Recovery of Sea Urchin Diadema Antillarum Populations is Correlated to Increased Coral and Reduced Macroalgal Cover

We surveyed the benthic community structure and population density of the long-spined sea urchinDiadema antillarum on the shallow fore-reefs of the Gandoca-Manzanillo Wildlife Refuge, Caribbean Costa Rica, in September and October 2004. In zones with high densities of D. antillarum (\u3e0.6 ind. m–2), the cover of non-calcareous macroalgae, known coral competitors, was low and that of live coral was high, whereas the opposite occurred in zones with low densities of D. antillarum (D. antillarum density was not related to the coverage of calcareous macroalgae, which are not viewed as coral competitors. Mean density of D. antillarum was 0.2 ind. m–2 and the total area covered by live coral was 14%. D. antillarum density and area covered by live coral were 2 and 7 times larger, respectively, than those reported 4 yr earlier for the study site. Within the same period, the proportion contributed by non-calcareous macroalgae to total algal cover declined from ~79 to 48%. Results indicate that various families of scleractinian corals in the Caribbean coast of Costa Rica have increased in abundance, that non-calcareous macroalgae have declined, and that recovering D. antillarum densities are correlated with these observations

Southern California margin benthic foraminiferal assemblages record recent centennial-scale changes in oxygen minimum zone

Microfossil assemblages provide valuable records to investigate variability in continental margin biogeochemical cycles, including dynamics of the oxygen minimum zone (OMZ). Analyses of modern assemblages across environmental gradients are necessary to understand relationships between assemblage characteristics and environmental factors. Five cores were analyzed from the San Diego margin (32∘42′00′′ N, 117∘30′00′′ W; 300–1175 m water depth) for core top benthic foraminiferal assemblages to understand relationships between community assemblages and spatial hydrographic gradients as well as for down-core benthic foraminiferal assemblages to identify changes in the OMZ through time. Comparisons of benthic foraminiferal assemblages from two size fractions (63–150 and \u3e150 µm) exhibit similar trends across the spatial and environmental gradient or in some cases exhibit more pronounced spatial trends in the \u3e150 µm fraction. A range of species diversity exists within the modern OMZ (1.910–2.586 H, Shannon index), suggesting that diversity is not driven by oxygenation alone. We identify two hypoxic-associated species (B. spissa and U. peregrina), one oxic-associated species (G. subglobosa) and one OMZ edge-associated species (B. argentea). Down-core analysis of indicator species reveals variability in the upper margin of the OMZ (528 m water depth) while the core of the OMZ (800 m) and below the OMZ (1175 m) remained stable in the last 1.5 kyr. We document expansion of the upper margin of the OMZ beginning 400 BP on the San Diego margin that is synchronous with other regional records of oxygenation

Improvement Science in Teacher Preparation at California State University: How teacher preparation partnerships are building capacity to learn to improve

One of the most pressing educational problems in the United States is improving the quality of teacher preparation (Goldhaber, Liddle, & Theobald, 2013; National Academy of Sciences, National Academy of Engineering, & Institute of Medicine, 2007). Over the last decade the education sector has begun to learn from other sectors -- especially health care -- about the potential power of improvement science as an approach to improving the quality and reliability of educational systems (Bryk, Gomez, Grunow, & LeMahieu, 2015; Coburn, Penuel, & Geil, 2013; Lewis, 2015). Evidence from an effort to improve how beginning teachers are supported in three large urban districts through development and testing of feedback systems demonstrates the promise of improvement science methods for tackling persistent challenges in teaching (Hannan, Russell, Takahashi, & Park, 2015).This Innovation Highlight describes a network-based effort -- the New Generation of Educators Initiative (NGEI), funded by the S.D. Bechtel, Jr. Foundation -- that applies the principles and methods of improvement science (Langley, Moen, Nolan, Nolan, Norman, & Provost, 2009) to the challenge of improving how new teachers are prepared in the California State University System. The initiative emphasizes data-driven, continuous improvement by funding teacher preparation programs to routinely collect and analyze the data needed to monitor teacher candidates' progress toward competency in prioritized skills and to use the results of that analysis to (a) inform clinical support and teaching during the school year and (b) identify meaningful programmatic changes.The NGEI-funded teacher preparation programs also receive support from WestEd and SRI, which have developed a multipronged technical assistance strategy that is informed by improvement science. The technical assistance includes in-person trainings, cross-site webinars, monthly coaching calls with each site, annual convenings, and occasional site visits.The first section of this Innovation Highlight explains the theory of improvement science and how approaches that are informed by improvement science differ from other improvement efforts. The second section describes how NGEI has put this theory into practice through improvement science technical assistance for the NGEI grantees. Examples from the NGEI grantees are included throughout to illustrate how improvement science principles have been applied in the teacher preparation context

