Agricultural Production in the 21st Century: Land-use, Diversity, Pests and Pesticides

Over the next 50 years, global food demand is forecast to double. Already it is estimated that agriculture covers about 40% of ice-free land, accounts for a third of greenhouse gas emissions, and contributes significantly to global biodiversity declines. One means to reduce the impact of agriculture on humans and natural systems is to ensure the efficient use of pesticides. Pesticides, especially insecticides, have numerous negative externalities for human and environmental health, and their efficient use is an economic, ecological and public health priority. How land use patterns influence insect pests and insecticide demand is of special concern, because productive and efficient land use is key to meeting future food demand. This research investigates the relationships between insecticide use and landscape configuration. It further investigates the importance of weather variability and data quality to understanding agriculture in the 21st Century. Finally, it explores ecological theory to understand how multiple natural enemies may coexist on a single resource species.Specifically, I address the following questions: 1) is landscape simplification a consistent driver of insecticide use across time, 2) is landscape simplification a consistent driver of insecticide use across space and throughout the varied growing regions of the US, and do annual weather patterns influence insecticide use? 3) Is satellite crop data sufficiently accurate to be applied to ecological and economic questions at the sub-county level? 4) Can coexistence be driven by non-consumptive ecological interactions?To address these questions I integrate ecological and economic theory, and apply multivariate statistical techniques to multi-year national or regional databases. I find that, contrary to expectations from ecological theory, landscape simplification does not consistently drive insecticide use over time (Chapter 1) or space (Chapter 2). This spatio-temporal variation helps explain the ambiguous results in the literature and implies that national land use policy will have very different effects on insecticide use if regional differences are ignored. To further understand the underlying mechanisms requires fine-scale spatial information of configuration and crop type. However, leveraging satellite data for sub-county information such as spatial configuration is well suited to simplified growing regions, but highly inaccurate elsewhere (Chapter 3). Lastly, I show natural enemies and other intermediate consumers can coexist with sufficiently strong non-consumptive effects of a top predator on the dominant consumer (Chapter 4).In 2007 US farmers applied ~70 million pounds of insecticide active ingredients. While farmers pay the purchase price, society pays for degradation of natural systems and harm to human health. To minimize the cost of insecticides to both farmers and society, now and under future climate change, we must understand what drives variation in insecticide use and what enables persistence of natural enemy diversity. My dissertation research informs these key gaps in our understanding

Chronology of dune development in the White River Badlands, northern Great Plains, USA

Aeolian dune field chronologies provide important information on drought history on the Great Plains. The White River Badlands (WRB) dunes are located approximately 60 km north of the Nebraska Sand Hills (NSH), in the western section of the northern Great Plains. Clifftop dunes, sand sheets, and stabilized northwest-southeast trending parabolic dunes are found on upland mesas and buttes, locally called tables. The result of this study is a dune stabilization history determined from samples collected from stratigraphic exposures and dune crests. Thirty-seven OSL ages, from this and previous investigations, show three periods of dune activity: 1) ~21,000 years ago to 12,000 years ago (a), 2) ~9 to 6 ka, and 3) post-700 a. Stratigraphic exposures and low-relief dune forms preserve evidence of late Pleistocene and middle Holocene dune development, while high-relief dune crests preserve evidence of late Holocene dune development. Results of 12 OSL ages from the most recent dune activation event indicate that Medieval Climate Anomaly (MCA) droughts and Little Ice Age (LIA) droughts caused dune reactivation on the tables. Dune reactivation was accompanied by other drought-driven geomorphological responses in the WRB, including fluvial incision of the prairie and formation of sod tables. Regional significance of the MCA and LIA droughts is supported by similarities in the aeolian chronologies of the NSH at 700–600 a and some western Great Plains dune fields at 420–210 a. Aerial photographs of the WRB show little activity during the Dust Bowl droughts of the 1930s

Crop Pests and Predators Exhibit Inconsistent Responses to Surrounding Landscape Composition

