Biomechanical analysis of a customized lumbar interspinous spacer based on transfacetopedicular screw fixation: A finite element study.

The interspinous spacer (ISP) is a minimally invasive surgical device implanted into the interspinal space to treat lumbar degenerative diseases. Unfortunately, ISPs sometimes cause device breakage and spinal process fracture. Our aim was to elaborate the design of lumbar customized posterior fixation system (CISP system), encompassing a customized ISP body and transfacetopedicular screws, and examine its biomechanical effect on the lumbar spine using finite element (FE) analysis. We constructed the CISP system, based on the interspinal anatomical data at the surgical level. We generated the L3-S1 FE models, implanted with the polyetheretherketone (PEEK) CISP system, titanium alloy (TI) CISP system, and Coflex device at the L4/L5 segment, and determined the lumbar segmental range of motions (ROMs), intervertebral discs (IVD) peak stress, and implant stresses. The CISP system enhanced mobility restriction at the surgical level, compared to the Coflex device. Furthermore, the IVD peak stress reduction was more obvious in the CISP system than the Coflex device, particularly during extension. Under the same motion mode, the maximum stress on the TI CISP system was smaller than on the Coflex device, but larger than the PEEK CISP system. Given these evidences, PEEK appeared to be a better material for the CISP body.

Recurrence or neurological loss? Resection mode selection for patients with large sacral chordoma: an analysis of prognostic factors and quality of life.

BACKGROUND: Surgical resection represents the main therapeutic method for sacral chordoma, but plans for resection mode must weigh neurological loss against complete tumor excision, a difficult balance to strike. The purpose of this study was to provide useful information contributing to surgical decision making in sacral chordoma. METHODS: A retrospective review was performed on 47 patients with large sacral chordoma. Prognostic factors affecting recurrence-free survival (RFS) and overall survival (OS) were analyzed using the Kaplan-Meier method and Cox proportional hazards model. Quality of life was assessed by the Functional Assessment of Cancer Therapy-General (FACT-G) questionnaire and compared using Student's t test. RESULTS: Resection mode was the independent prognostic factor affecting RFS, while independent prognostic factors affecting OS were resection mode and postoperative recurrence. As for quality of life, the en bloc resection group showed a higher score in emotional well-being, while the piecemeal resection group scored better in function well-being. No significant difference was identified in total the FACT-G score between two groups. CONCLUSIONS: On the one hand, en bloc resection showed huge advantages in disease control for sacral chordoma. On the other hand, despite the unsatisfaction in functional well-being, en bloc resection did not sacrifice quality of life significantly in terms of the total FACT-G score.

Symptomatic postoperative spinal epidural hematoma after spine tumor surgery: Incidence, clinical features, and risk factors.

STUDY DESIGN: Case-control study. OBJECTIVES: The objective of this study was to provide some useful information concerning the incidence, clinical features, and risk factors for symptomatic postoperative spinal epidural hematoma (SPSEH) in an isolated cohort of patients undergoing spine tumor surgery. SETTING: Hospital in Shanghai, China. METHODS: We retrospectively reviewed all patients who underwent surgery for spine tumors between August 2012 and August 2017, and conducted a case-control study involving 16 patients who received evacuation surgery due to SPSEH after spine tumor surgery and 48 controls without SPSEH. Case and control subjects were matched at 1:3 by pathological diagnosis, tumor size (±1 cm), resection mode, surgical approach, and the operation team. Data of SPSEH subjects along with 48 matched controls were further obtained from a detailed review of the medical records. Univariate and multivariate analyses were conducted to identify the risk factors for developing SPSEH. RESULTS: SPSEH evacuation surgery was performed after 16 of 5421 (0.30%) spine tumor surgeries. Angiogenic tumors were the most susceptible tumors developing SPSEH. Very large hematomas, continuous blood loss, and delayed hematomas were characteristic clinical presentations for SPSEH after spine tumor surgery. Multiple logistic regression analysis suggested that patients suffering from at least one medical comorbidity and patients with Frankel grade of A-C had a significantly higher risk of developing SPSEH. CONCLUSIONS: The incidence of SPSEH after spine tumor surgery requiring surgical evacuation was 0.30%. Medical comorbidity and Frankel grade were identified as independent risk factors for SPSEH development.

ILKAP Binding to and Dephosphorylating HIF-1α is Essential for Apoptosis Induced by Severe Hypoxia.

BACKGROUND/AIMS: Integrin-linked kinase-associated phosphatase (ILKAP), a serine/threonine phosphatase that belongs to the protein phosphatase 2C family, has a role in cell survival and apoptosis. Hypoxia-inducible factor 1α (HIF-1α) is the key transcription factor in the response to oxygen deficiency in mammals. Direct phosphorylation and dephosphorylation of HIF-1α affect its function. The present study investigated the role of ILKAP on HIF-1α dephosphorylation and cell behavior. METHODS: HIF-1α was induced by hypoxia. Physical binding between ILKAP and HIF-1α was demonstrated by a co-immunoprecipitation assay. HIF-1α transcriptional activity was investigated using a hypoxia-response element-containing luciferase reporter plasmid. Cell viability was evaluated by a trypan blue dye exclusion assay. ILKAP function was explored by a gain and loss assay with an overexpression plasmid and shRNA infection. RESULTS: ILKAP physically interacted with HIF-1α and induced its dephosphorylation. Both the HIF-1α-p53 interaction and apoptosis relied on ILKAP. CONCLUSION: The results indicated that the ILKAP directly binds and dephosphorylates HIF-1α and responsible for severe hypoxia-induced cell apoptosis.