An Adaptive Algorithm to Optimize the Dynamics of IEEE 802.15.4 Networks

Presentado en ICST 2013IEEE 802.15.4 standard is becoming one of the most popular technologies for the deployment of low rate Wireless Personal Area Networks with strong power constraints. In order to reduce the energy consumption, beacon-enabled networks with long network inactive periods can be employed. However, the duration of these inactivity periods, as some other configuration parameters, are conventionally set to default values and remain fixed during the whole network operation. This implies that if they are misconfigured the network will not adapt to changes in the conditions of the environment, particularly to the most determining one, i.e. the traffic load. This paper proposes a simple procedure for the dynamic adaptation of several key parameters of IEEE 802.15.4 networks. Under this procedure, the 802.15.4 parameters are modified as a function of the existing traffic conditions.Spanish National Project No.TEC2009-13763-C02-01

Financial Transaction Tax: Small is Beautiful

The case for taxing financial transactions merely to raise more revenues from the financial sector is not particularly strong. Better alternatives to tax the financial sector are likely to be available. However, a tax on financial transactions could be justified in order to limit socially undesirable transactions when more direct means of doing so are unavailable for political or practical reasons. Some financial transactions are indeed likely to do more harm than good, especially when they contribute to the systemic risk of the financial system. However, such a financial transaction tax should be very small, much smaller than the negative externalities in question, because it is a blunt instrument that also drives out socially useful transactions. There is a case for taxing over-the-counter derivative transactions at a somewhat higher rate than exchange-based derivative transactions. More targeted remedies to drive out socially undesirable transactions should be sought in parallel, which would allow, after their implementation, to reduce or even phase out financialtransaction taxes

Cellular connectivity for UAVs: Network modeling, performance analysis, and design guidelines

The growing use of aerial user equipments (UEs) in various applications requires ubiquitous and reliable connectivity for safe control and data exchange between these devices and ground stations. Key questions that need to be addressed when planning the deployment of aerial UEs are whether the cellular network is a suitable candidate for enabling such connectivity and how the inclusion of aerial UEs might impact the overall network efficiency. This paper provides an in-depth analysis of user and network-level performance of a cellular network that serves both unmanned aerial vehicles (UAVs) and ground users in the downlink. Our results show that the favorable propagation conditions that UAVs enjoy due to their height often backfire on them, as the increased load-dependent co-channel interference received from neighboring ground base stations (BSs) is not compensated by the improved signal strength. When compared with a ground user in an urban area, our analysis shows that a UAV flying at 100 m can experience a throughput decrease of a factor 10 and a coverage drop from 76% to 30%. Motivated by these findings, we develop UAV and network-based solutions to enable an adequate integration of UAVs into cellular networks. In particular, we show that an optimal tilting of the UAV antenna can increase the coverage from 23% to 89% and throughput from 3.5 to 5.8 b/s/Hz, outperforming ground UEs. Furthermore, our findings reveal that depending on the UAV altitude and its antenna configuration, the aerial user performance can scale with respect to the network density better than that of a ground user. Finally, our results show that network densification and the use of microcells limit the UAV performance. Although UAV usage has the potential to increase the area spectral efficiency (ASE) of cellular networks with a moderate number of cells, they might hamper the development of future ultradense networks

Genetic Modulation of Lipid Profiles following Lifestyle Modification or Metformin Treatment: the Diabetes Prevention Program

Weight-loss interventions generally improve lipid profiles and reduce cardiovascular disease risk, but effects are variable and may depend on genetic factors. We performed a genetic association analysis of data from 2,993 participants in the Diabetes Prevention Program to test the hypotheses that a genetic risk score (GRS) based on deleterious alleles at 32 lipid-associated single-nucleotide polymorphisms modifies the effects of lifestyle and/or metformin interventions on lipid levels and nuclear magnetic resonance (NMR) lipoprotein subfraction size and number. Twenty-three loci previously associated with fasting LDL-C, HDL-C, or triglycerides replicated (P=0.04–1×10$^{−17}$). Except for total HDL particles (r=−0.03, P=0.26), all components of the lipid profile correlated with the GRS (partial |r|=0.07–0.17, P=5×10$^{−5}$–1×10$^{−19}$). The GRS was associated with higher baseline-adjusted 1-year LDL cholesterol levels (β=+0.87, SEE±0.22 mg/dl/allele, P=8×10−5, P$_{interaction}$=0.02) in the lifestyle intervention group, but not in the placebo (β=+0.20, SEE±0.22 mg/dl/allele, P=0.35) or metformin (β=−0.03, SEE±0.22 mg/dl/allele, P=0.90; P$_{interaction}$=0.64) groups. Similarly, a higher GRS predicted a greater number of baseline-adjusted small LDL particles at 1 year in the lifestyle intervention arm (β=+0.30, SEE±0.012 ln nmol/L/allele, P=0.01, P$_{interaction}$=0.01) but not in the placebo (β=−0.002, SEE±0.008 ln nmol/L/allele, P=0.74) or metformin (β=+0.013, SEE±0.008 nmol/L/allele, P=0.12; P$_{interaction}$ = 0.24) groups. Our findings suggest that a high genetic burden confers an adverse lipid profile and predicts attenuated response in LDL-C levels and small LDL particle number to dietary and physical activity interventions aimed at weight loss

