Deterministic Polynomial-Time Algorithms for Designing Short DNA Words

Designing short DNA words is a problem of constructing a set (i.e., code) of n DNA strings (i.e., words) with the minimum length such that the Hamming distance between each pair of words is at least k and the n words satisfy a set of additional constraints. This problem has applications in, e.g., DNA self-assembly and DNA arrays. Previous works include those that extended results from coding theory to obtain bounds on code and word sizes for biologically motivated constraints and those that applied heuristic local searches, genetic algorithms, and randomized algorithms. In particular, Kao, Sanghi, and Schweller (2009) developed polynomial-time randomized algorithms to construct n DNA words of length within a multiplicative constant of the smallest possible word length (e.g., 9 max{log n, k}) that satisfy various sets of constraints with high probability. In this paper, we give deterministic polynomial-time algorithms to construct DNA words based on derandomization techniques. Our algorithms can construct n DNA words of shorter length (e.g., 2.1 log n + 6.28 k) and satisfy the same sets of constraints as the words constructed by the algorithms of Kao et al. Furthermore, we extend these new algorithms to construct words that satisfy a larger set of constraints for which the algorithms of Kao et al. do not work.Comment: 27 page

Networks and Our Limited Information Horizon

In this paper we quantify our limited information horizon, by measuring the information necessary to locate specific nodes in a network. To investigate different ways to overcome this horizon, and the interplay between communication and topology in social networks, we let agents communicate in a model society. Thereby they build a perception of the network that they can use to create strategic links to improve their standing in the network. We observe a narrow distribution of links when the communication is low and a network with a broad distribution of links when the communication is high.Comment: 5 pages and 5 figure

Self-Assembly of Infinite Structures

We review some recent results related to the self-assembly of infinite structures in the Tile Assembly Model. These results include impossibility results, as well as novel tile assembly systems in which shapes and patterns that represent various notions of computation self-assemble. Several open questions are also presented and motivated

Size-Dependent Tile Self-Assembly: Constant-Height Rectangles and Stability

We introduce a new model of algorithmic tile self-assembly called size-dependent assembly. In previous models, supertiles are stable when the total strength of the bonds between any two halves exceeds some constant temperature. In this model, this constant temperature requirement is replaced by an nondecreasing temperature function $\tau : \mathbb{N} \rightarrow \mathbb{N}$ that depends on the size of the smaller of the two halves. This generalization allows supertiles to become unstable and break apart, and captures the increased forces that large structures may place on the bonds holding them together. We demonstrate the power of this model in two ways. First, we give fixed tile sets that assemble constant-height rectangles and squares of arbitrary input size given an appropriate temperature function. Second, we prove that deciding whether a supertile is stable is coNP-complete. Both results contrast with known results for fixed temperature.Comment: In proceedings of ISAAC 201

The inflammatory process of gout and its treatment.

Gouty arthritis is a characteristically intense acute inflammatory reaction that erupts in response to articular deposits of monosodium urate (MSU) crystals. Important recent molecular biologic advances in this field have given us a clear picture of the mechanistic basis of gouty inflammation. The innate immune inflammatory response is critically involved in the pathology of gout. Specifically, MSU crystals promote inflammation directly by stimulating cells via Toll-like receptor signaling and by providing a surface for cleavage of C5 and formation of complement membrane attack complex (C5b-9), culminating in secretion of cytokines, chemokines, and other inflammatory mediators with a dramatic influx of neutrophils into the joint. Despite the detailed mechanistic picture for gouty inflammation, there are no placebo-controlled, randomized clinical studies for any of the therapies commonly used, although comparative studies have demonstrated that many nonsteroidal anti-inflammatory drugs are equivalent to indomethacin with respect to controlling acute gouty attacks. In general, the first line of anti-inflammatory therapy for acute gout is nonsteroidal anti-inflammatory drugs, and the selective cyclo-oxygenase-2 inhibitor celecoxib can be used where appropriate. The second line of treatment is glucocorticosteroids, given systemically (oral, intravenous, or intramuscular) or intra-articularly. Alternatively, synthetic adrenocorticotropic hormone is effective, partly via induction of adrenal glucocorticosteroids and partly via rapid peripheral suppression of leukocyte activation by melatonin receptor 3 signaling. The third line of treatment is oral colchicine, which is highly effective when given early in an acute gouty attack, but it is poorly tolerated because of predictable gastrointestinal side effects