Neuroradiologic Findings and Clinical Features of Meningiomas With Spontaneous Hemorrhagic Onset: A Single-center 10-year Experience.

OBJECTIVE: This study aimed to elucidate the clinicoradiologic features of spontaneous hemorrhagic meningiomas (HMs) and examine risk factors associated with meningioma hemorrhage. METHODS: We retrospectively reviewed 651 consecutive meningioma patients who underwent surgical resection in our hospital between January 2011 and January 2021. After exclusions, 169 patients were included for analysis. Patients were grouped according to presence of hemorrhage in the meningioma: the HM group (n = 19) and non-HM group (n = 150). Clinicoradiologic patient data were examined and compared using univariate and multivariate analysis. RESULTS: HMs accounted for 2.9% of the entire series of meningiomas. HMs were mainly located at the convexity (63.2%). Mean diameter of HMs was 4.8 cm. On computed tomography, most HMs appeared as mixed isodensity and hyperdensity (84.2%). On magnetic resonance imaging, most appeared as mixed isointensity and hyperintensity on T1-weighted imaging and mixed hypointesity and hyperintensity on T2-weighted imaging (52.6%). Seventeen tumors exhibited heterogeneous enhancement, a dural tail, and peritumoral brain edema. Thirteen showed intratumoral cystic change. The misdiagnosis rate was significantly higher in HMs than non-HMs (31.6% vs. 7.3%; P = 0.005). Intratumoral cystic change was the only independent predictor of meningioma hemorrhage in multivariate analysis (odds ratio 4.116; 95% confidence interval 1.138-14.894; P = 0.031). CONCLUSIONS: Mixed isodensity/intensity and hyperdensity/intensity on computed tomography/magnetic resonance imaging in conjunction with heterogenous enhancement, a dural tail, and varying degrees of peritumoral brain edema suggest a high possibility of HM. Presence of intratumoral cystic change was an independent risk factor associated with meningioma hemorrhage.

Misdiagnosis and Delay of Diagnosis in Hemorrhagic Meningioma: A Case Series and Review of the Literature.

OBJECTIVE: To evaluate the clinicoradiologic characteristics of hemorrhagic meningiomas (HMs) that are missed or misdiagnosed on radiologic imaging studies. METHODS: Clinical and radiologic data from 6 patients with HM who were initially misdiagnosed were collected and recorded respectively. In addition, we performed a literature review for misdiagnosed HM and summarized the results. RESULTS: Five of the 6 patients with misdiagnosed HM were female, and 1 was male. Both computed tomography (CT) and magnetic resonance imaging were performed in 4 patients, and CT alone was performed in 2. On CT, the HM was heterogeneously hyperdense in 5 patients and isodense in 1 patient. In all 4 patients who underwent magnetic resonance imaging, the HM was mixed iso- and hypointense on T1-weighted imaging and heterogeneously hyperintense on T2-weighted imaging. Marked heterogeneous contrast enhancement was observed in 2 patients, strong rim enhancement in 1, and peripheral enhancement in 1. The dural tail sign was seen in only 1 patient. The initial radiologic misdiagnoses were subdural hematoma (n = 1), malignant glioma (n = 1), ruptured arterial aneurysm (n = 1), metastasis (n = 2), and uncertain (n = 1). In the literature review, 22 cases of HM diagnostic error were collected. The main misdiagnoses were subdural hematoma (27.3%), traumatic hematoma (13.6%), vascular anomaly (13.6%), malignant glioma (4.5%), and metastasis (4.5%). CONCLUSIONS: Our study showed that in patients with HM with inadequate imaging evaluation, a small tumor associated with massive hematoma and atypical imaging features was more likely to be misdiagnosed.

MicroRNA-675 promotes glioma cell proliferation and motility by negatively regulating retinoblastoma 1.

