Search

Objective: The purpose of this study was to explore the effect of endovascular therapy on posterior communicating artery-infundibular dilatation aneurysms. Methods: A total of 15 patients with ruptured aneurysms caused by posterior communicating artery-infundibular dilatation who were treated in our neurosurgical center from January 2015 to December 2018were included in this study. They were performed with bilateral internal carotid angiography and vertebral angiography and treated with endovascular method. The modified Rankin Scale (mRS) was used for clinical follow-up for 18 months. Results: There were 10 patients in the posterior communicating artery-infundibular dilatation aneurysms with non-fetal posterior cerebral artery. Among them, 8 patients were treated with coil-alone embolization. Immediate imaging showed infundibular dilation residual in 6 cases and no contrast filling in either infundibular dilation or aneurysm in 2 case. Another 2 were treated with stent-assisted coiling embolization, and immediate imaging showed no contrast filling. Of the 5 patients in posterior communicating artery-infundibular dilatation aneurysms with fetal posterior cerebral artery, 4 were only coiled in the aneurysm sack with contrast filling in infundibular cones, and 2 were treated with stent assisted coiling. Among the 10 patients with non-fetal posterior cerebral artery, 3 showed recurrence, 4 showed stable images, 2 were also stable with no contrast filling in infundibular dilation or aneurysm and 1 was lost to follow-up. Among the 5 patients with fetal posterior cerebral artery, 1 showed stable images, 3 showed recurrence and 1 was lost to follow-up. Conclusions: For posterior communicating artery-infundibular dilatation aneurysms with non-fetal posterior cerebral artery, stent-assisted coiling of aneurysm embolization combined with occlusion of cones is effective to prevent or reduce recurrence.

Yang Yao,1,2,* Xinggen Fang,1,* Jinlong Yuan,1 Feiyun Qin,1 Tao Yu,1 Dayong Xia,1,3 Zhenbao Li,1 Niansheng Lai1,3 1Department of Neurosurgery, First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, Anhui Province, People’s Republic of China; 2Department of Nursing, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, Anhui Province, People’s Republic of China; 3Key Laboratory of Non-Coding RNA Transformation Research of Anhui Higher Education Institution (Wannan Medical College), Wuhu, 241001, Anhui Province, People’s Republic of China*These authors contributed equally to this workCorrespondence: Niansheng Lai; Zhenbao LiDepartment of Neurosurgery, First Affiliated Hospital of Wannan Medical College (Yijishan Hospital), 2 West Zheshan Road, Wuhu, 241001, Anhui Province, People’s Republic of ChinaTel +86-15155308793Fax +86-05535739594Email mlns@wnmc.edu.cn; zhenbaoli123@126.comObjective: Aneurysmal subarachnoid hemorrhage (aSAH) is a severe form of stroke characterized by high rates of mortality and disability. Identifying circulating biomarkers is helpful to improve outcomes. In this study, for the first time, we identify interleukin-6 (IL-6) in cerebrospinal fluid (CSF) small extracellular vesicles (sEVs) as potential biomarkers for prognosis of aSAH.Methods: We extracted small extracellular vesicles from the CSF of 103 aSAH patients and 40 healthy controls in a prospective observational study. Subsequently, we measured IL-6sEVs levels using an enzyme-linked immunosorbent assay. Results were statistically analyzed to determine the function of IL-6sEVs for disease monitoring of aSAH.Results: CSF IL-6 sEVs showed distinct pattern differences between healthy controls and aSAH patients. The concentration of IL-6sEVs in CSF is significantly correlated with the severity of aSAH patients. The areas under the receiver operating characteristic curves of IL-6sEVs for identifying severe aSAH patient from aSAH patients were 0.900. After multivariate logistic regression analysis, IL-6sEVs were associated with neurological outcome at 1 year. IL-6sEVs levels were greater and positively associated with disease processes and outcome.Conclusion: There is a neuroinflammatory cascade in aSAH patients. IL-6sEVs in CSF may be a biomarker for the progression of aSAH.Keywords: subarachnoid hemorrhage, cerebrospinal fluid, small extracellular vesicles, interleukin-6, biomarker

