Outcome of prosthesis exchange for infected knee arthroplasty: the effect of treatment approach: A systematic review of the literature

Background and purpose Two-stage revision remains the gold standard in the treatment of infected knee arthroplasty. Lately, good long-term results of direct exchange arthroplasty have been reported. The purpose of this literature review is to compare the clinical outcome achieved with one-stage revision and two-stage revision with different types of spacers

TRIM11 is overexpressed in high-grade gliomas and promotes proliferation, invasion, migration and glial tumor growth

TRIM11 (tripartite motif-containing protein 11), an E3 ubiquitin ligase, is known to be involved in the development of the central nervous system. However, very little is known regarding the role of TRIM11 in cancer biology. Here, we examined the expression profile of TRIM11, along with two stem cell markers CD133 and nestin, in multiple glioma patient specimens, glioma primary cultures derived from tumors taken at surgery, and normal neural stem/progenitor cells (NSCs). The oncogenic function of TRIM11 in glioma biology was investigated by knockdown and/or over-expression in vitro and in vivo experiments. Our results showed that TRIM11 expression levels were up-regulated in malignant glioma specimens and in high-grade glioma-derived primary cultures, while remaining low in glioblastoma multiforme (GBM) stable cell lines, low-grade glioma-derived primary cultures, and NSCs. The expression pattern of TRIM11 strongly correlated with that of CD133 and nestin, and differentiation status of malignant glioma cells. Knockdown of TRIM11 inhibited proliferation, migration and invasion of GBM cells, significantly decreased EGFR levels and MAPK activity, and down-regulated HB-EGF mRNA levels. Meanwhile, TRIM11 over-expression promoted a stem-like phenotype in vitro (tumorsphere formation) and enhanced glial tumor growth in immunocompromised mice. These findings suggest that TRIM11 might be an indicator of glioma malignancy, and has an oncogenic function mediated through the EGFR signaling pathway. TRIM11 over-expression potentially leads to a more aggressive glioma phenotype, along with increased malignant tumor growth and poor survival. Taken together, clarification of the biological function of TRIM11 and pathways it affects may provide novel therapeutic strategies for treating malignant glioma patients