Review of Privileged Documents in Trial and Deposition Preparation of Witnesses in New York: When, if Ever, Will the Privilege be Lost?

This article will examine New York’s refreshing recollection doctrine in the context of trial and deposition preparation of witnesses as to the consequences of the witness’s review of privileged writings. Initially, Part II will discuss Rule 612 of the Federal Rules of Evidence. The discussion will serve as the backdrop for the analysis of the above-mentioned issues under New York law. Part III will then examine the refreshing recollection doctrine as developed and applied to testifying witnesses at a trial or deposition by the New York courts. The examination will point out the doctrine’s key rules. Part IV discusses the treatment of these key rules by the New York courts in the witness preparation situation, both pre-trial and pre-deposition, showing the shortcomings of this judicial treatment and advocating for change. Lastly, Part V makes some suggestions to the attorney in light of current New York law as to avoidance in the preparation of witnesses before they testify at a trial or a deposition of the disclosure of otherwise privileged writings

Cellular automaton decoders of topological quantum memories in the fault tolerant setting

Active error decoding and correction of topological quantum codes—in particular the toric code—remains one of the most viable routes to large scale quantum information processing. In contrast, passive error correction relies on the natural physical dynamics of a system to protect encoded quantum information. However, the search is ongoing for a completely satisfactory passive scheme applicable to locally interacting two-dimensional systems. Here, we investigate dynamical decoders that provide passive error correction by embedding the decoding process into local dynamics. We propose a specific discrete time cellular-automaton decoder in the fault tolerant setting and provide numerical evidence showing that the logical qubit has a survival time extended by several orders of magnitude over that of a bare unencoded qubit. We stress that (asynchronous) dynamical decoding gives rise to a Markovian dissipative process. We hence equate cellular-automaton decoding to a fully dissipative topological quantum memory, which removes errors continuously. In this sense, uncontrolled and unwanted local noise can be corrected for by a controlled local dissipative process. We analyze the required resources, commenting on additional polylogarithmic factors beyond those incurred by an ideal constant resource dynamical decoder

The strong coupling constant at small momentum as an instanton detector

We present a study of $\alpha_{MOM}(p)$ at small p computed from the lattice. It shows a dramatic $\propto p^4$ law which can be understood within an instanton liquid model. In this framework the prefactor gives a direct measure of the instanton density in thermalised configurations. A preliminary result for this density is 5.27(4) fm^{-4}.Comment: 12 pages, 4 figure

Factor VIII gene inversions causing severe hemophilia A originate almost exclusively in male germ cells

The factor VIII gene, which is defective In hemophilia A, is located in the last megabase of the long arm of the X chromosome. Inversions due to intrachromosomal homologous recombination between mispaired copies of gene A located within intron 22 of the gene and about 500 kb telomeric to it account for nearly half of all cases of severe hemophilia A. We hypothesized that pairing of Xq with its homolog inhibits the Inversion process, and that, therefore, the event originates predominantly in male germ cells. In all 20 informative cases In which the inversion originated in a maternal grandparent, DNA polymorphism analysis determined that it occurred in the male germline. In addition, all but one of 50 mothers of sporadic cases due to an Inversion were carriers. Thus, these data support the hypothesis and Indicate that factor VIII gene inversions leading to severe hemophilia A occur almost exclusively In male germ cell

Validation of Kepler's Multiple Planet Candidates. III: Light Curve Analysis & Announcement of Hundreds of New Multi-planet Systems

The Kepler mission has discovered over 2500 exoplanet candidates in the first two years of spacecraft data, with approximately 40% of them in candidate multi-planet systems. The high rate of multiplicity combined with the low rate of identified false-positives indicates that the multiplanet systems contain very few false-positive signals due to other systems not gravitationally bound to the target star (Lissauer, J. J., et al., 2012, ApJ 750, 131). False positives in the multi- planet systems are identified and removed, leaving behind a residual population of candidate multi-planet transiting systems expected to have a false-positive rate less than 1%. We present a sample of 340 planetary systems that contain 851 planets that are validated to substantially better than the 99% confidence level; the vast majority of these have not been previously verified as planets. We expect ~2 unidentified false-positives making our sample of planet very reliable. We present fundamental planetary properties of our sample based on a comprehensive analysis of Kepler light curves and ground-based spectroscopy and high-resolution imaging. Since we do not require spectroscopy or high-resolution imaging for validation, some of our derived parameters for a planetary system may be systematically incorrect due to dilution from light due to additional stars in the photometric aperture. None the less, our result nearly doubles the number of verified exoplanets.Comment: 138 pages, 8 Figures, 5 Tables. Accepted for publications in the Astrophysical Journa

Probing host pathogen cross-talk by transcriptional profiling of both Mycobacterium tuberculosis and infected human dendritic cells and macrophages

This study provides the proof of principle that probing the host and the microbe transcriptomes simultaneously is a valuable means to accessing unique information on host pathogen interactions. Our results also underline the extraordinary plasticity of host cell and pathogen responses to infection, and provide a solid framework to further understand the complex mechanisms involved in immunity to M. tuberculosis and in mycobacterial adaptation to different intracellular environments

Discovery of a Third Transiting Planet in the Kepler-47 Circumbinary System

Of the nine confirmed transiting circumbinary planet systems, only Kepler-47 is known to contain more than one planet. Kepler-47 b (the "inner planet") has an orbital period of 49.5 days and a radius of about 3 R⊕. Kepler-47 c (the "outer planet") has an orbital period of 303.2 days and a radius of about 4.7 R⊕. Here we report the discovery of a third planet, Kepler-47 d (the "middle planet"), which has an orbital period of 187.4 days and a radius of about 7 R⊕. The presence of the middle planet allows us to place much better constraints on the masses of all three planets, where the 1σranges are less than 26 M⊕, between 7–43 M⊕, and between 2–5 M⊕ for the inner, middle, and outer planets, respectively. The middle and outer planets have low bulk densities, with ρ_(middle) < 0.68 g cm^(−3) and ρ_(outer) < 0.26 g cm^(−3) at the 1σ level. The two outer planets are "tightly packed," assuming the nominal masses, meaning no other planet could stably orbit between them. All of the orbits have low eccentricities and are nearly coplanar, disfavoring violent scattering scenarios and suggesting gentle migration in the protoplanetary disk

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts