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  • Open Access English
    Authors: 
    Laurent A. F. Frantz; James Haile; Audrey T. Lin; Amelie Scheu; Christina Geörg; Norbert Benecke; Michelle Alexander; Anna Linderholm; Victoria E. Mullin; Kevin G. Daly; +90 more
    Countries: Netherlands, United Kingdom, Portugal, Germany, United Kingdom, Germany, France, Belgium, United Kingdom, United Kingdom ...
    Project: NSF | Northern Narratives: Soci... (0638897), WT | Domestic animals as a mod... (210119), UKRI | Deciphering dog domestica... (NE/K003259/1), NSF | Conference on Global Long... (0947862), UKRI | Deciphering dog domestica... (NE/K005243/1), NSF | RAPID Gardar Collaborativ... (1119354), NSF | IPY: Long Term Human Ecod... (0732327), EC | Extinction Genomics (681396), NSF | The Origins of Equid Dome... (1311551), MESTD | Bioarchaeology of Ancient... (47001),...

    Archaeological evidence indicates that pig domestication had begun by ∼10,500 y before the present (BP) in the Near East, and mitochondrial DNA (mtDNA) suggests that pigs arrived in Europe alongside farmers ∼8,500 y BP. A few thousand years after the introduction of Near Eastern pigs into Europe, however, their characteristic mtDNA signature disappeared and was replaced by haplotypes associated with European wild boars. This turnover could be accounted for by substantial gene flow from local European wild boars, although it is also possible that European wild boars were domesticated independently without any genetic contribution from the Near East. To test these hypotheses, we obtained mtDNA sequences from 2,099 modern and ancient pig samples and 63 nuclear ancient genomes from Near Eastern and European pigs. Our analyses revealed that European domestic pigs dating from 7,100 to 6,000 y BP possessed both Near Eastern and European nuclear ancestry, while later pigs possessed no more than 4% Near Eastern ancestry, indicating that gene flow from European wild boars resulted in a near-complete disappearance of Near East ancestry. In addition, we demonstrate that a variant at a locus encoding black coat color likely originated in the Near East and persisted in European pigs. Altogether, our results indicate that while pigs were not independently domesticated in Europe, the vast majority of human-mediated selection over the past 5,000 y focused on the genomic fraction derived from the European wild boars, and not on the fraction that was selected by early Neolithic farmers over the first 2,500 y of the domestication process. Significance Archaeological evidence indicates that domestic pigs arrived in Europe, alongside farmers from the Near East ∼8,500 y ago, yet mitochondrial genomes of modern European pigs are derived from European wild boars. To address this conundrum, we obtained mitochondrial and nuclear data from modern and ancient Near Eastern and European pigs. Our analyses indicate that, aside from a coat color gene, most Near Eastern ancestry in the genomes of European domestic pigs disappeared over 3,000 y as a result of interbreeding with local wild boars. This implies that pigs were not domesticated independently in Europe, yet the first 2,500 y of human-mediated selection applied by Near Eastern Neolithic farmers played little role in the development of modern European pigs.

  • Open Access
    Authors: 
    Guzelmeric, Etil; Ristivojević, Petar; Trifković, Jelena; Dastan, Tugce; Yilmaz, Ozlem; Cengiz, Ozlem; Yesilada, Erdem;
    Publisher: Elsevier Science Bv, Amsterdam
    Country: Serbia
    Project: MESTD | Structure-properties rela... (172017)

    Supplementary data for: [https://doi.org/10.1016/j.lwt.2017.08.060] Related to published version: [http://cherry.chem.bg.ac.rs/handle/123456789/2552] Related to accepted version: [http://cherry.chem.bg.ac.rs/handle/123456789/2989]

  • Open Access English
    Authors: 
    Feigin V; Nichols E; Alam T; Bannick M; Beghi E; Blake N; Culpepper W; Dorsey E; Elbaz A; Ellenbogen R; +192 more
    Countries: Australia, Italy, Turkey, Netherlands, Spain, Iceland, Denmark, Sweden, Germany, United Kingdom ...
    Project: NHMRC | Prevention of stroke and ... (1042600), WT | Global Atlas of Podoconio... (201900), NIH | AdminSupp:Transforming Re... (3U01NS086090-02S1), NHMRC | Modifiable risk factors f... (1056929), NIH | Stroke Investigative Rese... (3U54HG007479-03S1), NIH | Systematic Investigation ... (1R01NS107900-01), MESTD | Epidemiological investiga... (175087), NIH | The Ohio State University... (5U10NS086484-03), NIH | African Neurobiobank for ... (1U01HG010273-01)

