Retracted: Long noncoding RNA MEG3 inhibits proliferation and migration but induces autophagy by regulation of Sirt7 and PI3K/AKT/mTOR pathway in glioma cells.

Glioma is a common primary brain tumor with high mortality rate and poor prognosis. Long noncoding RNA maternally expressed gene 3 (MEG3) is a tumor suppressor in diverse cancer types. However, the role of MEG3 in glioma remains unclear. We aimed to explore the effects of MEG3 on U251 cells as well as the underlying mechanisms. U251 cells were stably transfected with different recombined plasmids to overexpress or silence MEG3. Effects of aberrantly expressed MEG3 on cell viability, migration, apoptosis, expressions of apoptosis-associated and autophagy-associated proteins, and phosphorylated levels of key kinases in the PI3K/AKT/mTOR pathway were all evaluated. Then, messenger RNA (mRNA) and protein expression of Sirt7 in cells abnormally expressing MEG3 were estimated. In addition, effects of abnormally expressed MEG3 and Sirt7 on U251 cells were determined to reveal the underlying mechanism of MEG3-associated modulation. Cell viability and migration were significantly reduced by MEG3 overexpression whereas cell apoptosis as well as Bax and cleaved caspase-3/-9 proteins were obviously induced. Beclin-1 and LC3-II/LC3-I were upregulated and p62 was downregulated in MEG3 overexpressed cells. In addition, the autophagy pharmacological inhibitor (3-methyladenine, 3-MA) affected the effect of MEG3 overexpression on cell proliferation. Furthermore, the phosphorylated levels of key kinases in the PI3K/AKT/mTOR pathway were all reduced by MEG3 overexpression. Sirt7 was positively regulated by MEG3 expression, and effects of MEG3 overexpression on U251 cells were ameliorated by Sirt7 silence. MEG3 suppressed cell proliferation and migration but promoted autophagy in U251 cells through positively regulating Sirt7, involving in the inhibition of the PI3K/AKT/mTOR pathway.

Ligustrazine Inhibits Growth, Migration and Invasion of Medulloblastoma Daoy Cells by Up-Regulation of miR-211.

BACKGROUND/AIMS: Ligustrazine (LSZ) has been identified as an antitumor agent against some types of cancers. Nevertheless, its ability to inhibit growth, migration and invasion of medulloblastoma cells is still unclear. This study aimed to explore the effect of LSZ on Daoy cells. METHODS: The effects of LSZ on viability, proliferation, apoptosis, migration, and invasion of Daoy cells were analyzed by CCK-8, BrdU, flow cytometry and Transwell assays, respectively. The effect of LSZ on miR-211 expression was analyzed by qRT-PCR. miR-211 inhibitor transfection was performed to suppress miR-211 expression. The effects of LSZ on apoptosis-related factors, MMP-2, MMP-9, and Vimentin (Vim), as well as main factors of PI3K/AKT and mTOR pathways were analyzed by Western blot. RESULTS: LSZ inhibited viability but promoted apoptosis of Daoy cells. Additionally, the proliferative, migratory and invasive abilities of Daoy cells were decreased by LSZ. Meanwhile, LSZ promoted the activations of Caspase-3 and Caspase-9, increased Bax level, decreased Bcl-2 level, as well as inhibited the expressions of MMP-2, MMP-9 and Vim. Additionally, we found that LSZ enhanced miR-211 expression and exerted its anti-medulloblastoma effect by up-regulation of miR-211. Furthermore, LSZ inhibited PI3K/AKT and mTOR signaling pathways by up-regulating miR-211. CONCLUSION: LSZ suppressed medulloblastoma Daoy cells by up-regulating miR-211 and further modulating the activations of PI3K/AKT and mTOR signaling pathways.

Diagnosis and treatment of solitary fibrous tumor/hemangiopericytoma of central nervous system. Retrospective report of 17 patients and literature review.

