Multi-channel Hybrid Access Femtocells: A Stochastic Geometric Analysis

For two-tier networks consisting of macrocells and femtocells, the channel access mechanism can be configured to be open access, closed access, or hybrid access. Hybrid access arises as a compromise between open and closed access mechanisms, in which a fraction of available spectrum resource is shared to nonsubscribers while the remaining reserved for subscribers. This paper focuses on a hybrid access mechanism for multi-channel femtocells which employ orthogonal spectrum access schemes. Considering a randomized channel assignment strategy, we analyze the performance in the downlink. Using stochastic geometry as technical tools, we model the distribution of femtocells as Poisson point process or Neyman-Scott cluster process and derive the distributions of signal-to-interference-plus-noise ratios, and mean achievable rates, of both nonsubscribers and subscribers. The established expressions are amenable to numerical evaluation, and shed key insights into the performance tradeoff between subscribers and nonsubscribers. The analytical results are corroborated by numerical simulations.Comment: This is the final version, which was accepted in IEEE Transactions on Communication

Analytical investigation of sideband electromagnetic vibration in integral-slot PMSM drive with SVPWM technique

This paper provides a comprehensive investigation into the electromagnetic vibration associated with the sideband harmonic components introduced by space vector pulse width modulation applied in integral-slot permanent magnet synchronous machine drives. The critical permanent magnet, armature reaction, and sideband magnetic field components, which are the primary causes for sideband electromagnetic vibration in integral-slot permanent magnet synchronous machines, are identified. The analytical derivations of the magnetic field components are carried out, and amplitudes and frequencies of the resultant sideband radial electromagnetic force components are obtained. Furthermore, the proposed models of the sideband radial electromagnetic force components are incorporated into the vibration model to analytically evaluate the corresponding sideband electromagnetic vibrations of the machine. Experimental tests on an integral-slot permanent magnet synchronous machine drive are comprehensively performed to confirm the validity and accuracy of the analytical models. Not only can the validated analytical models offer insightful details in understanding the impacts of the key factors, such as operation conditions, machine geometry, electromagnetic and power converter parameters, on the sideband electromagnetic vibration, but also can be readily extended to assess and reduce noise in integral-slot permanent magnet synchronous machine drives

Protective effects of Zhuifeng tougu on collagen-induced arthritis in DBA/1 mice

Purpose: To investigate the protective effects of Zhuifengtougu (ZFTG) on rheumatoid arthritis (RA) using collagen-induced arthritis (CIA) mouse modelMethods: DBA/1 mice were randomly divided into 7 treatment groups (n = 8): normal, positive control (CIA mice), CIA mice + total glucosides of peony (TGP), CIA mice + cyclophosphamide (CPA), CIA mice + 100 mg/kg ZFTG, CIA mice + 200 mg/kg ZFTG, and CIA mice + 400 mg/kg ZFTG. The serum levels of interleukin (IL)-1β, IL-6, IL-10, IL-17 and tumor necrosis factor (TNF)-αwere measured by enzyme-linked immunosorbent assay (ELISA). Western blot was used to determine the protein expression of B-cell lymphoma 2 (BCL-2), p53 and first apoptosis signal receptor (Fas).Results: Following drug administration, the arthritic index in CIA mice administered low-dose, mediumdose, or high-dose ZFTG (1.53 – 1.87), TGP (1.75 ± 0.42), or CPA (1.52 ± 0.36) was reduced significantly (p < 0.05), compared with positive control group (5.66 ± 0.73; p < 0.01). Levels of IL-1β, IL-6, IL-17 and TNF-α in serum and expression of Bcl-2, p53, and Fas were also significantly decreased (p < 0.05) in CIA mice administered ZFTG, TGP, or CPA, whereas IL-10 levels increased.Conclusion: These results suggest that ZFTG exhibit anti-rheumatic activity in CIA mice via modulation of inflammatory cytokines (IL-1β, IL-6, IL-10, IL-17 and TNF-α) and downregulation of the expressions of Bcl-2, p53, and Fas. Thus, ZFTG is a potential candidate drug for the treatment of RA.Keywords: Zhuifengtougu pill, Rheumatoid arthritis, Cytokines, Bcl-2, Fas, p5

NO Reduction By Propane Over Monolithic Cordierite-based Fe/Al2O3 Catalyst: Reaction Mechanism And Effect Of H2O/SO2

The selective reduction of NO by C3H8and the sensitivity to H2O and SO2have been studied over monolithic cordierite-based Fe/Al2O3catalysts, which were prepared by the sol–gel and impregnation method. The catalysts were investigated by N2 adsorption, X-ray diffraction (XRD), scanning electron microscope (SEM), X-ray photoelectron spectroscopy (XPS) and in situ diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS) techniques. Results showed that NO reduction was more than 90% in the absence of oxygen at 500 °C and in the presence of oxygen at 600 °C respectively. In a continues test of 12 h at 600 °C, 0.02% of SO2caused an irrecoverable decrease of NO conversion from 94% to 85% and 2.5% of H2O caused a drop of NO conversion from 86% to 56%, while NO conversion totally recovered when H2O was removed. The catalysts lost 15% of the initial activity after a hydrothermal treatment due to the agglomeration of iron oxide nanorods. Sulphidation treatment caused about a loss of 30% of the initial activity because of the deposited SO42−species. In situ study by DRIFTS indicated that coexisting H2O influenced the formation NO2 ad species and unidentate nitrate, while SO2 slightly inhibited the formation of NO2/NO3−species but promoted the formation of acetate/formate species during NO reduction by C3H8. Based on the results, a preliminary mechanism was proposed and discussed. The results may help understand the fundamental performance of monolithic cordierite-based Fe/Al2O3catalysts and provide some reference for SCR-HC catalyst design

DNA damage-induced activation of ATM promotes β-TRCP-mediated Mdm2 ubiquitination and destruction

The Mdm2 oncoprotein promotes p53 ubiquitination and destruction. Yet, exact molecular mechanisms of Mdm2 destruction itself, under DNA damaging conditions, remain unclear. Recently, we identified SCFβ-TRCP as a novel E3 ligase that targets Mdm2 for ubiquitination and destruction in a Casein Kinase Iδ (CKIδ)-dependent manner. However, it remains elusive how the β-TRCP/CKIδ/Mdm2 signaling axis is regulated by DNA damage signals to govern p53 activity. Consistent with previous studies, we found that inactivation of the Ataxia Telangiectasia Mutated (ATM) kinase, in turn, impaired DNA damage-induced Mdm2 destruction. Although phosphorylation of Mdm2 at Ser395 (an ATM phosphorylation site) facilitated Mdm2 interaction with β-TRCP, Ser395A-Mdm2 was degraded non-distinguishably from WT-Mdm2 by SCFβ-TRCP upon DNA damaging treatments. This indicates that in addition to phosphorylating Mdm2 at Ser395, ATM may govern Mdm2 stability through other unknown mechanisms. We further demonstrated that DNA damage-induced activation of ATM directly phosphorylated CKIδ at two well-conserved S/TQ sites, which promotes CKIδ nuclear localization to increase CKIδ-mediated phosphorylation of Mdm2, thereby facilitating subsequent Mdm2 ubiquitination by SCFβ-TRCP. Our studies provide a molecular mechanism of how ATM could govern DNA damage-induced destruction of Mdm2 in part by phosphorylating both Mdm2 and CKIδ to modulate SCFβ-TRCP–mediated Mdm2 ubiquitination. Given the pivotal role of Mdm2 in the negative regulation of p53, this work will also provide a rationale for developing CKIδ or ATM agonists as anti-cancer agents

Identification of acetylation-dependent regulatory mechanisms that govern the oncogenic functions of Skp2

The Skp2 (S-phase kinase associated protein 2) oncoprotein is often highly expressed in various types of human cancers. However, the mechanistic basis of its oncogenic function, as well as the upstream regulatory pathway(s) that control Skp2 activities remains not fully understood. Recently, we reported that p300 acetylates Skp2 at two conserved lysine residues K68 and K71 within its NLS (Nuclear localization signal). This modification leads to increased Skp2 stability and cytoplasmic translocation, thus contributing to elevated Skp2 oncogenic potential. Moreover, we found that the SIRT3 tumor suppressor serves as the physiological deacetylase that antagonizes p300-mediated Skp2 acetylation. Furthermore, we showed that Skp2 governs E-cadherin ubiquitination and degradation in the cytosol. Consistent with this, we observed an inverse correlation between Skp2 and E-cadherin expression in clinical breast tumor samples. Therefore, our work elucidates a novel acetylation-dependent regulatory mechanism for Skp2 oncogenic functions

Propagation and Wireless Channel Modeling Development on Wide-Sense Vehicle-to-X Communications

The need for improving the safety and the efficiency of transportation systems has become of extreme importance. In this regard, the concept of vehicle-to-X (V2X) communication has been introduced with the purpose of providing wireless communication technology in vehicular networks. Not like the traditional views, the wide-sense V2X (WSV2X) communications in this paper are defined by including not only vehicle-to-vehicle (V2V) and vehicle-to-infrastructure (V2I) communications but also train-to-X (T2X) communications constituted of train-to-train (T2T) and train-to-infrastructure (T2I) communications. All the information related to the wide-sense V2X channels, such as the standardization, scenarios, characters, and modeling philosophies, is organized and summarized to form the comprehensive understanding of the development of the WSV2X channels

SCFβ-TRCP targets MTSS1 for ubiquitination-mediated destruction to regulate cancer cell proliferation and migration

Metastasis suppressor 1 (MTSS1) is an important tumor suppressor protein, and loss of MTSS1 expression has been observed in several types of human cancers. Importantly, decreased MTSS1 expression is associated with more aggressive forms of breast and prostate cancers, and with poor survival rate. Currently, it remains unclear how MTSS1 is regulated in cancer cells, and whether reduced MTSS1 expression contributes to elevated cancer cell proliferation and migration. Here we report that the SCFβ-TRCP regulates MTSS1 protein stability by targeting it for ubiquitination and subsequent destruction via the 26S proteasome. Notably, depletion of either Cullin 1 or β-TRCP1 led to increased levels of MTSS1. We further demonstrated a crucial role for Ser322 in the DSGXXS degron of MTSS1 in governing SCFβ-TRCP-mediated MTSS1 degradation. Mechanistically, we defined that Casein Kinase Iδ (CKIδ) phosphorylates Ser322 to trigger MTSS1's interaction with β-TRCP for subsequent ubiquitination and degradation. Importantly, introducing wild-type MTSS1 or a non-degradable MTSS1 (S322A) into breast or prostate cancer cells with low MTSS1 expression significantly inhibited cellular proliferation and migration. Moreover, S322A-MTSS1 exhibited stronger effects in inhibiting cell proliferation and migration when compared to ectopic expression of wild-type MTSS1. Therefore, our study provides a novel molecular mechanism for the negative regulation of MTSS1 by β-TRCP in cancer cells. It further suggests that preventing MTSS1 degradation could be a possible novel strategy for clinical treatment of more aggressive breast and prostate cancers