37 research outputs found
Three-Dimensional Phylogeny Explorer: Distinguishing paralogs, lateral transfer, and violation of "molecular clock" assumption with 3D visualization-0
<p><b>Copyright information:</b></p><p>Taken from "Three-Dimensional Phylogeny Explorer: Distinguishing paralogs, lateral transfer, and violation of "molecular clock" assumption with 3D visualization"</p><p>http://www.biomedcentral.com/1471-2105/8/213</p><p>BMC Bioinformatics 2007;8():213-213.</p><p>Published online 20 Jun 2007</p><p>PMCID:PMC1906840.</p><p></p
Performance analysis of IP<sub>0</sub> vs. ZD strategies.
<p>A: Stationary self-score </p><p></p><p></p><p></p><p><mi>S</mi></p><p><mi>G</mi><mi>G</mi></p><p></p><mo>ÂŻ</mo><p></p><p></p><p></p> of ZDR and ZD<sub><i>Ï</i></sub> (<i>Îș</i> = 0) at different levels of noise <i>Δ</i>. B: Invasion success of IP versus ZD strategies (log-scale, fixation probability of an IP<sub>0</sub> invader, normalized so 1.0 = neutral selection) for different levels of noise <i>Δ</i>. The top plot is extortionate (<i>Îș</i> = 0) while the lower three plots have <i>Îș</i> = <i>B</i> â <i>C</i> so the ZD strategies are cooperative [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0120625#pone.0120625.ref020" target="_blank">20</a>]. As the value of <i>Ï</i> increases, the fixation probability of IP increases. As the amount of noise decreases, the fixation of our implementation of IP approaches the neutral fixation. With no noise, an optimal IP player (ConSwitch, see text) can empirically invade ZDR at twice the neutral probability (20 out of 1000 simulations with the information phase replaced with tags).<p></p
Growth and Structure of Tb<sub>2</sub>O<sub>3</sub>(111) Films on Pt(111)
We
investigated the formation and structure of Tb<sub>2</sub>O<sub>3</sub>(111) thin films grown on Pt(111) using low-energy electron
diffraction (LEED) and scanning tunneling microscopy (STM). We find
that the Tb<sub>2</sub>O<sub>3</sub>(111) films adopt an oxygen-deficient
cubic fluorite structure, wherein the Tb cations form an approximately
(1.32 Ă 1.32) lattice in registry with the Pt(111) substrate.
STM shows that terbia film growth follows the StranskiâKrastanov
mechanism, in which Tb<sub>2</sub>O<sub>3</sub>(111) initially forms
a well-connected wetting layer up to a Tb<sub>2</sub>O<sub>3</sub> coverage of âŒ2 ML (monolayer), whereas multilayer Tb<sub>2</sub>O<sub>3</sub> islands develop as the coverage increases thereafter.
The Tb<sub>2</sub>O<sub>3</sub>(111) wetting layer yields a sharp
(3 Ă 3) LEED pattern relative to the primary Tb spots that we
attribute to diffraction from a 3/4 coincidence lattice formed at
the Tb<sub>2</sub>O<sub>3</sub>(111)âPtÂ(111) interface. STM
further shows that oxygen vacancies are randomly distributed within
the lattice of the Tb<sub>2</sub>O<sub>3</sub>(111) wetting layer.
The (3 Ă 3) LEED pattern diminishes during the transition to
island growth but re-emerges as the islands ripen at Tb<sub>2</sub>O<sub>3</sub> coverages beyond about 5 ML. We attribute the re-emergent
LEED pattern to a (3 Ă 3) superstructure of oxygen vacancies
within the Tb<sub>2</sub>O<sub>3</sub>(111) islands, the formation
of which is likely mediated by the (3 Ă 3) Tb<sub>2</sub>O<sub>3</sub>âPtÂ(111) coincidence lattice. The (3 Ă 3) structure
persists to Tb<sub>2</sub>O<sub>3</sub> coverages of at least 10 ML
and remains stable after annealing to temperatures up to 1100 K. An
implication of this study is that Tb<sub>2</sub>O<sub>3</sub>(111)
surfaces with well-defined, ordered oxygen vacancies can be stabilized
to better study the role of structure and oxygen vacancies on the
chemical reactivity of TbO<sub><i>x</i></sub> surfaces
Screening of a panel of normal tissues and tumor-derived cell lines using RTâPCR
<p><b>Copyright information:</b></p><p>Taken from "Evidence that public database records for many cancer-associated genes reflect a splice form found in tumors and lack normal splice forms"</p><p>Nucleic Acids Research 2005;33(16):5026-5033.</p><p>Published online 7 Sep 2005</p><p>PMCID:PMC1201329.</p><p>© The Author 2005. Published by Oxford University Press. All rights reserved</p> RTâPCR was performed on cDNAs from normal, non-cancerous tissues (lettered in black) and from tumor-derived cell lines (lettered in red). 2% agarose gels were run, and bands visualized by ethidium bromide staining. denotes the band corresponding to the novel splice form, and denotes the band corresponding to the known splice form. The genes shown are (upper gel) and (lower gel)
Positive Selection evidence for Top 10 gene groups.
<p>Positive Selection evidence for Top 10 gene groups.</p
Safety and Tolerability of Combinations of Empagliflozin and Linagliptin in Patients with Type 2 Diabetes: Pooled Data from Two Randomized Controlled Trials
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Estimated Causal Mutations in the Top 10 gene groups.
<p>Estimated Causal Mutations in the Top 10 gene groups.</p
Top 10 gene groups ranked by hypergeometric p-value (Bonferroni corrected for 28 tests).
<p>Top 10 gene groups ranked by hypergeometric p-value (Bonferroni corrected for 28 tests).</p
1000 Simulations of the Wright-Fisher Selective Dynamics [58] of a Randomly Mutagenized Population.
<p>A. (Top) a simulation of 26 strains of various fitnesses that grow exponentially from a founder population of individual mutants to a carrying capacity under Wright-Fisher selection dynamics. The results of a single simulation show that one mutant dominates the population after a small number of generations. Note diversity is lost due not only to selection, but also genetic drift. B. (Middle) As reproduction and selection proceeds, the mean number of distinct strains decreases very quickly. On average half of the strains are lost after just 6â7 generations. C. (Bottom) Similarly, the mean Shannon entropy <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0088072#pone.0088072-Cover1" target="_blank">[59]</a> of the population distribution also decreases quickly. This differs from (B) in that the population proportions are also taken into account.</p
Top 10 gene groups ranked by pathway-phenoseq p-value (Bonferroni corrected for 536 tests).
<p>Top 10 gene groups ranked by pathway-phenoseq p-value (Bonferroni corrected for 536 tests).</p