Increased importance of methane reduction for a 1.5 degree target

To understand the importance of methane on the levels of carbon emission reductions required to achieve temperature goals, a processed-based approach is necessary rather than reliance on the Transient Climate Response to Emissions. We show that plausible levels of methane (CH4) mitigation can make a substantial difference to the feasibility of achieving the Paris climate targets through increasing the allowable carbon emissions. This benefit is enhanced by the indirect effects of CH4 on ozone (O3). Here the differing effects of CH4 and CO2 on land carbon storage, including the effects of surface O3, lead to an additional increase in the allowable carbon emissions with CH4 mitigation. We find a simple robust relationship between the change in the 2100 CH4 concentration and the extra allowable cumulative carbon emissions between now and 2100 (0.27 ± 0.05 GtC per ppb CH4). This relationship is independent of modelled climate sensitivity and precise temperature target, although later mitigation of CH4 reduces its value and thus methane reduction effectiveness. Up to 12% of this increase in allowable emissions is due to the effect of surface ozone. We conclude early mitigation of CH4 emissions would significantly increase the feasibility of stabilising global warming below 1.5C, alongside having co-benefits for human and ecosystem health

Contribution of regional sources to atmospheric methane over the Amazon Basin in 2010 and 2011

We present an assessment of methane (CH4) atmospheric concentrations over the Amazon Basin for 2010 and 2011 using a 3-D atmospheric chemical transport model, two wetland emission models, and new observations made during biweekly flights made over four locations within the basin. We attempt to constrain basin-wide CH4 emissions using the observations, and since 2010 was an unusually dry year, we assess the effect of this drought on Amazonian methane emissions. We find that South American emissions contribute up to 150 ppb to concentrations at the sites, mainly originating from within the basin. Our atmospheric model simulations agree reasonably well with measurements at three of the locations (0.28 ≤ r2 ≤ 0.63, mean bias ≤ 9.5 ppb). Attempts to improve the simulated background CH4 concentration through analysis of simulated and observed sulphur hexafluoride concentrations do not improve the model performance, however. Through minimisation of seasonal biases between the simulated and observed atmospheric concentrations, we scale our prior emission inventories to derive total basin-wide methane emissions of 36.5–41.1 Tg(CH4)/yr in 2010 and 31.6–38.8 Tg(CH4)/yr in 2011. These totals suggest that the Amazon contributes significantly (up to 7%) to global CH4 emissions. Our analysis indicates that factors other than precipitation, such as temperature variations or tree mortality, may have affected microbial emission rates. However, given the uncertainty of our emission estimates, we cannot say definitively whether the noncombustion emissions from the region were different in 2010 and 2011, despite contrasting meteorological conditions between the two years

Genetic analysis of hyperemesis gravidarum reveals association with intracellular calcium release channel (RYR2)

Hyperemesis Gravidarum (HG), severe nausea/vomiting in pregnancy (NVP), can cause poor maternal/fetal outcomes. Genetic predisposition suggests the genetic component is essential in discovering an etiology. We performed whole-exome sequencing of 5 families followed by analysis of variants in 584 cases/431 controls. Variants in RYR2 segregated with disease in 2 families. The novel variant L3277R was not found in any case/control. The rare variant, G1886S was more common in cases (p = 0.046) and extreme cases (p = 0.023). Replication of G1886S using Norwegian/Australian data was supportive. Common variants rs790899 and rs1891246 were significantly associated with HG and weight loss. Copy-number analysis revealed a deletion in a patient. RYR2 encodes an intracellular calcium release channel involved in vomiting, cyclic-vomiting syndrome, and is a thyroid hormone target gene. Additionally, RYR2 is a downstream drug target of Inderal, used to treat HG and CVS. Thus, herein we provide genetic evidence for a pathway and therapy for HG

Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics

Funding Information: Researchers were funded by investment from the European Regional Development Fund (ERDF) and the European Social Fund (ESF) Convergence Programme for Cornwall and the Isles of Scilly [J.T.]; European Research Council (ERC) [grant: SZ-245 50371-GLUCOSEGENES-FP7-IDEAS-ERC to T.M.F., A.R.W.], [ERC Consolidator Grant, ERC-2014-CoG-648916 to V.W.V.J.], [P.R.N.]; University of Bergen, KG Jebsen and Helse Vest [P.R.N.]; Wellcome Trust Senior Investigator Awards [A.T.H. (WT098395), M.I.M. (WT098381)]; National Institute for Health Research (NIHR) Senior Investigator Award (NF-SI-0611–10219); Sir Henry Dale Fellowship (Wellcome Trust and Royal Society grant: WT104150) [R.M.F., R.N.B.]; 4-year studentship (Grant Code: WT083431MF) [R.C.R]; the European Research Council under the European Union’s Seventh Framework Programme (FP/2007– 2013)/ERC Grant Agreement (grant number 669545; Develop Obese) [D.A.L.]; US National Institute of Health (grant: R01 DK10324) [D.A.L, C.L.R]; Wellcome Trust GWAS grant (WT088806) [D.A.L] and NIHR Senior Investigator Award (NF-SI-0611–10196) [D.A.L]; Wellcome Trust Institutional Strategic Support Award (WT097835MF) [M.A.T.]; The Diabetes Research and Wellness Foundation Non-Clinical Fellowship [J.T.]; Australian National Health and Medical Research Council Early Career Fellowship (APP1104818) [N.M.W.]; Daniel B. Burke Endowed Chair for Diabetes Research [S.F.A.G.]; UK Medical Research Council Unit grants MC_UU_12013_5 [R.C.R, L.P, S.R, C.L.R, D.M.E., D.A.L.] and MC_UU_12013_4 [D.M.E.]; Medical Research Council (grant: MR/M005070/1) [M.N.W., S.E.J.]; Australian Research Council Future Fellowship (FT130101709) [D.M.E] and (FT110100548) [S.E.M.]; NIHR Oxford Biomedical Research Centre (BRC); Oak Foundation Fellowship and Novo Nordisk Foundation (12955) [B.F.]; FRQS research scholar and Clinical Scientist Award by the Canadian Diabetes Association and the Maud Menten Award from the Institute of Genetics– Canadian Institute of Health Research (CIHR) [MFH]; CIHR— Frederick Banting and Charles Best Canada Graduate Scholarships [C.A.]; FRQS [L.B.]; Netherlands Organization for Health Research and Development (ZonMw–VIDI 016.136.361) [V.W.V.J.]; National Institute on Aging (R01AG29451) [J.M.M.]; 2010–2011 PRIN funds of the University of Ferrara—Holder: Prof. Guido Barbujani, Supervisor: Prof. Chiara Scapoli—and in part sponsored by the European Foundation for the Study of Diabetes (EFSD) Albert Renold Travel Fellowships for Young Scientists, ‘5 per mille’ contribution assigned to the University of Ferrara, income tax return year 2009 and the ENGAGE Exchange and Mobility Program for ENGAGE training funds, ENGAGE project, grant agreement HEALTH-F4–2007-201413 [L.M.]; ESRC (RES-060–23-0011) [C.L.R.]; National Institute of Health Research ([S.D., M.I.M.], Senior Investigator Award (NF-SI-0611–10196) [D.A.L]); Australian NHMRC Fellowships Scheme (619667) [G.W.M]. For study-specific funding, please see Supplementary Material. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. Funding to pay the Open Access publication charges for this article was provided by the Charity Open Access Fund (COAF). Funding Information: We are extremely grateful to the participants and families who contributed to all of the studies and the teams of investigators involved in each one. These include interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists and nurses. This research has been conducted using the UK Biobank Resource (Application numbers 7036 and 12703). For additional study-specific acknowledgements, please see Supplementary Material. Conflict of Interest statement. D.A.L. has received support from Roche Diagnostics and Medtronic for biomarker research unrelated to the work presented here. Funding Researchers were funded by investment from the European Regional Development Fund (ERDF) and the European Social Fund (ESF) Convergence Programme for Cornwall and the Isles of Scilly [J.T.]; European Research Council (ERC) [grant: SZ-245 50371-GLUCOSEGENES-FP7-IDEAS-ERC to T.M.F., A.R.W.], [ERC Consolidator Grant, ERC-2014-CoG-648916 to V.W.V.J.], [P.R.N.]; University of Bergen, KG Jebsen and Helse Vest [P.R.N.]; Wellcome Trust Senior Investigator Awards [A.T.H. (WT098395), M.I.M. (WT098381)]; National Institute for Health Research (NIHR) Senior Investigator Award (NF-SI-0611-10219); Sir Henry Dale Fellowship (Wellcome Trust and Royal Society grant: WT104150) [R.M.F., R.N.B.]; 4-year studentship (Grant Code: WT083431MF) [R.C.R]; the European Research Council under the European Union's Seventh Framework Programme (FP/2007-2013)/ERC Grant Agreement (grant number 669545; Develop Obese) [D.A.L.]; US National Institute of Health (grant: R01 DK10324) [D.A.L, C.L.R]; Wellcome Trust GWAS grant (WT088806) [D.A.L] and NIHR Senior Investigator Award (NF-SI-0611-10196) [D.A.L]; Wellcome Trust Institutional Strategic Support Award (WT097835MF) [M.A.T.]; The Diabetes Research and Wellness Foundation Non-Clinical Fellowship [J.T.]; Australian National Health and Medical Research Council Early Career Fellowship (APP1104818) [N.M.W.]; Daniel B. Burke Endowed Chair for Diabetes Research [S.F.A.G.]; UK Medical Research Council Unit grants MC_UU_12013_5 [R.C.R, L.P, S.R, C.L.R, D.M.E., D.A.L.] and MC_UU_12013_4 [D.M.E.]; Medical Research Council (grant: MR/M005070/1) [M.N.W., S.E.J.]; Australian Research Council Future Fellowship (FT130101709) [D.M.E] and (FT110100548) [S.E.M.]; NIHR Oxford Biomedical Research Centre (BRC); Oak Foundation Fellowship and Novo Nordisk Foundation (12955) [B.F.]; FRQS research scholar and Clinical Scientist Award by the Canadian Diabetes Association and the Maud Menten Award from the Institute of Genetics-Canadian Institute of Health Research (CIHR) [MFH]; CIHR-Frederick Banting and Charles Best Canada Graduate Scholarships [C.A.]; FRQS [L.B.]; Netherlands Organization for Health Research and Development (ZonMw-VIDI 016.136.361) [V.W.V.J.]; National Institute on Aging (R01AG29451) [J.M.M.]; 2010-2011 PRIN funds of the University of Ferrara-Holder: Prof. Guido Barbujani, Supervisor: Prof. Chiara Scapoli-and in part sponsored by the European Foundation for the Study of Diabetes (EFSD) Albert Renold Travel Fellowships for Young Scientists, '5 per mille' contribution assigned to the University of Ferrara, income tax return year 2009 and the ENGAGE Exchange and Mobility Program for ENGAGE training funds, ENGAGE project, grant agreement HEALTH-F4-2007-201413 [L.M.]; ESRC (RES-060-23-0011) [C.L.R.]; National Institute of Health Research ([S.D., M.I.M.], Senior Investigator Award (NFSI-0611-10196) [D.A.L]); Australian NHMRC Fellowships Scheme (619667) [G.W.M]. For study-specific funding, please see Supplementary Material. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. Funding to pay the Open Access publication charges for this article was provided by the Charity Open Access Fund (COAF). Publisher Copyright: © The Author(s) 2018.Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P<5 x 10(-8). In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.Peer reviewe

Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors.

Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.The Fenland Study is funded by the Medical Research Council (MC_U106179471) and Wellcome Trust

Polygenic prediction of educational attainment within and between families from genome-wide association analyses in 3 million individuals

We conduct a genome-wide association study (GWAS) of educational attainment (EA) in a sample of ~3 million individuals and identify 3,952 approximately uncorrelated genome-wide-significant single-nucleotide polymorphisms (SNPs). A genome-wide polygenic predictor, or polygenic index (PGI), explains 12-16% of EA variance and contributes to risk prediction for ten diseases. Direct effects (i.e., controlling for parental PGIs) explain roughly half the PGI's magnitude of association with EA and other phenotypes. The correlation between mate-pair PGIs is far too large to be consistent with phenotypic assortment alone, implying additional assortment on PGI-associated factors. In an additional GWAS of dominance deviations from the additive model, we identify no genome-wide-significant SNPs, and a separate X-chromosome additive GWAS identifies 57

Genome-wide analysis identifies 12 loci influencing human reproductive behavior.

The genetic architecture of human reproductive behavior-age at first birth (AFB) and number of children ever born (NEB)-has a strong relationship with fitness, human development, infertility and risk of neuropsychiatric disorders. However, very few genetic loci have been identified, and the underlying mechanisms of AFB and NEB are poorly understood. We report a large genome-wide association study of both sexes including 251,151 individuals for AFB and 343,072 individuals for NEB. We identified 12 independent loci that are significantly associated with AFB and/or NEB in a SNP-based genome-wide association study and 4 additional loci associated in a gene-based effort. These loci harbor genes that are likely to have a role, either directly or by affecting non-local gene expression, in human reproduction and infertility, thereby increasing understanding of these complex traits