Aims Acyl‐CoA synthetase long chain family member 4 (ACSL4) is closely related to tumor genesis and development in certain tissues. However, the function of ACSL4 in early brain injury (EBI) caused by subarachnoid hemorrhage (SAH) is unclear. In this study, we investigated the expression patterns and role of ACSL4 in SAH and post‐SAH EBI using a rat model of SAH. Methods The rat model of SAH was induced by autologous blood injection into the prechiasmatic cistern of rats. We also used two specific inhibitors of ferroptosis (Ferrostatin‐1 and Liproxstatin‐1) to investigate the role of ferroptosis in EBI. Results We found that ACSL4 levels in brain tissue increased significantly in post‐SAH EBI. Inhibiting the expression of ACSL4 using small interfering RNAs alleviated inflammation, blood‐brain barrier (BBB) impairment, oxidative stress, brain edema, and behavioral and cognitive deficits, and increased the number of surviving neurons, after SAH. Similar effects were obtained by suppressing ferroptosis. Conclusions ACSL4 exacerbated SAH‐induced EBI by mediating ferroptosis. These findings may provide a theoretical basis for potential therapy aimed at alleviating post‐SAH EBI., ACSL4 levels in brain tissue of rats increase significantly in EBI and brain damage after SAH could be reduced by down‐regulation of ACSL4. ACSL4 could trigger ferroptosis and aggravate brain damage via catalyzing lipid metabolism. It may provide a theoretical basis for potential therapy to alleviate EBI after SAH

RAB7, a member of RAS oncogene family-like 1 (RAB7L1), is a GTPase belonging to the Rab family and acts as an upstream regulator to regulate the kinase activity of leucine-rich repeat kinase 2 (LRRK2). Although LRRK2 has been shown to aggravate secondary brain injury (SBI) after intracerebral hemorrhage (ICH), it is unknown whether RAB7L1 is also involved in this process. The purpose of the present study was to investigate the role of RAB7L1 in ICH-induced SBI in vivo. Autologous blood was injected into adult male Sprague-Dawley rats to induce an ICH model in vivo. The results showed that the protein levels of RAB7L1 increased after ICH. Overexpression of RAB7L1 induced neuronal apoptosis and damage, as demonstrated by TUNEL-positive and FJB-positive cells, and exacerbated ICH-induced learning and cognitive dysfunctions; in contrast, downregulation of RAB7L1 via RNA interference yielded comparatively opposite changes in these parameters. In summary, this study demonstrates that RAB7L1 promotes SBI after ICH and may represent a potential target for ICH therapy.

Objective Hemodynamic factors are thought to play important roles in the pathogenesis, progression, and rupture of cerebral aneurysms. Previous hemodynamic studies have been based on comparisons between post-ruptured and unruptured aneurysms. Nevertheless, changes of aneurysm morphology after rupture render these results unreliable. Moreover, pressure, age, gender, and the morphology of the parent artery also influence these results. Therefore, in the present study, we identified hemodynamic and morphological characteristics of aneurysms prior to rupture using twelve mirror aneurysms. Materials and methods From our database, we retrospectively analyzed twelve mirror aneurysms (MANs) prior to rupture. Each mirror aneurysm was divided into the prior to rupture or the unruptured group. Patient-specific models were reconstructed from three-dimensional (3D) images of all patients. Hemodynamic and morphological factors were analyzed and compared. Results Compared with the unruptured side of MANs, aneurysms prior to rupture were significantly larger and significantly more irregular in shape; they also had significantly higher aspect ratio (AR), size ratio (SR), undulation index (UI), ellipticity index (EI), percentage of low wall shear stress area (LSA) and significantly lower normal wall shear stress (NWSS). The oscillatory shear index (OSI) and nonsphericity index (NSI) in the aneurysms prior to rupture were non-significantly higher than those of the unruptured group. Conclusion MANs prior to rupture may be extremely useful models to assess the risk of aneurysm rupture. Larger size, irregular shape, higher AR, SR, UI, NI, and lower WSS may be associated with aneurysms at risk for rupture.

