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  • 1.
    Bachelet, Delphine
    et al.
    CESP, INSERM UMR 1018, Faculty of Medicine, Paris-Sud University, UVSQ, Paris-Saclay University, Villejuif, France.
    Albert, Thilo
    Institute of Experimental Haematology and Transfusion Medicine, University Clinic Bonn, Germany.
    Mbogning, Cyprien
    CESP, INSERM UMR 1018, Faculty of Medicine, Paris-Sud University, UVSQ, Paris-Saclay University, Villejuif, France.
    Hässler, Signe
    CESP, INSERM UMR 1018, Faculty of Medicine, Paris-Sud University, UVSQ, Paris-Saclay University, Villejuif, France.
    Zhang, Yuan
    CESP, INSERM UMR 1018, Faculty of Medicine, Paris-Sud University, UVSQ, Paris-Saclay University, Villejuif, France.
    Schultze-Strasser, Stephan
    University Hospital Frankfurt, Goethe University, Department of Pediatrics, Molecular Haemostasis and Immunodeficiency, Frankfurt am Main, Germany.
    Repessé, Yohann
    CHU Caen, Hématologie Biologique, Caen, Caen, France.
    Rayes, Julie
    Sorbonne Universités, UPMC Univ Paris 06, INSERM, Université Paris Descartes, Sorbonne Paris Cité, UMR_S 1138, Centre de Recherche des Cordeliers, Paris, France.
    Pavlova, Anna
    Institute of Experimental Haematology and Transfusion Medicine, University Clinic Bonn, Bonn, Germany.
    Pezeshkpoor, Behnaz
    Institute of Experimental Haematology and Transfusion Medicine, University Clinic Bonn, Bonn, Germany.
    Liphardt, Kerstin
    Institute of Experimental Haematology and Transfusion Medicine, University Clinic Bonn, Bonn, Germany.
    Davidson, Julie E.
    GlaxoSmithKline, Uxbridge, Middlesex, United Kingdom.
    Hincelin-Méry, Agnès
    Sanofi, Chilly-Mazarin, France.
    Dönnes, Pierre
    SciCross AB, Skövde, Sweden.
    Lacroix-Desmazes, Sébastien
    Sorbonne Universités, UPMC Univ Paris 06, INSERM, Université Paris Descartes, Sorbonne Paris Cité, UMR_S 1138, Centre de Recherche des Cordeliers, Paris, France.
    Königs, Christoph
    University Hospital Frankfurt, Goethe University, Department of Pediatrics, Molecular Haemostasis and Immunodeficiency, Frankfurt am Main, Germany.
    Oldenburg, Johannes
    Institute of Experimental Haematology and Transfusion Medicine, University Clinic Bonn, Bonn, Germany.
    Broët, Philippe
    CESP, INSERM UMR 1018, Faculty of Medicine, Paris-Sud University, UVSQ, Paris-Saclay University, Villejuif, France / AP-HP, Paris-Sud University Hospitals, Villejuif, France.
    Risk stratification integrating genetic data for factor VIII inhibitor development in patients with severe hemophilia A2019In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 14, no 6, article id e0218258Article in journal (Refereed)
    Abstract [en]

    Replacement therapy in severe hemophilia A leads to factor VIII (FVIII) inhibitors in 30% of patients. Factor VIII gene (F8) mutation type, a family history of inhibitors, ethnicity and intensity of treatment are established risk factors, and were included in two published prediction tools based on regression models. Recently investigated immune regulatory genes could also play a part in immunogenicity. Our objective is to identify bio-clinical and genetic markers for FVIII inhibitor development, taking into account potential genetic high order interactions. The study population consisted of 593 and 79 patients with hemophilia A from centers in Bonn and Frankfurt respectively. Data was collected in the European ABIRISK tranSMART database. A subset of 125 severely affected patients from Bonn with reliable information on first treatment was selected as eligible for risk stratification using a hybrid tree-based regression model (GPLTR). In the eligible subset, 58 (46%) patients developed FVIII inhibitors. Among them, 49 (84%) were "high risk" F8 mutation type. 19 (33%) had a family history of inhibitors. The GPLTR model, taking into account F8 mutation risk, family history of inhibitors and product type, distinguishes two groups of patients: a high-risk group for immunogenicity, including patients with positive HLA-DRB1*15 and genotype G/A and A/A for IL-10 rs1800896, and a low-risk group of patients with negative HLA-DRB1*15 / HLA-DQB1*02 and T/T or G/T for CD86 rs2681401. We show associations between genetic factors and the occurrence of FVIII inhibitor development in severe hemophilia A patients taking into account for high-order interactions using a generalized partially linear tree-based approach.

