Evaluating the Mechanisms of Landscape Change on White-Tailed Deer Populations

Understanding how landscape change influences the distribution and densities of species, and the consequences of these changes, is a central question in modern ecology. The distribution of white-tailed deer (Odocoileus virginianus) is expanding across North America, and in some areas, this pattern has led to an increase in predators and consequently higher predation rates on woodland caribou (Rangifer tarandus caribou)—an alternate prey species that is declining across western Canada. Understanding the factors influencing deer distribution has therefore become important for effective conservation of caribou in Canada. Changing climate and anthropogenic landscape alteration are hypothesized to facilitate white-tailed deer expansion. Yet, climate and habitat alteration are spatiotemporally correlated, making these factors difficult to isolate. Our study evaluates the relative effects of snow conditions and human-modified habitat (habitat alteration) across space on white-tailed deer presence and relative density. We modeled deer response to snow depth and anthropogenic habitat alteration across a large latitudinal gradient (49° to 60°) in Alberta, Canada, using motion-sensitive camera data collected in winter and spring from 2015 to 2019. Deer distribution in winter and spring were best explained by models including both snow depth and habitat alteration. Sites with shallower snow had higher deer presence regardless of latitude. Increased habitat alteration increased deer presence in the northern portion of the study area only. Winter deer density was best explained by snow depth only, whereas spring density was best explained by both habitat alteration and the previous winter's snow depth. Our results suggest that limiting future habitat alteration or restoring habitat can alter deer distribution, thereby potentially slowing or reversing expansion, but that climate plays a significant role beyond what managers can influence. © 2020 The Wildlife Society.     

Translating insights from the seed metabolome into improved prediction for lipid-composition traits in oat (Avena sativa L.)

Oat (Avena sativa L.) seed is a rich resource of beneficial lipids, soluble fiber, protein, and antioxidants, and is considered a healthful food for humans. Little is known regarding the genetic controllers of variation for these compounds in oat seed. We characterized natural variation in the mature seed metabolome using untargeted metabolomics on 367 diverse lines and leveraged this information to improve prediction for seed quality traits. We used a latent factor approach to define unobserved variables that may drive covariance among metabolites. One hundred latent factors were identified, of which 21% were enriched for compounds associated with lipid metabolism. Through a combination of whole-genome regression and association mapping, we show that latent factors that generate covariance for many metabolites tend to have a complex genetic architecture. Nonetheless, we recovered significant associations for 23% of the latent factors. These associations were used to inform a multi-kernel genomic prediction model, which was used to predict seed lipid and protein traits in two independent studies. Predictions for 8 of the 12 traits were significantly improved compared to genomic best linear unbiased prediction when this prediction model was informed using associations from lipid-enriched factors. This study provides new insights into variation in the oat seed metabolome and provides genomic resources for breeders to improve selection for health-promoting seed quality traits. More broadly, we outline an approach to distill high-dimensional “omics” data to a set of biologically meaningful variables and translate inferences on these data into improved breeding decisions.     

Integration of Sugar Metabolism and Proteoglycan Synthesis by UDP-glucose Dehydrogenase

Regulation of proteoglycan and glycosaminoglycan synthesis is critical throughout development, and to maintain normal adult functions in wound healing and the immune system, among others. It has become increasingly clear that these processes are also under tight metabolic control and that availability of carbohydrate and amino acid metabolite precursors has a role in the control of proteoglycan and glycosaminoglycan turnover. The enzyme uridine diphosphate (UDP)-glucose dehydrogenase (UGDH) produces UDP-glucuronate, an essential precursor for new glycosaminoglycan synthesis that is tightly controlled at multiple levels. Here, we review the cellular mechanisms that regulate UGDH expression, discuss the structural features of the enzyme, and use the structures to provide a context for recent studies that link post-translational modifications and allosteric modulators of UGDH to its function in downstream pathways:     

A quantitative trait variant in Gabra2 underlies increased methamphetamine stimulant sensitivity

