Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017: a systematic analysis for the Global Burden of Disease Study 2017.

BACKGROUND: Global development goals increasingly rely on country-specific estimates for benchmarking a nation's progress. To meet this need, the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 estimated global, regional, national, and, for selected locations, subnational cause-specific mortality beginning in the year 1980. Here we report an update to that study, making use of newly available data and improved methods. GBD 2017 provides a comprehensive assessment of cause-specific mortality for 282 causes in 195 countries and territories from 1980 to 2017. METHODS: The causes of death database is composed of vital registration (VR), verbal autopsy (VA), registry, survey, police, and surveillance data. GBD 2017 added ten VA studies, 127 country-years of VR data, 502 cancer-registry country-years, and an additional surveillance country-year. Expansions of the GBD cause of death hierarchy resulted in 18 additional causes estimated for GBD 2017. Newly available data led to subnational estimates for five additional countries-Ethiopia, Iran, New Zealand, Norway, and Russia. Deaths assigned International Classification of Diseases (ICD) codes for non-specific, implausible, or intermediate causes of death were reassigned to underlying causes by redistribution algorithms that were incorporated into uncertainty estimation. We used statistical modelling tools developed for GBD, including the Cause of Death Ensemble model (CODEm), to generate cause fractions and cause-specific death rates for each location, year, age, and sex. Instead of using UN estimates as in previous versions, GBD 2017 independently estimated population size and fertility rate for all locations. Years of life lost (YLLs) were then calculated as the sum of each death multiplied by the standard life expectancy at each age. All rates reported here are age-standardised

Wie geen vreemde talen kent, weet niets van zijn eigen taal

Van een taal kun je genieten, maar het is ook hard werken om hem onder de knie te krijgen. Een proces dat voor iedereen anders kan verlopen. Daarom is het van belang dat je je bewust wordt van je eigen leerproces en inzicht krijgt in wat het beste bij jou past. Dat kan door je eigen Language Learning History (LLH) te maken of die van anderen te lezen. Een Language Learning History is een persoonlijk verhaal over hoe je een vreemde taal (of meer dan één) hebt geleerd en hoe dat proces verder verloopt. Hoe komt het dat ik geen Duits durf te spreken en wat vind ik dan vooral lastig? Aan welke realistische eisen zou ik wel kunnen voldoen? Door een compleet verhaal krijg je meer grip op wat voor jezelf werkt en wat je doel precies is. Daardoor raak je bovendien gemotiveerder om je taalvaardigheid te verbeteren. Totstandkoming Studenten in de minor Toegepaste Taalwetenschap van de Rijksuniversiteit Groningen interviewden zo’n 120 taalcursisten van het Talencentrum. Deze interviews werkten ze uit tot taalportretten, waarin ze taalwetenschappelijke kennis verwerkten. Het Talencentrum en de Wetenschapswinkel Taal, Cultuur en Communicatie selecteerden elf gevarieerde taalportretten die u in dit boekje kunt terugvinden. Marijke Laan, studente Taalwetenschap, vulde deze portretten aan met interviews met Talencentrumdocenten. Daarmee wordt het boekje voor taaldocenten extra interessant. “Wat kun je nu praktisch doen met de persoonlijke verhalen over zelfvertrouwen en motivatie, of met de verschillen die je in een groep aantreft?” Ook geven deze docenten tal van inspirerende tips.

Systematic study of exciton diffusion length in organic semiconductors by six experimental methods

Six experimental methods have been used to investigate the exciton diffusion length in materials with systematic chemical modifications. We find that exciton diffusion length correlates with molecular ordering. We discuss situations in which certain experimental techniques are more appropriate

Genome-wide association study for circulating levels of PAI-1 provides novel insights into its regulation

We conducted a genome-wide association study to identify novel associations between genetic variants and circulating plasminogen activator inhibitor-1 (PAI-1) concentration, and examined functional implications of variants and genes that were discovered. A discovery meta-analysis was performed in 19 599 subjects, followed by replication analysis of genome-wide significant (P <5 x 10(-8)) single nucleotide polymorphisms (SNPs) in 10 796 independent samples. We further examined associations with type 2 diabetes and coronary artery disease, assessed the functional significance of the SNPs for gene expression in human tissues, and conducted RNA-silencing experiments for one novel association. We confirmed the association of the 4G/5G proxy SNP rs2227631 in the promoter region of SERPINE1 (7q22.1) and discovered genome-wide significant associations at 3 additional loci: chromosome 7q22.1 close to SERPINE1 (rs6976053, discovery P = 3.4 x 10(-10)); chromosome 11p15.2 within ARNTL (rs6486122, discovery P = 3.0 x 10(-8)); and chromosome 3p25.2 within PPARG (rs11128603, dis-covery P = 2.9 x 10(-8)). Replication was achieved for the 7q22.1 and 11p15.2 loci. There was nominal association with type 2 diabetes and coronary artery disease at ARNTL (P <.05). Functional studies identified MUC3 as a candidate gene for the second association signal on 7q22.1. In summary, SNPs in SERPINE1 and ARNTL and an SNP associated with the expression of MUC3 were robustly associated with circulating levels of PAI-1. (Blood. 2012;120(24):4873-4881

Genome-Wide Association Study for Circulating Tissue Plasminogen Activator Levels and Functional Follow-Up Implicates Endothelial STXBP5 and STX2

Objective Tissue plasminogen activator (tPA), a serine protease, catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for endogenous fibrinolysis. In some populations, elevated plasma levels of tPA have been associated with myocardial infarction and other cardiovascular diseases. We conducted a meta-analysis of genome-wide association studies to identify novel correlates of circulating levels of tPA. Approach and Results Fourteen cohort studies with tPA measures (N=26 929) contributed to the meta-analysis. Three loci were significantly associated with circulating tPA levels (P Conclusions We identified 3 loci associated with circulating tPA levels, the PLAT region, STXBP5, and STX2. Our functional studies implicate a novel role for STXBP5 and STX2 in regulating tPA release

The Pierre Auger Observatory: Contributions to the 33rd International Cosmic Ray Conference (ICRC 2013)

Contributions of the Pierre Auger Collaboration to the 33rd International Cosmic Ray Conference, Rio de Janeiro, Brazil, July 201