Larval connectivity and water quality explain spatial distribution of crown-of-thorns starfish outbreaks across the Great Barrier Reef.

Outbreaks of the coral eating crown-of-thorns starfish (COTS; Acanthasts cf. solaris) occur in cyclical waves along the Great Barrier Reef (GBR), contributing significantly to the decline in hard coral cover over the past 30 years. One main difficulty faced by scientists and managers alike, is understanding the relative importance of contributing factors to COTS outbreaks such as increased nutrients and water quality, larval connectivity, fishing pressure, and abiotic conditions. We analysed COTS abundances from the most recent outbreak (2010-2018) using both boosted regression trees and generalised additive models to identify key predictors of COTS outbreaks. We used this approach to predict the suitability of each reef on the GBR for COTS outbreaks at three different levels: (1) reefs with COTS present intermittently (Presence); (2) reefs with COTS widespread and present in most samples and (Prevalence) (3) reefs experiencing outbreak levels of COTS (Outbreak). We also compared the utility of two auto-covariates accounting for spatial autocorrelation among observations, built using weighted inverse distance and weighted larval connectivity to reefs supporting COTS populations, respectively. Boosted regression trees (BRT) and generalised additive mixed models (GAMM) were combined in an ensemble model to reduce the effect of model uncertainty on predictions of COTS presence, prevalence and outbreaks. Our results from best performing models indicate that temperature (Degree Heating Week exposure: relative importance=13.1%) and flood plume exposure (13.0%) are the best predictors of COTS presence, variability in chlorophyll concentration (12.6%) and flood plume exposure (8.2%) best predicted COTS prevalence and larval connectivity potential (22.7%) and minimum sea surface temperature (8.0%) are the best predictors of COTS outbreaks. Whether the reef was open or closed to fishing, however, had no significant effect on either COTS presence, prevalence or outbreaks in BRT results (<0.5%). We identified major hotspots of COTS activity primarily on the mid shelf central GBR and on the southern Swains reefs. This study provides the first empirical comparison of the major hypotheses of COTS outbreaks and the first validated predictions of COTS outbreak potential at the GBR scale incorporating connectivity, nutrients, biophysical and spatial variables, providing a useful aid to management of this pest species on the GBR.

COTSMod: A spatially explicit metacommunity model of outbreaks of crown-of-thorns starfish and coral recovery.

Outbreaks of the Pacific crown-of-thorns starfish (COTS; Acanthaster cf. solaris) have been responsible for 40% of the decline in coral cover on the GBR over the last 35 years. With the intensity and frequency of bleaching and cyclonic disturbances increasing, effectively managing these outbreaks may allow reefs an opportunity to recover from these cumulative impacts. Significant research effort has been directed toward developing regional scale models for COTS outbreaks, but these have yet to be fit explicitly to long term time series at the scale of the entire GBR, nor do previous research efforts incorporate explicit estimates of cumulative disturbance history. We developed a stage-based metapopulation model for COTS at a 1×1km resolution using long-term time series and modelled estimates of COTS larval connectivity, nutrient concentrations and important vital rates estimated from the literature. We coupled this metapopulation model to an existing spatially explicit model of coral cover growth, disturbance and recovery across the GBR from 1996 to 2017 to create a metacommunity model. Our results were validated against a spatially and temporally extensive dataset of COTS and coral cover across the GBR, predicting an average coral decline of 1.3% p.a. across the GBR, and accurately recreating coral cover trajectories (mean prediction error=7.1%) and COTS outbreak classification (accuracy=80%). Sensitivity analyses revealed that overall model accuracy was most sensitive to larval predation (boosted regression tree; relative importance=46.7%) and two parameters defining juvenile density dependent mortality (21.5% and 17.5%). The COTS model underestimated peak COTS densities particularly in the Swains and Townsville sectors of the reef, while overestimating COTS density during non-outbreak years. A better understanding of inter-annual variability in larval connectivity, and regionally variable density dependence for adult COTS life stages may improve model fit during these extreme outbreak events. Our model provides a platform to develop upon, and with improvements to estimates of larval connectivity and larval predation could be used to simulate the effects of implementing varying combinations of COTS interventions. This research highlights the importance of the early life history stages of COTS as drivers of outbreak dynamics, emphasizing the need for further empirical research to estimate these parameters.

