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Strategies to single-step edit the core skeleton of structurally complex compounds still remain highly desirable but challenging. Herein an unexpected discovery to access natural product dehydrocostus lactone/parthenolide-inspired bispiro[oxindole-oxazinane] hybrids enabled...

Silicon carbide (SiC) is regarded as a promising semiconductor owing to its wide band gap and high thermal conductivity. Meanwhile, it possesses issues such as interface properties, which may affect the performance of SiC substrate power devices (e.g. MOSFET), especially when compared with similarly structured silicon appliances. Given that the development of SiC semiconductor devices has a number of commonalities with conventional silicon-based semiconductors, titanium dioxide (TiO2), a material that has a great track record in Si-based semiconductor devices, has been chosen for investigation in this work. Although TiO2 is not capable of being a gate dielectric alone on the SiC substrate because of its relatively narrow band gap, it can be adopted into composite or multilayer gate dielectrics to reach satisfying characteristics. As such, the interfacial state and heterostructure between TiO2 and SiC remain worthy being researched. In the present study, the properties of atomic layer deposited (ALD) TiO2 films on silicon substrates were compared with those on 4H-SiC substrates via x-ray photoelectron spectroscopy, atomic force microscopy, and x-ray reflectometry. It is shown that the interface state between ALD TiO2 film and both types of substrates as-deposited have similar chemical conditions, whereby TiO2 layer barely react with substrates, containing great amount of oxygen vacancies. According to band alignment calculations, heterostructure of both samples are type-II heterojunctions with negatively shifted conduction band. Although the large bandwidth of 4H-SiC hinders the use of TiO2 as a gate dielectric in power devices, this structure has the potential for other semiconductor products.

Background: Glioma is the most common malignant tumor in the human central nervous system. Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) promotes oncogenesis in various tumors. In the present study, we aimed to examine the role of NEAT1 in altering the properties of gliomas.Methods: Quantitative real-time PCR technology was used to determine the expression levels of relevant genes in tumor tissues and cell lines. The protein expression levels were validated by Western blotting. Cell counting kit-8 (CCK-8) and colony formation assays were used to test the cell proliferation ability. A luciferase reporter assay was used to determine the interactions of the genes. Tumor xenografts were used to detect the role of NEAT1 in gliomas in vivo.Results: We demonstrated that NEAT1 up-regulated glioma cells and negatively correlated with miR-98-5p in glioma tissues. A potential binding region between NEAT1 and miR-98-5p was confirmed by dual-luciferase assays. NEAT1 knockdown inhibited glioma cell proliferation. The inhibition of miR-98-5p rescued the knockdown of NEAT1 in glioma cells. Basic leucine zipper and W2 domain containing protein 1 (BZW1) was identified as a direct target of miR-98-5p. We also identified that BZW1 was positively correlated with NEAT1 in glioma tissues. NEAT1 knockdown inhibited glioma cell proliferation in vivo via miR-98-5p/BZW1.Conclusion: Our results suggest that NEAT1 plays an oncogenic function in glioma progression. Targeting NEAT1/miR-98-5p/BZW1 may be a novel therapeutic treatment approach for glioma patients.

Xiao-Yong Han,1 Wei Wang,2 Lei-Lei Wang,1 Xi-Rui Wang,1 Gang Li1 1Department of Neurosurgery 3, Cangzhou Central Hospital, Cangzhou, 2Department of Ultrasound, Anqiu People’s Hospital, Weifang, China Purpose: Various genetic variants have been reported to be linked to an increased risk of meningioma. However, no confirmed conclusion has been obtained. The purpose of the study was to investigate potential meningioma-associated gene polymorphisms, based on published evidence. Materials and methods: An updated meta-analysis was performed in September 2016. After electronic database searching and study screening, we selected eligible case-control studies and extracted data for meta-analysis, using Mantel–Haenszel statistics. P-values, pooled odds ratios (ORs), and 95% confidence intervals were calculated. Results: We finally selected eight genes with ten polymorphisms: MLLT10 rs12770228, CASP8 rs1045485, XRCC1 rs1799782, rs25487, MTHFR rs1801133, rs1801131, MTRR rs1801394, MTR rs1805087, GSTM1 null/present, and GSTT1 null/present. Results of meta-analyses showed that there was increased meningioma risk in case groups under all models of MLLT10 rs12770228 (all OR >1, P1, P1, P

MicroRNAs (miRNAs) are highly evolutionarily-conserved non-coding small RNAs, which were first identified in Caenorhabditis elegans. Let-7 miRNA is involved in the regulation of gene expression in cells. Several novel factors and feedback loops involved in the regulation of the synthesis of let-7 have been identified and additional let-7 target genes have been found. Let-7 has also been shown to be significantly correlated with the occurrence and development of cancer and the results of preliminary studies suggest that it is involved in the regulation of oncogenic pathways in numerous types of tumors. Let-7 is, therefore, a potential molecular target for tumor therapy. Thus, this review examined let-7 and the correlation between let-7 and oncogenic pathways in cancer.

