Effect of Titanium Miniplate Fixation on Hinge Fracture and Hinge Fracture Displacement Following Cervical Open-Door Laminoplasty.

BACKGROUND: Cervical spondylotic myelopathy is a neuromotor disorder responsible for functional limitations and decreased daily activities. Expansive open-door laminoplasty is the widely accepted procedure for the treatment of multilevel cervical spondylotic myelopathy. Among the various fixation procedures to secure the open lamina, miniplate fixation provides better clinical and radiological outcomes. However, the immediate effects on hinge fracture and hinge fracture displacement following miniplate fixation have not been proven until now. The purpose of our study was to elucidate the impact of cervical open-door angle on the status of spinal cord expansion and hinge fracture, hinge fracture displacement, and the role of implants used during surgery. METHODS: For this retrospective study, 122 patients who had undergone surgery from September 2016 to November 2017 with preoperative and postoperative radiographs were enrolled. Clinical and radiological outcomes were assessed before and after surgery. RESULTS: There were no significant differences in demographics, surgery time, blood loss, medical comorbidities, or perioperative and postoperative complications between 2 groups. The recovery rate and Nurick score before and at the follow-up show no statistical significance between the 2 groups, P value > .05 (P = .672) and P > .05 (P = .553), respectively. The statistical analysis shows that the mean hinge fracture in the miniplate group with a cervical open angle >30° was 2.42 ± 1.68 and with a <30° open angle, 0.05 ± 0.23; whereas, in the anchor group the mean hinge fracture in >30° cervical open angle was 2.227 ± 2.50 and in <30° was 0.409 ± 0.503. The results revealed statistical significance between 2 implant groups, P = .024 in the aspect of hinge fracture displacement and implant used. CONCLUSION: Laminoplasty by titanium miniplate fixation holds the laminae securely, prevents hinge fracture displacement, and promotes spinal cord expansion better than suture anchor fixation.

Brief report: benchmarking human pluripotent stem cell markers during differentiation into the three germ layers unveils a striking heterogeneity: all markers are not equal.

Pluripotent stem cells (PSC) are functionally characterized by their capacity to differentiate into all the cell types from the three germ layers. A wide range of markers, the expression of which is associated with pluripotency, has been used as surrogate evidence of PSC pluripotency, but their respective relevance is poorly documented. Here, we compared by polychromatic flow cytometry the kinetics of loss of expression of eight widely used pluripotency markers (SSEA3, SSEA4, TRA-1-60, TRA-1-81, CD24, OCT4, NANOG, and alkaline phosphatase [AP]) at days 0, 5, 7, and 9 after induction of PSC differentiation into cells representative of the three germ layers. Strikingly, each marker showed a different and specific kinetics of disappearance that was similar in all the PSC lines used and for all the induced differentiation pathways. OCT4, SSEA3, and TRA-1-60 were repeatedly the first markers to be downregulated, and their expression was completely lost at day 9. By contrast, AP activity, CD24, and NANOG proteins were still detectable at day 9. In addition, we show that differentiation markers are coexpressed with pluripotency markers before the latter begin to disappear. These results suggest that OCT4, SSEA3, and TRA-1-60 might be better to trace in vitro the emergence of pluripotent cells during reprogramming.