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.

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.

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.

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.

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.

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.

Thiabendazole, a well-known antifungal drug, exhibits anti-metastatic melanoma B16F10 activity via inhibiting VEGF expression and inducing apoptosis.

Thiabendazole, an orally available antifungal drug, has been used in clinical practice for 40 years. Previous studies indicated its potential in inhibiting angiogenesis in both animal models and in human cells. Malignant melanoma is associated with angiogenesis and it is unknown whether thiabendazole is effective for malignant melanoma or not. In our research, the effects of thiabendazole on the proliferation of the murine metastatic melanoma cell line B16F10 in vitro and in vivo and the molecular mechanism were investigated. Assay of cell viability, chick embryo chorioallantoic membrane assay, quantitative real-time PCR, Western blot, wound healing assay, annexin V/propidium iodide (AV/PI) assay and B16F10-xenograft model were applied to elucidate the mechanism of thiabendazole on B16F10 cells. Thiabendazole inhibited B16F10 proliferation in vitro in a dose- and time-dependent manner with an IC50 of 532.4 +/- 32.6, 322.9 +/- 28.9, 238.5 +/- 19.8 microM at 24, 48, and 72 h, respectively. Moreover, thiabendazole inhibited the angiogenesis and the migration of B16F10 cells in vitro. Furthermore, thiabendazole restrained transcription and translation of the VEGF gene in B16F10 in vitro, and the apoptotic percentage of B16F10 cells was increased after exposure to thiabendazole. Finally, in the B16F10-bearing mice model, thiabendazole significantly suppressed tumor growth with inhibitory rates of 16.5%, 35.4% and 48.7% at the treatment of thiabendazole 20, 40 and 80 mg/kg, respectively. These results further indicated that thiabendazole may be a potential candidate for the treatment of malignant melanoma.

Remote peritentorial hemorrhage complicating supratentorial aneurysmal surgery: a report of three cases and literature review.

We herein coin the term "remote peritentorial hemorrhage (RPTH)" and present three cases with "RPTH" after supratentorial aneurysmal surgeries, including two with remote cerebellar hemorrhage (RCH) and one with remote temporobasal hemorrhage. The RCH may result from rupture of the superior cerebellar veins due to excessive cerebrospinal fluid (CSF) loss. The mechanism behind the remote temporobasal hemorrhage may be similar to that of RCH. It can be explained by tearing of the temporobasal veins as a result of brain shift owing to intracranial hypotension stemming from intensive loss of CSF. As far as we know, this is the first report of such a bleeding pattern of probable venous origin. The results of this study could shed light on the "RPTH" physiopathology.

Neuronavigation used for the transsphenoidal resection of a pituitary adenoma accompanied by a concha sphenoid sinus.

A concha non-pneumatized sphenoid is considered to be a contraindication for the transsphenoidal resection of a pituitary adenoma. Specifically, this anatomical variation makes it difficult to approach the sella turcica. However, in this report, an intra-operative navigational system was used as a guide to access the sella through the sphenoid sinus. This procedure was found to be both reasonable and safe.

[Up regulation of phenylacetate to glioma homeobox gene expression].

OBJECTIVE: Even though phenylacetate (PA) bas been shown to inhibit the growth and induce differentiation in rat C6 glioma cell line, its mechanisms are still poorly understood. This study is aimed to identify which Hox gene is related to glioma and to observe the change in expression on mRNA level as treated by phenylasetate. METHODS: Twenty-two kinds of Hox gene were divided into 3 groups according to their primer sequence. Semiquantitative reverse transcription- polymerase chain reaction (RT-PCR) was used to investigate the mRNA expression of Hox gene groups and some Hox gene in rat C6 glioma cell line following differentiation induced by PA. The level of Hox gene expression was expressed as ratio expression rate (RER) of Hox gene/beta-actin according to computer image analysis and the difference between C6 cells and PA treated C6 cells was analyzed by student t-test. RESULTS: It was found that Hox genes matching to primers P2 were mildly expressed in C6 cells and the expression of HoxB2 mRNA was significantly up-regulated in PA treated C6 cells (P < 0.001). CONCLUSION: The weak expression of HoxB2 may be involved in glioma origin and the mechanisms of PA action are correlated with transcription process in the glioma cells.