    ROA is funded by the National Institutes of Health (U01HG010273). SMA acknowledges the International Centre for Casemix and Clinical Coding, Faculty of Medicine, National University of Malaysia and Department of Health Policy and Management, Faculty of Public Health, Kuwait University for the approval and support to participate in this research project. AAw acknowledges funding support from Department of Science and Technology, Government of India, New Delhi, through INSPIRE Faculty scheme. TBA acknowledges partial funding from the Institute of Medical Research and Medicinal Plant Studies. ABa is supported by the Public Health Agency of Canada. TWB was supported by the Alexander von Humboldt Foundation through the Alexander von Humboldt Professor Award, funded by the Federal Ministry of Education and Research. MSBS acknowledges support from the Australian Government Research and Training Program scholarship for a PhD degree at the Australian National University, Australia. JJC is supported by the Swedish Heart and Lung Foundation. FCar is supported by the European Union (FEDER funds POCI/01/0145/FEDER/007728 and POCI/01/0145/FEDER/007265) and National Funds (FCT/MEC, Fundacao para a Ciencia e a Tecnologia and Ministerio da Educacao e Ciencia) under the Partnership Agreements PT2020 UID/MULTI/04378/2013 and PT2020UID/QUI/50006/2013. EC is supported by an Australian Research Council Future Fellowship (FT3 140100085). KD is supported by a Wellcome Trust [Grant Number 201900] as part of his International Intermediate Fellowship. EF is supported by the European Union (FEDER funds POCI/01/0145/FEDER/007728 and POCI/01/0145/FEDER/007265) and National Funds (FCT/MEC, Fundacao para a Ciencia e a Tecnologia and Ministerio da Educacao e Ciencia) under the Partnership Agreements PT2020 UID/MULTI/04378/2013 and PT2020UID/QUI/50006/2013. SMSI is funded by the Institute for Physical Activity and Nutrition (IPAN), Deakin University and received funding from High Blood Pressure Research Council of Australia. YKa is a DBT/Wellcome Trust India Alliance Fellow in Public Health. YJK is supported by the Office of Research and Innovation at Xiamen University Malaysia. BL acknowledges funding from the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre. WDL is supported in part by U10NS086484 NINDS. SLo is funded by the German Federal Ministry of Education and Research (nutriCARD, grant agreement number 01EA1411A). RML is supported by a National Health and Medical Research Council (NHMRC) of Australia Senior Research Fellowship. AMa and the Imperial College London are grateful for support from the NW London NIHR Collaboration for Leadership in Applied Health Research and Care. JJM is supported by the Danish National Research Foundation (Niels Bohr Professorship), and the John Cade Fellowship (APP1056929) from NHMRC. TMei acknowledges additional institutional support from the Competence Cluster for Nutrition and Cardiovascular Health (nutriCARD), Jena-Halle-Leipzig. IMV is supported by the Sistema Nacional de Investigacion (Panama). MOO is supported by SIREN U54 U54HG007479 and SIBS Genomics R01NS107900 grants. AMS was supported by a fellowship from the Egyptian Fulbright Mission Program. MMSM acknowledges the support from the Ministry of Education, Science and Technological Development, Republic of Serbia (contract no 175087). AShe is supported by Health Data Research UK. MBS' work on traumatic brain injury is supported by grants NIH U01 NS086090 (PI G Manley) from the National Institutes of Health (NIH) and DoD W81XWH-14-2-0176 (PI G Manley) from the United States Department of Defense. RTS is supported in part by grant number PROMETEOII/2015/021 from Generalitat Valenciana and the national grant PI17/00719 from ISCIIIFEDER. AGT was supported by a Fellowship from the NHMRC (Australia; 1042600. KBT acknowledges funding supports from the Maurice Wilkins Centre for Biodiscovery, Cancer Society of New Zealand, Health Research Council, Gut Cancer Foundation, and the University of Auckland. CY acknowledges support from the National Natural Science Foundation of China (grant number 81773552) and the Chinese NSFC International Cooperation and Exchange Program (grant number 71661167007). Background Neurological disorders are increasingly recognised as major causes of death and disability worldwide. The aim of this analysis from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 is to provide the most comprehensive and up-to-date estimates of the global, regional, and national burden from neurological disorders.Methods We estimated prevalence, incidence, deaths, and disability-adjusted life-years (DALYs; the sum of years of life lost [YLLs] and years lived with disability [YLDs]) by age and sex for 15 neurological disorder categories (tetanus, meningitis, encephalitis, stroke, brain and other CNS cancers, traumatic brain injury, spinal cord injury, Alzheimer’s disease and other dementias, Parkinson’s disease, multiple sclerosis, motor neuron diseases, idiopathic epilepsy, migraine, tension-type headache, and a residual category for other less common neurological disorders) in 195 countries from 1990 to 2016. DisMod-MR 2.1, a Bayesian meta-regression tool, was the main method of estimation of prevalence and incidence, and the Cause of Death Ensemble model (CODEm) was used for mortality estimation. We quantified the contribution of 84 risks and combinations of risk to the disease estimates for the 15 neurological disorder categories using the GBD comparative risk assessment approach.Findings Globally, in 2016, neurological disorders were the leading cause of DALYs (276 million [95% UI 247–308]) and second leading cause of deaths (9·0 million [8·8–9·4]). The absolute number of deaths and DALYs from all neurological disorders combined increased (deaths by 39% [34–44] and DALYs by 15% [9–21]) whereas their age-standardised rates decreased (deaths by 28% [26–30] and DALYs by 27% [24–31]) between 1990 and 2016. The only neurological disorders that had a decrease in rates and absolute numbers of deaths and DALYs were tetanus, meningitis, and encephalitis. The four largest contributors of neurological DALYs were stroke (42·2% [38·6–46·1]), migraine (16·3% [11·7–20·8]), Alzheimer’s and other dementias (10·4% [9·0–12·1]), and meningitis (7·9% [6·6–10·4]). For the combined neurological disorders, age-standardised DALY rates were significantly higher in males than in females (male-to-female ratio 1·12 [1·05–1·20]), but migraine, multiple sclerosis, and tension-type headache were more common and caused more burden in females, with male-to-female ratios of less than 0·7. The 84 risks quantified in GBD explain less than 10% of neurological disorder DALY burdens, except stroke, for which 88·8% (86·5–90·9) of DALYs are attributable to risk factors, and to a lesser extent Alzheimer’s disease and other dementias (22·3% [11·8–35·1] of DALYs are risk attributable) and idiopathic epilepsy (14·1% [10·8–17·5] of DALYs are risk attributable).Interpretation Globally, the burden of neurological disorders, as measured by the absolute number of DALYs, continues to increase. As populations are growing and ageing, and the prevalence of major disabling neurological disorders steeply increases with age, governments will face increasing demand for treatment, rehabilitation, and support services for neurological disorders. The scarcity of established modifiable risks for most of the neurological burden demonstrates that new knowledge is required to develop effective prevention and treatment strategies. Publisher´s version (útgefin grein). "Peer Reviewed"

  • Open Access
    Authors: 
    Mosić, Mirjana D.; Trifković, Jelena; Vovk, Irena; Gašić, Uroš M.; Tešić, Živoslav Lj.; Šikoparija, Branko; Milojković-Opsenica, Dušanka;
    Publisher: MDPI AG
    Country: Serbia
    Project: MESTD | Structure-properties rela... (172017), EC | FCUB-ERA (256716)

    Supplementary material for: [https://doi.org/10.3390/biom9120783] Related to published version: [http://cherry.chem.bg.ac.rs/handle/123456789/3774]

  • Open Access English
    Authors: 
    Christopher J L Murray; Mohsen Abbasi-Kangevari; Hassan Abolhassani; Victor Adekanmbi; Olatunji O. Adetokunboh; Tauseef Ahmad; Keivan Ahmadi; Mehdi Ahmadi; Hamid Ahmadieh; Fares Alahdab; +274 more
    Publisher: Elsevier BV
    Countries: United Kingdom, Denmark, Sweden, Finland, Norway, Denmark, Peru, Netherlands, United Kingdom, Norway ...
    Project: MESTD | Epidemiological investiga... (175087), WT | Using linked electronic h... (205039), FCT | UID/QUI/50006/2019 (UID/QUI/50006/2019), EC | SHARE_M4 (261982), NIH | Health and Retirement Stu... (3U01AG009740-24S2), NIH | Cumulative and synergisti... (1K23AG056638-01), EC | SHARE_LEAP (227822), AKA | Paths to early labour mar... (319200), NIH | Health and Retirement Sur... (1R21AG032572-01), NHMRC | The natural history of di... (1137969),...

