The Kite technique: a new all-arthroscopic technique for the treatment of acute acromioclavicular joint dislocation.

PURPOSE: Although many open techniques have been developed, no all-arthroscopic technique has been introduced to reduce acute acromioclavicular joint dislocation (ACJD) and augment both coracoclavicular (CC) ligaments. The Kite technique is the first all arthroscopic technique with this aim. METHODS: Forty-one consecutive patients [35M-6F; median: 29.2 years (range 23-36)] with acute type III and V acromioclavicular joint dislocation were treated with the Kite technique: it consists of positioning three titanium buttons connected by heavy sutures in an 8-strand configuration between clavicle and coracoid to restore the anatomy of CC ligaments. Patients were followed up for a median of 35 months (range 30-43 months). RESULTS: Median operation time was 70.6 min (range 58-82), with no cases of intra-operative complications. At the final follow-up, the median post-operative Constant Score and SST were 94.1 (range 89-98) and 11.6 (range 10-12), respectively. At the final follow-up reduction maintenance was present in 39 patients; in one patient, signs of acromioclavicular joint dislocation recurrence were present 3 months post-op. In another patient, medial suture ruptures occurred 4 months after surgery with type II acromioclavicular joint dislocation recurrence but with scarce symptoms and full recovery to sport activity. Clavicle osteolysis was observed in four patients. Cosmetics of the arm were judged as excellent in 39/41. All patients, except two, were satisfied with the final result. CONCLUSIONS: The kite technique is a safe and reproducible arthroscopic procedure to treat acute ACJD. In daily clinical practice, due to the excellent results and the low complication rate, this technique might be considered by surgeons when operative treatment of an acute acromioclavicular joint dislocation is planned. LEVEL OF EVIDENCE: IV.

Pur-alpha functionally interacts with FUS carrying ALS-associated mutations.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder due to motor neuron loss. Fused in sarcoma (FUS) protein carrying ALS-associated mutations localizes to stress granules and causes their coalescence into larger aggregates. Here we show that Pur-alpha physically interacts with mutated FUS in an RNA-dependent manner. Pur-alpha colocalizes with FUS carrying mutations in stress granules of motoneuronal cells differentiated from induced pluripotent stem cells and that are derived from ALS patients. We observe that both Pur-alpha and mutated FUS upregulate phosphorylation of the translation initiation factor eukaryotic translation initiation factor 2 alpha and consistently inhibit global protein synthesis. In vivo expression of Pur-alpha in different Drosophila tissues significatively exacerbates the neurodegeneration caused by mutated FUS. Conversely, the downregulation of Pur-alpha in neurons expressing mutated FUS significatively improves fly climbing activity. All these findings suggest that Pur-alpha, through the control of mRNA translation, might be involved in the pathogenesis of ALS associated with the mutation of FUS, and that an alteration of protein synthesis may be directly implicated in the disease. Finally, in vivo RNAi-mediated ablation of Pur-alpha produced locomotion defects in Drosophila, indicating a pivotal role for this protein in the motoneuronal function.