Comparative breeding ecology in arctic-geese of different body size : an example in ross's and lesser snow geese

Two closely-related, different-sized species of geese nest sympatrically south of the Queen Maud Gulf (QMG) in Canada’s central arctic. Following a period of high population growth rate in both species within the QMG, the population growth rate of larger-bodied lesser snow geese (Chen caerulescens caerulescens; hereafter snow geese) has slowed most recently to roughly half that observed in smaller-bodied Ross’s geese (Chen rossii). I focused on factors that influence productivity and recruitment in these two species, to improve our understanding of life history variation associated with interspecific differences in body size, and to test for density-dependent population responses. I used long-term data (1991 to 2008) to compare spring nutrient reserves, breeding strategies, clutch sizes, nest success, and juvenile survival in Ross’s and snow geese breeding at Karrak Lake, Nunavut; a large breeding colony located within the QMG. Long-term patterns of spring body condition (i.e., fat and protein reserves) diverged in prospective breeding female Ross’s and snow geese implying that differences in food acquisition ability had become more acute. Snow geese displayed larger reductions in protein and fat reserves through time compared to Ross’s geese thereby suggesting a differential density-dependent response in the ability to store nutrient reserves, a prerequisite for breeding in both species. Decreased per capita food availability influenced the timing of reproduction in both species. Nesting phenologies of Ross’s and snow geese, adjusted for variation in phenology of local spring climate, have become later by 6.5 and 5.0 days, respectively, since 1991. Nutritional strategies (i.e., reliance on reserves versus local food) used for clutch formation differed between species. Ross’s geese displayed greater reliance on stored reserves (i.e., capital breeding) than did snow geese, though both used endogenous reserves (> 62% of yolk protein, > 48% of albumen, and > 73% of yolk lipid) for clutch formation. Ross’s and snow geese experienced declines of 28% and 23% in body masses from arrival to post-laying and also until hatch demonstrating that endogenous reserves are the main nutrient sources for incubation. Still, constraints of small size forced Ross’s geese to use a mixture of local food plants and reserves for incubation metabolism. I then examined differences in clutch size, nest success, and juvenile survival to understand of the role of recruitment in the interspecific divergence of population trajectories. I did not find strong interspecific differences in clutch size and nest success. Overall, snow geese had a larger mean clutch size, which was expected based on benefits of a larger-body size. Clutch sizes decreased with delays in breeding and decreasing protein reserves of arriving females, although Ross’s geese displayed larger declines with decreasing protein reserves. Mean apparent nest success for Ross’s geese was 4.5% higher compared to snow geese. Nest success showed large declines (11%) in both species with increasing population size at the breeding colony. However, nest success of snow geese decreased twice as fast with delays in breeding compared to Ross’s geese. Last, I found no evidence of negative density dependence in juvenile survival over time. Juvenile survival was higher in snow geese (48%) compared to Ross’s geese (38%), consistent with a life history prediction based on body size differences. Despite lower juvenile survival, recruitment by Ross’s geese is likely greater than that of snow geese because of earlier sexual maturity, higher breeding probability and/or greater nest success. Ultimately, small body size of Ross’s geese may produce an ideal life history schedule under resource limitation at this colony i.e., one that maximizes fitness compared to larger snow geese. Life history characteristics of Ross’s geese (e.g., absolutely lower energy requirement, have a flexible breeding strategy, higher reproductive effort, an earlier age of sexual maturity, a shorter breeding cycle allowing delayed arrival and nest initiation on arctic breeding areas, and shorter time required by goslings to attain adult size), in addition to their smaller bill morphology may allow exploitation of a wider niche space (i.e., one that includes marginal quality and low quantity vegetation) relative to snow geese. Because there were no large differences in components of recruitment considered here, other components of recruitment (age of sexual maturity, breeding probability) may be affected more strongly by diminished spring nutrition in snow geese and thus have a larger influence on local population dynamics

Nesting and duckling ecology of white-winged scoters (melanitta fusca deglandi) at Redberry Lake, Saskatchewan

