Temperature-nutrient interactions exacerbate sensitivity to warming in phytoplankton.

Temperature and nutrients are fundamental, highly nonlinear drivers of biological processes, but we know little about how they interact to influence growth. This has hampered attempts to model population growth and competition in dynamic environments, which is critical in forecasting species distributions, as well as the diversity and productivity of communities. To address this, we propose a model of population growth that includes a new formulation of the temperature-nutrient interaction and test a novel prediction: that a species' optimum temperature for growth, Topt , is a saturating function of nutrient concentration. We find strong support for this prediction in experiments with a marine diatom, Thalassiosira pseudonana: Topt decreases by 3-6 °C at low nitrogen and phosphorus concentrations. This interaction implies that species are more vulnerable to hot, low-nutrient conditions than previous models accounted for. Consequently the interaction dramatically alters species' range limits in the ocean, projected based on current temperature and nitrate levels as well as those forecast for the future. Ranges are smaller not only than projections based on the individual variables, but also than those using a simpler model of temperature-nutrient interactions. Nutrient deprivation is therefore likely to exacerbate environmental warming's effects on communities.

Visualizing locus-specific sister chromatid exchange reveals differential patterns of replication stress-induced fragile site breakage.

Chromosomal fragile sites are genomic loci sensitive to replication stress which accumulate high levels of DNA damage, and are frequently mutated in cancers. Fragile site damage is thought to arise from the aberrant repair of spontaneous replication stress, however successful fragile site repair cannot be calculated using existing techniques. Here, we report a new assay measuring recombination-mediated repair at endogenous genomic loci by combining a sister chromatid exchange (SCE) assay with fluorescent in situ hybridization (SCE-FISH). Using SCE-FISH, we find that endogenous and exogenous replication stress generated unrepaired breaks and SCEs at fragile sites. We also find that distinct sources of replication stress induce distinct patterns of breakage: ATR inhibition induces more breaks at early replicating fragile sites (ERFS), while ERFS and late-replicating common fragile sites (CFS) are equally fragile in response to aphidicolin. Furthermore, SCEs were suppressed at fragile sites near centromeres in response to replication stress, suggesting that genomic location influences DNA repair pathway choice. SCE-FISH also measured successful recombination in human primary lymphocytes, and identificed the proto-oncogene BCL2 as a replication stress-induced fragile site. These findings demonstrate that SCE-FISH frequency at fragile sites is a sensitive indicator of replication stress, and that large-scale genome organization influences DNA repair pathway choice.

Simulation Use in Acute Care Hospitals in the United States.

Three national nursing associations formed a collaborative partnership to research simulation use in acute care hospitals in the United States and military hospitals abroad. An electronic survey was used to determine simulation modalities used, participants engaged, space allocation, purposes of use, commonly taught skills, logistics, and barriers to use. Data from 521 respondents revealed widespread use of a variety of simulation modalities. However, use of this educational strategy could be expanded to patients and families.