The safety and clinical outcomes of endovascular treatment versus microsurgical clipping of ruptured anterior communicating artery aneurysms: a 2-year follow-up, multicenter, observational study.

Background and objective: Current data on the optimal treatment modality for ruptured anterior communicating artery (AComA) aneurysms are limited. We conducted this multicenter retrospective study to evaluate the safety and clinical outcomes of endovascular treatment (EVT) and microsurgical clipping (MC) for the treatment of ruptured AComA patients. Methods: Patients with ruptured AComA aneurysms were screened from the Chinese Multicenter Cerebral Aneurysm Database. Propensity score matching (PSM) was used to adjust for baseline characteristic imbalances between the EVT and MC groups. The safety outcomes included total procedural complications, procedure-related morbidity/death and remedial procedure for complication. The primary clinical outcome was 2-year functional independence measured by the modified Rankin scale (mRS) score. Results: The analysis included 893 patients with ruptured AComA aneurysms (EVT: 549; MC: 346). PSM yielded 275 pairs of patients in the EVT and MC cohorts for comparison. Decompressive craniectomy being more prevalent in the MC group (19.3% vs. 1.5%, p < 0.001). Safety data revealed a lower rate of total procedural complications (odds ratio [OR] = 0.62, 95% CI 0.39-0.99; p = 0.044) in the EVT group and similar rates of procedure-related morbidity/death (OR = 0.91, 95% CI 0.48-1.73; p = 0.880) and remedial procedure for complication (OR = 1.35, 95% CI 0.51-3.69, p = 0.657) between the groups. Compared with that of MC patients, EVT patients had a greater likelihood of functional independence (mRS score 0-2) at discharge (OR = 1.68, 95% CI 1.14-2.50; p = 0.008) and at 2 years (OR = 1.89, 95% CI 1.20-3.00; p = 0.005), a lower incidence of 2-year all-cause mortality (OR = 0.54, 95% CI 0.31-0.93; p = 0.023) and a similar rate of retreatment (OR = 1.00, 95% CI 0.23-4.40; p = 1.000). Conclusion: Clinical outcomes after treatment for ruptured AComA aneurysms appear to be superior to those after treatment with MC, with fewer overall procedure-related complications and no increase in the retreatment rate. Additional studies in other countries are needed to verify these findings.

Integrate prediction of machine learning for single ACoA rupture risk: a multicenter retrospective analysis.

Background: Statistically, Anterior communicating aneurysm (ACoA) accounts for 30 to 35% of intracranial aneurysms. ACoA, once ruptured, will have an acute onset and cause severe neurological dysfunction and even death. Therefore, clinical analysis of risk factors related to ACoA and the establishment of prediction model are the benefits to the primary prevention of ACoA. Methods: Among 1,436 cases of single ACoA patients, we screened 1,325 valid cases, classified risk factors of 1,124 cases in the ruptured group and 201 cases in the unruptured group, and assessed the risk factors, respectively, and predicted the risk of single ACoA rupture by using the logistic regression and the machine learning. Results: In the ruptured group (84.8%) of 1,124 cases and the unruptured group (15.2%) of 201 cases, the multivariable logistic regression (MLR) model shows hemorrhagic stroke history (OR 95%CI, p:0.233 (0.120-0.454),<0.001) and the age stratification of 60-69 years (OR 95%CI, p:0.425 (0.271-0.668),<0.001) has a significant statistic difference. In the RandomForest (RF) model, hemorrhagic stroke history and age are the best predictive factors. Conclusion: We combined the analysis of MLR, RF, and PCA models to conclude that hemorrhagic stroke history and gender affect single ACoA rupture. The RF model with web dynamic nomogram, allows for real-time personalized analysis based on different patients' conditions, which is a tremendous advantage for the primary prevention of single ACoA rupture. Clinical trial registration: https://www.chictr.org.cn/showproj.html?proj=178501.

Association of CDKN2A/CDKN2B Gene Polymorphisms with Increased Susceptibility to Intracranial Aneurysm in a Chinese Han Population.

OBJECTIVE: Several studies have reported that single-nucleotide polymorphisms (SNPs) of the CDKN2A/CDKN2B gene on chromosome 9p21.3 are associated with increased risk of intracranial aneurysm (IA). However, the association between IAs and SNPs of CDKN2A/CDKN2B in Chinese Han people is yet to be evaluated. This study examined the association of the SNPs rs10811661 and rs4977574 with IA in the Chinese Han population. METHODS: A total of 595 IA patients and 600 sex- and age-matched controls were enrolled in the study. Peripheral blood was collected and stored at -80°C until use. CDKN2A/CDKN2B was identified using polymerase chain reaction-ligase detection reaction. SNP genotyping was performed for rs10811661 and rs4977574 using a MassArray system. Associations between these two SNPs and IAs was tested with χ2 or Fisher's exact tests and multivariate logistic regression. RESULTS: rs10811661 and rs4977574 were significantly associated with IA. The frequency of rs10811661-T in IA was higher than in controls (OR 1.26, 95% CI 1.07-1.49; P<0.01). There was no significant difference in frequency of haplotype between control subjects and IA patients. CONCLUSION: rs10811661 and rs4977574 on 9p21.3 were strongly associated with genetic susceptibility to IA in the Chinese Han population, which emphasizes a need for further investigation.

