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Butelman ER, Maremmani AGI, Bacciardi S, Chen CY, da Rosa JC, Kreek MJ
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Non-medical Cannabis Self-Exposure as a Dimensional Predictor of Opioid Dependence Diagnosis: A Propensity Score Matched Analysis
FRONTIERS IN PSYCHIATRY 2018 JUN 27; 9(?):? Article 283
Background: The impact of increasing non-medical cannabis use on vulnerability to develop opioid use disorders has received considerable attention, with contrasting findings. A dimensional analysis of self-exposure to cannabis and other drugs, in individuals with and without opioid dependence (OD) diagnoses, may clarify this issue. Objective: To examine the age of onset of maximal self-exposure to cannabis, alcohol, cocaine, and heroin, in volunteers diagnosed with OD, using a rapidly administered instrument (the KMSK scales). To then determine whether maximal self-exposure to cannabis, alcohol, and cocaine is a dimensional predictor of odds of OD diagnoses. Methods: This outpatient observational study examined maximal self-exposure to these drugs, in volunteers diagnosed with DSM-IV OD or other drug diagnoses, and normal volunteers. In order to focus more directly on opioid dependence diagnosis as the outcome, volunteers who had cocaine dependence diagnoses were excluded. Male and female adults of diverse ethnicity were consecutively ascertained from the community, and from local drug treatment programs, in 2002-2013 (n = 574, of whom n = 94 had OD diagnoses). The age of onset ofmaximal self-exposure of these drugs was examined. After propensity scorematching for age at ascertainment, gender, and ethnicity, amultiple logistic regression examined how increasing self-exposure to non-medical cannabis, alcohol and cocaine affected odds of OD diagnoses. Results: Volunteers with OD diagnoses had the onset of heaviest use of cannabis in the approximate transition between adolescence and adulthood (mean age = 18.9 years), and onset of heaviest use of alcohol soon thereafter (mean age = 20.1 years). Onset of heaviest use of heroin and cocaine was detected later in the lifespan (mean ages = 24.7 and 25.3 years, respectively). After propensity score matching for demographic variables, we found that the maximal self-exposure to cannabis and cocaine, but not to alcohol, was greater in volunteers with OD diagnoses, than in those without this diagnosis. Also, a multiple logistic regression detected that increasing self-exposure to cannabis and cocaine, but not alcohol, was a positive predictor of OD diagnosis. Conclusions/Importance: Increasing self-exposure to non-medical cannabis, as measured with a rapid dimensional instrument, was a predictor of greater odds of opioid dependence diagnosis, in propensity score-matched samples.
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Alexander J, Chaves J, Chu J, Dittmer S, Mcdermott K, Mirman N, Patterson JR, Quach D, Rinkevicius A, Ryd A, Skinnari L, Soffi L, Tan SM, Tao Z, Thom J, Tucker J, Wittich P, Zientek M, Abdullin S, Albrow M, Alyari M, Apollinari G, Apresyan A, Apyan A, Banerjee S, Bauerdick LAT, Beretvas A, Berryhill J, Bhat PC, Bolla G, Burkett K, Butler JN, Canepa A, Cerati GB, Cheung HWK, Chlebana F, Cremonesi M, Duarte J, Elvira VD, Freeman J, Geese