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Objective The aim of the present study was to retrospectively analyze and investigate the clinical and morphological data of 204 cases of ruptured intracranial aneurysms (RIAs) and unruptured intracranial aneurysms (UIAs). The risk factors predicting aneurysm rupture were explored from the perspective of the clinical and geometric morphology of small and medium-sized(Methods The geometric morphological parameters, including the condition of the aneurysm-carrying vessels, the shape of the daughter aneurysm, the distribution and size of the aneurysm location, the height of the aneurysm, the wide diameter of the aneurysm, the width of the aneurysm neck, AR, SR, BN, and HWR. A comprehensive and detailed analysis, ROC curve analysis and multifactor logistic regression analysis, were performed to explore the risk factors for small and medium-sized aneurysm rupture, including the incidence angle, aneurysm angle.Results Multifactor logistic regression analysis suggested that there were significant differences between Groups RIA and UIA regarding age(OR 2.458), atherosclerosis, bifurcation-type IA(OR 5.523), and SR(OR 4.695) (P Conclusions Age( 0.86) and aneurysm at the bifurcation could be used as risk factors for small and medium-sized(

The glymphatic system (GS) plays an important role in subarachnoid hemorrhage (SAH). Nimodipine treatment provides SAH patients with short-term neurological benefits. However, no trials have been conducted to quantify the relationship between nimodipine and GS. We hypothesized that nimodipine could attenuate early brain injury (EBI) after SAH by affecting the function of the GS. In this study, we assessed the effects of nimodipine, a dihydropyridine calcium channel antagonist, on mice 3 days after SAH. The functions of GS were assessed by immunofluorescence and western blot. The effects of nimodipine were assessed behaviorally. Concurrently, correlation analysis was performed for the functions of GS, immunofluorescence and behavioral function. Our results indicated that nimodipine improved GS function and attenuated neurological deficits and brain edema in mice with SAH. Activation of the cAMP/PKA pathway was involved in this process. GS function was closely associated with perivascular AQP4 polarization, cortical GFAP/AQP4 expression, brain edema and neurobehavioral function. In conclusion, this study shows for the first time that nimodipine plays a neuroprotective role in the period of EBI after SAH in mice through the GS.

BACKGROUND In an atherosclerotic artery wall, monocyte-derived macrophages are the principal mediators that respond to pathogens and inflammation. The present study aimed to investigate potential genetic changes in gene expression between normal tissue-resident macrophages and atherosclerotic macrophages in the human body. MATERIAL AND METHODS The expression profile data of GSE7074 acquired from the Gene Expression Omnibus (GEO) database, which includes the transcriptome of 4 types of macrophages, was downloaded. Differentially expressed genes (DEGs) were identified using R software, then we performed functional enrichment, protein‑protein interaction (PPI) network construction, key node and module analysis, and prediction of microRNAs (miRNAs)/transcription factors (TFs) targeting genes. RESULTS After data processing, 236 DEGs were identified, including 21 upregulated genes and 215 downregulated genes. The DEG set was enriched in 22 significant Gene Ontology (GO) terms and 25 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, and the PPI network constructed with these DEGs comprised 6 key nodes with degrees ≥8. Key nodes in the PPI network and simultaneously involved in the prime modules, including rhodopsin (RHO), coagulation factor V (F5), and bestrophin-1 (BEST1), are promising for the prediction of atherosclerotic plaque formation. Furthermore, in the miRNA/TF-target network, hsa-miR-3177-5p might be involved in the pathogenesis of -atherosclerosis via regulating BEST1, and the transcription factor early growth response-1 (EGR1) was found to be a potential promoter in atherogenesis. CONCLUSIONS The identified key hub genes, predicted miRNAs/TFs, and underlying molecular mechanisms may be involved in atherogenesis, thus potentially contributing to the treatment and diagnosis of patients with atherosclerotic disease.

Ubiquitin-specific protease 22 (USP22), a potential marker of cancer stem cells, significantly influences stem cell fate choices. However, its functions in neural stem cells (NSCs) and adult neurogenesis, especially following traumatic brain injury (TBI), remain only partially understood. Here, we found that aberrant USP22 expression could affect NSC proliferation and stemness maintenance, as assessed by the generation of neurospheres, cell counting kit-8 (CCK-8) and immunofluorescence staining in vitro. Moreover, USP22 depletion promotes the differentiation of NSCs, both in vitro and in vivo. In contrast, USP22 overexpression inhibits NSC differentiation into neurons. Interestingly, our data showed that USP22 promotes the proliferation but inhibits the differentiation of NSCs in the dentate gyrus (DG) of the hippocampus soon after TBI. The Morris water maze (MWM) test was adopted to evaluate neurological function, which confirmed that USP22 could improve the learning and memory capacity that was already compromised following TBI. Overall, this study uncovers a potentially novel regulatory role of USP22 in the proliferation and differentiation ability of NSCs, contributing to the hippocampus-dependent cognitive function of TBI mice and may be a novel target for future therapeutic approaches.

