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University of Gothenburg
Country: Sweden
Funder (6)
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523 Projects, page 1 of 105
  • Funder: NIH Project Code: 5R01NS040863-06
    Funder Contribution: 233,152 USD
  • Funder: NIH Project Code: 5R01DA010765-05
    Funder Contribution: 135,000 USD
  • Funder: NWO Project Code: 462-14-076

    Cutting across the five research themes of this Call, HEALTHDOX aims to explore future trajectories of European health politics and policies through an investigation of the impact of recent health reforms on health inequalities, health expenditures, and public attitudes towards both the health system and the welfare state. At its broadest level, the project poses the question of whether there is a paradox of health state futures. Europeanization and globalization processes may be putting National Health Service types of health systems under increasing pres-sure to converge to the Continental health insurance model. But, para-doxically, National Health Services may be the type of health system best suited both to cope with the rising health costs associated with population aging, and to regenerate public support for the welfare state amongst increasingly diverse populations. This project will investigate health policy developments from 1990 to the present in Estonia, Germany, Ireland, the Netherlands, Portugal and Sweden. The impact of these policy changes will be analysed using quantitative data found in both national and international sources. Our team is comprised of qualitative and quantitative researchers from the fields of Political Science and Sociology, whose combined expertise in-cludes health politics, health policy, demography, migration, compara-tive and European politics, and the politics and sociology of the welfare state. The comparative and transnational design of the project will al-low us to provide insights into health inequalities, the meaning of the welfare state for individuals, and the future politics of the welfare state, as well as to provide health policy-makers with important feedback on their policies.

  • Funder: EC Project Code: 844909
    Overall Budget: 191,852 EURFunder Contribution: 191,852 EUR

    Diatoms are unicellular eukaryotic algae (microalgae) and one of the most common and diverse type of marine phytoplankton. Thanks to a flexible cell metabolism, they dominate in environmental conditions normally unfavorable for photosynthesis, i.e. freezing seawater, low light intensity and short photoperiod. Moreover, diatoms are able to synthesize storage lipids (20-50% of cell dry weight) that can be used for production of renewable biomass and high-value fatty acids. However, the success of these microalgae as feedstock depends on lowering the production cost. The proposed project aims to develop mixotrophic cultivation (i.e. the simultaneous use of light and carbon dioxide for photosynthesis and organic carbon for respiration) to maximize growth and outdoor productivity for selected strains from the Swedish west coast. The focus will be on the bloom-forming coastal diatom Skeletonema marinoi (S. marinoi) whose sequence annotation is ongoing, and the recent knowledge on mixotrophic growth of the model diatom Phaeodactylum tricornutum will be employed. The main objectives will be: i) using the bloom-forming S. marinoi to better understand mixotrophic metabolism in diatoms; ii) exploring the optimal mixotrophic conditions for enhanced productivity of S. marinoi; iii) investigating the potential industrial applications of S. marinoi when cultivated under mixotrophy. To achieve these objectives, an interdisciplinary approach including computational, biophysical, analytical, biotechnological and biological methods will be employed. A mixotrophic outdoor cultivation of marine microalgae in the dynamic climate of the Swedish west coast could provide a higher total production of renewable biomass for industry.

  • Funder: EC Project Code: 681712
    Overall Budget: 1,985,090 EURFunder Contribution: 1,985,090 EUR

    Critical to our understanding of Alzheimer’s disease (AD) and also to finding therapies is determining how key pathological factors interact and relate to neuronal toxicity, symptoms and disease progression. My research has focussed on amyloid beta (Aβ) moities and demonstrated that cerebrospinal fluid (CSF) Aβ42 correlates with cerebral Aβ pathology; that Aβ accumulates in the brain 10-20 years prior to onset of symptoms; and that CSF Aβ abnormalities precede CSF tau changes. However, it is increasingly clear that a simple linear model of AD aetiology and progression is inadequate. This proposal aims at developing and validating new diagnostic and prognostic biomarker tools to examine the AD pathogenesis in humans taking a broad view of AD’s multiple pathophysiological features and their putative biomarkers. The major questions, all relevant to therapeutic research, that will be addressed in my proposal include: (i) how are different forms of Aβ produced and modified; (ii) what is the toxicity of these different forms; (iii) how is this toxicity mediated; and iv) what other pathologies may contribute to or modify AD-like phenotypes? We and others have shown that Aβ monomers are relatively non-toxic. We will address the hypothesis that Aβ starts to accumulate in the brains of certain individuals due to defective clearance of the peptide. Once aggregated, Aβ acquires chemical modifications during brain incubation over years. These modified Aβ forms then induce tau hyperphosphorylation and concomitantly over-activate the immune system, resulting in neurotoxicity. Other pathologies, including α-synuclein and TDP-43, may contribute in this process. In PATHAD, we will develop and validate new diagnostic and prognostic tools using a combination of groundbreaking technologies and unique clinical materials to dissect the underlying molecular pathogenesis of AD in much greater detail than what has been possible before and facilitate the development of effective treatments.

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