Modern to millennium-old greenhouse gases emitted from ponds and lakes of the Eastern Canadian Arctic (Bylot Island, Nunavut)

Ponds and lakes are widespread across the rapidly changing permafrost environments. Aquatic systems play an important role in global biogeochemical cycles, especially in greenhouse gas (GHG) exchanges between terrestrial systems and the atmosphere. The source, speciation and emission rate of carbon released from permafrost landscapes are strongly influenced by local conditions, hindering pan-Arctic generalizations. This study reports on GHG ages and emission rates from aquatic systems located on Bylot Island, in the continuous permafrost zone of the Eastern Canadian Arctic. Dissolved and ebullition gas samples were collected during the summer season from different types of water bodies located in a highly dynamic periglacial valley: polygonal ponds, collapsed ice-wedge trough ponds, and larger lakes. The results showed strikingly different ages and fluxes depending on aquatic system types. Polygonal ponds were net sinks of dissolved CO2, but variable sources of dissolved CH4. They presented the highest ebullition fluxes, 1 or 2 orders of magnitude higher than from other ponds and lakes. Trough ponds appeared as substantial GHG sources, especially when their edges were actively eroding. Both types of ponds produced modern to hundreds of years old (< 550 yr BP) GHG, even if trough ponds could contain much older carbon (> 2000 yr BP) derived from freshly eroded peat. Lakes had small dissolved and ebullition fluxes, however they released much older GHG, including millennium-old CH4 (up to 3500 yr BP) from lake central areas. Acetoclastic methanogenesis dominated at all study sites and there was minimal, if any, methane oxidation in gas emitted through ebullition. These findings provide new insights on GHG emissions by permafrost aquatic systems and their potential positive feedback effect on climate

Vesicoureteral Reflux and Other Urinary Tract Malformations in Mice Compound Heterozygous for Pax2 and Emx2

Congenital anomalies of the kidney and urinary tract (CAKUT) are the most common cause of chronic kidney disease in children. This disease group includes a spectrum of urinary tract defects including vesicoureteral reflux, duplex kidneys and other developmental defects that can be found alone or in combination. To identify new regulators of CAKUT, we tested the genetic cooperativity between several key regulators of urogenital system development in mice. We found a high incidence of urinary tract anomalies in Pax2;Emx2 compound heterozygous mice that are not found in single heterozygous mice. Pax2+/−;Emx2+/− mice harbor duplex systems associated with urinary tract obstruction, bifid ureter and a high penetrance of vesicoureteral reflux. Remarkably, most compound heterozygous mice refluxed at low intravesical pressure. Early analysis of Pax2+/−;Emx2+/− embryos point to ureter budding defects as the primary cause of urinary tract anomalies. We additionally establish Pax2 as a direct regulator of Emx2 expression in the Wolffian duct. Together, these results identify a haploinsufficient genetic combination resulting in CAKUT-like phenotype, including a high sensitivity to vesicoureteral reflux. As both genes are located on human chromosome 10q, which is lost in a proportion of VUR patients, these findings may help understand VUR and CAKUT in humans

Eosinophilic Enteritis Confined to an Ileostomy Site

Eosinophilic enteritis is a rather rare condition that can manifest anywhere from esophagus to rectum. Its description in the literature is sparse, but associations have been made with collagen vascular disease, malignancy, food allergy, parasitic or viral infections, inflammatory bowel disease, and drug sensitivity. We present the case of a 41-year-old male diagnosed with ulcerative colitis who underwent proctocolectomy with ileal pouch anal anastomosis and loop ileostomy formation utilizing Seprafilm®, who later developed eosinophilic enteritis of the loop ileostomy site. This is the first report of eosinophilic enteritis and its possible link to the use of bioabsorbable adhesion barriers

Condensin I Recruitment to Base Damage-Enriched DNA Lesions Is Modulated by PARP1

