A trophic cascade initiated by an invasive vertebrate alters the structure of native reptile communities.

Invasive vertebrates are frequently reported to have catastrophic effects on the populations of species which they directly impact. It follows then, that if invaders exert strong suppressive effects on some species then other species will indirectly benefit due to ecological release from interactions with directly impacted species. However, evidence that invasive vertebrates trigger such trophic cascades and alter community structure in terrestrial ecosystems remains rare. Here, we ask how the cane toad, a vertebrate invader that is toxic to many of Australia's vertebrate predators, influences lizard assemblages in a semi-arid rangeland. In our study area, the density of cane toads is influenced by the availability of water accessible to toads. We compared an index of the abundance of sand goannas, a large predatory lizard that is susceptible to poisoning by cane toads and the abundances of four lizard families preyed upon by goannas (skinks, pygopods, agamid lizards and geckos) in areas where cane toads were common or rare. Consistent with the idea that suppression of sand goannas by cane toads initiates a trophic cascade, goanna activity was lower and small lizards were more abundant where toads were common. The hypothesis that suppression of sand goannas by cane toads triggers a trophic cascade was further supported by our findings that small terrestrial lizards that are frequently preyed upon by goannas were more affected by toad abundance than arboreal geckos, which are rarely consumed by goannas. Furthermore, the abundance of at least one genus of terrestrial skinks benefitted from allogenic ecosystem engineering by goannas where toads were rare. Overall, our study provides evidence that the invasion of ecosystems by non-native species can have important effects on the structure and integrity of native communities extending beyond their often most obvious and frequently documented direct ecological effects

Interactions between corticosterone phenotype, environmental stressor pervasiveness and irruptive movement-related survival in the cane toad

© 2018. Published by The Company of Biologists Ltd Animals use irruptive movement to avoid exposure to stochastic and pervasive environmental stressors that impact fitness. Beneficial irruptive movements transfer individuals from high-stress areas (conferring low fitness) to alternative localities that may improve survival or reproduction. However, being stochastic, environmental stressors can limit an animal’s preparatory capacity to enhance irruptive movement performance. Thus individuals must rely on pre-existing, or rapidly induced, physiological and behavioural responses. Rapid elevation of glucocorticoid hormones in response to environmental stressors are widely implicated in adjusting physiological and behaviour processes that could influence irruptive movement capacity. However, there remains little direct evidence demonstrating that corticosterone-regulated movement performance or interaction with pervasiveness of environmental stress, confers adaptive movement outcomes. Here, we compared how movement-related survival of cane toads (Rhinella marina) varied with three different experimental corticosterone phenotypes across four increments of increasing environmental stressor pervasiveness (i.e. distance from water in a semi-arid landscape). Our results indicated that toads with phenotypically increased corticosterone levels attained higher movement-related survival compared with individuals with control or lowered corticosterone phenotypes. However, the effects of corticosterone phenotypes on movement-related survival to some extent co-varied with stressor pervasiveness. Thus, our study demonstrates how the interplay between an individual’s corticosterone phenotype and movement capacity alongside the arising costs of movement and the pervasiveness of the environmental stressor can affect survival outcomes

Chronic insulin treatment of diabetes does not fully normalize alterations in the retinal transcriptome

<p>Abstract</p> <p>Background</p> <p>Diabetic retinopathy (DR) is a leading cause of blindness in working age adults. Approximately 95% of patients with Type 1 diabetes develop some degree of retinopathy within 25 years of diagnosis despite normalization of blood glucose by insulin therapy. The goal of this study was to identify molecular changes in the rodent retina induced by diabetes that are not normalized by insulin replacement and restoration of euglycemia.</p> <p>Methods</p> <p>The retina transcriptome (22,523 genes and transcript variants) was examined after three months of streptozotocin-induced diabetes in male Sprague Dawley rats with and without insulin replacement for the later one and a half months of diabetes. Selected gene expression changes were confirmed by qPCR, and also examined in independent control and diabetic rats at a one month time-point.</p> <p>Results</p> <p>Transcriptomic alterations in response to diabetes (1376 probes) were clustered according to insulin responsiveness. More than half (57%) of diabetes-induced mRNA changes (789 probes) observed at three months were fully normalized to control levels with insulin therapy, while 37% of probes (514) were only partially normalized. A small set of genes (5%, 65 probes) was significantly dysregulated in the insulin-treated diabetic rats. qPCR confirmation of findings and examination of a one month time point allowed genes to be further categorized as prevented or rescued with insulin therapy. A subset of genes (Ccr5, Jak3, Litaf) was confirmed at the level of protein expression, with protein levels recapitulating changes in mRNA expression.</p> <p>Conclusions</p> <p>These results provide the first genome-wide examination of the effects of insulin therapy on retinal gene expression changes with diabetes. While insulin clearly normalizes the majority of genes dysregulated in response to diabetes, a number of genes related to inflammatory processes, microvascular integrity, and neuronal function are still altered in expression in euglycemic diabetic rats. Gene expression changes not rescued or prevented by insulin treatment may be critical to the pathogenesis of diabetic retinopathy, as it occurs in diabetic patients receiving insulin replacement, and are prototypical of metabolic memory.</p

