Conservation Genetics of North Island Kōkako (Callaeas wilsoni)

Conservation genetics has recently been recognised as an important, although often overlooked, aspect of wildlife management. Applying molecular techniques and genetic concepts to management strategies has the potential to significantly improve current and future recovery efforts. Wildlife translocations are often used for threatened species management in New Zealand, in which the selection of appropriate source populations is an important decision. North Island kōkako (Callaeas wilsoni) are an endemic, threatened songbird distributed across 24 relict and translocated populations in the North Island of New Zealand. Translocations have significantly influenced kōkako recovery. As such, kōkako are one of the most commonly translocated species in New Zealand. Integrating genetic techniques and recommendations into source population selection will help ensure the long-term success of future translocation projects. Te Hauturu-o-Toi is currently the largest population of kōkako but is thought to have been established by a founding population of as few as nine individuals. The aim of this research was to assess the suitability of the Hauturu kōkako population as a future source for translocations using molecular methods. In particular, the aim was to address two aspects of a source population that contribute to the overall success of a translocation; genetic diversity and disease status. To do so, the level of genetic variation across six populations and the presence of Psittacine Beak and Feather Disease on Hauturu was examined. Such research provides conservation managers with important genetic information that can be applied to best protect kōkako in future. Conserving genetic diversity is important for long-term survival of endangered species. As translocations involve a small number of individuals and create a genetic bottleneck, sourcing founder birds from genetically diverse populations helps ensure long-term translocation success. I developed 21 kōkako-specific microsatellite primers using a whole kōkako genome, that were then multiplexed to infer genetic diversity and population structure in one translocated (Hauturu) and five relict (Mapara, Mangatutu, Te Urewera, Waipapa and Bay of Plenty) kōkako populations. A similar level of genetic diversity was apparent across all populations, providing evidence to support the use of Hauturu as a source for future translocations. Both multivariate and Bayesian methods recognised a clear population structure (K=3), identifying kōkako from Hauturu and Mapara as genetically distinct from the other four sites. Understanding the differentiation between kōkako populations will allow managers to plan translocations that maximise genetic diversity and hence translocation success. Disease risk and spread has the potential to induce a translocation failure. A kōkako on Hauturu developed aberrant coloured plumage and features (claws, legs, beak) between sampling seasons (2013–2015), reminiscent of Psittacine Beak and Feather Disease (PBFD). PBFD typically infects psittacine species, but due to high recombination rates can host-switch for infection in non-psittacine species. The Hauturu population was screened for PBFD using polymerase chain reaction, with all individuals (n=31) testing negative. There is no evidence for a host switching event from red-crowned parakeets (Cyanoramphus novaezelandiae) on Hauturu into kōkako, therefore, a translocation from Hauturu is unlikely to facilitate PBFD spread. Following this result, the melanocortin-1 receptor (MC1R) gene was amplified as an alternative explanation, looking for sequence variants between the before (normal), after (aberrant) and seven normal kōkako (also from Hauturu). The MC1R gene was selected as it has a pleiotropic role in regulating both melanin deposition and physiological stress responses. No mutational differences were found, and it is recommended that future research includes screening of alternative candidate genes or explores epigenetic mechanisms to provide an explanation for the observed phenotype

Risk of Mortality (including Sudden Cardiac Death) and Major Cardiovascular Events in Users of Olanzapine and Other Antipsychotics: A Study with the General Practice Research Database.

Objective. Assess risk of cardiac events and mortality among users of olanzapine and other antipsychotics relative to nonusers. Methods. The General Practice Research Database was used to identify cohorts of antipsychotic users and nonusers with psychiatric illness. Outcomes included cardiac mortality, sudden cardiac death (SCD), all-cause mortality (excluding suicide), coronary heart disease (CHD), and ventricular arrhythmias (VA). Results. 183,392 antipsychotic users (including 20,954 olanzapine users) and 193,920 psychiatric nonusers were identified. There was a significantly higher rate of cardiac mortality (adjusted RR [aRR]: 1.53, CI, 1.12-2.09) in olanzapine users relative to psychiatric nonusers, consistent with findings for both atypical and typical antipsychotics. Relative to psychiatric nonusers, no increased risk of all-cause mortality was observed among olanzapine users (aRR: 1.04, CI, 0.93-1.17), but elevated all-cause mortality risk was observed when compared to all antipsychotic users (aRR: 1.75, CI, 1.64-1.87). There was no increased risk of CHD or VA among olanzapine users relative to psychiatric nonusers, consistent with findings for atypical but not typical antipsychotics. SCD cases were uncommon. Conclusions. Use of antipsychotic agents was associated with increased risk of all-cause and cardiac mortality. Patients treated with olanzapine were found to be at increased risk of cardiac mortality versus psychiatric nonusers

