114 research outputs found
Open and Hidden Charm Production in 920 GeV Proton-Nucleus Collisions
The HERA-B collaboration has studied the production of charmonium and open
charm states in collisions of 920 GeV protons with wire targets of different
materials. The acceptance of the HERA-B spectrometer covers negative values of
xF up to xF=-0.3 and a broad range in transverse momentum from 0.0 to 4.8
GeV/c. The studies presented in this paper include J/psi differential
distributions and the suppression of J/psi production in nuclear media.
Furthermore, production cross sections and cross section ratios for open charm
mesons are discussed.Comment: 5 pages, 9 figures, to be published in the proceedings of the 6th
International Conference on Hyperons, Charm & Beauty Hadrons (BEACH04),
Chicago, IL, June 27 - July 3, 200
Search for the Flavor-Changing Neutral Current Decay with the HERA-B Detector
We report on a search for the flavor-changing neutral current decay using events recorded with a dimuon trigger in
interactions of 920 GeV protons with nuclei by the HERA-B experiment. We find
no evidence for such decays and set a 90% confidence level upper limit on the
branching fraction .Comment: 17 pages, 4 figures (of which 1 double), paper to be submitted to
Physics Letters
Measurement of the J/Psi Production Cross Section in 920 GeV/c Fixed-Target Proton-Nucleus Interactions
The mid-rapidity (dsigma_(pN)/dy at y=0) and total sigma_(pN) production
cross sections of J/Psi mesons are measured in proton-nucleus interactions.
Data collected by the HERA-B experiment in interactions of 920 GeV/c protons
with carbon, titanium and tungsten targets are used for this analysis. The
J/Psi mesons are reconstructed by their decay into lepton pairs. The total
production cross section obtained is sigma_(pN)(J/Psi) = 663 +- 74 +- 46
nb/nucleon. In addition, our result is compared with previous measurements
Three long period transiting giant planets from TESS
We report the discovery and orbital characterization of three new transiting
warm giant planets. These systems were initially identified as presenting
single transit events in the light curves generated from the full frame images
of the Transiting Exoplanet Survey Satellite (TESS). Follow-up radial velocity
measurements and additional light curves were used to determine the orbital
periods and confirm the planetary nature of the candidates. The planets orbit
slightly metal-rich late F- and early G-type stars. We find that TOI 4406b has
a mass of = 0.30 0.04 , a radius of = 1.00 0.02
, and a low eccentricity orbit (e=0.15 0.05) with a period of P=
30.08364 0.00005 d . TOI 2338b has a mass of = 5.98 0.20
, a radius of = 1.00 0.01 , and a highly eccentric orbit (e=
0.676 0.002 ) with a period of P= 22.65398 0.00002 d . Finally, TOI
2589b has a mass of = 3.50 0.10 , a radius of = 1.08
0.03 , and an eccentric orbit (e = 0.522 0.006 ) with a
period of P= 61.6277 0.0002 d . TOI 4406b and TOI 2338b are enriched in
metals compared to their host stars, while the structure of TOI 2589b is
consistent with having similar metal enrichment to its host star.Comment: 24 pages, 16 figures, accepted in A
Why Does Exercise “Triggerâ€? Adaptive Protective Responses in the Heart?