    Background Rigorous analysis of levels and trends in exposure to leading risk factors and quantification of their effect on human health are important to identify where public health is making progress and in which cases current efforts are inadequate. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 provides a standardised and comprehensive assessment of the magnitude of risk factor exposure, relative risk, and attributable burden of disease. Methods GBD 2019 estimated attributable mortality, years of life lost (YLLs), years of life lived with disability (YLDs), and disability-adjusted life-years (DALYs) for 87 risk factors and combinations of risk factors, at the global level, regionally, and for 204 countries and territories. GBD uses a hierarchical list of risk factors so that specific risk factors (eg, sodium intake), and related aggregates (eg, diet quality), are both evaluated. This method has six analytical steps. (1) We included 560 risk-outcome pairs that met criteria for convincing or probable evidence on the basis of research studies. 12 risk-outcome pairs included in GBD 2017 no longer met inclusion criteria and 47 risk-outcome pairs for risks already included in GBD 2017 were added based on new evidence. (2) Relative risks were estimated as a function of exposure based on published systematic reviews, 81 systematic reviews done for GBD 2019, and meta-regression. (3) Levels of exposure in each age-sex-location-year included in the study were estimated based on all available data sources using spatiotemporal Gaussian process regression, DisMod-MR 2.1, a Bayesian meta-regression method, or alternative methods. (4) We determined, from published trials or cohort studies, the level of exposure associated with minimum risk, called the theoretical minimum risk exposure level. (5) Attributable deaths, YLLs, YLDs, and DALYs were computed by multiplying population attributable fractions (PAFs) by the relevant outcome quantity for each age-sex-location-year. (6) PAFs and attributable burden for combinations of risk factors were estimated taking into account mediation of different risk factors through other risk factors. Across all six analytical steps, 30 652 distinct data sources were used in the analysis. Uncertainty in each step of the analysis was propagated into the final estimates of attributable burden. Exposure levels for dichotomous, polytomous, and continuous risk factors were summarised with use of the summary exposure value to facilitate comparisons over time, across location, and across risks. Because the entire time series from 1990 to 2019 has been re-estimated with use of consistent data and methods, these results supersede previously published GBD estimates of attributable burden. Findings The largest declines in risk exposure from 2010 to 2019 were among a set of risks that are strongly linked to social and economic development, including household air pollution; unsafe water, sanitation, and handwashing; and child growth failure. Global declines also occurred for tobacco smoking and lead exposure. The largest increases in risk exposure were for ambient particulate matter pollution, drug use, high fasting plasma glucose, and high body-mass index. In 2019, the leading Level 2 risk factor globally for attributable deaths was high systolic blood pressure, which accounted for 10.8 million (95% uncertainty interval [UI] 9.51-12.1) deaths (19.2% [16.9-21.3] of all deaths in 2019), followed by tobacco (smoked, second-hand, and chewing), which accounted for 8.71 million (8.12-9.31) deaths (15.4% [14.6-16.2] of all deaths in 2019). The leading Level 2 risk factor for attributable DALYs globally in 2019 was child and maternal malnutrition, which largely affects health in the youngest age groups and accounted for 295 million (253-350) DALYs (11.6% [10.3-13.1] of all global DALYs that year). The risk factor burden varied considerably in 2019 between age groups and locations. Among children aged 0-9 years, the three leading detailed risk factors for attributable DALYs were all related to malnutrition. Iron deficiency was the leading risk factor for those aged 10-24 years, alcohol use for those aged 25-49 years, and high systolic blood pressure for those aged 50-74 years and 75 years and older. Interpretation Overall, the record for reducing exposure to harmful risks over the past three decades is poor. Success with reducing smoking and lead exposure through regulatory policy might point the way for a stronger role for public policy on other risks in addition to continued efforts to provide information on risk factor harm to the general public. Copyright (C) 2020 The Author(s). Published by Elsevier Ltd.

  • Open Access
    Authors: 
    James A. Fellows Yates; Irina M. Velsko; Franziska Aron; Cosimo Posth; Courtney A. Hofman; Rita M. Austin; Cody Parker; Allison E. Mann; Kathrin Nägele; Kathryn Weedman Arthur; +39 more
    Countries: Spain, France, Serbia, Sweden, United Kingdom, Netherlands, United Kingdom, Italy, Spain
    Project: EC | HARVEST (677576), MESTD | Cultural changes and popu... (177023), EC | ADAPT (617627)

    The oral microbiome plays key roles in human biology, health, and disease, but little is known about the global diversity, variation, or evolution of this microbial community. To better understand the evolution and changing ecology of the human oral microbiome, we analyzed 124 dental biofilm metagenomes from humans, including Neanderthals and Late Pleistocene to present-day modern humans, chimpanzees, and gorillas, as well as New World howler monkeys for comparison. We find that a core microbiome of primarily biofilm structural taxa has been maintained throughout African hominid evolution, and these microbial groups are also shared with howler monkeys, suggesting that they have been important oral members since before the catarrhine–platyrrhine split ca. 40 Mya. However, community structure and individual microbial phylogenies do not closely reflect host relationships, and the dental biofilms of Homo and chimpanzees are distinguished by major taxonomic and functional differences. Reconstructing oral metagenomes from up to 100 thousand years ago, we show that the microbial profiles of both Neanderthals and modern humans are highly similar, sharing functional adaptations in nutrient metabolism. These include an apparent Homo-specific acquisition of salivary amylase-binding capability by oral streptococci, suggesting microbial coadaptation with host diet. We additionally find evidence of shared genetic diversity in the oral bacteria of Neanderthal and Upper Paleolithic modern humans that is not observed in later modern human populations. Differences in the oral microbiomes of African hominids provide insights into human evolution, the ancestral state of the human microbiome, and a temporal framework for understanding microbial health and disease. Significance The microbiome plays key roles in human health, but little is known about its evolution. We investigate the evolutionary history of the African hominid oral microbiome by analyzing dental biofilms of humans and Neanderthals spanning the past 100,000 years and comparing them with those of chimpanzees, gorillas, and howler monkeys. We identify 10 core bacterial genera that have been maintained within the human lineage and play key biofilm structural roles. However, many remain understudied and unnamed. We find major taxonomic and functional differences between the oral microbiomes of Homo and chimpanzees but a high degree of similarity between Neanderthals and modern humans, including an apparent Homo-specific acquisition of starch digestion capability in oral streptococci, suggesting microbial coadaptation with host diet.