To investigate the diagnosis, treatment and prognosis of solitary fibrous tumor (SFT)/ hemangiopericytoma (HPC) of central nervous system (CNS), we retrospectively reviewed records of 17 patients who were treated for CNS SFT/HPC at the Department of Neurosurgery, China-Japan Union Hospital of Jilin University from December 2010 to June 2016, and reevaluated their pathological diagnoses according to the 2016 WHO classification of CNS tumors. We then analyzed their clinical symptoms, imaging characteristics, treatments and outcomes. Clinical manifestations of CNS SFT/HPC were diverse, but mainly included headache, increased intracranial pressure, seizures, and focal neurological deficits. In MRI, CNS SFT/HPC usually shows heterogeneous signals, and unusual enhancements; we saw lobulated shapes in 13 patients and necrotic or cystic changes in 12 patients. Tumors of all 17 patients were resected surgically; 9 patients also received postoperative adjuvant radiotherapy. Mean follow-up time was 21 months (range: 2-67 months). The 17 surgeries included 11 total resections, 4 subtotal resection, and 2 partial resections. We followed up 12 patients; 9 of the patients who received total resections had no disease progression; among the 6 patients who did not receive total resections, 2 died of tumor recurrence, 1 has not shown any disease progression. Thus, extent of resection has an apparently crucial influence on prognosis. Postoperative radiotherapy should be chosen carefully, based on resection extent and pathologic grade.

Intracerebral schwannoma: A case report and literature review.

Intracranial schwannoma accounts for between 5 and 8% of intracranial tumors, whereas intracerebral schwannoma, a rare disease, accounts for <1% of intracranial schwannomas. In addition to the present case report, a total of 84 cases reported within China and elsewhere were reviewed and summarized, and the age of the tumor onset, the site of disease, imaging results, clinical presentation, pathological classification and prognosis were analyzed. The present case report described a 12-year-old female with an intracerebral schwannoma in the brainstem, who was followed-up for 5 years using magnetic resonance imaging after a surgical resection without recurrence, and clinical symptoms were reported to have completely resolved. The incidence of intracerebral schwannoma was low among cases, and the correct diagnosis was not able to be made preoperatively, and the majority of cases were diagnosed on the basis of postoperative pathology. The majority of cases analyzed were supratentorial, occurring at an age ≤40 according to previous literature. In addition, 33% of patients presented with subtentorial schwannoma, occurring at an age >40. The prognosis was classified as good (patient can live independently) for the majority of patients if surgery was able to completely resect the lesion.

Hemodynamics in Ruptured Intracranial Aneurysms with Known Rupture Points.

BACKGROUND: Hemodynamics plays an important role in aneurysm rupture. Microsurgical clipping provides the best chance to confirm the rupture point. The aim of this study was to explore the associations between the rupture point and hemodynamics. METHODS: Computational fluid dynamic simulations were performed on 16 intracranial aneurysms. The rupture point was detected at the time of clipping by 3 independent neurosurgeons. Hemodynamic parameters, including wall shear stress (WSS) and oscillatory shear index (OSI), were calculated at the rupture point and the whole aneurysm sac. Intra-aneurysmal flow patterns and flow impingement were also studied. RESULTS: The time-averaged WSS was 3.4855 ± 3.8881 Pa at the aneurysm sac, which was significantly larger than that at the rupture point (1.5403 ± 2.3688 Pa, P = 0.002). The OSI at the rupture point (0.0354 ± 0.0459) was larger than at the sac (0.0220 ± 0.0232) without difference. Thirteen aneurysms (81.3%) showed a complex flow pattern in the aneurysm sac; however, more than two thirds of the cases (68.7%) did not show a flow impact at the rupture point. Of these cases with daughter blebs, the rupture points were confirmed at the blebs in 6 cases. Two cases did not show association between blebs and rupture point. CONCLUSIONS: The hemodynamic characteristics at the rupture point were different from the aneurysm sac, and the WSS was significantly lower at the rupture point. Further study on the rupture risk assessment is still needed with more data and detailed information.

Lnc-SNHG1 Activates the TGFBR2/SMAD3 and RAB11A/Wnt/ß-Catenin Pathway by Sponging MiR-302/372/373/520 in Invasive Pituitary Tumors.

