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Many surgical approaches have been described for hip hemiarthroplasty (HHA) treating femur neck fractures (FNFs). Direct lateral approach (DLA) is one of the most used. Today, the direct anterior approach (DAA) has become very attractive, but it seems to involve more intra-operative fractures. Our main endpoint was to demonstrate that the DAA may be a valid alternative comparing to the DLA.Patients affected by FNFs and treated with HHA between the years 2016 and 2020 were studied. We divided the treatment of the fractures according to the surgical approach. The analysis was focused on perioperative complications and radiological outcomes.There were a total of 166 patients. The DLA group included patients with an average age of 83.5 years and the DAA group of 83 years. We found similar surgical times (DLA 67 min vs DAA 61 min; p = 0,55), number of transfusions (DLA 3/person vs DAA 4/person; p = 0,91), perioperative complications (fractures: DLA 0 vs DAA 0 - dislocations: DLA 2,50% vs DAA 0) and functional outcomes (HHS: DLA 83 points vs DAA 87 points; p = 0,71). There were no statistical differences comparing diaphyseal filling (Canal Fill Index at the proximal third: DLA 0,79 vs DAA 0,78; p= 0,24), bone loss (Paprosky I: DLA 96,25% vs DAA 91,86%; p = 0,47) and prevalence of heterotopic ossification (Broker low degree: DLA 93,75% vs 95, 34%; p = 0,87).Analysing perioperative complications and studying post-operative radiographic evolution, our results suggest that the DAA is a valid alternative to the DLA in HHA treating FNFs.

Highlights:\ud \ud • NMN deamidase delays Wallerian degeneration in vivo in mice and zebrafish\ud \ud • NMN deamidase reduces NMN accumulation in transected nerves\ud \ud • NMN deamidase protects axons against non-injury insults\ud \ud • NMN deamidase rescues axonal defects and lethality in NMNAT2-deficient mice.\ud \ud Summary:\ud \ud Axons require the axonal NAD-synthesizing enzyme NMNAT2 to survive. Injury or genetically induced depletion of NMNAT2 triggers axonal degeneration or defective axon growth. We have previously proposed that axonal NMNAT2 primarily promotes axon survival by maintaining low levels of its substrate NMN rather than generating NAD; however, this is still debated. NMN deamidase, a bacterial enzyme, shares NMN-consuming activity with NMNAT2, but not NAD-synthesizing activity, and it delays axon degeneration in primary neuronal cultures. Here we show that NMN deamidase can also delay axon degeneration in zebrafish larvae and in transgenic mice. Like overexpressed NMNATs, NMN deamidase reduces NMN accumulation in injured mouse sciatic nerves and preserves some axons for up to three weeks, even when expressed at a low level. Remarkably, NMN deamidase also rescues axonal outgrowth and perinatal lethality in a dose-dependent manner in mice lacking NMNAT2. These data further support a pro-degenerative effect of accumulating NMN in axons in vivo. The NMN deamidase mouse will be an important tool to further probe the mechanisms underlying Wallerian degeneration and its prevention.

Hyaloglide® is a hyaluronan-based gel based on a novel auto-crosslinked technology designed to reduce postsurgical adhesions. Its efficacy was assessed in a multicentred randomized controlled trial comparing the results of flexor tenolysis in zone 2 following failed flexor tendon repairs. In the control group a standard release was performed. In the treated group, Hyaloglide® was applied into the flexor sheath and around the site of tenolysis. Forty-five patients, 19 controls and 26 treated with Hyaloglide®, were enrolled in 13 centres. All the patients were evaluated at 30, 60, 90 and 180 days after surgery by testing Total Active Motion, Quick-DASH questionnaire and number of working days lost after surgery. Patients in the Hyaloglide® group had a statistically better recovery of finger motion at all time intervals and returned earlier to work and daily activities. The use of Hyaloglide® did not appear to increase the complication rate.