  • Open Access
    Authors: 
    Mladenović , Milan; Arsić , Biljana B.; Stanković , Nevena; Mihović , Nezrina; Ragno, Rino; Regan, Andrew; +9 more
    Publisher: MDPI AG
    Countries: Italy, Serbia, United Kingdom
    Project: MESTD | Simultaneous Bioremediati... (43004), MESTD | Functional analysis, stoc... (174007), MESTD | Physics and Chemistry wit... (45006)

    Commercially available pesticides were examined as Mus musculus and Homo sapiens acetylcholinesterase (mAChE and hAChE) inhibitors by means of ligand-based (LB) and structure-based (SB) in silico approaches. Initially, the crystal structures of simazine, monocrotophos, dimethoate, and acetamiprid were reproduced using various force fields. Subsequently, LB alignment rules were assessed and applied to determine the inter synaptic conformations of atrazine, propazine, carbofuran, carbaryl, tebufenozide, imidacloprid, diuron, monuron, and linuron. Afterwards, molecular docking and dynamics SB studies were performed on either mAChE or hAChE, to predict the listed pesticides&rsquo acute toxicities (i.e., the LD50 values) against mice, as well to generate the model that could predict the LD50s against humans. Although for most of the pesticides the low Eglob_min correlates with the high acute toxicity, it is the ∆Gbinding that conditions the LD50 values for all the evaluated pesticides. Derived pLD50 = f(∆Gbinding) mAChE model may predict the pLD50 against hAChE, too. The hAChE inhibition by atrazine, propazine, and simazine (the most toxic pesticides) was elucidated by SB quantum mechanics (QM) DFT mechanistic and concentration-dependent kinetic studies, enriching the knowledge for design of less toxic pesticides. binding modes. Calculated energies of global minima (Eglob_min) and free energies of binding (∆Gbinding) were correlated with the pesticides&rsquo

  • Open Access
    Authors: 
    Reitze N. Rodseth; Bruce M Biccard; Yannick Le Manach; Daniel I. Sessler; Giovana A. Lurati Buse; Lehana Thabane; Robert C. Schutt; Daniel Bolliger; Lucio Cagini; Daniela Cardinale; +17 more
    Publisher: Elsevier BV
    Project: CIHR , MESTD | Biomarkers for kidney dis... (175089)

    Objectives The objective of this study was to determine whether measuring post-operative B-type natriuretic peptides (NPs) (i.e., B-type natriuretic peptide [BNP] and N-terminal fragment of proBNP [NT-proBNP]) enhances risk stratification in adult patients undergoing noncardiac surgery, in whom a pre-operative NP has been measured. Background Pre-operative NP concentrations are powerful independent predictors of perioperative cardiovascular complications, but recent studies have reported that elevated post-operative NP concentrations are independently associated with these complications. It is not clear whether there is value in measuring post-operative NP when a pre-operative measurement has been done. Methods We conducted a systematic review and individual patient data meta-analysis to determine whether the addition of post-operative NP levels enhanced the prediction of the composite of death and nonfatal myocardial infarction at 30 and ≥180 days after surgery. Results Eighteen eligible studies provided individual patient data (n = 2,179). Adding post-operative NP to a risk prediction model containing pre-operative NP improved model fit and risk classification at both 30 days (corrected quasi-likelihood under the independence model criterion: 1,280 to 1,204; net reclassification index: 20%; p Conclusions Additional post-operative NP measurement enhanced risk stratification for the composite outcomes of death or nonfatal myocardial infarction at 30 days and ≥180 days after noncardiac surgery compared with a pre-operative NP measurement alone.

  • Restricted
    Authors: 
    Antonio Politano; Ivan Radović; Duško Borka; Zoran L. Mišković; Gennaro Chiarello;
    Publisher: Elsevier BV
    Country: Serbia
    Project: NSERC , MESTD | Functional, Functionalize... (45005)

    We present a theoretical modeling of the energy-loss spectroscopy data for monolayer graphene (MLG) supported by Pt(111), Ru(0001) and Ni(111) substrates. To reproduce the experimental loss function, we have used a two-dimensional, two-fluid hydrodynamic model for interband transitions of graphenes pi and sigma electrons and an empirical Drude-Lorentz model in the local approximation for metal substrates. The electronic response from the visible to the ultraviolet frequency range has been nicely reproduced for MLG/Pt(111) and MLG/Ru(0001). For graphene nanodomes on Ru(0001), the loss function of valleys shows an additional mode at 8-9 eV. By contrast, this models fails for the case of MLG/Ni(111), presumably due to the strong hybridization between the pi states of graphene and the d bands of Ni, which is not accounted for in the model. (C) 2015 Elsevier Ltd. All rights reserved.

  • Open Access
    Authors: 
    Antonio Politano; Ivan Radović; Duško Borka; Zoran L. Mišković; Hak Ki Yu; Daniel Farías; Gennaro Chiarello;
    Publisher: Elsevier BV
    Country: Serbia
    Project: NSERC , MESTD | Functional, Functionalize... (45005)

    By means of angle-resolved electron energy loss spectroscopy, we have measured the interband it plasmon in high-quality graphene grown on peeled-off epitaxial Cu(111) foils. Experimental loss spectra have been reproduced by means of a hydrodynamic model. The dispersion relation of the plasmon frequency shows a nearly-flat dispersion up to a critical wave-vector of 0.3 angstrom(-1). We propose that the observed behavior could be originated by confinement effects in ripples in the strained graphene sheet. Strain also limits the dispersion at higher momenta, as a consequence of the increased effective mass of charge carriers. The analysis of momentum dependence of the line-width and of the inverse quality factor indicates that damping processes are dominated by decay in electron-hole pairs via indirect interband transitions. (C) 2016 Elsevier Ltd. All rights reserved.

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The following results are related to Canada. Are you interested to view more results? Visit OpenAIRE - Explore.
16 Research products, page 1 of 2
  • Open Access English
    Authors: 
    Laurent A. F. Frantz; James Haile; Audrey T. Lin; Amelie Scheu; Christina Geörg; Norbert Benecke; Michelle Alexander; Anna Linderholm; Victoria E. Mullin; Kevin G. Daly; +90 more
    Countries: Netherlands, United Kingdom, Portugal, Germany, United Kingdom, Germany, France, Belgium, United Kingdom, United Kingdom ...
    Project: NSF | Northern Narratives: Soci... (0638897), WT | Domestic animals as a mod... (210119), UKRI | Deciphering dog domestica... (NE/K003259/1), NSF | Conference on Global Long... (0947862), UKRI | Deciphering dog domestica... (NE/K005243/1), NSF | RAPID Gardar Collaborativ... (1119354), NSF | IPY: Long Term Human Ecod... (0732327), EC | Extinction Genomics (681396), NSF | The Origins of Equid Dome... (1311551), MESTD | Bioarchaeology of Ancient... (47001),...

    Archaeological evidence indicates that pig domestication had begun by ∼10,500 y before the present (BP) in the Near East, and mitochondrial DNA (mtDNA) suggests that pigs arrived in Europe alongside farmers ∼8,500 y BP. A few thousand years after the introduction of Near Eastern pigs into Europe, however, their characteristic mtDNA signature disappeared and was replaced by haplotypes associated with European wild boars. This turnover could be accounted for by substantial gene flow from local European wild boars, although it is also possible that European wild boars were domesticated independently without any genetic contribution from the Near East. To test these hypotheses, we obtained mtDNA sequences from 2,099 modern and ancient pig samples and 63 nuclear ancient genomes from Near Eastern and European pigs. Our analyses revealed that European domestic pigs dating from 7,100 to 6,000 y BP possessed both Near Eastern and European nuclear ancestry, while later pigs possessed no more than 4% Near Eastern ancestry, indicating that gene flow from European wild boars resulted in a near-complete disappearance of Near East ancestry. In addition, we demonstrate that a variant at a locus encoding black coat color likely originated in the Near East and persisted in European pigs. Altogether, our results indicate that while pigs were not independently domesticated in Europe, the vast majority of human-mediated selection over the past 5,000 y focused on the genomic fraction derived from the European wild boars, and not on the fraction that was selected by early Neolithic farmers over the first 2,500 y of the domestication process. Significance Archaeological evidence indicates that domestic pigs arrived in Europe, alongside farmers from the Near East ∼8,500 y ago, yet mitochondrial genomes of modern European pigs are derived from European wild boars. To address this conundrum, we obtained mitochondrial and nuclear data from modern and ancient Near Eastern and European pigs. Our analyses indicate that, aside from a coat color gene, most Near Eastern ancestry in the genomes of European domestic pigs disappeared over 3,000 y as a result of interbreeding with local wild boars. This implies that pigs were not domesticated independently in Europe, yet the first 2,500 y of human-mediated selection applied by Near Eastern Neolithic farmers played little role in the development of modern European pigs.

  • Open Access
    Authors: 
    Guzelmeric, Etil; Ristivojević, Petar; Trifković, Jelena; Dastan, Tugce; Yilmaz, Ozlem; Cengiz, Ozlem; Yesilada, Erdem;
    Publisher: Elsevier Science Bv, Amsterdam
    Country: Serbia
    Project: MESTD | Structure-properties rela... (172017)

    Supplementary data for: [https://doi.org/10.1016/j.lwt.2017.08.060] Related to published version: [http://cherry.chem.bg.ac.rs/handle/123456789/2552] Related to accepted version: [http://cherry.chem.bg.ac.rs/handle/123456789/2989]

  • Open Access English
    Authors: 
    Feigin V; Nichols E; Alam T; Bannick M; Beghi E; Blake N; Culpepper W; Dorsey E; Elbaz A; Ellenbogen R; +192 more
    Countries: Australia, Italy, Turkey, Netherlands, Spain, Iceland, Denmark, Sweden, Germany, United Kingdom ...
    Project: NHMRC | Prevention of stroke and ... (1042600), WT | Global Atlas of Podoconio... (201900), NIH | AdminSupp:Transforming Re... (3U01NS086090-02S1), NHMRC | Modifiable risk factors f... (1056929), NIH | Stroke Investigative Rese... (3U54HG007479-03S1), NIH | Systematic Investigation ... (1R01NS107900-01), MESTD | Epidemiological investiga... (175087), NIH | The Ohio State University... (5U10NS086484-03), NIH | African Neurobiobank for ... (1U01HG010273-01)

