The impact of damming on riverine fluxes to the ocean: A case study from Eastern Iceland

Anthropogenic water management has extensively altered the world's river systems through impoundments and channel diversions to meet the human's need for water, energy and transportation. To illuminate the effect of such activities on the environment, this study describes the impact of the installation of the Kárahnjúkar Dam in Eastern Iceland on the transport of riverine dissolved- and particulate material to the ocean by the Jökulsá á Dal and the Lagarfljót rivers. This dam, completed in 2007, collects water into the 2.2 km3 Hálslón reservoir and diverts water from the glacial Jökulsá á Dal river into the partially glaciated Lagarfljót lagoon via a headrace tunnel. The impact of the damming was evaluated by sampling water from both the Jökulsá á Dal and the Lagarfljót rivers over a 15 year period spanning from 1998 to 2013. The annual flux of most dissolved elements increased substantially due to the damming. The fluxes of dissolved Zn, Al, Co, Ti and Fe increased most by damming; these fluxes increased by 46–391%. These differences can be attributed to changed saturation states of common secondary minerals in the Jökulsá á Dal due to reduced discharge, increased residence time and dissolution of suspended material, and, to a lesser degree, reduced photosynthesis due to less transparency in the Lagarfljót lagoon. The removal of particulate material and thus decreasing adsorption potential in the Jökulsá á Dal is the likely reason for the Fe flux increase. In contrast, approximately 85% of the original riverine transported mass of particulate material is trapped by the dam; that which passes tends to be relatively fine grained, increasing the average specific surface area of that which continues to flow towards the ocean. Consequently, the particulate geometric surface area flux is decreased by only 50% due to the damming. The blooming of silica diatoms during the spring consumes dissolved silica from the coastal waters until it becomes depleted; making the riverine spring dissolved silica flux an important source of this nutrient. Despite extensive riverine flux changes due to the Kárahnjúkar dam construction, the total spring dissolved silica flux increased, and thus so too the potential for a silica diatom spring bloom in the coastal waters. This is likely because the spring flux is dominated by snow melting downstream of the dam

Pollution from the 2014–15 Bárðarbunga eruption monitored by snow cores from the Vatnajökull glacier, Iceland

The chemical composition of Icelandic rain and snow is dominated by marine aerosols, however human and volcanic activity can also affect these compositions. The six month long 2014-15 Bárdarbunga volcanic eruption was the largest in Iceland for more than 200years and it released into the atmosphere an average of 60kt/day SO 2 , 30kt/day CO 2 , 500t/day HCl and 280t/day HF. To study the effect of this eruption on the winter precipitation, snow cores were collected from the Vatnajökull glacier and the highlands northeast of the glacier. In addition to 29 bulk snow cores from that precipitated from September 2014 until March 2015, two cores were sampled in 21 and 44 increments to quantify the spatial and time evolution of the chemical composition of the snow.The pH and chemical compositions of melted snow samples indicate that snow has been affected by the volcanic gases emitted during the Bárdarbunga eruption. The pH of the melted bulk snow cores ranged from 4.41 to 5.64 with an average value of 5.01. This is four times greater H + activity than pure water saturated with the atmospheric CO 2 . The highest concentrations of volatiles in the snow cores were found close to the eruption site as predicted from CALPUFF SO 2 gas dispersion quality model. The anion concentrations (SO 4 , Cl, and F) were higher and the pH was lower compared to equivalent snow samples collected during 1997-2006 from the unpolluted Icelandic Langjökull glacier. Higher SO 4 and Cl concentrations in the snow compared with the unpolluted rainwater of marine origin confirm the addition of a non-seawater SO 4 and Cl. The δ 34 S isotopic composition confirms that the sulphur addition is of volcanic aerosol origin.The chemical evolution of the snow with depth reflects changes in the lava effusion and gas emission rates. Those rates were the highest at the early stage of the eruption. Snow that fell during that time, represented by samples from the deepest part of the snow cores, had the lowest pH and highest concentrations of SO 4 , F, Cl and metals, compared with snow that fell later in the winter. Also the Al concentration, did exceed World Health Organisation drinking water standard of 3.7μmol/kg in the lower part of the snow core closest to the eruption site.Collected snow represents the precipitation that fell during the eruption period. Nevertheless, only minor environmental impacts are evident in the snow due to its interaction with the volcanic aerosol gases. In addition, the microbial communities identified in the snow that fell during the eruption were similar to those found in snow from other parts of the Arctic, confirming an insignificant impact of this eruption on the snow microecology

Similar decline in mortality rate of older persons with and without type 2 diabetes between 1993 and 2004 the Icelandic population-based Reykjavik and AGES-Reykjavik cohort studies.

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Files. This article is open access.A decline in mortality rates due to cardiovascular diseases and all-cause mortality has led to increased life expectancy in the Western world in recent decades. At the same time, the prevalence of type 2 diabetes, a disease associated with a twofold excess risk of cardiovascular disease and mortality, has been increasing. The objective of this study was to estimate the secular trend of cardiovascular and all-cause mortality rates in two population-based cohorts of older persons, with and without type 2 diabetes, examined 11 years apart.1506 participants (42% men) from the population-based Reykjavik Study, examined during 1991-1996 (median 1993), mean age 75.0 years, and 4814 participants (43% men) from the AGES-Reykjavik Study, examined during 2002-2006 (median 2004), mean age 77.2 years, age range in both cohorts 70-87 years. The main outcome measures were age-specific mortality rates due to cardiovascular disease and all causes, over two consecutive 5.7- and 5.3-year follow-up periods.A 32% decline in cardiovascular mortality rate and a 19% decline in all-cause mortality rate were observed between 1993 and 2004. The decline was greater in those with type 2 diabetes, as illustrated by the decline in the adjusted hazard ratio of cardiovascular mortality in individuals with diabetes compared to those without diabetes, from 1.88 (95% CI 1.24-2.85) in 1993 to 1.46 (95% CI 1.11-1.91) in 2004. We also observed a concurrent decrease in major cardiovascular risk factors in both those with and without diabetes. A higher proportion of persons with diabetes received glucose-lowering, hypertensive and lipid-lowering medication in 2004.A decline in cardiovascular and all-cause mortality rates was observed in older persons during the period 1993-2004, in both those with and without type 2 diabetes. This decline may be partly explained by improvements in cardiovascular risk factors and medical treatment over the period studied. However, type 2 diabetes still persists as an independent risk factor for cardiovascular mortality.National Institute of Health/N01-AG-1-2100 NIA Intramural Research Program Icelandic Heart Association (Hjartavernd) Icelandic Parliament (Althingi

Ice sheets as a missing source of silica to the polar oceans

Ice sheets play a more important role in the global silicon cycle than previously appreciated. Input of dissolved and amorphous particulate silica into natural waters stimulates the growth of diatoms. Here we measure dissolved and amorphous silica in Greenland Ice Sheet meltwaters and icebergs, demonstrating the potential for high ice sheet export. Our dissolved and amorphous silica flux is 0.20 (0.06-0.79) Tmol year(-1), ∼50% of the input from Arctic rivers. Amorphous silica comprises >95% of this flux and is highly soluble in sea water, as indicated by a significant increase in dissolved silica across a fjord salinity gradient. Retreating palaeo ice sheets were therefore likely responsible for high dissolved and amorphous silica fluxes into the ocean during the last deglaciation, reaching values of ∼5.5 Tmol year(-1), similar to the estimated export from palaeo rivers. These elevated silica fluxes may explain high diatom productivity observed during the last glacial-interglacial period

The trans-ancestral genomic architecture of glycemic traits

Glycemic traits are used to diagnose and monitor type 2 diabetes and cardiometabolic health. To date, most genetic studies of glycemic traits have focused on individuals of European ancestry. Here we aggregated genome-wide association studies comprising up to 281,416 individuals without diabetes (30% non-European ancestry) for whom fasting glucose, 2-h glucose after an oral glucose challenge, glycated hemoglobin and fasting insulin data were available. Trans-ancestry and single-ancestry meta-analyses identified 242 loci (99 novel; P < 5 × 10−8), 80% of which had no significant evidence of between-ancestry heterogeneity. Analyses restricted to individuals of European ancestry with equivalent sample size would have led to 24 fewer new loci. Compared with single-ancestry analyses, equivalent-sized trans-ancestry fine-mapping reduced the number of estimated variants in 99% credible sets by a median of 37.5%. Genomic-feature, gene-expression and gene-set analyses revealed distinct biological signatures for each trait, highlighting different underlying biological pathways. Our results increase our understanding of diabetes pathophysiology by using trans-ancestry studies for improved power and resolution

