Spatiotemporal Variability in Biomass and Forage Quality Across a Temperate Landscape with Heterogeneous Phenology Patterns (Poster)

Although spatial and temporal heterogeneity in grassland biomass and forage quality is well-recognized to play an important role in migratory ungulate population dynamics, attempts to directly quantify biomass and forage quality across temperate landscapes throughout the growing season are limited. It is generally recognized that biomass and forage quality are directly related to phenology, but little is known about how seasonal biomass and forage quality differs across land use and biophysical gradients with varying phenology patterns. This study uses field estimates of biomass, chlorophyll concentration, crude protein, and in vitro dry matter digestibility collected from 20, 250m2 grassland plots throughout the summers of 2013 and 2014 to quantify how biomass and forage quality differ across land uses and biophysical gradients in the migratory elk (Cervus elaphus) range in the Upper Yellowstone River Basin. Key findings were that irrigated agriculture had overall greater and longer available biomass and forage quality throughout the growing season compared to private and public grasslands with natural phenology patterns. And that areas that begin growth later in the season had overall greater biomass and forage quality than areas with mid and early phenology characteristics, but availability was shorter. These results suggest that seasonal patterns of biomass and forage quality differ with phenological characteristics across temperate landscapes. This information should be incorporated in our understanding of spatiotemporal patterns of vegetation important for studying migratory ungulate ecology and predicting the effects of climate change and human land use on vegetation dynamics in temperate landscapes

Lotic-SIPCO2: Adaptation of an open-source CO2 sensor system and examination of associated emission uncertainties across a range of stream sizes and land uses

River networks play a crucial role in the global carbon cycle, as relevant sources of carbon dioxide (CO2) to the atmosphere. Advancements in high-frequency monitoring in aquatic environments have enabled measurement of dissolved CO2 concentration at temporal resolutions essential for studying carbon variability and evasion from these dynamic ecosystems. Here, we describe the adaptation, deployment, and validation of an open-source and relatively low-cost in situ pCO2 sensor system for lotic ecosystems, the lotic-SIPCO2. We tested the lotic-SIPCO2 in 10 streams that spanned a range of land cover and basin size. Key system adaptations for lotic environments included prevention of biofouling, configuration for variable stage height, and reduction of headspace equilibration time. We then examined which input parameters contribute the most to uncertainty in estimating CO2 emission rates and found scaling factors related to the gas exchange velocity were the most influential when CO2 concentration was significantly above saturation. Near saturation, sensor measurement of pCO2 contributed most to uncertainty in estimating CO2 emissions. We also found high-frequency measurements of pCO2 were not necessary to accurately estimate median emission rates given the CO2 regimes of our streams, but daily to weekly sampling was sufficient. High-frequency measurements of pCO2 remain valuable for exploring in-stream metabolic variability, source partitioning, and storm event dynamics. Our adaptations to the SIPCO2 offer a relatively affordable and robust means of monitoring dissolved CO2 in lotic ecosystems. Our findings demonstrate priorities and related considerations in the design of monitoring projects of dissolved CO2 and CO2 evasion dynamics more broadly

Dominance of Diffusive Methane Emissions From Lowland Headwater Streams Promotes Oxidation and Isotopic Enrichment

Inland waters are the largest natural source of methane (CH4) to the atmosphere, yet the contribution from small streams to this flux is not clearly defined. To fully understand CH4 emissions from streams and rivers, we must consider the relative importance of CH4 emission pathways, the prominence of microbially-mediated production and oxidation of CH4, and the isotopic signature of emitted CH4. Here, we construct a complete CH4 emission budgets for four lowland headwater streams by quantifying diffusive CH4 emissions and comparing them to previously published rates of ebullitive emissions. We also examine the isotopic composition of CH4 along with the sediment microbial community to investigate production and oxidation across the streams. We find that all four streams are supersaturated with respect to CH4 with diffusive emissions accounting for approximately 78–100% of total CH4 emissions. Isotopic and microbial data suggest CH4 oxidation is prevalent across the streams, depleting approximately half of the dissolved CH4 pool before emission. We propose a conceptual model of CH4 production, oxidation, and emission from small streams, where the dominance of diffusive emissions is greater compared to other aquatic ecosystems, and the impact of CH4 oxidation is observable in the emitted isotopic values. As a result, we suggest the CH4 emitted from small streams is isotopically heavy compared to lentic ecosystems. Our results further demonstrate streams are important components of the global CH4 cycle yet may be characterized by a unique pattern of cycling and emission that differentiate them from other aquatic ecosystems

Maternal health conditions during pregnancy and acute leukemia in children with Down syndrome: A Children's Oncology Group study

Children with Down syndrome (DS) have about a 20-fold increased risk of developing leukemia. Early childhood infections may protect against acute lymphoid leukemia (ALL) in children with and without DS. We examined whether maternal infections and health conditions during pregnancy were associated with acute leukemia in children with DS