The idea that noncrop habitat enhances pest control and represents a win–win opportunity to conserve biodiversity and bolster yields has emerged as an agroecological paradigm. However, while noncrop habitat in landscapes surrounding farms sometimes benefits pest predators, natural enemy responses remain heterogeneous across studies and effects on pests are inconclusive. The observed heterogeneity in species responses to noncrop habitat may be biological in origin or could result from variation in how habitat and biocontrol are measured. Here, we use a pest-control database encompassing 132 studies and 6,759 sites worldwide to model natural enemy and pest abundances, predation rates, and crop damage as a function of landscape composition. Our results showed that although landscape composition explained significant variation within studies, pest and enemy abundances, predation rates, crop damage, and yields each exhibited different responses across studies, sometimes increasing and sometimes decreasing in landscapes with more noncrop habitat but overall showing no consistent trend. Thus, models that used landscape-composition variables to predict pest-control dynamics demonstrated little potential to explain variation across studies, though prediction did improve when comparing studies with similar crop and landscape features. Overall, our work shows that surrounding noncrop habitat does not consistently improve pest management, meaning habitat conservation may bolster production in some systems and depress yields in others. Future efforts to develop tools that inform farmers when habitat conservation truly represents a win–win would benefit from increased understanding of how landscape effects are modulated by local farm management and the biology of pests and their enemies

Range expansion and the origin of USA300 north american epidemic methicillin-resistant Staphylococcus aureus

The USA300 North American epidemic (USA300-NAE) clone of methicillin-resistant Staphylococcus aureus has caused a wave of severe skin and soft tissue infections in the United States since it emerged in the early 2000s, but its geographic origin is obscure. Here we use the population genomic signatures expected from the serial founder effects of a geographic range expansion to infer the origin of USA300-NAE and identify polymorphisms associated with its spread. Genome sequences from 357 isolates from 22 U.S. states and territories and seven other countries are compared. We observe two significant signatures of range expansion, including decreases in genetic diversity and increases in derived allele frequency with geographic distance from the Pennsylvania region. These signatures account for approximately half of the core nucleotide variation of this clone, occur genome wide, and are robust to heterogeneity in temporal sampling of isolates, human population density, and recombination detection methods. The potential for positive selection of a gyrA fluoroquinolone resistance allele and several intergenic regions, along with a 2.4 times higher recombination rate in a resistant subclade, is noted. These results are the first to show a pattern of genetic variation that is consistent with a range expansion of an epidemic bacterial clone, and they highlight a rarely considered but potentially common mechanism by which genetic drift may profoundly influence bacterial genetic variation. IMPORTANCE The process of geographic spread of an origin population by a series of smaller populations can result in distinctive patterns of genetic variation. We detect these patterns for the first time with an epidemic bacterial clone and use them to uncover the clone’s geographic origin and variants associated with its spread. We study the USA300 clone of methicillin-resistant Staphylococcus aureus, which was first noticed in the early 2000s and subsequently became the leading cause of skin and soft tissue infections in the United States. The eastern United States is the most likely origin of epidemic USA300. Relatively few variants, which include an antibiotic resistance mutation, have persisted during this clone’s spread. Our study suggests that an early chapter in the genetic history of this epidemic bacterial clone was greatly influenced by random subsampling of isolates during the clone’s geographic spread

Preterm birth: inflammation, fetal injury and treatment strategies

Preterm birth (PTB) is the leading cause of childhood mortality in children under 5 and accounts for approximately 11% of births worldwide. Premature babies are at risk of a number of health complications, notably cerebral palsy, but also respiratory and gastrointestinal disorders. Preterm deliveries can be medically indicated/elective procedures or they can occur spontaneously. Spontaneous PTB is commonly associated with intrauterine infection/inflammation. The presence of inflammatory mediators in utero has been associated with fetal injury, particularly affecting the fetal lungs and brain. This review will outline (i) the role of inflammation in term and PTB, (ii) the effect infection/inflammation has on fetal development and (iii) recent strategies to target PTB. Further research is urgently required to develop effective methods for the prevention and treatment of PTB and above all, to reduce fetal injury

Progress of Crew Autonomous Scheduling Test (CAST) on the ISS

No abstract availabl

SLC30A3 Responds to Glucose- and Zinc Variations in ß-Cells and Is Critical for Insulin Production and In Vivo Glucose-Metabolism During ß-Cell Stress

