Contribution of the Bioball head-neck adapter to the restoration of femoral offset in hip revision arthroplasty with retention of a well-fixed cup and stem.

Purpose: Failure to restore the femoral offset of the native hip is a potential cause of dysfunctional hip arthroplasty. The aim of this study was to report our experience of using a modular head-neck adapter in revision THA, specifically analyzing its usefulness as a tool to correct a slightly diminished femoral offset.

Materials And Methods: This was a retrospective single-center study including all hip revisions performed at our institution from January 2017 to March 2022 where the BioBall head-neck metal adapter was used.

Multiple epigenetic factors co-localize with HMGN proteins in A-compartment chromatin.

Background: Nucleosomal binding proteins, HMGN, is a family of chromatin architectural proteins that are expressed in all vertebrate nuclei. Although previous studies have discovered that HMGN proteins have important roles in gene regulation and chromatin accessibility, whether and how HMGN proteins affect higher order chromatin status remains unknown.

Results: We examined the roles that HMGN1 and HMGN2 proteins play in higher order chromatin structures in three different cell types.

H3K27ac nucleosomes facilitate HMGN localization at regulatory sites to modulate chromatin binding of transcription factors.

Nucleosomes containing acetylated H3K27 are a major epigenetic mark of active chromatin and identify cell-type specific chromatin regulatory regions which serve as binding sites for transcription factors. Here we show that the ubiquitous nucleosome binding proteins HMGN1 and HMGN2 bind preferentially to H3K27ac nucleosomes at cell-type specific chromatin regulatory regions. HMGNs bind directly to the acetylated nucleosome; the H3K27ac residue and linker DNA facilitate the preferential binding of HMGNs to the modified nucleosomes.

[Opposite Effects of Histone H1 and HMGN5 Protein on Distant Interactions in Chromatin].

Transcriptional enhancers in the cell nuclei typically interact with the target promoters over long stretches of chromatin, but the mechanism of this communication remains unknown. Previously we have developed a defined system for quantitative analysis of the rate of distant enhancer-promoter communication (EPC) and have shown that the chromatin fibers maintain efficient distant EPC . Here we investigate the roles of linker histone H1 and HMGN5 protein in EPC.

Binding of HMGN proteins to cell specific enhancers stabilizes cell identity.

The dynamic nature of the chromatin epigenetic landscape plays a key role in the establishment and maintenance of cell identity, yet the factors that affect the dynamics of the epigenome are not fully known. Here we find that the ubiquitous nucleosome binding proteins HMGN1 and HMGN2 preferentially colocalize with epigenetic marks of active chromatin, and with cell-type specific enhancers. Loss of HMGNs enhances the rate of OSKM induced reprogramming of mouse embryonic fibroblasts (MEFs) into induced pluripotent stem cells (iPSCs), and the ASCL1 induced conversion of fibroblast into neurons.