Background Inflammation is a potential crucial factor in the pathogenesis of subarachnoid hemorrhage (SAH). Circulating microRNAs (miRNAs) are involved in the regulation of diverse aspects of neuronal dysfunction. The therapeutic potential of miRNAs has been demonstrated in several CNS disorders and is thought to involve modulation of neuroinflammation. Here, we found that peripherally injected modified exosomes (Exos) delivered miRNAs to the brains of mice with SAH and that the potential mechanism was regulated by regulation of neuroinflammation. Methods Next-generation sequencing (NGS) and qRT-PCR were used to define the global miRNA profile of plasma exosomes in aSAH patients and healthy controls. We peripherally injected RVG/Exos/miR-193b-3p to achieve delivery of miR-193b-3p to the brain of mice with SAH. The effects of miR-193b-3p on SAH were assayed using a neurological score, brain water content, blood-brain barrier (BBB) injury, and Fluoro-Jade C (FJC) staining. Western blotting analysis, enzyme-linked immunosorbent assay (ELISA), and qRT-PCR were used to measure various proteins and mRNA levels. Results NGS and qRT-PCR revealed that four circulating exosomal miRNAs were differentially expressed. RVG/Exos exhibited improved targeting to the brains of SAH mice. MiR-193b-3p suppressed the expression and activity of HDAC3, upregulating the acetylation of NF-κB p65. Finally, miR-193b-3p treatment mitigated the neurological behavioral impairment, brain edema, BBB injury, and neurodegeneration induced by SAH, and reduced inflammatory cytokine expression in the brains of mice after SAH. Conclusions Exos/miR-193b-3p treatment attenuated the inflammatory response by acetylation of the NF-κB p65 via suppressed expression and activity of HDAC3. These effects alleviated neurobehavioral impairments and neuroinflammation following SAH.

This meeting abstract was removed due to the OA licensing requirements of this journal. The full abstract is listed here : https://www.svin.org/files/SVIN_2021_Abstracts_for_Web.pdf

To investigate the relationship between the dynamic changes of pro-inflammatory cytokines in cerebrospinal fluid (CSF) and headache in patients with aneurysmal subarachnoid hemorrhage (aSAH)at hospital admission.CSF was collected from patients with aSAH at four time points (days 1, 3, 5, and 7; n = 216) from January 2017 to August 2017 at the Department of Neurosurgery of the First Affiliated Hospital of Wannan Medical College. We measured CSF levels ofinterleukin-1β (IL-1β), IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α) levels using an enzyme-linked immunosorbent assay. Results were statistically analyzed to determine the relationship between the dynamic changes of pro-inflammatory cytokines in CSF and headache after aSAH.The concentrations of IL-1β, IL-6, IL-8, and TNF-α in CSF showed dynamic changes after aSAH. Spearman correlation coefficient analysis revealed that high Hunt-hess grade and modified Fisher scale were associated with a worse headache after aSAH on days 1 and 7 (all P 0.05). High values of intracranial pressure (ICP) and high levels of CSF pro-inflammatory cytokines were associated with a worse headache after aSAH at four time points (all P 0.05). However, no significant associations were found between headache and sex, and age. After multiple regression analysis, the Hunt-hess grade, the levels of IL-6 and the levels of TNF-α were associated with headache severity at day 1 (all P 0.05). The ICP, the levels of IL-1β and the levels of TNF-α were associated with headache severity on day 3, 5 and 7 (all P 0.05).Pro-inflammatory cytokines in CSF are closely associated with a headache after aSAH, and therefore may be a therapeutic target in the future.

