Clustering with multiple receiving antennas in downlink FDD CoMP systems

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Prevalence of thoracic vertebral fractures in hospitalized elderly patients with heart failure

ObjectiveHeart failure (HF) has been associated with increased risk of fragility fractures. Indeed, most literature data on fractures were based on an historical and clinical approach focused on the identification of peripheral fractures, whereas the risk of vertebral fractures in this clinical setting is still unclear.DesignCross-sectional study.AimTo evaluate the prevalence and determinants of radiological thoracic vertebral fractures in patients with HF.MethodsThe study includes 1031 elderly hospitalized patients (491 females and 540 males; median age, 75 years; range, 65–90; 430 patients with HF) who were evaluated for the presence of thoracic vertebral fractures by quantitative morphometric analysis, using chest X-ray routinely performed in the diagnostic work-up of HF.ResultsVertebral fractures were found in 166 patients (16.1%), the prevalence being significantly higher in patients with HF as compared with those without HF, both in females (30.9 vs 15.8%; P<0.001) and in males (16.4 vs 7.4%; P=0.001). The association between HF and vertebral fractures remained statistically significant (odds ratio, 2.14; 95% CI, 1.25–3.66; P=0.01) even after adjustment for age, sex, loop diuretic therapy, anticoagulant therapy, proton pump therapy, coexistent chronic obstructive pulmonary disease, diabetes mellitus, renal insufficiency, and chronic liver diseases. In patients with HF, vertebral fractures were positively correlated with female sex, duration of HF, ischemic heart disease, cigarette smoking, and treatment with anti-osteoporotic drugs, and inversely correlated with left ventricular ejection fraction.ConclusionsHospitalized patients suffering from HF are at higher risk of vertebral fractures than patients without HF in the same clinical context

Chiral Perturbation Theory Predictions for η→π+π−π0γ\eta \to \pi^+ \pi^- \pi^0 \gamma

The $\eta \to \pi^+ \pi^- \pi^0 \gamma$ decay is discussed in the general context of Chiral Perturbation Theory (ChPT), assuming that the low--energy constants (counter--terms) are saturated by vector-meson resonances. The $\eta \to \pi^+ \pi^- \pi^0 \gamma$ amplitude can be separated in two distinct pieces: the inner bremsstrahlung, $A^{(IB)}$, and the structure dependent (or direct emission), $A^{(SD)}$, amplitudes. The former -- which essentially contains the same physics as $A(\eta \to \pi^+ \pi^- \pi^0)$ -- is found to dominate over the second one -- which looks more interesting from the ChPT point of view.Comment: 14 pages, 4 figures. PS file (96/8 N/P) available at http://www.nordita.dk/locinfo/preprints.htm

The Mixed Vector Current Correlator <0|T(V^3_\mu V^8_\nu )|0> To Two Loops in Chiral Perturbation Theory

The isospin-breaking correlator of the product of flavor octet vector currents, $V^3_\mu$ and $V^8_\nu$, $\Pi^{38}_{\mu\nu}(q^2)$ is computed to next-to-next- to-leading (two-loop) order in Chiral Perturbation Theory. Large corrections to both the magnitude and $q^2$-dependence of the one-loop result are found, and the reasons for the slow convergence of the chiral series for the correlator given. The two-loop expression involves a single ${\cal O}(q^6)$ counterterm, present also in the two-loop expressions for $\Pi^{33}_{\mu\nu}(q^2)$ and $\Pi^{88}_{\mu\nu}(q^2)$, which counterterm contributes a constant to the scalar correlator $\Pi^{38}(q^2)$. The feasibility of extracting the value of this counterterm from other sources is discussed. Analysis of the slope of the correlator with respect to $q^2$ using QCD sum rules is shown to suggest that, even to two-loop order, the chiral series for the correlator may not yet be well-converged.Comment: 32 pages, uses REVTEX and epsfig.sty with 7 uuencoded figures. Entire manuscript available as a ps file at http://www.physics.adelaide.edu.au/theory/home.html Also available via anonymous ftp at ftp://adelphi.adelaide.edu.au/pub/theory/ADP-95-27.T181.p

Novel Role of NOX in Supporting Aerobic Glycolysis in Cancer Cells with Mitochondrial Dysfunction and as a Potential Target for Cancer Therapy

NAD(P)H oxidase plays a role in cancer metabolism by providing NAD+ to support increased glycolysis

Mutant Kras copy number defines metabolic reprogramming and therapeutic susceptibilities.

The RAS/MAPK (mitogen-activated protein kinase) signalling pathway is frequently deregulated in non-small-cell lung cancer, often through KRAS activating mutations. A single endogenous mutant Kras allele is sufficient to promote lung tumour formation in mice but malignant progression requires additional genetic alterations. We recently showed that advanced lung tumours from Kras(G12D/+);p53-null mice frequently exhibit Kras(G12D) allelic enrichment (Kras(G12D)/Kras(wild-type) > 1) (ref. 7), implying that mutant Kras copy gains are positively selected during progression. Here we show, through a comprehensive analysis of mutant Kras homozygous and heterozygous mouse embryonic fibroblasts and lung cancer cells, that these genotypes are phenotypically distinct. In particular, Kras(G12D/G12D) cells exhibit a glycolytic switch coupled to increased channelling of glucose-derived metabolites into the tricarboxylic acid cycle and glutathione biosynthesis, resulting in enhanced glutathione-mediated detoxification. This metabolic rewiring is recapitulated in mutant KRAS homozygous non-small-cell lung cancer cells and in vivo, in spontaneous advanced murine lung tumours (which display a high frequency of Kras(G12D) copy gain), but not in the corresponding early tumours (Kras(G12D) heterozygous). Finally, we demonstrate that mutant Kras copy gain creates unique metabolic dependences that can be exploited to selectively target these aggressive mutant Kras tumours. Our data demonstrate that mutant Kras lung tumours are not a single disease but rather a heterogeneous group comprising two classes of tumours with distinct metabolic profiles, prognosis and therapeutic susceptibility, which can be discriminated on the basis of their relative mutant allelic content. We also provide the first, to our knowledge, in vivo evidence of metabolic rewiring during lung cancer malignant progression.We thank T. Jacks (Kras^LSL-G12D), A. Berns (p53^Fx) and the NIH Mouse repository for mice. We also thank Sam Kleeman and Patricia Ogger for assistance with redox cell profiling and cell viability assays, respectively. We are very thankful to CRUK CI BRU staff for support with in vivo work and all the members of the Martins lab for critical comments and advice. This work was supported by the Medical Research Council.This is the author accepted manuscript. The final version is available at http://www.nature.com/nature/journal/v531/n7592/full/nature16967.html

Factor graph based detection approach for high-mobility OFDM systems with large FFT modes

In this article, a novel detector design is proposed for orthogonal frequency division multiplexing (OFDM) systems over frequency selective and time varying channels. Namely, we focus on systems with large OFDM symbol lengths where design and complexity constraints have to be taken into account and many of the existing ICI reduction techniques can not be applied. We propose a factor graph (FG) based approach for maximum a posteriori (MAP) symbol detection which exploits the frequency diversity introduced by the ICI in the OFDM symbol. The proposed algorithm provides high diversity orders allowing to outperform the free-ICI performance in high-mobility scenarios with an inherent parallel structure suitable for large OFDM block sizes. The performance of the mentioned near-optimal detection strategy is analyzed over a general bit-interleaved coded modulation (BICM) system applying low-density parity-check (LDPC) codes. The inclusion of pilot symbols is also considered in order to analyze how they assist the detection process