Numerous epidemiological studies suggest that individuals who exercise have decreased cardiac morbidity and mortality. Pre-clinical studies in animal models also find clear cardioprotective phenotypes in animals that exercise, specifically characterized by lower myocardial infarction and arrhythmia. Despite the clear benefits, the underlying cellular and molecular mechanisms that are responsible for exercise preconditioning are not fully understood. In particular, the adaptive signaling events that occur during exercise to “trigger� cardioprotection represent emerging paradigms. In this review, we discuss recent studies that have identified several different factors that appear to initiate exercise preconditioning. We summarize the evidence for and against specific cellular factors in triggering exercise adaptations and identify areas for future study
The ReCoDe addiction research consortium:Losing and regaining control over drug intake-Findings and future perspectives
Substance use disorders (SUDs) are seen as a continuum ranging from goal-directed and hedonic drug use to loss of control over drug intake with aversive consequences for mental and physical health and social functioning. The main goals of our interdisciplinary German collaborative research centre on Losing and Regaining Control over Drug Intake (ReCoDe) are (i) to study triggers (drug cues, stressors, drug priming) and modifying factors (age, gender, physical activity, cognitive functions, childhood adversity, social factors, such as loneliness and social contact/interaction) that longitudinally modulate the trajectories of losing and regaining control over drug consumption under real-life conditions. (ii) To study underlying behavioural, cognitive and neurobiological mechanisms of disease trajectories and drug-related behaviours and (iii) to provide non-invasive mechanism-based interventions. These goals are achieved by: (A) using innovative mHealth (mobile health) tools to longitudinally monitor the effects of triggers and modifying factors on drug consumption patterns in real life in a cohort of 900 patients with alcohol use disorder. This approach will be complemented by animal models of addiction with 24/7 automated behavioural monitoring across an entire disease trajectory; i.e. from a naïve state to a drug-taking state to an addiction or resilience-like state. (B) The identification and, if applicable, computational modelling of key molecular, neurobiological and psychological mechanisms (e.g., reduced cognitive flexibility) mediating the effects of such triggers and modifying factors on disease trajectories. (C) Developing and testing non-invasive interventions (e.g., Just-In-Time-Adaptive-Interventions (JITAIs), various non-invasive brain stimulations (NIBS), individualized physical activity) that specifically target the underlying mechanisms for regaining control over drug intake. Here, we will report on the most important results of the first funding period and outline our future research strategy.</p
Limits for the central production of Θ+ and Ξ−− pentaquarks in 920-GeV pA collisions
We have searched for Θ+(1540) and Ξ−−(1862) pentaquark candidates in proton-inducedreactions on C, Ti, and W targets at midrapidity and s√=41.6 GeV. In 2×108 inelastic eventswe find no evidence for narrow (σ≈5 MeV) signals in the Θ+→pK0S and Ξ−−→Ξ−π− channels; our 95% C.L. upper limits (UL) forthe inclusive production cross section times branching fraction B dσ/dy $y ≈0 are (4-16) μb/N for a Θ+ mass between 1521 and 1555 MeV,and 2.5μb/N for the Ξ−−. The UL of the yield ratio of Θ+/Λ(1520)<(3-12)% is significantly lower than model predictions.Our UL of B Ξ−−/Ξ(1530)0<4% is at variance with the results that have provided the first evidencefor the Ξ−−
Association of genetic variation with systolic and diastolic blood pressure among African Americans: the Candidate Gene Association Resource study
The prevalence of hypertension in African Americans (AAs) is higher than in other US groups; yet, few have performed genome-wide association studies (GWASs) in AA. Among people of European descent, GWASs have identified genetic variants at 13 loci that are associated with blood pressure. It is unknown if these variants confer susceptibility in people of African ancestry. Here, we examined genome-wide and candidate gene associations with systolic blood pressure (SBP) and diastolic blood pressure (DBP) using the Candidate Gene Association Resource (CARe) consortium consisting of 8591 AAs. Genotypes included genome-wide single-nucleotide polymorphism (SNP) data utilizing the Affymetrix 6.0 array with imputation to 2.5 million HapMap SNPs and candidate gene SNP data utilizing a 50K cardiovascular gene-centric array (ITMAT-Broad-CARe [IBC] array). For Affymetrix data, the strongest signal for DBP was rs10474346 (P= 3.6 × 10−8) located near GPR98 and ARRDC3. For SBP, the strongest signal was rs2258119 in C21orf91 (P= 4.7 × 10−8). The top IBC association for SBP was rs2012318 (P= 6.4 × 10−6) near SLC25A42 and for DBP was rs2523586 (P= 1.3 × 10−6) near HLA-B. None of the top variants replicated in additional AA (n = 11 882) or European-American (n = 69 899) cohorts. We replicated previously reported European-American blood pressure SNPs in our AA samples (SH2B3, P= 0.009; TBX3-TBX5, P= 0.03; and CSK-ULK3, P= 0.0004). These genetic loci represent the best evidence of genetic influences on SBP and DBP in AAs to date. More broadly, this work supports that notion that blood pressure among AAs is a trait with genetic underpinnings but also with significant complexit
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