Vitamin supplement use among children with Down syndrome and risk of leukemia: A Children’s Oncology Group (COG) Study

Vitamin supplements have been proposed for children with Down syndrome (DS) with claims of improving cognitive abilities, or immune or thyroid function. Several studies have shown decreased levels of zinc in this population. Because children with DS have a 50-fold increased risk of developing acute leukemia during the first 5 years of life, we explored the relation between child vitamin and herbal supplement use and the risk for leukemia in a case-control study. During the period 1997–2002, we enrolled 158 children with DS aged 0–18 years that were diagnosed with acute lymphoblastic leukemia (ALL) (n=97) or acute myeloid leukemia (AML) (n=61) at participating COG institutions. We enrolled 173 DS children without leukemia (controls), selected from the cases’ primary care clinic and frequency matched on age. Data were collected via telephone interviews with mothers of the index child regarding use of multivitamins, zinc, vitamin C, iron, and herbal supplements, including age at first use, frequency and duration. Among controls, 57% reported regular multivitamin use (≥ 3 times/week for ≥ 3 months) compared with 48% of ALL cases and 61% of AML cases. We found no evidence of an association between child’s regular multivitamin use and ALL or AML (adjusted odds ratios (ORs)=0.94 [95% confidence interval 0.52, 1.70] and 1.90 [0.73, 4.91], respectively. There was a suggestion of an increased risk for AML associated with regular multivitamin use during the first year of life or for an extended duration (ORs = 2.38 [0.94, 5.76] and 2.59 [1.02, 6.59], respectively). Despite being the largest study of DS-leukemia, our sample size was small, resulting in imprecise effect estimates. Future research should include larger sample sizes as well as a full assessment of diet including vitamin supplementation to adequately examine the relation between nutritional status and childhood leukemia

Integrated genomics of ovarian xenograft tumor progression and chemotherapy response

<p>Abstract</p> <p>Background</p> <p>Ovarian cancer is the most deadly gynecological cancer with a very poor prognosis. Xenograft mouse models have proven to be one very useful tool in testing candidate therapeutic agents and gene function <it>in vivo</it>. In this study we identify genes and gene networks important for the efficacy of a pre-clinical anti-tumor therapeutic, MT19c.</p> <p>Methods</p> <p>In order to understand how ovarian xenograft tumors may be growing and responding to anti-tumor therapeutics, we used genome-wide mRNA expression and DNA copy number measurements to identify key genes and pathways that may be critical for SKOV-3 xenograft tumor progression. We compared SKOV-3 xenografts treated with the ergocalciferol derived, MT19c, to untreated tumors collected at multiple time points. Cell viability assays were used to test the function of the PPARγ agonist, Rosiglitazone, on SKOV-3 cell growth.</p> <p>Results</p> <p>These data indicate that a number of known survival and growth pathways including Notch signaling and general apoptosis factors are differentially expressed in treated vs. untreated xenografts. As tumors grow, cell cycle and DNA replication genes show increased expression, consistent with faster growth. The steroid nuclear receptor, PPARγ, was significantly up-regulated in MT19c treated xenografts. Surprisingly, stimulation of PPARγ with Rosiglitazone reduced the efficacy of MT19c and cisplatin suggesting that PPARγ is regulating a survival pathway in SKOV-3 cells. To identify which genes may be important for tumor growth and treatment response, we observed that MT19c down-regulates some high copy number genes and stimulates expression of some low copy number genes suggesting that these genes are particularly important for SKOV-3 xenograft growth and survival.</p> <p>Conclusions</p> <p>We have characterized the time dependent responses of ovarian xenograft tumors to the vitamin D analog, MT19c. Our results suggest that PPARγ promotes survival for some ovarian tumor cells. We propose that a combination of regulated expression and copy number can identify genes that are likely important for chemotherapy response. Our findings suggest a new approach to identify candidate genes that are critical for anti-tumor therapy.</p

Class dynamics of development: a methodological note

This article argues that class relations are constitutive of developmental processes and central to understanding inequality within and between countries. In doing so it illustrates and explains the diversity of the actually existing forms of class relations, and the ways in which they interplay with other social relations such as gender and ethnicity. This is part of a wider project to re- vitalise class analysis in the study of development problems and experiences

Establishment of the epithelial-specific transcriptome of normal and malignant human breast cells based on MPSS and array expression data