Background Intracranial aneurysm (IA) is a serious disease. Analyze and review the cases of anterior circulation ruptured IA by supraorbital lateral keyhole approach, and summarize the experiences of this approach. Methods Retrospective analysis of 16 cases of ruptured anterior circulation IA in our department from January 2019 to June 2020, CT angiography (CTA) was performed before operation. Analyzing the IA’s parameters by 3D-CT reconstruction. The IA was clipped by supraorbital lateral keyhole approach combined with the 3D-skull reconstruction. Extraventricular drainage was performed before craniotomy. Intraoperative neurophysiological monitoring was performed during the operation. After operation, fluorescein angiography and vascular ultrasound were performed to check the clipping effect. Intracranial pressure monitor was performed postoperatively. CTA was reexamined one week after operation. The modified Rankin Scale (MRS) was performed 6 months after operation. Results There were 7 males (43.8%) and 9 females (56.2%), and the average age is 52.31 ± 11.12 years old. Among them, 11 patients (68.8%) were anterior communicating artery aneurysms and 5 (31.2%) were middle cerebral artery aneurysms. All patients were out of hospital within 10 days without any death, without cerebral infarction, cerebrospinal fluid leakage and neurological impairments. About mRS score, after 6 months follow-up, 8 cases (50%) had 0 point, 4 cases (25%) had 1 point, and 4 cases (25%) had 2 points. Conclusions For ruptured anterior circulation IA, the supraorbital lateral keyhole approach combined with ventricular drainage, intraoperative electrophysiological monitoring, and intraoperative vascular ultrasound is a safe and minimally invasive treatment. The application of reconstruction clipping can reconstruct the diameter of parent vessel and reduce the recurrence rate of IA.

Xiaopeng Cui,1,2,* Wen-Qiang Xin,1,* Bangyue Wang,1 Yan Zhao,1 Changkai Hou,1 Shifei Cai,1 Chao Peng,1 Zhen Wang,1 Jian Li,1 Linchun Huan,3 Lei Chen,2 Xinyu Yang1 1Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, People’s Republic of China; 2Department of Neurosurgery, Tianjin Fifth Central Hospital, Tianjin, People’s Republic of China; 3Department of Neurosurgery, Linyi People’s Hospital, Shandong, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xinyu YangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin Medical University, 154 Anshan Road, Peace Zone, Tianjin, 300041, People’s Republic of ChinaEmail yangxinyu@tmu.edu.cnLei ChenDepartment of Neurosurgery, Tianjin Fifth Central Hospital, 41 Zhejiang Road, Binhai New Area, Tianjin, 300450, People’s Republic of ChinaEmail chenlei1130@163.comObjective: 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.Keywords: intracranial aneurysm, CDKN2A/CDKN2B gene, Chinese Han population, SNP

Background and purpose Blood that enters the subarachnoid space (SAS) and its breakdown products are neurotoxic and are the principal inducers of brain injury after subarachnoid hemorrhage (SAH). Recently, meningeal lymphatic vessels (MLVs) have been proven to play an important role in clearing erythrocytes that arise from SAH, as well as other macromolecular solutes. However, evidence demonstrating the relationship between MLVs and brain injury after SAH is still limited. Therefore, we performed this study to observe the effects of meningeal lymphatic impairment on early brain injury (EBI) after experimental SAH. Methods The MLVs of C57BL/6 male adult mice were ablated by injecting Visudyne into the cisterna magna and transcranially photoconverting it with laser light. The MLVs were then examined by immunofluorescence staining for lyve-1. Next, both the MLV-ablated group and the control group (normal mice) underwent filament perforation to model SAH or sham operation. We assessed the cortical perfusion of all the mice before SAH induction, 5 min after SAH and 24 h after SAH. In addition, we evaluated neurological function deficits by Garcia scores and measured brain water content at 24 h post SAH. Then, neuroinflammation and neural apoptosis in the mouse brain were also examined. Results Visudyne and transcranial photoconversion treatment notably ablated mouse MLVs. Five minutes after SAH induction, cortical perfusion was significantly impaired, and after 24 h, this impairment was ameliorated considerably in the control group but ameliorated only slightly or worsened in the MLV-ablated group. Additionally, the MLVablated group presented worse neurological function deficits and more severe brain edema than the control group. More notably, neuroinflammation and neural apoptosis were also observed. Conclusion Ablation of MLVs by Visudyne treatment exacerbated EBI after experimental SAH in mice. The worsening of EBI may have arisen from limited drainage of blood and other breakdown products, which are thought to cause brain edema, neuroinflammation, neuronal apoptosis and other pathological processes.