BACKGROUND: Unstable cases of Hangman’s fracture or traumatic spondylilisthesis which are type II, IIa and III should be treated surgicaly. Retropharyngeal approach was employed in exposure of anterior upper cervical region. However, dissection and traction around important structures make the procedure complicated and increase the chance of nerve injury.
OBJECTIVE:To evaluate the clinical curative effect and safety of an innovative operative technique in which a polyetheretherketone cage was used to perform cervical spinal fusion for the treatment of Hangman’s fracture.
METHODS: Eight patients with type II or IIa Hangman’s fracture were enroled in this study and received cervical fusions at C2/3 levels. During folow-up postoperatively, they received X-ray examination. Fusion time and implant position were evaluated. The angle of deformity (α) and the displacement distance (β) were compared pre-operatively and 6-month post-operatively to measure reduction. The functional outcomes were also compared using the Post-Traumatic Neck Score (Mayo) pre-operatively and 6-month post-operatively, while neck pain was further investigated by Visual Analogue Scale score.
RESULTS AND CONCLUSION:Al eight patients were folowed-up successfuly, with an average folow-up of 13 months (range 6-26 months). Compared with pre-operatively, Clinical Post-Traumatic Neck Score (Mayo) was increased, Visual Analogue Scale score, angle deformity (α) and displacement distance (β) were reduced at 6-month post-operatively (P < 0.05). Neck activity was not limited in final folow-up. Bone fusion was found in al patients at 3 or 6 months post-operatively, and no complication was detected. Results confirm that polyetheretherketone cage for type II and IIa Hangman’s fracture could achieve good outcomes and safety.

Nowadays potential preclinical drugs for the treatment of nonalcoholic steatohepatitis (NASH) have failed to achieve expected therapeutic efficacy because the pathogenic mechanisms are underestimated. Inactive rhomboid protein 2 (IRHOM2), a promising target for treatment of inflammation-related diseases, contributes to deregulated hepatocyte metabolism-associated nonalcoholic steatohepatitis (NASH) progression. However, the molecular mechanism underlying Irhom2 regulation is still not completely understood. In this work, we identify the ubiquitin-specific protease 13 (USP13) as a critical and novel endogenous blocker of IRHOM2, and we also indicate that USP13 is an IRHOM2-interacting protein that catalyzes deubiquitination of Irhom2 in hepatocytes. Hepatocyte-specific loss of the Usp13 disrupts liver metabolic homeostasis, followed by glycometabolic disorder, lipid deposition, increased inflammation, and markedly promotes NASH development. Conversely, transgenic mice with Usp13 overexpression, lentivirus (LV)- or adeno-associated virus (AAV)-driven Usp13 gene therapeutics mitigates NASH in 3 models of rodent. Mechanistically, in response to metabolic stresses, USP13 directly interacts with IRHOM2 and removes its K63-linked ubiquitination induced by ubiquitin-conjugating enzyme E2N (UBC13), a ubiquitin E2 conjugating enzyme, and thus prevents its activation of downstream cascade pathway. USP13 is a potential treatment target for NASH therapy by targeting the Irhom2 signaling pathway.