Causal association between years of schooling and the risk of traumatic brain injury: A two-sample mendelian randomization analysis.

OBJECTIVE: To investigate whether the number of years of schooling are causally associated traumatic brain injury (TBI). We aimed to investigate whether the number of years of schooling are causally associated TBI. METHODS: We investigate the prospective causal effect of years of schooling on TBI using summary statistical data. The statistical dataset comprising years of schooling (n = 293,723) from genome-wide association studies (GWASs) deposited in the UK Biobank was used for exposure. We used the following GWAS available in the FinnGen dataset: individuals with TBI (total = 13,165; control = 136,576; number of single nucleotide polymorphisms [SNPs] = 16,380,088). RESULTS: Seventy significant genome-wide SNPs from GWAS datasets with annotated years of schooling were selected as instrumental variables. The inverse variance weighted method results supported a causal relationship between years of schooling and TBI (odds ratio (OR), 0.78; 95 % confidence interval (CI), 0.62-0.98; P = 0.029). MR-Egger regression showed that polydirectionality was unlikely to bias the results (intercept = 0.007, SE = 0.01, P = 0.484) and demonstrated no causal relationship between years of schooling and TBI (OR, 0.52; 95%CI, 0.17-1.64; P = 0.270). The weighted median method revealed a causal relationship with TBI (OR, 0.73; 95%CI, 0.55-0.98; P = 0.047). A Cochran's Q test and funnel plot did not show heterogeneity nor asymmetry, indicating no directional pleiotropy. CONCLUSIONS: The current investigation yields substantiation of a causal association between years of schooling and TBI development. More years of schooling may be causally associated with a reduced risk of TBI, which has implications for clinical and public health practices and policies.

Migration-inducing gene-7 promotes glioma cell proliferation and invasiveness via activating the MAPK signaling pathway.

Glioma is a highly aggressive primary malignant tumor. Migration-inducing gene-7 (Mig-7) is closely related to tumor invasion and metastasis. However, the detailed molecular mechanism of Mig-7-mediated promotion of glioma cell invasion requires further investigation. Therefore, this study aimed to investigate the molecular mechanism by which Mig-7 promotes invasion and growth of glioma tumor cells. After collecting 65 glioma tissues and 16 non-tumor tissues, the expression difference of Mig-7 between tumor tissues and non-tumor tissues was analyzed. The molecular mechanism of Mig-7 in tumor cells was investigated by knockdown or overexpression of Mig-7 in U87MG cells. Specifically, the expression levels of mitogen-activated protein kinase (MAPK) signaling pathway-related molecules were detected in cells that knocked down Mig-7. MTT, Transwell, and three-dimensional cell culture assays were used to detect the survival, migration, invasion, and tube formation of U87MG cells that overexpressed Mig-7 were treated with the MAPK signaling pathway inhibitors (SP600125, SCH772984, and SB202190). The effect of Mig-7 on the tumorigenic ability of U87MG cells was investigated by subcutaneous tumorigenic experiment in nude mice. The corresponding results indicated that Mig-7 expression was significantly higher in glioma tissues and cell lines compared to that in non-neoplastic brain tissues and normal glial cell lines. In U87MG cells, downregulation or overexpression of Mig-7 inhibited or promoted the expression of MMP-2, MMP-9, LAMC2, EphA2, and VE-cadherin, and phosphorylation levels of ERK1/2, JNK, and p38. Mig-7 overexpression promoted migration, invasion, cell viability, and tube formation, which were reversed by the MAPK signaling pathway inhibitors. Mig-7 overexpression promoted subcutaneous tumor growth in mice and upregulated the phosphorylation levels of ERK1/2, JNK, and p38 and the expression of Ki-67. These effects of Mig-7 overexpression were reversed by MAPK pathway inhibitors. Overall, these results suggest that Mig-7 may be a novel biomarker and potential therapeutic target for glioma, with the MAPK pathway playing a key role in the corresponding Mig-7 mechanism of action.