    ROA is funded by the National Institutes of Health (U01HG010273). SMA acknowledges the International Centre for Casemix and Clinical Coding, Faculty of Medicine, National University of Malaysia and Department of Health Policy and Management, Faculty of Public Health, Kuwait University for the approval and support to participate in this research project. AAw acknowledges funding support from Department of Science and Technology, Government of India, New Delhi, through INSPIRE Faculty scheme. TBA acknowledges partial funding from the Institute of Medical Research and Medicinal Plant Studies. ABa is supported by the Public Health Agency of Canada. TWB was supported by the Alexander von Humboldt Foundation through the Alexander von Humboldt Professor Award, funded by the Federal Ministry of Education and Research. MSBS acknowledges support from the Australian Government Research and Training Program scholarship for a PhD degree at the Australian National University, Australia. JJC is supported by the Swedish Heart and Lung Foundation. FCar is supported by the European Union (FEDER funds POCI/01/0145/FEDER/007728 and POCI/01/0145/FEDER/007265) and National Funds (FCT/MEC, Fundacao para a Ciencia e a Tecnologia and Ministerio da Educacao e Ciencia) under the Partnership Agreements PT2020 UID/MULTI/04378/2013 and PT2020UID/QUI/50006/2013. EC is supported by an Australian Research Council Future Fellowship (FT3 140100085). KD is supported by a Wellcome Trust [Grant Number 201900] as part of his International Intermediate Fellowship. EF is supported by the European Union (FEDER funds POCI/01/0145/FEDER/007728 and POCI/01/0145/FEDER/007265) and National Funds (FCT/MEC, Fundacao para a Ciencia e a Tecnologia and Ministerio da Educacao e Ciencia) under the Partnership Agreements PT2020 UID/MULTI/04378/2013 and PT2020UID/QUI/50006/2013. SMSI is funded by the Institute for Physical Activity and Nutrition (IPAN), Deakin University and received funding from High Blood Pressure Research Council of Australia. YKa is a DBT/Wellcome Trust India Alliance Fellow in Public Health. YJK is supported by the Office of Research and Innovation at Xiamen University Malaysia. BL acknowledges funding from the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre. WDL is supported in part by U10NS086484 NINDS. SLo is funded by the German Federal Ministry of Education and Research (nutriCARD, grant agreement number 01EA1411A). RML is supported by a National Health and Medical Research Council (NHMRC) of Australia Senior Research Fellowship. AMa and the Imperial College London are grateful for support from the NW London NIHR Collaboration for Leadership in Applied Health Research and Care. JJM is supported by the Danish National Research Foundation (Niels Bohr Professorship), and the John Cade Fellowship (APP1056929) from NHMRC. TMei acknowledges additional institutional support from the Competence Cluster for Nutrition and Cardiovascular Health (nutriCARD), Jena-Halle-Leipzig. IMV is supported by the Sistema Nacional de Investigacion (Panama). MOO is supported by SIREN U54 U54HG007479 and SIBS Genomics R01NS107900 grants. AMS was supported by a fellowship from the Egyptian Fulbright Mission Program. MMSM acknowledges the support from the Ministry of Education, Science and Technological Development, Republic of Serbia (contract no 175087). AShe is supported by Health Data Research UK. MBS' work on traumatic brain injury is supported by grants NIH U01 NS086090 (PI G Manley) from the National Institutes of Health (NIH) and DoD W81XWH-14-2-0176 (PI G Manley) from the United States Department of Defense. RTS is supported in part by grant number PROMETEOII/2015/021 from Generalitat Valenciana and the national grant PI17/00719 from ISCIIIFEDER. AGT was supported by a Fellowship from the NHMRC (Australia; 1042600. KBT acknowledges funding supports from the Maurice Wilkins Centre for Biodiscovery, Cancer Society of New Zealand, Health Research Council, Gut Cancer Foundation, and the University of Auckland. CY acknowledges support from the National Natural Science Foundation of China (grant number 81773552) and the Chinese NSFC International Cooperation and Exchange Program (grant number 71661167007). Background Neurological disorders are increasingly recognised as major causes of death and disability worldwide. The aim of this analysis from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 is to provide the most comprehensive and up-to-date estimates of the global, regional, and national burden from neurological disorders.Methods We estimated prevalence, incidence, deaths, and disability-adjusted life-years (DALYs; the sum of years of life lost [YLLs] and years lived with disability [YLDs]) by age and sex for 15 neurological disorder categories (tetanus, meningitis, encephalitis, stroke, brain and other CNS cancers, traumatic brain injury, spinal cord injury, Alzheimer’s disease and other dementias, Parkinson’s disease, multiple sclerosis, motor neuron diseases, idiopathic epilepsy, migraine, tension-type headache, and a residual category for other less common neurological disorders) in 195 countries from 1990 to 2016. DisMod-MR 2.1, a Bayesian meta-regression tool, was the main method of estimation of prevalence and incidence, and the Cause of Death Ensemble model (CODEm) was used for mortality estimation. We quantified the contribution of 84 risks and combinations of risk to the disease estimates for the 15 neurological disorder categories using the GBD comparative risk assessment approach.Findings Globally, in 2016, neurological disorders were the leading cause of DALYs (276 million [95% UI 247–308]) and second leading cause of deaths (9·0 million [8·8–9·4]). The absolute number of deaths and DALYs from all neurological disorders combined increased (deaths by 39% [34–44] and DALYs by 15% [9–21]) whereas their age-standardised rates decreased (deaths by 28% [26–30] and DALYs by 27% [24–31]) between 1990 and 2016. The only neurological disorders that had a decrease in rates and absolute numbers of deaths and DALYs were tetanus, meningitis, and encephalitis. The four largest contributors of neurological DALYs were stroke (42·2% [38·6–46·1]), migraine (16·3% [11·7–20·8]), Alzheimer’s and other dementias (10·4% [9·0–12·1]), and meningitis (7·9% [6·6–10·4]). For the combined neurological disorders, age-standardised DALY rates were significantly higher in males than in females (male-to-female ratio 1·12 [1·05–1·20]), but migraine, multiple sclerosis, and tension-type headache were more common and caused more burden in females, with male-to-female ratios of less than 0·7. The 84 risks quantified in GBD explain less than 10% of neurological disorder DALY burdens, except stroke, for which 88·8% (86·5–90·9) of DALYs are attributable to risk factors, and to a lesser extent Alzheimer’s disease and other dementias (22·3% [11·8–35·1] of DALYs are risk attributable) and idiopathic epilepsy (14·1% [10·8–17·5] of DALYs are risk attributable).Interpretation Globally, the burden of neurological disorders, as measured by the absolute number of DALYs, continues to increase. As populations are growing and ageing, and the prevalence of major disabling neurological disorders steeply increases with age, governments will face increasing demand for treatment, rehabilitation, and support services for neurological disorders. The scarcity of established modifiable risks for most of the neurological burden demonstrates that new knowledge is required to develop effective prevention and treatment strategies. Publisher´s version (útgefin grein). "Peer Reviewed"

  • Open Access
    Authors: 
    Mosić, Mirjana D.; Trifković, Jelena; Vovk, Irena; Gašić, Uroš M.; Tešić, Živoslav Lj.; Šikoparija, Branko; Milojković-Opsenica, Dušanka;
    Publisher: MDPI AG
    Country: Serbia
    Project: MESTD | Structure-properties rela... (172017), EC | FCUB-ERA (256716)

    Supplementary material for: [https://doi.org/10.3390/biom9120783] Related to published version: [http://cherry.chem.bg.ac.rs/handle/123456789/3774]

  • Open Access English
    Authors: 
    Christopher J L Murray; Mohsen Abbasi-Kangevari; Hassan Abolhassani; Victor Adekanmbi; Olatunji O. Adetokunboh; Tauseef Ahmad; Keivan Ahmadi; Mehdi Ahmadi; Hamid Ahmadieh; Fares Alahdab; +274 more
    Publisher: Elsevier BV
    Countries: United Kingdom, Denmark, Sweden, Finland, Norway, Denmark, Peru, Netherlands, United Kingdom, Norway ...
    Project: MESTD | Epidemiological investiga... (175087), WT | Using linked electronic h... (205039), FCT | UID/QUI/50006/2019 (UID/QUI/50006/2019), EC | SHARE_M4 (261982), NIH | Health and Retirement Stu... (3U01AG009740-24S2), NIH | Cumulative and synergisti... (1K23AG056638-01), EC | SHARE_LEAP (227822), AKA | Paths to early labour mar... (319200), NIH | Health and Retirement Sur... (1R21AG032572-01), NHMRC | The natural history of di... (1137969),...

