Modular Well-Fixed Hip Revision Stem Fracture: A Case Report and Literature Review.

This study presents a case of repeated prosthetic fractures in a modular hip prosthesis in a 56-year-old male patient. After the initial implantation of a modular total hip prosthesis in 2006, the patient experienced two instances of prosthetic implant fractures over seventeen years. In this study, we analyze the clinical case, explore potential underlying causes of this complication, and delve into current indications and strategies for the revision of fractured prosthesis stems.

Enrichment of DNA replication intermediates by EdU pull down.

Analysis of replication fork structures in electron microscopy (EM) can provide important mechanistic insights in DNA replication studies. A major challenge in this type of analysis is the paucity of replication intermediates. At any given time only a small fraction of the restriction fragments of genomic DNA will contain a replication fork.

Clinical outcomes and complications of S53P4 bioactive glass in chronic osteomyelitis and septic non-unions: a retrospective single-center study.

Introduction: Dead space management following debridement surgery in chronic osteomyelitis or septic non-unions is one of the most crucial and discussed steps for the success of the surgical treatment of these conditions. In this retrospective clinical study, we described the efficacy and safety profile of surgical debridement and local application of S53P4 bioactive glass (S53P4 BAG) in the treatment of bone infections.

Methods: A consecutive single-center series of 38 patients with chronic osteomyelitis (24) and septic non-unions (14), treated with bioactive glass S53P4 as dead space management following surgical debridement between May 2015 and November 2020, were identified and evaluated retrospectively.

Isolated, displaced, talar body fracture: a case report and literature review.

Talar body fractures are uncommon fractures of the foot and its management results to be very hard due to retrograde vascularization and wide articular cartilage coverage of talar surface, which could easily lead to poor functional outcomes, avascular osteonecrosis and early post traumatic arthritis. We describe a case of displaced, vertical, talar body fracture in a 41-year-old patient treated with reduction and fixation by talar anteromedial approach coupled to medial malleolar osteotomy to better expose the fracture. Our literature review has found few studies, in addition with a low level of statistical evidence.

Rehabilitative treatment of patients with COVID-19 infection: the P.A.R.M.A. evidence based clinical practice protocol.

Background: The impact of the SARS-CoV-2 on the National Health System (NHS) required a reorganization of the various levels of care, which also involved the rehabilitation reality.

Aim Of The Work: A clinical practice review of the literature was conducted to provide operational-rehabilitation guidelines adapted to the local reality and to the recent corporate reorganization in the context of the COVID-19 emergency.

Methods: A practice review of the available scientific evidence was regularly conducted from the start of the COVID-19 pandemic to periodically update the clinical practice guidelines.

Telomere damage induces internal loops that generate telomeric circles.

Extrachromosomal telomeric circles are commonly invoked as important players in telomere maintenance, but their origin has remained elusive. Using electron microscopy analysis on purified telomeres we show that, apart from known structures, telomeric repeats accumulate internal loops (i-loops) that occur in the proximity of nicks and single-stranded DNA gaps. I-loops are induced by single-stranded damage at normal telomeres and represent the majority of telomeric structures detected in ALT (Alternative Lengthening of Telomeres) tumor cells.

DNA Damage Triggers a New Phase in Neurodegeneration.

Subcellular compartmentalization contributes to the organization of a plethora of molecular events occurring within cells. This can be achieved in membraneless organelles generated through liquid-liquid phase separation (LLPS), a demixing process that separates and concentrates cellular reactions. RNA is often a critical factor in mediating LLPS.

Damage-induced lncRNAs control the DNA damage response through interaction with DDRNAs at individual double-strand breaks.

The DNA damage response (DDR) preserves genomic integrity. Small non-coding RNAs termed DDRNAs are generated at DNA double-strand breaks (DSBs) and are critical for DDR activation. Here we show that active DDRNAs specifically localize to their damaged homologous genomic sites in a transcription-dependent manner.

Recent Advancements in DNA Damage-Transcription Crosstalk and High-Resolution Mapping of DNA Breaks.

Until recently, DNA damage arising from physiological DNA metabolism was considered a detrimental by-product for cells. However, an increasing amount of evidence has shown that DNA damage could have a positive role in transcription activation. In particular, DNA damage has been detected in transcriptional elements following different stimuli.

Correction: The RSF1 Histone-Remodelling Factor Facilitates DNA Double Strand Break Repair by Recruiting Centromeric and Fanconi Anaemia Proteins.

[This corrects the article DOI: 10.1371/journal.pbio.

The RSF1 histone-remodelling factor facilitates DNA double-strand break repair by recruiting centromeric and Fanconi Anaemia proteins.

ATM is a central regulator of the cellular responses to DNA double-strand breaks (DSBs). Here we identify a biochemical interaction between ATM and RSF1 and we characterise the role of RSF1 in this response. The ATM-RSF1 interaction is dependent upon both DSBs and ATM kinase activity.

ATR-ATRIP kinase complex triggers activation of the Fanconi anemia DNA repair pathway.

ATR kinase activates the S-phase checkpoint when replication forks stall at sites of DNA damage. This event also causes phosphorylation of the Fanconi anemia (FA) protein FANCI, triggering its monoubiquitination of the key DNA repair factor FANCD2 by the FA core E3 ligase complex, thereby promoting this central pathway of DNA repair which permits replication to be restarted. However, the interplay between ATR and the FA pathway has been unclear.