44 research outputs found

    EVIDENCE-FEDERAL CRIMINAL PROCEDURE-ADMISSIBILITY OF CONFESSION OBTAINED DURING ILLEGAL DETENTION

    Get PDF
    Petitioner was arrested without a warrant on suspicion of larceny. He was held without commitment for a period of thirty hours during which he was intermittently questioned but was not subjected to any form of physical coercion. At the end of this period, he signed a confession which was the basis for his conviction in the district court. On certiorari to the United States Supreme Court, following affirmation in the court of appeals, held, reversed. The detention was unlawful as a violation of rule 5 (a) of the Federal Rules of Criminal Procedure, and the confession thus obtained was inadmissible in evidence. Upshaw v. United States, (U.S. 1948) 69 S.Ct. 170

    FEDERAL COURTS-GRANTING OF NEW TRIAL ON INITIATIVE OF THE COURT

    Get PDF
    Following conviction for violation of a federal statute, petitioner was granted his release on a writ of habeas corpus by a federal district court, on the basis of uncontroverted testimony that his counsel had not been present when the jury returned its verdict. Within ten days of this release, a motion for rehearing was filed, supported by affidavits that his counsel actually had been present. On subsequent hearing, the court set aside its former order and remanded petitioner to custody, on the theory that his release was obtained by means of a fraud on the Court. The present action was a habeas corpus proceeding challenging the remanding order. Held, the remanding order amounted to the granting of a new trial on the court\u27s initiative and, being made after the statutory period had expired, was void. Thomas v. Hunter, (D.C. Kan. 1948) 78 F. Supp. 925

    An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers

    Get PDF
    Introduction: Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods: We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results: We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions: This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects.Peer reviewe

    The ATLAS inner detector trigger performance in pp collisions at 13 TeV during LHC Run 2

    Get PDF
    The design and performance of the inner detector trigger for the high level trigger of the ATLAS experiment at the Large Hadron Collider during the 2016-18 data taking period is discussed. In 2016, 2017, and 2018 the ATLAS detector recorded 35.6 fb1^{-1}, 46.9 fb1^{-1}, and 60.6 fb1^{-1} respectively of proton-proton collision data at a centre-of-mass energy of 13 TeV. In order to deal with the very high interaction multiplicities per bunch crossing expected with the 13 TeV collisions the inner detector trigger was redesigned during the long shutdown of the Large Hadron Collider from 2013 until 2015. An overview of these developments is provided and the performance of the tracking in the trigger for the muon, electron, tau and bb-jet signatures is discussed. The high performance of the inner detector trigger with these extreme interaction multiplicities demonstrates how the inner detector tracking continues to lie at the heart of the trigger performance and is essential in enabling the ATLAS physics programme

    Measurement of jet fragmentation in Pb+Pb and pppp collisions at sNN=2.76\sqrt{{s_\mathrm{NN}}} = 2.76 TeV with the ATLAS detector at the LHC

    Get PDF

    Measurement of the charge asymmetry in top-quark pair production in the lepton-plus-jets final state in pp collision data at s=8TeV\sqrt{s}=8\,\mathrm TeV{} with the ATLAS detector

    Get PDF

    Measurements of top-quark pair differential cross-sections in the eμe\mu channel in pppp collisions at s=13\sqrt{s} = 13 TeV using the ATLAS detector

    Get PDF
    corecore