Lawson criterion for ignition exceeded in an inertial fusion experiment

For more than half a century, researchers around the world have been engaged in attempts to achieve fusion ignition as a proof of principle of various fusion concepts. Following the Lawson criterion, an ignited plasma is one where the fusion heating power is high enough to overcome all the physical processes that cool the fusion plasma, creating a positive thermodynamic feedback loop with rapidly increasing temperature. In inertially confined fusion, ignition is a state where the fusion plasma can begin "burn propagation" into surrounding cold fuel, enabling the possibility of high energy gain. While "scientific breakeven" (i.e., unity target gain) has not yet been achieved (here target gain is 0.72, 1.37 MJ of fusion for 1.92 MJ of laser energy), this Letter reports the first controlled fusion experiment, using laser indirect drive, on the National Ignition Facility to produce capsule gain (here 5.8) and reach ignition by nine different formulations of the Lawson criterion

Interactions between corticosterone phenotype, environmental stressor pervasiveness and irruptive movement-related survival in the cane toad

Animals use irruptive movement to avoid exposure to stochastic and pervasive environmental stressors that impact fitness. Beneficial irruptive movements transfer individuals from high-stress areas (conferring low fitness) to alternate localities that may improve survival or reproduction. However, being stochastic, environmental stressors can limit an animal's preparatory capacity to enhance irruptive movement performance. Thus individuals must rely on standing, or rapidly induced, physiological and behavioural responses. Rapid elevation of glucocorticoid hormones in response to environmental stressors are widely implicated in adjusting physiological and behaviour processes that could influence irruptive movement capacity. However, there remains little direct evidence to demonstrate that corticosterone regulated movement performance, nor the interaction with the pervasiveness of environmental stress, confers adaptive movement outcomes. Here we compared how movement-related survival of cane toads (Rhinella marina) varied with three different experimental corticosterone phenotypes across four increments of increasing environmental stressor pervasiveness (i.e. distance from water in a semi-arid landscape). Our results indicated that toads with phenotypically increased corticosterone levels attained higher movement-related survival compared to individuals with control or lowered corticosterone phenotypes. However, the effects of corticosterone phenotypes on movement-related survival to some extent co-varied with stressor pervasiveness. Thus our study demonstrates how the interplay among an individual's corticosterone phenotype and movement capacity alongside the arising costs of movement and the pervasiveness of the environmental stressor can affect survival outcomes

Retinal Thickness Normative Data in Wild-Type Mice Using Customized Miniature SD-OCT

OBJECTIVE: To report normative data for retinal thickness in wild-type C57BL/6 mouse utilizing a miniature SD-OCT system. METHODS: Thirty adult mice (range: 3–5 months) were anesthetized and secured into the Bioptigen Spectral Domain Ophthalmic Imaging System. Right eye SD-OCT images were standardized by centralizing the optic nerve head (ONH) prior to image acquisition. Global and quadrant total retinal thickness (TRT) values were measured from retinal nerve fiber layer to retinal pigment epithelial layer. Posterior segment analyses also included the outer retinal layer (ORL) and inner retinal layer (IRL). Further sublayer analyses of four layers from the ORL and three layers comprising the IRL were also performed. RESULTS: The overall mean±SD global TRT in a C57BL/6 mouse model was 204.41±5.19 µm. Quadrant mean TRT values were 204.85±5.81 µm inferiorly, 204.97±6.71 µm nasally, 205.08±5.44 µm temporally, and 202.74±4.85 µm superiorly. Mean±SD thickness for ORL, and IRL were 126.37±10.01 µm, and 107.03±10.98 µm respectively. The mean±SD estimates for the four layers of the ORL were 18.23±2.73 µm, 26.04±4.21 µm, 63.8±6.23 µm, and 19.22±4.34 µm. Mean±SD values for the three IRL sublayers were 27.82±4.04 µm, 59.62±6.66 µm and 19.12±3.71 µm. CONCLUSION: This study established normative values for the total retinal thickness and sublayer thickness for the wild-type C57BL/6 mice. Moreover, it provides a standard of retinal morphology, in a commonly used animal model, for evaluating therapeutic interventions and retinal disease pathophysiology

Interventricular coupling coefficients in a thick shell model of passive cardiac chamber deformation

Mechanical interplay between the adjacent ventricles is one of the principal modulators of physiopathological heart function, and the underlying mechanisms of interaction are only partially understood, hence hampering clinically useful interpretation of imaging data. In order to characterize the influence of chamber geometry on ventricular coupling, the ventricles and septum are modeled as portions of ellipsoidal shells, and configuration is derived as a function of pressure gradients by combining shell element equilibrium equations through static boundary conditions applied at the sulcus. Diastolic volume (v) surfaces are calculated as a function of pressure (p), contralateral pressure (clp) and intrathoracic pressure (pt) and match literature data where available. Ventricular interaction is characterized in terms of partial derivatives in v-p-clp-pt space both under physiological and altered (selectively stiffened walls) conditions. The model allows prediction of diastolic ventricular v-p-clp-pt interplay in a variety of physiopathological circumstances. © International Federation for Medical and Biological Engineering 2008