In this paper, we examine the use of Monte Carlo Tree Search (MCTS) for a variant of one of the most popular and profitable games in the world: the card game Magic: The Gathering (M:TG). The game tree for M:TG has a range of distinctive features, which we discuss here, and has incomplete information through the opponent's hidden cards, and randomness through card drawing from a shuffled deck. We investigate a wide range of approaches that use determinization, where all hidden and random information is assumed known to all players, alongside Monte Carlo Tree Search. We consider a number of variations to the rollout strategy using a range of levels of sophistication and expert knowledge, and decaying reward to encourage play urgency. We examine the effect of utilising various pruning strategies in order to increase the information gained from each determinization, alongside methods that increase the relevance of random choices. Additionally we deconstruct the move generation procedure into a binary yes/no decision tree and apply MCTS to this finer grained decision process. We compare our modifications to a basic MCTS approach for Magic: The Gathering using fixed decks, and show that significant improvements in playing strength can be obtained.

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The protein release factor 2 (RF2) participates in Escherichia coli polypeptide chain termination with codon specificity (UAA or UGA). A colicin E1 recombinant identified in the Carbon and Clarke E. coli bank contains the protein release factor 2 gene. A 1.7-kilobase E. coli fragment has been subcloned into the plasmid pUC9 vector. Bacterial cells, containing the plasmid recombinant, produce elevated levels of protein release factor 2 as detected by an immune precipitation assay and in vitro measurement of UGA-directed peptide chain termination and [3H]UGA codon recognition.

The Escherichia coli ribosomal proteins, L7/L12, are dominant over L11 in modulating the binding of RF‐1 and RF‐2 to ribosomes. The elevated activity of RF‐2 on L11‐lacking ribosomes over those containing L11 is abolished by IgG against L7/L12 or by removing the L7/L12 proteins. Adding back L7/L12 restores the original phenotype. The stimulatory factor, RF‐3, is active on ribosomes depleted of L7/L12 but on those which lack L11 the stimulatory effects are less pronounced or often not seen. RF‐3 cannot restore activity with RF‐1 or RF‐2 to ribosomes lacking both these sets of proteins. The stimulatory effects of an absence of either L11 or RF‐3 on the activity of RF‐2 are not additive or synergistic.

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