Detection of selfish manipulation of carrier sensing in 802.11 networks

Recently, tuning the clear channel assessment (CCA) threshold in conjunction with power control has been considered for improving the performance of WLANs. However, we show that, CCA tuning can be exploited by selfish nodes to obtain an unfair share of the available bandwidth. Specifically, a selfish entity can manipulate the CCA threshold to ignore ongoing transmissions; this increases the probability of accessing the medium and provides the entity a higher, unfair share of the bandwidth. We experiment on our 802.11 testbed to characterize the effects of CCA tuning on both isolated links and in 802.11 WLAN configurations. We focus on AP-client(s) configurations, proposing a novel approach to detect this misbehavior. A misbehaving client is unlikely to recognize low power receptions as legitimate packets; by intelligently sending low power probe messages, an AP can efficiently detect a misbehaving node. Our key contributions are: 1) We are the first to quantify the impact of selfish CCA tuning via extensive experimentation on various 802.11 configurations. 2) We propose a lightweight scheme for detecting selfish nodes that inappropriately increase their CCAs. 3) We extensively evaluate our system on our testbed; its accuracy is 95 percent while the false positive rate is less than 5 percent. © 2012 IEEE

A case for adaptive sub-carrier level power allocation in OFDMA networks

In today's OFDMA networks, the transmission power is typically fixed and the same for all the sub-carriers that compose a channel. The sub-carriers though, experience different degrees of fading and thus, the received power is different for different sub-carriers; while some frequencies experience deep fades, others are relatively unaffected. In this paper, we make a case of redistributing the power across the sub-carriers (subject to a fixed power budget constraint) to better cope with this frequency selectivity. Specifically, we design a joint power and rate adaptation scheme (called JPRA for short) wherein power redistribution is combined with sub-carrier level rate adaptation to yield significant throughput benefits. We further consider two variants of JPRA: (a) JPRA-CR where, the power is redistributed across sub-carriers so as to support a maximum common rate (CR) across sub-carriers and (b) JPRA-MT where, the goal is to redistribute power such that the transmission time of a packet is minimized. While the first variant decreases transceiver complexity and is simpler, the second is geared towards achieving the maximum throughput possible. We implement both variants of JPRA on our WARP radio testbed. Our extensive experiments demonstrate that our scheme provides a 35% improvement in total network throughput in testbed experiments compared to FARA, a scheme where only sub-carrier level rate adaptation is used. We also perform simulations to demonstrate the efficacy of JPRA in larger scale networks. © 2012 ACM

Enhanced photoelectrochemical response of 1D TiO₂ by atmospheric pressure plasma surface modification

In this paper we demonstrate the use of atmospheric pressure plasma jet (APPJ) to functionalize the surface of hydrothermally synthesized vertically aligned TiO2 nanorods (TNRs) for photo electrochemical (PEC) application. The TNRs functionalized with the atmospheric pressure He-plasma showed relatively higher crystallinity, improved light absorption, and change in the morphology with additional surface area, leading to an enhanced photocurrent density than that of the untreated. Achieving the PEC performance on par with the best in the literature, this APPJ treatment is shown to be a promising technique to obtain better functionality with TNR kind of materials and many other nano-micro systems for various applications such as PEC hydrogen generation

Electrochemically Top Gated Graphene: Monitoring Dopants by Raman Scattering

We demonstrate electrochemical top gating of graphene by using a solid polymer electrolyte. This allows to reach much higher electron and hole doping than standard back gating. In-situ Raman measurements monitor the doping. The G peak stiffens and sharpens for both electron and hole doping, while the 2D peak shows a different response to holes and electrons. Its position increases for hole doping, while it softens for high electron doping. The variation of G peak position is a signature of the non-adiabatic Kohn anomaly at $\Gamma$. On the other hand, for visible excitation, the variation of the 2D peak position is ruled by charge transfer. The intensity ratio of G and 2D peaks shows a strong dependence on doping, making it a sensitive parameter to monitor charges.Comment: 7 pages, 8 figure

Modelling survival : exposure pattern, species sensitivity and uncertainty

The General Unified Threshold model for Survival (GUTS) integrates previously published toxicokinetic-toxicodynamic models and estimates survival with explicitly defined assumptions. Importantly, GUTS accounts for time-variable exposure to the stressor. We performed three studies to test the ability of GUTS to predict survival of aquatic organisms across different pesticide exposure patterns, time scales and species. Firstly, using synthetic data, we identified experimental data requirements which allow for the estimation of all parameters of the GUTS proper model. Secondly, we assessed how well GUTS, calibrated with short-term survival data of Gammarus pulex exposed to four pesticides, can forecast effects of longer-term pulsed exposures. Thirdly, we tested the ability of GUTS to estimate 14-day median effect concentrations of malathion for a range of species and use these estimates to build species sensitivity distributions for different exposure patterns. We find that GUTS adequately predicts survival across exposure patterns that vary over time. When toxicity is assessed for time-variable concentrations species may differ in their responses depending on the exposure profile. This can result in different species sensitivity rankings and safe levels. The interplay of exposure pattern and species sensitivity deserves systematic investigation in order to better understand how organisms respond to stress, including humans

