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Sökning: WFRF:(Swietlicki Erik)

  • Resultat 201-210 av 319
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201.
  • Massad, Eduardo, et al. (författare)
  • Estimated Zika virus importations to Europe by travellers from Brazil
  • 2016
  • Ingår i: Global Health Action. - : Informa UK Limited. - 1654-9716 .- 1654-9880. ; 9, s. 1-7
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Given the interconnectivity of Brazil with the rest of the world, Zika virus (ZIKV) infections have the potential to spread rapidly around the world via viremic travellers. The extent of spread depends on the travel volume and the endemicity in the exporting country. In the absence of reliable surveillance data, we did mathematical modelling to estimate the number of importations of ZIKV from Brazil into Europe.DESIGN: We applied a previously developed mathematical model on importations of dengue to estimate the number of ZIKV importations into Europe, based on the travel volume, the probability of being infected at the time of travel, the population size of Brazil, and the estimated incidence of ZIKV infections.RESULTS: Our model estimated between 508 and 1,778 imported infections into Europe in 2016, of which we would expect between 116 and 355 symptomatic Zika infections; with the highest number of importations being into France, Portugal and Italy.CONCLUSIONS: Our model identified high-risk countries in Europe. Such data can assist policymakers and public health professionals in estimating the extent of importations in order to prepare for the scale up of laboratory diagnostic assays and estimate the occurrence of Guillain-Barré Syndrome, potential sexual transmission, and infants with congenital ZIKV syndrome.
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202.
  • Massad, Eduardo, et al. (författare)
  • Estimating the size of Aedes aegypti populations from dengue incidence data : Implications for the risk of yellow fever outbreaks
  • 2017
  • Ingår i: Infectious Disease Modelling. - : Elsevier. - 2468-0427. ; 2:4, s. 441-454
  • Tidskriftsartikel (refereegranskat)abstract
    • In this paper we present a model to estimate the density of aedes mosquitoes in a community affected by dengue. The method consists in fitting a continuous function to the incidence of dengue infections, from which the density of infected mosquitoes is derived straightforwardly. Further derivations allow the calculation of the latent and susceptible mosquitoes’ densities, the sum of the three equals the total mosquitoes’ density. The method is illustrated with the case of the risk of urban yellow fever resurgence in dengue infested areas but the same procedures apply for other aedes-transmitted infections like Zika and chikungunya viruses.
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203.
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204.
  • Massad, Eduardo, et al. (författare)
  • Modelling an optimum vaccination strategy against ZIKA virus for outbreak use
  • 2019
  • Ingår i: Epidemiology and Infection. - : Cambridge University Press. - 0950-2688 .- 1469-4409. ; 147
  • Tidskriftsartikel (refereegranskat)abstract
    • We present a model to optimise a vaccination campaign aiming to prevent or to curb a Zika virus outbreak. We show that the optimum vaccination strategy to reduce the number of cases by a mass vaccination campaign should start when the Aedes mosquitoes' density reaches the threshold of 1.5 mosquitoes per humans, the moment the reproduction number crosses one. The maximum time it is advisable to wait for the introduction of a vaccination campaign is when the first ZIKV case is identified, although this would not be as effective to minimise the number of infections as when the mosquitoes' density crosses the critical threshold. This suboptimum strategy, however, would still curb the outbreak. In both cases, the catch up strategy should aim to vaccinate at least 25% of the target population during a concentrated effort of 1 month immediately after identifying the threshold. This is the time taken to accumulate the herd immunity threshold of 56.5%. These calculations were done based on theoretical assumptions that vaccine implementation would be feasible within a very short time frame.
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205.
  • Mathieu, Roland, et al. (författare)
  • The nanoscale phase separation in hole-doped manganites
  • 2007
  • Ingår i: Journal of the Physical Society of Japan. - 0031-9015 .- 1347-4073. ; 76:12, s. 124706-
  • Tidskriftsartikel (refereegranskat)abstract
    • A macroscopic phase separation, in which ferromagnetic clusters are observed in an insulating matrix, is sometimes observed, and believed to be essential to the colossal magnetoresistive (CMR) properties of manganese oxides. The application of a magnetic field may indeed trigger large magnetoresistance effects due to the percolation between clusters allowing the movement of the charge carriers. However, this macroscopic phase separation is mainly related to extrinsic defects or impurities, which hinder the long-ranged charge-orbital order of the system. We show in the present article that rather than the macroscopic phase separation, an homogeneous short-ranged charge-orbital order accompanied by a spin glass state occurs, as an intrinsic result of the uniformity of the random potential perturbation induced by the solid solution of the cations on the A-sites of the structure of these materials. Hence the phase separation does occur, but in a more subtle and interesting nanoscopic form, here referred as "homogeneous". Remarkably, this "nanoscale phase separation" alone is able to bring forth the colossal magnetoresistance in the perovskite manganites, and is potentially relevant to a wide variety of other magnetic and/or electrical properties of manganites, as well as many other transition metal oxides, in bulk or thin film form as we exemplify throughout the article.
