11 research outputs found
Folkets val
Denna kvantitativa teoriprövande uppsats undersöker hur ekonomisk röstning påverkar utfallet av svenska riksdagsval. Fokus ligger främst på val efter kriser eftersom det är här som ekonomin borde påverka valen mest. Undersökningar om väljarpreferenser från SOM-institutet ligger till grund för denna analys. Statistiken har sedan tabellerats och analyserats utifrån två dimensioner: samhällsmotiv kontra plånboksmotiv och retrospektiva kontra prospektiva perspektiv på ekonomin. Det mesta av den tidigare forskningen har varit på makronivå och analyserat väljarbeteende utifrån t.ex. arbetslöshet, BNP/capita och tillväxt. Vi har valt att gå ner på individnivå för att tillföra mer forskning på en nivå närmare väljarna. Vi finner att både samhällsmotiv och plånboksmotiv ligger bakom väljarnas preferenser men att det är samhällsmotiven som väger tyngst. Vi finner också att tiden före valet påverkar väljarna mer än vad de tror komma skall. Detta ligger i linje med tidigare forskning. Uppsatsen når slutsatsen att den ekonomiska röstningsteorin kan tänkas förklara valresultaten i Sverige 1994 och 2010, men att den är alldeles för enkel för att kunna förklara dagens allt mer komplexa, globaliserade ekonomi
Förändring eller Kontinuitet - SD:s plats i den svenska politiken
Is the rise of Sverigedemokraterna (SD) something new in Swedish politics, or is it just a modern incarnation of an old phenomenon? Sverigedemokraterna have sometimes been portrayed as a foreign entity in Swedish politics. It’s claimed it came out of nowhere and it’s policies are seen as something that no true democratic, lagom, Swede could ever agree to. And yet, they are the third largest party in the Riksdag. If you take a closer look at Swedish political history, the ideas and ideals of SD are not so special after all. Through an idealtype analysis and an overview of post-WWII Swedish politics I set out to prove not only that the SD have had a predecessor in the Riksdag in the form of Ny Demokrati but also that their ideals stretch back decades. I will show that SD did not come from nowhere, but owe the existence to developments that have taken place over decades. Even though the success of the party might be unprecedented in the Swedish context, we should not be surprised at all over their existence. In fact we should ask ourselves why did it take the radikal right such a long time to blossom in Sweden
Antechamber to the Bosphorus: In point, line, surface
Architecture, Urbanism and Building Sciences | Borders and Territorie
The use of sequential mark-release-recapture experiments to estimate population size, survival and dispersal of male mosquitoes of the Anopheles gambiae complex in Bana, a west African humid savannah village
Experimentelle und Theoretische Untersuchungen Ăśber die Entdifferenzierung und Teilung Pflanzlicher Dauerzellen
Clinical phenotypes and quality of life to define post-COVID-19 syndrome: a cluster analysis of the multinational, prospective ORCHESTRA cohortResearch in context
Summary: Background: Lack of specific definitions of clinical characteristics, disease severity, and risk and preventive factors of post-COVID-19 syndrome (PCS) severely impacts research and discovery of new preventive and therapeutics drugs. Methods: This prospective multicenter cohort study was conducted from February 2020 to June 2022 in 5 countries, enrolling SARS-CoV-2 out- and in-patients followed at 3-, 6-, and 12-month from diagnosis, with assessment of clinical and biochemical features, antibody (Ab) response, Variant of Concern (VoC), and physical and mental quality of life (QoL). Outcome of interest was identification of risk and protective factors of PCS by clinical phenotype, setting, severity of disease, treatment, and vaccination status. We used SF-36 questionnaire to assess evolution in QoL index during follow-up and unsupervised machine learning algorithms (principal component analysis, PCA) to explore symptom clusters. Severity of PCS was defined by clinical phenotype and QoL. We also used generalized linear models to analyse the impact of PCS on QoL and associated risk and preventive factors. CT registration number: NCT05097677. Findings: Among 1796 patients