Academic literature on the topic 'Johan Lundborg'

On October 1, 1936 the Stockholm economists hosted a very distinguished guest, John Maynard Keynes. Homeward bound from a visit to the Soviet Union, Keynes appeared at the Political Economy Club. The minutes, as recorded by Ingvar Svennilson, relate:1.At the invitation of the club, Mr. J.M. Keynes lectured at the Institute of Social Science on the subject “My grounds for departure from orthodox economic traditions.” The lecture was arranged with support from J.H. Palme's fund for economic education and economic research. Some 100 persons attended the lecture.2.Following the lecture, the club arranged a dinner at the student union building. In addition to Mr. and Mrs. Keynes, the dinner was attended by: the chairman Professor Ohlin, Miss Kock, Messrs. Björ, Böök, Cederwall, Dahlgren, Hammarskjöld, Helger, Johansson, Lagercrantz (guest), Lundberg, Myrdal, Rothlieb, Rooth, Suoviranta (Finland, guest) and Wigforss, as well as the undersigned. After dinner there was a discussion that continued until midnight.

Background:Idiopathic inflammatory myopathies (IIM) are rare chronic inflammatory diseases associated with high mortality and morbidity [1]. One sub-group of IIM, anti-synthetase syndrome (ASS), is characterized by the presence of autoantibodies that target aminoacyl transfer(t) RNA synthetases (aaRS), together with specific clinical manifestations such as myositis, interstitial lung disease (ILD), arthritis, mechanic’s hand, Raynaud’s syndrome and fever [2]. The most common anti-aaRS autoantibody, anti-Jo1 targeting histidyl tRNA synthetase (HisRS), is present in up to 20-30% of patients with IIM, and up to 90% of patients with myositis and ILD [3, 4]. Besides Jo1, there are today seven other identified autoantigens within the aaRS family.Objectives:A large part of patients with IIM, including individuals with clinical manifestations indicating ASS, test seronegative to all known myositis specific autoantibodies. However, these patients could potentially harbor autoantibodies against targets not tested for in clinic. In this study, we aimed at extending the detection of autoantibodies by including all cytoplasmic aaRS in the analysis of patients with IIM. We hypothesized the existence of new potential autoantigens within this protein family.Methods:The presence of anti-aaRS autoantibodies was determined using a multiplex suspension bead array assay on 242 IIM patients from the Karolinska University Hospital myositis cohort. A panel of 186 recombinant constructs, representing 57 proteins that included full-length or partial sequence overlaps between constructs of all cytoplasmic aaRS as well as other myositis related proteins, were coupled to magnetic color-coded beads and each plasma sample was tested against the complete antigen panel.Results:By the use of this multiplex method we identified patients with autoantibodies against many of the tested aaRS. Autoantibodies binding to HisRS have previously been shown to bind with higher reactivity to the WHEP domain of HisRS and this was also confirmed in this study. We confirmed reactivity against three of the other aaRS tested for in the clinic (PL-12, PL-7, and EJ). In addition, we identified patients positive for anti-Zo, -KS and -HA, autoantibodies usually not screened for in routine. Finally, our data indicates that there are autoantibodies binding to other aaRS than the previously known eight autoantigens, which will be presented.Conclusion:In this study, we could detect autoantibodies in plasma from patients with IIM, both against the most common aaRS autoantigens, but also against other aaRS that are usually not tested for in clinic. We conclude that it is important to continue the studies of anti-aaRS autoantibodies, and their correlation to clinical manifestations, and in the long run also include more aaRS autoantigens in clinical practice.References:[1]Dobloug, G.C., et al., Mortality in idiopathic inflammatory myopathy: results from a Swedish nationwide population-based cohort study. Ann Rheum Dis, 2018. 77(1): p. 40-47.[2]Barsotti, S. and I.E. Lundberg, Myositis an evolving spectrum of disease. Immunol Med, 2018. 41(2): p. 46-54.[3]Vencovsky, J., H. Alexanderson, and I.E. Lundberg, Idiopathic Inflammatory Myopathies. Rheum Dis Clin North Am, 2019. 45(4): p. 569-581.[4]Richards, T.J., et al., Characterization and peripheral blood biomarker assessment of anti-Jo-1 antibody-positive interstitial lung disease. Arthritis Rheum, 2009. 60(7): p. 2183-92.Disclosure of Interests:Charlotta Preger: None declared, Antonella Notarnicola: None declared, Cecilia Hellström: None declared, Edvard Wigren: None declared, Catia Cerqueira: None declared, Peter Nilsson: None declared, Ingrid E. Lundberg Grant/research support from: Bristol Meyer Squibb, Corbus Pharmaceuticals, Inc and Astra Zeneca, Helena Persson: None declared, Susanne Gräslund: None declared, Per-Johan Jakobsson Shareholder of: Gesynta Pharma, Grant/research support from: Gesynta Pharma, AstraZeneca,

Background:Seropositive rheumatoid arthritis (RA) is characterized by the presence of rheumatoid factor (RF) and anti-citrullinated protein autoantibodies (ACPA) with different fine-specificities. Yet, other serum anti-modified protein autoantibodies (AMPA), e.g. anti-carbamylated (Carb), anti-acetylated (KAc), and anti-malondialdehyde acetaldehyde (MAA) modified protein antibodies, have been described. By using RA patient single-cell derived monoclonal antibodies we have previously shown that individual ACPA clones recognize small distinct citrulline-containing epitopes giving them extensive multireactivity when these epitopes are found in many peptides and proteins. Moreover, certain CCP2+ multireactive ACPA clones bind also to cabamylated and acetylated autoantigens [1].Objectives:To provide a comprehensive evaluation of serum IgG and IgA autoreactivity to different post-translational modifications in RA.Methods:We analyzed 30 different IgG and IgA AMPA reactivities to modified antigens by ELISA and autoantigen arrays, in N=1985 newly diagnosed RA patients and population controls. The study utilized both previously established (i.e IgG and IgA CCP2; IgG ACPA fine-specificities; IgG anti-Carb fibrinogen and Carb FCS; IgG and IgA Cit/Carb/KAc/Orn(Ac)-vimentin), and novel assays (e.g. IgG anti-MAA and IgG anti-acetylated histones). Association with patient characteristics such as smoking and disease activity were explored. The newly developed assays were also evaluated in SLE disease controls and CCP2+ RA-risk individuals without arthritis.Results:Carb and KAc reactivities by different assays were primarily seen in patients also positive for citrulline-reactivity. Modified vimentin (mod-Vim) peptides were used for direct comparison of different AMPA reactivities, revealing that IgA AMPA recognizing mod-Vim was mainly detected in subsets of patients with high IgG anti-Cit-Vim levels and a history of smoking. IgG acetylation reactivity was mainly detected in a subset of patients with Cit and Carb reactivity. Anti-acetylated histone 2B reactivity was RA-specific and associated with high anti-CCP2 IgG levels, multiple ACPA fine-specificities, and smoking. This reactivity was also found to be present in CCP2+ RA-risk individuals without arthritis. Our data further demonstrate that IgG autoreactivity to MAA was increased in RA compared to controls with highest levels in CCP2+ RA, but was not RA-specific, and showed low correlation with other AMPA. Anti-MAA was instead associated with disease activity and was not significantly increased in CCP2+ individuals at risk of RA. Notably, RA patients could be subdivided into four different subsets based on their AMPA IgG and IgA reactivity profiles.Conclusion:We conclude that autoantibodies exhibiting different patterns of ACPA fine-specificities as well as Carb and KAc reactivity are present in RA and may be derived from multireactive B-cell clones. Anti-Carb and anti-KAc could be considered reactivities within the “Cit-umbrella” similar to ACPA fine-specificities, while MAA is distinctly different.References:[1]Sahlström P, Hansson M, Steen J, Amara K, Titcombe PJ, Forsström B, Stålesen R, Israelsson L, Piccoli L, Lundberg K, Klareskog L, Mueller DL, Catrina AI, Skriner K, Malmström V, Grönwall C. Different Hierarchies of Anti-Modified Protein Autoantibody Reactivities in Rheumatoid Arthritis. Arthritis Rheumatol. 2020 Oct;72(10):1643-1657. PMID: 32501655Caroline Grönwall: None declared, Lisa Liljefors: None declared, Holger Bang Employee of: Employee at ORGENTEC Diagnostika GmbH, Aase Hensvold: None declared, Monika Hansson: None declared, Linda Mathsson-Alm Employee of: Employee at Thermo Fisher Scientific, Lena Israelsson: None declared, Anna Svärd: None declared, Cyril CLAVEL: None declared, Elisabet Svenungsson: None declared, Iva Gunnarsson: None declared, Guy Serre: None declared, Saedis Saevarsdottir: None declared, Alf Kastbom: None declared, Lars Alfredsson: None declared, Vivianne Malmström: None declared, Johan Rönnelid: None declared, Anca Catrina: None declared, Karin Lundberg: None declared, Lars Klareskog: None declared