Four Novel Loci (19q13, 6q24, 12q24, and 5q14) Influence the Microcirculation In Vivo

Jaakko Tuomilehto Global BPgen Consortium'n jäsenPeer reviewe

Low-frequency and rare exome chip variants associate with fasting glucose and type 2 diabetes susceptibility.

Fasting glucose and insulin are intermediate traits for type 2 diabetes. Here we explore the role of coding variation on these traits by analysis of variants on the HumanExome BeadChip in 60,564 non-diabetic individuals and in 16,491 T2D cases and 81,877 controls. We identify a novel association of a low-frequency nonsynonymous SNV in GLP1R (A316T; rs10305492; MAF=1.4%) with lower FG (β=-0.09±0.01 mmol l(-1), P=3.4 × 10(-12)), T2D risk (OR[95%CI]=0.86[0.76-0.96], P=0.010), early insulin secretion (β=-0.07±0.035 pmolinsulin mmolglucose(-1), P=0.048), but higher 2-h glucose (β=0.16±0.05 mmol l(-1), P=4.3 × 10(-4)). We identify a gene-based association with FG at G6PC2 (pSKAT=6.8 × 10(-6)) driven by four rare protein-coding SNVs (H177Y, Y207S, R283X and S324P). We identify rs651007 (MAF=20%) in the first intron of ABO at the putative promoter of an antisense lncRNA, associating with higher FG (β=0.02±0.004 mmol l(-1), P=1.3 × 10(-8)). Our approach identifies novel coding variant associations and extends the allelic spectrum of variation underlying diabetes-related quantitative traits and T2D susceptibility.CHARGE: Funding support for ‘Building on GWAS for NHLBI-diseases: the U.S. CHARGE consortium’ was provided by the NIH through the American Recovery and Reinvestment Act of 2009 (ARRA) (5RC2HL102419). Sequence data for ‘Building on GWAS for NHLBI-diseases: the U.S. CHARGE consortium’ was provided by Eric Boerwinkle on behalf of the Atherosclerosis Risk in Communities (ARIC) Study, L. Adrienne Cupples, principal investigator for the Framingham Heart Study, and Bruce Psaty, principal investigator for the Cardiovascular Health Study. Sequencing was carried out at the Baylor Genome Center (U54 HG003273). Further support came from HL120393, ‘Rare variants and NHLBI traits in deeply phenotyped cohorts’ (Bruce Psaty, principal investigator). Supporting funding was also provided by NHLBI with the CHARGE infrastructure grant HL105756. In addition, M.J.P. was supported through the 2014 CHARGE Visiting Fellow grant—HL105756, Dr Bruce Psaty, PI. ENCODE: ENCODE collaborators Ben Brown and Marcus Stoiber were supported by the LDRD# 14-200 (B.B. and M.S.) and 4R00HG006698-03 (B.B.) grants. AGES: This study has been funded by NIA contract N01-AG-12100 with contributions from NEI, NIDCD and NHLBI, the NIA Intramural Research Program, Hjartavernd (the Icelandic Heart Association) and the Althingi (the Icelandic Parliament). ARIC: The Atherosclerosis Risk in Communities (ARIC) Study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute (NHLBI) contracts (HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C and HHSN268201100012C), R01HL087641, R01HL59367 and R01HL086694; National Human Genome Research Institute contract U01HG004402; and National Institutes of Health contract HHSN268200625226C. We thank the staff and participants of the ARIC study for their important contributions. Infrastructure was partly supported by Grant Number UL1RR025005, a component of the National Institutes of Health and NIH Roadmap for Medical Research. CARDIA: The CARDIA Study is conducted and supported by the National Heart, Lung, and Blood Institute in collaboration with the University of Alabama at Birmingham (HHSN268201300025C & HHSN268201300026C), Northwestern University (HHSN268201300027C), University of Minnesota (HHSN268201300028C), Kaiser Foundation Research Institute (HHSN268201300029C), and Johns Hopkins University School of Medicine (HHSN268200900041C). CARDIA is also partially supported by the Intramural Research Program of the National Institute on Aging. Exome chip genotyping and data analyses were funded in part by grants U01-HG004729, R01-HL093029 and R01-HL084099 from the National Institutes of Health to Dr Myriam Fornage. This manuscript has been reviewed by CARDIA for scientific content. CHES: This work was supported in part by The Chinese-American Eye Study (CHES) grant EY017337, an unrestricted departmental grant from Research to Prevent Blindness, and the Genetics of Latinos Diabetic Retinopathy (GOLDR) Study grant EY14684. CHS: This CHS research was supported by NHLBI contracts HHSN268201200036C, HHSN268200800007C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086; and NHLBI grants HL080295, HL087652, HL103612, HL068986 with additional contribution from the National Institute of Neurological Disorders and Stroke (NINDS). Additional support was provided through AG023629 from the National Institute on Aging (NIA). A full list of CHS investigators and institutions can be found at http://www.chs-nhlbi.org/pi.htm. The provision of genotyping data was supported in part by the National Center for Advancing Translational Sciences, CTSI grant UL1TR000124, and the National Institute of Diabetes and Digestive and Kidney Disease Diabetes Research Center (DRC) grant DK063491 to the Southern California Diabetes Endocrinology Research Center. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. The CoLaus Study: We thank the co-primary investigators of the CoLaus study, Gerard Waeber and Peter Vollenweider, and the PI of the PsyColaus Study Martin Preisig. We gratefully acknowledge Yolande Barreau, Anne-Lise Bastian, Binasa Ramic, Martine Moranville, Martine Baumer, Marcy Sagette, Jeanne Ecoffey and Sylvie Mermoud for their role in the CoLaus data collection. The CoLaus study was supported by research grants from GlaxoSmithKline and from the Faculty of Biology and Medicine of Lausanne, Switzerland. The PsyCoLaus study was supported by grants from the Swiss National Science Foundation (#3200B0–105993) and from GlaxoSmithKline (Drug Discovery—Verona, R&D). CROATIA-Korcula: The CROATIA-Korcula study would like to acknowledge the invaluable contributions of the recruitment team in Korcula, the administrative teams in Croatia and Edinburgh and the people of Korcula. Exome array genotyping was performed at the Wellcome Trust Clinical Research Facility Genetics Core at Western General Hospital, Edinburgh, UK. The CROATIA-Korcula study on the Croatian island of Korucla was supported through grants from the Medical Research Council UK and the Ministry of Science, Education and Sport in the Republic of Croatia (number 108-1080315-0302). EFSOCH: We are extremely grateful to the EFSOCH study participants and the EFSOCH study team. The opinions given in this paper do not necessarily represent those of NIHR, the NHS or the Department of Health. The EFSOCH study was supported by South West NHS Research and Development, Exeter NHS Research and Development, the Darlington Trust, and the Peninsula NIHR Clinical Research Facility at the University of Exeter. Timothy Frayling, PI, is supported by the European Research Council grant: SZ-245 50371-GLUCOSEGENES-FP7-IDEAS-ERC. EPIC-Potsdam: We thank all EPIC-Potsdam participants for their invaluable contribution to the study. The study was supported in part by a grant from the German Federal Ministry of Education and Research (BMBF) to the German Center for Diabetes Research (DZD e.V.). The recruitment phase of the EPIC-Potsdam study was supported by the Federal Ministry of Science, Germany (01 EA 9401) and the European Union (SOC 95201408 05 F02). The follow-up of the EPIC-Potsdam study was supported by German Cancer Aid (70-2488-Ha I) and the European Community (SOC 98200769 05 F02). Furthermore, we thank Ellen Kohlsdorf for data management as well as the follow-up team headed by Dr Manuala Bergmann for case ascertainment. ERF: The ERF study was supported by grants from the Netherlands Organization for Scientific Research (NWO) and a joint grant from NWO and the Russian Foundation for Basic research (Pionier, 047.016.009, 047.017.043), Erasmus MC, and the Centre for Medical Systems Biology (CMSB; National Genomics Initiative). Exome sequencing analysis in ERF was supported by the ZonMw grant (91111025). For the ERF Study, we are grateful to all participants and their relatives, to general practitioners and neurologists for their contributions, to P. Veraart for her help in genealogy and to P. Snijders for his help in data collection. FamHS: The Family Heart Study (FamHS) was supported by NIH grants R01-HL-087700 and R01-HL-088215 (Michael A. Province, PI) from NHLBI; and R01-DK-8925601 and R01-DK-075681 (Ingrid B. Borecki, PI) from NIDDK. FENLAND: The Fenland Study is funded by the Medical Research Council (MC_U106179471) and Wellcome Trust. We are grateful to all the