Warming shifts the biomass distribution of soil microarthropod communities

Climate warming is often more detrimental to large body sized organisms than small body sized organisms. Yet, how such differential effects of warming at organismal levels affect aggregate community properties, such as community biomass, remains little understood. Here, using geothermally warmed sub-Arctic grassland soils, we investigate how total biomass (product of density and individual body mass) of two major groups of soil microarthropods (Collembola and mites), which are composed of both large and small body sized species, shift in warmed soils when warmed by ∼3–∼6 °C. Our results show that total biomass of Collembola significantly decreased in warmed soils predominantly due to a decline in the density of large body sized species. In contrast, total mite biomass showed a unimodal response to warming. As a result, there was a shift towards mite biomass dominated microarthropod communities in warmed soils. Within Collembola, the deep soil living eu-edaphic functional group declined the most in total biomass, whereas the unimodal response in mites was most pronounced in oribatid mites. Our study highlights that warming induced shifts in total community biomass of soil microarthropods are likely due to greater detrimental effects of warming on several large body sized Collembola

Age related macular degeneration

Hægt er að lesa greinina í heild sinni með því að smella á hlekkinn View/OpenAge-related macular degeneration (AMD) is the main reason for blindness today in the western hemisphere. According to Björn Olafsson, who was the first ophthalmologist in Iceland a century ago, this disease was not found in Iceland. In the blindness-registry of 1950 6% blindness was due to this disease. Today, AMD is responsible for 54% of legal blindness in Iceland. The incidence of the disease increases with age. Heredity and environmental factors are thought to influence its etiology. Indirect methods, including twin studies and increased frequency of this disease in some families, have demonstrated that hereditary factors may be important. This has been confirmed recently by demonstrating that genes on chromosome 1 and chromosome10 play a role. This disease is classified as early stage, with drusen and pigmentary changes and insignificant visual loss. Treatment options for this stage are limited. The use of vitamin E and C and Zinc has, however, been shown to delay its progress. The second and end stage involves visual loss, either as a dry form with pigment epithelial atrophy or wet form, with new vessel formation. Treatment options for the dry form are limited. The second form is more common in Iceland than in other countries. Treatment options for the wet form have increased. Localised laser and drug treatment to neovascular membranes, either alone or as a combination treatment with drugs that have anti-proliferate effect on new vessels (anti-VEGF) are increasingly used. New treatment methods are also used in assisting those that are already visually handicapped. The use of computers is increasing as are the patients' computer skills. As the number of the elderly increases, AMD will be an increasing health problem in Iceland as in other Western countries. It is therefore important to improve the treatment options and the service and counselling of patients.Aldursbundin hrörnun í augnbotnum (AMD) er algengasta ástæðan fyrir blindu í hinum vestræna heimi í dag. Þessum sjúkdómi er ekki lýst í gögnum Björns Ólafssonar fyrir rúmlega öld síðan en hann var fyrsti augnlæknirinn á Íslandi. Á blinduskrá 1950 eru 6% blindir vegna þessa sjúkdóms. Í dag veldur sjúkdómurinn 54% af lögblindu á Íslandi samkvæmt blinduskrá Sjónstöðvar Íslands. Algengi sjúkdómsins eykst með hækkandi aldri. Erfðir og umhverfisþættir eru talin hafa áhrif á tilurð sjúkdómsins. Óbeinar aðferðir, svo sem tvíburarannsóknir og aukin lægni í ákveðnum ættum, hafa bent til að erfðir hafi áhrif. Nýverið hafa litningarannsóknir staðfest þennan grun með því að finna svæði á litningi 1 og 10 sem virðast hafa áhrif á tilurð sjúkdómsins. AMD flokkast annars vegar í byrjunarstig sem einkennist af drúsen og litarefnistilfærslum í augnbotni og samfara því óverulegri sjónskerðingu. Meðferðarform við byrjunarstigi eru fá, þó hafa rannsóknir sýnt fram á notagildi andoxunarefna, svo sem vitamín E og C ásamt zinki. Hitt form AMD er lokastigið með verulegri sjónskerðingu. Það er ýmist þurrt með rýrnun í makúlu eða vott með æðanýmyndun undir sjónhimnu og blæðingum. Meðferðarmöguleikar við þurra formið eru í dag litlir, en þetta form er mun algengara hér á landi miðað við önnur lönd án þess að fyrir því liggi haldbærar skýringar. Aftur á móti eru verulegar vonir bundnar við nýja meðferðarmöguleika í vota forminu. Staðbundin leysimeðferð á fyrirfram lyfja merkta himnu í sambland við lyfjameðferð sem gefin er inn í augað. Það lyf hindrar vaxtarþátt nýæðamyndar (anti-VEGF) . Nýjungar í meðferð sjónskertra þar sem nýjasta tölvutækni er notuð reynist þeim sem nú eru með sjúkdóminn betur, tækin eru betri og þeir einstaklingar sem fá sjúkdóminn í dag hafa oft náð valdi á tölvutækni. Með fjölgun aldraðra er þó ljóst að þessi sjúkdómur verður vaxandi heilbrigðisvandamál á Íslandi, sem og í hinum vestræna heimi, og er því mikilvægt að bæta meðferð, þjónustu og ráðgjöf fyrir þennan sjúklingahóp. Aldursbundin hrörnun í augnbotnum (Age-Related Macular Degeneration) AMD er sjúkdómur í litþekju augans, Bruch´s himnu og ljósnemum í sjónhimnu og veldur gjarnan sjónskerðingu. Algengi sjúkdómsins eykst með hækkandi aldri. "Macula" er latneskt orð og þýðir blettur eða díll og er í raun stytting á "macula lutea", það er guli díllinn eða bletturinn í sjónhimnu auga þar sem sjónskynjun er sterkust. "Macula" hefur verið þýtt sem makúla á íslensku og er það orð notað í þessari grein (1). Í gegnum árin hefur sjúkdómsástandinu verið lýst á mismunandi hátt og gefin mörg nöfn. Árið 1885 lýsti Haab þessu sjúkdómsástandi og kallaði það ellihrörnun í augnbotnum "senile macular degeneration" (2). Nú meira en 100 árum seinna eru fræðimenn ekki á eitt sáttir um hvernig eigi að skilgreina og flokka þetta sjúkdómsástand. Í þessari grein er stuðst við alþjóðaskilgreiningu á aldursbundinni hrörnun í augnbotnum frá 1995 frá The International ARM Epidemiological Study Group (3). Með hækkandi aldri verða ákveðnar breytingar í makúlu, æðahimnan þykknar og magn og þéttleiki litarefnisins melanín í litþekju minnkar og litþekjufrumum fækkar. Auk þess verður þykknun á Bruch?s himnu, og ljósnemum í makúlu fækkar. Við byrjunarstig á AMD safnast niðurbrotsefni frá diskum ljósnema upp og myndar svonefnd drúsen

