Intraneural hemangioma of spinal nerve roots: a Case Report and literature review.

Intraneural hemangiomas are rare benign neoplasms. We report the case of a 53­year­old female with a hemangioma in a spinal nerve root. The patient presented with muscular atropy of the right arm wihout obvious predisposing factors one year ago. MRI demonstrated a heterogeneously enhanced lesion adjacent to the right C4/5 intervertebral foramen. The lesion was considered to be a schwannoma preoperatively. Histologically, the lesion was abundant with intervening malformed vascular mass lined by simple squamous epithelial cells, and CD31 was positively stained at these epithelial cells by immunohistochemistry. The patient underwent microsurgical resection and recovered without complications.

Ferroptosis and Its Potential Role in Glioma: From Molecular Mechanisms to Therapeutic Opportunities.

Glioma is the most common intracranial malignant tumor, and the current main standard treatment option is a combination of tumor surgical resection, chemotherapy and radiotherapy. Due to the terribly poor five-year survival rate of patients with gliomas and the high recurrence rate of gliomas, some new and efficient therapeutic strategies are expected. Recently, ferroptosis, as a new form of cell death, has played a significant role in the treatment of gliomas. Specifically, studies have revealed key processes of ferroptosis, including iron overload in cells, occurrence of lipid peroxidation, inactivation of cysteine/glutathione antiporter system Xc- (xCT) and glutathione peroxidase 4 (GPX4). In the present review, we summarized the molecular mechanisms of ferroptosis and introduced the application and challenges of ferroptosis in the development and treatment of gliomas. Moreover, we highlighted the therapeutic opportunities of manipulating ferroptosis to improve glioma treatments, which may improve the clinical outcome.

Intracerebral hemorrhage associated with brucellosis: A case report.

Background: Intracerebral hemorrhage is a common disease, but cases of intracerebral hemorrhage with brucellosis are very rare. Here, we are presenting a case of a 60-year-old male patient diagnosed with brucellosis who has a right basal ganglia hemorrhage ruptured into bilateral lateral ventricles. Case presentation: A 60-year-old male patient with symptoms of intracerebral hemorrhage who had no common risk factors for intracerebral hemorrhage, but having been diagnosed with brucellosis 2 months earlier and telling a shepherd history for 3 years. Cranial computed tomography (CT) and cranial magnetic resonance angiography (MRA) revealed that an intracerebral hemorrhage in the right basal ganglia had broken into bilateral lateral ventricles, and a Brucella serology test was positive. The patient's condition improved significantly after receiving bilateral lateral ventricle cone drainage, hematoma cavity cone drainage and anti-brucellosis treatment. Conclusions: Herein, we discuss the possible mechanisms and clinical implications between brucellosis and intracerebral hemorrhage. This case suggests whether we can use brucellosis as a routine examination for disease diagnosis and prevention in patients with intracerebral hemorrhage from pastoral areas.

CASP4 can be a diagnostic biomarker and correlated with immune infiltrates in gliomas.

Background: Gliomas are the most common and invasive malignant tumors that originate in the central nervous system. Currently, the primary treatment modality for gliomas is maximum surgical resection, supplemented by radiotherapy and chemotherapy. However, the long-term survival rate has not signifificantly increased. Pyroptosis is a new form of programmed lytic death that has been recently discovered. Caspase 4 (CASP4) plays a key role in pyroptosis. Many studies have shown that pyroptosis is not only related to inflflammation but is also closely related to the occurrence and development of most tumors. This study aimed to prove that CASP4 has a key role in the mechanism of gliomas. Methods: We used expression data from The Cancer Genome Atlas and the Chinese Glioma Genome Atlas to explore the relationship between CASP4 expression and glioma prognosis. The differential expression of CASP4 in gliomas and normal tissues was fifirst tested, and then the connection between CASP4 and tumor prognosis was explored. The relationship between CASP4 expression and immune cell infifiltration was also investigated. Finally, the possible pathways were analyzed using Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Gene Set Enrichment Analysis. Results: CASP4 was highly expressed and associated with a signifificantly lower survival rate in patients with glioma. It could also inflfluence immune cell infifiltration by releasing cytokines. Conclusion: CASP4 can be a diagnostic biomarker and is a promising therapeutic target for gliomas.

OLFML2A Downregulation Inhibits Glioma Proliferation Through Suppression of Wnt/ß-Catenin Signaling.

Glioma is a highly heterogeneous and lethal tumor with an extremely poor prognosis. Through analysis of TCGA data, we identified that OLFML2A is a key promotor of gliomagenesis. However, the molecular function of OLFML2A and its underlying mechanism of action in glioma remain unclear. In this study, we found that OLFML2A expression was significantly upregulated in glioma specimens and positively correlated with pathological grades in glioma patients. Moreover, Kaplan-Meier survival analysis of TCGA data revealed that glioma patients with higher OLFML2A expression had shorter overall survival. Importantly, OLFML2A knockdown in glioma cells inhibited cell proliferation and promoted apoptosis. Mechanistically, OLFML2A downregulation inhibits Wnt/ß-catenin signaling by upregulating amyloid precursor protein (APP) expression and reducing stabilized ß-catenin levels, leading to the repression of MYC, CD44, and CSKN2A2 expression. Furthermore, OLFML2A downregulation suppressed the growth of transplanted glioma subcutaneously and intracranially by inhibiting Wnt/ß-catenin pathway-dependent cell proliferation. By uncovering the oncogenic effects in human and rodent gliomas, our data support OLFML2A as a potential therapeutic target for glioma.