Z, Gottschalk E, Gray L, Green D, Grunendahl S, Gutsche O, Harris RM, Hasegawa S, Hirschauer J, Hu Z, Jayatilaka B, Jindariani S, Johnson M, Joshi U, Klima B, Kreis B, Lammel S, Lincoln D, Lipton R, Liu M, Liu T, De Sa RL, Lykken J, Maeshima K, Magini N, Marraffino JM, Mason D, McBride P, Merkel P, Mrenna S, Nahn S, O'Dell V, Pedro K, Prokofyev O, Rakness G, Ristori L, Schneider B, Sexton-Kennedy E, Soha A, Spalding WJ, Spiegel L, Stoynev S, Strait J, Strobbe N, Taylor L, Tkaczyk S, Tran NV, Uplegger L, Vaandering EW, Vernieri C, Verzocchi M, Vidal R, 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Blumenfeld B, Cocoros A, Eminizer N, Fehling D, Feng L, Gritsan AV, Maksimovic P, Roskes J, Sarica U, Swartz M, Xiao M, You C, Al-Bataineh A, Baringer P, Bean A, Boren S, Bowen J, Castle J, Khalil S, Kropivnitskaya A, Majumder D, Mcbrayer W, Murray M, Royon C, Sanders S, Schmitz E, Takaki JDT, Wang Q, Ivanov A, Kaadze K, Maravin Y, Mohammadi A, Saini LK, Skhirtladze N, Toda S, Rebassoo F, Wright D, Anelli C, Baden A, Baron O, Belloni A, Calvert B, Eno SC, Feng Y, Ferraioli C, Hadley NJ, Jabeen S, Jeng GY, Kellogg RG, Kunkle J, Mignerey AC, -Tam FR, Shin YH, Skuja A, Tonwar SC, Abercrombie D, Allen B, Azzolini V, Barbieri R, Baty A, Bi R, Brandt S, Busza W, Cali IA, D'Alfonso M, Demiragli Z, Ceballos GG, Goncharov M, Hsu D, Hu M, Iiyama Y, Innocenti GM, Klute M, Kovalskyi D, Lai YS, Lee YJ, Levin A, Luckey PD, Maier B, Marini AC, Mcginn C, Mironov C, Narayanan S, Niu X, Paus C, Roland C, Roland G, Salfeld-Nebgen J, Stephans GSF, Tatar K, Velicanu D, Wang J, Wang TW, Wyslouch B, 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Hebda P, Higginbotham S, Lange D, Luo J, Marlow D, Mei K, Ojalvo I, Olsen J, Palmer C, Piroue P, Stickland D, Tully C, Malik S, Norberg S, Barker A, Barnes VE, Das S, Folgueras S, Gutay L, Jha MK, Jones M, Jung AW, Khatiwada A, Miller DH, Neumeister N, Peng CC, Qiu H, Schulte JF, Sun J, Wang F, Xie W, Cheng T, Parashar N, Stupak J, Adair A, Chen Z, Ecklund KM, Freed S, Geurts FJM, Guilbaud M, Kilpatrick M, Li W, Michlin B, Northup M, Padley BP, Roberts J, Rorie J, Shi W, Tu Z, Zabel J, Zhang A, Bodek A, de Barbaro P, Demina R, Duh YT, Ferbel T, Galanti M, Garcia-Bellido A, Han J, Hindrichs O, Khukhunaishvili A, Lo KH, Tan P, Verzetti M, Ciesielski R, Goulianos K, Mesropian C, Agapitos A, Chou JP, Gershtein Y, Espinosa TAG, Halkiadakis E, Heindl M, Hughes E, Kaplan S, Elayavalli RK, Kyriacou S, Lath A, Montalvo R, Nash K, Osherson M, Saka H, Salur S, Schnetzer S, Sheffield D, Somalwar S, Stone R, Thomas S, Thomassen P, Walker M, Delannoy AG, Foerster M, Heideman J, Riley G, Rose K, Spanier S, Thapa K, Bouhali O, Hernandez AC, Celik A, Dalchenko M, De Mattia M, Delgado A, Dildick S, Eusebi R, Gilmore J, Huang T, Kamon T, Mueller R, Pakhotin Y, Patel R, Perloff A, Pernie L, Rathjens D, Safonov A, Tatarinov A, Ulmer KA, Akchurin N, Damgov J, De Guio F, Dudero PR, Faulkner J, Gurpinar E, Kunori S, Lamichhane K, Lee SW, Libeiro T, Mengke T, Muthumuni S, Peltola T, Undleeb S, Volobouev I, Wang Z, Greene S, Gurrola A, Janjam R, Johns W, Maguire C, Melo A, Ni H, Padeken K, Sheldon P, Tuo S, Velkovska J, Xu Q, Arenton MW, Barria P, Cox B, Hirosky R, Joyce M, Ledovskoy A, Li H, Neu C, Sinthuprasith T, Wang Y, Wolfe E, Xia F, Harr R, Karchin PE, Poudyal N, Sturdy J, Thapa P, Zaleski S, Brodski M, Buchanan J, Caillol C, Dasu S, Dodd L, Duric S, Gomber B, Grothe M, Herndon M, Herve A, Hussain U, Klabbers P, Lanaro A, Levine A, Long K, Loveless R, Polese G, Ruggles T, Savin A, Smith N, Smith WH, Taylor D, Woods N