Jinlong Yuan,1,&ast; Chenlei Huang,2,&ast; Zhenbao Li,1 Xiaochun Jiang,1 Xintong Zhao,1 Niansheng Lai,1 Dayong Xia,1 Degang Wu,1 Bingbing Zhang,1 Xuanzhi Wang,3 Xinggen Fang1 1Department of Neurosurgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, People’s Republic of China; 2Department of Clinical Laboratory, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, People’s Republic of China; 3Department of Neurosurgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Xinggen FangDepartment of Neurosurgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Zheshan West Road 2, Wuhu, 241001, People’s Republic of ChinaEmail 18805536056@163.comObjective: Hemodynamic parameters are associated with the recurrence of intracranial aneurysms (IAs). Studies showed that high velocity and wall shear stress (WSS) were associated with IAs recurrence after endovascular treatment; nevertheless, factors such as small sample size, locations of IAs, and types of IAs (ie, sidewall or bifurcation) were neglected. The purpose of this study was to identify the hemodynamic characteristics associated with recurrence of middle cerebral artery bifurcation aneurysms (MCABAs) after total embolization by the method of computer fluid dynamics (CFD).Methods: Following inclusion criteria, we included 92 MCABAs treated with coils only after total embolization from January 2014 to January 2019. We segmented into recurrent and non-recurrent groups according to follow-up digital subtraction angiography (DSA). The MCABA models, including pre-operatively and immediate post-operatively, were reconstructed using 3D-DSAs. The hemodynamic parameters pre-operatively and immediately post-operatively between the groups were calculated and analyzed.Results: There were no significant differences between the recurrent and non-recurrent groups for spatially averaged wall shear stress (SAWSS), maximum wall shear stress (MWSS), velocity, or oscillatory shear index (OSI) at the neck pre-operatively. In the recurrent group, the WSS (22.02± 5.11 vs 37.43± 8.27 pa, p < 0.001), MWSS (42.59± 17.02 vs 66.98± 18.61 pa, p=0.014), velocity (0.86± 0.19 vs 1.44± 0.61 m/s, p=0.01) preoperatively were significantly higher than postoperative values. By contrast, in the non-recurrent group, the WSS (26.53± 8.18 vs 22.29± 8.64pa, p=0.002), MWSS (42.71± 14.01 vs 37.15± 15.56 pa, p=0.013), velocity (1.08± 0.43 vs 0.23 (0.52, 0.57) m/s, p < 0.001) postoperatively were significantly lower than preoperative values. The OSI, whether in the recurrent group or the non-recurrent group, did not differ significantly between groups (p=0.79 and p=0.19).Conclusion: Higher WSS (SAWSS, MWSS) and flow velocity at the aneurysm neck after embolization might be related to recurrence of bifurcation IAs. These might be applied to clinical post-embolization management for the evaluation of bifurcation IAs recanalization.Keywords: computational fluid dynamic, hemodynamics, middle cerebral artery bifurcation aneurysms, recurrence

Background: Aneurismal subarachnoid hemorrhage (aSAH) is a serious type of stroke with high mortality and disability. Identifying circulating biomarkers is helpful to improve theranostics of aSAH. In this study, we are for the first time to report circulating interleukin-6(IL-6) in neuron-derived small extracellular vesicles(NDSEVs) were identified to be the potential biomarkers in prognosis of aSAH. Methods: We extracted small extracellular vesicles from the plasma of aSAH patients and healthy controls and were enriched by sequential precipitation and anti-L1CAM antibody immunoabsorption. Subsequently,we determined IL-6 levels by an enzyme-linked immunosorbent assay (ELISA). Result: Plasma IL-6 NDSEVs showed distinct pattern differences between aSAH patients and healthy controls. The IL-6NDSEVs levels were increased and positively associated with disease monitoring and prognosis of aSAH patients. These data suggest an elevated neuroinflammatory cascade in aSAH patients.Conclusion: The IL-6NDSEVs maybe prospective biomarkers to indicate its progression, and thus may own great potential in applications such as prognostic evaluation of aSAH in the near future.