Population surveys indicate a declining trend in abundance for the scoter genus at the continental level. Little is known about changes in life history traits responsible for the recent population decline of white-winged scoters (Melanitta fusca deglandi, hereafter scoters). Therefore, I studied nesting and duckling ecology of scoters at Redberry Lake, Saskatchewan, Canada during summers 2000-2001 when I found 198 nests. To examine nest-site selection, I compared habitat features between successful nests, failed nests, and random sites. Discriminant function analysis differentiated habitat features, measured at hatch, between successful nests, failed nests, and random sites; lateral (r = 0.65) and overhead (r = 0.35) concealment were microhabitat variables most correlated with canonical discriminant functions. I also modeled daily survival rate (DSR) of nests as a function of year, linear and quadratic trends with nest age, nest initiation date, and seven microhabitat variables. Nest survival from a time constant model (i.e., Mayfield nest success estimate) was 0.35 (95% CL: 0.27, 0.43). Estimates of nest success were lower than those measured at Redberry Lake in the 1970s and 1980s. In addition to nest survival increasing throughout the laying period and stabilizing during incubation, nest survival showed positive relationships with nest concealment and distance to water, and a negative relationship with distance to edge. Considering these factors, a model-averaged estimate of nest survival was 0.24 (95% CL: 0.09, 0.42). I conclude that scoters selected nesting habitat adaptively because (1) successful sites were more concealed than failed sites, (2) nest sites (i.e., successful and failed) had higher concealment than random sites, and (3) nest sites were on islands where success is greater than mainland. I then estimated duckling and brood survival with Cormack-Jolly-Seber models, implemented in Program Mark, from observations of 94 and 664 individually marked adult hens and ducklings, respectively. I tested hypotheses about duckling survival and (1) hatch date, (2) initial brood size at hatch, (3) duckling size and body condition at hatch, (4) offspring sex, (5) maternal female size and body condition at hatch, and (6) weather conditions within one week of hatching. Most mortality occurred during the first six days of duckling age. Variation in both duckling and brood survival were best modeled with effects of hatch date and initial brood size, while effects of female condition, female size, duckling size, and duckling condition were inconsistent. Survival probability clearly decreased with advancing hatch date and increased with larger initial brood sizes. Effects of weather and offspring sex in 2001, the only year such information was collected, suggested survival was negatively related to poor weather, but sex of ducklings, beyond size-related differences (i.e., sexual-size dimorphism), was unimportant. Estimates of survival to 28 days of age (30-day period), whether for ducklings (0.016, 0.021) or broods (0.084, 0.138) in 2000 or 2001, respectively, are the lowest of published studies and first for scoter broods in North America. I suspect intense gull predation shortly after hatch had the largest influence on duckling survival. Further research is needed to ascertain if low nesting success and duckling survival as well as other life cycle components are limiting scoter populations locally and throughout the rest of their breeding range

IMPROVING NAVAL AVIATION MAINTENANCE OPERABILITY IN SUPPORT OF CONUS DETACHMENTS

Naval Aviation currently operates as complete, internally supported squadrons responsible for their own maintenance equipment for operations. In this capacity, a squadron conducting training detachments away from its home station is required to transport all imperative equipment and personnel via contracted ground and government air transport. Because there is no additional equipment capacity to draw from for detachments, flight operations at the home station are reduced during the ground transportation period. This proposal assesses if it is beneficial for the Naval Aviation enterprise to continue the current transportation procedures of aviation maintenance equipment to detachments within the continental United States.Outstanding ThesisCommander, United States NavyLieutenant, United States NavyApproved for public release. Distribution is unlimited

Genomic survey of candidate stress-response genes in the estuarine anemone Nematostella vectensis

