Object: The minimally invasive transpsoas interbody fusion technique requires dissection through the psoas muscle, which contains the nerves of the lumbosacral plexus posteriorly and genitofemoral nerve anteriorly. Retraction of the psoas is becoming recognized as a cause of transient postoperative thigh pain, numbness, paresthesias, and weakness. However, few reports have described the nature of thigh symptoms after this procedure. Methods: The authors performed a review of patients who underwent the transpsoas technique for lumbar spondylotic disease, disc degeneration, and spondylolisthesis treated at a single academic medical center. A review of patient charts, including the use of detailed patient-driven pain diagrams performed at equal preoperative and follow-up intervals, investigated the survival of postoperative thigh pain, numbness, paresthesias, and weakness of the iliopsoas and quadriceps muscles in the follow-up period on the ipsilateral side of the surgical approach. Results: Over a 3.2-year period, 59 patients underwent transpsoas interbody fusion surgery. Of these, 62.7% had thigh symptoms postoperatively. New thigh symptoms at first follow-up visit included the following: burning, aching, stabbing, or other pain (39.0%); numbness (42.4%); paresthesias (11.9%); and weakness (23.7%). At 3 months postoperatively, these percentages decreased to 15.5%, 24.1%, 5.6%, and 11.3%, respectively. Within the patient sample, 44% underwent a 1-level, 41% a 2-level, and 15% a 3-level transpsoas operation. While not statistically significant, thigh pain, numbness, and weakness were most prevalent after L4–5 transpsoas interbody fusion at the first postoperative follow-up. The number of lumbar levels that were surgically treated had no clear association with thigh symptoms but did correlate directly with surgical time, intraoperative blood loss, and length of hospital stay. Conclusions: Transpsoas interbody fusion is associated with high rates of immediate postoperative thigh symptoms. While larger, prospective studies are necessary to validate these findings, the authors found that half of the patients had symptom resolution at approximately 3 months postoperatively and more than 90% by 1 year.

Object: Minimally invasive spine (MIS) procedures are increasingly being recognized as equivalent to open procedures with regard to clinical and radiographic outcomes. These techniques are also believed to result in less pain and disability in the immediate postoperative period. There are, however, little data to assess whether these procedures produce their intended result and even fewer objective data to demonstrate that they are cost effective when compared with open surgery.Methods: The authors performed a retrospective analysis of hospital charges for 1- and 2-level MIS and open posterior interbody fusion for lumbar spondylotic disease, disc degeneration, and spondylolisthesis treated at a single academic medical center. Patients presenting with bilateral neurological symptoms were treated with open surgery, and those with unilateral symptoms were treated with MIS. Overall hospital charges and surgical episode–related charges, length of stay (LOS), and discharge status were obtained from the hospital finance department and adjusted for multi-/single-level surgeries.Results: During a 14-month period, 74 patients (mean age 55 years) were treated. The series included 59 single-level operations (75% MIS and 25% open), and 15 2-level surgeries (53% MIS and 47% open). The demographic profile, including age and Charlson Comorbidity Index, were similar between the 4 groups. The mean LOS for patients undergoing single-level surgery was 3.9 and 4.8 days in the MIS and open cases, respectively (p = 0.017). For those undergoing 2-level surgery, the mean LOS was 5.1 for MIS versus 7.1 for open surgery (p = 0.259). With respect to hospital charges, single-level MIS procedures were associated with an average of $70,159 compared with $78,444 for open surgery (p = 0.027). For 2-level surgery, mean charges totalled $87,454 for MIS versus $108,843 for open surgery (p = 0.071). For single-level surgeries, 5 and 20% of patients undergoing MIS and open surgery, respectively, were discharged to inpatient rehabilitation. For 2-level surgeries, the rates were 13 and 29%, respectively.Conclusions: While hospital setting, treatment population, patient selection, and physician expectation play major roles in determining hospital charges and LOS, this pilot study at an academic teaching hospital shows trends for quicker discharge, reduced hospital charges, and lower transfer rates to inpatient rehabilitation with MIS. However, larger multicenter studies are necessary to validate these findings and their relevance across diverse US practice environments.

Long noncoding RNAs (lncRNAs) get great involvements in the development of countless cancers. Nonetheless, the deep molecular mechanism by which lncRNA regulates the formation of glioma is unclear. In our study, the expression of PSMB8-AS1 was dramatically upregulated in glioma tissues and cells, further, PSMB8-AS1 silencing restrained cell proliferation in glioma, and the results of PSMB8-AS1 overexpression were opposite. Moreover, PSMB8-AS1 could bind with miR-574-5p, which was low expressed in glioma cells. In addition, RAB10 acted the target gene of miR-574-5p, and PSMB8-AS1 could regulate RAB10 via modulating miR-574-5p. Besides, miR-574-5p inhibitor/mimics remedied the repressive/simulative role of PSMB8-AS1 depletion/overexpression, and RAB10 downregulation/upregulation reversed the encouraging/blocked function caused by miR-574-5p inhibitor/mimics in PSMB8-AS1 depletion/overexpression transfected glioma cells. Additionally, ELK1, a transcription factor, could active PSMB8-AS1 expression. To be concluded, PSMB8-AS1 activated by ELK1 promotes cell proliferation in glioma via regulating miR-574-5p/RAB10, which may be contributory to find new targets to treat glioma.

Studies have revealed the aberrant expression of lncRNAs is responsible for human carcinogenesis. MIR4697 host gene (MIR4697HG) is an upregulated lncRNA that promoted cell growth and metastasis in other cancers. In this study, we tested the expression of MIR4697HG in glioma cells and detected the comparatively down-regulated expression. RAD1 is an upstream regulator for MIR4697HG. This study aimed at exploring the regulatory mechanism and function of RAD1/MIR4697HG/PRR12 axis in glioma. We profiled the expression of MIR4697HG in glioblastoma multiforme (GBM) tissues according to GEPIA database as well as in glioma cells by qPCR. Functional experiments confirmed relevant role of MIR4697HG in regulating glioma cell proliferation and migration. We also carried out luciferase reporter assay, pull down assay and RIP assay to verify the location and interaction among the indicated RNA molecules. The expression of MIR4697HG is down-regulated significantly in glioma cells due to the up-regulated expression of RAD21. MiR-766-5p was identified functioning as a sponge for MIR4697HG and is sequestered by MIR4697HG. We also found either miR-766-5p inhibitor or PRR12 knockdown rescued the function depletion caused by MIR4697HG overexpression. In all, the down-regulated expression of MIR4697HG inhibited PRR12 to suppress glioma and led to the deterioration of glioma. RAD21-induced down-regulated expression of MIR4697HG is correlated with aggravation of glioma. The MIR4697HG/miR-766-5p/PRR12 axis predicts poor results in glioma and MIR4697HG could be considered as a promising biomarker for diagnosis and treatment of glioma.