volunteers for their time and help, and to the General Practitioners and practice staff for assistance with recruitment. We thank the Fenland Study Investigators, Fenland Study Co-ordination team and the Epidemiology Field, Data and Laboratory teams. The Fenland Study is funded by the Medical Research Council (MC_U106179471) and Wellcome Trust. FHS: Genotyping, quality control and calling of the Illumina HumanExome BeadChip in the Framingham Heart Study was supported by funding from the National Heart, Lung and Blood Institute Division of Intramural Research (Daniel Levy and Christopher J. O’Donnell, Principle Investigators). A portion of this research was conducted using the Linux Clusters for Genetic Analysis (LinGA) computing resources at Boston University Medical Campus. Also supported by National Institute for Diabetes and Digestive and Kidney Diseases (NIDDK) R01 DK078616, NIDDK K24 DK080140 and American Diabetes Association Mentor-Based Postdoctoral Fellowship Award #7-09-MN-32, all to Dr Meigs, a Canadian Diabetes Association Research Fellowship Award to Dr Leong, a research grant from the University of Verona, Italy to Dr Dauriz, and NIDDK Research Career Award K23 DK65978, a Massachusetts General Hospital Physician Scientist Development Award and a Doris Duke Charitable Foundation Clinical Scientist Development Award to Dr Florez. FIA3: We are indebted to the study participants who dedicated their time and samples to these studies. We thank Åsa Ågren (Umeå Medical Biobank) for data organization and Kerstin Enquist and Thore Johansson (Västerbottens County Council) for technical assistance with DNA extraction. This particular project was supported by project grants from the Swedish Heart-Lung Foundation, Umeå Medical Research Foundation and Västerbotten County Council. The Genetics Epidemiology of Metabolic Syndrome (GEMS) Study: We thank Metabolic Syndrome GEMs investigators: Scott Grundy, Jonathan Cohen, Ruth McPherson, Antero Kesaniemi, Robert Mahley, Tom Bersot, Philip Barter and Gerard Waeber. We gratefully acknowledge the contributions of the study personnel at each of the collaborating sites: John Farrell, Nicholas Nikolopoulos and Maureen Sutton (Boston); Judy Walshe, Monica Prentice, Anne Whitehouse, Julie Butters and Tori Nicholls (Australia); Heather Doelle, Lynn Lewis and Anna Toma (Canada); Kari Kervinen, Seppo Poykko, Liisa Mannermaa and Sari Paavola (Finland); Claire Hurrel, Diane Morin, Alice Mermod, Myriam Genoud and Roger Darioli (Switzerland); Guy Pepin, Sibel Tanir, Erhan Palaoglu, Kerem Ozer, Linda Mahley and Aysen Agacdiken (Turkey); and Deborah A. Widmer, Rhonda Harris and Selena Dixon (United States). Funding for the GEMS study was provided by GlaxoSmithKline. GeneSTAR: The Johns Hopkins Genetic Study of Atherosclerosis Risk (GeneSTAR) Study was supported by NIH grants through the National Heart, Lung, and Blood Institute (HL58625-01A1, HL59684, HL071025-01A1, U01HL72518, HL112064, and HL087698) and the National Institute of Nursing Research (NR0224103) and by M01-RR000052 to the Johns Hopkins General Clinical Research Center. Genotyping services were provided through the RS&G Service by the Northwest Genomics Center at the University of Washington, Department of Genome Sciences, under U.S. Federal Government contract number HHSN268201100037C from the National Heart, Lung, and Blood Institute. GLACIER: We are indebted to the study participants who dedicated their time, data and samples to the GLACIER Study as part of the Västerbottens hälsoundersökningar (Västerbottens Health Survey). We thank John Hutiainen and Åsa Ågren (Northern Sweden Biobank) for data organization and Kerstin Enquist and Thore Johansson (Västerbottens County Council) for extracting DNA. We also thank M. Sterner, M. Juhas and P. Storm (Lund University Diabetes Center) for their expert technical assistance with genotyping and genotype data preparation. The GLACIER Study was supported by grants from Novo Nordisk, the Swedish Research Council, Påhlssons Foundation, The Heart Foundation of Northern Sweden, the Swedish Heart Lung Foundation, the Skåne Regional Health Authority, Umeå Medical Research Foundation and the Wellcome Trust. This particular project was supported by project grants from the Swedish Heart-Lung Foundation, the Swedish Research Council, the Swedish