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

Calculation of Heavy Ion Inactivation and Mutation Rates in Radial Dose Model of Track Structure

In the track structure model, the inactivation cross section is found by summing an inactivation probability over all impact parameters from the ion to the sensitive sites within the cell nucleus. The inactivation probability is evaluated by using the dose response of the system to gamma rays and the radial dose of the ions and may be equal to unity at small impact parameters. We apply the track structure model to recent data with heavy ion beams irradiating biological samples of E. Coli, Bacillus Subtilis spores, and Chinese hamster (V79) cells. Heavy ions have observed cross sections for inactivation that approach and sometimes exceed the geometric size of the cell nucleus in mammalian cells. We show how the effects of inactivation may be taken into account in the evaluation of the mutation cross sections from heavy ions in the track structure model through correlation of sites for gene mutation and cell inactivation. The model is fit to available data for HPRT (hypoxanthine guanine phosphoribosyl transferase) mutations in Chinese hamster cells, and good agreement is found. The resulting calculations qualitatively show that mutation cross sections for heavy ions display minima at velocities where inactivation cross sections display maxima. Also, calculations show the high probability for mutation by relativistic ions due to the radial extension of the ion track from delta rays in agreement with the microlesion concept. The effects of inactivation on mutation rates make it very unlikely that a single parameter such as LET (linear energy transfer) or Z*2/ β2&#;(where Z*is effective charge number and β is ion velocity) can be used to specify radiation quality for heavy ion bombardment

Calculation of Heavy Ion Inactivation and Mutation Rates in Radial Dose Model of Track Structure

In the track structure model, the inactivation cross section is found by summing an inactivation probability over all impact parameters from the ion to the sensitive sites within the cell nucleus. The inactivation probability is evaluated by using the dose response of the system to gamma rays and the radial dose of the ions and may be equal to unity at small impact parameters. We apply the track structure model to recent data with heavy ion beams irradiating biological samples of E. Coli, B. Subtilis spores, and Chinese hamster (V79) cells. Heavy ions have observed cross sections for inactivation that approach and sometimes exceed the geometric size of the cell nucleus. We show how the effects of inactivation may be taken into account in the evaluation of the mutation cross sections in the track structure model through correlation of sites for gene mutation and cell inactivation. The model is fit to available data for HPRT (hypoxanthine guanine phosphoribosyl transferase) mutations in V79 cells, and good agreement is found. Calculations show the high probability for mutation by relativistic ions due to the radial extension of ions track from delta rays. The effects of inactivation on mutation rates make it very unlikely that a single parameter such as LET (linear energy transfer) can be used to specify radiation quality for heavy ion bombardment

Calculation of Heavy Ion Inactivation and Mutation Rates in Radial Dose Model of Track Structure

In the track structure model, the inactivation cross section is found by summing an inactivation probability over all impact parameters from the ion to the sensitive sites within the cell nucleus. The inactivation probability is evaluated by using the dose response of the system to gamma rays and the radial dose of the ions and may be equal to unity at small impact parameters. We apply the track structure model to recent data with heavy ion beams irradiating biological samples of E. Coli, Bacillus Subtilis spores, and Chinese hamster (V79) cells. Heavy ions have observed cross sections for inactivation that approach and sometimes exceed the geometric size of the cell nucleus in mammalian cells. We show how the effects of inactivation may be taken into account in the evaluation of the mutation cross sections from heavy ions in the track structure model through correlation of sites for gene mutation and cell inactivation. The model is fit to available data for HPRT (hypoxanthine guanine phosphoribosyl transferase) mutations in Chinese hamster cells, and good agreement is found. The resulting calculations qualitatively show that mutation cross sections for heavy ions display minima at velocities where inactivation cross sections display maxima. Also, calculations show the high probability for mutation by relativistic ions due to the radial extension of the ion track from delta rays in agreement with the microlesion concept. The effects of inactivation on mutation rates make it very unlikely that a single parameter such as LET (linear energy transfer) or Z*2/ β2&#;(where Z*is effective charge number and β is ion velocity) can be used to specify radiation quality for heavy ion bombardment

