Aller au contenu principal
Profil bibliographique

Minna Turkkila

Informations fournies par OpenAlex. Research Africa ne déduit ni nationalité, ni poste, ni coordonnées personnelles.

24Publications signalées
739Citations signalées
1Affiliations récentes

Les institutions déclarées

Les domaines associés

Rheumatoid Arthritis Research and TherapiesMonoclonal and Polyclonal Antibodies ResearchSystemic Lupus Erythematosus ResearchCystic Fibrosis Research AdvancesT-cell and B-cell Immunology

Les publications récentes

Accès ouvert 2018 article OpenAlex

Survivin Measurement improves Clinical Prediction of Transition From Arthralgia to RA—Biomarkers to Improve Clinical Sensitivity of Transition From Arthralgia to RA

Malin C. Erlandsson, Minna Turkkila, Rille Pullerits, Maria I Bokarewa

Background: Arthralgia often predates development of rheumatoid arthritis (RA). A set of clinical joint symptoms assisting recognition of patients during their transition from arthralgia to RA, has been recently proposed. Aim: To combine clinical and serological markers aiming to improve recognition of …

se (code pays fourni par la source)

11 citations Frontiers in Medicine
Accès ouvert 2017 article OpenAlex

Survivin improves the early recognition of rheumatoid arthritis among patients with arthralgia: A population-based study within two university cities of Sweden

Malin C. Erlandsson, Minna Turkkila, Filip Siljehult, Rille Pullerits et autres

OBJECTIVES: The aim of this study was to validate the use of survivin for preclinical recognition of rheumatoid arthritis (RA) among patients with unexplained arthralgia. METHODS: Serum levels of survivin and the arthritis-specific autoantibodies RF and ACPA were measured in total of …

se (code pays fourni par la source)

19 citations Seminars in Arthritis and Rheumatism
Accès ouvert 2017 article OpenAlex

Smoking activates cytotoxic CD8+ T cells and causes survivin release in rheumatoid arthritis

Caroline Wasén, Minna Turkkila, Apostolos Bossios, Malin C. Erlandsson et autres

CD8+ T cells have an emerging role in RA. Resent research indicates a causal relationship between the non-exhausted state of CD8+ T cells, defined by lost function of PD-1, and development of arthritis. We investigated how smoking contributes to the non-exhausted phenotype …

se (code pays fourni par la source)

46 citations Journal of Autoimmunity
Accès ouvert 2016 article OpenAlex

Survivin controls biogenesis of microRNA in smokers: A link to pathogenesis of rheumatoid arthritis

Karin M Andersson, Minna Turkkila, Malin C. Erlandsson, Apostolos Bossios et autres

MicroRNAs (miRs) represent a part of epigenetic control of autoimmunity gaining increasing attention in rheumatoid arthritis (RA). Since cigarette smoking plays important role in RA pathogenesis and reprograms transcriptional profile of miRNAs, we ask if the onco-protein survivin, a novel biomarker of …

se, us (code pays fourni par la source)

25 citations Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Accès ouvert 2016 article OpenAlex

A randomised, double-blind, placebo-controlled trial of repeated nebulisation of non-viral cystic fibrosis transmembrane conductance regulator (CFTR) gene therapy in patients with cystic fibrosis

Eric W.F.W. Alton, David K Armstrong, Deborah Ashby, Katie J Bayfield et autres

Background Cystic fibrosis (CF) is a chronic, life-limiting disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene leading to abnormal airway surface ion transport, chronic lung infections, inflammation and eventual respiratory failure. With the exception of the small-molecule potentiator, …

gb, us, fr (code pays fourni par la source)

45 citations Efficacy and Mechanism Evaluation

BNTIC News n’est pas le producteur de ces données. Les publications sont interrogées à la demande dans Crossref, OpenAIRE, DOAJ, Europe PMC, HAL, DataCite, AfricArXiv, ROR et la Banque mondiale, sans clé d’accès. OpenAlex reste optionnel. Aucun service payant n’est nécessaire et aucune donnée externe n’est enregistrée en base. Consulter les sources et leurs limites.