Current, future and potential use of mobile and wearable technologies and social media data in the ABCD study to increase understanding of contributors to child health.

Mobile and wearable technologies and novel methods of data collection are innovating health-related research. These technologies and methods allow for multi-system level capture of data across environmental, physiological, behavioral, and psychological domains. In the Adolescent Brain Cognitive Development (ABCD) Study, there is great potential for harnessing the acceptability, accessibility, and functionality of mobile and social technologies for in-vivo data capture to precisely measure factors, and interactions between factors, that contribute to childhood and adolescent neurodevelopment and psychosocial and health outcomes. Here we discuss advances in mobile and wearable technologies and methods of analysis of geospatial, ecologic, social network and behavioral data. Incorporating these technologies into the ABCD study will allow for interdisciplinary research on the effects of place, social interactions, environment, and substance use on health and developmental outcomes in children and adolescents.

Observations and Modelling of the Pre-flare Period of the 29 March 2014 X1 Flare.

On 29 March 2014, NOAA Active Region (AR) 12017 produced an X1 flare that was simultaneously observed by an unprecedented number of observatories. We have investigated the pre-flare period of this flare from 14:00 UT until 19:00 UT using joint observations made by the Interface Region Imaging Spectrometer (IRIS) and the Hinode Extreme Ultraviolet Imaging Spectrometer (EIS). Spectral lines providing coverage of the solar atmosphere from the chromosphere to the corona were analysed to investigate pre-flare activity within the AR. The results of the investigation have revealed evidence of strongly blue-shifted plasma flows, with velocities up to 200 km s - 1 , being observed 40 minutes prior to flaring. These flows are located along the filament present in the active region and are both spatially discrete and transient. In order to constrain the possible explanations for this activity, we undertake non-potential magnetic field modelling of the active region. This modelling indicates the existence of a weakly twisted flux rope along the polarity inversion line in the region where a filament and the strong pre-flare flows are observed. We then discuss how these observations relate to the current models of flare triggering. We conclude that the most likely drivers of the observed activity are internal reconnection in the flux rope, early onset of the flare reconnection, or tether-cutting reconnection along the filament.

The Pan-University Network for Global Health: framework for collaboration and review of global health needs.

In the current United Nations efforts to plan for post 2015-Millennium Development Goals, global partnership to address non-communicable diseases (NCDs) has become a critical goal to effectively respond to the complex global challenges of which inequity in health remains a persistent challenge. Building capacity in terms of well-equipped local researchers and service providers is a key to bridging the inequity in global health. Launched by Penn State University in 2014, the Pan University Network for Global Health responds to this need by bridging researchers at more than 10 universities across the globe. In this paper we outline our framework for international and interdisciplinary collaboration, as well the rationale for our research areas, including a review of these two themes. After its initial meeting, the network has established two central thematic priorities: 1) urbanization and health and 2) the intersection of infectious diseases and NCDs. The urban population in the global south will nearly double in 25 years (approx. 2 billion today to over 3.5 billion by 2040). Urban population growth will have a direct impact on global health, and this growth will be burdened with uneven development and the persistence of urban spatial inequality, including health disparities. The NCD burden, which includes conditions such as hypertension, stroke, and diabetes, is outstripping infectious disease in countries in the global south that are considered to be disproportionately burdened by infectious diseases. Addressing these two priorities demands an interdisciplinary and multi-institutional model to stimulate innovation and synergy that will influence the overall framing of research questions as well as the integration and coordination of research.

Results of surgical treatment of colic in miniature breed horses: 11 cases.