Condensin I is important for chromosome organization and segregation in mitosis. We previously showed that condensin I also interacts with PARP1 in response to DNA damage and plays a role in single-strand break repair. However, whether condensin I physically associates with DNA damage sites and how PARP1 may contribute to this process were unclear. We found that condensin I is preferentially recruited to DNA damage sites enriched for base damage. This process is dictated by PARP1 through its interaction with the chromosome-targeting domain of the hCAP-D2 subunit of condensin I

Associations of iron metabolism genes with blood manganese levels: a population-based study with validation data from animal models

<p>Abstract</p> <p>Background</p> <p>Given mounting evidence for adverse effects from excess manganese exposure, it is critical to understand host factors, such as genetics, that affect manganese metabolism.</p> <p>Methods</p> <p>Archived blood samples, collected from 332 Mexican women at delivery, were analyzed for manganese. We evaluated associations of manganese with functional variants in three candidate iron metabolism genes: <it>HFE </it>[hemochromatosis], <it>TF </it>[transferrin], and <it>ALAD </it>[δ-aminolevulinic acid dehydratase]. We used a knockout mouse model to parallel our significant results as a novel method of validating the observed associations between genotype and blood manganese in our epidemiologic data.</p> <p>Results</p> <p>Percentage of participants carrying at least one copy of <it>HFE C282Y</it>, <it>HFE H63D</it>, <it>TF P570S</it>, and <it>ALAD K59N </it>variant alleles was 2.4%, 17.7%, 20.1%, and 6.4%, respectively. Percentage carrying at least one copy of either <it>C282Y </it>or <it>H63D </it>allele in <it>HFE </it>gene was 19.6%. Geometric mean (geometric standard deviation) manganese concentrations were 17.0 (1.5) μg/l. Women with any <it>HFE </it>variant allele had 12% lower blood manganese concentrations than women with no variant alleles (β = -0.12 [95% CI = -0.23 to -0.01]). <it>TF </it>and <it>ALAD </it>variants were not significant predictors of blood manganese. In animal models, <it>Hfe</it>^-/-mice displayed a significant reduction in blood manganese compared with <it>Hfe</it>^+/+mice, replicating the altered manganese metabolism found in our human research.</p> <p>Conclusions</p> <p>Our study suggests that genetic variants in iron metabolism genes may contribute to variability in manganese exposure by affecting manganese absorption, distribution, or excretion. Genetic background may be critical to consider in studies that rely on environmental manganese measurements.</p

The effects of spatial legacies following shifting management practices and fire on boreal forest age structure

Forest age structure and its spatial arrangement are important elements of sustainable forestry because of their effects on biodiversity and timber availability. Forest management objectives that include specific forest age structure may not be easily attained due to constraints imposed by the legacies of historical management and natural disturbance. We used a spatially explicit stochastic model to explore the synergetic effects of forest management and fire on boreal forest age structure. Specifically, we examined (1) the duration of spatial legacies of different management practices in the boreal forest, (2) how multiple shifts in management practices affect legacy duration and the spatial trajectories of forest age structure, and (3) how fire influences legacy duration and pattern development in combination with harvesting. Results based on 30 replicates of 500 years for each scenario indicate that (1) spatial legacies persist over 200 years and the rate at which legacies are overcome depends on whether new management targets are in synchrony with existing spatial pattern; (2) age specific goals were met faster after multiple management shifts due to the similar spatial scale of the preceding management types; (3) because large fires can erase the spatial pattern created by smaller disturbances, scenarios with fire had shorter lags than scenarios without fire. These results suggest that forest management goals can be accelerated by applying management at a similar spatial scale as existing spatial patterns. Also, management planning should include careful consideration of historical management as well as current and likely future disturbances

The use of group dynamics strategies to enhance cohesion in a lifestyle intervention program for obese children