Interleukin-1 signaling in the basolateral amygdala is necessary for heroin-conditioned immunosuppression

Heroin administration suppresses the production of inducible nitric oxide (NO), as indicated by changes in splenic inducible nitric oxide synthase (iNOS) and plasma nitrate/nitrite. Since NO is a measure of host defense against infection and disease, this provides evidence that heroin can increase susceptibility to pathogens by directly interacting with the immune system. Previous research in our laboratory has demonstrated that these immunosuppressive effects of heroin can also be conditioned to environmental stimuli by repeatedly pairing heroin administration with a unique environmental context. Re-exposure to a previously drug-paired context elicits immunosuppressive effects similar to heroin administration alone. In addition, our laboratory has reported that the basolateral amygdala (BLA) and medial nucleus accumbens shell (mNAcS) are critical neural substrates that mediate this conditioned effect. However, our understanding of the contributing mechanisms within these brain regions is limited. It is known that the cytokine interleukin-1 (IL-1) plays an important role in learning and memory. In fact, our laboratory has demonstrated that inhibition of IL-1β expression in the dorsal hippocampus (DH) prior to reexposure to a heroin-paired context prevents the suppression of measures of NO production. Therefore, the present studies sought to further investigate the role of IL-1 in heroin-conditioned immunosuppression. Blockade of IL-1 signaling in the BLA, but not in the caudate putamen or mNAcS, using IL-1 receptor antagonist (IL-1Ra) attenuated heroin-conditioned immunosuppression of NO production as measured by plasma nitrate/nitrite and iNOS mRNA expression in spleen tissue. Taken together, these findings suggest that IL-1 signaling in the BLA is necessary for the expression of heroin-conditioned immunosuppression of NO production and may be a target for interventions that normalize immune function in heroin users and patient populations exposed to opiate regimens

Acquisition of heroin conditioned immunosuppression requires IL-1 signaling in the dorsal hippocampus

Opioid users experience increased incidence of infection, which may be partially attributable to both direct opiate-immune interactions and conditioned immune responses. Previous studies have investigated the neural circuitry governing opioid conditioned immune responses, but work remains to elucidate the mechanisms mediating this effect. Our laboratory has previously shown that hippocampal IL-1 signaling, specifically, is required for the expression of heroin conditioned immunosuppression following learning. The current studies were designed to further characterize the role of hippocampal IL-1 in this phenomenon by manipulating IL-1 during learning. Experiment 1 tested whether hippocampal IL-1 is also required for the acquisition of heroin conditioned immunosuppression, while Experiment 2 tested whether hippocampal IL-1 is required for the expression of unconditioned heroin immunosuppression. We found that blocking IL-1 signaling in the dorsal hippocampus with IL-1RA during each conditioning session, but not on interspersed non-conditioning days, significantly attenuated the acquisition of heroin conditioned immunosuppression. Strikingly, we found that the same IL-1RA treatment did not alter unconditioned immunosuppression to a single dose of heroin. Thus, IL-1 signaling is not a critical component of the response to heroin but rather may play a role in the formation of the association between heroin and the context. Collectively, these studies suggest that IL-1 signaling, in addition to being involved in the expression of a heroin conditioned immune response, is also involved in the acquisition of this effect. Importantly, this effect is likely not due to blocking the response to the unconditioned stimulus since IL-1RA did not affect heroin’s immunosuppressive effects

Risk of mortality (including sudden cardiac death) and major cardiovascular events in atypical and typical antipsychotic users: a study with the general practice research database.