Objective: Posterior communicating artery bifurcation aneurysms (PcomA-BAs) and infundibular dilations (PcomA-IDs) are found at the junction between the internal carotid artery (ICA) and the posterior communicating artery (PcomA). Several studies found that PcomA-IDs potentially progress to aneurysms and can even rupture. In our clinical practice, digital subtraction angiography (DSA) helps differentiate PcomA-IDs from unruptured PcomA-BAs. However, when PcomA-IDs are >3 mm in diameter or PcomA are absent on DSA, it is challenging to use DSA to differentiate PcomA-IDs from unruptured PcomA-BAs. Hemodynamic and morphological factors are thought to play important roles in the pathogenesis, progression, and rupture of cerebral aneurysms. We compared hemodynamic and morphological differences in unruptured PcomA-BAs and PcomA-IDs to better manage PcomA-IDs.Methods: We included 83 PcomA-IDs and 115 unruptured PcomA-BAs dignosed and measured using DSA from January 2015 to January 2019. Computational fluid dynamics was performed on these patient-specific models reconstructed using axial slices in DICOM format. Clinical, hemodynamic, and morphological factors were compared between the PcomA-IDs and PcomA-BAs. Significant parameters were analyzed using binary logistic regression analysis to identify independent risk factors. Receiver operating characteristic (ROC) analysis was performed on the independent risk factors to acquire cutoff values.Results: One hemodynamic and four morphyological parameters were significantly different between PcomA-IDs and PcomA-BAs: normalized wall shear stress (NWSS), size, the angle between the ophthalmic segment of the ICA and the PcomA (APcomA), the angle between the ophthalmic and the communicating segment of the ICA (AICA) and the diameter of the PcomA (DPcomA). Binary logistic regression analysis showed that small size and DPcomA as well as APcomA were all independent significant factors characterizing the status of PcomA-IDs and the ROC analysis for independent risk factors indicated the cutoff values of size, APcomA, and DPcomA were 3.45 mm, 66.27°, and 1.24 mm, respectively.Conclusions: Size, DpcomA, and ApcomA could independently characterize the status of PcomA-IDs. These might help us better differentiate them from real aneurysms and guide its management.

Background Aneurysmal subarachnoid hemorrhage (aSAH) is a severe type of stroke characterized by high rates of mortality and disability. Identifying circulating biomarkers is helpful to improve prognosis. In this study, for the first time, we identify circulating interleukin-6 (IL-6) levels in neuron-derived small extracellular vesicles (NDSEVs) as potential biomarkers in prognosis of aSAH.Methods We extracted small extracellular vesicles from the plasma of aSAH patients and healthy controls and enriched them using sequential precipitation and anti-L1CAM antibody immunoabsorption. Subsequently, we determined IL-6 levels using an enzyme-linked immunosorbent assay (ELISA).Results Plasma IL-6 NDSEVs showed distinct pattern differences between aSAH patients and healthy controls. There were significant correlations of IL-6concentrations in plasma with severity in aSAH. The AUCs of IL-6 for distinguishing the severe aSAH patients from mild aSAH patients were 0.961. After multivariate logistic regression analysis, only age, acute hydrocephalus,and the levels of IL-6 NDSEVs enabled prediction of neurological outcome at 1 year. The IL-6 NDSEVs levels were greater and positively associated with disease and prognosis of aSAH patients.Conclusions These data suggest a neuroinflammatory cascade in aSAH patients. IL-6 NDSEVs may be a biomarkers to monitor the progression of aSAH.