Psychostimulant (methamphetamine, cocaine) use disorders have a genetic component that remains mostly unknown. We conducted genome-wide quantitative trait locus (QTL) analysis of methamphetamine stimulant sensitivity. To facilitate gene identification, we employed a Reduced Complexity Cross between closely related C57BL/6 mouse substrains and examined maximum speed and distance traveled over 30 min following methamphetamine (2 mg/kg, i.p.). For maximum methamphetamine-induced speed following the second and third administration, we identified a single genome-wide significant QTL on chromosome 11 that peaked near the Cyfip2 locus (LOD = 3.5, 4.2; peak = 21 cM [36 Mb]). For methamphetamine-induced distance traveled following the first and second administration, we identified a genome-wide significant QTL on chromosome 5 that peaked near a functional intronic indel in Gabra2 coding for the alpha-2 subunit of the GABA-A receptor (LOD = 3.6–5.2; peak = 34–35 cM [66–67 Mb]). Striatal cis-expression QTL mapping corroborated Gabra2 as a functional candidate gene underlying methamphetamine-induced distance traveled. CRISPR/Cas9-mediated correction of the mutant intronic deletion on the C57BL/6J background to the wild-type C57BL/6NJ allele was sufficient to reduce methamphetamine-induced locomotor activity toward the wild-type C57BL/6NJ-like level, thus validating the quantitative trait variant (QTV). These studies show the power and efficiency of Reduced Complexity Crosses in identifying causal variants underlying complex traits. Functionally restoring Gabra2 expression decreased methamphetamine stimulant sensitivity and supports preclinical and human genetic studies implicating the GABA-A receptor in psychostimulant addiction-relevant traits. Importantly, our findings have major implications for studying psychostimulants in the C57BL/6J strain—the gold standard strain in biomedical research.     

Health and economic burden estimates of snakebite management upon health facilities in three regions of southern Burkina Faso

BackgroundSnakebite has become better recognized as a significant cause of death and disability in Sub-Saharan Africa, but the health economic consequences to victims and health infrastructures serving them remain poorly understood. This information gap is important as it provides an evidence-base guiding national and international health policy decision making on the most cost-effective interventions to better manage snakebite. Here, we assessed hospital-based data to estimate the health economic burden of snakebite in three regions of Burkina Faso (Centre-Ouest, Hauts Bassins and Sud-Ouest).MethodologyPrimary data of snakebite victims admitted to regional and district health facilities (eg, number of admissions, mortality, hospital bed days occupied) was collected in three regions over 17 months in 2013/14. The health burden of snakebite was assessed using Disability-Adjusted Life Years (DALYs) calculations based upon hospitalisation, mortality and disability data from admitted patients amongst other inputs from secondary sources (eg, populations, life-expectancy and age-weighting constants). An activity-based costing approach to determine the direct cost of snake envenoming included unit costs of clinical staff wages, antivenom, supportive care and equipment extracted from context-relevant literature.FindingsThe 10,165 snakebite victims admitted to hospital occupied 28,164 hospital bed days over 17 months. The annual rate of hospitalisation and mortality of admitted snakebite victims was 173 and 1.39/100,000 population, respectively. The estimated annual (i) DALYs lost was 2,153 (0.52/1,000) and (ii) cost to hospitals was USD 506,413 (USD 49/hospitalisation) in these three regions of Burkina Faso. These costs appeared to be influenced by the number of patients receiving antivenom (10.90% in total) in each area (highest in Sud-Ouest) and the type of health facility.ConclusionThe economic burden of snake envenoming is primarily shouldered by the rural health centres closest to snakebite victims–facilities that are typically least well equipped or resourced to manage this burden. Our study highlights the need for more research in other regions/countries to demonstrate the burden of snakebite and the socioeconomic benefits of its management. This evidence can guide the most cost-effective intervention from government and development partners to meet the snakebite-management needs of rural communities and their health centres.     

