Preliminary calculation of solar cosmic ray dose to the female breast in space mission

No regulatory dose limits are specifically assigned for the radiation exposure of female breasts during manned space flight. However, the relatively high radiosensitivity of the glandular tissue of the breasts and its potential exposure to solar flare protons on short- and long-term missions mandate a priori estimation of the associated risks. A model for estimating exposure within the breast is developed for use in future NASA missions. The female breast and torso geometry is represented by a simple interim model. A recently developed proton dose-buildup procedure is used for estimating doses. The model considers geomagnetic shielding, magnetic-storm conditions, spacecraft shielding, and body self-shielding. Inputs to the model include proton energy spectra, spacecraft orbital parameters, STS orbiter-shielding distribution at a given position, and a single parameter allowing for variation in breast size

Analyses of risks associated with radiation exposure from past major solar particle events

Radiation exposures and cancer induction/mortality risks were investigated for several major solar particle events (SPE's). The SPE's included are: February 1956, November 1960, August 1972, October 1989, and the September, August, and October 1989 events combined. The three 1989 events were treated as one since all three could affect a single lunar or Mars mission. A baryon transport code was used to propagate particles through aluminum and tissue shield materials. A free space environment was utilized for all calculations. Results show the 30-day blood forming organs (BFO) limit of 25 rem was surpassed by all five events using 10 g/sq cm of shielding. The BFO limit is based on a depth dose of 5 cm of tissue, while a more detailed shield distribution of the BFO's was utilized. A comparison between the 5 cm depth dose and the dose found using the BFO shield distribution shows that the 5 cm depth value slightly higher than the BFO dose. The annual limit of 50 rem was exceeded by the August 1972, October 1989, and the three combined 1989 events with 5 g/sq cm of shielding. Cancer mortality risks ranged from 1.5 to 17 percent at 1 g/sq cm and 0.5 to 1.1 percent behind 10 g/sq cm of shielding for five events. These ranges correspond to those for a 45 year old male. It is shown that secondary particles comprise about 1/3 of the total risk at 10 g/sq cm of shielding. Utilizing a computerized Space Shuttle shielding model to represent a typical spacecraft configuration in free space at the August 1972 SPE, average crew doses exceeded the BFO dose limit

Multi-Wavelength Variability of the Synchrotron Self-Compton Model for Blazar Emission

Motivated by recent reports of strongly correlated radio and X-ray variability in 3C279 (Grandi, etal 1995), we have computed the relative amplitudes of variations in the synchrotron flux at $\nu$ and the self-Compton X-ray flux at 1 keV ($R(\nu)$) for a homogeneous sphere of relativistic electrons orbiting in a tangled magnetic field. Relative to synchrotron self-Compton scattering without induced Compton scattering, stimulated scattering reduces the amplitude of $R(\nu)$ by as much as an order of magnitude when \tau_T \gtwid 1. When $\tau_T$ varies in a fixed magnetic field, $R_{\tau}$ increases monotonically from 0.01 at $\nu_o$, the self-absorption turnover frequency, to $0.5$ at $100 \nu_o$. The relative amplitudes of the correlated fluctuations in the radio-mm and X-ray fluxes from 3C279 are consistent with the synchrotron self-Compton model if $\tau_T$ varies in a fixed magnetic field and induced Compton scattering is the dominant source of radio opacity. The variation amplitudes are are too small to be produced by the passage of a shock through the synchrotron emission region unless the magnetic field is perpendicular to the shock front.Comment: 21 pages, 4 fig

Radiation risk predictions for Space Station Freedom orbits

Risk assessment calculations are presented for the preliminary proposed solar minimum and solar maximum orbits for Space Station Freedom (SSF). Integral linear energy transfer (LET) fluence spectra are calculated for the trapped proton and GCR environments. Organ dose calculations are discussed using the computerized anatomical man model. The cellular track model of Katz is applied to calculate cell survival, transformation, and mutation rates for various aluminum shields. Comparisons between relative biological effectiveness (RBE) and quality factor (QF) values for SSF orbits are made

Characterisation of an Advanced Nickel Based Superalloy Post Cold Work by Swaging

Cylindrical bars of the advanced nickel based superalloy RR1000 were subjected to swaging to induce approximately 30% cold work. Grain size analysis demonstrated a distinct modification to the microstructure whilst electron back scattered diffraction (EBSD) measurements confirmed the evolution of a relatively strong texture parallel with the longitudinal bar axis. Intragranular strain damage was identified. The effects of the swaging on bulk mechanical properties are illustrated across a range of test temperatures

Functional immunoglobulin transgenes guide ordered B-cell differentiation in Rag-1-deficient mice