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206.
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207.
  • Mir, Bilal Ahmad, et al. (författare)
  • MicroRNA‐100 Reduced Fetal Bovine Muscle Satellite Cell Myogenesis and Augmented Intramuscular Lipid Deposition by Modulating IGF1R
  • 2022
  • Ingår i: Cells. - : MDPI AG. - 2073-4409. ; 11:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Previously, microRNA‐100 (miR‐100) and its putative mRNA target, insulin‐like growth factor receptor‐1 (IGF1R) were identified as differentially and inversely expressed in bovine longissimus dorsi (LD) muscles with divergent intramuscular fat (IMF) content by our group. While IGF1R signaling is implicated in myogenesis and muscle lipid metabolism, the underlying regulatory mechanisms are poorly understood. In the present study, we aimed to investigate the regulation of IGF1R by miR‐100 during bovine muscle satellite cell (BMSC) myogenesis and lipid deposition. MiR‐100 was confirmed to target the IGF1R 3′‐untranslated region (3′‐UTR) by luciferase reporter assay. Furthermore, expression of miR‐100 and IGF1R was reciprocal during BMSC differentiation, suggesting a crosstalk between the two. Correspondingly, miR‐100 mimic (agomiR) suppressed the levels of IGF1R, PI3K/AKT pathway signaling, myogenic gene MYOG, muscle structural components MYH7 and MYH8, whereas the inhibitor (antagomiR) had no clear stimulating effects. The IGF1R inhibitor (BMS‐754807) curtailed receptor levels and triggered atrophy in muscle myotubes but did not influence miR‐100 expression. AgomiR increased oleic acid‐induced lipid deposition in BMSC myotubes supporting its involvement in intramuscular fat deposition, while antagomiR had no effect. Moreover, mitochondrial beta‐oxidation and long‐chain fatty acid synthesis‐related genes were modulated by agomiR addition. Our results demonstrate modulatory roles of miR‐100 in BMSC development, lipid deposition, and metabolism and suggest a role of miR‐100 in marbling characteristics of meat animals and fat oxidation in muscle.
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208.
  • Mravinacová, Sára, et al. (författare)
  • CSF protein ratios with enhanced potential to reflect Alzheimer’s disease pathology and neurodegeneration
  • 2024
  • Ingår i: Molecular Neurodegeneration. - : Springer Nature. - 1750-1326. ; 19:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Amyloid and tau aggregates are considered to cause neurodegeneration and consequently cognitive decline in individuals with Alzheimer’s disease (AD). Here, we explore the potential of cerebrospinal fluid (CSF) proteins to reflect AD pathology and cognitive decline, aiming to identify potential biomarkers for monitoring outcomes of disease-modifying therapies targeting these aggregates. Method: We used a multiplex antibody-based suspension bead array to measure the levels of 49 proteins in CSF from the Swedish GEDOC memory clinic cohort at the Karolinska University Hospital. The cohort comprised 148 amyloid- and tau-negative individuals (A-T-) and 65 amyloid- and tau-positive individuals (A+T+). An independent sample set of 26 A-T- and 26 A+T+ individuals from the Amsterdam Dementia Cohort was used for validation. The measured proteins were clustered based on their correlation to CSF amyloid beta peptides, tau and NfL levels. Further, we used support vector machine modelling to identify protein pairs, matched based on their cluster origin, that reflect AD pathology and cognitive decline with improved performance compared to single proteins. Results: The protein-clustering revealed 11 proteins strongly correlated to t-tau and p-tau (tau-associated group), including mainly synaptic proteins previously found elevated in AD such as NRGN, GAP43 and SNCB. Another 16 proteins showed predominant correlation with Aβ42 (amyloid-associated group), including PTPRN2, NCAN and CHL1. Support vector machine modelling revealed that proteins from the two groups combined in pairs discriminated A-T- from A+T+ individuals with higher accuracy compared to single proteins, as well as compared to protein pairs composed of proteins originating from the same group. Moreover, combining the proteins from different groups in ratios (tau-associated protein/amyloid-associated protein) significantly increased their correlation to cognitive decline measured with cognitive scores. The results were validated in an independent cohort. Conclusions: Combining brain-derived proteins in pairs largely enhanced their capacity to discriminate between AD pathology-affected and unaffected individuals and increased their correlation to cognitive decline, potentially due to adjustment of inter-individual variability. With these results, we highlight the potential of protein pairs to monitor neurodegeneration and thereby possibly the efficacy of AD disease-modifying therapies.
