Power adaptation for cognitive radio systems under an average sinr loss constraint in the absence of path loss information

An upper bound is derived on the capacity of a cognitive radio system by considering the effects of path loss and log-normal shadowing simultaneously for a single-cell network. Assuming that the cognitive radio is informed only of the shadow fading between the secondary (cognitive) transmitter and primary receiver, the capacity is achieved via the water-filling power allocation strategy under an average primary signal to secondary interference plus noise ratio loss constraint. Contrary to the perfect channel state information requirement at the secondary system (SS), the transmit power control of the SS is accomplished in the absence of any path loss estimates. For this purpose, a method for estimating the instantaneous value of the shadow fading is also presented. A detailed analysis of the proposed power adaptation strategy is conducted through various numerical simulations. © 2013 Springer Science+Business Media New York

Bulk Fermi surface and momentum density in heavily doped La2−x_{2-x}Srx_xCuO4_4 using high resolution Compton scattering and positron annihilation spectroscopies

We have observed the bulk Fermi surface (FS) in an overdoped ($x$=0.3) single crystal of La$_{2-x}$Sr$_x$CuO$_4$ by using Compton scattering. A two-dimensional (2D) momentum density reconstruction from measured Compton profiles yields a clear FS signature in the third Brillouin zone along [100]. The quantitative agreement between density functional theory (DFT) calculations and momentum density experiment suggests that Fermi-liquid physics is restored in the overdoped regime. In particular the predicted FS topology is found to be in good accord with the corresponding experimental data. We find similar quantitative agreement between the measured 2D angular correlation of positron annihilation radiation (2D-ACAR) spectra and the DFT based computations. However, 2D-ACAR does not give such a clear signature of the FS in the extended momentum space in either the theory or the experiment.Comment: 9 pages, 8 figure

High resolution Compton scattering as a Probe of the Fermi surface in the Iron-based superconductor LaO1−xFxFeAsLaO_{1-x}F_xFeAs

We have carried out first principles all-electron calculations of the (001)-projected 2D electron momentum density and the directional Compton profiles along the [100], [001] and [110] directions in the Fe-based superconductor LaOFeAs within the framework of the local density approximation. We identify Fermi surface features in the 2D electron momentum density and the directional Compton profiles, and discuss issues related to the observation of these features via Compton scattering experiments.Comment: 4 pages, 3 figure

Characterization of preplasma produced by an ultrahigh intensity laser system

Copyright 2004 American Institute of Physics. This article may be downloaded for personal use only. Any other use requires prior permission of the author and the American Institute of Physics. The following article appeared in Physics of Plasmas, 11(8), 3721-3725, 2004 and may be found at http://dx.doi.org/10.1063/1.176077

Source parameters of the great Sumatran megathrust earthquakes of 1797 and 1833 inferred from coral microatolls

Large uplifts and tilts occurred on the Sumatran outer arc islands between 0.5° and 3.3°S during great historical earthquakes in 1797 and 1833, as judged from relative sea level changes recorded by annually banded coral heads. Coral data for these two earthquakes are most complete along a 160-km length of the Mentawai islands between 3.2° and 2°S. Uplift there was as great as 0.8 m in 1797 and 2.8 m in 1833. Uplift in 1797 extended 370 km, between 3.2° and 0.5°S. The pattern and magnitude of uplift imply megathrust ruptures corresponding to moment magnitudes (M_w) in the range 8.5 to 8.7. The region of uplift in 1833 ranges from 2° to at least 3.2°S and, judging from historical reports of shaking and tsunamis, perhaps as far as 5°S. The patterns and magnitude of uplift and tilt in 1833 are similar to those experienced farther north, between 0.5° and 3°N, during the giant Nias-Simeulue megathrust earthquake of 2005; the outer arc islands rose as much as 3 m and tilted toward the mainland. Elastic dislocation forward modeling of the coral data yields megathrust ruptures with moment magnitudes ranging from 8.6 to 8.9. Sparse accounts at Padang, along the mainland west coast at latitude 1°S, imply tsunami runups of at least 5 m in 1797 and 3–4 m in 1833. Tsunamis simulated from the pattern of coral uplift are roughly consistent with these reports. The tsunami modeling further indicates that the Indian Ocean tsunamis of both 1797 and 1833, unlike that of 2004, were directed mainly south of the Indian subcontinent. Between about 0.7° and 2.1°S, the lack of vintage 1797 and 1833 coral heads in the intertidal zone demonstrates that interseismic submergence has now nearly equals coseismic emergence that accompanied those earthquakes. The interseismic strains accumulated along this reach of the megathrust have thus approached or exceeded the levels relieved in 1797 and 1833

Evolution of Robustness to Noise and Mutation in Gene Expression Dynamics

Phenotype of biological systems needs to be robust against mutation in order to sustain themselves between generations. On the other hand, phenotype of an individual also needs to be robust against fluctuations of both internal and external origins that are encountered during growth and development. Is there a relationship between these two types of robustness, one during a single generation and the other during evolution? Could stochasticity in gene expression have any relevance to the evolution of these robustness? Robustness can be defined by the sharpness of the distribution of phenotype; the variance of phenotype distribution due to genetic variation gives a measure of `genetic robustness' while that of isogenic individuals gives a measure of `developmental robustness'. Through simulations of a simple stochastic gene expression network that undergoes mutation and selection, we show that in order for the network to acquire both types of robustness, the phenotypic variance induced by mutations must be smaller than that observed in an isogenic population. As the latter originates from noise in gene expression, this signifies that the genetic robustness evolves only when the noise strength in gene expression is larger than some threshold. In such a case, the two variances decrease throughout the evolutionary time course, indicating increase in robustness. The results reveal how noise that cells encounter during growth and development shapes networks' robustness to stochasticity in gene expression, which in turn shapes networks' robustness to mutation. The condition for evolution of robustness as well as relationship between genetic and developmental robustness is derived through the variance of phenotypic fluctuations, which are measurable experimentally.Comment: 25 page

The MRN complex is transcriptionally regulated by MYCN during neural cell proliferation to control replication stress

The MRE11/RAD50/NBS1 (MRN) complex is a major sensor of DNA double strand breaks, whose role in controlling faithful DNA replication and preventing replication stress is also emerging. Inactivation of the MRN complex invariably leads to developmental and/or degenerative neuronal defects, the pathogenesis of which still remains poorly understood. In particular, NBS1 gene mutations are associated with microcephaly and strongly impaired cerebellar development, both in humans and in the mouse model. These phenotypes strikingly overlap those induced by inactivation of MYCN, an essential promoter of the expansion of neuronal stem and progenitor cells, suggesting that MYCN and the MRN complex might be connected on a unique pathway essential for the safe expansion of neuronal cells. Here, we show that MYCN transcriptionally controls the expression of each component of the MRN complex. By genetic and pharmacological inhibition of the MRN complex in a MYCN overexpression model and in the more physiological context of the Hedgehog-dependent expansion of primary cerebellar granule progenitor cells, we also show that the MRN complex is required for MYCN-dependent proliferation. Indeed, its inhibition resulted in DNA damage, activation of a DNA damage response, and cell death in a MYCN- and replication-dependent manner. Our data indicate the MRN complex is essential to restrain MYCN-induced replication stress during neural cell proliferation and support the hypothesis that replication-born DNA damage is responsible for the neuronal defects associated with MRN dysfunctions.Cell Death and Differentiation advance online publication, 12 June 2015; doi:10.1038/cdd.2015.81