One of us? Negotiating multiple legal identities across the Viking diaspora

Migrations from mainland Scandinavia during the Viking age resulted in the establishment of colonies across the North Atlantic. Evidence of sustained sociocultural contact between these colonies has encouraged scholars to recognise the Viking world as a diaspora. Medieval Iceland, by way of its poets, writers, and learned men, was the locus of the memorialisation of this diaspora. Laws provide historians with a way in which to understand the creation of identity in a past society and the criteria that formed the basis of these identities. In the Viking world, where separate identities were emerging while still being connected through the diaspora, the manner in which identity was constructed and negotiated is of special interest. This paper uses Grágás, the medieval Icelandic law code, along with laws from other parts of the diaspora and Icelandic sagas to unpick how Viking diasporans negotiated identity, where they ‘belonged’, and where they were excluded

The Wellesley News (12-01-1966)

https://repository.wellesley.edu/wcnews/1090/thumbnail.jp

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes

The population genomic legacy of the second plague pandemic

SummaryHuman populations have been shaped by catastrophes that may have left long-lasting signatures in their genomes. One notable example is the second plague pandemic that entered Europe in ca. 1,347 CE and repeatedly returned for over 300 years, with typical village and town mortality estimated at 10%–40%.1 It is assumed that this high mortality affected the gene pools of these populations. First, local population crashes reduced genetic diversity. Second, a change in frequency is expected for sequence variants that may have affected survival or susceptibility to the etiologic agent (Yersinia pestis).2 Third, mass mortality might alter the local gene pools through its impact on subsequent migration patterns. We explored these factors using the Norwegian city of Trondheim as a model, by sequencing 54 genomes spanning three time periods: (1) prior to the plague striking Trondheim in 1,349 CE, (2) the 17th–19th century, and (3) the present. We find that the pandemic period shaped the gene pool by reducing long distance immigration, in particular from the British Isles, and inducing a bottleneck that reduced genetic diversity. Although we also observe an excess of large FST values at multiple loci in the genome, these are shaped by reference biases introduced by mapping our relatively low genome coverage degraded DNA to the reference genome. This implies that attempts to detect selection using ancient DNA (aDNA) datasets that vary by read length and depth of sequencing coverage may be particularly challenging until methods have been developed to account for the impact of differential reference bias on test statistics.Results and discussion STAR★Method

