Background: The presence of the blood–brain barrier (BBB) uniquely distinguishes the brain from other organs, and various brain pathologies, including cancer, can disrupt or breach the BBB. The specific implications of BBB alterations in glioma have not been sufficiently clarified. Methods: In this study, statistical analysis of the TCGA pan-glioma dataset and four other validation cohorts was used to investigate the infiltration of BBB constituent cells (endothelial cells, pericytes and astrocytes) in the glioma tumor microenvironment (TME). Results: We found that the infiltration proportions of the three BBB constituent cell types were highly collinear, which implied alteration of the BBB. Hence, we developed an index, the BBB score, which is calculated based on the infiltration proportion of BBB constituent cells. Furthermore, we observed that patients with higher BBB scores were more likely to be diagnosed with more malignant entities in the TCGA database according to significant molecular features, such as IDH mutation status and 1p/19q deletion. The BBB score was also strikingly positively correlated with WHO grade in other cohorts. More importantly, a higher BBB score correlated with shorter survival time and unfavorable prognosis in glioma patients. Finally, we showed that TME-related pathways may regulate BBB alterations and that coinhibitory immune checkpoints were enriched in samples with higher BBB scores. Conclusions: We showed that TME-related pathways may regulate BBB alterations and that coinhibitory immune checkpoints were enriched in samples with higher BBB scores. Assessing BBB alterations may help elucidate the complex role of the glioma TME and suggest new combination treatment strategies.

Background: Data regarding the association between anthropometric factors and meningioma risk are inconsistent. Our aim was to investigate the association of body mass index (BMI), height, waist to hip ratio (WHR), waist circumference, and meningioma risk through a comprehensive meta-analysis. Methods: An extensive review of literature was conducted in PubMed and Embase databases. Random-effects models were used to pool the study-specific relative risk estimates (RRs) and 95% confidence intervals (CIs). Moreover, we employed a dose-response meta-analysis with a one-stage robust error meta-regression (REMR) model. Results: We included nine prospective studies for four anthropometric factors listed above and meningioma risk. Compared with normal weight, both overweight (RR:1.11, 95% CI: 1.04, 1.19; P = 0.003, I² = 0.0%) and obesity (RR: 1.38, 95% CI:1.16, 1.64; P < 0.001, I² = 54.7%) were statistically significantly associated with meningioma risk. Dose-response analysis showed a nonlinear relationship between BMI and meningioma risk (P = 0.038). For height, a positive association was identified for men (RR:1.30, 95% CI:1.08, 1.56; P = 0.005, I² = 0.0%) but not women (RR:1.13, 95% CI: 0.94,1.36; P = 0.186, I² = 49.8%). Highest vs. lowest levels analyses also showed a positive association between meningioma risk and waist circumference (RR:1.89, 95% CI:1.34, 2.66; P < 0.001, I² = 0.0%) and WHR (RR:1.40, 95% CI:1.00, 1.94; P = 0.048, I² = 0.0%). Conclusion: Our meta-analysis indicates greater height (in men) and excess weight and body fat mass were associated with an increased risk of meningioma. Further prospective studies with particular attention to sex disparity and dose-response analysis are warranted to confirm our observation.

Objective. To study the effect of circ_0000512 (circRPPH1_025) on the tumorigensis and development of glioblastoma and its molecular mechanism. Methods. The expression levels of circ_0000512 in normal astrocytes (NHA) and human glioblastoma cell lines (U87, U251, and A172) and the expression levels of circ_0000512 and linear RNA RPPH1 in U87 cells after RNase R treatment were detected by qRT-PCR. The effects of circ_0000512 knockdown or overexpression on the proliferation, migration, invasion, and epithelial-mesenchymal transition of U87 cells were detected by CCK-8 assay, cell colony formation assay, transwell invasion assay, wound healing assay, and western blot. Results. The expression of circ_0000512 was upregulated in glioblastoma cells, and the overexpression of circ_0000512 was beneficial to the proliferation, migration, invasion, and epithelial-mesenchymal transition of U87 cells, while knockdown of circ_0000512 showed the opposite results. Conclusion. circ_0000512 can be used as a potential target for early diagnosis and targeted therapy of glioblastoma multiforme.

Subarachnoid hemorrhage (SAH), a severe cerebrovascular disorder, is principally instigated by the rupture of an aneurysm. Early brain injury (EBI), which gives rise to neuronal demise, microcirculation impairments, disruption of the blood-brain barrier, cerebral edema, and the activation of oxidative cascades, has been established as the predominant cause of mortality among patients with SAH. These pathophysiological processes hinge on the activation of inflammasomes, specifically the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)and absent in melanoma 2 (AIM2) inflammasomes. These inflammasomes assume a crucial role in downstream intracellular signaling pathways and hold particular significance within the nervous system. The activation of inflammasomes can be modulated, either by independently regulating these two entities or by influencing their engagement at specific target loci within the pathway, thereby attenuating EBI subsequent to SAH. Although certain clinical instances lend credence to this perspective, more in-depth investigations are essential to ascertain the optimal treatment regimen, encompassing dosage, timing, administration route, and frequency. Consequently, targeting the ensuing early brain injury following SAH represents a potentially efficacious therapeutic approach.