We have examined the regulatory role of the individual components of the immunoglobulin antigen receptor in B-cell development by transgenic complementation of Rag-1 deficient (Rag-1⁻) mice. Complementation with a membrane µ heavy chain (µHC) gene allows progression of developmentally arrested Rag-1⁻ pro-B-cells to the small pre-B cell stage, whereas the introduction of independently integrated µHC and κ light chain (κLC) transgenes promotes the appearance of peripheral lymphocytes which, however, remain unresponsive to external stimuli. Complete reconstitution of the B-cell lineage and the emergence of functionally nature Rag-1⁻ peripheral B cells is achieved by the introduction of cointegrated heavy and light chain transgenes encoding an anti-H-2^k antibody. This experimental system demonstrates the competence of the µHC and κLC to direct and regulate the sequential stages of B-cell differentiation, defines the time at which negative selection of self-reactive B cells occurs, and shows that elimination of these cells occurs equally well in the absence of Rag-1 as in its presence. These data also support the hypothesis that Rag-1 directly participates in the V(D)J recombination process

The microstructure and hardness of Ni-Co-Al-Ti-Cr quinary alloys

The effects of Ni:Co and Al:Ti ratios on the room temperature microstructure, hardness and lattice parameter of twenty-seven quinary Ni-Co-Al-Ti-Cr alloys have been evaluated. All of the alloys exhibited a uniform $\gamma$-$\gamma ^\prime$ microstructure. Differential scanning calorimetry (DSC) showed that the liquidus and solidus temperatures of the alloys increased with greater Al:Ti ratios, decreased with Cr concentration and remained largely unchanged with respect to the Ni:Co ratio. Neutron diffraction measurements of the $\gamma$ and $\gamma ^\prime$ lattice parameters revealed that the lattice misfit in all of the alloys was positive and increased with Ti concentration (i.e. lower Al:Ti ratio) regardless of the concentration of Cr, or the ratio of Ni:Co. Importantly, alloys with a Ni:Co ratio of 1:1, were found to have consistently greater lattice misfits than alloys with Ni:Co ratios of either 1:3 or 3:1. The measured lattice misfits were found to be strongly correlated with the Vickers hardness of the alloys, suggesting that lattice misfit plays a key role in the strengthening of $\gamma$-$\gamma ^\prime$ alloys of this type.Rolls-Royce/EPSRC Strategic Partnership (Grant IDs: EP/H022309/1, EP/H500375/1 and EP/ M005607/1)This is the author accepted manuscript. The final version is available from Elsevier via http://dx.doi.org/10.1016/j.jallcom.2016.07.15

Cortisol shifts financial risk preferences.

Risk taking is central to human activity. Consequently, it lies at the focal point of behavioral sciences such as neuroscience, economics, and finance. Many influential models from these sciences assume that financial risk preferences form a stable trait. Is this assumption justified and, if not, what causes the appetite for risk to fluctuate? We have previously found that traders experience a sustained increase in the stress hormone cortisol when the amount of uncertainty, in the form of market volatility, increases. Here we ask whether these elevated cortisol levels shift risk preferences. Using a double-blind, placebo-controlled, cross-over protocol we raised cortisol levels in volunteers over 8 d to the same extent previously observed in traders. We then tested for the utility and probability weighting functions underlying their risk taking and found that participants became more risk-averse. We also observed that the weighting of probabilities became more distorted among men relative to women. These results suggest that risk preferences are highly dynamic. Specifically, the stress response calibrates risk taking to our circumstances, reducing it in times of prolonged uncertainty, such as a financial crisis. Physiology-induced shifts in risk preferences may thus be an underappreciated cause of market instability.This research was supported by a Programme Grant from the Economic and Social Research Council.This is the version of record of the article "Cortisol shifts financial risk preferences" published in PNAS on March 2104 under the PNAS Open Access option. The published version of record is available on the journal website at http://www.pnas.org/cgi/doi/10.1073/pnas.131790811

The WD40 Domain Is Required for LRRK2 Neurotoxicity

BACKGROUND:Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson disease (PD). LRRK2 contains an "enzymatic core" composed of GTPase and kinase domains that is flanked by leucine-rich repeat (LRR) and WD40 protein-protein interaction domains. While kinase activity and GTP-binding have both been implicated in LRRK2 neurotoxicity, the potential role of other LRRK2 domains has not been as extensively explored. PRINCIPAL FINDINGS:We demonstrate that LRRK2 normally exists in a dimeric complex, and that removing the WD40 domain prevents complex formation and autophosphorylation. Moreover, loss of the WD40 domain completely blocks the neurotoxicity of multiple LRRK2 PD mutations. CONCLUSION:These findings suggest that LRRK2 dimerization and autophosphorylation may be required for the neurotoxicity of LRRK2 PD mutations and highlight a potential role for the WD40 domain in the mechanism of LRRK2-mediated cell death

Position-momentum local realism violation of the Hardy type

We show that it is, in principle, possible to perform local realism violating experiments of the Hardy type in which only position and momentum measurements are made on two particles emanating from a common source. In the optical domain, homodyne detection of the in-phase and out-of-phase amplitude components of an electromagnetic field is analogous to position and momentum measurement. Hence, local realism violations of the Hardy type are possible in optical systems employing only homodyne detection.Comment: 10 pages, no figures, to be published in Physical Review