Jingping Liu

Broadband enhancement of spontaneous emission from nitrogen-vacancy centers in nanodiamonds by hyperbolic metamaterials

We experimentally demonstrate a broadband enhancement of emission from nitrogen-vacancy centers in nanodiamonds. The enhancement is achieved by using a multilayer metamaterial with hyperbolic dispersion.

MicroRNA-200b inhibits the growth and metastasis of glioma cells via targeting ZEB2

MicroRNAs (miRs) have been found to play important roles in mediating a variety of biological processes in human cancers, including tumor cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). In the present study, we aimed to investigate the putative role of miR‑200b in the progression of glioma. Real-time RT-PCR data showed that the miR‑200b levels were frequently reduced in primary glioma tissues (n=88) and cell lines, when compared to normal brain tissues (n=25). Moreover, decreased miR‑200b level was tightly associated with the malignant progression of glioma. Overexpression of miR‑200b significantly suppressed cell proliferation, migration, invasion and EMT in glioma U251 and U87 cells. Luciferase reporter assay data further identified ZEB2 as a direct target of miR‑200b, and the protein expression of ZEB2 was markedly reduced after overexpression of miR‑200b in U251 and U87 cells. Furthermore, restoration of ZEB2 effectively reversed the reduced expression of ZEB2, as well as the suppressive effects of miR‑200b overexpression on the proliferation, migration, invasion and EMT in glioma U251 and U87 cells. Moreover, in vivo study showed that overexpression of miR‑200b significantly inhibited tumorigenesis as well as the tumor growth of glioma cells, and effectively protected nude mice from tumor-induced death. Taken together these findings suggest that miR‑200b has suppressive effects on the proliferation, migration, invasion and EMT of glioma cells, partly at least, via targeting ZEB2. Therefore, miR‑200b acts as a novel tumor suppressor in glioma, and thus may become a promising therapeutic candidate for glioma.

Surviving the Largest Atypical Parasagittal Meningioma in a 2-Year-Old Child: A Case Report and a Brief Review of the Literature

BACKGROUND Meningiomas arising in pediatric populations are rare neoplasms with distinct biological and clinical features. A rare case of a 2-year-old boy with extremely large intracranial parasagittal meningioma is presented. To our knowledge, this case is the largest parasagittal meningioma to be reported to date in the pediatric age group. CASE DESCRIPTION The tumor size at its largest diameter was 14.2 cm. Two-stage craniotomy was performed within 3 weeks to resect the tumor totally by Simpson grade II while preserving the superior sagittal sinus. Three months after the second resection, the patient had a complication of subdural hematoma, which was managed by external drainage and urokinase. CONCLUSIONS The patients postoperative recovery was unremarkable, and the previously compressed brain rebounded. There was no evidence of recurrence after two years of follow-up. Every effort should be exerted to achieve radical resection of the tumor, which can result in a satisfactory prognosis and a low recurrence rate.

Clinical features of 417 patients with chronic subdural hematoma

OBJECTIVE To discuss the clinical features of chronic subdural hematoma (CSDH) in different age groups. METHOD A total of 417 patients with CSDH were divided into 3 groups: 0 to 39, 40 to 59 and elder than 60 years. We analyzed the clinical features in different groups, including sex, trauma history, potential hemorrhage factors, trauma to symptoms interval, encephalatrophy, onset symptom and hematoma volume. RESULTS The incidence of trauma, potential hemorrhage factors, encephalatrophy, consciousness disorders and paralysis increased with age, while the incidence of intracranial hypertension symptoms and seizures decreased with age (P<0.001). The trauma to symptom interval in the group elder than 60 was longer than in other groups (P<0.05) and the hematoma volume increased with age(P<0.05). CONCLUSION The clinical features of CSDH including onset symptoms, trauma history, potential hemorrhage factors, encephalatrophy, trauma to symptoms interval and hematoma volume vary in different age groups.

Effect of epidural drainage and dural tenting suture on epidural hematoma in 145 cases of craniotomy

OBJECTIVE To evaluate the efficacy of dural tenting suture and epidural drainage in craniotomy. METHODS In 145 cases of intracranial lesions, dural tenting suture and epidural drainage were performed to prevent epidural hematoma. RESULTS Postoperative computed tomography (CT) showed no epidural hematoma required surgery in both groups. CONCLUSION Both dural tenting suture and epidural drainage are effective in preventing epidural hematoma. Hemostasis is the key step. Dural tenting suture without epidural drainage relieves psychological stress. It decreases the risk of intracranial infection and avoids some unusual complications.

