141 research outputs found
Revolutionaries and Spies
Let be a graph and let be positive integers.
"Revolutionaries and Spies", denoted \cG(G,r,s,k), is the following
two-player game. The sets of positions for player 1 and player 2 are and
respectively. Each coordinate in gives the location of a
"revolutionary" in . Similarly player 2 controls "spies". We say are adjacent, , if for all , or . In round 0 player 1 picks and
then player 2 picks . In each round player 1 moves to
and then player 2 moves to . Player 1 wins
the game if he can place revolutionaries on a vertex in such a way that
player 1 cannot place a spy on in his following move. Player 2 wins the
game if he can prevent this outcome.
Let be the minimum such that player 2 can win \cG(G,r,s,k).
We show that for , .
Here with are connected by an edge if and only if
for all with .Comment: This is the version accepted to appear in Discrete Mathematic
Ontario Lifestyle, Alcohol, and Drug Questionnaire
The variable list from the Canadian database along with rewriting of the Canadian variables, a sample calculation for comparing the two countries, and sample calculation for extracting the Midwestern data from the Engs sample are found with the data bases for this study. Data Bases and CALCULATIONS using this instrument are found in the IU repository under databases at:
The American questionnaire is found at IUScholarWorks repository: http://hdl.handle.net/2022/17206.
Several data bases are associated with this questionnaire. These include data collected by the Ontario researchers (ALLCAN.DAT), data collected by the American researchers (MIDWEST88.DAT) and the two data based combined for comparison between the two countries (XUSACAN.DAT). Data for this study were collected in the United States and in Canada during 1977-1988.
ALL QUESTIONNAIRES developed by Engs are found in the repository at: https://scholarworks.iu.edu/dspace/handle/2022/17141/browse?type=dateissuedThe Ontario Lifestyle, Alcohol, and Drug Questionnaire adapts items from the SAQ including 9 demographic, 6 drinking behaviors and 20 problems related to alcohol. in addition it includes 13 lifestyle items and 17 drug related ietms developed by Glicksman and Smyth.
First-Order Definability of Trees and Sparse Random Graphs
This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively.Let D(G) be the smallest quantifier depth of a first-order formula which is true for a graph G but false for any other non-isomorphic graph. This can be viewed as a measure for the descriptive complexity of G in first-order logic.
We show that almost surely , where G is a random tree of order n or the giant component of a random graph with constant c<1. These results rely on computing the maximum of D(T) for a tree T of order n and maximum degree l, so we study this problem as well.Peer Reviewe
Src-family kinases mediate an outside-in signal necessary for β2 integrins to achieve full activation and sustain firm adhesion of polymorphonuclear leucocytes tethered on E-selectin
In cell suspensions subjected to high-shear rotatory motion, human PMN (polymorphonuclear cells) adhered to E-selectin-expressing CHO (Chinese-hamster ovary) cells (CHO-E), and formed homotypic aggregates when challenged by E-selectin–IgG fusion protein, by a mechanism that involved β2 integrins. Both heterotypic and homotypic PMN adhesion was accompanied by tyrosine phosphorylation of a 110 kDa protein (P110). This event was prevented by blocking anti-(β2 integrin) antibodies and by inhibitors of Src-family kinases, suggesting that it was part of an ‘outside-in’ signalling that was initiated by integrin engagement. Interestingly, Src-family kinase inhibitors prevented β2-integrin-mediated (i) homotypic PMN adhesion triggered by E-selectin–IgG, (ii) heterotypic CHO-E/PMN adhesion in mixed-cell suspensions, and (iii) firm adhesion of PMN to CHO-E monolayers under physiological flow. Similarly to PMN treated with Src-family kinase inhibitors, PMN from hck−/−fgr−/− and hck−/−fgr−/−lyn−/− mice showed significant impairment of β2-integrin-mediated adhesion to CHO-E. Moreover, the expression of β2 integrin activation epitopes at the sites of cell–cell contact in CHO-E/PMN conjugates was abolished by Src-family kinase inhibitors. One component of P110 was identified as the FAK (focal adhesion kinase) Pyk2 (proline-rich tyrosine kinase 2), which was phosphorylated in a β2 integrin- and Src-family-kinase-dependent manner. Thus, Src-family kinases, and perhaps Pyk2, mediate a signal necessary for β2 integrin function in PMN tethered by E-selectin
A putative lipase gene EXTRA GLUME1 regulates both empty-glume fate and spikelet development in rice
Recent studies have shown that molecular control of inner floral organ identity appears to be largely conserved between monocots and dicots, but little is known regarding the molecular mechanism underlying development of the monocot outer floral organ, a unique floral structure in grasses. In this study, we report the cloning of the rice EXTRA GLUME1 (EG1) gene, a putative lipase gene that specifies empty-glume fate and floral meristem determinacy. In addition to affecting the identity and number of empty glumes, mutations in EG1 caused ectopic floral organs to be formed at each organ whorl or in extra ectopic whorls. Iterative glume-like structures or new floral organ primordia were formed in the presumptive region of the carpel, resulting in an indeterminate floral meristem. EG1 is expressed strongly in inflorescence primordia and weakly in developing floral primordia. We also found that the floral meristem and organ identity gene OsLHS1 showed altered expression with respect to both pattern and levels in the eg1 mutant, and is probably responsible for the pleiotropic floral defects in eg1. As a putative class III lipase that functionally differs from any known plant lipase, EG1 reveals a novel pathway that regulates rice empty-glume fate and spikelet development
Network-based functional enrichment
<p>Abstract</p> <p>Background</p> <p>Many methods have been developed to infer and reason about molecular interaction networks. These approaches often yield networks with hundreds or thousands of nodes and up to an order of magnitude more edges. It is often desirable to summarize the biological information in such networks. A very common approach is to use gene function enrichment analysis for this task. A major drawback of this method is that it ignores information about the edges in the network being analyzed, i.e., it treats the network simply as a set of genes. In this paper, we introduce a novel method for functional enrichment that explicitly takes network interactions into account.</p> <p>Results</p> <p>Our approach naturally generalizes Fisher’s exact test, a gene set-based technique. Given a function of interest, we compute the subgraph of the network induced by genes annotated to this function. We use the sequence of sizes of the connected components of this sub-network to estimate its connectivity. We estimate the statistical significance of the connectivity empirically by a permutation test. We present three applications of our method: i) determine which functions are enriched in a given network, ii) given a network and an interesting sub-network of genes within that network, determine which functions are enriched in the sub-network, and iii) given two networks, determine the functions for which the connectivity improves when we merge the second network into the first. Through these applications, we show that our approach is a natural alternative to network clustering algorithms.</p> <p>Conclusions</p> <p>We presented a novel approach to functional enrichment that takes into account the pairwise relationships among genes annotated by a particular function. Each of the three applications discovers highly relevant functions. We used our methods to study biological data from three different organisms. Our results demonstrate the wide applicability of our methods. Our algorithms are implemented in C++ and are freely available under the GNU General Public License at our supplementary website. Additionally, all our input data and results are available at <url>http://bioinformatics.cs.vt.edu/~murali/supplements/2011-incob-nbe/</url>.</p
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