BACKGROUND/AIMS: Long noncoding RNAs (lncRNAs) are critical regulators in various diseases including human cancer and could function as competing endogenous RNAs (ceRNAs) to regulate microRNAs (miRNAs). METHODS: Quantitative real-time PCR (qRT-PCR) was used to analyze the expression of lnc-SNHG1 and miR-302/372/373/520 in pituitary tumor tissues and cell lines. Cell proliferation was investigated using MTT and cell count assays. The mechanisms by which lnc-SNHG1 affects pituitary tumor progression were investigated using Western blot assays, transwell migration assays, immunohistochemistry, immunofluorescence, luciferase reporter assays, tumor xenografts, and flow cytometry Results: We found that lnc-SNHG1 was overexpressed in invasive pituitary tumor tissues and cell lines. Ectopic expression of lnc-SNHG1 promoted cell proliferation, migration, and invasion, as well as the epithelial-mesenchymal transition (EMT), by affecting the cell cycle and cell apoptosis in vitro and tumor growth in vivo. Further study indicated that overexpression of lnc-SNHG1 markedly inhibited the expression of miR-302/372/373/520 (miRNA-pool) which is down-regulated in invasive pituitary tumor cells. Moreover, overexpression of lnc-SNHG1 significantly promoted the expression of TGFBR2 and RAB11A, the direct targets of miR-302/372/373/520. Finally, lnc-SNHG1 activates the TGFBR2/SMAD3 and RAB11A/Wnt/ß-catenin pathways in pituitary tumor cells via sponging miR-302/372/373/520. CONCLUSIONS: Our data suggest that lnc-SNHG1 promotes the progression of pituitary tumors and is a potential therapeutic target for invasive pituitary tumor.

Meningeal carcinomatosis: three case-reports.

BACKGROUND: Meningeal carcinomatosis (MC) is characterized by diffuse infiltration of tumor cells in meninges. There is no tumor mass in the brain and parenchyma of the spinal cord. MC is divided into primary and metastatic types. MC cases were previously diagnosed postoperatively or at autopsy. Recent advances in spinal abbreviation cytology and imaging have led to increase in number of reported cases. In this study, we discuss the manifestations of MC patients based on magnetic resonance imaging (MRI) findings, as well as the correlation between the manifestations and pathology. CASE PRESENTATION: MC was confirmed in all three cases by lumbar puncture and gadopentetate dimeglumine-enhanced magnetic resonance imaging. Due to different primary diseases, the patients had specific imaging manifestations. CONCLUSION: Enhanced MRI examination is extremely sensitive for detecting abnormalities in meninges, which plays a very important role in the diagnosis of MC. Since meninges of some MC patients cannot be enhanced, the enhanced MRI examination cannot be replaced by conventional cerebrospinal abbreviation examination. Attribute to the diversity of MR contrast agents, which could provide higher lesion conspicuity and enhances lesion detection, there may be some more choices to improve the detection rate of MC patients and prolong their survival lifetime.

Cortical blindness as a rare presentation of hemorrhagic cerebral hyperperfusion syndrome following vertebral angioplasty.

Cerebral hyperperfusion syndrome (CHS) is a well-documented complication after carotid endarterectomy or stenting. In contrast, CHS following vertebral revascularization is extremely rare. Here we present a case of a 77-year-old man with high-grade vertebral stenosis who subsequently underwent balloon angioplasty, complicated by hemorrhagic CHS manifesting as cortical blindness, although strict postoperative blood pressure control was administered. To our knowledge, cortical blindness as a presentation of hemorrhagic CHS has not previously been reported. This study highlights the fact that identifying high-risk patients, as well as making an individual therapeutic plan, is important prior to revascularization. Further studies are needed to elucidate the exact mechanism of this condition and thereby prevent it.

Cortical blindness as a rare presentation of hemorrhagic cerebral hyperperfusion syndrome following vertebral angioplasty.

Cerebral hyperperfusion syndrome (CHS) is a well-documented complication after carotid endarterectomy or stenting. In contrast, CHS following vertebral revascularization is extremely rare. Here we present a case of a 77-year-old man with high-grade vertebral stenosis who subsequently underwent balloon angioplasty, complicated by hemorrhagic CHS manifesting as cortical blindness, although strict postoperative blood pressure control was administered. To our knowledge, cortical blindness as a presentation of hemorrhagic CHS has not previously been reported. This study highlights the fact that identifying high-risk patients, as well as making an individual therapeutic plan, is important prior to revascularization. Further studies are needed to elucidate the exact mechanism of this condition and thereby prevent it.

Intraoperative neurophysiological monitoring to protect the facial nerve during microsurgery for large vestibular schwannomas.