The expression of Wnt‑1 inducible signaling pathway protein‑2 in astrocytoma: Correlation between pathological grade and clinical outcome

Wnt-1 inducible signaling pathway protein-2 (WISP-2) is a member of the CCN family, which is critical for the control of cell morphology, motion, adhesion and other processes involved in tumorigenesis. The expression pattern and clinical significance of WISP-2 in astrocytomas remains unclear. In this study, reverse transcription-polymerase chain reaction was performed to systematically investigate the expression of WISP-2 in 47 astrocytoma tissues of different pathological grades and 10 normal brain tissues. The mRNA expression levels of WISP-2 in the astrocytoma tissues were observed to be significantly higher than those in the normal brain tissues. Furthermore, the upregulation of WISP-2 was found to be associated with astrocytomas of higher pathological grades. Subsequently, 154 astrocytoma and 15 normal brain tissues were analyzed using immunohistochemistry and similar results were obtained. Univariate and multivariate survival analyses were used to determine the correlations between WISP-2 expression and overall survival (OS) and progression-free survival (PFS). The results indicated that the expression of WISP-2 was found to negatively correlate with patient PFS and OS. These results demonstrated that the WISP-2 protein is involved in the pathogenesis and progression of human astrocytomas and may serve as a malignant biomarker of this disease.

A brain-specific isoform of apoptosis-inducing factor 2 attenuates ischemia-induced oxidative stress in HT22 cells

&NA; Apoptosis‐inducing factor (AIF) is a family of conserved mitochondrial flavoproteins that have both vital and lethal functions in cells. The function and regulation of AIF‐1, the original described and most abundant isoform, has been extensively studied, whereas three other AIF isoforms have not been further characterized. Here, we investigated the role of AIF‐2, a brain‐specific isoform of AIF, in an in vitro ischemia model in neuronal HT22 cells. We showed that AIF‐2 was constitutively expressed in HT22 cells, and the oxygen and glucose deprivation (OGD) did not alter AIF‐2 expression. Downregulation of AIF‐2 with specific siRNA aggravated OGD‐induced lactate dehydrogenase (LDH) release, apoptosis and loss of cell viability, whereas overexpression of AIF‐2 through lentivirus transfection exerted the opposite effects. In OGD‐treated cells, AIF‐2 overexpression promoted the endogenous antioxidant enzyme activities, preserved mitochondrial membrane potential (MMP), inhibited cytochrome c release, and thereby prevented reactive oxygen species (ROS) generation and lipid peroxidation. In addition, AIF‐2 significantly prevented the OGD‐induced AIF‐1 translocation from cytoplasm to the nuclei. In view of these considerations, AIF‐2 might represent an ideal strategy to avoid AIF‐1 associated neurotoxicity, and could be tested against brain ischemia in animal models. HighlightsAIF‐2 attenuates OGD‐induced cytotoxicity in HT22 cells.AIF‐2 suppresses OGD‐induced oxidative stress.AIF‐2 preserves mitochondrial function after OGD.AIF‐2 prevents OGD‐induced AIF‐1 translocation.

Multidrug Resistant Brain Abscess Due to Acinetobacter baumannii Ventriculitis Cleared by Intraventricular and Intravenous Tigecycline Therapy: A Case Report and Review of Literature

Objective: Ventricular infection from multidrug-resistant (MDR) Acinetobacter baumannii (A. baumannii) is one of the most severe complications of craniotomy. However, the availability of effective therapeutic options for these infections is limited. Thus, this report aims to describe the efficacy of abscess clearance by intraventricular and intravenous tigecycline therapy in managing patients with multidrug-resistant A. baumannii ventriculitis after neurosurgery. Moreover, the current literature on the use of tigecycline therapy for these life-threatening infections is reviewed and summarized, and a treatment regimen based on the available data is proposed. Methods: A patient with multidrug-resistant A. baumannii ventriculitis was admitted in our hospital and was provided with a detailed therapeutic schedule. Tigecycline treatments for multidrug-resistant A. baumannii ventriculitis that were reported in the literature were also reviewed and summarized. Results: The patient in our hospital underwent abscess clearance on a ventriculoscope and was subsequently subjected to multi-route tigecycline therapy 14 days after the start of the continuous ventricular irrigation (CVI) tigecycline and 3 days after the intraventricular (IVT) tigecycline. The signs of ventriculitis disappeared, and the Acinetobacter cerebrospinal fluid (CSF) load steadily decreased until CSF sterilization. Literature review identified seven cases of ventricular infection from multidrug-resistant A. baumannii treated with tigecycline. In the eight cases, all patients were male adults (>18 years), with a mean age of 46.1 (range: 22–75) years. Meningitis/ventriculitis was secondary to neurosurgery procedures for the management of various central nervous system diseases in all cases. A good clinical outcome was achieved in all eight patients with multidrug-resistant A. baumannii meningitis/ventriculitis treated with CVI and/or IVT tigecycline, and any relevant complications were not observed. Conclusions: CVI and IVT tigecycline and IVT colistin could be considered as the first-line therapy in patients with ventricular infections from MDR/extreme drug-resistant A. baumannii. However, more studies should be conducted to confirm our observation.

