Description: The Cosmic Ray Telescope for the Effects of Radiation (CRaTER) measures linear energy transfer by Galactic Cosmic Rays (GCRs) and Solar Energetic Particles (SEPs) on the Lunar Reconnaissance Orbiter (LRO) Mission in a circular, polar lunar orbit. GCR fluxes remain at the highest levels ever observed during the space age. One of the largest SEP events observed by CRaTER during the LRO mission occurred on June 7, 2011. We compare model predictions by the Earth-Moon-Mars Radiation Environment Module (EMMREM) for both dose rates from GCRs and SEPs during this event with results from CRaTER. We find agreement between these models and the CRaTER dose rates, which together demonstrate the accuracy of EMMREM, and its suitability for a real-time space weather system. We utilize CRaTER to test forecasts made by the Relativistic Electron Alert System for Exploration (REleASE), which successfully predicts the June 7th event. At the maximum CRaTER-observed GCR dose rate (∼11.7 cGy/yr where Gy is a unit indicating energy deposition per unit mass, 1 Gy = 1 J/kg), GCRs deposit ∼88 eV/molecule in water over 4 billion years, causing significant change in molecular composition and physical structure (e.g., density, color, crystallinity) of water ice, loss of molecular hydrogen, and production of more complex molecules linking carbon and other elements in the irradiated ice. This shows that space weathering by GCRs may be extremely important for chemical evolution of ice on the Moon. Thus, we show comprehensive observations from the CRaTER instrument on the Lunar Reconnaissance Orbiter that characterizes the radiation environment and space weathering on the Moon.

Description: Fetal growth restriction (FGR) is the inability of a fetus to reach its genetically predetermined growth potential. In the absence of a genetic anomaly or maternal undernutrition, FGR is attributable to "placental insufficiency": inappropriate maternal/fetal blood flow, reduced nutrient transport or morphological abnormalities of the placenta (e.g., altered barrier thickness). It is not known whether these diverse factors act singly, or in combination, having additive effects that may lead to greater FGR severity. We suggest that multiplicity of such dysfunction might underlie the diverse FGR phenotypes seen in humans. Pregnant endothelial nitric oxide synthase knockout (eNOS –/– ) dams exhibit dysregulated vascular adaptations to pregnancy, and eNOS –/– fetuses of such dams display FGR. We investigated the hypothesis that both altered vascular function and placental nutrient transport contribute to the FGR phenotype. eNOS –/– dams were hypertensive prior to and during pregnancy and at embryonic day (E) 18.5 were proteinuric. Isolated uterine artery constriction was significantly increased, and endothelium-dependent relaxation significantly reduced, compared with wild-type (WT) mice. eNOS –/– fetal weight and abdominal circumference were significantly reduced compared with WT. Unidirectional maternofetal 14 C-methylaminoisobutyric acid (MeAIB) clearance and sodium-dependent 14 C-MeAIB uptake into mouse placental vesicles were both significantly lower in eNOS –/– fetuses, indicating diminished placental nutrient transport. eNOS –/– mouse placentas demonstrated increased hypoxia at E17.5, with elevated superoxide compared with WT. We propose that aberrant uterine artery reactivity in eNOS –/– mice promotes placental hypoxia with free radical formation, reducing placental nutrient transport capacity and fetal growth. We further postulate that this mouse model demonstrates "uteroplacental hypoxia," providing a new framework for understanding the etiology of FGR in human pregnancy.