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209.
  • Mravinacová, Sára, 1994- (författare)
  • Multiplexed protein analysis in neurodegenerative diseases
  • 2024
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Proteins are essential biomolecules that perform a vast array of functions within the human body. The abundance of proteins within cells, tissues, and bodily fluids is dy- namic and can be associated with different physiological and disease states. As such, studying proteins and protein profiles in health and disease can provide insights into the mechanisms and pathological processes associated with different diseases as well as different disease stages. Furthermore, protein biomarkers identified in research have the potential to aid clinical diagnostics and therapeutic development, leading to im- provement of patient care and outcomes. The majority of the work included in this thesis, revolves around the analysis of protein profiles in the context of neurodegenerative diseases, with the main focus on demen- tias. In the studies, preselected protein panels were measured in cerebrospinal fluid (CSF) samples employing the multiplexed high-throughput antibody-based suspension bead array technology. In paper I, the potential of using protein pairs to reflect Alzheimer’s disease pathology and cognitive decline was explored, with the aim to identify biomarkers which could possibly aid in monitoring the efficacy of disease-modifying treatments in clinical tri- als. A number of protein pairs was identified providing significantly higher performance compared to single proteins, likely due to adjustment for inter-individual variability in general protein levels. Paper II built upon the findings from paper I, expanding the investigation of CSF protein patterns across multiple neurodegenerative diseases. This study demonstrated that the performance of single brain-derived proteins in disease prediction is affected by variability in general protein levels, accounting for 70 % of protein variability be- tween individuals irrespective of disease. Adjusting for the general protein levels directly or through combining proteins in pairs improved the performance of proteins as biomarkers. However, the majority of the proteins with altered levels in CSF were not specific for a single disease, suggesting their association to processes common for the diseases, and highlighting the need for disease comparisons in biomarker studies. While paper I and II established the presence of variability in general CSF levels of brain-derived proteins between individuals, the factors underlying this variability re- mained unclear. Paper III explored whether the levels of proteins in CSF are influenced by CSF volume in a cohort of healthy individuals. The findings revealed negative correlations of brain-derived proteins with brain ventricular volumes, sug- gesting a dilution effect of proteins in CSF potentially contributing to differences in CSF levels of brain-derived proteins between individuals. In summary, these three Abstract i Abstract studies shed light on CSF protein patterns and their relevance in neurodegenerative diseases, pushing the boundaries of our current knowledge a step forward. A specific group of proteins present in the human body; the antibodies, are involved in the defense mechanisms against pathogens. These large molecules are produced by our immune system upon infection (or vaccination), and provide protection against future reinfections. However, the amount of antibodies produced and their protective effect through virus neutralization varies between individuals. Paper IV included in this thesis involved the development of a cell-free and virus-free bead-based assay for assessment of the neutralization capability of antibodies produced against the SARS- COV-2 virus. While this study can be considered an outlier in the theme of this thesis, it represents our contribution to the global research efforts which necessitated other activities to be put on hold in favor of endeavors in response to the rise of the Covid- 19 pandemic. 
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210.
  • Mráz, Attila (författare)
  • Does Political Equality Require Equal Power? A Pluralist Account
  • 2023
  • Ingår i: Ethical Theory and Moral Practice. - 1386-2820 .- 1572-8447.
  • Tidskriftsartikel (refereegranskat)abstract
    • In this paper, I criticize two views on how political equality is related to equally distributed political power, and I offer a novel, pluralist account of political equality to address their shortcomings—in particular, concerning their implications for affirmative action in the political domain, political representation, and the situation of permanent minorities. The Equal Power View holds that political equality requires equally distributed political power. It considers affirmative action—e.g., racial or gender electoral quotas—, representation, and more-than-equal power to permanent minorities pro tanto objectionable. The Equal Status View, in contrast, holds that political equality concerns equal relations and status, and it is only contingently related to equally distributed power. I argue that while the Equal Status View is right that equal power can be insufficient for—or even objectionable from the viewpoint of—political equality, it is wrong to conclude that equal power has no independent significance in an account of political equality. My pluralist account shows that political equality entails not only status-based requirements but also independent egalitarian requirements to distribute political power equally. This account provides a finer-grained understanding of affirmative action in the political domain. It justifies affirmative action but holds that it should only be used to realize equal political status until thorough-going social reform allows us to maintain both equal political status and equally distributed political power at the same time. Similarly, representation should be amended with power-balancing institutions, and permanent minorities should enjoy equal status with minimal compromise to power equality.
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