Institution
Tallinn University of Technology
Education•Tallinn, Estonia•
About: Tallinn University of Technology is a education organization based out in Tallinn, Estonia. It is known for research contribution in the topics: European union & Oil shale. The organization has 3688 authors who have published 10313 publications receiving 145058 citations. The organization is also known as: Tallinn Technical University & Tallinna Tehnikaülikool.
Topics: European union, Oil shale, Thin film, Nonlinear system, Microstructure
Papers published on a yearly basis
Papers
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TL;DR: The findings suggest that partner specificity in AM symbiosis may occur at the level of ecological groups, rather than at the species level, of both plant and fungal partners.
Abstract: * Knowledge of the diversity of arbuscular mycorrhizal fungi (AMF) in natural ecosystems is a major bottleneck in mycorrhizal ecology. Here, we aimed to apply 454 sequencing--providing a new level of descriptive power--to assess the AMF diversity in a boreonemoral forest. * 454 sequencing reads of the small subunit ribosomal RNA (SSU rRNA) gene of Glomeromycota were assigned to sequence groups by blast searches against a custom-made annotated sequence database. * We detected 47 AMF taxa in the roots of 10 plant species in a 10 x 10 m plot, which is almost the same as the number of plant species in the whole studied forest. There was a significant difference between AMF communities in the roots of forest specialist plant species and in the roots of habitat generalist plant species. Forest plant species hosted 22 specialist AMF taxa, and the generalist plants shared all but one AMF taxon with forest plants, including globally distributed generalist fungi. These AMF taxa that have been globally recorded only in forest ecosystems were significantly over-represented in the roots of forest plant species. * Our findings suggest that partner specificity in AM symbiosis may occur at the level of ecological groups, rather than at the species level, of both plant and fungal partners.
477 citations
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TL;DR: It is explored how the risk of infection would vary with several influential factors: ventilation rate, duration of event, and deposition onto surfaces, to better understand the factors that promote superspreading events.
Abstract: During the 2020 COVID-19 pandemic, an outbreak occurred following attendance of a symptomatic index case at a weekly rehearsal on 10 March of the Skagit Valley Chorale (SVC). After that rehearsal, 53 members of the SVC among 61 in attendance were confirmed or strongly suspected to have contracted COVID-19 and two died. Transmission by the aerosol route is likely; it appears unlikely that either fomite or ballistic droplet transmission could explain a substantial fraction of the cases. It is vital to identify features of cases such as this to better understand the factors that promote superspreading events. Based on a conditional assumption that transmission during this outbreak was dominated by inhalation of respiratory aerosol generated by one index case, we use the available evidence to infer the emission rate of aerosol infectious quanta. We explore how the risk of infection would vary with several influential factors: ventilation rate, duration of event, and deposition onto surfaces. The results indicate a best-estimate emission rate of 970 ± 390 quanta/h. Infection risk would be reduced by a factor of two by increasing the aerosol loss rate to 5 h-1 and shortening the event duration from 2.5 to 1 h.
465 citations
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University of Auckland1, Uppsala University2, GlaxoSmithKline3, Stanford University4, Imperial College London5, French Institute of Health and Medical Research6, University of Paris7, University of Parma8, University of Alberta9, University of São Paulo10, Peking University11, National Taiwan University12, Pontifical Catholic University of Chile13, Milpark Hospital14, University of Amsterdam15, University of Ioannina16, University of East Anglia17, Norfolk and Norwich University Hospital18, Duke University19, University of Buenos Aires20, New York University21, Seoul National University22, University of Ulm23, Charles University in Prague24, Population Health Research Institute25, Autonomous University of Madrid26, University of Pennsylvania27, St. John's University28, University of Oslo29, St George's Hospital30, Katholieke Universiteit Leuven31, Mahidol University32, University of the Philippines33, University of Hong Kong34, Henry Ford Health System35, Tallinn University of Technology36, Carol Davila University of Medicine and Pharmacy37, Fudan University38, Harvard University39
TL;DR: In patients with stable coronary heart disease, darapladib did not significantly reduce the risk of the primary composite end point of cardiovascular death, myocardial infarction, or stroke.
Abstract: Background Elevated lipoprotein-associated phospholipase A2 activity promotes the development of vulnerable atherosclerotic plaques, and elevated plasma levels of this enzyme are associated with an increased risk of coronary events. Darapladib is a selective oral inhibitor of lipoprotein-associated phospholipase A2. Methods In a double-blind trial, we randomly assigned 15,828 patients with stable coronary heart disease to receive either once-daily darapladib (at a dose of 160 mg) or placebo. The primary end point was a composite of cardiovascular death, myocardial infarction, or stroke. Secondary end points included the components of the primary end point as well as major coronary events (death from coronary heart disease, myocardial infarction, or urgent coronary revascularization for myocardial ischemia) and total coronary events (death from coronary heart disease, myocardial infarction, hospitalization for unstable angina, or any coronary revascularization). Results During a median follow-up period of 3.7 years, the primary end point occurred in 769 of 7924 patients (9.7%) in the darapladib group and 819 of 7904 patients (10.4%) in the placebo group (hazard ratio in the darapladib group, 0.94; 95% confidence interval [CI], 0.85 to 1.03; P=0.20). There were also no significant between-group differences in the rates of the individual components of the primary end point or in all-cause mortality. Darapladib, as compared with placebo, reduced the rate of major coronary events (9.3% vs. 10.3%; hazard ratio, 0.90; 95% CI, 0.82 to 1.00; P=0.045) and total coronary events (14.6% vs. 16.1%; hazard ratio, 0.91; 95% CI, 0.84 to 0.98; P=0.02). Conclusions In patients with stable coronary heart disease, darapladib did not significantly reduce the risk of the primary composite end point of cardiovascular death, myocardial infarction, or stroke. (Funded by GlaxoSmithKline; STABILITY ClinicalTrials.gov number, NCT00799903.).
456 citations
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TL;DR: In this paper, a forward-to-French translation of How rich countries got rich and why poor countries stay poor is presented. But the translation is limited to the French language.
Abstract: This article is a forward to French translation of How rich countries got rich and why poor countries stay poor.
454 citations
Authors
Showing all 3757 results
Name | H-index | Papers | Citations |
---|---|---|---|
James Chapman | 82 | 483 | 36468 |
Alexandre Alexakis | 67 | 540 | 17247 |
Bernard Waeber | 56 | 370 | 35335 |
Peter A. Andrekson | 54 | 573 | 12042 |
Charles S. Peirce | 51 | 167 | 11998 |
Lars M. Blank | 49 | 301 | 8011 |
Fushuan Wen | 49 | 465 | 9189 |
Mati Karelson | 48 | 207 | 10210 |
Ago Samoson | 46 | 119 | 8807 |
Zebo Peng | 45 | 359 | 7312 |
Petru Eles | 44 | 300 | 6749 |
Vijai Kumar Gupta | 43 | 301 | 6901 |
Eero Vasar | 43 | 263 | 6930 |
Rik Ossenkoppele | 42 | 192 | 6839 |
Tõnis Timmusk | 41 | 105 | 11056 |