    Background Rigorous analysis of levels and trends in exposure to leading risk factors and quantification of their effect on human health are important to identify where public health is making progress and in which cases current efforts are inadequate. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 provides a standardised and comprehensive assessment of the magnitude of risk factor exposure, relative risk, and attributable burden of disease. Methods GBD 2019 estimated attributable mortality, years of life lost (YLLs), years of life lived with disability (YLDs), and disability-adjusted life-years (DALYs) for 87 risk factors and combinations of risk factors, at the global level, regionally, and for 204 countries and territories. GBD uses a hierarchical list of risk factors so that specific risk factors (eg, sodium intake), and related aggregates (eg, diet quality), are both evaluated. This method has six analytical steps. (1) We included 560 risk-outcome pairs that met criteria for convincing or probable evidence on the basis of research studies. 12 risk-outcome pairs included in GBD 2017 no longer met inclusion criteria and 47 risk-outcome pairs for risks already included in GBD 2017 were added based on new evidence. (2) Relative risks were estimated as a function of exposure based on published systematic reviews, 81 systematic reviews done for GBD 2019, and meta-regression. (3) Levels of exposure in each age-sex-location-year included in the study were estimated based on all available data sources using spatiotemporal Gaussian process regression, DisMod-MR 2.1, a Bayesian meta-regression method, or alternative methods. (4) We determined, from published trials or cohort studies, the level of exposure associated with minimum risk, called the theoretical minimum risk exposure level. (5) Attributable deaths, YLLs, YLDs, and DALYs were computed by multiplying population attributable fractions (PAFs) by the relevant outcome quantity for each age-sex-location-year. (6) PAFs and attributable burden for combinations of risk factors were estimated taking into account mediation of different risk factors through other risk factors. Across all six analytical steps, 30 652 distinct data sources were used in the analysis. Uncertainty in each step of the analysis was propagated into the final estimates of attributable burden. Exposure levels for dichotomous, polytomous, and continuous risk factors were summarised with use of the summary exposure value to facilitate comparisons over time, across location, and across risks. Because the entire time series from 1990 to 2019 has been re-estimated with use of consistent data and methods, these results supersede previously published GBD estimates of attributable burden. Findings The largest declines in risk exposure from 2010 to 2019 were among a set of risks that are strongly linked to social and economic development, including household air pollution; unsafe water, sanitation, and handwashing; and child growth failure. Global declines also occurred for tobacco smoking and lead exposure. The largest increases in risk exposure were for ambient particulate matter pollution, drug use, high fasting plasma glucose, and high body-mass index. In 2019, the leading Level 2 risk factor globally for attributable deaths was high systolic blood pressure, which accounted for 10.8 million (95% uncertainty interval [UI] 9.51-12.1) deaths (19.2% [16.9-21.3] of all deaths in 2019), followed by tobacco (smoked, second-hand, and chewing), which accounted for 8.71 million (8.12-9.31) deaths (15.4% [14.6-16.2] of all deaths in 2019). The leading Level 2 risk factor for attributable DALYs globally in 2019 was child and maternal malnutrition, which largely affects health in the youngest age groups and accounted for 295 million (253-350) DALYs (11.6% [10.3-13.1] of all global DALYs that year). The risk factor burden varied considerably in 2019 between age groups and locations. Among children aged 0-9 years, the three leading detailed risk factors for attributable DALYs were all related to malnutrition. Iron deficiency was the leading risk factor for those aged 10-24 years, alcohol use for those aged 25-49 years, and high systolic blood pressure for those aged 50-74 years and 75 years and older. Interpretation Overall, the record for reducing exposure to harmful risks over the past three decades is poor. Success with reducing smoking and lead exposure through regulatory policy might point the way for a stronger role for public policy on other risks in addition to continued efforts to provide information on risk factor harm to the general public. Copyright (C) 2020 The Author(s). Published by Elsevier Ltd.

  • Open Access
    Authors: 
    James A. Fellows Yates; Irina M. Velsko; Franziska Aron; Cosimo Posth; Courtney A. Hofman; Rita M. Austin; Cody Parker; Allison E. Mann; Kathrin Nägele; Kathryn Weedman Arthur; +39 more
    Countries: Spain, France, Serbia, Sweden, United Kingdom, Netherlands, United Kingdom, Italy, Spain
    Project: EC | HARVEST (677576), MESTD | Cultural changes and popu... (177023), EC | ADAPT (617627)

    The oral microbiome plays key roles in human biology, health, and disease, but little is known about the global diversity, variation, or evolution of this microbial community. To better understand the evolution and changing ecology of the human oral microbiome, we analyzed 124 dental biofilm metagenomes from humans, including Neanderthals and Late Pleistocene to present-day modern humans, chimpanzees, and gorillas, as well as New World howler monkeys for comparison. We find that a core microbiome of primarily biofilm structural taxa has been maintained throughout African hominid evolution, and these microbial groups are also shared with howler monkeys, suggesting that they have been important oral members since before the catarrhine–platyrrhine split ca. 40 Mya. However, community structure and individual microbial phylogenies do not closely reflect host relationships, and the dental biofilms of Homo and chimpanzees are distinguished by major taxonomic and functional differences. Reconstructing oral metagenomes from up to 100 thousand years ago, we show that the microbial profiles of both Neanderthals and modern humans are highly similar, sharing functional adaptations in nutrient metabolism. These include an apparent Homo-specific acquisition of salivary amylase-binding capability by oral streptococci, suggesting microbial coadaptation with host diet. We additionally find evidence of shared genetic diversity in the oral bacteria of Neanderthal and Upper Paleolithic modern humans that is not observed in later modern human populations. Differences in the oral microbiomes of African hominids provide insights into human evolution, the ancestral state of the human microbiome, and a temporal framework for understanding microbial health and disease. Significance The microbiome plays key roles in human health, but little is known about its evolution. We investigate the evolutionary history of the African hominid oral microbiome by analyzing dental biofilms of humans and Neanderthals spanning the past 100,000 years and comparing them with those of chimpanzees, gorillas, and howler monkeys. We identify 10 core bacterial genera that have been maintained within the human lineage and play key biofilm structural roles. However, many remain understudied and unnamed. We find major taxonomic and functional differences between the oral microbiomes of Homo and chimpanzees but a high degree of similarity between Neanderthals and modern humans, including an apparent Homo-specific acquisition of starch digestion capability in oral streptococci, suggesting microbial coadaptation with host diet.