Author Posting. © Marine Biological Laboratory, 2008. This article is posted here by permission of Marine Biological Laboratory for personal use, not for redistribution. The definitive version was published in Biological Bulletin 214 (2008): 233-254.Salt marshes are challenging habitats due to natural variability in key environmental parameters including temperature, salinity, ultraviolet light, oxygen, sulfides, and reactive oxygen species. Compounding this natural variation, salt marshes are often heavily impacted by anthropogenic insults including eutrophication, toxic contamination, and coastal development that alter tidal and freshwater inputs. Commensurate with this environmental variability, estuarine animals generally exhibit broader physiological tolerances than freshwater, marine, or terrestrial species. One factor that determines an organism's physiological tolerance is its ability to upregulate "stress-response genes" in reaction to particular stressors. Comparative studies on diverse organisms have identified a number of evolutionarily conserved genes involved in responding to abiotic and biotic stressors. We used homology-based scans to survey the sequenced genome of Nematostella vectensis, the starlet sea anemone, an estuarine specialist, to identify genes involved in the response to three kinds of insult—physiochemical insults, pathogens, and injury. Many components of the stress-response networks identified in triploblastic animals have clear orthologs in the sea anemone, meaning that they must predate the cnidarian-triploblast split (e.g., xenobiotic receptors, biotransformative genes, ATP-dependent transporters, and genes involved in responding to reactive oxygen species, toxic metals, osmotic shock, thermal stress, pathogen exposure, and wounding). However, in some instances, stress-response genes known from triploblasts appear to be absent from the Nematostella genome (e.g., many metal-complexing genes). This is the first comprehensive examination of the genomic stress-response repertoire of an estuarine animal and a member of the phylum Cnidaria. The molecular markers of stress response identified in Nematostella may prove useful in monitoring estuary health and evaluating coastal conservation efforts. These data may also inform conservation efforts on other cnidarians, such as the reef-building corals.AMR was supported by a Postdoctoral Scholar Program at the Woods Hole Oceanographic Institution, with funding provided by The Beacon Institute for Rivers and Estuaries, and the J. Seward Johnson Fund. NTK was supported by a graduate research training grant from the National Institutes of Health. This research was also supported by NSF grant FP-91656101-0 to JCS and JRF, EPA grant F5E11155 to AMR and JRF, and a grant from the Conservation International Marine Management Area Science Program to JRF

In vivo regulation of the heme oxygenase-1 gene in humanized transgenic mice

Heme oxygenase-1 (HO-1) catalyzes the rate-limiting step in heme degradation, producing equimolar amounts of carbon monoxide, iron, and biliverdin. Induction of HO-1 is a beneficial response to tissue injury in diverse animal models of diseases including acute kidney injury. In vitro analysis has shown that the human HO-1 gene is transcriptionally regulated by changes in chromatin conformation, but whether such control occurs in vivo is not known. To enable such an analysis, we generated transgenic mice, harboring an 87-kb bacterial artificial chromosome expressing human HO-1 mRNA and protein and bred these mice with HO-1 knockout mice to generate humanized BAC transgenic mice. This successfully rescued the phenotype of the knockout mice including reduced birth rates, tissue iron overload, splenomegaly, anemia, leukocytosis, dendritic cell abnormalities, and survival after acute kidney injury induced by rhabdomyolysis or cisplatin nephrotoxicity. Transcription factors such as USF1/2, JunB, Sp1, and CTCF were found to associate with regulatory regions of the human HO-1 gene in the kidney following rhabdomyolysis. Chromosome conformation capture and ChIP-loop assays confirmed this in the formation of chromatin looping in vivo. Thus, these bacterial artificial chromosome humanized HO-1 mice are a valuable model to study the human HO-1 gene, providing insight to the in vivo architecture of the gene in acute kidney injury and other diseases

Common NOTCH3 Variants and Cerebral Small-Vessel Disease.