Recently, several microRNAs (miRNAs) were reported to be involved in the modulation of glioma development. The aim of our study was to determine the effect of miR-181d on the growth of glioma and to investigate whether this growth is modulated by targeting K-ras and Bcl-2. Real-time PCR was used to analyze the expression of miR-181d in human glioma samples and glioma cell lines. Apoptosis, cell cycle, and proliferation (MTT) assays were performed to assess the phenotypic changes in glioma cells. Immunohistochemistry was used to determine the expression of K-ras and Bcl-2 in glioma tissues, and a luciferase reporter assay was carried out to confirm whether K-ras and Bcl-2 are direct targets of miR-181d. Western blotting was used to identify the potential signaling pathways affected glioma cell growth by miR-181d. In vivo, xenograft tumors were examined for an anti-glioma effect of miR-181d. MiR-181d was down-regulated in human glioma samples and up-regulated in transfected glioma cells. Ectopic expression of miR-181d suppressed proliferation and triggered cell cycle arrest and apoptosis in glioma cell lines. K-ras and Bcl-2 were identified as direct targets of miR-181d and were up-regulated in glioma samples. The results showed evidence linking the tumor suppressor activity of miR-181d in glioma cells with the K-ras-related PI3K/AKT and MAPK/ERK pathways. Furthermore, xenograft tumors from miR-181d-treated U251 cells were suppressed in vivo. MiR-181d may act as a glioma suppressor by targeting K-ras and Bcl-2.

Human interleukin-24 (IL-24) has been found recently to play a tumor-suppressor role in a variety of tumors, including gliomas. However, the exact mechanism of glioma tumor suppression by IL-24 remains unclear. We collected by surgery 30 gliomas at different grades and evaluated IL-24 and double-stranded RNA-activated protein kinase (PKR) expression using fluorescence quantitative real-time PCR and immunohistochemical techniques. Two human glioma cell lines, U87 and U251, were transfected with Ad5F35-IL24 via recombinant adenovirus-mediated gene transfer and apoptosis, as well as PKR and eIF-2α expression analyzed. The results showed that IL-24 and PKR expression decreased with increasing tumor grade. Compared with cells of the control groups, Ad5F35-IL24-infected U87 and U251 cells exhibited a significantly increased apoptosis and elevated PKR, eIF-2α, p-PKR, and p-eIF-2α levels, while the expression of Bcl-2 was decreased. Finally, IL-24 also sensitized apoptosis of glioma cells to temozolomide (TMZ). This study indicates that IL-24 upregulates expression and activation of PKR, further increasing expression and activation of eIF-2α, and decreasing Bcl-2 to promote apoptosis. IL-24 also increases chemosensitivity of glioma cells to TMZ.

Machine-to-machine (M2M) communications are to exchange information between a subscriber station and a server in the core network through a base station or between subscriber stations which may be realized without any human interaction or intervention. There are some requirements when designing M2M communication systems such resource allocation for large number of M2M devices or users. In this paper the authors propose a design way for the large set of user uplink codes in M2M communications. The zero-correlation-zone (ZCZ) sequences and Gold sequence have been applied as spreading sequences in this code division multiplexing access (CDMA)-like system according to different correlation characteristics. This system supports number of simultaneous users up to 256 and the total synchronization time is about 200 ms under reasonable chip rate 2.5 Mcps. Compared with previous systems for ranging process, it only requires 33% cycles of IEEE 802.16e and 16.7% cycles of IEEE 802.16m. Besides, the logic design and FPGA emulation based on low complexity are presented and the estimated about 11k total gate counts.

Survivin is an inhibitor of apoptosis protein and has a crucial role in the development of cancer. The survivin −31G>C (rs9904341) promoter polymorphism influences survivin expression and has been implicated in cancer risk. However, conflicting results have been published from studies on the association between survivin −31G>C polymorphism and the risk of cancer. To clarify the role of this polymorphism in cancer, we performed a meta-analysis of all available and relevant published studies, involving a total of 3485 cancer patients and 3964 control subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of the associations. The overall results indicated that the variant genotypes were associated with a significantly increased cancer risk (CC vs GG: OR=1.58, 95% CI=1.20–2.10; CC/GC vs GG: OR=1.23, 95% CI=1.00–1.51; CC vs GG/GC: OR=1.51, 95% CI=1.23–1.85). In the stratified analyses, significantly increased risk was associated with the Asian populations (CC vs GG: OR=1.67, 95% CI=1.16–2.40; CC vs GG/GC: OR=1.50, 95% CI=1.17–1.91). We also performed the analyses by cancer type, and no statistical association was observed. The results suggest that the survivin −31G>C promoter polymorphism might be associated with an increased risk of cancer, especially in the Asian populations.

Invasion growth is the most characteristic biological phenotype of glioblastoma, but the molecular mechanism in glioma cell invasion is poorly understood. Recent data have showed that microRNA plays an essential role in tumor invasion. Our study aimed to explore the mechanism of miR-7 involved in the control of glioblastoma cell invasion.Glioma cell invasion was evaluated by transwell and scratch assays after up-regulation of miR-7 using miR-7 mimics in U87 and U251 cells. Luciferase reporter assay was used to determine focal adhesion kinase (FAK) as a target of miR-7. The levels of miR-7, matrix metalloproteinases (MMP)-2 and MMP-9 mRNA were detected by PCR assay, and the levels of FAK, MMP-2, MMP-9, total and phosphorylation serine/threonine kinase (AKT), and extracellular signal-regulated kinase (ERK) 1/2 were measured by Western blotting analysis.Over-expression of miR-7 inhibited the invasion and migration activity of U87 and U251 cells. And up-regulation of miR-7 reduced FAK protein expression, Further, luciferase reporter assay showed that miR-7 modulated FAK expression directly by binding 3'UTR of FAK mRNA. In addition, miR-7 repressed p-ERK1/2 and p-AKT level, MMP-2 and MMP-9 expression. Finally, the inverse relationship between FAK and miR-7 expression was certificated in human glioma tissues.To our knowledge, these data indicate for the first time that miR-7 directly regulates cell invasion by targeting FAK in glioblastoma and that miR-7 could be a potential therapeutic target for glioblastoma intervention.