<p>Abstract</p> <p>Background</p> <p>Most research pertaining to childhood obesity has assessed the effectiveness of preventative interventions, while relatively little has been done to advance knowledge in the treatment of obesity. Thus, a 4-week family- and group-based intervention utilizing group dynamics strategies designed to increase cohesion was implemented to influence the lifestyles and physical activity levels of obese children.</p> <p>Methods/Design</p> <p>This paper provides an overview of the rationale for and implementation of the intervention for obese children and their families. Objectives of the intervention included the modification of health behaviors and cohesion levels through the use of group dynamics strategies. To date, a total of 15 children (7 boys and 8 girls, mean age = 10.5) and their families have completed the intervention (during the month of August 2008). Physiological and psychological outcomes were assessed throughout the 4-week intervention and at 3-, 6-, and 12-month follow-up periods.</p> <p>Discussion</p> <p>It is believed that the information provided will help researchers and health professionals develop similar obesity treatment interventions through the use of evidence-based group dynamics strategies. There is also a need for continued research in this area, and it is our hope that the Children's Health and Activity Modification Program (C.H.A.M.P.) will provide a strong base from which others may build.</p

Evidence of maternal QTL affecting growth and obesity in adult mice

Most quantitative trait loci (QTL) studies fail to account for the effect that the maternal genotype may have on an individual’s phenotypes, even though maternal effect QTL have been shown to account for considerable variation in growth and obesity traits in mouse models. Moreover, the fetal programming theory suggests that maternal effects influence an offspring’s adult fitness, although the genetic nature of fetal programming remains unclear. Within this context, our study focused on mapping genomic regions associated with maternal effect QTL by analyzing the phenotypes of chromosomes 2 and 7 subcongenic mice from genetically distinct dams. We analyzed 12 chromosome 2 subcongenic strains that spanned from 70 to 180 Mb with CAST/EiJ donor regions on the background of C57BL/6 J, and 14 chromosome 7 subcongenic strains that spanned from 81 to 111 Mb with BALB/cByJ donor regions on C57BL/6ByJ background. Maternal QTL analyses were performed on the basis of overlapping donor regions between subcongenic strains. We identified several highly significant (P < 5 × 10−4) maternal QTL influencing total body weight, organ weight, and fat pad weights in both sets of subcongenics. These QTL accounted for 1.9-11.7% of the phenotypic variance for growth and obesity and greatly narrowed the genomic regions associated with the maternal genetic effects. These maternal effect QTL controlled phenotypic traits in adult mice, suggesting that maternal influences at early stages of development may permanently affect offspring performance. Identification of maternal effects in our survey of two sets of subcongenic strains, representing approximately 5% of the mouse genome, supports the hypothesis that maternal effects represent significant sources of genetic variation that are largely ignored in genetic studies

Effects of Light, Food Availability and Temperature Stress on the Function of Photosystem II and Photosystem I of Coral Symbionts

Background: Reef corals are heterotrophic coelenterates that achieve high productivity through their photosynthetic dinoflagellate symbionts. Excessive seawater temperature destabilises this symbiosis and causes corals to "bleach," lowering their photosynthetic capacity. Bleaching poses a serious threat to the persistence of coral reefs on a global scale. Despite expanding research on the causes of bleaching, the mechanisms remain a subject of debate.\ud \ud Methodology/Principal Findings: This study determined how light and food availability modulate the effects of temperature stress on photosynthesis in two reef coral species. We quantified the activities of Photosystem II, Photosystem I and whole chain electron transport under combinations of normal and stressful growth temperatures, moderate and high light levels and the presence or absence of feeding of the coral hosts. Our results show that PS1 function is comparatively robust against temperature stress in both species, whereas PS2 and whole chain electron transport are susceptible to temperature stress. In the symbiotic dinoflagellates of Stylophora pistillata the contents of chlorophyll and major photosynthetic complexes were primarily affected by food availability. In Turbinaria reniformis growth temperature was the dominant influence on the contents of the photosynthetic complexes. In both species feeding the host significantly protected photosynthetic function from high temperature stress.\ud \ud Conclusions/Significance: Our findings support the photoinhibition model of coral bleaching and demonstrate that PS1 is not a major site for thermal damage during bleaching events. Feeding mitigates bleaching in two scleractinian corals, so that reef responses to temperature stresses will likely be influenced by the coinciding availabilities of prey for the host