SYT14 (Synaptotagmin 14) participates in pathomechanical neurodegeneration and contributes to abnormal neurodevelopment. However, the functional mechanism of SYT14 in human glioma tumorigenesis remains unclear. In the present study, we measured the expression levels of SYT14 mRNA in human glioma cell lines, U373MG, U178, and U87MG and neural stem cells (NSC) cell line by RT-PCR, and used lentivirus-mediated small hairpin RNAs (shRNAs) to knock down SYT14 expression in U87MG cells. Changes in SYT14 expression were determined by real-time PCR. Cell proliferation and colony formation assays were used to analyze the role of SYT14 in U87MG cell proliferation, and cell apoptosis was assessed by flow cytometry. SYT14 mRNA expression was detected in the three glioma cell lines, and was highest in the U87MG cell line. The RNAi-mediated knockdown of SYT14 significantly decreased cell proliferation and colony formation in U87MG cells, and caused a moderate increase in apoptosis. Fewer S phase cells and more G2/M phase cells were observed. These data indicate that SYT14 is highly expressed in glioma cells, and may participate in glioma cell proliferation, apoptosis, and colony formation.

RAB7, a member of RAS oncogene family-like 1 (RAB7L1), is a GTPase belonging to the Rab family and acts as an upstream regulator to regulate the kinase activity of leucine-rich repeat kinase 2 (LRRK2). Although LRRK2 has been shown to aggravate secondary brain injury (SBI) after intracerebral hemorrhage (ICH), it is unknown whether RAB7L1 is also involved in this process. The purpose of the present study was to investigate the role of RAB7L1 in ICH-induced SBI in vivo. Autologous blood was injected into adult male Sprague-Dawley rats to induce an ICH model in vivo. The results showed that the protein levels of RAB7L1 increased after ICH. Overexpression of RAB7L1 induced neuronal apoptosis and damage, as demonstrated by TUNEL-positive and FJB-positive cells, and exacerbated ICH-induced learning and cognitive dysfunctions; in contrast, downregulation of RAB7L1 via RNA interference yielded comparatively opposite changes in these parameters. In summary, this study demonstrates that RAB7L1 promotes SBI after ICH and may represent a potential target for ICH therapy.

Background Intracerebral hemorrhage (ICH) is the common brain diseases in middle-aged and elderly people, with high disability and/or mortality rate, and is a serious public health concern. Both WNK3 kinase and the WNK3/SPAK/NKCC1 signaling pathway play an integral role in maintaining normal cell homeostasis. However, their role and underlying mechanisms in ICH-induced secondary brain injury (SBI) have yet to be elucidated. Methods We established an ICH model using male Sprague-Dawley (SD) rats by injecting autologous arterial blood into the unilateral basal ganglia. To establish ICH model in vitro, oxyhemoglobin (OxyHb; 20 μM) and neurons were cultured for 6 h at 37 °C, 5% CO2 atmosphere. To investigate the role of WNK3 and the WNK3/SPAK/NKCC1 signaling pathway in SBI, after genetic interventions, rotation and water maze test, brain edema and neuroinflammation were detected, and terminal-deoxynucleoitidyl transferase mediated dUTP nick end labeling (TUNEL), Fluoro-Jade C (FJC), and Nissl staining were performed. Results Our data showed that WNK3 expression in brain tissue were upregulated after ICH induction. In addition, silencing of WNK3 reduced neuronal apoptosis, and inflammatory responses in rats that underwent ICH. Inhibition of WNK3 expression reduced the damaged blood-brain barrier (BBB), alleviated the impaired degree of cerebral edema, and improved disruptive neurobehavioral cognition caused by ICH. Moreover, overexpression of WNK3 had the opposite effects. Finally, WNK3/SPAK/NKCC1 signaling pathway may be involved in the above-mentioned processes. Conclusions In conclusion, our findings showed that WNK3 and WNK3/SPAK/NKCC1 signaling pathway play a vital biological function in ICH-induced SBI. Depletion of WNK3 attenuated brain injury after ICH both in vivo and in vitro. Thus, WNK3 and WNK3/SPAK/NKCC1 signaling pathway are potential targets for treating SBI after ICH.