In the fall of 1997 George D. Lundberg and John E. Wennberg wrote an editorial in JAMA calling for comprehensive quality improvement programs to become the driver of the American health care system. The suggestion came during the Second European Forum on Quality Improvement in Health Care held in Paris, France, in April 1997 and was based on comments made by Donald Berwick. The concept was to focus on an organized response to problem identification and proposed solutions to improve patient care and protect the health of the public. Critical care medicine represents a large segment of health care and is undergoing dramatic changes during our managed care revolution. General ICU severity of illness models have been developed, tested, and shown to provide a useful estimate of hospital mortality for populations of critically ill patients. These systems have captured the imagination of clinical researchers and have become an integral component of a large number of publications as well as a part of many ICU databases. These risk adjustment severity models are remarkably robust for heterogeneous patient populations but the models have not been shown to validate well in new settings. We feel that by focusing on the episode of critical illness rather than each individual ICU admission and by going beyond the traditional acute hospital discharge to determine whether the patient lives or dies, we can better evaluate critical care system performance and cost-effectiveness. The incentives for high quality/low cost should favor integrated comprehensive critical care delivery systems. Programs that score well should be identified as high quality and be honored as medallion level 1 ICUs. We challenge national and international critical care societies to evaluate and then debate the described definitions and recommendations as a call to action.

Background:Autoantibodies that target aminoacyl transfer(t) RNA synthetases (aaRS) represent the serological marker of the anti-synthetase syndrome (ASS), a major subgroup of the idiopathic inflammatory myopathies (IIM) (1). Among the anti-aaRS, anti-histidyl tRNA synthetase (HisRS) autoantibodies (anti-Jo1) are the most common. Up to 90% of IIM/ASS patients diagnosed with interstitial lung disease (ILD) harbor anti-Jo1 autoantibodies (2).Objectives:Reactivity and affinity of anti-Jo1 autoantibodies from serum and broncheoalveolar lavage fluid (BALF) were investigated against HisRS autoantigen. Associations with clinical data from patients IIM/ASS were addressed.Methods:Total IgGs were purified by affinity chromatography. Samples and clinical data were obtained from: i) 26 anti-Jo1+patients (19 at diagnosis, 16/19 at follow-up, 7 BALF/matching serum at baseline; ii) 29 anti-Jo1-(25 serum at diagnosis, 4 BALF/matching serum at baseline); iii) 24 age/gender matched healthy controls. Anti-Jo1 IgG and IgA response against HisRS was evaluated by ELISA and western blot. Affinity was measured by surface plasmon resonance. HisRS full-length (HisRS-FL), two HisRS domains (ABD and CD), and two HisRS splice variants (WHEP and WHEP + ABD splice variant (SV)) were tested. Correlations between autoantibody reactivity and clinical data, at baseline and over disease course, were evaluated.Results:Anti-Jo1 autoantibodies from serum and lung bound HisRS-FL, WHEP and SV with high reactivity and affinity already at diagnosis and recognized both conformational and linear HisRS epitopes (Fig. 1). Levels of autoantibodies (against HisRS-FL, -domains and -splice variants) varied among patients and overtime. Patients with ILD, arthritis and less skin involvement presented higher anti-Jo1 titers compared to those with lower anti-Jo1 titers and to the anti-Jo1 negative group (Fig. 2). Anti-WHEP reactivity in BALF strongly correlated with poor pulmonary function.Conclusion:High reactivity and affinity at time of diagnosis indicates that autoimmunity against HisRS is most likely initiated before IIM/ASS diagnosis. Reactivity to specific splice variants of HisRS may be employed as diagnostic and prognostic markers.References:[1]Marguerie C, Bunn CC, Beynon HL, Bernstein RM, Hughes JM, So AK, Walport MJ: Polymyositis, pulmonary fibrosis and autoantibodies to aminoacyl-tRNA synthetase enzymes. Q J Med 1990, 77(282):1019-1038[2]Richards TJ, Eggebeen A, Gibson K, Yousem S, Fuhrman C, Gochuico BR, Fertig N, Oddis CV, Kaminski N, Rosas IO et al: Characterization and peripheral blood biomarker assessment of anti-Jo-1 antibody-positive interstitial lung disease. Arthritis Rheum 2009, 60(7):2183-2192.Fig. 1.Anti-Jo1 reactivity in total IgG purified from the first available serum sampleFig. 2.Reactivity of total anti-Jo1+ IgG purified from the first available serum close to IIM/ASS diagnosis in relation to clinical dataDisclosure of Interests:Antonella Notarnicola: None declared, Charlotta Preger: None declared, Susanna Lundström: None declared, Nuria Renard: None declared, Edvard Wigren: None declared, Eveline Van Gompel: None declared, Angeles Shunashy Galindo-Feria: None declared, Helena Persson: None declared, Maryam Fathi: None declared, Johan Grunewald: None declared, Per-Johan Jakobsson Shareholder of: Gesynta Pharma, Grant/research support from: Gesynta Pharma, AstraZeneca,, Susanne Gräslund: None declared, Ingrid E. Lundberg Grant/research support from: Bristol Meyer Squibb, Corbus Pharmaceuticals, Inc and Astra Zeneca, Catia Cerqueira: None declared