Previous studies indicated that microRNA (miR)-675 and its precursor lncRNA H19 were both overexpressed in glioma tissues, and H19 might play an oncogenic role. To investigate the involvement of miR-675 in gliomas and its underlying mechanisms, we here collected candidate target genes of miR-675-5p from miRTarBase (http://mirtarbase.mbc.nctu.edu.tw/, Release 6.0), which contains the experimentally validated microRNA-target interactions. Then, regulatory effects of miR-675 on its target genes were validated using clinical samples and glioma cell lines. Involvement of the miR-675-target axis deregulation in cell proliferation, migration and invasion of glioma was demonstrated by both gain- and loss-of-function experiments. As a result, retinoblastoma 1 (RB1) was identified as a candidate target gene of miR-675-5p. Expression levels of miR-675-5p in glioma tissues and cells were negatively correlated with RB1 expression at both mRNA and protein levels. Importantly, deregulation of the miR-675-5p-RB1 axis was significantly associated with advanced World Health Organization (WHO) grade and low Karnofsky performance score (KPS) score of glioma patients. Luciferase reporter assay verified that RB1 was a direct target gene of miR-675 in glioma cells. Functionally, miR-675 promoted glioma cell proliferation, migration and invasion. Notably, simulation of RB1 antagonized the effects induced by miR-675 up-regulation in glioma cells. In conclusion, our data suggest that miR-675 may be a key negative regulator of RB1 and the imbalance of the miR-675-RB1 axis may be clinically associated with aggressive progression of glioma patients. In addition, miR-675 may act as an oncogenic miRNA in glioma cells via regulating its target gene RB1.

microRNA-328 is a favorable prognostic marker in human glioma via suppressing invasive and proliferative phenotypes of malignant cells.

OBJECTIVE: microRNA (miR)-328 has been reported to be implicated into tumorigenesis and tumor progression in human gliomas. However, there were controversial study results in relation to its expression pattern as well as functions in this disease. The aim of the current study was to determine the clinical significance of miR-328 expression in patients with gliomas and its effect in tumor cell malignant phenotypes. METHODS: Quantitative real-time PCR was performed to detect the expression levels of miR-328 in 116 glioma and 15 non-neoplastic brain tissues. Then, the correlations of miR-328 expression with selected clinicopathologic parameters and clinical outcome of glioma patients were statistically evaluated. Moreover, CCK-8 and transwell assays were performed to investigate the functions of miR-328 in cell proliferation, invasion and migration, respectively. RESULTS: Compared to non-neoplastic brain tissues, the expression levels of miR-328 were significantly downregulated in glioma tissues (p < 0.001). In addition, miR-328 downregulation was significantly associated with WHO grade (p < 0.001) and Karnofsky performance status score (p = 0.02). Moreover, glioma patients with low miR-328 expression exhibited markedly shorter overall survival than those with high expression (p < 0.001). Furthermore, functional assays in vitro system demonstrated that enforced expression of miR-328 could notably attenuate cell proliferation, invasion and migration of two glioma cell lines, including U251 and U87. CONCLUSIONS: Our data offer the convincing evidence that loss of miR-328 expression may stimulate advanced tumor progression and adverse outcome via promoting cellular proliferation and invasion. We propose a tumor suppressive role of miR-328 and its potential therapeutic value in human glioma.

MicroRNA-144 suppresses tumorigenesis and tumor progression of astrocytoma by targeting EZH2.

Our previous study demonstrated that enhancer of zeste homolog 2 (EZH2) overexpression may be associated with aggressive tumor progression and poor prognosis in human astrocytoma. The aim of this study was to investigate the underlying mechanisms of EZH2 on astrocytoma tumorigenesis. An online program miRWalk (http://www.umm.uni-heidelberg.de/apps/zmf/mirwalk/) was used to predict possible microRNAs (miRNAs) that might target EZH2 messenger RNA (mRNA). Then the functions of the miRNA-EZH2 mRNA axis in astrocytoma cell proliferation, invasion, and migration were also assessed. We further evaluated the clinical value of the miRNA-EZH2 mRNA axis in astrocytomas. As a result, we identified EZH2 as a target gene of miR-144. In addition, forced expression of miR-144 suppressed astrocytoma cell proliferation, invasion, and migration by down-regulating EZH2. Moreover, miR-144 down-regulation and EZH2 mRNA up-regulation were both significantly associated with advanced World Health Organization grades and low Karnofsky performance status score of astrocytoma patients. Importantly, survival analysis identified the combined expression of miR-144 and EZH2 (miR-144/EZH2) as an independent prognostic factor for overall survival in astrocytoma patients. In conclusion, miR-144 may function as a tumor suppressor by regulating EZH2 expression, and miR-144/EZH2 expression may be a highly sensitive marker for the prognosis in astrocytoma patients.

