Oxygen: the universal currency on coral reefs

Coral Reefs - Coral reefs are suffering unprecedented declines worldwide. Most studies focus on stressors such as rising temperatures, nutrient pollution, overfishing, and ocean acidification as...     

Focus: The Science of Stress: The Impact of Maternal Antioxidants on Prenatal Stress Effects on Offspring Neurobiology and Behavior

Prenatal stress is a neuropsychiatric risk factor, and effects may be mediated by prenatal oxidative stress. Cell types in the brain sensitive to oxidative stress—cortical microglia and cortical and hippocampal interneurons—may be altered by oxidative stress generated during prenatal stress and may be neurobiological substrates for altered behavior. Our objective was to determine the critical nature of oxidative stress in prenatal stress effects by manipulating prenatal antioxidants. CD1 mouse dams underwent restraint embryonic day 12 to 18 three times daily or no stress and received intraperitoneal injections before each stress period of vehicle, N-acetylcysteine (200 mg/kg daily), or astaxanthin (30 mg/kg before first daily stress, 10 mg/kg before second/third stresses). Adult male and female offspring behavior, microglia, and interneurons were assessed. Results supported the hypothesis that prenatal stress-induced oxidative stress affects microglia; microglia ramification increased after prenatal stress, and both antioxidants prevented these effects. In addition, N-acetylcysteine or astaxanthin was effective in preventing distinct male and female interneuron changes; decreased female medial frontal cortical parvalbumin interneurons was prevented by either antioxidant; increased male medial frontal cortical parvalbumin interneurons was prevented by N-acetylcysteine and decreased male hippocampal GAD67GFP+ cells prevented by astaxanthin. Prenatal stress-induced increased anxiety-like behavior and decreased sociability were not prevented by prenatal antioxidants. Sensorimotor gating deficits in males was partially prevented by prenatal astaxanthin. This study demonstrates the importance of oxidative stress for persistent impacts on offspring cortical microglia and interneurons, but did not link these changes with anxiety-like, social, and sensorimotor gating behaviors.     

Health care cost of crusted scabies in Aboriginal communities in the Northern Territory,Australia

BackgroundCrusted scabies is a debilitating dermatological condition. Although still relatively rare in the urban areas of Australia, rates of crusted scabies in remote Aboriginal communities in the Northern Territory (NT) are reported to be among the highest in the world.ObjectiveTo estimate the health system costs associated with diagnosing, treating and managing crusted scabies.MethodsA disease pathway model was developed to identify the major phases of managing crusted scabies. In recognition of the higher resource use required to treat more severe cases, the pathway differentiates between crusted scabies severity grades. The disease pathway model was populated with data from a clinical audit of 42 crusted scabies patients diagnosed in the Top-End of Australia’s Northern Territory between July 1, 2016 and May 1, 2018. These data were combined with standard Australian unit costs to calculate the expected costs per patient over a 12-month period, as well as the overall population cost for treating crusted scabies.FindingsThe expected health care cost per patient diagnosed with crusted scabies is $35,418 Australian dollars (AUD) (95% CI: $27,000 to $43,800), resulting in an overall cost of $1,558,392AUD (95% CI: $1,188,000 to $1,927,200) for managing all patients diagnosed in the Northern Territory in a given year (2018). By far, the biggest component of the health care costs falls on the hospital system.DiscussionThis is the first cost-of-illness analysis for treating crusted scabies. Such analysis will be of value to policy makers and researchers by informing future evaluations of crusted scabies prevention programs and resource allocation decisions. Further research is needed on the wider costs of crusted scabies including non-financial impacts such as the loss in quality of life as well as the burden of care and loss of well-being for patients, families and communities.     

Individual small in‐stream barriers contribute little to strong local population genetic structure five strictly aquatic macroinvertebrate taxa

Water flow in river networks is frequently regulated by man‐made in‐stream barriers. These obstacles can hinder dispersal of aquatic organisms and isolate populations leading to the loss of genetic diversity. Although millions of small in‐stream barriers exist worldwide, their impact on dispersal of macroinvertebrates remains unclear. Therefore, we, therefore, assessed the effects of such barriers on the population structure and effective dispersal of five macroinvertebrate species with strictly aquatic life cycles: the amphipod crustacean Gammarus fossarum (clade 11), three snail species of the Ancylus fluviatilis species complex and the flatworm Dugesia gonocephala. We studied populations at nine weirs and eight culverts (3 pipes, 5 tunnels), built 33–109 years ago, mainly in the heavily fragmented catchment of the river Ruhr (Sauerland, Germany). To assess fragmentation and barrier effects, we generated genome‐wide SNP data using ddRAD sequencing and evaluated clustering, differentiation between populations up‐ and downstream of each barrier and effective migration rates among sites and across barriers. Additionally, we applied population genomic simulations to assess expected differentiation patterns under different gene flow scenarios. Our data show that populations of all species are highly isolated at regional and local scales within few kilometers. While the regional population structure likely results from historical processes, the strong local differentiation suggests that contemporary dispersal barriers exist. However, we identified significant barrier effects only for pipes (for A. fluviatilis II and III) and few larger weirs (>1.3 m; for D. gonocephala). Therefore, our data suggest that most small in‐stream barriers can probably be overcome by all studied taxa frequently enough to prevent fragmentation. However, it remains to be tested if the strong local differentiation is a result of a cumulative effect of small barriers, or if larger in‐stream barriers, land use, chemical pollution, urbanization, or a combination of these factors impede gene flow.     

Viral protein instability enhances host-range evolvability

Viruses are highly evolvable, but what traits endow this property? The high mutation rates of viruses certainly play a role, but factors that act above the genetic code, like protein thermostability, are also expected to contribute. We studied how the thermostability of a model virus, bacteriophage λ, affects its ability to evolve to use a new receptor, a key evolutionary transition that can cause host-range evolution. Using directed evolution and synthetic biology techniques we generated a library of host-recognition protein variants with altered stabilities and then tested their capacity to evolve to use a new receptor. Variants fell within three stability classes: stable, unstable, and catastrophically unstable. The most evolvable were the two unstable variants, whereas seven of eight stable variants were significantly less evolvable, and the two catastrophically unstable variants could not grow. The slowly evolving stable variants were delayed because they required an additional destabilizing mutation. These results are particularly noteworthy because they contradict a widely supported contention that thermostabilizing mutations enhance evolvability of proteins by increasing mutational robustness. Our work suggests that the relationship between thermostability and evolvability is more complex than previously thought, provides evidence for a new molecular model of host-range expansion evolution, and identifies instability as a potential predictor of viral host-range evolution.