To determine the clinical, biomechanical, and financial impact of the use of subacromial balloon spacers in the surgical management of massive, irreparable rotator cuff tears (RCTs). Methods: All studies assessing the use of implantable subacromial balloon spacers for management of massive, irreparable RCTs were systematically searched. Risk of bias was assessed using Methodological Index for Non-Randomized Studies criteria. Data extraction and analysis was performed for pain and function scores, shoulder range of motion (ROM), glenohumeral contact pressure and vertical migration of humeral head, and cost. Subjective synthesis was performed with forest plots when outcomes were reported in 3 or more studies. Results: In total, 19 studies met inclusion criteria for analysis; 337 patients (mean age 68 years) had 343 subacromial balloon spacer implantations. Throughout a mean follow-up of 33 months, there was significant

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Using syngeneic BALB/c mouse breast cancer models, we show that the chromatin remodeling subunit bromodomain PHD finger transcription factor (BPTF) suppresses natural killer (NK) cell antitumor activity in the tumor microenvironment (TME). In culture, BPTF suppresses direct natural cytotoxicity receptor (NCR) mediated NK cell cytolytic activity to mouse and human cancer cell lines, demonstrating conserved functions. Blocking mouse NCR1 in vivo rescues BPTF KD tumor weights, demonstrating its importance for the control of tumor growth. We discovered that BPTF occupies heparanase (Hpse) regulatory elements, activating its expression. Increased heparanase activity results in reduced cell surface abundance of the NCR co-ligands: heparan sulfate proteoglycans (HSPGs). Using gain and loss of function approaches we show that elevated heparanase levels suppress NK cell cytolytic activity to tumor cells in culture. These results suggest that BPTF activates heparanase expression, which in turn reduces cell surface HSPGs and NCR co-ligands, inhibiting NK cell activity. Furthermore, gene expression data from human breast cancer tumors shows that elevated BPTF expression correlates with reduced antitumor immune cell signatures, supporting conserved roles for BPTF in suppressing antitumor immunity. Conditional BPTF depletion in established mouse breast tumors enhances antitumor immunity, suggesting that inhibiting BPTF could provide a novel immunotherapy.

A 79-year-old woman with a history of osteoporosis treated with alendronate presented to the orthopaedic clinic with persistent left hip pain. X-ray and bone scan revealed an atypical femoral fracture associated with bisphosphonate use. The fracture was repaired with antegrade femoral intramedullary fixation. Her postoperative course was complicated by acute blood loss anaemia requiring several packed red blood cell transfusions and progressive thigh ecchymosis. CT angiography demonstrated extravasation of contrast from the superior gluteal artery (SGA). Subsequent angiography revealed an SGA pseudoaneurysm above the intramedullary nail, which was coil embolised. Iatrogenic SGA injury secondary to femoral intramedullary fixation is a rare complication, with only one previous case reported in the literature. Therefore, successful identification of the injury required attention to patient reported symptoms, neurovascular examinations and laboratory values to determine the cause of the patient’s postoperative anaemia. The patient made a full recovery and did not have any long-term adverse effects following the embolisation.

Using syngeneic BALB/c mouse breast cancer models, we show that the chromatin remodeling subunit bromodomain PHD finger transcription factor (BPTF) suppresses natural killer (NK) cell antitumor activity in the tumor microenvironment (TME). In culture, BPTF suppresses direct natural cytotoxicity receptor (NCR) mediated NK cell cytolytic activity to mouse and human cancer cell lines, demonstrating conserved functions. Blocking mouse NCR1 in vivo rescues BPTF KD tumor weights, demonstrating its importance for the control of tumor growth. We discovered that BPTF occupies heparanase (Hpse) regulatory elements, activating its expression. Increased heparanase activity results in reduced cell surface abundance of the NCR co-ligands: heparan sulfate proteoglycans (HSPGs). Using gain and loss of function approaches we show that elevated heparanase levels suppress NK cell cytolytic activity to tumor cells in culture. These results suggest that BPTF activates heparanase expression, which in turn reduces cell surface HSPGs and NCR co-ligands, inhibiting NK cell activity. Furthermore, gene expression data from human breast cancer tumors shows that elevated BPTF expression correlates with reduced antitumor immune cell signatures, supporting conserved roles for BPTF in suppressing antitumor immunity. Conditional BPTF depletion in established mouse breast tumors enhances antitumor immunity, suggesting that inhibiting BPTF could provide a novel immunotherapy. Citation Format: Kimberly Mayes, Zeinab Elsayed, Aiman Alhazmi, Michael Waters, Suehyb Alkhatib, Mark Roberts, Carolyn Song, Kristen Peterson, Vivian Chan, Nikhil Ailaney, Pumoli Malapati, Tana Blevins, Berislav Lisnic, Catherine Dumur, Joseph Landry. Tumor cell intrinsic BPTF inhibits NK cell activity and the abundance of natural cytotoxicity receptor co-ligands [abstract]. In: Proceedings of the AACR Special Conference on Tumor Immunology and Immunotherapy; 2017 Oct 1-4; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2018;6(9 Suppl):Abstract nr A28.