  • Open Access
    Authors: 
    Mladenović , Milan; Arsić , Biljana B.; Stanković , Nevena; Mihović , Nezrina; Ragno, Rino; Regan, Andrew; +9 more
    Publisher: MDPI AG
    Countries: Italy, Serbia, United Kingdom
    Project: MESTD | Simultaneous Bioremediati... (43004), MESTD | Functional analysis, stoc... (174007), MESTD | Physics and Chemistry wit... (45006)

    Commercially available pesticides were examined as Mus musculus and Homo sapiens acetylcholinesterase (mAChE and hAChE) inhibitors by means of ligand-based (LB) and structure-based (SB) in silico approaches. Initially, the crystal structures of simazine, monocrotophos, dimethoate, and acetamiprid were reproduced using various force fields. Subsequently, LB alignment rules were assessed and applied to determine the inter synaptic conformations of atrazine, propazine, carbofuran, carbaryl, tebufenozide, imidacloprid, diuron, monuron, and linuron. Afterwards, molecular docking and dynamics SB studies were performed on either mAChE or hAChE, to predict the listed pesticides&rsquo acute toxicities (i.e., the LD50 values) against mice, as well to generate the model that could predict the LD50s against humans. Although for most of the pesticides the low Eglob_min correlates with the high acute toxicity, it is the ∆Gbinding that conditions the LD50 values for all the evaluated pesticides. Derived pLD50 = f(∆Gbinding) mAChE model may predict the pLD50 against hAChE, too. The hAChE inhibition by atrazine, propazine, and simazine (the most toxic pesticides) was elucidated by SB quantum mechanics (QM) DFT mechanistic and concentration-dependent kinetic studies, enriching the knowledge for design of less toxic pesticides. binding modes. Calculated energies of global minima (Eglob_min) and free energies of binding (∆Gbinding) were correlated with the pesticides&rsquo

  • Open Access
    Authors: 
    Reitze N. Rodseth; Bruce M Biccard; Yannick Le Manach; Daniel I. Sessler; Giovana A. Lurati Buse; Lehana Thabane; Robert C. Schutt; Daniel Bolliger; Lucio Cagini; Daniela Cardinale; +17 more
    Publisher: Elsevier BV
    Project: CIHR , MESTD | Biomarkers for kidney dis... (175089)

    Objectives The objective of this study was to determine whether measuring post-operative B-type natriuretic peptides (NPs) (i.e., B-type natriuretic peptide [BNP] and N-terminal fragment of proBNP [NT-proBNP]) enhances risk stratification in adult patients undergoing noncardiac surgery, in whom a pre-operative NP has been measured. Background Pre-operative NP concentrations are powerful independent predictors of perioperative cardiovascular complications, but recent studies have reported that elevated post-operative NP concentrations are independently associated with these complications. It is not clear whether there is value in measuring post-operative NP when a pre-operative measurement has been done. Methods We conducted a systematic review and individual patient data meta-analysis to determine whether the addition of post-operative NP levels enhanced the prediction of the composite of death and nonfatal myocardial infarction at 30 and ≥180 days after surgery. Results Eighteen eligible studies provided individual patient data (n = 2,179). Adding post-operative NP to a risk prediction model containing pre-operative NP improved model fit and risk classification at both 30 days (corrected quasi-likelihood under the independence model criterion: 1,280 to 1,204; net reclassification index: 20%; p Conclusions Additional post-operative NP measurement enhanced risk stratification for the composite outcomes of death or nonfatal myocardial infarction at 30 days and ≥180 days after noncardiac surgery compared with a pre-operative NP measurement alone.

  • Restricted
    Authors: 
    Antonio Politano; Ivan Radović; Duško Borka; Zoran L. Mišković; Gennaro Chiarello;
    Publisher: Elsevier BV
    Country: Serbia
    Project: NSERC , MESTD | Functional, Functionalize... (45005)

    We present a theoretical modeling of the energy-loss spectroscopy data for monolayer graphene (MLG) supported by Pt(111), Ru(0001) and Ni(111) substrates. To reproduce the experimental loss function, we have used a two-dimensional, two-fluid hydrodynamic model for interband transitions of graphenes pi and sigma electrons and an empirical Drude-Lorentz model in the local approximation for metal substrates. The electronic response from the visible to the ultraviolet frequency range has been nicely reproduced for MLG/Pt(111) and MLG/Ru(0001). For graphene nanodomes on Ru(0001), the loss function of valleys shows an additional mode at 8-9 eV. By contrast, this models fails for the case of MLG/Ni(111), presumably due to the strong hybridization between the pi states of graphene and the d bands of Ni, which is not accounted for in the model. (C) 2015 Elsevier Ltd. All rights reserved.

  • Open Access
    Authors: 
    Antonio Politano; Ivan Radović; Duško Borka; Zoran L. Mišković; Hak Ki Yu; Daniel Farías; Gennaro Chiarello;
    Publisher: Elsevier BV
    Country: Serbia
    Project: NSERC , MESTD | Functional, Functionalize... (45005)

    By means of angle-resolved electron energy loss spectroscopy, we have measured the interband it plasmon in high-quality graphene grown on peeled-off epitaxial Cu(111) foils. Experimental loss spectra have been reproduced by means of a hydrodynamic model. The dispersion relation of the plasmon frequency shows a nearly-flat dispersion up to a critical wave-vector of 0.3 angstrom(-1). We propose that the observed behavior could be originated by confinement effects in ripples in the strained graphene sheet. Strain also limits the dispersion at higher momenta, as a consequence of the increased effective mass of charge carriers. The analysis of momentum dependence of the line-width and of the inverse quality factor indicates that damping processes are dominated by decay in electron-hole pairs via indirect interband transitions. (C) 2016 Elsevier Ltd. All rights reserved.