OBJECTIVE: Microsurgery is the preferred treatment for large vestibular schwannomas (VSs). However, anatomical and functional preservation of the facial nerve (FN) remains a challenge during this surgery. The aim of this study was to determine whether it is beneficial to the preservation rates of the FN during microsurgical treatment of large VSs using intraoperative neurophysiological monitoring (IONM). METHODS: We retrospectively reviewed 53 patients with large VSs that underwent microsurgical resection via the retrosigmoid approach in our department during April 2009 to March 2016. IONM was used in 29 cases. Postoperative FN function was evaluated using the House-Brankmann (HB) FN grading scale at 2 weeks and 3 and 6 months after surgery. RESULTS: There were two cases (8.3%) of subtotal resection in the monitored group, compared with one case (3.4%) among the controls (p>0.05). The anatomical integrity rate for FNs was 100% in the monitored group, which was significantly different from 83.3% in the controls (p<0.05), which included four cases the FN was injured, mostly around the internal auditory foramen. Functional preservation of the FN in the monitored group differed significantly from that in the controls at 2 weeks and 3 and 6 months postoperatively (p<0.05). CONCLUSIONS: IONM contributes to FN anatomical integrity and functional preservation rates during microsurgery of large VSs. It has no significant effect on differences in the total VS resection rates.

Effect of estrogen administration on middle cerebral arterial viscoelastic properties in aged female rats.

PURPOSE:: To develop a model for studying cerebrovascular disease prevention in elderly women. METHODS:: Sixty 18-month-old Sprague Dawley (SD) rats were randomly divided into an estrogen administration group (EA, n=30) and a non-administration group (NA, n=30); thirty 4-month-old SD rats were allocated to a control group. The EA group received estradiol benzoate starting on the 5th day of a 34-day breeding period, and the serum levels of estradiol (E2), estrogen receptor (ER), and malondialdehyde (MDA) were measured. The MCA of each group was then sampled for viscoelastic experiments. RESULTS:: The serum levels of E2 and MDA in the EA group showed significant differences compared to those in the control group (p<0.05), while the difference in ER between the EA and control groups was not significant (p>0.05). The decrease in MCA stress at 7,200 s and the increase in strain at 7,200 s in the EA group showed no significant differences compared to the control group (p>0.05). CONCLUSION:: Estradiol administration inhibited the formation of lipid peroxidation products and restored middle cerebral arterial viscoelasticity in aged female rats.

Effect of estrogen administration on middle cerebral arterial viscoelastic properties in aged female rats

ABSTRACT PURPOSE: To develop a model for studying cerebrovascular disease prevention in elderly women. METHODS: Sixty 18-month-old Sprague Dawley (SD) rats were randomly divided into an estrogen administration group (EA, n=30) and a non-administration group (NA, n=30); thirty 4-month-old SD rats were allocated to a control group. The EA group received estradiol benzoate starting on the 5th day of a 34-day breeding period, and the serum levels of estradiol (E2), estrogen receptor (ER), and malondialdehyde (MDA) were measured. The MCA of each group was then sampled for viscoelastic experiments. RESULTS: The serum levels of E2 and MDA in the EA group showed significant differences compared to those in the control group (p<0.05), while the difference in ER between the EA and control groups was not significant (p>0.05). The decrease in MCA stress at 7,200 s and the increase in strain at 7,200 s in the EA group showed no significant differences compared to the control group (p>0.05). CONCLUSION: Estradiol administration inhibited the formation of lipid peroxidation products and restored middle cerebral arterial viscoelasticity in aged female rats.

Endovascular treatment of ruptured vertebrobasilar dissecting aneurysms: Review of 40 consecutive cases.

AIMS: To evaluate the safety and efficacy of endovascular intervention in the treatment of ruptured vertebrobasilar dissecting aneurysms (VBDAs) with the aim of developing endovascular treatment standards for this disorder. MATERIALS AND METHODS: The results of 40 consecutive patients with ruptured VBDAs, who were treated with internal trapping (n = 7), stent(s)-assisted coiling (n = 26), and solely stenting (n = 7) from January 2010 to June 2014, were retrospectively reviewed and analyzed. RESULTS: A treatment protocol for the ruptured VBDAs was created and proved to be effective. All 7 patients treated with internal trapping had satisfactory outcomes; none had treatment-related complications, rebleeding, or recanalization after treatment. Of the 26 patients treated with stent-assisted coiling, one patient suffered from an acute in-stent thrombosis during the operation, one had a small cerebral cortical infarction, one had rebleeding, and one had recanalization of his obliterated aneurysm after surgery. Of the seven patients treated solely with stenting, one patient had recanalization and two patients suffered rebleeding, of whom one patient died. CONCLUSIONS: The treatment protocol for ruptured VBDAs proposed in this study proved to be a simple and effective method in selecting the requisite treatment. If a proper endovascular strategy is in place, an effective treatment outcome for ruptured VBDAs can be obtained.

