with fewer than 11 (0.7%–6.7%) from the fusion subgroup (values not precise due to privacy limitations). CONCLUSIONS Fusion surgery for thoracic fracture does not appear to increase the likelihood of undergoing future surgery. In the lumbar region, initial fusion surgery appears to increase the incidence of disc degeneration and could potentially necessitate future surgeries.