Tissue-specific dose equivalents of secondary mesons and leptons during galactic cosmic ray exposures for mars exploration.

During a human mission to Mars, astronauts would be continuously exposed to galactic cosmic rays (GCR) consisting of high energy protons and heavier ions coming from outside our solar system. Due to their high energy, GCR ions can penetrate spacecraft and space habitat structures, directly reaching human organs. Additionally, they generate secondary particles when interacting with shielding materials and human tissues. Baryon secondaries have been the focus of many previous studies, while meson and lepton secondaries have been considered to a much lesser extent. In this work, we focus on assessing the tissue-specific dose equivalents and the effective dose for males of secondary mesons and leptons for the interplanetary cruise phase and the surface phase on Mars. We also provide the energy distribution of the secondary pions in each human organ since they are dominant compared to other mesons and leptons. For this calculation, the PHITS3.27 Monte Carlo simulation toolkit is used to compute the energy spectra of particles in organs in a realistic human phantom. Based on the simulation data, the dose equivalent has been estimated with radiation quality factors in ICRP Publication 60 and in the latest NASA Space Cancer Risk model (NSCR-2022). The effective dose is then assessed with the tissue weighting factors in ICRP Publication 103 and in the NSCR model, separately. The results indicate that the contribution of secondary mesons and leptons to the total effective dose is 6.1 %, 9.1 %, and 11.3 % with the NSCR model in interplanetary space behind 5, 20, and 50 g/cm2 aluminum shielding, respectively, with similar values using the ICRP model. The outcomes of this work lead to an improved understanding of the potential health risks induced by secondary particles for exploration missions to Mars and other destinations.

Cancer and circulatory disease risks for the largest solar particle events in the space age.

In this paper we use the NASA Space Cancer Risk (NSCR version 2022) model to predict cancer and circulatory disease risks using energy spectra representing the largest SPE's observed in the space age. Because tissue dose-rates behind shielding for large SPE's lead to low dose-rates (<0.2 Gy/h) we consider the integrated risk for several historical periods of high solar activity, including July-November, 1960 events and August-October 1989 events along with the February 1956 and August 1972 events. The galactic cosmic ray (GCR) contribution to risks is considered in predictions. Results for these largest historical events show risk of exposure induced death (REID) are mitigated to < 1.2 % with a 95 % confidence interval with passive radiation shielding of 20 g/cm2 aluminum, while larger amounts would support the application of the ALARA principle. Annual GCR risks are predicted to surpass the risks from large SPEs by ∼30 g/cm2 of aluminum shielding.

Isotopic production cross sections in proton-16O and proton-12C interactions for energies from 10 MeV/u to 100 GeV/u.

Proton interactions with 16O or 12C nuclei are frequent nuclear interaction leading to secondary radiation in tissues for space radiation and cancer therapy with protons or ion beams. The fragmentation of these ions by protons produces a large number of heavy ion (A>4) target or projectile fragments often with high ionization density. Here we develop an analytical model of energy dependent proton-16O and proton-12C cross sections for isotopic nuclei production. Using experimental data and a 2nd order optical model an accurate formula for the absorption cross section from <10 MeV/u to >10 GeV/u is obtained. The energy dependence of the elemental and isotopic cross sections is modeled as multiplicities scaled to absorption cross section with average isotopic fractions estimated from experimental data. We show that this approach results in accurate analytic formulae for isotopic fragmentation cross sections over the full energy range in hadron therapy and space radiation protection studies.

Tentonin 3/TMEM150C regulates glucose-stimulated insulin secretion in pancreatic ß-cells.

Glucose homeostasis is initially regulated by the pancreatic hormone insulin. Glucose-stimulated insulin secretion in ß-cells is composed of two cellular mechanisms: a high glucose concentration not only depolarizes the membrane potential of the ß-cells by ATP-sensitive K+ channels but also induces cell inflation, which is sufficient to release insulin granules. However, the molecular identity of the stretch-activated cation channel responsible for the latter pathway remains unknown. Here, we demonstrate that Tentonin 3/TMEM150C (TTN3), a mechanosensitive channel, contributes to glucose-stimulated insulin secretion by mediating cation influx. TTN3 is expressed specifically in ß-cells and mediates cation currents to glucose and hypotonic stimulations. The glucose-induced depolarization, firing activity, and Ca2+ influx of ß-cells were significantly lower in Ttn3-/- mice. More importantly, Ttn3-/- mice show impaired glucose tolerance with decreased insulin secretion in vivo. We propose that TTN3, as a stretch-activated cation channel, contributes to glucose-stimulated insulin secretion.

Comparison between PHITS and GEANT4 Simulations of the Heavy Ion Beams at the BEVALAC at LBNL and the Booster Accelerator at BNL.

Heavy charged particles have been discussed for clinical use due to their superior dose-depth distribution compared to conventional radiation such as X-rays. In addition, high-charge and energy (HZE) ions in galactic cosmic rays (GCR) present important health risks for crewed space missions to the Earth's moon or Mars. Experiments at heavy ion accelerators are used in radiobiology studies; however, numerical simulations of track segment or Bragg peak irradiations are complicated by the details of the beam-line and dosimetry systems. The goal of the present work is in support of biophysics modeling of historical radiobiology data at Lawrence Berkeley National Laboratory (LBNL) and more recent results from the Brookhaven National Lab (BNL) facility (NASA Space Radiation Lab (NSRL)). In this work, the Spread-Out Bragg Peak (SOBP) of 4He, 12C, and 20Ne particles, and a Bragg curve of 56Fe ion have been simulated numerically in the geometries of LBNL and BNL using the Monte-Carlo based PHITS and GEANT4 simulation toolkits. The dose contributions of primary particles and secondary particles, including neutrons and photons, in the target material are computed and discussed as well. Comparisons suggest more contributions of secondaries in GEANT4 simulations compared to PHITS simulations, and less statistical fluctuation and better prediction of neutrons in PHITS simulations. Neutrons and gamma-rays are estimated to make minor contributions to absorbed doses for these beams.

Tentonin 3/TMEM150C senses blood pressure changes in the aortic arch.

The baroreceptor reflex is a powerful neural feedback that regulates arterial pressure (AP). Mechanosensitive channels transduce pulsatile AP to electrical signals in baroreceptors. Here we show that tentonin 3 (TTN3/TMEM150C), a cation channel activated by mechanical strokes, is essential for detecting AP changes in the aortic arch. TTN3 was expressed in nerve terminals in the aortic arch and nodose ganglion (NG) neurons. Genetic ablation of Ttn3 induced ambient hypertension, tachycardia, AP fluctuations, and impaired baroreflex sensitivity. Chemogenetic silencing or activation of Ttn3+ neurons in the NG resulted in an increase in AP and heart rate, or vice versa. More important, overexpression of Ttn3 in the NG of Ttn3-/- mice reversed the cardiovascular changes observed in Ttn3-/- mice. We conclude that TTN3 is a molecular component contributing to the sensing of dynamic AP changes in baroreceptors.