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At least 199 records · Page 11
All sourcesNASA NTRSDOE OSTI
DOE OSTI2015

First determination of the $CP$ content of D → π + π – π + π – and updated determination of the $CP$ contents of D → π + π – π 0 and D → K + K – π 0

Quantum-correlated ψ(3770)→DD¯ decays collected by the CLEO-c experiment are used to perform a first measurement of $F$ $^{4π}_{+}$, the fractional CP-even content of the self-conjugate decay D → π + π – π + π – , obtaining a value of 0.737 ± 0.028. An important input to the measurement comes from the use of D → $K$ $^{0}_{S}$π + π – and D → $K$ $^{0}_{L}$π + π – decays to tag the signal mode. This same technique is applied to the channels D → π + π – π 0 and D → K + K – π 0 , yielding $F$ $^{πππ0}_{+}$ =1.014 ± 0.045 ± 0.022 and $F$ $^{KKπ0}_{+}$ = 0.734 ± 0.106 ± 0.054, where the first uncertainty is statistical and the second systematic. These measurements are consistent with those of an earlier analysis, based on CP-eigenstate tags, and can be combined to give values of $F$ $^{πππ0}_{+}$ = 0.973 ± 0.017 and $F$ $^{KKπ0}_{+}$ = 0.732 ± 0.055. The results will enable the three modes to be included in a model-independent manner in measurements of the unitarity triangle angle γ using B ∓ → DK ∓ decays, and in time-dependent studies of CP violation and mixing in the D 0 D¯ 0 system.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗
DOE OSTI2019

Toxicokinetics of benzo[a]pyrene in humans: Extensive metabolism as determined by UPLC-accelerator mass spectrometry following oral micro-dosing

Benzo[a]pyrene (BaP), produces tumors of skin, lung, liver, kidney and stomach in animals, enhances lung cancer in epidemiological studies and is a known human carcinogen. The EPA cancer slope risk factor for oral BaP exposure is 1 per mg/kg-day. The remarkable sensitivity (attomole 14C; precision 0.5-2% in biological samples) of accelerator mass spectrometry (AMS) makes possible [14C]-BaP dosing of humans with de minimus risk. A micro-dose of 46 ng (5 nCi), was given in 3 separate cycles to 5 human volunteers with a minimum 2 weeks between dosing. Blood was collected over 72 hours and BaP and BaP metabolites ([14C]-BaPeq) measured using AMS. [14C]-BaPeq appeared in plasma with an average Tmax of 75 minutes and Cmax 116-326 fM (29-82 fg/mL). Non-compartmental half-lives in plasma ranged from 30.7-114.2 hours and area under the curve values (AUC0-72 hr) 649-2060 fg x hr x mL-1. A two compartmental model yielded first-order rate constants (Ka, K12, K21, Kela and Kelß) of 0.92, 0.49, 0.12, 0.05 and 0.01 fg/hr, respectively. The T1/2a and T1/2ß were 1.14 and 89 hours, respectively. The actual interval between dosing was 20-420 days with no impact on a low intra-individual variation. No covalent [14C]-BaPeq-DNA adducts from peripheral blood mononuclear cells (PBMCs) were detected (LLOD of 10 fg [14C]-BaPeq adducts/mg DNA) 12-72 hours post-dosing negating the use of this cancer biomarker in risk assessment. We assert that the most relevant model for humans is humans. AMS and micro-dosing could be used to enhance the accuracy of pharmacokinetics and potentially risk assessments.

pharmacokinetcs, Polycyclic aromatic hydrocarbons↗