Optimal Timing of Cranioplasty After Decompressive Craniectomy: Timing or Collapse Ratio.

BACKGROUND AND OBJECTIVES: Although cranioplasty (CP) is a relatively straightforward surgical procedure, it is associated with a high complication rate. The optimal timing for this surgery remains undetermined. This study aimed to identify the most suitable timing for CP to minimize postoperative complications. METHODS: We conducted a retrospective analysis of all CP cases performed in our department from August 2015 to March 2022. Data were gathered through case statistics and categorized based on the occurrence of complications. The collapse ratio was determined using 3-dimensional Slicer software. RESULTS: In our retrospective study of 266 patients, 51 experienced postoperative complications, including hydrocephalus, epidural effusion, subdural hematoma, epilepsy, and subcutaneous infection. Logistic regression analysis identified independent predictors of postcranioplasty complications, and a nomogram was developed. The predictive value of the logistic regression model, collapse ratio, and decompression craniotomy-CP operation interval for post-skull repair complications was assessed using receiver operating characteristic curve analysis. No significant differences were observed in postoperative complications and decompression craniotomy-CP intervals between the groups (P = .07, P > .05). However, significant differences were noted in postoperative collapse ratios and CP complications between the groups (P = .023, P < .05). Logistic regression revealed that the collapse ratio (odds ratio = 1.486; 95% CI: 1.001-2.008; P = .01) and CP operation time (odds ratio = 1.017; 95% CI: 1.008-1.025, P < .001) were independent risk factors for postoperative complications. Receiver operating characteristic curve analysis indicated that the collapse ratio could predict CP postoperative complications, with a cutoff value of 0.274, an area under the curve of 0.621, a sensitivity of 62.75%, and a specificity of 63.26%. CONCLUSION: The post-skull repair collapse ratio is a significant predictor of postoperative complications. It is advisable to base the timing of surgery on the extent of brain tissue collapse, rather than solely on the duration between cranial decompression and CP.

CircNUP98 Suppresses the Maturation of miR-519a-3p in Glioblastoma.

Circular RNA (circNUP98) has been reported to promote renal cancer; however, its role in other cancers is unknown. The function of circNUP98 in glioblastoma (GB) cancer was explored in this study. A total of 58 GB tissue samples were collected to study the expression of circNUP98 and miR-519a-3p [both the mature and pre-mature microRNA (miRNA)] by quantitative real-time PCR (RT-qPCR) and heatmap analysis. The subcellular location that expresses circNUP98 was analyzed by nuclear fractionation assay. RNA pull-down assay was performed to evaluate the interaction between circNUP98 and pre-mature miR-519a-3p. Overexpression assays were performed to investigate the role of circNUP98 in the regulation of both the mature and pre-mature miR-519a-3p. The role of circNUP98 and miR-519a-3p in GB cell proliferation was explored by 5-bromo-2-deoxyuridine (BrdU) assay and was assessed in mouse xenograft model. Heatmap analysis showed that circNUP98 and pre-mature miR-519a-3p were upregulated in GB, while mature miR-519a-3p was downregulated in GB. Across the cancer tissues, circNUP98 was inversely correlated with mature miR-519a-3p, but positively correlated with pre-mature miR-519a-3p. In GB cells, circNUP98 was localized to both the nucleus and cytoplasm and it interacted with pre-mature miR-519a-3p. In GB cells, circNUP98 increased the expression levels of pre-mature miR-519a-3p and decreased the expression levels of mature miR-519a-3p. BrdU and cholecystokinin octapeptide (CCK-8) assays illustrated that overexpression of circNUP98 reduced the inhibitory effects of miR-519a-3p on cell proliferation. CircNUP98 contributed to larger tumors, which resulted in significantly reduced mice survival. CircNUP98 suppresses the maturation of miR-519a-3p to promote GB cell proliferation.

[Construction and screening of neurite outgrowth inhibitory 66 eukaryotic expression vectors].

OBJECTIVE: To construct and screen neurite outgrowth inhibitory 66-small interfering RNA (nogo66-siRNA) eukaryotic expression vectors of effective interference, so as to lay a foundation for further reconstruction of related viral vector. METHODS: The nogo66-siRNA fragments were designed and cloned into pGenesil-1.1, 4 plasmids of pGenesil-nogo66-siRNA-1, pGenesil-nogo66-siRNA-2, pGenesil-nogo66-siRNA-hk, and pGenesil-nogo66-siRNA-kb were obtained, sequenced and identified, then were transfected into C6 cell line. The transfection efficiency was measured by fluorescence microscope. RT-PCR and Western blot were used to detect the expression of nogo gene and select the plasmid of effective interference. RESULTS: DNA sequencing results showed interference sequences were correct. The bands of 800 bp and 4.3 kb were detected when pGenesil-nogo66-siRNAs were digested by Kpn I/Xho I. The expression of green fluorescent protein could be detected under fluorescence microscope, and the transfection efficiency was about 73%. RT-PCR and Western blot results showed that compared to non-transfected cells, the transfection of pGenesil-nogo66-siRNA-1 made the expression of nogo gene decline 22% and the expression of nogo protein decline 73%; the transfection of pGenesil-nogo66-siRNA-2 made the expression of nogo gene decline 28% and the expression of nogo protein decline 78%; the differences were significant (P < 0.05); and the transfection of pGenesil-nogo66-siRNA-hk and pGenesil-nogo66-siRNA-kb did not make the expressions of nogo gene and nogo protein decrease significantly (P > 0.05). CONCLUSION: Nogo66-siRNA eukaryotic expression vector is successfully constructed, it lays an experimental foundation for repair of spinal cord injury.