Objective. Antipsychotics have been associated with increased cardiac events including mortality. This study assessed cardiac events including mortality among antipsychotic users relative to nonusers. Methods. The General Practice Research Database (GPRD) was used to identify antipsychotic users, matched general population controls, and psychiatric diseased nonusers. Outcomes included cardiac mortality, sudden cardiac death (SCD), all-cause mortality (excluding suicide), coronary heart disease (CHD), and ventricular arrhythmias (VA). Sensitivity analyses were conducted for age, dose, duration, antipsychotic type, and psychiatric disease. Results. 183,392 antipsychotic users (115,491 typical and 67,901 atypical), 544,726 general population controls, and 193,920 psychiatric nonusers were identified. Nonusers with schizophrenia, dementia, or bipolar disorder had increased risks of all-cause mortality compared to general population controls, while nonusers with major depression had comparable risks. Relative to psychiatric nonusers, the adjusted relative ratios (aRR) of all-cause mortality in antipsychotic users was 1.75 (95% CI: 1.64-1.87); cardiac mortality 1.72 (95% CI: 1.42-2.07); SCD primary definition 5.76 (95% CI: 2.90-11.45); SCD secondary definition 2.15 (95% CI: 1.64-2.81); CHD 1.16 (95% CI: 0.94-1.44); and VA 1.16 (95% CI: 1.02-1.31). aRRs of the various outcomes were lower for atypical versus typical antipsychotics (all-cause mortality 0.83 (95% CI: 0.80-0.85); cardiac mortality 0.89 (95% CI: 0.82-0.97); and SCD secondary definition 0.76 (95% CI: 0.55-1.04). Conclusions. Antipsychotic users had an increased risk of cardiac mortality, all-cause mortality, and SCD compared to a psychiatric nonuser cohort

The Role of Brain Interleukin-1 in Stress-Enhanced Fear Learning

Posttraumatic stress disorder (PTSD) has been shown to be associated with pro-inflammatory markers, including elevated plasma levels of interleukin-1β (IL-1β). However, the precise role of neuroinflammation and central immune signaling on the development of this debilitating psychological disorder is not known. Here, we used stress-enhanced fear learning (SEFL), an animal model of the disorder, to examine the role of central IL-1β in PTSD. The results show that the severe stressor in SEFL induces a time-dependent increase in IL-1β immunoreactivity and mRNA expression within the dentate gyrus of the dorsal hippocampus (DH). There was no increase in IL-1β in the basolateral amygdala or the perirhinal cortex. Moreover, blocking the action of IL-1β following the severe stressor with IL-1 receptor antagonist (10 μg, intracerebroventricular (i.c.v.), 24 and 48 h after the stressor) prevented the development of SEFL. To provide further support for the role of IL-1β in the development of SEFL, we show that systemic morphine, a treatment which is known to reduce both PTSD and SEFL, also reduces IL-1β expression in the DH induced by the severe stressor. These studies provide the first evidence that IL-1 is involved SEFL and suggest that IL-1 signaling in the brain may have a critical role in the development of PTSD

Root microbiota drive direct integration of phosphate stress and immunity

Plants live in biogeochemically diverse soils that harbor extraordinarily diverse microbiota. Plant organs associate intimately with a subset of these microbes; this community’s structure can be altered by soil nutrient content. Plant-associated microbes can compete with the plant and with each other for nutrients; they can also provide traits that increase plant productivity. It is unknown how the plant immune system coordinates microbial recognition with nutritional cues during microbiome assembly. We establish that a genetic network controlling phosphate stress response influences root microbiome community structure, even under non-stress phosphate conditions. We define a molecular mechanism regulating coordination between nutrition and defense in the presence of a synthetic bacterial community. We demonstrate that the master transcriptional regulators of phosphate stress response in Arabidopsis also directly repress defense, consistent with plant prioritization of nutritional stress over defense. Our work will impact efforts to define and deploy useful microbes to enhance plant performance

Design of synthetic bacterial communities for predictable plant phenotypes

Specific members of complex microbiota can influence host phenotypes, depending on both the abiotic environment and the presence of other microorganisms. Therefore, it is challenging to define bacterial combinations that have predictable host phenotypic outputs. We demonstrate that plant-bacterium binary-association assays inform the design of small synthetic communities with predictable phenotypes in the host. Specifically, we constructed synthetic communities that modified phosphate accumulation in the shoot and induced phosphate starvation-responsive genes in a predictable fashion. We found that bacterial colonization of the plant is not a predictor of the plant phenotypes we analyzed. Finally, we demonstrated that characterizing a subset of all possible bacterial synthetic communities is sufficient to predict the outcome of untested bacterial consortia. Our results demonstrate that it is possible to infer causal relationships between microbiota membership and host phenotypes and to use these inferences to rationally design novel communitie

