Virtual reality (VR) over wireless is emerging as an important use case of 5G networks. Immersive VR experience requires the delivery of huge data at ultra-low latency, thus demanding ultra-high transmission rate. This challenge can be largely addressed by the recent network architecture known as mobile edge computing (MEC), which enables caching and computing capabilities at the edge of wireless networks. This paper presents a novel MEC-based mobile VR delivery framework that is able to cache parts of the field of views (FOVs) in advance and run certain post-processing procedures at the mobile VR device. To optimize resource allocation at the mobile VR device, we formulate a joint caching and computing decision problem to minimize the average required transmission rate while meeting a given latency constraint. When FOVs are homogeneous, we obtain a closed-form expression for the optimal joint policy which reveals interesting communicationscaching-computing tradeoffs. When FOVs are heterogeneous, we obtain a local optima of the problem by transforming it into a linearly constrained indefinite quadratic problem then applying concave convex procedure. Numerical results demonstrate great promises of the proposed mobile VR delivery framework in saving communication bandwidth while meeting low latency requirement.

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Systemic inflammation responses have been associated with cancer development and progression. C-reactive protein (CRP), Glasgow prognostic score (GPS), neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), lymphocyte-monocyte ratio (LMR), and neutrophil-platelet score (NPS) have been shown to be independent risk factors in various types of malignant tumors. This retrospective analysis of 162 osteosarcoma cases was performed to estimate their predictive value of survival in osteosarcoma. All statistical analyses were performed by SPSS statistical software. Receiver operating characteristic (ROC) analysis was generated to set optimal thresholds; area under the curve (AUC) was used to show the discriminatory abilities of inflammation-based scores; Kaplan-Meier analysis was performed to plot the survival curve; cox regression models were employed to determine the independent prognostic factors. The optimal cut-off points of NLR, PLR, and LMR were 2.57, 123.5 and 4.73, respectively. GPS and NLR had a markedly larger AUC than CRP, PLR and LMR. High levels of CRP, GPS, NLR, PLR, and low level of LMR were significantly associated with adverse prognosis (P < 0.05). Multivariate Cox regression analyses revealed that GPS, NLR, and occurrence of metastasis were top risk factors associated with death of osteosarcoma patients.

Mobile virtual reality (VR) delivery is gaining increasing attention from both industry and academia due to its ability to provide an immersive experience. However, achieving mobile VR delivery requires ultra-high transmission rate, deemed as a first killer application for 5G wireless networks. In this paper, in order to alleviate the traffic burden over wireless networks, we develop an implementation framework for mobile VR delivery by utilizing caching and computing capabilities of mobile VR device. We then jointly optimize the caching and computation offloading policy for minimizing the required average transmission rate under the latency and local average energy consumption constraints. In a symmetric scenario, we obtain the optimal joint policy and the closed-form expression of the minimum average transmission rate. Accordingly, we analyze the tradeoff among communication, computing and caching, and then reveal analytically the fact that the communication overhead can be traded by the computing and caching capabilities of mobile VR device, and also what conditions must be met for it to happen. Finally, we discuss the optimization problem in a heterogeneous scenario, and propose an efficient suboptimal algorithm with low computation complexity, which is shown to achieve good performance in the numerical results.

Vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) have been widely used in advanced cancers. Concerns have arisen regarding the risk of venous thromboembolism with the use of these drugs. Currently, the contribution of VEGFR-TKIs to venous thromboembolism is still unknown. We performed a meta-analysis to determine the incidence and relative risk (RR) of venous thromboembolism events (VTEs) associated with these agents. Eligible studies included phase II and III prospective trials evaluating US Food and Drug Administration approved VEGFR-TKIs (pazopanib, sunitinib, sorafenib and vandetanib), and data on VTEs were available. Overall incidence rates, RR and 95% confidence intervals (CI) were calculated employing fixed-or random-effects models depending on the heterogeneity of included trials. A total of 14 studies (4,430 patients) were selected for this meta-analysis. The incidence of VTEs related to VEGFR-TKIs was 3% (95%CI: 1.7-5.1%), and there was no statistically significant increase in the risk of VTEs for VEGFR-TKIs versus controls in overall population (RR0.912, 95%CI: 0.617-1.348, p 5 0.643). On subgroup analysis, no significant increase in the risk of VTEs was found among different VEGFR-TKIs or tumor types. No evidence of publication bias was observed. The use of VEGFRTKIs does not significantly increase the risk of VTEs, the risk of VTEs in patients with cancer is driven predominantly by tumor types, host factors and concomitant usage of anticancer agents. These results would provide important information for clinicians who use VEGFR-TKIs to treat patients with solid cancer.

PurposeThe aims of this study were to determine the effect of curcumin on osteosarcoma (OS) cells due to inactivation of the p-JAK2/p-STAT3 pathway and evaluate the prognostic value of this pathway in OS.Materials and methodsWe exposed a human OS cell line (MG-63) to different concentrations of curcumin. Then, we characterized the effects on MG-63 cells using assays (cell viability, colony formation, cell cycle, wound healing, invasion), flow cytometry, Western blot, immunohistochemical analyses, and tumor xenograft.ResultsThe half-maximal inhibitory of curcumin for MG-63 cells at 24 hours was 27.6 µM. The number of colonies of MG-63 cells was decreased obviously upon curcumin (10 and 20 µM) treatment. We also found increased accumulation of MG-63 cells in the G2/M phase upon curcumin (10 and 20 µM) treatment. Apoptosis was increased in 10 and 20 µM curcumin-treated MG-63 cells. After incubation of physically wounded cells for 24 hours, the percentage wound width increased upon curcumin exposure. Curcumin obviously decreased the expression of pJAK-2 and pSTAT-3 in MG-63 cells in a dose-dependent manner. Curcumin dose-dependently inhibited the proliferation, migration, and invasion of MG-63 cells and induced arrest of the G0/G1 phase and apoptosis by inhibiting the p-JAK2/p-STAT3 pathway. The linear correlativity between expression of p-JAK2 and STAT3 was very prominent, and both were closely associated with lung metastasis. In vivo study suggested that curcumin suppressed tumor growth through JAK2/STAT3 signaling.ConclusionCurcumin-mediated inhibition of the proliferation and migration of MG-63 cells was associated with inactivation of JAK/STAT signaling.

Treatment with EGFR-TKIs is associated with a significantly increased risk of developing ILD.

The use of pazopanib is associated with a significantly increased risk of developing hypertension. Close monitoring and appropriate managements are recommended during the therapy. Future studies are still needed to investigate the risk reduction and possible use of pazopanib in selected patients.