Diabetes Association, Påhlssons Foundation and Novo nordisk (all grants to P. W. Franks). GOMAP (Genetic Overlap between Metabolic and Psychiatric Disease): This work was funded by the Wellcome Trust (098051). We thank all participants for their important contribution. We are grateful to Georgia Markou, Laiko General Hospital Diabetes Centre, Maria Emetsidou and Panagiota Fotinopoulou, Hippokratio General Hospital Diabetes Centre, Athina Karabela, Dafni Psychiatric Hospital, Eirini Glezou and Marios Matzioros, Dromokaiteio Psychiatric Hospital, Angela Rentari, Harokopio University of Athens, and Danielle Walker, Wellcome Trust Sanger Institute. Generation Scotland: Scottish Family Health Study (GS:SFHS): GS:SFHS is funded by the Chief Scientist Office of the Scottish Government Health Directorates, grant number CZD/16/6 and the Scottish Funding Council. Exome array genotyping for GS:SFHS was funded by the Medical Research Council UK and performed at the Wellcome Trust Clinical Research Facility Genetics Core at Western General Hospital, Edinburgh, UK. We also acknowledge the invaluable contributions of the families who took part in the Generation Scotland: Scottish Family Health Study, the general practitioners and Scottish School of Primary Care for their help in recruiting them, and the whole Generation Scotland team, which includes academic researchers, IT staff, laboratory technicians, statisticians and research managers. The chief investigators of Generation Scotland are David J. Porteous (University of Edinburgh), Lynne Hocking (University of Aberdeen), Blair Smith (University of Dundee), and Sandosh Padmanabhan (University of Glasgow). GSK (CoLaus, GEMS, Lolipop): We thank the GEMS Study Investigators: Philip Barter, PhD; Y. Antero Kesäniemi, PhD; Robert W. Mahley, PhD; Ruth McPherson, FRCP; and Scott M. Grundy, PhD. Dr Waeber MD, the CoLaus PI’s Peter Vollenweider MD and Gerard Waeber MD, the LOLIPOP PI’s, Jaspal Kooner MD and John Chambers MD, as well as the participants in all the studies. The GEMS study was sponsored in part by GlaxoSmithKline. The CoLaus study was supported by grants from GlaxoSmithKline, the Swiss National Science Foundation (Grant 33CSCO-122661) and the Faculty of Biology and Medicine of Lausanne. Health ABC: The Health, Aging and Body Composition (HABC) Study is supported by NIA contracts N01AG62101, N01AG62103 and N01AG62106. The exome-wide association study was funded by NIA grant 1R01AG032098-01A1 to Wake Forest University Health Sciences and was supported in part by the Intramural Research Program of the NIH, National Institute on Aging (Z01 AG000949-02 and Z01 AG007390-07, Human subjects protocol UCSF IRB is H5254-12688-11). Portions of this study utilized the high-performance computational capabilities of the Biowulf Linux cluster at the National Institutes of Health, Bethesda, MD. (http:/biowulf.nih.gov). Health2008: The Health2008 cohort was supported by the Timber Merchant Vilhelm Bang’s Foundation, the Danish Heart Foundation (Grant number 07-10-R61-A1754-B838-22392F), and the Health Insurance Foundation (Helsefonden) (Grant number 2012B233). HELIC: This work was funded by the Wellcome Trust (098051) and the European Research Council (ERC-2011-StG 280559-SEPI). The MANOLIS cohort is named in honour of Manolis Giannakakis, 1978–2010. We thank the residents of Anogia and surrounding Mylopotamos villages, and of the Pomak villages, for taking part. The HELIC study has been supported by many individuals who have contributed to sample collection (including Antonis Athanasiadis, Olina Balafouti, Christina Batzaki, Georgios Daskalakis, Eleni Emmanouil, Chrisoula Giannakaki, Margarita Giannakopoulou, Anastasia Kaparou, Vasiliki Kariakli, Stella Koinaki, Dimitra Kokori, Maria Konidari, Hara Koundouraki, Dimitris Koutoukidis, Vasiliki Mamakou, Eirini Mamalaki, Eirini Mpamiaki, Maria Tsoukana, Dimitra Tzakou, Katerina Vosdogianni, Niovi Xenaki, Eleni Zengini), data entry (Thanos Antonos, Dimitra Papagrigoriou, Betty Spiliopoulou), sample logistics (Sarah Edkins, Emma Gray), genotyping (Robert Andrews, Hannah Blackburn, Doug Simpkin, Siobhan Whitehead), research administration (Anja Kolb-Kokocinski, Carol Smee, Danielle Walker) and informatics (Martin Pollard, Josh Randall). INCIPE: NIcole Soranzo’s research is supported by the Wellcome