OBJECTIVE: To report on the outcome of surgical treatment of acute abdominal crises in miniature breed horses. DESIGN: Retrospective case series of miniature horses presented to the University Veterinary Centre, Camden with an acute abdominal crisis. METHODS: Hospital records of all miniature horses that underwent ventral midline laparotomy for acute abdominal crisis between 1997 and 2001 were reviewed. The signalment, history, clinical signs, results of ancillary diagnostic procedures, location and type of intestinal lesion, treatment and outcome were retrieved from each case record. Long-term survival was determined by telephone interview of owners. RESULTS: Eleven miniature horses including five females and six males underwent ventral midline laparotomies for acute abdominal crisis during the study period. Ages ranged between 1 month and 19 years. Surgical findings included faecalith obstruction (seven horses), enterolith (one horse), strangulating lipoma of the descending colon (one horse), jejunal infarction (one horse), and caecal infarction (one horse). Long-term survival rate (minimum 12 months post surgery) was 55%. Six of eight horses with simple intraluminal obstructions survived, while the three horses with gastrointestinal lesions associated with vascular compromise were euthanased either at surgery (caecal infarction), or postoperatively, due to complications (strangulating lipoma of the descending colon, jejunal infarction). Postoperative complications in this study included impaction of the descending colon (two horses), diarrhoea (two horses), peritonitis (one horse), hyperlipaemia (two horses), incisional infection (two horses) and abdominal adhesions (one horse). Hyperlipidaemia was present in five of seven horses in which serum triglycerides were measured at presentation. CONCLUSIONS: Simple intraluminal obstructions of the large intestine were frequently encountered during exploratory laparotomy in miniature horses presented for acute abdominal crises, and their surgical treatment was associated with a good prognosis. In contrast, this study suggested that abdominal pain associated with vascular compromise of gastrointestinal tissues in miniature horses was associated with a poorer prognosis, consistent with reports in other horse breeds. Possible contributing factors to faecalith formation, including poor quality roughage, dental disease, and inadequate water consumption, should be recognised and avoided in miniature horses. Serum triglyceride concentrations should be measured in miniature horses presented for acute abdominal pain. If elevated, nutritional supplementation should be provided.

Protein kinase D. A selective target for antigen receptors and a downstream target for protein kinase C in lymphocytes.

Protein kinase Cs (PKCs) are activated by antigen receptors in lymphocytes, but little is known about proximal targets for PKCs in antigen receptor-mediated responses. In this report, we define a role for diacylglycerol-regulated PKC isoforms in controlling the activity of the serine/threonine kinase protein kinase D (PKD; also known as PKC mu) in T cells, B cells, and mast cells. Antigen receptor activation of PKD is a rapid and sustained response that can be seen in T cells activated via the T cell antigen receptor, B cells activated via the B cell antigen receptor, and in mast cells triggered via the high-affinity receptor for IgE (FcepsilonR1). Herein, we show that antigen receptor activation of PKD requires the activity of classical/novel PKCs. Moreover, PKC activity is sufficient to bypass the requirement for antigen receptor signals in the induction of PKD activity. These biochemical and genetic studies establish a role for antigen receptor-regulated PKC enzymes in the control of PKD activity. Regulation of PKD activity through upstream PKCs reveals a signaling network that exists between different members of the PKC superfamily of kinases that can operate to amplify and disseminate antigen receptor signals generated at the plasma membrane.

Spatial and temporal regulation of protein kinase D (PKD).

Protein kinase D (PKD; also known as PKCmicro) is a serine/threonine kinase activated by diacylglycerol signalling pathways in a variety of cells. PKD has been described previously as Golgi-localized, but herein we show that it is present within the cytosol of quiescent B cells and mast cells and moves rapidly to the plasma membrane after antigen receptor triggering. The membrane redistribution of PKD requires the diacylglycerol-binding domain of the enzyme, but is independent of its catalytic activity and does not require the integrity of the pleckstrin homology domain. Antigen receptor signalling initiates in glycosphingolipid-enriched microdomains, but membrane-associated PKD does not co-localize with these specialized structures. Membrane targeting of PKD is transient, the enzyme returns to the cytosol within 10 min of antigen receptor engagement. Strikingly, the membrane-recycled PKD remains active in the cytosol for several hours. The present work thus characterizes a sustained antigen receptor-induced signal transduction pathway and establishes PKD as a serine kinase that temporally and spatially disseminates antigen receptor signals away from the plasma membrane into the cytosol.

Characterization of serine 916 as an in vivo autophosphorylation site for protein kinase D/Protein kinase Cmu.

