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Objective. This study aimed to explore the roles and mechanisms of lncRNA FAM225B and PDIA4 in ovarian cancer. Methods. RT-qPCR and Western blot assays were performed to detect the expression levels of the lncRNAs FAM225B, DDX17, and PDIA4 in the serum of patients with ovarian cancer and cell lines. Cells were transfected with lncRNA FAM225B- and PDIA4-related vectors to determine the malignant phenotypes using functional experiments. The mutual binding of lncRNA FAM225B and DDX17 was verified using RNA pull-down and RIP assays. Results. The expression of lncRNAs FAM225B and PDIA4 was decreased in the serum of patients with ovarian cancer and cell lines. Restoration of lncRNA FAM225B or PDIA4 reduced cell proliferation, migration, and invasion abilities and elevated the apoptosis rate, whereas suppression of lncRNA FAM225B or PDIA4 exhibited an inverse trend. RNA pull-down and RIP assays revealed a direct interaction between lncRNA FAM225B and DDX17. ChIP assay revealed a relationship between DDX17 and the PDIA4 promoter. LncRNA FAM225B and DDX17 positively regulate PDIA4 expression. Downregulation of PDIA4 expression counteracts the suppressive effect of lncRNA FAM225B overexpression in ovarian cancer cells. Conclusion. This research study supports the fact that lncRNA FAM225B in ovarian cancer can upregulate PDIA4 by directly binding to DDX17, inhibiting the activities of ovarian cancer cells.

ObjectiveAn early onset of menarche and, later, menopause are well-established risk factors for the development of breast cancer and endometrial cancer. Although the largest GWASs have identified 389 independent signals for age at menarche (AAM) and 44 regions for age at menopause (ANM), GWAS can only identify the associations between variants and traits. The aim of this study was to identify genes whose expression levels were associated with AAM or ANM due to pleiotropy or causality by integrating GWAS data with genome-wide expression quantitative trait loci (eQTLs) data. We also aimed to identify the pleiotropic genes that influenced both phenotypes.MethodWe employed GWAS data of AAM and ANM and genome-wide eQTL data from whole blood. The summary data-based Mendelian randomization method was used to prioritize the associated genes for further study. The colocalization analysis was used to identify the pleiotropic genes associated with both phenotypes.ResultsWe identified 31 genes whose expression was associated with AAM and 24 genes whose expression was associated with ANM due to pleiotropy or causality. Two pleiotropic genes were identified to be associated with both phenotypes.ConclusionThe results point out the most possible genes which were responsible for the association. Our study prioritizes the associated genes for further functional mechanistic study of AAM and ANM and illustrates the benefit of integrating different omics data into the study of complex traits.

Objective: MicroRNAs, as essential players in tumorigenesis, have been demonstrated to have a revolutionary effect on human cancer research. Ovarian cancer is the primary reason of death among gynecologic malignancies. In view of this, it is significant to identify prognostic and predictive markers for treatment of ovarian cancer. The aim of this study was to probe into the effects of miR‐378a‐3p and protein disulfide‐isomerase A4 (PDIA4) on the biological functions of ovarian cancer cells. Methods: miR‐378a‐3p expression and PDIA4 messenger RNA expression in human ovarian cancer cells, normal human ovarian epithelial cells, and serum of both ovarian cancer patients and healthy people were detected by reverse transcription‐quantitative polymerase chain reaction, and the PDIA4 protein expression was tested by Western blot analysis. Ovarian cancer OVCAR3 and SKOV3 cells were transfected or cotransfected with miR‐378a‐3p mimic or pcDNA3.1‐PDIA4 or their negative control plasmids to explore their roles in biological functions in ovarian cancer cells. Luciferase activity and RIPA assays were implemented to validate the interaction between miR‐378a‐3p and PDIA4. Western blot analysis was utilized to detect phosphatidylinositol‐3 kinase/serine/threonine kinase (PI3K/AKT) signaling pathway‐related protein expression and their phosphate expression levels. Results: miR‐378a‐3p was elevated and PDIA4 was decreased in ovarian cancer cells and serum. In addition, miR‐378a‐3p mimic induced ovarian cancer cell growth, while miR‐378a‐3p inhibitor and pcDNA3.1‐PDIA4 presented an inverse trend. pcDNA3.1‐PDIA4 partially eliminated the capabilities of miR‐378a‐3p mimic on ovarian cancer progression. Meanwhile, miR‐378a‐3p was found to negatively regulate PDIA4, and miR‐378a‐3p mimic increased the phosphorylation levels of AKT and PI3K, while pcDNA3.1‐PDIA4 exhibited an opposite tendency. Furthermore, pcDNA3.1‐PDIA4 largely eliminated the functions of miR‐378a‐3p mimic on phosphorylation levels of AKT and PI3K. Conclusion: This study provides evidences that miR‐378a‐3p activates PI3K/AKT signaling pathway by modulating PDIA4 expression, thereby playing a role in promoting the growth of ovarian cancer cells. This study provides novel directions for targeted therapy of ovarian cancer. [ABSTRACT FROM AUTHOR]

Presents a study that investigated the effects of a combined link adaptation and power control scheme for achieving a target error rate and reducing error variability in an enhanced general packet radio services (EGPRS) cellular network. Relevant aspects of EGPRS and advanced audio coder design under consideration in the study; Description of Automatic Repeat Request and packet shuffling techniques used in the study; Details of the link adaptation and power control algorithm of the study.

The Enhanced General Packet Radio Services is one of the proposals submitted to the IMT-2000 initiative of the ITU for third-generation wireless services. EGPRS is also the evolutionary path chosen by the Universal Wireless Communications Consortium, leading toward the convergence of GSM and IS-136 standards for their next-generation wireless systems. We discuss the feasibility of supporting integrated services, such as packet voice, Web browsing, and best-effort data, using EGPRS. We first describe the relevant capabilities offered by the currently proposed standard, and then outline additional capabilities at the radio link control/medium access control layer that are necessary to support integrated services in a spectrally efficient manner. In summary, these needed capabilities are: fast uplink access during an ongoing session; fast resource assignment for both uplink and downlink; and the ability to differentiate services at the base station subsystem. To realize these capabilities, we propose enhancements to the RLC/MAC layer. These enhancements include a new set of packet control channels (namely, a fast packet access channel in the uplink, and a fast packet access grant channel and a fast packet polling channel in the downlink); uplink access protocols that utilize these control channels; and a modified fast uplink access channel structure. These changes would enable EGPRS to offer a wide range of services through a single packet-based network. Similar ideas are also applicable to other third-generation systems [ABSTRACT FROM PUBLISHER]

In this paper, we study the interference management and resource allocation problem in a packet-switched, fixed, broadband, Time Division Multiple Access (TDMA) wireless system. These systems have the potential to provide high-speed data access to the home and therefore are of current interest. The system capacity is limited by the co-channel interference, which arises from both intercell and intracell transmissions. The intracell interference management and resource allocation, which significantly impacts the system performance, is the focus of this study. The goal is to design efficient resource allocation schemes to combat intracell interference so as to improve the system capacity and service quality. We address the following issues: (1) estimating the optimal capacity of the system; (2) proposing resource allocation schemes with reasonable complexity that are close to optimal; and (3) proposing a new class of power control schemes that are suited to intracell interference management. Two resource allocation schemes are proposed: Max-Min Scheduling Protocol (MMSP) and Revisited Max-Min Scheduling Protocol (RMMSP). We show via simulations that these schemes combined with the new power control provide close to optimal performance. [ABSTRACT FROM AUTHOR]