Background Although multiple signaling cascades and molecules contributing to the pathophysiological process have been studied, the treatments for stroke against present targets have not acquired significant clinical progress. Although CARD3 (caspase activation and recruitment domain 3) protein is an important factor involved in regulating immunity, inflammation, lipid metabolism, and apoptosis, its role in cerebral stroke is currently unknown. Methods and Results Using a mouse model of ischemia‐reperfusion (I‐R) injury based on transient blockage of the middle cerebral artery, we have found that CARD3 expression is upregulated in a time‐dependent manner during I‐R injury. Further animal study revealed that, relative to control mice, CARD3‐knockout mice exhibited decreased inflammatory response and neuronal apoptosis, with reduced infarct volume and lower neuropathological scores. In contrast, neuron‐specific CARD3‐overexpressing transgenic (CARD3‐TG) mice exhibited increased I‐R induced injury compared with controls. Mechanistically, we also found that the activation of TAK1 (transforming growth factor‐β–activated kinase 1) was enhanced in CARD3‐TG mice. Furthermore, the increased inflammation and apoptosis seen in injured CARD3‐TG brains were reversed by intravenous administration of the TAK1 inhibitor 5Z‐7‐oxozeaenol. Conclusions These results indicate that CARD3 promotes I‐R injury via activation of TAK1, which not only reveals a novel regulatory axis of I‐R induced brain injury but also provides a new potential therapeutic approach for I‐R injury.

Background: Glioblastoma (GBM), which has a poor prognosis, accounts for 31% of all cancers in the brain and central nervous system. There is a paucity of research on prognostic indicators associated with the tumor immune microenvironment in GBM patients. Accurate tools for risk assessment of GBM patients are urgently needed. Methods: In this study, we used weighted gene co-expression network analysis (WGCNA) and differentially expressed gene (DEG) methods to screen out GBM-related genes among immune-related genes (IRGs). Then, we used survival analysis and Cox regression analysis to identify prognostic genes among the GBM-related genes to further establish a risk signature, which was validated using methods including ROC analysis, stratification analysis, protein expression level validation (HPA), gene expression level validation based on public cohorts, and RT-qPCR. In order to provide clinicians with a useful tool to predict survival, a nomogram based on an assessment of IRGs and clinicopathological features was constructed and further validated using DCA, time-dependent ROC curve, etc. Results: Three immune-related genes were found: PPP4C (p < 0.001, HR = 0.514), C5AR1 (p < 0.001, HR = 1.215), and IL-10 (p < 0.001, HR = 1.047). An immune-related prognostic signature (IPS) was built to calculate risk scores for GBM patients; patients classified into different risk groups had significant differences in survival (p = 0.006). Then, we constructed a nomogram based on an assessment of the IRG-based signature, which was validated as a potential prediction tool for GBM survival rates, showing greater accuracy than the nomogram without the IPS when predicting 1-year (0.35 < Pt < 0.50), 3-year (0.65 < Pt < 0.80), and 5-year (0.65 < Pt < 0.80) survival. Conclusions: In conclusion, we integrated bioinformatics and experimental approaches to construct an IPS and a nomogram based on IPS for predicting GBM prognosis. The signature showed strong potential for prognostic prediction and could help in developing more precise diagnostic approaches and treatments for GBM.

Introduction: Primary central nervous system (CNS) vasculitis is a rare immune inflammatory disease confined to the blood vessels of the brain and spinal cord. The total number reported in the world is about 500[1]. Most are negative in cerebral angiography or vascular stenosis and only 1 case of aortic aneurysms reported. Patient concerns: A 12-year-old female experienced sudden headache and vomiting. Previous findings of vascular stenosis. Diagnosed as a ruptured aneurysm bleeding. The aneurysm recurred a short time after treatment. Diagnosis: Multiple recurrent aneurysms with angiitis of the central nervous system Interventions: The patient underwent 2 aneurysm clipping operations, both of which completely clipped the aneurysm. Outcomes: The patient recovered well after surgery. Three months after discharge, DSA reexamination in our hospital showed that the aneurysm was completely clipped without recurrence. Conclusion: Subarachnoid hemorrhage after acute cerebral infarction is rare. In addition, the patient had recurrent aneurysms after the first aneurysm clipping, which emphasized the importance of postoperative drug therapy and blood pressure control.

Glioma is the most common malignant tumor in the central nervous system. The clinical treatment strategy is mainly surgery combined with concurrent temozolomide chemotherapy, but patients can develop drug resistance during treatment, which severely limits its therapeutic efficacy. Epigenetic regulation at the RNA level is plastic and adaptable, and it can induce a variety of tumor responses to drugs. The regulators of RNA modification include methyltransferases, demethylases, and methylation binding proteins; these are also considered to play an important role in the development, prognosis, and therapeutic response of gliomas, which provides a basis for finding new targets of epigenetic drugs and resetting the sensitivity of tumor cells to temozolomide. This review discusses the relationship between the development of adaptive drug resistance and RNA modification in glioma and summarizes the progress of several major RNA modification strategies in this field, especially RNA m6A modification, m5C modification, and adenosine-to-inosine editing.