Self-consistent long-time simulation of chirping and beating energetic particle modes in JT-60U plasmas

Recurring bursts of chirping Alfvén modes that were observed in JT-60U tokamak plasmas driven by negative-ion-based neutral beams (N-NB) are reproduced in first-principle simulations performed with an extended version of the hybrid code MEGA. This code simulates the interactions between gyrokinetic fast ions and magnetohydrodynamic (MHD) modes in the presence of a realistic fast ion source and collisions, so that it self-consistently captures dynamics across a wide range of time scales (0.01–100 ms). The simulation confirms that the experimentally observed phenomena known as \u27fast frequency sweeping (fast FS) modes\u27 are caused by bursts of energetic particle modes (EPM) with dominant toroidal mode number n  =  1. On the long time scale (1–10 ms), the simulation reproduces the chirping range (40–60 kHz), the burst duration (few ms) and intervals (5–10 ms). On the short time scale (0.01–0.1 ms), it reproduces pulsations and phase jumps, which we interpret as the result of beating between multiple resonant wave packets. Having reproduced at multiple levels of detail the dynamics of low-amplitude long-wavelength Alfvén modes driven by N-NB ions, the next goal is to reproduce and explain abrupt large-amplitude events (ALE) that were seen in the same experiments at longer time intervals (10–100 ms)

Measurement of low-energy antiproton detection efficiency in BESS below 1 GeV

An accelerator experiment was performed using a low-energy antiproton beam to measure antiproton detection efficiency of BESS, a balloon-borne spectrometer with a superconducting solenoid. Measured efficiencies showed good agreement with calculated ones derived from the BESS Monte Carlo simulation based on GEANT/GHEISHA. With detailed verification of the BESS simulation, the relative systematic error of detection efficiency derived from the BESS simulation has been determined to be $\pm$5%, compared with the previous estimation of $\pm$15% which was the dominant uncertainty for measurements of cosmic-ray antiproton flux.Comment: 13 pages, 7 figure

Use of the index of pulmonary vascular disease for predicting long-term outcome of pulmonary arterial hypertension associated with congenital heart disease

AimsLimited data exist on risk factors for the long-term outcome of pulmonary arterial hypertension (PAH) associated with congenital heart disease (CHD-PAH). We focused on the index of pulmonary vascular disease (IPVD), an assessment system for pulmonary artery pathology specimens. The IPVD classifies pulmonary vascular lesions into four categories based on severity: (1) no intimal thickening, (2) cellular thickening of the intima, (3) fibrous thickening of the intima, and (4) destruction of the tunica media, with the overall grade expressed as an additive mean of these scores. This study aimed to investigate the relationship between IPVD and the long-term outcome of CHD-PAH.MethodsThis retrospective study examined lung pathology images of 764 patients with CHD-PAH aged <20 years whose lung specimens were submitted to the Japanese Research Institute of Pulmonary Vasculature for pulmonary pathological review between 2001 and 2020. Clinical information was collected retrospectively by each attending physician. The primary endpoint was cardiovascular death.ResultsThe 5-year, 10-year, 15-year, and 20-year cardiovascular death-free survival rates for all patients were 92.0%, 90.4%, 87.3%, and 86.1%, respectively. The group with an IPVD of ≥2.0 had significantly poorer survival than the group with an IPVD <2.0 (P = .037). The Cox proportional hazards model adjusted for the presence of congenital anomaly syndromes associated with pulmonary hypertension, and age at lung biopsy showed similar results (hazard ratio 4.46; 95% confidence interval: 1.45–13.73; P = .009).ConclusionsThe IPVD scoring system is useful for predicting the long-term outcome of CHD-PAH. For patients with an IPVD of ≥2.0, treatment strategies, including choosing palliative procedures such as pulmonary artery banding to restrict pulmonary blood flow and postponement of intracardiac repair, should be more carefully considered

Analytical estimation of drift-orbit island-width for passing ions in static magnetic perturbation