INTRODUCTION: Diverse microarray and sequencing technologies have been widely used to characterise the molecular changes in malignant epithelial cells in breast cancers. Such gene expression studies to identify markers and targets in tumour cells are, however, compromised by the cellular heterogeneity of solid breast tumours and by the lack of appropriate counterparts representing normal breast epithelial cells. METHODS: Malignant neoplastic epithelial cells from primary breast cancers and luminal and myoepithelial cells isolated from normal human breast tissue were isolated by immunomagnetic separation methods. Pools of RNA from highly enriched preparations of these cell types were subjected to expression profiling using massively parallel signature sequencing (MPSS) and four different genome wide microarray platforms. Functional related transcripts of the differential tumour epithelial transcriptome were used for gene set enrichment analysis to identify enrichment of luminal and myoepithelial type genes. Clinical pathological validation of a small number of genes was performed on tissue microarrays. RESULTS: MPSS identified 6,553 differentially expressed genes between the pool of normal luminal cells and that of primary tumours substantially enriched for epithelial cells, of which 98% were represented and 60% were confirmed by microarray profiling. Significant expression level changes between these two samples detected only by microarray technology were shown by 4,149 transcripts, resulting in a combined differential tumour epithelial transcriptome of 8,051 genes. Microarray gene signatures identified a comprehensive list of 907 and 955 transcripts whose expression differed between luminal epithelial cells and myoepithelial cells, respectively. Functional annotation and gene set enrichment analysis highlighted a group of genes related to skeletal development that were associated with the myoepithelial/basal cells and upregulated in the tumour sample. One of the most highly overexpressed genes in this category, that encoding periostin, was analysed immunohistochemically on breast cancer tissue microarrays and its expression in neoplastic cells correlated with poor outcome in a cohort of poor prognosis estrogen receptor-positive tumours. CONCLUSION: Using highly enriched cell populations in combination with multiplatform gene expression profiling studies, a comprehensive analysis of molecular changes between the normal and malignant breast tissue was established. This study provides a basis for the identification of novel and potentially important targets for diagnosis, prognosis and therapy in breast cancer

Rescue of deficits by Brwd1 copy number restoration in the Ts65Dn mouse model of Down syndrome

With an incidence of ~1 in 800 births, Down syndrome (DS) is the most com- mon chromosomal condition linked to intellectual disability worldwide. While the genetic basis of DS has been identified as a triplication of chromosome 21 (HSA21), the genes encoded from HSA 21 that directly contribute to cognitive de fi cits remain incompletely understood. Here, we found that the HSA21- encoded chromatin effector, BRWD1, was upregulated in neurons derived from iPS cells from an individual with Down syndrome and brain of trisomic mice. We showed that selective copy number restoration of Brwd1 in trisomic animals rescued de fi cits in hippocampal LTP, cognition and gene expression. We demonstrated that Brwd1 tightly binds the BAF chromatin remodeling complex, and that increased Brwd1 expression promotes BAF genomic mistargeting. Importantly, Brwd1 renormalization rescued aberrant BAF localization, along with associated changes in chromatin accessibility and gene expression. These findings establish BRWD1 as a key epigenomic mediator of normal neurodevelopment and an important contributor to DS-related phenotypes

Sex differences in the traumatic stress response: the role of adult gonadal hormones

Abstract Background Our previous study revealed that adult female rats respond differently to trauma than adult males, recapitulating sex differences in symptoms of post-traumatic stress disorder (PTSD) exhibited by women and men. Here, we asked two questions: does the female phenotype depend on (1) social housing condition and/or (2) circulating gonadal hormones? Methods For the first study, the effects of single prolonged stress (SPS) were compared for females singly or pair-housed. For the second study, adult male and female rats were gonadectomized or sham-gonadectomized 2 weeks prior to exposure to SPS, with half the gonadectomized rats given testosterone. In addition to the typical measures of the trauma response in rats, acoustic startle response (ASR), and the dexamethasone suppression test (DST), we also used two other measures typically used to assess depressive-like responses, social interaction and sucrose preference. Glucocorticoid receptor (GR) expression in the hypothalamus was also examined. Results We now report that the distinct trauma response of female rats is not influenced by social housing condition. Moreover, sex differences in the response to SPS based on ASR and DST, replicated in the current study, are independent of adult gonadal hormones. Regardless of hormonal status, traumatized males show a hyper-responsive phenotype whereas traumatized females do not. Moreover, testosterone treatment in adulthood did not masculinize the response to trauma in females. Notably, both sucrose preference and social interaction tests revealed an effect of trauma in females but not in males, with the effects of SPS on sucrose preference dependent on ovarian hormones. Effects of SPS on GR expression in the hypothalamus also depended on gonadal hormones in females. Conclusions We propose that the trauma response for female rats is depressive in nature, recapitulating the female bias in PTSD for internalizing symptoms and major depression in contrast to the externalizing symptoms of males. Presumed core markers of PTSD (enhanced ASR and negative feedback control of corticosterone) are apparently relevant only to males and are independent of adult gonadal hormones. Such sex differences in trauma responding are likely determined earlier in life. We conclude that males and females show fundamentally different responses to trauma that do not simply reflect differences in resilience