  • 2.
    Carlström, Karl E.
    et al.
    Department of Clinical Neurosciences, Section of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Ewing, Ewoud
    Department of Clinical Neurosciences, Section of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Granqvist, Mathias
    Department of Clinical Neurosciences, Section of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Gyllenberg, Alexandra
    Department of Clinical Neurosciences, Section of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Aeinehband, Shahin
    Department of Clinical Neurosciences, Section of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Enoksson, Sara Lind
    Department of Clinical Immunology Karolinska University Hospital, Stockholm, Sweden.
    Checa, Antonio
    Division of Physiological Chemistry II, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
    Badam, Tejaswi
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Department of Physics, Chemistry & Biology (IFM), Bioinformatics, Linköping University, Sweden.
    Huang, Jesse
    Department of Clinical Neurosciences, Section of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Gomez-Cabrero, David
    Translational Bioinformatics Unit, Navarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Publica de Nevarra (UPNA), IdiSNA, Pamplona, Spain.
    Gustafsson, Mika
    Department of Physics, Chemistry and Biology, Linköping University, Sweden.
    Al Nimer, Faiez
    Department of Clinical Neurosciences, Section of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Wheelock, Craig E.
    Division of Physiological Chemistry II, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
    Kockum, Ingrid
    Department of Clinical Neurosciences, Section of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Olsson, Tomas
    Department of Clinical Neurosciences, Section of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Jagodic, Maja
    Department of Clinical Neurosciences, Section of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Piehl, Fredrik
    Department of Clinical Neurosciences, Section of Neurology, Karolinska Institutet, Stockholm, Sweden.
    Therapeutic efficacy of dimethyl fumarate in relapsing-remitting multiple sclerosis associates with ROS pathway in monocytes2019In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 10, no 1, p. 1-13, article id 3081Article in journal (Refereed)
    Abstract [en]

    Dimethyl fumarate (DMF) is a first-line-treatment for relapsing-remitting multiple sclerosis (RRMS). The redox master regulator Nrf2, essential for redox balance, is a target of DMF, but its precise therapeutic mechanisms of action remain elusive. Here we show impact of DMF on circulating monocytes and T cells in a prospective longitudinal RRMS patient cohort. DMF increases the level of oxidized isoprostanes in peripheral blood. Other observed changes, including methylome and transcriptome profiles, occur in monocytes prior to T cells. Importantly, monocyte counts and monocytic ROS increase following DMF and distinguish patients with beneficial treatment-response from non-responders. A single nucleotide polymorphism in the ROS-generating NOX3 gene is associated with beneficial DMF treatment-response. Our data implicate monocyte-derived oxidative processes in autoimmune diseases and their treatment, and identify NOX3 genetic variant, monocyte counts and redox state as parameters potentially useful to inform clinical decisions on DMF therapy of RRMS.

  • 3.
    Tapp, Eve
    University of Skövde, School of Health and Education.
    Kommunikation med sjuksköterskor vid vård av maligna hematologiska sjukdomar: En enkätstudie om patienters upplevelser2019Independent thesis Basic level (degree of Bachelor), 10 credits / 15 HE creditsStudent thesis
    Abstract [en]

    Background: Malignant hematologic diseases can occur both among children and the elderly. Successful communication is a central part of satisfying and safe person-centered care, hence nurses need to be informed about how patients experience communication with nurses. Aim and objectives: To examine patients’ experience of communication with nurses during their hospital stay while being treated for malignant hematologic diseases. Method: Quantitative design with qualitative elements - a prospective cross-sectional study where data comprised a patient questionnaire survey of their treatment in a hematology ward at a hospital in Western Sweden. Results: Patients were overall satisfied with the communication with nurses; however, signs of insufficient nursing staff and stress were eminent. Patients desired more time for conversations with nurses. Occasionally other patients were present in shared patient rooms while private matters were discussed with nurses and doctors. Discussion: Integrity emerges as an important aspect, as conversations with nurses in shared patient rooms can leave patients exposed. Conclusion: Larger comparable reoccurring studies are needed to outline patients’ experiences of communication with nurses in different wards, to get a clear perception of what can be improved and how. This research would provide consistency and improvements related to communication between patients and nurses.

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