The fast ion transport plays a key role in the simulation for developing operational scenarios. But the transport of fast ions in the perturbed field is complex compared with that of thermal ions since the transport depends on energy and pitch angle as well as a spatial coordinate. The Monte-Carlo approach can handle the transport in the straight forward way, however the approach is computationally expensive and is not suitable for scenario simulators. We need a computationally low-cost method or a reduced transport model. The island width in the phase space can be a characteristic scale of the transport. Thus, a simple method to determine the island width is useful to construct a reduced model. In this paper, we present a method to estimate the drift-orbit island-width from the velocity perturbation. We have derived an analytic expression for the drift-orbit island-width on a resonant toroidal canonical angular momentum surface in the same way how we estimate the magnetic island width from the magnetic perturbation on a resonant magnetic poloidal flux surface. Thus, we can avoid the issue, in our previous work, on the difference between the magnetic perturbation and velocity perturbation. We can also eliminate the cost for the Poincaré-map calculation of the magnetic perturbation. The estimated drift orbit island widths were compared with those from Poincaré maps obtained from a drift-orbit-following calculation. The estimated island widths well correlate with those from Poincaré maps within the error of about 15%. The island overlaps are also explained by the estimated island position and its width. The estimation method can provide an indicator to evaluate an overlapping threshold for chaotic orbits in the same way with the magnetic perturbation.The 16th IAEA Technical Meeting on Energetic Particles in Magnetic Confinement Systems - Theory of Plasma Instabilities (EPPI2019

Lidar measurements of stratospheric aerosols enhanced after the eruption of Mt. Pinatubo: Alaska, winter 1991/1992

Lidar measurements made at Poker Flat, Alaska in winter 1991/1992 suggest that stratospheric aerosols were extremely enhanced after the volcanic eruption of Pinatubo. The vertical profile of aerosol concentration had maxima 16-17km, and 22-23km. An additional aerosol layer was identified only in the measurements of December 15,1991

PDIP38/PolDIP2 controls the DNA damage tolerance pathways by increasing the relative usage of translesion DNA synthesis over template switching

International audienceReplicative DNA polymerases are frequently stalled at damaged template strands. Stalled replication forks are restored by the DNA damage tolerance (DDT) pathways, error-prone translesion DNA synthesis (TLS) to cope with excessive DNA damage, and error-free template switching (TS) by homologous DNA recombination. PDIP38 (Pol-delta interacting protein of 38 kDa), also called Pol δ-interacting protein 2 (PolDIP2), physically associates with TLS DNA polymerases, polymerase η (Polη), Polλ, and PrimPol, and activates them in vitro. It remains unclear whether PDIP38 promotes TLS in vivo, since no method allows for measuring individual TLS events in mammalian cells. We disrupted the PDIP38 gene, generating PDIP38-/- cells from the chicken DT40 and human TK6 B cell lines. These PDIP38-/- cells did not show a significant sensitivity to either UV or H2O2, a phenotype not seen in any TLS-polymerase-deficient DT40 or TK6 mutants. DT40 provides a unique opportunity of examining individual TLS and TS events by the nucleotide sequence analysis of the immunoglobulin variable (Ig V) gene as the cells continuously diversify Ig V by TLS (non-templated Ig V hypermutation) and TS (Ig gene conversion) during in vitro culture. PDIP38-/- cells showed a shift in Ig V diversification from TLS to TS. We measured the relative usage of TLS and TS in TK6 cells at a chemically synthesized UV damage (CPD) integrated into genomic DNA. The loss of PDIP38 also caused an increase in the relative usage of TS. The number of UV-induced sister chromatid exchanges, TS events associated with crossover, was increased a few times in PDIP38-/- human and chicken cells. Collectively, the loss of PDIP38 consistently causes a shift in DDT from TLS to TS without enhancing cellular sensitivity to DNA damage. We propose that PDIP38 controls the relative usage of TLS and TS increasing usage of TLS without changing the overall capability of DDT