Propagation of Cross-Section Uncertainties in Criticality Calculations in the Framework of UAM-Phase I Using MCNPX-2.7e and SCALE-6.1

In the framework of the OECD/NEA project on Benchmark for Uncertainty Analysis in Modeling (UAM) for Design, Operation, and Safety Analysis of LWRs, several approaches and codes are being used to deal with the exercises proposed in Phase I, “Specifications and Support Data for Neutronics Cases.” At UPM, our research group treats these exercises with sensitivity calculations and the “sandwich formula” to propagate cross-section uncertainties. Two different codes are employed to calculate the sensitivity coefficients of to cross sections in criticality calculations: MCNPX-2.7e and SCALE-6.1. The former uses the Differential Operator Technique and the latter uses the Adjoint-Weighted Technique. In this paper, the main results for exercise I-2 “Lattice Physics” are presented for the criticality calculations of PWR. These criticality calculations are done for a TMI fuel assembly at four different states: HZP-Unrodded, HZP-Rodded, HFP-Unrodded, and HFP-Rodded. The results of the two different codes above are presented and compared. The comparison proves a good agreement between SCALE-6.1 and MCNPX-2.7e in uncertainty that comes from the sensitivity coefficients calculated by both codes. Differences are found when the sensitivity profiles are analysed, but they do not lead to differences in the uncertainty.

Cyclooxygenase-2 mediates the cardioprotective effects of the late phase of ischemic preconditioning in conscious rabbits

We examined the role of cyclooxygenase-2 (COX-2) in the late phase of ischemic preconditioning (PC). A total of 176 conscious rabbits were used. Ischemic PC (six cycles of 4-min coronary occlusions/4-min reperfusions) resulted in a rapid increase in myocardial COX-2 mRNA levels (+231 ± 64% at 1 h; RNase protection assay) followed 24 h later by an increase in COX-2 protein expression (+216 ± 79%; Western blotting) and in the myocardial content of prostaglandin (PG)E2 and 6-keto-PGF1α (+250 ± 85% and +259 ± 107%, respectively; enzyme immunoassay). Administration of two unrelated COX-2 selective inhibitors (NS-398 and celecoxib) 24 h after ischemic PC abolished the ischemic PC-induced increase in tissue levels of PGE2 and 6-keto-PGF1α. The same doses of NS-398 and celecoxib, given 24 h after ischemic PC, completely blocked the cardioprotective effects of late PC against both myocardial stunning and myocardial infarction, indicating that COX-2 activity is necessary for this phenomenon to occur. Neither NS-398 nor celecoxib lowered PGE2 or 6-keto-PGF1α levels in the nonischemic region of preconditioned rabbits, indicating that constitutive COX-1 activity was unaffected. Taken together, these results demonstrate that, in conscious rabbits, up-regulation of COX-2 plays an essential role in the cardioprotection afforded by the late phase of ischemic PC. Therefore, this study identifies COX-2 as a cardioprotective protein. The analysis of arachidonic acid metabolites strongly points to PGE2 and/or PGI2 as the likely effectors of COX-2-dependent protection. The recognition that COX-2 mediates the antistunning and antiinfarct effects of late PC impels a reassessment of current views regarding this enzyme, which is generally regarded as detrimental.

Modulation of Sarco/Endoplasmic Reticulum Ca2+-ATPase 2 (SERCA2) function by acetylation following the treatment with histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA)