The largest deep-ocean silicic volcanic eruption of the past century

© The Author(s), 2018. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Science Advances 4 (2018): e1701121, doi:10.1126/sciadv.1701121.The 2012 submarine eruption of Havre volcano in the Kermadec arc, New Zealand, is the largest deep-ocean eruption in history and one of very few recorded submarine eruptions involving rhyolite magma. It was recognized from a gigantic 400-km2 pumice raft seen in satellite imagery, but the complexity of this event was concealed beneath the sea surface. Mapping, observations, and sampling by submersibles have provided an exceptionally high fidelity record of the seafloor products, which included lava sourced from 14 vents at water depths of 900 to 1220 m, and fragmental deposits including giant pumice clasts up to 9 m in diameter. Most (>75%) of the total erupted volume was partitioned into the pumice raft and transported far from the volcano. The geological record on submarine volcanic edifices in volcanic arcs does not faithfully archive eruption size or magma production.This research was funded by Australian Research Council Postdoctoral fellowships (DP110102196 and DE150101190 to R. Carey), a short-term postdoctoral fellowship grant from the Japan Society for the Promotion of Science (to R. Carey), National Science Foundation grants (OCE1357443 to B.H., OCE1357216 to S.A.S., and EAR1447559 to J.D.L.W.), and a New Zealand Marsden grant (U001616 to J.D.L.W.). J.D.L.W. and A.M. were supported by a research grant and PhD scholarship from the University of Otago. R.W. was supported by NIWA grant COPR1802. J.D.L.W. and F.C.-T. were supported by GNS Science grants CSA-GHZ and CSA-EEZ. M.J. was supported by the U.S. Department of Defense (DoD) through the National Defense Science and Engineering Graduate Fellowship (NDSEG) Program

Autonomous Seawater \u3ci\u3ep\u3c/i\u3eCO\u3csub\u3e2\u3c/sub\u3e and pH Time Series From 40 Surface Buoys and the Emergence of Anthropogenic Trends

Ship-based time series, some now approaching over 3 decades long, are critical climate records that have dramatically improved our ability to characterize natural and anthropogenic drivers of ocean carbon dioxide (CO2) uptake and biogeochemical processes. Advancements in autonomous marine carbon sensors and technologies over the last 2 decades have led to the expansion of observations at fixed time series sites, thereby improving the capability of characterizing sub-seasonal variability in the ocean. Here , we present a data product of 40 individual autonomous moored surface ocean pCO2 (partial pressure of CO2) time series established between 2004 and 2013, 17 also include autonomous pH measurements. These time series characterie a wide range of surface ocean carbonate conditions in diffferent oceanic (17 sites), coastal (13 sites), and coral reef (10 sites) regimes. A time of trend emergence (ToE) methodology applied ot the time series that exhibit well-constrained daily to interannual variability and an estimate of decadal variability indicates that the length of sustained observations necessary to detect statistically significant anthropogenic trends varies by marine environment. The ToE estisites, and 9 to 22 years at the coral reef sites. Only two open ocean pCO2 and pH range from 8 to 15 years at the open ocean sites, 16 to 41 years at the coastal sites, and 9 to 22 years at the coral reef sites. Only two open ocean pCO2 time series, Woods Hole Oceanographic Institution Hawaii Ocean Time-series Station (WHOTS) in the subtropical North Pacific and Stratus n the South Pacific gyre, have been deployed longer than the estimated trend detection time and, for these, deseasoned monthly means show estimated anthropogenic trends of 1.9 ± 0.3 and 1.6 ± 0.3 μatm yr-1, respectively. In the future, it is possible that updates to this product will allow for the estimation of anthropogenic trends at more sites; however, the product currently provides a valuable tool in an accessible format for evaluating climatology and natural variability of surface ocean carbonate chemistry in a variety of regions. Data are available at https://doi.org/10.7289/V5DB8043 and https://www.nodc.noaa.gov/ocads/oceans/Moorings/ndp097.html (Sutton et al., 2018)