Efficacy of Personalized Postoperative Epilepsy Management in Patients with Glioblastoma Utilizing IDH1 Gene Assessment.

Objective: We explored the correlation between the presence of isocitrate dehydrogenase-1 (IDH1) mutations and the incidence of postoperative epilepsy in patients with glioblastoma, as well as assessed the efficacy of preemptive administration of antiepileptic medications in mitigating the occurrence of postoperative epilepsy. Methods: Fifty-three patients who received a postoperative pathological diagnosis of glioblastoma, were enrolled in this study. Tumor specimens were subjected to IDH1 gene analysis. The patient cohort was stratified based on their IDH1 mutation status and the administration of prophylactic antiepileptic drugs during the postoperative phase. We subsequently conducted a comparative analysis of postoperative epileptic complications within each patient subgroup. Results: In the cohort of 53 patients under study, the occurrence of epilepsy was observed in 10 out of 21 patients carrying IDH1 mutations, while 5 out of 32 patients with wild-type IDH1 also experienced epilepsy, revealing a statistically significant difference (P < 0.05). Among the 27 patients who received prophylactic antiepileptic drugs, 6 of them developed epilepsy, whereas 9 out of 26 patients who did not receive prophylactic antiepileptic drugs exhibited concurrent epilepsy, with no statistically significant difference (P > 0.05). However, when performing a subgroup analysis, it was found that 3 out of 12 patients with IDH1 mutations who received prophylactic antiepileptic drugs experienced epilepsy, whereas 7 out of 9 patients who did not receive prophylactic antiepileptic drugs developed epilepsy, demonstrating a statistically significant difference (P < 0.05). Furthermore, within the group of 15 patients with wild-type IDH1, 3 patients who received prophylactic antiepileptic drugs developed epilepsy, while 2 cases of epilepsy occurred among the 17 patients who did not receive prophylactic antiepileptic drugs, with no statistically significant difference (P > 0.05). Conclusion: In individuals with IDH1 mutant glioblastoma who have undergone surgical resection, the implementation of preventive antiepileptic therapy demonstrates a potential to diminish the occurrence of postoperative epilepsy.

Identification of key genes in spontaneous cerebral hemorrhage and prevention of disease damage: LASSO and SVM regression.

Prevention is more important than treatment, and the incidence of intracerebral hemorrhage can be effectively reduced by intervening on the risk factors of intracerebral hemorrhage. By studying the risk factors of spontaneous intracerebral hemorrhage, we can identify the risk factors to achieve the target of treatment and prevention. Through the use of the Least Absolute Shrinkage and Selection Operator (LASSO) and the Support Vector Machine (SVM), the two essential SICH-related genes, NUAK1 and ERO1L, were eliminated from consideration. A Venn analysis was performed, and based on the two important modules, it found that SICH was related with four critical genes: VCM1, CRNDE, COL6A2, and HSPB6. One gene (NUAK1) was dramatically downregulated in the illness group compared to the control group, whereas three essential genes (ERO1L, VCAM1, and COL6A2) were significantly upregulated in the disease group. In the end, the genes ERO1L, VCAM1, COL6A2, and NUAK1 were shown to be the most important ones for SICH. It is anticipated that these genes will become novel biomarkers as well as targets for the development of new pharmacotherapies for SICH.

Bioinformatics analysis of BIRC5 in human cancers.

Background: An inhibitor of apoptosis (IAP) family member, baculoviral IAP repeat containing five (BIRC5) plays an important role in the occurrence and development of tumors. However, the underlying mechanism in human cancers remains unclear. Methods: In this study, we investigated BIRC5 expression and explored the prognostic value of BIRC5 in different human cancers via bioinformatics analysis, including the databases of Oncomine, Gene Expression Profiling Interactive Analysis (GEPIA), UALCAN, GEPIA, DriverDBv3, GeneMANIA, WEB-based Gene Set Analysis Tool (WebGestalt) and TIMER. Results: In most human cancers, BIRC5 usually had higher expression compared to normal human tissues. High expression of BIRC5 could increase the mortality of patients with adrenocortical carcinoma (ACC), kidney renal clear cell carcinoma (KIRC), low-grade glioma (LGG), liver hepatocellular carcinoma (LIHC), and lung adenocarcinoma (LUAD) (P<0.05). Cox analysis demonstrated that high BIRC5 expression was an independent factor for poor overall survival (OS) [hazard ratio, (HR) >1, P<0.05]. There were differences in BIRC5 expression in the case of TP53 mutation, different tumor grades, and stages. Interactive genes for BIRC5 mainly participated in apoptosis, cell division, cell cycle, and cancer pathways, strongly suggesting its oncogenic role in promoting cancer cell proliferation and cancer development. In addition, BIRC5 expression exhibited a close correlation with immune infiltration, which was related to the cumulative survival rate, especially in LGG. The elevated expression of BIRC5 could be regulated through TP53 mutation, tumor stage, and tumor grade (P<0.05). Conclusions: As a result of our findings, BIRC5 appears to be an independent unfavourable prognostic biomarker in human cancers. BIRC5 may become a potential clinical target in the future for the treatment of cancers.