D25V apolipoprotein C-III variant causes dominant hereditary systemic amyloidosis and confers cardiovascular protective lipoprotein profile

Apolipoprotein C-III deficiency provides cardiovascular protection, but apolipoprotein C-III is not known to be associated with human amyloidosis. Here we report a form of amyloidosis characterized by renal insufficiency caused by a new apolipoprotein C-III variant, D25V. Despite their uremic state, the D25V-carriers exhibit low triglyceride (TG) and apolipoprotein C-III levels, and low very-low-density lipoprotein (VLDL)/high high-density lipoprotein (HDL) profile. Amyloid fibrils comprise the D25V-variant only, showing that wild-type apolipoprotein C-III does not contribute to amyloid deposition in vivo. The mutation profoundly impacts helical structure stability of D25V-variant, which is remarkably fibrillogenic under physiological conditions in vitro producing typical amyloid fibrils in its lipid-free form. D25V apolipoprotein C-III is a new human amyloidogenic protein and the first conferring cardioprotection even in the unfavourable context of renal failure, extending the evidence for an important cardiovascular protective role of apolipoprotein C-III deficiency. Thus, fibrate therapy, which reduces hepatic APOC3 transcription, may delay amyloid deposition in affected patients

Evaluation of the association between the common E469K polymorphism in the ICAM-1 gene and diabetic nephropathy among type 1 diabetic patients in GoKinD population

<p>Abstract</p> <p>Background</p> <p>The ICAM-1 gene is a strong positional and biological candidate for susceptibility to the development of T1D and DN. We have recently demonstrated that SNP rs5498(E469K) confers susceptibility to the development of T1D and might be associated with DN in Swedish Caucasians. The present study aimed to further evaluate the association between the ICAM-1 genetic polymorphisms and DN.</p> <p>Methods</p> <p>Two common non-synonymous SNPs, including rs5498(E469K) and rs1799969(R241G), in the ICAM-1 gene were genotyped in 662 (312 female/350 male) T1D patients with DN and 620 (369/251) without DN. All patients were selected from the GoKinD study.</p> <p>Results</p> <p>Genotype distributions of both SNPs were in Hardy-Weinberg equilibrium but SNP rs5498(E469K) had high heterozygous index. In this SNP, the heterozygosity and positivity for the allele G were found to be significantly associated with DN in female T1D patients (P = 0.010, OR = 0.633, CI 95% 0.447–0.895 and P = 0.026, OR = 0.692, CI 95% 0.500–0.958). Furthermore, the female patients without DN carrying three genotypes A/A, A/G and G/G had different cystatin levels (0.79 ± 0.17, 0.81 ± 0.14 and 0.75 ± 0.12 mg/L, P = 0.021). No significant association of SNP rs1799969 (R241G) with DN was found.</p> <p>Conclusion</p> <p>The present study provides further evidence that SNP rs5498(E469K) in the ICAM-1 gene presents a high heterozygous index and the allele G of this polymorphism may confers the decreased risk susceptibility to the development of DN in female T1D patients among the GoKinD population.</p

In the dedicated pursuit of dedicated capital: restoring an indigenous investment ethic to British capitalism

Tony Blair’s landslide electoral victory on May 1 (New Labour Day?) presents the party in power with a rare, perhaps even unprecedented, opportunity to revitalise and modernise Britain’s ailing and antiquated manufacturing economy.* If it is to do so, it must remain true to its long-standing (indeed, historic) commitment to restore an indigenous investment ethic to British capitalism. In this paper we argue that this in turn requires that the party reject the very neo-liberal orthodoxies which it offered to the electorate as evidence of its competence, moderation and ‘modernisation’, which is has internalised, and which it apparently now views as circumscribing the parameters of the politically and economically possible