A new unique form of microRNA from human heart,microRNA-499c,promotes myofibril formation and rescues cardiac development in mutant axolotl embryos

Background

A recessive mutation “c” in the Mexican axolotl, Ambystoma mexicanum, results in the failure of normal heart development. In homozygous recessive embryos, the hearts do not have organized myofibrils and fail to beat. In our previous studies, we identified a noncoding Myofibril-Inducing RNA (MIR) from axolotls which promotes myofibril formation and rescues heart development.

Results

We randomly cloned RNAs from fetal human heart. RNA from clone #291 promoted myofibril formation and induced heart development of mutant axolotls in organ culture. This RNA induced expression of cardiac markers in mutant hearts: tropomyosin, troponin and α-syntrophin. This cloned RNA matches in partial sequence alignment to human microRNA-499a and b, although it differs in length. We have concluded that this cloned RNA is unique in its length, but is still related to the microRNA-499 family. We have named this unique RNA, microRNA-499c. Thus, we will refer to this RNA derived from clone #291 as microRNA-499c throughout the rest of the paper.

Conclusions

This new form, microRNA-499c, plays an important role in cardiac development.     

Portrayals of Canine Obesity in English-Language Newspapers and in Leading Veterinary Journals, 2000–2009: Implications for Animal Welfare Organizations and Veterinarians as Public Educators

In industrialized societies, more than 1 in 3 dogs and people currently qualify as overweight or obese. Experts in public health expect both these figures to rise. Although clinical treatment remains important, so are public perceptions and social norms. This article presents a thematic analysis of English-language mass media coverage on canine obesity from 2000 through 2009 and compares these results with a thematic analysis of articles on canine obesity in leading veterinary journals during the same time period. Drawing on Giddens's theory of structuration, this study identified articles that emphasized individual agency, environmental structure, or both as contributors to canine obesity. Comparisons with weight-related health problems in human populations were virtually absent from the veterinary sample. Although such comparisons were almost always present in the media sample, quotations from veterinarians and other spokespeople for the welfare of nonhuman animals emphasized the agency of individual caregivers (owners) over structural influences. Now that weight gain and obesity have been established as a pressing animal welfare problem, these results suggest a need for research and for interventions, such as media advocacy, that emphasize intersections between animal-owner agency, socioenvironmental determinants, and connections between animal welfare and human health.     

The oxidative burst reaction in mammalian cells depends on gravity

Gravity has been a constant force throughout the Earth’s evolutionary history. Thus, one of the fundamental biological questions is if and how complex cellular and molecular functions of life on Earth require gravity. In this study, we investigated the influence of gravity on the oxidative burst reaction in macrophages, one of the key elements in innate immune response and cellular signaling. An important step is the production of superoxide by the NADPH oxidase, which is rapidly converted to H₂O₂ by spontaneous and enzymatic dismutation. The phagozytosis-mediated oxidative burst under altered gravity conditions was studied in NR8383 rat alveolar macrophages by means of a luminol assay. Ground-based experiments in “functional weightlessness” were performed using a 2 D clinostat combined with a photomultiplier (PMT clinostat). The same technical set-up was used during the 13th DLR and 51st ESA parabolic flight campaign. Furthermore, hypergravity conditions were provided by using the Multi-Sample Incubation Centrifuge (MuSIC) and the Short Arm Human Centrifuge (SAHC). The results demonstrate that release of reactive oxygen species (ROS) during the oxidative burst reaction depends greatly on gravity conditions. ROS release is 1.) reduced in microgravity, 2.) enhanced in hypergravity and 3.) responds rapidly and reversible to altered gravity within seconds. We substantiated the effect of altered gravity on oxidative burst reaction in two independent experimental systems, parabolic flights and 2D clinostat / centrifuge experiments. Furthermore, the results obtained in simulated microgravity (2D clinorotation experiments) were proven by experiments in real microgravity as in both cases a pronounced reduction in ROS was observed. Our experiments indicate that gravity-sensitive steps are located both in the initial activation pathways and in the final oxidative burst reaction itself, which could be explained by the role of cytoskeletal dynamics in the assembly and function of the NADPH oxidase complex.