Sulfur Amino Acid Supplementation Abrogates Protective Effects of Caloric Restriction for Enhancing Bone Marrow Regrowth Following Ionizing Radiation.

Radiation therapy damages and depletes total bone marrow (BM) cellularity, compromising safety and limiting effective dosing. Aging also strains total BM and BM hematopoietic stem and progenitor cell (HSPC) renewal and function, resulting in multi-system defects. Interventions that preserve BM and BM HSPC homeostasis thus have potential clinical significance. Here, we report that 50% calorie restriction (CR) for 7-days or fasting for 3-days prior to irradiation improved mouse BM regrowth in the days and weeks post irradiation. Specifically, one week of 50% CR ameliorated loss of total BM cellularity post irradiation compared to ad libitum-fed controls. CR-mediated BM protection was abrogated by dietary sulfur amino acid (i.e., cysteine, methionine) supplementation or pharmacological inhibition of sulfur amino acid metabolizing and hydrogen sulfide (H <sub>2</sub> S) producing enzymes. Up to 2-fold increased proliferative capacity of ex vivo-irradiated BM isolated from food restricted mice relative to control mice indicates cell autonomy of the protective effect. Pretreatment with H <sub>2</sub> S in vitro was sufficient to preserve proliferative capacity by over 50% compared to non-treated cells in ex vivo-irradiated BM and BM HSPCs. The exogenous addition of H <sub>2</sub> S inhibited Ten eleven translocation 2 (TET2) activity in vitro, thus providing a potential mechanism of action. Short-term CR or fasting therefore offers BM radioprotection and promotes regrowth in part via altered sulfur amino acid metabolism and H <sub>2</sub> S generation, with translational implications for radiation treatment and aging

Mapping Bathymetry and Depositional Facies on Great Bahama Bank

Satellite imagery and an extensive set of water-depth measurements have been used to map and critically evaluate the magnitude and patterns of bathymetry across Great Bahama Bank. Descriptions of previously collected sediment samples were combined with satellite imagery to map and refine the interpreted distribution of surficial carbonate sediments (depositional facies). Data reveal that 60% of Great Bahama Bank lies in 5 m or less of water. The deep portion occurs mainly in a generally east–west trending area in the southern portion of the platform. The re-evaluation of the facies reveals that Great Bahama Bank is essentially a very grainy platform with muddier accumulations primarily in the lee of Andros Island. This area of Great Bahama Bank also experiences currents related to an excursion of the Florida Current onto the platform top; possibly enhancing sediment mud production through the generation of whitings. Sediment equivalents to mudstones, wackestones and mud-rich packstones cover 8%, 5% and 14%, respectively, of the platform top, whereas sediment equivalents to mud-poor packstones, grainstones and rudstones account for 20%, 45% and 3% of the surface area. Boundstones (reefs) were not specifically mapped in this study due to the resolution of the mapping. There is a poor relationship between the occurrence of the depositional texture and water depth, in that the grainier sediment types are abundant across the full range of water depths. The most abrupt lateral facies changes portrayed on the facies maps are observed leeward of islands, areas which also hold the highest diversity in facies type. The majority of the islands on the platform align with the north-west/south-east strike of the platform margin and these islands, in turn, exert control on the shape and orientation of facies belts that develop in proximity to them. For this reason, regions of the platform that contain principal islands host facies belts that align with the principal axis of the platform, whereas for regions lacking islands, the facies belts adopt an east–west trend consistent with prevailing winds and currents. There is a clear trend that the wide southern portion of the platform hosts the most continuous expanses of grain-rich sediments

Subarachnoid CSF hyperintensities at 7 tesla FLAIR MRI: A novel marker in cerebral amyloid angiopathy

Background: We observed subarachnoid cerebrospinal fluid (CSF) hyperintensities at non-contrast 7-tesla (T) fluid-attenuated inversion recovery (FLAIR) MRI, frequently topographically associated with cortical superficial siderosis (cSS), in participants with cerebral amyloid angiopathy (CAA). To systemically evaluate these CSF hyperintensities we investigated their frequency and anatomical and temporal relationship with cSS on 7T and 3T MRI in hereditary Dutch-type CAA (D-CAA), sporadic CAA (sCAA), and non-CAA controls. Methods: CAA participants were included from two prospective natural history studies and non-CAA controls from a 7T study in healthy females and females with ischemic stroke. CSF hyperintensities were scored by two independent observers. Results: We included 38 sCAA participants (mean age 72y), 50 D-CAA participants (mean age 50y) and 44 non-CAA controls (mean age 53y, 15 with stroke). In total 27/38 (71 %, 95 %CI 56–84) sCAA and 23/50 (46 %, 95 %CI 33–60) D-CAA participants had subarachnoid CSF hyperintensities at baseline 7T. Most (96 %) of those had cSS, in 54 % there was complete topographical overlap with cSS. The remaining 46 % had ≥1 sulcus with CSF hyperintensities without co-localizing cSS. None of the healthy controls and 2/15 (13 %, 95 %CI 2–41, 100 % cSS overlap) of the stroke controls had CSF hyperintensities. In 85 % of the CAA participants CSF hyperintensities could retrospectively be identified at 3T. Of the 35 CAA participants with follow-up 7T after two years, 17/35 (49 %) showed increase and 6/35 (17 %) decrease of regional CSF hyperintensities. In 2/11 (18 %) of participants with follow-up who had baseline CSF hyperintensities without overlapping cSS, new cSS developed at those locations. Conclusions: Subarachnoid CSF hyperintensities at 7T FLAIR MRI occur frequently in CAA and are associated with cSS, although without complete overlap. We hypothesize that the phenomenon could be a sign of subtle plasma protein or blood product leakage into the CSF, resulting in CSF T1-shortening