Background: Acetylation and deacetylation at specific lysine (K) residues is mediated by histone acetylases (HATs) and deacetylases (HDACs), respectively. HATs and HDACs act on both histone and non-histone proteins, regulating various processes, including cardiac impulse propagation. Aim of the present work was to establish whether the function of the Ca2+ ATPase SERCA2, one of the major players in Ca2+ reuptake during excitation-contraction coupling in cardiac myocytes (CMs), could be modulated by direct K acetylation. Materials and methods: HL-1 atrial mouse cells (donated by Prof. Claycomb), zebrafish and Streptozotocin-induced diabetic rat CMs were treated with the pan-inhibitor of class I and II HDACs suberanilohydroxamic acid (SAHA) for 1.5 hour. Evaluation of SERCA2 acetylation was analyzed by co-immunoprecipitation. SERCA2 activity was measured on microsomes by pyruvate/NADH coupled reaction assay. SERCA2 mutants were obtained after cloning wild-type and mutated sequences into the pCDNA3 vector and transfected into HEK cells. Ca2+ transients in CMs (loading with Fluo3-AM, field stimulation, 0.5 Hz) and in transfected HEK cells (loading with FLUO-4, caffeine pulse) were recorded. Results: Co-Immunoprecipitation experiments performed on HL-1 cells demonstrated a significant increase in the acetylation of SERCA2 after SAHA-treatment (2.5 µM, n=3). This was associated with an increase in SERCA2 activity in microsomes obtained from HL-1 cells, after SAHA exposure (n=5). Accordingly, SAHA-treatment significantly shortened the Ca2+ reuptake time of adult zebrafish CMs. Further, SAHA 2.5 nM restored to control values the recovery time of Ca2+ transients decay in diabetic rat CMs. HDAC inhibition also improved contraction parameters, such as fraction of shortening, and increased pump activity in microsomes isolated from diabetic CMs (n=4). Notably, the K464, identified by bioinformatic tools as the most probable acetylation site on human SERCA2a, was mutated into Glutamine (Q) or Arginine (R) mimicking acetylation and deacetylation respectively. Measurements of Ca2+ transients in HEK cells revealed that the substitution of K464 with R significantly delayed the transient recovery time, thus indicating that deacetylation has a negative impact on SERCA2 function. Conclusions: Our results indicate that SERCA2 function can be improved by pro-acetylation interventions and that this mechanism of regulation is conserved among species. Therefore, the present work provides the basis to open the search for novel pharmacological tools able to specifically improve SERCA2 activity in diseases where its expression and/or function is impaired, such as diabetic cardiomyopathy.

Pulse phase-coherent timing and spectroscopy of CXOU J164710.2−45521 outbursts

We present a long-term phase-coherent timing analysis and pulse-phase resolved spectroscopy for the two outbursts observed from the transient anomalous X-ray pulsar CXOU J164710.2−455216. For the first outburst we used 11 Chandra and XMM–Newton observations between 2006 September and 2009 August, the longest baseline yet for this source. We obtain a coherent timing solution with P = 10.61065583(4) s, Ṗ = 9.72(1) × 10−13 s s−1 and P̈ = –1.05(5) × 10−20 s s−2. Under the standard assumptions this implies a surface dipolar magnetic field of ∼1014 G, confirming this source as a standard B magnetar. We also study the evolution of the pulse profile (shape, intensity and pulsed fraction) as a function of time and energy. Using the phase-coherent timing solution we perform a phase-resolved spectroscopy analysis, following the spectral evolution of pulse-phase features, which hints at the physical processes taking place on the star. The results are discussed from the perspective of magnetothermal evolution models and the untwisting magnetosphere model. Finally, we present similar analysis for the second, less intense, 2011 outburst. For the timing analysis we used Swift data together with 2 XMM–Newton and Chandra pointings. The results inferred for both outbursts are compared and briefly discussed in a more general framework.

Integrated traffic simulation model - phase I. Volume 2: design of the TRAF system (TOS). Final report.

Federal Highway Administration, Washington, D.C.

Integrated motorist information system (IMIS) feasibility and design study. Phase I: feasibility study. Volume 2 - appendices. Final report.

Federal Highway Administration, Office of Research and Development, Washington, D.C.

Integrated motorist information (IMIS) feasibility and design study. Phase II: generalized methodology for IMIS feasibility studies. Volume 2--validation and application of feasibility study handbook. Final report.

Federal Highway Administration, Office of Research and Development, Washington, D.C.

Construction of a comprehensive causal network. Volume 2: literature review and bibliographies. Phase II report.

National Highway Traffic Safety Administration, Washington, D.C.

Fox River Watershed investigation : Stratton Dam to the Illinois River, Phase II : hydrologic models and water quality simulation models, part 2 : Blackberry and Poplar Creek HSPF models, calibration and initial simulation results /

"June 2007."

Operator's, organizational, direct support, and general support maintenance manual : air conditioner, split package, 18,000 Btu/hr cooling, 30,000 Btu/hr heating, 208 volt, 3 phase, 400 hertz, Keco model F18H4-2 (4120-01-069-1321).

"25 February 1982."