Intra-arterial microguidewire electrocoagulation to treat intracranial vascular diseases.

OBJECTIVE: To investigate the therapeutic effect of intra-arterial microguidewire electrocoagulation on intracranial vascular diseases. METHODS: Data from 10 patients with cerebral aneurysms between May 2018 and September 2022 were analysed. Patients were treated with endovascular coil embolisation and microguidewire electrocoagulation. XperCT scans were conducted to identify new intracranial haemorrhage, infarction and hydrocephalus. Follow-up examinations were conducted 1, 3, 6 and 12 months after discharge. RESULTS: After the patients received electrocoagulation for different durations, Raymond Grade 1 embolisation was achieved in all 10 patients. No complications, such as haemorrhage, infarction or hydrocephalus, were found during or after surgery. Ten patients were followed up for 6-12 months, and none had any symptoms or new neurological dysfunction 1 month after their operation. Among them, nine were followed up for 12 months, and digital subtraction angiography showed no recurrence of aneurysms or occlusion of parent arteries. CONCLUSION: Intra-arterial microguidewire electrocoagulation can be used as a supplementary treatment for cerebral aneurysms. In cases of incomplete lesion embolisation and cases where tamponade treatment cannot continue, immediate thrombosis may occur. Thus, intra-arterial microguidewire electrocoagulation can help achieve patients' treatment goals.

Case report: emergent endovascular treatment for carotid cavernous fistulas presenting as intracranial hemorrhage.

Objectives: This study aimed to discuss the clinical characteristics and emergent endovascular treatment of carotid cavernous fistulas presenting as intracranial hemorrhage. Methods: The clinical data of five patients with carotid cavernous fistulas, who presented with intracranial hemorrhage and who were admitted from January 2010 to April 2017, were analyzed retrospectively, and the diagnoses were confirmed by head computed tomography. Digital subtraction angiography was carried out in all the patients for the diagnosis and further emergent endovascular procedures. All patients were followed up to assess the clinical outcomes. Results: In total, five patients harbored five mono-lateral lesions; two of them were obliterated by detachable balloons, two by detachable coils, and one by detachable coils and Onyx glue. Only one patient was cured by another detachable balloon in the second session, and the other four patients were cured in the first session. At the 3- to 10-year follow-up, there was no intracranial re-hemorrhage in any of the patients; there was no recurrence of symptoms; and delayed occlusion of the parent artery was noted in one case. Conclusion: Emergent endovascular therapy is indicated for carotid cavernous fistulas presenting as intracranial hemorrhage. Individualized treatment according to the characteristics of different lesions is safe and effective.

Glioma stem cells reconstruct similar immunoinflammatory microenvironment in different transplant sites and induce malignant transformation of tumor microenvironment cells.

PURPOSE: This study aimed to examine whether the different tumor-transplanted sites could construct a similar immunoinflammatory microenvironment and to investigate the interactions between tumor microenvironment cells. METHODS: The red fluorescent protein-SU3 (SU3-RFP) or SU3 glioma stem cells (GSC) were inoculated into the brain, liver, abdominal cavity, and subcutis of green fluorescent protein (GFP)-nude mice. The tumor tissues were taken to observe the tissue cell distribution. The single cell suspension of tumor tissues was prepared and cultured, while the SU3-RFP cells were co-cultured with the cells from GFP-transgenic mice. The RFP+, GFP+, and RFP+/GFP+ cells were traced by fluorescence microscope, and their protein expressions were determined by Western blot analysis. The markers of immunoinflammatory cells, including F4/80, CD11b, CD11c, CD80, CD47, and SIRP-α, were determined by RT-PCR and immunocytochemistry assays, respectively. RESULTS: The xenograft models of all transplant sites were inducible, and the red tumor cells of tumor tissues were encircled by a great quantity of host-derived green cells, including immunoinflammatory cells with CD80, F4/80, CD11b, and CD11c expressions, which might generate the cell colonies and possess the pseudopodia. Additionally, the interactions between red tumor cells and green immunoinflammatory cells, including cell fusion process and yellow fusion cell formation, were observed in cultured cells. The fusion cells-derived B4 cells with expressions of CD47 and SIRP-α proteins had the strong proliferation ability and tumorigenic effect. CONCLUSIONS: The similar tumor immunoinflammatory microenvironment was constructed by GSC in different transplant sites, and the cell fusion indicated a malignant transformation of the tumor microenvironment cells.

Establishment of a green fluorescent protein tracing murine model focused on the functions of host components in necrosis repair and the niche of subcutaneously implanted glioma.

Due to progress in the research of glioma stem cells and the glioma niche, development of an animal model that facilitates the elucidation of the roles of the host tissue and cells is necessary. The aim of the present study was to develop a subcutaneous xenograft green fluorescent protein nude mouse model and use this model to analyze the roles of host cells in tumor necrosis repair. Tumors derived from the human glioma stem/progenitor cell line SU3 were subcutaneously implanted in green fluorescent protein nude mice. The implanted tumors were then passed from animal to animal for 10 generations. Finally, subcutaneous xenografts were assayed with traditional pathology, immunopathological techniques and fluorescence photography. For each generation, the tumorigenicity rate was 100%. Subcutaneous xenografts were rich in blood vessels, and necrotic and hemorrhagic foci, which highly expressed hypoxia-inducible factor-1α, tumor necrosis factor, Ki-67, CD68 and CD11b. In the interstitial tissue, particularly in old hemorrhagic foci, there were numerous cells expressing green fluorescent protein, CD68 and CD11b. Green fluorescent protein nude mouse subcutaneous xenografts not only consistently maintained the high invasiveness and tumorigenicity of glioma stem/progenitor cells, but also consisted of a high concentration of tumor blood vessels and necrotic and hemorrhagic foci. Subcutaneous xenografts also expressed high levels of tumor microenvironment-related proteins and host-derived tumor interstitial molecules. The model has significant potential for further research on tumor tissue remodeling and the tumor microenvironment.