BACKGROUND:Ion transporters of the Slc30A- (ZnT-) family regulate zinc fluxes into sub-cellular compartments. beta-cells depend on zinc for both insulin crystallization and regulation of cell mass. METHODOLOGY/PRINCIPAL FINDINGS:This study examined: the effect of glucose and zinc chelation on ZnT gene and protein levels and apoptosis in beta-cells and pancreatic islets, the effects of ZnT-3 knock-down on insulin secretion in a beta-cell line and ZnT-3 knock-out on glucose metabolism in mice during streptozotocin-induced beta-cell stress. In INS-1E cells 2 mM glucose down-regulated ZnT-3 and up-regulated ZnT-5 expression relative to 5 mM. 16 mM glucose increased ZnT-3 and decreased ZnT-8 expression. Zinc chelation by DEDTC lowered INS-1E insulin content and insulin expression. Furthermore, zinc depletion increased ZnT-3- and decreased ZnT-8 gene expression whereas the amount of ZnT-3 protein in the cells was decreased. Zinc depletion and high glucose induced apoptosis and necrosis in INS-1E cells. The most responsive zinc transporter, ZnT-3, was investigated further; by immunohistochemistry and western blotting ZnT-3 was demonstrated in INS-1E cells. 44% knock-down of ZnT-3 by siRNA transfection in INS-1E cells decreased insulin expression and secretion. Streptozotocin-treated mice had higher glucose levels after ZnT-3 knock-out, particularly in overt diabetic animals. CONCLUSION/SIGNIFICANCE:Zinc transporting proteins in beta-cells respond to variations in glucose and zinc levels. ZnT-3, which is pivotal in the development of cellular changes as also seen in type 2 diabetes (e.g. amyloidosis in Alzheimer's disease) but not previously described in beta-cells, is present in this cell type, up-regulated by glucose in a concentration dependent manner and up-regulated by zinc depletion which by contrast decreased ZnT-3 protein levels. Knock-down of the ZnT-3 gene lowers insulin secretion in vitro and affects in vivo glucose metabolism after streptozotocin treatment

Higher risk of gastrointestinal parasite infection at lower elevation suggests possible constraints in the distributional niche of Alpine marmots

Alpine marmots Marmota marmota occupy a narrow altitudinal niche within high elevation alpine environments. For animals living at such high elevations where resources are limited, parasitism represents a potential major cost in life history. Using occupancy models, we tested if marmots living at higher elevation have a reduced risk of being infected with gastrointestinal helminths, possibly compensating the lower availability of resources (shorter feeding season, longer snow cover and lower temperature) than marmots inhabiting lower elevations. Detection probability of eggs and oncospheres of two gastro-intestinal helminthic parasites, Ascaris laevis and Ctenotaenia marmotae, sampled in marmot feces, was used as a proxy of parasite abundance. As predicted, the models showed a negative relationship between elevation and parasite detectability (i.e. abundance) for both species, while there appeared to be a negative effect of solar radiance only for C. marmotae. Site-occupancy models are used here for the first time to model the constrains of gastrointestinal parasitism on a wild species and the relationship existing between endoparasites and environmental factors in a population of free-living animals. The results of this study suggest the future use of site-occupancy models as a viable tool to account for parasite imperfect detection in ecoparasitological studies, and give useful insights to further investigate the hypothesis of the contribution of parasite infection in constraining the altitudinal niche of Alpine marmots

Neuronal sensitivity to TDP-43 overexpression is dependent on timing of induction

Ubiquitin-immunoreactive neuronal inclusions composed of TAR DNA binding protein of 43 kDa (TDP-43) are a major pathological feature of frontotemporal lobar degeneration (FTLD-TDP). In vivo studies with TDP-43 knockout mice have suggested that TDP-43 plays a critical, although undefined role in development. In the current report, we generated transgenic mice that conditionally express wild-type human TDP-43 (hTDP-43) in the forebrain and established a paradigm to examine the sensitivity of neurons to TDP-43 overexpression at different developmental stages. Continuous TDP-43 expression during early neuronal development produced a complex phenotype, including aggregation of phospho-TDP-43, increased ubiquitin immunoreactivity, mitochondrial abnormalities, neurodegeneration and early lethality. In contrast, later induction of hTDP-43 in the forebrain of weaned mice prevented early death and mitochondrial abnormalities while yielding salient features of FTLD-TDP, including progressive neurodegeneration and ubiquitinated, phospho-TDP-43 neuronal cytoplasmic inclusions. These results suggest that neurons in the developing forebrain are extremely sensitive to TDP-43 overexpression and that timing of TDP-43 overexpression in transgenic mice must be considered when distinguishing normal roles of TDP-43, particularly as they relate to development, from its pathogenic role in FTLD-TDP and other TDP-43 proteinopathies. Finally, our adult induction of hTDP-43 strategy provides a mouse model that develops critical pathological features that are directly relevant for human TDP-43 proteinopathies