Automation of PCXMC and ImPACT for NASA Astronaut Medical Imaging Dose and Risk Tracking

To automate astronaut organ and effective dose calculations from occupational X-ray and computed tomography (CT) examinations incorporating PCXMC and ImPACT tools and to estimate the associated lifetime cancer risk per the National Council on Radiation Protection & Measurements (NCRP) using MATLAB(R). Methods: NASA follows guidance from the NCRP on its operational radiation safety program for astronauts. NCRP Report 142 recommends that astronauts be informed of the cancer risks from reported exposures to ionizing radiation from medical imaging. MATLAB(R) code was written to retrieve exam parameters for medical imaging procedures from a NASA database, calculate associated dose and risk, and return results to the database, using the Microsoft .NET Framework. This code interfaces with the PCXMC executable and emulates the ImPACT Excel spreadsheet to calculate organ doses from X-rays and CTs, respectively, eliminating the need to utilize the PCXMC graphical user interface (except for a few special cases) and the ImPACT spreadsheet. Results: Using MATLAB(R) code to interface with PCXMC and replicate ImPACT dose calculation allowed for rapid evaluation of multiple medical imaging exams. The user inputs the exam parameter data into the database and runs the code. Based on the imaging modality and input parameters, the organ doses are calculated. Output files are created for record, and organ doses, effective dose, and cancer risks associated with each exam are written to the database. Annual and post-flight exposure reports, which are used by the flight surgeon to brief the astronaut, are generated from the database. Conclusions: Automating PCXMC and ImPACT for evaluation of NASA astronaut medical imaging radiation procedures allowed for a traceable and rapid method for tracking projected cancer risks associated with over 12,000 exposures. This code will be used to evaluate future medical radiation exposures, and can easily be modified to accommodate changes to the risk calculation procedure

Differences in the Tumor Microenvironment between African-American and European-American Breast Cancer Patients

Background: African-American breast cancer patients experience higher mortality rates than European-American patients despite having a lower incidence of the disease. We tested the hypothesis that intrinsic differences in the tumor biology may contribute to this cancer health disparity. Methods and Results: Using laser capture microdissection, we examined genome-wide mRNA expression specific to tumor epithelium and tumor stroma in 18 African-American and 17 European-American patients. Numerous genes were differentially expressed between these two patient groups and a two-gene signature in the tumor epithelium distinguished between them. To identify the biological processes in tumors that are different by race/ethnicity, Gene Ontology and disease association analyses were performed. Several biological processes were identified which may contribute to enhanced disease aggressiveness in African-American patients, including angiogenesis and chemotaxis. African-American tumors also contained a prominent interferon signature. The role of angiogenesis in the tumor biology of African-American

Science Fiction Studies 102. Volume 34, Part 2: Special 'Afrofuturism' issue

Mark Bould and Rone Shavers edited this special issue of the journal Fiction Studies, devoted to afrofuturism and black sf

Time-integrated radiation risk metrics and interpopulation variability of survival

Task Group 115 of the International Commission on Radiological Protection is focusing on mission-related exposures to space radiation and concomitant health risks for space crew members including, among others, risk of cancer development. Uncertainties in cumulative radiation risk estimates come from the stochastic nature of the considered health outcome (i.e., cancer), uncertainties of statistical inference and model parameters, unknown secular trends used for projections of population statistics and unknown variability of survival properties between individuals or population groups. The variability of survival is usually ignored when dealing with large groups, which can be assumed well represented by the statistical data for the contemporary general population, either in a specific country or world averaged. Space crew members differ in many aspects from individuals represented by the general population, including, for example, their lifestyle and health status, nutrition, medical care, training and education. The individuality of response to radiation and lifespan is explored in this modelling study. Task Group 115 is currently evaluating applicability and robustness of various risk metrics for quantification of radiation-attributed risks of cancer for space crew members. This paper demonstrates the impact of interpopulation variability of survival curves on values and uncertainty of the estimates of the time-integrated radiation risk of cancer