A homozygous loss-of-function mutation leading to CYBC1 deficiency causes chronic granulomatous disease

Publisher's version (útgefin grein) Publisher’s note: Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.Mutations in genes encoding subunits of the phagocyte NADPH oxidase complex are recognized to cause chronic granulomatous disease (CGD), a severe primary immunodeficiency. Here we describe how deficiency of CYBC1, a previously uncharacterized protein in humans (C17orf62), leads to reduced expression of NADPH oxidase’s main subunit (gp91phox) and results in CGD. Analyzing two brothers diagnosed with CGD we identify a homozygous loss-of-function mutation, p.Tyr2Ter, in CYBC1. Imputation of p.Tyr2Ter into 155K chipgenotyped Icelanders reveals six additional homozygotes, all with signs of CGD, manifesting as colitis, rare infections, or a severely impaired PMA-induced neutrophil oxidative burst. Homozygosity for p.Tyr2Ter consequently associates with inflammatory bowel disease (IBD) in Iceland (P = 8.3 × 10−8; OR = 67.6), as well as reduced height (P = 3.3 × 10−4; −8.5 cm). Overall, we find that CYBC1 deficiency results in CGD characterized by colitis and a distinct profile of infections indicative of macrophage dysfunction.We wish to thank the family of the two probands, as well as all the other individuals who participated in the study and whose contribution made this work possible.Peer Reviewe

Identification of candidate pelagic marine protected areas through a seabird seasonal-, multispecific- and extinction risk-based approach

With increasing pressure on the oceans from environmental change, there has been a global call for improved protection of marine ecosystems through the implementation of marine protected areas (MPAs). Here, we used species distribution modelling (SDM) of tracking data from 14 seabird species to identify key marine areas in the southwest Atlantic Ocean, valuing areas based on seabird species occurrence, seasonality and extinction risk. We also compared overlaps between the outputs generated by the SDM and layers representing important human threats (fishing intensity, ship density, plastic and oil pollution, ocean acidification), and calculated loss in conservation value using fishing and ship density as cost layers. The key marine areas were located on the southern Patagonian Shelf, overlapping extensively with areas of high fishing activity, and did not change seasonally, while seasonal areas were located off south and southeast Brazil and overlapped with areas of high plastic pollution and ocean acidification. Non-seasonal key areas were located off northeast Brazil on an area of high biodiversity, and with relatively low human impacts. We found support for the use of seasonal areas depending on the seabird assemblage used, because there was a loss in conservation value for the seasonal compared to the non-seasonal approach when using ‘cost’ layers. Our approach, accounting for seasonal changes in seabird assemblages and their risk of extinction, identified additional candidate areas for incorporation in the network of pelagic MPAs

The population genomic legacy of the second plague pandemic

Human populations have been shaped by catastrophes that may have left long-lasting signatures in their genomes. One notable example is the second plague pandemic that entered Europe in ca. 1,347 CE and repeatedly returned for over 300 years, with typical village and town mortality estimated at 10%-40%.1 It is assumed that this high mortality affected the gene pools of these populations. First, local population crashes reduced genetic diversity. Second, a change in frequency is expected for sequence variants that may have affected survival or susceptibility to the etiologic agent (Yersinia pestis).2 Third, mass mortality might alter the local gene pools through its impact on subsequent migration patterns. We explored these factors using the Norwegian city of Trondheim as a model, by sequencing 54 genomes spanning three time periods: (1) prior to the plague striking Trondheim in 1,349 CE, (2) the 17th-19th century, and (3) the present. We find that the pandemic period shaped the gene pool by reducing long distance immigration, in particular from the British Isles, and inducing a bottleneck that reduced genetic diversity. Although we also observe an excess of large FST values at multiple loci in the genome, these are shaped by reference biases introduced by mapping our relatively low genome coverage degraded DNA to the reference genome. This implies that attempts to detect selection using ancient DNA (aDNA) datasets that vary by read length and depth of sequencing coverage may be particularly challenging until methods have been developed to account for the impact of differential reference bias on test statistics