miRNAs are important regulators of translation and have been associated with the pathogenesis of a number of cardiovascular diseases including stroke and may be possible prognostic biomarkers. The purpose of the present study was to determine the expression levels of miRNAs in the sera of subarachnoid haemorrhage (SAH) patients and to evaluate their relationships with the severity and clinical outcome of SAH. Serum samples on day 3 after the onset of SAH were subjected to microarray analysis with Exqion miRCURYTM LNA array and quantitative PCR analysis. Serum samples from SAH patients (n=60) and healthy controls (n=10) were subjected to quantitative PCR analysis. The severities and clinical outcomes of the SAH patients were evaluated with the WFNS grade and the Modified Rankin Scale (mRS). Three miRNAs, miR-502-5p, miR-1297 and miR-4320 were significantly up-regulated in the sera of SAH patients when compared with the healthy controls. The serum miR-502-5p and miR-1297 levels were significantly higher in the patients with severe SAH and a poor outcome than in those with mild SAH and a good outcome (P

Introduction: The microRNA, miR-210, is frequently associated with hypoxia induction, and an increase in its levels is often correlated with poor prognosis in many solid tumours. The present study examines the levels of miR-210 in glioma tumours of multiple origins to determine if an association can be established with disease progression. Material and methods: Tissue samples were acquired from normal brain tissue, oligodendroglial tumours and astrocytic tumours. The astrocytic tumours were further divided by grade: diffuse astrocytomas (WHO grade II), anaplastic astrocytomas (WHO grade III), and glioblastoma (WHO grade IV). The expression of miR-210 was examined by realtime quantitative RT-PCR. The correlation of the expression of miR-210 and astrocytic tumour grade was analyzed by the Spearman correlation test. Results: MiR-210 presents a differential expression depending on the origin of the glioma. Oligodendroglial tumours exhibit a significantly reduced level of miR-210 as compared with normal brain tissue. In contrast, astrocytic tumours demonstrate significantly increased levels of miR-210. Furthermore, the expression of miR-210 is positively correlated with the grade of astrocytic tumour, in the following order: grade IV > grade III > grade II > normal brain tissue (p < 0.05). Conclusions: MiR-210 levels can be potentially established as a biomarker for pathological diagnosis of malignant astrocytic tumour progression. In addition, the expression of miR-210 can be utilized as an additional identification measure of glioma tumour origin.

The optimal treatment modalities of ruptured middle cerebral artery aneurysm are still controversial. The objective of this study is to analyze the outcomes of patients with ruptured middle cerebral artery aneurysms treated by endovascular coiling.From October 2011 to October 2015, 67 patients with 71 ruptured middle cerebral artery aneurysms received endovascular coiling in our hospital. We retrospectively reviewed the clinical, radiologic records and outcomes.Of all the 71 aneurysms (67 patients), 42 were treated by coil embolization merely, 27 by stent-assisted coiling and 2 unruptured aneurysms in patients with bilateral middle cerebral artery aneurysms without receiving treatment. Complete occlusion was achieved in 82.6% (57/69) of all the procedures. Each of incomplete and partial occlusion rates was 8.7% (6/69). Intraoperative rupture of aneurysms occurred in two procedures (2.9%). Thrombogenesis occurred in eight procedures (11.6%). Brain infarction occurred in eight patients (11.9%). Post-operative rebleeding occurred in seven patients (10.4%). Sixty-three patients were followed at a mean follow-up of 8.24 ± 7.16 months. The mortality and good outcome rate were 3.2% and 90.5%, respectively. Aneurysm recurrence occurred in 6 (13.3%) of the 45 aneurysms at a mean follow-up of 8.44 ± 7.83 months.Endovascular coiling is effective for patients with ruptured middle cerebral artery aneurysms. Individualized treatment should be assessed by experienced specialist. It is essential to perform randomized large trials to confirm the efficiency of endovascular coiling.