Effects of Fibronectin 1 on Cell Proliferation, Senescence and Apoptosis of Human Glioma Cells Through the PI3K/AKT Signaling Pathway

Background/Aims: The current study aimed to investigate the role by which fibronectin 1 (FN1) influences the cell cycle, senescence and apoptosis in human glioma cells through the PI3K/ AKT signaling pathway. Methods: Differentially expressed genes (DEGs) were identified based on gene expression data (GSE12657, GSE15824 and GSE45921 datasets) and probe annotation files from Gene Expression Omnibus. The DEGs were identified in connection with gene ontology (GO) enrichment analysis and with the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. The positive expression of the FN1 protein was detected by immunohistochemistry. The glioma cell lines U251 and T98G were selected and assigned into blank, negative control (NC) and siRNA-FN1 groups. A dual luciferase reporter gene assay was used to investigate the effects of FN1 on transcriptional activity through the PI3K/AKT signaling pathway. An MTT assay was applied for the detection of cell proliferation, while flow cytometry was employed for cell cycle stage and cellular apoptosis detection. β-galactosidase staining was utilized to detect cellular senescence, a scratch test was applied to evaluate cell migration, and a transwell assay was used to analyze cell invasion. Western blotting and qRT-PCR methods were used to detect the protein and mRNA expression levels, respectively, of the FN1 gene and the related genes in the PI3K/AKT pathway (PI3K, AKT and PTEN), the cell cycle (pRb, CDK4 and Cyclin D1) and cell senescence (p16 and p21) among the collected tissues and cells. Results: GSE12657 profiling revealed FN1 to be the most upregulated gene in glioma. Regarding the GSE12657 and GSE15824 datasets, FN1 gene expression was higher in glioma tissues than in normal tissues. GO enrichment analysis and KEGG pathway enrichment analysis indicated that FN1 is involved in the synthesis of extracellular matrix (ECM) components and the PI3K/AKT signaling pathway. Verification was provided, indicating the role played by the FN1 gene in the regulation of the PI3K/AKT signaling pathway, as silencing the FN1 gene was found to inhibit cell proliferation, promote cell apoptosis and senescence, and reduce migration and invasion through the down-regulation of FN1 gene expression and disruption of the PI3K-AKT signaling pathway. Conclusion: The findings of this study provide evidence highlighting the prominent role played by FN1 in stimulating glioma growth, invasion, and survival through the activation of the PI3K/AKT signaling pathway.

Regulatory landscape and clinical implication of MBD3 in human malignant glioma

In this article we inspect the roles and functions of the methyl-CpG-binding domain protein 3 (MBD3) in human malignant glioma, to assess its potential as an epigenetic biomarker for prognosis. The regulatory effects of MBD3 on glioma transcriptome were first profiled by high-throughput microarray. Our results indicate that MBD3 is involved in both transcriptional activation and repression. Furthermore, MBD3 fine-controls a spectrum of proteins critical for cellular metabolism and proliferation, thereby contributing to an exquisite anti-glioma network. Specifically, the expression of MHC class II molecules was found to positively correlate with MBD3, which provides new insight into the immune escape of gliomagenesis. In addition, MBD3 participates in constraining a number of oncogenic non-coding RNAs whose over-activation could drive cells into excessive growth and higher malignancy. Having followed up a pilot cohort, we noted that the survival of malignant glioma patients was proportional to the content of MBD3 and 5-hydroxymethylcytosine (5hmC) in their tumor cells. The progression-free survival (PFS) and overall survival (OS) were relatively poor for patients with lower amount of MBD3 and 5hmC in the tissue biopsies. Taken together, this work enriches our understanding of the mechanistic involvement of MBD3 in malignant glioma.