Background:LDL-levels are increased by Proprotein convertase subtilisin kexin 9 (PCSK9) which targets the LDL-receptor (LDLR). We reported that PCSK9 has immune modulatory properties in addition to LDL-lowering and ameliorates dendritic cell (DC) activation by oxidized LDL (OxLDL)1, which is abundant in atherosclerotic plaques. OxLDL is also raised and associated with cardiovascular disease (CVD) in SLE.1-3Objectives:We here investigate the role of PCSK9 in SLE both in a clinical context and in experimental ex vivo studies. The objective is to investigate if PCSK9 and its inhibition could be of relevance in SLE in addition to LDL-level related propertiesMethods:PCSK9-levels were determined by ELISA among SLE patients (n=109) and age- and sex-matched population-based controls (n=91). Common carotid intima-media thickness (IMT) and plaque occurrence were determined by B-mode ultrasound. Plaques were graded by echogenicity. Human peripheral blood monocytes from SLE patients or controls were differentiated into DCs. Effects of PCSK9 and its inhibition by silencing were studied.Results:PCSK9-levels were non-significantly higher among SLE-patients as compared to controls but associated significantly with SLE disease activity, as determined by SLAM (0.020) or SLEDAI (0.0178). There was no association between PCSK9-levels and atherosclerosis as determined by IMT, prevalence of plaques or echolucent (potentially vulnerable) plaques. PCSK9 levels were significantly associated with CVD among SLE-patients but not after adjustment for age.OxLDL induced PCSK9 in DCs and DC-maturation with increased expression of CD86 and HLA-DR. The effects were significantly stronger in DC from SLE patients than from controls. Silencing of PCSK9 abolished OxLDL-induced DC-maturation.Conclusion:PCSK9 is associated with disease activity in SLE. One underlying cause could be OxLDL, promoting DC-activation which depends on PCSK9. OxLDL induces PCSK9, an effect which is higher among SLE-patients.PCSK9 could play an unexpected immunological role in SLE and inhibition of PCSK9 could potentially play a role in disease amelioration, pending on clinical studies.References:[1]Liu A and Frostegard J. PCSK9 plays a novel immunological role in oxidized LDL-induced dendritic cell maturation and activation of T cells from human blood and atherosclerotic plaque.J Intern Med. 2018.[2]Frostegard J, Svenungsson E, Wu R, Gunnarsson I, Lundberg IE, Klareskog L, Horkko S and Witztum JL. Lipid peroxidation is enhanced in patients with systemic lupus erythematosus and is associated with arterial and renal disease manifestations.Arthritis Rheum. 2005;52:192-200.[3]Frostegard J. Immunity, atherosclerosis and cardiovascular disease.BMC Med. 2013;11:117.Disclosure of Interests:Anquan Liu: None declared, Mizanur Rahman: None declared, Ingiäld Hafström: None declared, Sofia Ajeganova: None declared, Johan Frostegård Grant/research support from: Unconditional competitive grant from Amgen, related only to PCSK9, not the topic of this abstract

Denna uppsats behandlar ämnet Ingemar Hedenius och hans syn på kristendomen och religion. Dessa två frågeställningar är vad uppsatsen är byggd på. Vilken filosofisk kritik har riktats mot Hedenius behandling av gudsbegreppet? Hur ska denna kritik mot Hedenius värderas? Vilken roll spelar retorik i Hedenius argumentering? Jag har besvarat dessa frågor med hjälp ifrån relevant litteratur, videoklipp samt sökt information på nätet. Hedenius valde på ett provokativt vis skriva en bok om tro och vetande, dels för att filosofi intresserade honom men också som revolt mot sina föräldrars kristna tro. Han möttes av mycket kritik för sin bok men stod upp för sina åsikter och argumenterade gärna för dessa. Slutsatsen jag har kommit fram till genom detta arbete är att Hedenius bakgrund spelar en ganska stor roll till varför han valde att börja med religionskritik samt att hans sätt att framföra kritiken var speciell och kontroversiell för hans tid.