BACKGROUND AND PURPOSE: The most common monogenic cause of cerebral small-vessel disease is cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, caused by NOTCH3 gene mutations. It has been hypothesized that more common variants in NOTCH3 may also contribute to the risk of sporadic small-vessel disease. Previously, 4 common variants (rs10404382, rs1043994, rs10423702, and rs1043997) were found to be associated with the presence of white matter hyperintensity in hypertensive community-dwelling elderly. METHODS: We investigated the association of common single nucleotide polymorphisms (SNPs) in NOTCH3 in 1350 patients with MRI-confirmed lacunar stroke and 7397 controls, by meta-analysis of genome-wide association study data sets. In addition, we investigated the association of common SNPs in NOTCH3 with MRI white matter hyperintensity volumes in 3670 white patients with ischemic stroke. In each analysis, we considered all SNPs within the NOTCH3 gene, and within 50-kb upstream and downstream of the coding region. A total of 381 SNPs from the 1000 genome population with a mean allele frequency>0.01 were included in the analysis. A significance level of P<0.0015 was used, adjusted for the effective number of independent SNPs in the region using the Galwey method. RESULTS: We found no association of any common variants in NOTCH3 (including rs10404382, rs1043994, rs10423702, and rs1043997) with lacunar stroke or white matter hyperintensity volume. We repeated our analysis stratified for hypertension but again found no association. CONCLUSIONS: Our study does not support a role for common NOTCH3 variation in the risk of sporadic small-vessel disease.Collection of the UK Young Lacunar Stroke DNA Study (DNA lacunar) was primarily supported by the Wellcome Trust (WT072952) with additional support from the Stroke Association (TSA 2010/01). Genotyping of the DNA lacunar samples, and Dr Traylor, was supported by a Stroke Association Grant (TSA 2013/01). Funding for the genotyping at Massachusetts General Hospital was provided by the Massachusetts General Hospital- Deane Institute for the Integrative Study of Atrial Fibrillation and Stroke and the National Institute of Neurological Disorders and Stroke (U01 NS069208). Dr Rutten-Jacobs was supported by a project grant from the Stroke Association/British Heart Foundation grant (TSA BHF 2010/01). Dr Adib-Samii was supported by a Medical Research Council (United Kingdom) training fellowship. Drs Markus and Bevan were supported by the National Institute for Health Research Cambridge University Hospitals Comprehensive Biomedical Research Centre. Dr Markus was supported by a National Institute for Health Research Senior Investigator award. Dr Thijs was supported by a Clinical Investigator Grant from the scientific research fund, Fonds Wetenschappelijk Onderzoek Flanders. Dr Rost was supported by a National Institute of Neurological Disorders and Stroke grant (R01 NS082285-01).This is the final published version. It first appeared at http://stroke.ahajournals.org/content/46/6/1482.long

Exome array analysis of adverse reactions to fluoropyrimidine-based therapy for gastrointestinal cancer.

Fluoropyrimidines, including 5-fluororacil (5FU) and its pro-drug Capecitabine, are the common treatment for colorectal, breast, neck and head cancers-either as monotherapy or in combination therapy. Adverse reactions (ADRs) to the treatment are common and often result in treatment discontinuation or dose reduction. Factors contributing to ADRs, including genetic variation, are poorly characterized. We performed exome array analysis to identify genetic variants that contribute to adverse reactions. Our final dataset consisted of 504 European ancestry individuals undergoing fluoropyrimidine-based therapy for gastrointestinal cancer. A subset of 254 of these were treated with Capecitabine. All individuals were genotyped on the Illumina HumanExome Array. Firstly, we performed SNP and gene-level analyses of protein-altering variants on the array to identify novel associations the following ADRs, which were grouped into four phenotypes based on symptoms of diarrhea, mucositis, and neutropenia and hand-and-foot syndrome. Secondly, we performed detailed analyses of the HLA region on the same phenotypes after imputing the HLA alleles and amino acids. No protein-altering variants, or sets of protein-altering variants collapsed into genes, were associated with the main outcomes after Bonferroni correction. We found evidence that the HLA region was enriched for associations with Hand-and-Foot syndrome (p = 0.023), but no specific SNPs or HLA alleles were significant after Bonferroni correction. Larger studies will be required to characterize the genetic contribution to ADRs to 5FU. Future studies that focus on the HLA region are likely to be fruitful