Organisation in two series of low-dimensional polymer electrolytes with high ambient lithium salt conductivity.

The amphiphilic polymers poly[2,5,8,11,14-pentaoxapentadecamethylene(5-hexadecyloxy-1,3-phenylene)] I (abbrev. C16O5), its homologues C16On, n = 1-4, and its copolymers with C16O1 have been synthesised by two Williamson procedures. Method X gives polyether-esters; method Y gives pure polyethers. DSC, optical microscopy, small-to-wide angle X-ray diffraction and complex impedance spectroscopy have been used to investigate organisation and ionic conductivities of the C16On and the C16O5-C16O1 copolymer series and their complexes with LiClO4 and LiBF4. Four-component mixtures of the latter systems (polymers I) with polyoxytetramethylene-decamethylene copolymer (II) and an octadecyl-terminated ABA block copolymer (III) (interfacial stabiliser) ('type D' systems) gave high ambient conductivities ( > or = 10(-4) S cm(-1)) with low temperature dependence. Highest conductivities (8 x 10(-4) S cm(-1) at 20 degrees C) were observed with a type D system based upon C12C18O5X.

Structure and inter-phase stability in solvent-free low-dimensional polymer electrolytes with high lithium conductivity.

Two Williamson procedures for the synthesis of the amphiphilic polymers poly[2,5,8,11,14-pentaoxapentadecamethylene(5-alkyloxy-1,3-phenylene)]I(abbrev. CmO5) are compared. Method X gives polyether-esters; method Y gives pure polyethers. In both, a dehydration reaction gives rise to CmO5-CmO1 copolymers. Two-phase systems of I with polyoxytetramethylene and polyoxytrimethylene copolymers (II) and LiBF(4) have been prepared with and without an interfacial stabiliser copolymer III. Highest and most stable conductivities (>5 x 10(-4) S cm(-1) at ambient) with low temperature dependence were observed with III, but I from method Y showed a tendency to phase separate at ambient.

Solvent-free low-dimensional polymer electrolytes for lithium-polymer batteries.

The development of solvent-free low-dimensional polymer electrolytes intended for use in solvent-free lithium batteries operating at ambient or sub-ambient temperatures is described. The synthetic routes to the amphiphilic polymers I having 5-alkoxy-3,4-phenylene units connected with oligoethoxy segments via polyester-ether or pure polyether links (abbrev. CmOn, m = 12, 16, 18, n = 1-5) and to the copolymers CmO1-CmOn are described. The structures, thermal properties and SAXS long spacings of their complexes with lithium salts (type A) and with long chain n-alkane or alkyl side chain intercalation (type B) are discussed. However, high ambient conductivities (10(-4)-10(-3) S cm(-1)) are observed in type C systems when a second copolymer based on polytetramethylene oxide segments (II) is incorporated as a microphase between the lamellae of I and serving as an ion bridge or "glue". DC polarization between Li electrodes also gives ambient conductivities >/=ca.10(-3) S cm(-1). In type D systems the I/II interface is stabilized by including a copolymer III, promoting high reproducibility in performance. Copolymers I of CmO1-CmO5 having CmO1 in excess give optimum conductivities with low temperature-dependence. This, together with molecular modeling, suggests uncoupled ion mobilities by hopping between small aggregates in the interlamellar spaces.