Detta är en presentation av den namibiske konstnären John Ndevasia Muafangejos (1943 - 1987) konstnärliga gärning. Syftet med undersökningen har varit att utöver en tolkning av hans bilder försöka förstå vad han har betytt för landet Namibia under deras befrielsekamp och efteråt, men även hur han kunde utvecklas till konstnär under apartheidregimens Sydafrika.För min undersökning har jag använt tidigare gjorda analyser av hans verk men också en del intervjuer med bland annat hans lärare Peder Gowenius och Otto Lundbohm. Muafangejo utbildades på den av svenskar drivna konstskolan Rorkes Drift i Sydafrika, en skola som haft stort inflytande på skapandet av en rad svarta konstnärer.Min teoretiska ingång har varit hermeneutisk med en postkolonial vinkling. Jag har grundat mig på Hans-Georg Gadamers idéer om att förstå ett konstverk utifrån våra erfarenheter. En ingång som har utmanat då jag hade väldigt lite erfarenhet av och kunskap om Namibia när jag startade min undersökning. Den postkoloniala ingången har varit Frantz Fanon där främst hans resonemang kring hur den förtryckta befolkningen tar över förtryckarens syn på dem och deras kultur och genom det skapar ett självförakt. Frantz Fanons tankar har på ett mer konkret sätt hjälpt mig i analysen av Muafangejos bilder och liv.Muafangejo arbetade främst i grafiska tekniker där linoleumsnittet blev det han använde mest. Bilderna är oftast berättande med mängder av detaljer och mönster som flödar över bildrummet. Han använder gärna text för att ytterligare förstärka det han vill uttrycka. Bilderna speglar hans liv men också samtida händelse eller historiska och bibliska berättelser. Det finns även bilder som berättar om traditioner, djur och föremål från hans hembygd Ovamboland i norra Namibia. I min analys har jag sökt svara på vad det är han berättar i sina bilder och hur medvetet han gjorde det. Jag har även försökt sätta mig in i vad bilderna har betytt för Namibia och vilken betydelse de fått när de presenterats i ett internationellt sammanhang. Slutligen har jag försökt förstå hur han kunde utvecklas till en internationellt verkande konstnär.Muafangejo är den första kända svarta konstnären i Namibia och jag visar i min undersökning att hans bilder har haft betydelse för utvecklingen av konsten i Namibia. Något som även påtalas i litteraturen. Vilken betydelse hans bilder har haft på andra plan har varit svårare att se. Han gavs en möjlighet en möjlighet att verka internationellt tack vare ett svenskt utvecklingsprojekt, konstskolan Rorkes Drift i Sydafrika. Han har genom sina bilder synliggjort den förtryckta svarta befolkningens levnadsvillkor i apartheidregimens Sydafrika.

Sweden has 10 million inhabitants of which more than 30% are members of at least one sports club. Typically, sports clubs are organized under the Swedish Sports Confederation (Riksidrottsförbundet). On a national level, approximately 19,000 sports clubs exist, distributed over 72 specialist sports federations. Each club usually stages one or several sport events every year. For example, specialist sports federations organize all championships at national and international levels. From a sports club perspective, these events constitute important sources of income. From a societal perspective, clubs and events create considerable economic impacts, foster public health, and facilitate integration contributing with substantial social values (Brown et al., 2015; Pettersson & Wallstam, 2017; Wallstam, Ioannides, & Pettersson, 2020). During the Covid-19 pandemic, most governments restricted individuals’ possibilities for gatherings and movements. On March 12th the Swedish government responded to the pandemic by limiting the number of participants to events to no more than 500 people. Starting March 29th gatherings were limited to 50 people. During the end of year 2020 and the second virus wave, further actions were taken. The government limited the number of visitors and participants to eight people. These restrictions had considerable negative effects on many sport-related activities, events, and thus clubs.