Genetic polymorphisms in Sox17 associated with intracranial aneurysm in Chinese Han people: a genotype-phenotype study.

PURPOSE: Genetic factors play a vital role in intracranial aneurysm (IA) onset and development. Studying the relationship between IA and the Sox17 polymorphisms in diverse populations is essential for establishing credibility. PATIENTS AND METHODS: We collected blood samples derived from a total of 596 sporadic IA patients and 600 individual controls in several medical institutes in China. We used the Sequenom MassArray system for single nucleotide polymorphisms (SNPs) genotyping after DNA extraction. The SNPs data was tested and analyzed in PLINK (version 1.9). Multiple-testing was performed in PLINK to make the statistics more rigorous and accurate. RESULTS: We found that the allelic G of rs1072737 (OR=1.303, genomic-control corrected P-value =0.001032) is a risk allele, while the allelic G of rs9298506 (OR=0.7253, genomic-control corrected P-value =0.01559) is a protective allele in Chinese Han people. CONCLUSION: The allelic G of rs1072737 is a risk factor for IA, while the allelic G of rs9298506 serves as a protective factor for IA in Chinese Han people.

Rho Guanine Nucleotide Exchange Factor ARHGEF17 Is a Risk Gene for Intracranial Aneurysms.

BACKGROUND: Intracranial aneurysm (IA) is usually a late-onset disease, affecting 1% to 3% of the general population and leading to life-threatening subarachnoid hemorrhage. Genetic susceptibility has been implicated in IAs, but the causative genes remain elusive. METHODS: We performed next-generation sequencing in a discovery cohort of 20 Chinese IA patients. Bioinformatics filters were exploited to search for candidate deleterious variants with rare and low allele frequency. We further examined the candidate variants in a multiethnic sample collection of 86 whole exome sequenced unsolved familial IA cases from 3 previously published studies. RESULTS: We identified that the low-frequency variant c.4394C>A_p.Ala1465Asp (rs2298808) of ARHGEF17 was significantly associated with IA in our Chinese discovery cohort (P=7.3×10-4; odds ratio=7.34). It was subsequently replicated in Japanese familial IA patients (P=0.039; odds ratio=4.00; 95% confidence interval=0.832-14.8) and was associated with IA in the large Chinese sample collection comprising 832 sporadic IA-affected and 599 control individuals (P=0.041; odds ratio=1.51; 95% confidence interval=1.02-Inf). When combining the sequencing data of all familial IA patients from 4 different ethnicities (ie, Chinese, Japanese, European American, and French-Canadian), we identified a significantly increased mutation burden for ARHGEF17 (21/106 versus 11/306; P=8.1×10-7; odds ratio=6.6; 95% confidence interval=2.9-15.8) in cases as compared with controls. In zebrafish, arhgef17 was highly expressed in the brain blood vessel. arhgef17 knockdown caused blood extravasation in the brain region. Endothelial lesions were identified exclusively on cerebral blood vessels in the arhgef17-deficient zebrafish. CONCLUSIONS: Our results provide compelling evidence that ARHGEF17 is a risk gene for IA.

Alveolar soft part sarcoma associated with lung and brain metastases: A case report.

The present case report aimed to improve the understanding of alveolar soft part sarcoma (ASPS) by investigating the clinical characteristics, diagnosis and therapeutic methods used to treat ASPS associated with lung and brain metastases. The clinical data of a single patient diagnosed with ASPS by postoperative pathology was studied retrospectively, and additional associated reports and previous studies of similar cases were reviewed. Clinical symptoms were markedly alleviated following surgical treatment, followed by a chemotherapy regime. During post-treatment follow-up, no tumor recurrence was observed.

Hes1, a Notch signaling downstream target, regulates adult hippocampal neurogenesis following traumatic brain injury.

Hairy and enhancer of split 1 (Hes1), a downstream target of Notch signaling, has long been recognized as crucial in inhibiting neuronal differentiation. However, the role of Hes1 following traumatic brain injury (TBI) in adult neurogenesis in the mouse dentate gyrus (DG) remains partially understood. Here, we investigate the role of Hes1 in regulating neurogenesis in the DG of the adult hippocampus after TBI by up- or downregulating Hes1 expression. First, adenovirus-mediated gene transfection was employed to upregulate Hes1 in vivo. The mice were then subjected to TBI, and the hippocampal tissue was collected for Western blot analysis at designated times, pre- and post-injury. Moreover, the brain slices were stained for BrdU and doublecortin (DCX). We show that enhancing Hes1 inhibits the proliferation and differentiation of neural precursor cells (NPCs) in the DG of the hippocampus soon after TBI. Second, downregulation of Hes1 via RNA interference (RNAi) results in a significant increase in neuronal production and promotes the differentiation of NPCs into mature neurons in the DG, as assessed by BrdU and NeuN double staining. Furthermore, a Morris water maze (MWM) test clearly confirmed that the knockdown of Hes1 improves the spatial learning and memory capacity of adult mice following injury. Taken together, these observations suggest that Hes1 represents a negative regulator of adult neurogenesis post-TBI and that the precise space-time regulation of Hes1 expression in the DG may promote the recovery of neural function following TBI.