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Search for lepton flavour violating decays of the Higgs boson to mu tau and e tau in proton-proton collisions at root s=13 TeV
JOURNAL OF HIGH ENERGY PHYSICS 2018 JUN 1; ?(6):? Article 001
A search for lepton flavour violating decays of the Higgs boson in the mu tau and e tau decay modes is presented. The search is based on a data set corresponding to an integrated luminosity of 35.9 fb(-1) of proton-proton collisions collected with the CMS detector in 2016, at a centre-of-mass energy of 13 TeV. No significant excess over the standard model expectation is observed. The observed (expected) upper limits on the lepton flavour violating branching fractions of the Higgs boson are B(H -> mu tau) < 0.25% (0.25%) and B(H -> e tau) < 0.61% (0.37%), at 95% confidence level. These results are used to derive upper limits on the off-diagonal mu tau and e tau Yukawa couplings root vertical bar Y-mu tau vertical bar(2) + vertical bar Y-mu tau vertical bar(2) < 1.43 x 10(-3) and root vertical bar Y-e tau vertical bar(2) + vertical bar Y-tau e vertical bar(2) < 2.26 x 10(-3) at 95% confidence level. The limits on the lepton flavour violating branching fractions of the Higgs boson and on the associated Yukawa couplings are the most stringent to date.
Breker M, Lieberman K, Cross FR
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Comprehensive Discovery of Cell-Cycle-Essential Pathways in Chlamydomonas reinhardtii
PLANT CELL 2018 JUN; 30(6):1178-1198
We generated a large collection of temperature-sensitive lethal mutants in the unicellular green alga Chlamydomonas reinhardtii, focusing on mutations specifically affecting cell cycle regulation. We used UV mutagenesis and robotically assisted phenotypic screening to isolate candidates. To overcome the bottleneck at the critical step of molecular identification of the causative mutation ("driver"), we developed MAPS-SEQ (meiosis-assisted purifying selection sequencing), a multiplexed genetic/bioinformatics strategy. MAPS-SEQ allowed us to perform multiplexed simultaneous determination of the driver mutations from hundreds of neutral "passenger" mutations in each member of a large pool of mutants. This method should work broadly, including in multicellular diploid genetic systems, for any scorable trait. Using MAPS-SEQ, we identified essential genes spanning a wide range of molecular functions. Phenotypic clustering based on DNA content analysis and cell morphology indicated that the mutated genes function in the cell cycle at multiple points and by diverse mechanisms. The collection is sufficiently complete to allow specific conditional inactivation of almost all cell-cycle-regulatory pathways. Approximately seventy-five percent of the essential genes identified in this project had clear orthologs in land plant genomes, a huge enrichment compared with the value of similar to 20% for the Chlamydomonas genome overall. Findings about these mutants will likely have direct relevance to essential cell biology in land plants.