Protective effects of monosialotetrahexosylganglioside sodium on H2O2-induced human vascular endothelial cells.

Monosialotetrahexosylganglioside sodium (GM1) is widely used in the treatment of central and peripheral neurological injuries. In addition to its neuroprotective activity, GM1 exerts protective effects on brain microvascular endothelial cells, although the mechanisms underlying these effects remain unclear. The aim of the present study was to clarify the protective effects and underlying mechanisms of GM1 on human umbilical vein endothelial cells (HUVECs). In this study, hydrogen peroxide (H2O2) was applied to induce the HUVEC injury. HUVECs in a logarithmic growth phase were divided into five groups, namely the control, H2O2-treated, 10-mg/l GM1, 5-mg/l GM1 and 1-mg/l GM1 groups. In all the groups, cell proliferation was detected using a Cell Counting Kit-8 assay, a flow cytometric method was applied to analyze the cell cycle and nuclear factor (NF)-κB expression was evaluated using immunofluorescence analysis. In addition, the protein expression levels of NF-κB, phosphatidylinositol 3-kinase (PI3K) and glycogen synthase kinase (GSK)-3 were detected via western blot analysis. The results indicated that GM1 exerted significant protective effects on H2O2-injured cells by increasing the ratio of cells in the S/G2 phase. Furthermore, western blot analysis revealed that PI3K expression levels were markedly increased after 24 h, as a result of the GM1 treatment, while the expression of both GSK-3 markedly decreased. In addition, the ratio of nuclear-to-cytoplasmic NF-κB expression increased in the GM1-treated cells. In summary, GM1 exhibited marked protective effects on the HUVECs, possibly due to the ability of GM1 in maintaining the integrity of the endothelium and increasing the proportion of cells undergoing mitosis, a process in which the PI3K/GSK-3 and NF-κB pathways are crucially involved.

Surgical Resection of a Progressive Giant Arteriovenous Malformation After 13-year Follow-Up.

Giant arteriovenous malformation (AVM) is a complex and relatively rare congenital lesion with high morbidity and mortality. Its optimal treatment, however, remains controversial. Normal perfusion pressure breakthrough (NPPB) is a potentially devastating complication following surgical resection. Generally, strict blood pressure control is particularly recommended for preventing this phenomenon. Here we present a case of a 21-year-old patient with a progressive giant AVM who developed frequent seizures and subsequently underwent microsurgical total resection after 13-year follow-up, complicated by NPPB. Hypertensive hypervolemic treatment rather than strict blood pressure control was administrated postoperatively; however thalamic infarction occurred. During the 1 year of follow-up, the patient remained seizure-free with only mild right-sided hemiparesis.This case highlights that, in view of potential growth of the lesion, early intervention is necessary when possible. Microsurgical resection is challenging but remains to be an effective option for eliminating such giant AVM, and it is vital to keep risks associated with surgery in mind, such as NPPB. Moreover, whether blood pressure control is needed or not should be individualized.

Growing dissecting aneurysm of basilar trunk treated with stent-assisted coiling.

Growing basilar dissecting aneurysm is a scarce but increasingly recognized entity, accounting for a significant risk of death and disability. Controversy exists regarding the optimal management. A 61-year-old man presented with dysarthria and left hemiparesis attributable to a basilar trunk dissecting aneurysm. Antiplatelet therapy was instituted, and the patient's clinical condition markedly improved. However, he developed severe headache, dysarthria, and left hemiparesis 35 days later. Angiography revealed significant enlargement of the aneurysm, and stent-assisted coiling was then uneventfully performed. The patient remained clinically stable with only mild left-sided hemiparesis at the 2-year clinical follow-up.