enrolled, 1030 (57%) suffered from at least one symptom at 12-month. PCA identified 4 clinical phenotypes: chronic fatigue-like syndrome (CFs: fatigue, headache and memory loss, 757 patients, 42%), respiratory syndrome (REs: cough and dyspnoea, 502, 23%); chronic pain syndrome (CPs: arthralgia and myalgia, 399, 22%); and neurosensorial syndrome (NSs: alteration in taste and smell, 197, 11%). Determinants of clinical phenotypes were different (all comparisons p < 0.05): being female increased risk of CPs, NSs, and CFs; chronic pulmonary diseases of REs; neurological symptoms at SARS-CoV-2 diagnosis of REs, NSs, and CFs; oxygen therapy of CFs and REs; and gastrointestinal symptoms at SARS-CoV-2 diagnosis of CFs. Early treatment of SARS-CoV-2 infection with monoclonal Ab (all clinical phenotypes), corticosteroids therapy for mild/severe cases (NSs), and SARS-CoV-2 vaccination (CPs) were less likely to be associated to PCS (all comparisons p < 0.05). Highest reduction in QoL was detected in REs and CPs (43.57 and 43.86 vs 57.32 in PCS-negative controls, p < 0.001). Female sex (p < 0.001), gastrointestinal symptoms (p = 0.034) and renal complications (p = 0.002) during the acute infection were likely to increase risk of severe PCS (QoL <50). Vaccination and early treatment with monoclonal Ab reduced the risk of severe PCS (p = 0.01 and p = 0.03, respectively). Interpretation: Our study provides new evidence suggesting that PCS can be classified by clinical phenotypes with different impact on QoL, underlying possible different pathogenic mechanisms. We identified factors associated to each clinical phenotype and to severe PCS. These results might help in designing pathogenesis studies and in selecting high-risk patients for inclusion in therapeutic and management clinical trials. Funding: The study received funding from the Horizon 2020 ORCHESTRA project, grant 101016167; from the Netherlands Organisation for Health Research and Development (ZonMw), grant 10430012010023; from Inserm, REACTing (REsearch & ACtion emergING infectious diseases) consortium and the French Ministry of Health, grant PHRC 20-0424
Comparative Analysis of Protocols to Induce Human CD4+Foxp3+ Regulatory T Cells by Combinations of IL-2, TGF-beta, Retinoic Acid, Rapamycin and Butyrate
Rare predicted loss-of-function variants of type I IFN immunity genes are associated with life-threatening COVID-19
BackgroundWe previously reported that impaired type I IFN activity, due to inborn errors of TLR3- and TLR7-dependent type I interferon (IFN) immunity or to autoantibodies against type I IFN, account for 15-20% of cases of life-threatening COVID-19 in unvaccinated patients. Therefore, the determinants of life-threatening COVID-19 remain to be identified in similar to 80% of cases.MethodsWe report here a genome-wide rare variant burden association analysis in 3269 unvaccinated patients with life-threatening COVID-19, and 1373 unvaccinated SARS-CoV-2-infected individuals without pneumonia. Among the 928 patients tested for autoantibodies against type I IFN, a quarter (234) were positive and were excluded.ResultsNo gene reached genome-wide significance. Under a recessive model, the most significant gene with at-risk variants was TLR7, with an OR of 27.68 (95%CI 1.5-528.7, P=1.1x10(-4)) for biochemically loss-of-function (bLOF) variants. We replicated the enrichment in rare predicted LOF (pLOF) variants at 13 influenza susceptibility loci involved in TLR3-dependent type I IFN immunity (OR=3.70[95%CI 1.3-8.2], P=2.1x10(-4)). This enrichment was further strengthened by (1) adding the recently reported TYK2 and TLR7 COVID-19 loci, particularly under a recessive model (OR=19.65[95%CI 2.1-2635.4], P=3.4x10(-3)), and (2) considering as pLOF branchpoint variants with potentially strong impacts on splicing among the 15 loci (OR=4.40[9%CI 2.3-8.4], P=7.7x10(-8)). Finally, the patients with pLOF/bLOF variants at these 15 loci were significantly younger (mean age [SD]=43.3 [20.3] years) than the other patients (56.0 [17.3] years; P=1.68x10(-5)).ConclusionsRare variants of TLR3- and TLR7-dependent type I IFN immunity genes can underlie life-threatening COVID-19, particularly with recessive inheritance, in patients under 60 years old