Trust (Grant Codes WT098051 and WT091310), the EU FP7 (EPIGENESYS Grant Code 257082 and BLUEPRINT Grant Code HEALTH-F5-2011-282510). Inter99: The Inter99 was initiated by Torben Jørgensen (PI), Knut Borch-Johnsen (co-PI), Hans Ibsen and Troels F. Thomsen. The steering committee comprises the former two and Charlotta Pisinger. The study was financially supported by research grants from the Danish Research Council, the Danish Centre for Health Technology Assessment, Novo Nordisk Inc., Research Foundation of Copenhagen County, Ministry of Internal Affairs and Health, the Danish Heart Foundation, the Danish Pharmaceutical Association, the Augustinus Foundation, the Ib Henriksen Foundation, the Becket Foundation and the Danish Diabetes Association. Genetic studies of both Inter99 and Health 2008 cohorts were funded by the Lundbeck Foundation and produced by The Lundbeck Foundation Centre for Applied Medical Genomics in Personalised Disease Prediction, Prevention and Care (LuCamp, www.lucamp.org ). The Novo Nordisk Foundation Center for Basic Metabolic Research is an independent Research Center at the University of Copenhagen partially funded by an unrestricted donation from the Novo Nordisk Foundation (www.metabol.ku.dk). InterAct Consortium: Funding for the InterAct project was provided by the EU FP6 programme (grant number LSHM_CT_2006_037197). We thank all EPIC participants and staff for their contribution to the study. We thank the lab team at the MRC Epidemiology Unit for sample management and Nicola Kerrison for data management. IPM BioMe Biobank: The Mount Sinai IPM BioMe Program is supported by The Andrea and Charles Bronfman Philanthropies. Analyses of BioMe data was supported in part through the computational resources and staff expertise provided by the Department of Scientific Computing at the Icahn School of Medicine at Mount Sinai. The Insulin Resistance Atherosclerosis Family Study (IRASFS): The IRASFS was conducted and supported by the National Institute of Diabetes and Digestive and Kidney Diseases (HL060944, HL061019, and HL060919). Exome chip genotyping and data analyses were funded in part by grants DK081350 and HG007112. A subset of the IRASFS exome chips were contributed with funds from the Department of Internal Medicine at the University of Michigan. Computing resources were provided, in part, by the Wake Forest School of Medicine Center for Public Health Genomics. The Insulin Resistance Atherosclerosis Study (IRAS): The IRAS was conducted and supported by the National Institute of Diabetes and Digestive and Kidney Diseases (HL047887, HL047889, HL047890 and HL47902). Exome chip genotyping and data analyses were funded in part by grants DK081350 and HG007112). Computing resources were provided, in part, by the Wake Forest School of Medicine Center for Public Health Genomics. JHS: The JHS is supported by contracts HHSN268201300046C, HHSN268201300047C, HHSN268201300048C, HHSN268201300049C, HHSN268201300050C from the National Heart, Lung and Blood Institute and the National Institute on Minority Health and Health Disparities. ExomeChip genotyping was supported by the NHLBI of the National Institutes of Health under award number R01HL107816 to S. Kathiresan. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. The London Life Sciences Prospective Population (LOLIPOP) Study: We thank the co-primary investigators of the LOLIPOP study: Jaspal Kooner, John Chambers and Paul Elliott. The LOLIPOP study is supported by the National Institute for Health Research Comprehensive Biomedical Research Centre Imperial College Healthcare NHS Trust, the British Heart Foundation (SP/04/002), the Medical Research Council (G0700931), the Wellcome Trust (084723/Z/08/Z) and the National Institute for Health Research (RP-PG-0407-10371). MAGIC: Data on glycaemic traits were contributed by MAGIC investigators and were downloaded from www.magicinvestigators.org. MESA: The Multi-Ethnic Study of Atherosclerosis (MESA) and MESA SHARe project are conducted and supported by contracts N01-HC-95159 through N01-HC-95169 and RR-024156 from the National Heart, Lung, and Blood Institute (NHLBI). Funding for MESA SHARe genotyping was provided by NHLBI Contract N02-HL-6-4278. MESA Family is conducted and supported in collaboration with MESA investigators; support is provided by grants and co