Shifting the Paradigm: The Putative Mitochondrial Protein ABCB6 Resides in the Lysosomes of Cells and in the Plasma Membrane of Erythrocytes

ABCB6, a member of the adenosine triphosphate–binding cassette (ABC) transporter family, has been proposed to be responsible for the mitochondrial uptake of porphyrins. Here we show that ABCB6 is a glycoprotein present in the membrane of mature erythrocytes and in exosomes released from reticulocytes during the final steps of erythroid maturation. Consistent with its presence in exosomes, endogenous ABCB6 is localized to the endo/lysosomal compartment, and is absent from the mitochondria of cells. Knock-down studies demonstrate that ABCB6 function is not required for de novo heme biosynthesis in differentiating K562 cells, excluding this ABC transporter as a key regulator of porphyrin synthesis. We confirm the mitochondrial localization of ABCB7, ABCB8 and ABCB10, suggesting that only three ABC transporters should be classified as mitochondrial proteins. Taken together, our results challenge the current paradigm linking the expression and function of ABCB6 to mitochondria

BCRP expression does not result in resistance to STX140 in vivo, despite the increased expression of BCRP in A2780 cells in vitro after long-term STX140 exposure

The anti-proliferative and anti-angiogenic properties of the endogenous oestrogen metabolite, 2-methoxyoestradiol (2-MeOE2), are enhanced in a series of sulphamoylated derivatives of 2-MeOE2. To investigate possible mechanisms of resistance to these compounds, a cell line, A2780.140, eightfold less sensitive to the 3,17-O,O-bis-sulphamoylated derivative, STX140, was derived from the A2780 ovarian cancer cell line by dose escalation. Other cell lines tested did not develop STX140 resistance. RT–PCR and immunoblot analysis demonstrated that breast cancer resistance protein (BCRP) expression is dramatically increased in A2780.140 cells. The cells are cross-resistant to the most structurally similar bis-sulphamates, and to BCRP substrates, mitoxantrone and doxorubicin; but they remain sensitive to taxol, an MDR1 substrate, and to all other sulphamates tested. Sensitivity can be restored using a BCRP inhibitor, and this pattern of resistance is also seen in a BCRP-expressing MCF-7-derived cell line, MCF-7.MR. In mice bearing wild-type (wt) and BCRP-expressing tumours on either flank, both STX140 and mitoxantrone inhibited the growth of the MCF-7wt xenografts, but only STX140 inhibited growth of the MCF-7.MR tumours. In conclusion, STX140, a promising orally bioavailable anti-cancer agent in pre-clinical development, is highly efficacious in BCRP-expressing xenografts. This is despite an increase in BCRP expression in A2780 cells in vitro after chronic dosing with STX140

Cancer stem cell metabolism: A potential target for cancer therapy

© 2016 The Author(s). Cancer Stem cells (CSCs) are a unipotent cell population present within the tumour cell mass. CSCs are known to be highly chemo-resistant, and in recent years, they have gained intense interest as key tumour initiating cells that may also play an integral role in tumour recurrence following chemotherapy. Cancer cells have the ability to alter their metabolism in order to fulfil bio-energetic and biosynthetic requirements. They are largely dependent on aerobic glycolysis for their energy production and also are associated with increased fatty acid synthesis and increased rates of glutamine utilisation. Emerging evidence has shown that therapeutic resistance to cancer treatment may arise due to dysregulation in glucose metabolism, fatty acid synthesis, and glutaminolysis. To propagate their lethal effects and maintain survival, tumour cells alter their metabolic requirements to ensure optimal nutrient use for their survival, evasion from host immune attack, and proliferation. It is now evident that cancer cells metabolise glutamine to grow rapidly because it provides the metabolic stimulus for required energy and precursors for synthesis of proteins, lipids, and nucleic acids. It can also regulate the activities of some of the signalling pathways that control the proliferation of cancer cells. This review describes the key metabolic pathways required by CSCs to maintain a survival advantage and highlights how a combined approach of targeting cellular metabolism in conjunction with the use of chemotherapeutic drugs may provide a promising strategy to overcome therapeutic resistance and therefore aid in cancer therapy