A Risk Model Based on Ferroptosis-Related Genes OSMR, G0S2, IGFBP6, IGHG2, and FMOD Predicts Prognosis in Glioblastoma Multiforme.

Background: Glioblastoma multiforme (GBM) is a common and highly aggressive brain tumor with a poor prognosis. However, the prognostic value of ferroptosis-related genes (FRGs) and their classification remains insufficiently studied.

Objective: This study aims to explore the significance of ferroptosis classification and its risk model in GBM using multi-omics approaches and to evaluate its potential in prognostic assessment.

An inflammatory gene-related prognostic risk score model for prognosis and immune infiltration in glioblastoma.

This study aimed to screen for key genes related to the prognosis of patients with glioblastoma (GBM). First, bioinformatics analysis was performed based on databases such as TCGA and MSigDB. Inflammatory-related genes were obtained from the MSigDB database.

Uncover DNA damage and repair-related gene signature and risk score model for glioma.

Background: Glioma is a common primary central nervous system tumor with complex pathogenesis. DNA damage and repair (DDR) is widely involved in regulating cell proliferation and tumorigenesis by correcting and repairing DNA damage mechanisms. Recent studies have reported the following properties in cancer cells in glioma, increased DNA damage and reduced DNA repair capacity.

Extracellular vesicles derived from bone marrow mesenchymal stem cells alleviate neurological deficit and endothelial cell dysfunction after subarachnoid hemorrhage via the KLF3-AS1/miR-83-5p/TCF7L2 axis.

Background: New data are accumulating on the effects of mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) in cerebrovascular diseases. We explored the potential role of KLF3-AS1-containing bone marrow MSC-EVs (BMSC-EVs) in a rat model of subarachnoid hemorrhage (SAH).

Methods: A rat model of SAH was established by endovascular perforation method, into which KLF3-AS1-containing EVs from BMSCs or miR-183-5p mimic were injected.

Mesenchymal stem cell-derived extracellular vesicles prevent glioma by blocking M2 polarization of macrophages through a miR-744-5p/TGFB1-dependent mechanism.

Aim: Our current study is conducted with intention to explore the regulatory mechanism of mesenchymal stem cell (MSC)-derived extracellular vesicle (EV)-miR-744-5p in glioma.

Methods: Expression patterns of TGFB1, TGFBR1, and miR-744-5p were determined. EVs were isolated from human MSCs, which were characterized.

Transcription Factor ELF1 Activates MEIS1 Transcription and Then Regulates the GFI1/FBW7 Axis to Promote the Development of Glioma.

Glioma is the most common malignancy in the central nervous system with no immediate prospect of a cure. Comprehensive understanding on the pathogenesis of the disorder contributes to a better outcome. Herein, we aimed to investigate whether transcription factors erythroblast transformation-specific (ETS) transcription factor (ELF1), myeloid ecotropic viral integration site 1 (MEIS1), and growth factor independence 1 (GFI1)/F-box/WD repeat-containing protein 7 (FBW7) mediate progression of glioma.

Endovascular Intervention with a Low-profile Visualized Intraluminal Support Stent Versus Surgical Clipping for Blood Blister-like Aneurysms : A Retrospective Study.

Purpose: Blood blister-like aneurysms (BBAs) have a high risk of early recurrence and postoperative rebleeding. This study compared the clinical outcomes and complications between endovascular intervention with low-profile visualized intraluminal support (LVIS) stent-assisted coiling and the surgical clipping in patients with BBAs.

Methods: This retrospective study enrolled 39 patients with BBAs who underwent endovascular intervention with LVIS stent-assisted coiling (n = 21) or surgical clipping (n = 18) between January 2013 and July 2018.

Exome Sequencing Identifies LOXL2 Mutation as a Cause of Familial Intracranial Aneurysm.

Background: Genetic risk factors can contribute to the etiology of intracranial aneurysms (IAs), and the genetic predisposition of IAs is largely unknown. Our study aimed to explore the role of rare variations in IA susceptibility.

Methods: Whole-exome sequencing (WES) was performed in a representative family with a history of multiple cases of IAs.