Activation of the serine kinase protein kinase D (PKD)/PKCmicro is controlled by the phosphorylation of two serine residues within its activation loop via a PKC-dependent signaling cascade. In this study we have identified the C-terminal serine 916 residue as an in vivo phosphorylation site within active PKD/PKCmu. An antibody that recognized PKD/PKCmu proteins specifically phosphorylated on the serine 916 residue was generated and used to show that phosphorylation of Ser-916 is induced by phorbol ester treatment of cells. Thus, the pS916 antibody is a useful tool to study the regulation of PKD/PKCmu activity in vivo. Antigen receptor ligation of T and B lymphocytes also induced phosphorylation of the serine 916 residue of PKD/PKCmu. Furthermore the regulatory FcgammaRIIB receptor, which mediates vital negative feedback signals to the B cell antigen receptor complex, inhibited the antigen receptor-induced activation and serine 916 phosphorylation of PKD/PKCmu. The degree of serine 916 phosphorylation during lymphocyte activation and inhibition exactly correlated with the activation status of PKD/PKCmu. Moreover, using different mutants of PKD/PKCmu, we show that serine 916 is not trans-phosphorylated by an upstream kinase but is rather an autophosphorylation event that occurs following activation of PKD/PKCmu.

Bryostatin 1 induces biphasic activation of protein kinase D in intact cells.

Bryostatin 1 and phorbol esters are both potent activators of protein kinase C (PKC), although their specific biological effects can differ in many systems. Here, we report that bryostatin 1 activates protein kinase D (PKD), a novel serine/threonine protein kinase, in intact Swiss 3T3 cells and secondary mouse embryo fibroblasts and in COS-7 cells transiently transfected with a PKD expression construct. The dose response of PKD activation induced by bryostatin 1 follows a striking biphasic pattern with maximal activation achieved at a concentration of 10 nM. Higher concentrations of bryostatin 1 (100 nM) reduced PKD activation induced by phorbol 12,13-dibutyrate to levels stimulated by bryostatin 1 alone. Bryostatin 1-induced PKD activation was markedly attenuated by treatment of cells with the PKC inhibitors bisindolylmaleimide I and Ro 31-8220. However, these agents did not inhibit PKD activity when added directly to in vitro kinase assays, suggesting that bryostatin 1 stimulates PKD activation through a PKC-dependent pathway in intact cells. Our results raise the possibility that activated PKD in intact cells could mediate some of the multiple biphasic biological responses induced by bryostatin 1.

Gastric cancer: an epidemiological review.

An attempt is made to synthesize the epidemiological literature and identify salient factors from the multitude of potential antecedents of gastric cancer, factors which to a greater or lesser degree create nonrandom variations in the distribution of the disease. Implicit in this approach is the notion that observation of spatial variations in the incidence of gastric cancer may lead to hypotheses relating to the biological, personal and physical environmental factors. An extensive bibliography accompanies the text.

Effects of long and short photoperiod on the ultrastructure of pinealocytes of the cotton rat (Sigmodon hispidus).

The ultrastructure of the pinealocytes of wild-captured cotton rats (Sigmodon hispidus) housed in either long or short photoperiod was examined. Quantitative comparison of selected pinealocyte organelles revealed larger relative volumes of mitochondria, granular endoplasmic reticulum and ribosomes, Golgi apparatus, and inclusion bodies, as well as a higher number of dense-core vesicles in the animals kept in short photoperiod (LD 8:16) as compared to those in animals kept in long photoperiod (LD 16:8). These observations suggest that restricting the amount of light to which animals are exposed activates pinealocytes of the cotton rat.

Day:night variations of melatonin, 5-hydroxyindole acetic acid, serotonin, serotonin N-acetyltransferase, tryptophan, norepinephrine and dopamine in the rabbit pineal gland.

Pineal tryptophan, serotonin, serotonin-N-acetyltransferase (NAT), melatonin, 5-hydroxyindole acetic acid (5HIAA), norepinephrine and dopamine were measured in 5 castrated rabbits each at 11.00, 00.30 and 03.00 hours. The rabbits were housed in an L:D 14:10 (lights on 07.00 hours). Significant day:night variations were found in NAT, melatonin, dopamine and norepinephrine. These results were compared to data concerning rhythms of pineal constituents in other species.

The influence of various irradiances of artificial light, twilight, and moonlight on the suppression of pineal melatonin content in the Syrian hamster.