Tromp AT, Van Gent M, Abrial P, Martin A, Jansen JP, De Haas CJC, Van Kessel KPM, Bardoel BW, Kruse E, Bourdonnay E, Boettcher M, McManus MT, Day CJ, Jennings MP, Lina G, Vandenesch F, Van Strijp JAG, Lebbink RJ, Haas PJA, Henry T, Spaan AN
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Human CD45 is an F-component-specific receptor for the staphylococcal toxin Panton-Valentine leukocidin
NATURE MICROBIOLOGY 2018 JUN; 3(6):708-717
The staphylococcal bi-component leukocidins Panton-Valentine leukocidin (PVL) and gamma-haemolysin CB (HlgCB) target human phagocytes. Binding of the toxins' S-components to human complement C5a receptor 1 (C5aR1) contributes to cellular tropism and human specificity of PVL and HlgCB. To investigate the role of both leukocidins during infection, we developed a human C5aR1 knock-in (hC5aR1(KI)) mouse model. HlgCB, but unexpectedly not PVL, contributed to increased bacterial loads in tissues of hC5aR1(KI) mice. Compared to humans, murine hC5aR1(KI) neutrophils showed a reduced sensitivity to PVL, which was mediated by the toxin's F-component LukF-PV. By performing a genome-wide CRISPR-Cas9 screen, we identified CD45 as a receptor for LukF-PV. The human-specific interaction between LukF-PV and CD45 provides a molecular explanation for resistance of hC5aR1(KI) mouse neutrophils to PVL and probably contributes to the lack of a PVL-mediated phenotype during infection in these mice. This study demonstrates an unsuspected role of the F-component in driving the sensitivity of human phagocytes to PVL.
Mak ACY, White MJ, Eckalbar WL, Szpiech ZA, Oh SS, Pino-Yanes M, Hu DL, Goddard P, Huntsman S, Galanter J, Wu AC, Himes BE, Germer S, Vogel JM, Bunting KL, Eng C, Salazar S, Keys KL, Liberto J, Nuckton TJ, Nguyen TA, Torgerson DG, Kwok PY, Levin AM, Celedon JC, Forno E, Hakonarson H, Sleiman PM, Dahlin A, Tantisira KG, Weiss ST, Serebrisky D, Brigino-Buenaventura E, Farber HJ, Meade K, Lenoir MA, Avila PC, Sen S, Thyne SM, Rodriguez-Cintron W, Winkler CA, Moreno-Estrada A, Sandoval K, Rodriguez-Santana JR, Kumar R, Williams LK, Ahituv N, Ziv E, Seibold MA, Darnell RB, Zaitlen N, Hernandez RD, Burchard EG
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Whole-Genome Sequencing of Pharmacogenetic Drug Response in Racially Diverse Children with Asthma
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE 2018 JUN 15; 197(12):1552-1564
Rationale: Albuterol, a bronchodilator medication, is the first-line therapy for asthma worldwide. There are significant racial/ethnic differences in albuterol drug response. Objectives: To identify genetic variants important for bronchodilator drug response (BDR) in racially diverse children. Methods: We performed the first whole-genome sequencing pharmacogenetics study from 1,441 children with asthma from the tails of the BDR distribution to identify genetic association with BDR. Measurements and Main Results: We identified population-specific and shared genetic variants associated with BDR, including genome-wide significant (P < 3.53 X 10(-7)) and suggestive (P < 7.06 X 10(-6)) loci near genes previously associated with lung capacity (DNAH5), immunity (NFKB1 and PLCB1), and beta-adrenergic signaling (ADAMTS3 and COX18). Functional analyses of the BDR-associated SNP in NFKB1 revealed potential regulatory function in bronchial smooth muscle cells. The SNP is also an expression quantitative trait locus for a neighboring gene, SLC39A8. The lack of other asthma study populations with BDR and whole-genome sequencing data on minority children makes it impossible to perform replication of our rare variant associations. Minority underrepresentation also poses significant challenges to identify age-matched and population-matched cohorts of sufficient sample size for replication of our common variant findings. Conclusions: The lack of minority data, despite a collaboration of eight universities and 13 individual laboratories, highlights the urgent need for a dedicated national effort to prioritize diversity in research. Our study expands the understanding of pharmacogenetic analyses in racially/ethnically diverse populations and advances the foundation for precision medicine in at-risk and understudied minority populations.
