4,972 research outputs found
Rejoinder: Bayesian Checking of the Second Levels of Hierarchical Models
Rejoinder: Bayesian Checking of the Second Levels of Hierarchical Models
[arXiv:0802.0743]Comment: Published in at http://dx.doi.org/10.1214/07-STS235REJ the
Statistical Science (http://www.imstat.org/sts/) by the Institute of
Mathematical Statistics (http://www.imstat.org
Ripples in Tapped or Blown Powder
We observe ripples forming on the surface of a granular powder in a container
submitted from below to a series of brief and distinct shocks. After a few
taps, the pattern turns out to be stable against any further shock of the same
amplitude. We find experimentally that the characteristic wavelength of the
pattern is proportional to the amplitude of the shocks. Starting from
consideration involving Darcy's law for air flow through the porous granulate
and avalanche properties, we build up a semi-quantitative model which fits
satisfactorily the set of experimental observations as well as a couple of
additional experiments.Comment: 7 pages, four postscript figures, submitted PRL 11/19/9
A comprehensive study of high-metallicity giant extragalactic H II regions: ionizing populations
This is an electronic version of an article published in Revista Mexicana de Astronomía y Astrofísica. Castellanos, M., Díaz, A.I., and E. Terlevich. A comprehensive study of high-metallicity giant extragalactic H II regions: ionizing populations. Revista Mexicana de Astronomía y Astrofísica 12 (2002): 25
A very fast inference algorithm for finite-dimensional spin glasses: Belief Propagation on the dual lattice
Starting from a Cluster Variational Method, and inspired by the correctness
of the paramagnetic Ansatz (at high temperatures in general, and at any
temperature in the 2D Edwards-Anderson model) we propose a novel message
passing algorithm --- the Dual algorithm --- to estimate the marginal
probabilities of spin glasses on finite dimensional lattices. We show that in a
wide range of temperatures our algorithm compares very well with Monte Carlo
simulations, with the Double Loop algorithm and with exact calculation of the
ground state of 2D systems with bimodal and Gaussian interactions. Moreover it
is usually 100 times faster than other provably convergent methods, as the
Double Loop algorithm.Comment: 23 pages, 12 figures. v2: improved introductio
Adaptive resistance is not responsible for long-term drug resistance in a cellular model of triple negative breast cancer
Resistance to cancer therapeutics represents a leading cause of mortality and is particularly important in cancers, such as triple negative breast cancer, for which no targeted therapy is available, as these are only treated with traditional chemotherapeutics. Cancer, as well as bacterial, drug resistance can be intrinsic, acquired or adaptive. Adaptive cancer drug resistance is gaining attention as a mechanism for the generation of long-term drug resistance as is the case with bacterial antibiotic resistance. We have used a cellular model of triple negative breast cancer (CAL51) and its drug resistance derivative (CALDOX) to gain insight into genome-wide expression changes associated with long-term doxorubicin (a widely used anthracycline for cancer treatment) resistance and doxorubicin-induced stress. Previous work indicates that both naïve and resistance cells have a functional p53-p21 axis controlling cell cycle at G1, although this is not a driver for drug resistance, but down-regulation of TOP2A (topoisomerase IIα). As expected, CALDOX cells have a signature characterized, in addition to down-regulation of TOP2A, by genes and pathways associated with drug resistance, metastasis and stemness. Both CAL51 and CALDOX stress signatures share 12 common genes (TRIM22, FAS, SPATA18, SULF2, CDKN1A, GDF15, MYO6, CXCL5, CROT, EPPK1, ZMAT3 and CD44), with roles in the above-mentioned pathways, indicating that these cells have similar functional responses to doxorubicin relaying on the p53 control of apoptosis. Eight genes are shared by both drug stress signatures (in CAL51 and CALDOX cells) and CALDOX resistant cells (FAS, SULF2, CDKN1A, CXCL5, CD44, SPATA18, TRIM22 and CROT), many of them targets of p53. This corroborates experimental data indicating that CALDOX cells, even in the absence of drug, have activated, at least partially, the p53-p21 axis and DNA damage response. Although this eight-gene signature might be an indicator of adaptive resistance, as this transient phenomenon due to short-term stress may not revert to its original state upon withdrawal of the stressor, previous experimental data indicates that the p53-p21 axis is not responsible for doxorubicin resistance. Importantly, TOP2A is not responsive to doxorubicin treatment and thus absent in both drug stress signatures. This indicates that during the generation of doxorubicin resistance, cells acquire genetic changes likely to be random, leading to down regulation of TOP2A, but selected during the generation of cells due to the presence of drug in the culture medium. This poses a considerable constraint for the development of strategies aimed at avoiding the emergence of drug resistance in the clinic
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