The purpose of the present studies using artificial light was to determine how the timing and duration of exposure influence the light-induced suppression of pineal melatonin levels in hamsters. An 8-min exposure to 0.186 microW/cm2 of cool white fluorescent light caused a continued depression of pineal melatonin even when animals were returned to darkness. In addition, the pineal gland does not appear to change its sensitivity to light throughout the night. A 20-min exposure to 0.019 microW/cm2 of cool white fluorescent light did not significantly suppress pineal melatonin during any time of the melatonin peak, whereas a 20-min exposure to 0.186 microW/cm2 was capable of always suppressing melatonin. Furthermore, increasing the duration of 0.019-microW/cm2 exposure to 30, 60, 120, or 180 min does not increase the capacity of this irradiance to depress melatonin. Similar to artifical light, natural light has a variable capacity for suppressing nocturnal levels of pineal melatonin. Twilight irradiances of 0.138 microW/cm2 or less did not suppress nocturnal melatonin whereas twilight irradiances of 3.0 microW/cm2 or greater did suppress pineal melatonin. A few animals did have lower melatonin after a 40-min exposure to full moonlight during July (0.045 microW/cm2) or January (0.240 microW/cm2). However, pineal melatonin levels remained high in the majority of animals exposed to full moonlight.

The suppression of pineal melatonin content and N-acetyltransferase activity by different light irradiances in the Syrian hamster: a dose-response relationship.

The purpose of this study was to test the influence of various irradiances of cool white fluorescent light on the suppression of pineal N-acetyltransferase activity (NAT) and melatonin content in hamsters. Groups of animals were exposed to light irradiances ranging from 0.00-1.86 microwatts (microW)/cm2 for 20 min during the night. Both pineal NAT and melatonin were similarly depressed by the light irradiances in a dose-related manner. The shape of the resultant dose-response curves and the calculated ED50 for NAT (0.066 microW/cm2) and melatonin (0.058 microW/cm2) were remarkably similar. These findings may be relevant to the physiological control of the pineal by natural illumination.

Rhythms in immunoreactive melatonin in the retina and Harderian gland of rats: persistence after pinealectomy.

Immunoreactive melatonin levels were measured in the retina and Harderian gland of adult male rats throughout a 24 hour period. The animals were maintained under a light:dark cycle of 14:10 (lights on at 0600h). In intact animals, immunoreactive melatonin values in both organs exhibited a 24h rhythm with peak levels being measured at 0800h, 2 hours after lights on. Pinealectomy significantly increased peak levels at 0800h in both the retina and the Harderian gland. Gonadectomy abolished the peak retinal melatonin levels at 0800h. Likewise, continual light exposure for 1 week depressed the melatonin peak in the retina but not in the Harderian gland.

Pineal indoleamine metabolism in the cotton rat, Sigmodon hispidus: studies on norepinephrine, serotonin, N-acetyltransferase activity and melatonin.

The purpose of this study was to examine the levels of norepinephrine (NE), serotonin, melatonin and N-acetyltransferase (NAT) activity in the cotton rat pineal gland in relationship to environmental lighting. In each of two experiments cotton rats were collected from the wild and housed indoors in a 14:10 light:dark (LD) cycle (lights on at 0600) for a period of at least two weeks. Pineal glands were removed from animals in groups of eight at 0800, 1200, 1600, 2000, 2400, 0200 and 0400 hours over a 24 hour period for each experiment. Collection was done under a dim red light during the nighttime hours. In the first experiment pineal melatonin production showed a striking circadian rhythm with nighttime levels 20 times greater than that of daytime levels. In the second experiment pineal NE, serotonin and NAT activity were measured in aliquots from the same gland. NE showed no circadian rhythm whereas serotonin values were significantly depressed at night. The nighttime NAT activity rose to 10 times that of the daytime level. The NAT peak was concurrent with the melatonin peak. These data indicate that the neural and the biochemical control of the cotton rat pineal may be similar to that of other mammalian species.

An objective assessment of synovitis of the knee: measurement of the size of the suprapatellar pouch on xeroradiography.

Measurement of the size of the suprapatellar pouch of the knee appears to be a simple, useful, objective, and reproducible assessment of synovitis of the knee. Changes in the apparent size of the suprapatellar pouch have been shown to correlate closely with the volume of synovial fluid aspirated from the knee and with changes in circumferential measurements. Aspiration of 20 ml of fluid will produce a change in size significant at the 1% level. Lateral xeroradiographs were used in this study, as soft-tissue planes are more closely defined on xeroradiographs than on standard radiographs.