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- Koundouri, P., et al.
(author)
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Methodology for Integrated Socio-economic Assessment of Multi-use Offshore Platforms.
- 2017
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In: In: Koundouri P. (eds) The Ocean of Tomorrow. Environment & Policy, vol 56. Springer, Cham. - 9783319557700 ; , s. 11-26
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Book chapter (other academic/artistic)abstract
- This chapter presents the methodology employed for the Integrated Socio-Economic Assessment (MISEA) of different designs of Multi-Use Offshore Platforms (MUOPs). The methodology allows for the identification, the valuationand the assessment of the potential impacts and their magnitude. The analysis considers a number of feasible designs of MUOP investments, and the likely responsesof those impacted by the investment project. The approach provides decision-makers with a valuable tool to assess whether a MUOP project increases the overall social welfare and hence should be undertaken. This is performed under alternative specifications regarding platform design, the discount rate and the stream of net benefits, if a Cost-Benefit Analysis (CBA) is to be followed or a sensitivity analysis of selected criteria in a Multi-Criteria Decision Analysis (MCDA) framework. Themethodology can support the implementation of policies aiming at achieving a goodenvironmental status of the EU’s marine waters and the protection of the resource base upon which marine-related economic and social activities depend.
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| 2. |
- Oikonomou, Vasileios, et al.
(author)
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The Role of Interferon-γ in Autoimmune Polyendocrine Syndrome Type 1.
- 2024
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In: The New England journal of medicine. - 1533-4406. ; 390:20, s. 1873-1884
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Journal article (peer-reviewed)abstract
- Autoimmune polyendocrine syndrome type 1 (APS-1) is a life-threatening, autosomal recessive syndrome caused by autoimmune regulator (AIRE) deficiency. In APS-1, self-reactive T cells escape thymic negative selection, infiltrate organs, and drive autoimmune injury. The effector mechanisms governing T-cell-mediated damage in APS-1 remain poorly understood.We examined whether APS-1 could be classified as a disease mediated by interferon-γ. We first assessed patients with APS-1 who were participating in a prospective natural history study and evaluated mRNA and protein expression in blood and tissues. We then examined the pathogenic role of interferon-γ using Aire-/-Ifng-/- mice and Aire-/- mice treated with the Janus kinase (JAK) inhibitor ruxolitinib. On the basis of our findings, we used ruxolitinib to treat five patients with APS-1 and assessed clinical, immunologic, histologic, transcriptional, and autoantibody responses.Patients with APS-1 had enhanced interferon-γ responses in blood and in all examined autoimmunity-affected tissues. Aire-/- mice had selectively increased interferon-γ production by T cells and enhanced interferon-γ, phosphorylated signal transducer and activator of transcription 1 (pSTAT1), and CXCL9 signals in multiple organs. Ifng ablation or ruxolitinib-induced JAK-STAT blockade in Aire-/- mice normalized interferon-γ responses and averted T-cell infiltration and damage in organs. Ruxolitinib treatment of five patients with APS-1 led to decreased levels of T-cell-derived interferon-γ, normalized interferon-γ and CXCL9 levels, and remission of alopecia, oral candidiasis, nail dystrophy, gastritis, enteritis, arthritis, Sjögren's-like syndrome, urticaria, and thyroiditis. No serious adverse effects from ruxolitinib were identified in these patients.Our findings indicate that APS-1, which is caused by AIRE deficiency, is characterized by excessive, multiorgan interferon-γ-mediated responses. JAK inhibition with ruxolitinib in five patients showed promising results. (Funded by the National Institute of Allergy and Infectious Diseases and others.).
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