Kang JY, Mooney RA, Nedialkov Y, Saba J, Mishanina TV, Artsimovitch I, Landick R, Darst SA
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Structural Basis for Transcript Elongation Control by NusG Family Universal Regulators
CELL 2018 JUN 14; 173(7):1650-1662.e14 Article 1662.e14
NusG/RfaH/Spt5 transcription elongation factors are the only transcription regulators conserved across all life. Bacterial NusG regulates RNA polymerase (RNAP) elongation complexes (ECs) across most genes, enhancing elongation by suppressing RNAP backtracking and coordinating r-dependent termination and translation. The NusG paralog RfaH engages the EC only at operon polarity suppressor (ops) sites and suppresses both backtrack and hairpin-stabilized pausing. We used single-particle cryoelectron microscopy (cryo-EM) to determine structures of ECs at ops with NusG or RfaH. Both factors chaperone base-pairing of the upstream duplex DNA to suppress backtracking, explaining stimulation of elongation genome-wide. The RfaHopsEC structure reveals how RfaH confers operon specificity through specific recognition of an ops hairpin in the single-stranded nontemplate DNA and tighter binding to the EC to exclude NusG. Tight EC binding by RfaH sterically blocks the swiveled RNAP conformation necessary for hairpin-stabilized pausing. The universal conservation of NusG/RfaH/Spt5 suggests that the molecular mechanisms uncovered here are widespread.
Galea S, Vaughan RD
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On Looking Ahead to Mitigate Threats to Population Health: A Public Health of Consequence, June 2018
AMERICAN JOURNAL OF PUBLIC HEALTH 2018 JUN; 108(6):722-723
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Litov L, Pavlov B, Petkov P, Fang W, Gao X, Yuan L, Ahmad M, Bian JG, Chen GM, Chen HS, Chen M, Chen Y, Jiang CH, Leggat D, Liao H, Liu Z, Romeo F, Shaheen SM, Spiezia A, Tao J, Wang C, Wang Z, Yazgan E, Zhang H, Zhang S, Zhao J, Ban Y, Chen G, Li Q, Liu S, Mao Y, Qian SJ, Wang D, Xu Z, Avila C, Cabrera A, Sierra LFC, Florez C, Hernandez CFG, Alvarez JDR, Courbon B, Godinovic N, Lelas D, Puljak I, Cipriano PMR, Sculac T, Antunovic Z, Kovac M, Brigljevic V, Ferencek D, Kadija K, Mesic B, Starodumov A, Susa T, Ather MW, Attikis A, Mavromanolakis G, Mousa J, Nicolaou C, Ptochos F, Razis PA, Rykaczewski H, Finger M, Finger M, Jarrin EC, Assran Y, Elgammal S, Mahrous A, Dewanjee RK, Kadastik M, Perrini L, Raidal M, Tiko A, Veelken C, Eerola P, Kirschenmann H, Pekkanen J, Voutilainen M, Jarvinen T, Karimaki V, Kinnunen R, Lampen T, Lassila-Perini K, Lehti S, Linden T, Luukka P, Tuominen E, Tuominiemi J, Talvitie J, Tuuva T, Besancon M, Couderc F, Dejardin M, Denegri D, Faure JL, Ferri F, 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Measurement of b hadron lifetimes in pp collisions at root s=8TeV
EUROPEAN PHYSICAL JOURNAL C 2018 JUN 7; 78(6):? Article 457
Measurements are presented of the lifetimes of the B-0, B-s(0), Lambda(0)(b), and B-c(+) hadrons using the decay channels B-0 -> J/psi K*(892)(0), B-0 -> J/psi K-S(0), B-s(0) -> J/psi pi(+)pi(-), B-s(0) -> J/psi phi(1020), Lambda(0)(b) -> J/psi Lambda(0), and B-c(+) -> J/psi pi(+). The data sample, corresponding to an integrated luminosity of 19.7 fb(-1), was collected by the CMS detector at the LHC in proton-proton collisions at root s = 8TeV. The B-0 life-time is measured to be 453.0 +/- 1.6 (stat) +/- 1.8 (syst) mu m in J/psi K*(892)(0) and 457.8 +/- 2.7 (stat) +/- 2.8 (syst) mu m in J/psi K-S(0), which results in a combined measurement