MTHFR C677T genotype and small vessel disease

BACKGROUND AND PURPOSE: Elevated plasma homocysteine levels are associated with stroke. However, this might be a reflection of bias or confounding because trials have failed to demonstrate an effect from homocysteine lowering in stroke patients, although a possible benefit has been suggested in lacunar stroke. Genetic studies could potentially overcome these issues because genetic variants are inherited randomly and are fixed at conception. Therefore, we tested the homocysteine levels-associated genetic variant MTHFR C677T for association with magnetic resonance imaging-confirmed lacunar stroke and compared this with associations with large artery and cardioembolic stroke subtypes. METHODS: We included 1359 magnetic resonance imaging-confirmed lacunar stroke cases, 1824 large artery stroke cases, 1970 cardioembolic stroke cases, and 14 448 controls, all of European ancestry. Furthermore, we studied 3670 ischemic stroke patients in whom white matter hyperintensities volume was measured. We tested MTHFR C677T for association with stroke subtypes and white matter hyperintensities volume. Because of the established association of homocysteine with hypertension, we additionally stratified for hypertension status. RESULTS: MTHFR C677T was associated with lacunar stroke (P=0.0003) and white matter hyperintensity volume (P=0.04), but not with the other stroke subtypes. Stratifying the lacunar stroke cases for hypertension status confirmed this association in hypertensive individuals (P=0.0002), but not in normotensive individuals (P=0.30). CONCLUSIONS: MTHFR C677T was associated with magnetic resonance imaging-confirmed lacunar stroke, but not large artery or cardioembolic stroke. The association may act through increased susceptibility to, or interaction with, high blood pressure. This heterogeneity of association might explain the lack of effect of lowering homocysteine in secondary prevention trials which included all strokes.Collection of the UK Young Lacunar Stroke DNA Study (DNA Lacunar) was primarily supported by the Wellcome Trust (WT072952) with additional support from the Stroke Association (TSA 2010/01). Genotyping of the DNA Lacunar samples, and Dr Traylor, were supported by a Stroke Association Grant (TSA 2013/01). Genotyping of WTCCC2 ischaemic stroke study was funded by the Wellcome Trust. The Oxford Vascular Study has been funded by Wellcome Trust, Wolfson Foundation, UK Stroke Association, British Heart Foundation, Dunhill Medical Trust, National Institute of Health Research (NIHR), Medical Research Council, and the NIHR Oxford Biomedical Research Centre. Funding for the genotyping at Massachusetts General Hospital was provided by the Massachusetts General Hospital-Deane Institute for the Integrative Study of Atrial Fibrillation and Stroke and the National Institute of Neurological Disorders and Stroke (U01 NS069208). Dr Rutten-Jacobs was supported by a Stroke Association / British Heart Foundation programme grant (TSA BHF 2010/01). Dr Adib-Samii was supported by a Medical Research Council (United Kingdom) training fellowship. Dr Markus and Dr Bevan are supported by the National Institute for Health Research Cambridge University Hospitals Comprehensive Biomedical Research Centre. Dr Markus is supported by a National Institute for Health Research Senior Investigator award. Dr Thijs is supported by a Clinical Investigator Grant from the scientific research fund, Fonds Wetenschappelijk Onderzoek Flanders. Dr Levi is supported by a National Health and Medical Research Council (NHMRC Australia) Practitioner Fellowship and the Australian Stroke Genetics Collaboration has received Project Grant support from the NHMRC (App 1010287). Dr Rost was supported by a National Institute of Neurological Disorders and Stroke grant (R01 NS082285-01). Professor Rothwell is in receipt of an NIHR Senior Investigator Award and a Wellcome Trust Senior Investigator Award. We also acknowledge the use of the facilities of the Acute Vascular Imaging Centre, Oxford and the Cardiovascular Clinical Research Facility, Oxford. The sponsors of the study had no role in the study design, data collection, data analysis, interpretation, writing of the manuscript, or the decision to submit the manuscript for publication.This is the final version of the article. It first appeared from the American Heart Association via http://dx.doi.org/10.1161/STROKEAHA.115.01154