Quantifying the impact of freshwater diatom productivity on silicon isotopes and silicon fluxes

Diatom productivity in the oceans plays a crucial role in the carbon cycle, but is strongly dependent upon the continental silicon supply. However, the relative influence of weathering and biological processes on continental Si fluxes remains poorly constrained. This study aims to quantify the impact of terrestrial diatom productivity on Si fluxes to the ocean. Lake Myvatn in North Iceland is one of the most productive lakes in the Northern Hemisphere, with nutrient-rich waters almost uniquely sourced by groundwater. The primary production is mainly controlled by diatom growth but also by cyanobacteria, and the lake output is via a single river, thereby providing a relatively simple natural laboratory to quantify the impact of diatom growth on the chemistry and Si budget of lake waters. Silicon stable isotopes (δ30Si) provide a tracer of this biocycling, and have been measured in groundwater inputs to the lake, and in time-series monitoring of waters at the lake outlet. The δ30Si values at the outlet range from +0.70±0.08 to +1.42±0.06%, which is significantly heavier than the groundwater input (average cold and hot springs: +0.50±0.17%, 2SD) and consistent with the preferential uptake of light Si isotopes by diatoms. The δ30Si value at the outlet increases by up to 0.9% in spring and autumn relative to the Si isotope composition of the inflow. These seasonal diatom blooms can be modeled by an open system of Si uptake and affect Si fluxes at the outlet of the lake by up to 79%, or 53% integrated over the year. In the summer a shift to lighter δ30Si values is correlated with a higher pH, which results in dissolution of diatoms releasing light Si isotopes. From mass balance, this seasonal diatom dissolution affects Si fluxes by up to 33%, but is limited to 3.7% integrated over the year. These results clearly illustrate that biological activity can have a significant impact on both isotope composition and elemental abundance of continental derived Si. They also demonstrate the pH dependency of diatom dissolution and/or preservation, which is likely to affect not only the continental Si fluxes to the ocean but also the Si recycling in the oceans themselves. © 2011 Elsevier B.V