of c tau(0) = 454.1 +/- 1.4 (stat) +/- 1.7 (syst) mu m. The effective lifetime of the B-s(0) meson is measured in two decay modes, with contributions from different amounts of the heavy and light eigenstates. This results in two different measured lifetimes: c tau(0)(Bs) -> J/psi pi(+)pi(-) = 502.7 +/- 10.2 (stat) +/- 3.4 (syst) mu m and c tau(0)(Bs) -> J/psi phi(1020) = 443.9 +/- 2.0 (stat) +/- 1.5 (syst) mu m. The Lambda(0)(b) lifetime is found to be 442.9 +/- 8.2 (stat) +/- 2.8 (syst) mu m. The precision from each of these channels is as good as or better than previous measurements. The B-c(+) lifetime, measured with respect to the B+ to reduce the systematic uncertainty, is 162.3 +/- 7.8 (stat) +/- 4.2 (syst) +/- 0.1 (tau(B+)) mu m. All results are in agreement with current world-average values.
Zhang YX, Danner OS, Nakadai T, Fayzikhodjaeva G, Lu YH, Lazar MA, Roeder RG, Friedman JM
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A noncanonical PPAR gamma/RXR alpha-binding sequence regulates leptin expression in response to changes in adipose tissue mass
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2018 JUN 26; 115(26):E6039-E6047
Leptin expression decreases after fat loss and is increased when obesity develops, and its proper quantitative regulation is essential for the homeostatic control of fat mass. We previously reported that a distant leptin enhancer 1 (LE1), 16 kb upstream from the transcription start site (TSS), confers fat-specific expression in a bacterial artificial chromosome transgenic (BACTG) reporter mouse. However, this and the other elements that we identified do not account for the quantitative changes in leptin expression that accompany alterations of adipose mass. In this report, we used an assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) to identify a 17-bp noncanonical peroxisome proliferator-activated receptor gamma (PPAR gamma)/retinoid X receptor alpha (RXR alpha)-binding site, leptin regulatory element 1 (LepRE1), within LE1, and show that it is necessary for the fat-regulated quantitative control of reporter (luciferase) expression. While BACTG reporter mice with mutations in this sequence still show fat-specific expression, luciferase is no longer decreased after food restriction and weight loss. Similarly, the increased expression of leptin reporter associated with obesity in oWob mice is impaired. A functionally analogous LepRE1 site is also found in a second, redundant DNA regulatory element 13 kb downstream of the TSS. These data uncouple the mechanisms conferring qualitative and quantitative expression of the leptin gene and further suggest that factor(s) that bind to LepRE1 quantitatively control leptin expression and might be components of a lipid-sensing system in adipocytes.
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Measurements of differential cross sections of top quark pair production as a function of kinematic event variables in proton-proton collisions at root s=13 TeV
JOURNAL OF HIGH ENERGY PHYSICS 2018 JUN 1; ?(6):? Article 002
Measurements of differential t (t) over bar production cross sections are presented in the single-lepton decay channel, as a function of a number of kinematic event variables. The measurements are performed with proton-proton collision data at root s = 13 TeV, collected by the CMS experiment at the LHC during 2016, with an integrated luminosity of 35.9 fb(-1). The data are compared to a variety of state-of-the-art leading-order and next-to-leading order t (t) over bar simulations.