MicroRNAs (miRNAs) are small noncoding RNAs that negatively regulate protein biosynthesis and participate in the pathogenesis of various tumours. Previous studies have shown that miR-210 is highly expressed in different types of human cancers, including glioblastoma multiforme (GBM). However, the role that miR-210 plays in GBM remains unclear. Here, we detected the expression and examined the function of miRNA-210 in GBM cells. Furthermore, we investigated the possible molecular mechanisms by which miRNA-210 mediates cell proliferation and apoptosis. Fifteen GBM and five normal brain tissues, in addition to the U87MG and U251 GBM cell lines, were analysed in this study. We found that miR-210 was upregulated in GBM tissues and cell lines when compared to normal brain tissue. Cell counting and flow cytometric assay results demonstrated that upregulation of miR-210 induced cell proliferation and decreased cell apoptosis, respectively. In addition, downregulation of miR-210 inhibited cell proliferation and induced apoptosis. We also detected a miR-210 target, regulator of differentiation 1 (ROD1), which is involved in GBM progression. Knockdown of ROD1 reversed the growth arrest and apoptosis that were originally induced by miR-210 inhibition. We propose that miR-210 regulates cell proliferation and apoptosis in GBM cells by targeting ROD1. Our findings may provide a new potential therapeutic target for the treatment of GBM.

Enterprise stent has been widespread used in wide-necked intracranial aneurysms and good efficacy has been achieved, but there are few reports on its applications in very small ruptured intracranial aneurysms in literatures. This study aimed to evaluate the safety and efficacy of Enterprise stent-assisted coiling embolization of very small ruptured intracranial aneurysms. We retrospectively reviewed the clinical and imaging data from 37 patients with very small ruptured intracranial aneurysms who had SAC using Enterprise stents performed from February 2012 to July 2016 in our department. Data collected and analyzed included patient demographics, morphologic features of the aneurysm, treatment results, and follow-up results. Clinical outcomes were evaluated by the Glasgow Outcome Scale (GOS). Enterprise stents were successfully implanted in all 37 patients with very small ruptured intracranial aneurysms. Of the 37 individuals, 28 patients exhibited complete occlusion at Raymond grade I, 5 patients exhibited occlusion at Raymond grade II, and 4 patients at Raymond grade III. Procedure-related complications occurred in 3 of 37 patients (8.1%), including 1 case of intraprocedure aneurysm rupture who died from cerebral herniation caused by severe postoperative cerebral ischemia during the hospital stay, and the other 2 complications were acute in-stent thrombosis, and occlusion of parent artery caused by falling-off internal carotid artery plaque, respectively. A total of 36 patients underwent postoperative clinical follow-up visits for 6 to 24 months of which 31 patients recovered (GOS ≥ 4). One patient had hemiplegic paralysis, and no rehemorrhage was found. A total of 25 patients underwent follow-up digital subtraction angiography (DSA) at 3–21 months postintervention, in whom there were 22 cases with complete occlusion, 2 cases with recurrence of aneurysm neck, and 1 case with in-stent restenosis, but there was no patient with neurologic deficits. The Enterprise stent-assisted coiling embolization can be a safe and effective technique for treatment of very small ruptured intracranial aneurysms.

MicroRNA-155 is highly expressed in many malignant tumors with poor prognosis, which regulates cell apoptosis, proliferation, invasion, metastasis, tumor angiogenesis, and metabolism. This study aims at investigating the clinical significance of miR-155 expression in human gliomas. Real-time quantitative PCR was used to detect the expression levels of miR-155 in 131 glioma and 16 normal brain tissues. The association of miR-155 expression with clinicopathological factors and prognosis of glioma patients were analyzed. The expression levels of miR-155 were significantly higher in glioma tissues than that in normal brain tissues (P < 0.001), which was associated with high pathological grade (P < 0.001) and low Karnofsky Performance Status score (P = 0.022). As a result of Kaplan-Meier survival and Cox regression analyses, overall survival (OS) rates and progression-free survival were significantly poorer in high-expression group relative to low-expression group (both P < 0.001). Furthermore, miR-155 expression was significantly associated with poor OS (P < 0.001) and PFS (P = 0.001) in glioma patients who had high pathological grades (III-IV) as calculated by subgroup analyses. These findings reveal that miR-155 expression might be an independent prognostic factor and a therapeutic target for human glioma.