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  SIRI-OUSLY? FREE SPEECH RIGHTS AND ARTIFICIAL INTELLIGENCE

  Massaro, Toni M.; Norton, Helen; Univ Arizona, James E Rogers Coll Law; Univ Arizona, James E Rogers Coll Law, Constitut Law (NORTHWESTERN UNIV, 2016)

  Computers with communicative artificial intelligence (AI) are pushing First Amendment theory and doctrine in profound and novel ways. They are becoming increasingly self-directed and corporal in ways that may one day make it difficult to call the communication ours versus theirs. This, in turn, invites questions about whether the First Amendment ever will (or ever should) cover AI speech or speakers even absent a locatable and accountable human creator. In this Article, we explain why current free speech theory and doctrine pose surprisingly few barriers to this counterintuitive result; their elasticity suggests that speaker humanness no longer may be a logically essential part of the First Amendment calculus. We further observe, however, that free speech theory and doctrine provide a basis for regulating, as well as protecting, the speech of nonhuman speakers to serve the interests of their human listeners should strong AI ever evolve to this point. Finally, we note that the futurist implications we describe are possible, but not inevitable. Moreover, contemplating these outcomes for AI speech may inspire rethinking of the free speech theory and doctrine that make them plausible.
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  A Theorem at the Core of Colliding Bias

  Shahar, Doron J.; Shahar, Eyal; Univ Arizona, Dept Math; Univ Arizona, Dept Epidemiol & Biostat, Mel & Enid Zuckerman Coll Publ Hlth (WALTER DE GRUYTER GMBH, 2017-05)

  Conditioning on a shared outcome of two variables can alter the association between these variables, possibly adding a bias component when estimating effects. In particular, if two causes are marginally independent, they might be dependent in strata of their common effect. Explanations of the phenomenon, however, do not explicitly state when dependence will be created and have been largely informal. We prove that two, marginally independent, causes will be dependent in a particular stratum of their shared outcome if and only if they modify each other's effects, on a probability ratio scale, on that value of the outcome variable. Using our result, we also qualify the claim that such causes will "almost certainly" be dependent in at least one stratum of the outcome: dependence must be created in one stratum of a binary outcome, and independence can be maintained in every stratum of a trinary outcome.
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  Gle1 Regulates RNA Binding of the DEAD-Box Helicase Ded1 in Its Complex Role in Translation Initiation

  Aryanpur, Peyman P.; Regan, Chelsea A.; Collins, John M.; Mittelmeier, Telsa M.; Renner, David M.; Vergara, Ashley M.; Brown, Nicolette P.; Bolger, Timothy A.; Univ Arizona, Dept Mol & Cellular Biol (AMER SOC MICROBIOLOGY, 2017-11)

  DEAD-box proteins (DBPs) are required in gene expression to facilitate changes to ribonucleoprotein complexes, but the cellular mechanisms and regulation of DBPs are not fully defined. Gle1 is a multifunctional regulator of DBPs with roles in mRNA export and translation. In translation, Gle1 modulates Ded1, a DBP required for initiation. However, DED1 overexpression causes defects, suggesting that Ded1 can promote or repress translation in different contexts. Here we show that GLE1 expression suppresses the repressive effects of DED1 in vivo and Gle1 counteracts Ded1 in translation assays in vitro. Furthermore, both Ded1 and Gle1 affect the assembly of preinitiation complexes. Through mutation analysis and binding assays, we show that Gle1 inhibits Ded1 by reducing its affinity for RNA. Our results are consistent with a model wherein active Ded1 promotes translation but inactive or excess Ded1 leads to translation repression. Gle1 can inhibit either role of Ded1, positioning it as a gatekeeper to optimize Ded1 activity to the appropriate level for translation. This study suggests a paradigm for finely controlling the activity of DEAD-box proteins to optimize their function in RNA-based processes. It also positions the versatile regulator Gle1 as a potential node for the coordination of different steps of gene expression.
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  Search for diboson resonances in hadronic final states in 139 fb(-1) of pp collisions at root s=13 TeV with the ATLAS detector

  Berlendis, S.; Cheu, E.; Johns, K.A.; Jones, S.; Lampl, W.; LeBlanc, M.; Leone, R.; Loch, P.; Nayyar, R.; Varnes, E.W.; et al. (SPRINGER, 2019-09-12)

  Narrow resonances decaying into WW, WZ or ZZ boson pairs are searched for in 139 fb(-1) of proton-proton collision data at a centre-of-mass energy of root s = 13TeV recorded with the ATLAS detector at the Large Hadron Collider from 2015 to 2018. The diboson system is reconstructed using pairs of high transverse momentum, large-radius jets. These jets are built from a combination of calorimeter- and tracker-inputs compatible with the hadronic decay of a boosted W or Z boson, using jet mass and substructure properties. The search is performed for diboson resonances with masses greater than 1.3TeV. No significant deviations from the background expectations are observed. Exclusion limits at the 95% confidence level are set on the production cross-section times branching ratio into dibosons for resonances in a range of theories beyond the Standard Model, with the highest excluded mass of a new gauge boson at 3.8TeV in the context of mass-degenerate resonances that couple predominantly to gauge bosons.
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  What's New in Musculoskeletal Infection: Update Across Orthopaedic Subspecialties

  Chen, Antonia F.; Nana, Arvind D.; Nelson, Sandra B.; McLaren, Alex; Univ Arizona, Coll Med Phoenix (LIPPINCOTT WILLIAMS & WILKINS, 2017-07-19)

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