Subperiosteal/subgaleal drainage vs. subdural drainage for chronic subdural hematoma: A meta-analysis of postoperative outcomes.

BACKGROUND: Chronic subdural hematoma (CSDH) is commonly treated via surgical removal of the hematoma, placement of a routine indwelling drainage tube, and continuous drainage to ensure that the blood does not re-aggregate following removal. However, the optimal location for placement of the drainage tube remains to be determined. OBJECTIVES: To aid in establishing a reference for selecting the optimal method, we compared the effects of different drainage tube placements on CSDH prognosis via a systematic review and meta-analysis of previous clinical studies. DATA SOURCES: PubMed, Embase, and Cochrane databases. STUDY ELIGIBILITY CRITERIA: We searched for clinical studies comparing the outcomes of subperiosteal/subgaleal drainage (SPGD) and subdural drainage (SDD) for CSDH published in English prior to April 1, 2022. PARTICIPANTS: The final analysis included 15 studies involving 4,318 patients. RESULTS: Our analysis of the pooled results revealed no significant differences in recurrence rate between the SDD and SPGD groups. We also observed no significant differences in mortality or rates of postoperative complications (infection, pneumocephalus, or epilepsy) between the SDD and SPGD groups. CONCLUSIONS: These results suggest that the choice of SDD vs. SPGD has no significant effect on CSDH prognosis, highlighting SPGD as an alternative treatment option for CSDH.

Transradial versus transfemoral access for endovascular therapy of intracranial aneurysms: a systematic review and meta-analysis of cohort studies.

Endovascular treatment is widely used in the treatment of intracranial aneurysms. However, neurosurgeons are sceptical about endovascular access via the radial artery. We performed a systematic review and meta-analysis to compare the effectiveness and safety of transradial and transfemoral artery access in patients with intracranial aneurysms. We systematically searched the PubMed, Embase, and Cochrane databases for studies comparing the two approaches. The primary outcome was total complications, and the secondary outcomes were access site complications, intracranial haemorrhage, stroke, thromboembolism, silent infarct, re-treatment rate, mortality, complete occlusion of intracranial aneurysms, procedure duration, and length of hospital stay. A random-effects model was used to assess the pooled data. Of the 100 identified studies, 6 were eligible (a total of 3764 participants). There were no significant differences in total complications(odds ratio [OR] = 0.69, 95% confidence interval [CI] [0.33, 1.45], p = 0.32), complete occlusion of intracranial aneurysms (OR = 1.02, 95%CI [0.77,1.37], p = 0.87), procedure duration (mean difference [MD] = - 6.24, 95%CI [- 14.75, - 1.54], p = 0.95), or length of hospital stay (MD = 2.204, 95%CI [- 0.05, 4.45], p = 0.95), access site complications (OR = 0.49, 95%CI [0.16, 1.52], p = 0.22), intracranial haemorrhage (OR = 1.07, 95%CI [0.49, 2.34], p = 0.86), stroke (OR = 0.59, 95%CI [0.20, 1.77], p = 0.35), thromboembolism (OR = 0.85, 95%CI [0.33, 2.17], p = 0.74), silent infarct (OR = 0.69, 95%CI [0.04, 11.80], p = 0.80), retreatment rate (OR = 1.32, 95%CI [0.70, 2.48], p = 0.39), mortality (OR = 1.41, 95%CI [0.06, 5.20], p = 0.61), immediate occlusion (OR = 0.99, 95%CI [0.64, 1.51], p = 0.95), and occlusion during follow-up (OR = 1.10, 95%CI [0.56, 2.16], p = 0.74) between the transradial and transfemoral groups. This study showed comparable safety and efficacy outcomes between transradial and transfemoral access in patients with intracranial aneurysms treated endovascularly. Future large randomised trials are warranted to confirm these findings.