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Search: WFRF:(Björkander I.)

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  • Björkander, I., et al. (author)
  • Differential index, a novel graphical method for measurements of heart rate variability
  • 2005
  • In: International Journal of Cardiology. - : Elsevier BV. - 0167-5273 .- 1874-1754. ; 98:3, s. 493-499
  • Journal article (peer-reviewed)abstract
    • Background: Commonly used methods to evaluate heart rate variability require extensive filtering of the registrations in order to exclude artefacts and ectopic beats. We developed and validated a novel graphical method for time-domain measurements of heart rate variability, the differential index, which does not require filtering and is simple to use. Methods: The 24-h ambulatory long-term electrocardiogram recordings from 120 patients with angina pectoris and 49 control subjects were computerised without any filtering process. Sample density histograms of differences in the RR interval for successive beats were constructed and the widths of the histograms were used to obtain the differential index. For comparison, the same registrations were analysed by conventional methods. Results: The differential index was most closely related (P < 0.001) to conventional short-term time domain (e.g. percent of differences between adjacent normal RR intervals > 50 ms, pNN50, r = 0.81) and frequency-domain (e.g. high frequency power, r = 0.84) components, but also to long-term time domain (e.g. standard deviation of all normal-to-normal RR intervals for all 5-min segments of the entire registration, SDNNIDX, r = 0.72) and frequency-domain (e.g. low frequency power, r = 0.64) components. Conclusion: The differential index method shows good agreement with established indices of heart rate variability. The insensitivity to recording artefacts and short-lasting disturbances of sinus rhythm make the differential index method particularly suited when data quality is imperfect. The simplicity of the method is valuable when large numbers of registrations are to be evaluated.
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  • Björkander, Sofia, et al. (author)
  • Peripheral Monocyte Expression of the Chemokine Receptors CCR2, CCR5 and CXCR3 is Altered at Parturition in Healthy Women and in Women with Systemic Lupus Erythematosus
  • 2013
  • In: Scandinavian Journal of Immunology. - : Wiley. - 0300-9475 .- 1365-3083. ; 77:3, s. 200-212
  • Journal article (peer-reviewed)abstract
    • Monocytes are precursors of macrophages and recruited to the uterus throughout pregnancy to perform important immunological functions. In this study, we hypothesized that pregnant women have reduced peripheral monocyte expression of chemokine receptors and alterations in PBMC responses to microbial stimuli as an adaption to pregnancy and that these changes are less pronounced in women with autoimmunity. We therefore investigated the chemokine receptor expression, migratory behaviour and responses to microbial stimulation of peripheral monocytes from pregnant women at parturition (n=13) and from non-pregnant women (n=9). In addition, we compared healthy pregnant women with women suffering from SLE (n=5), a condition with pronounced systemic inflammation increasing the risk for pregnancy complications. We demonstrate that peripheral monocytes are affected by pregnancy with reduced percentages of CCR2+, CCR5+ and CXCR3+ monocytes of both classical (CD16) and inflammatory (CD16+) subsets and that the trophoblast-secreted chemokine CCL2/MCP-1 recruited monocytes of both subsets in vitro. Further, PBMCs from pregnant women had a divergent response to microbial stimulation with lower CCL5/RANTES and higher CCL2/MCP-1 secretion compared with non-pregnant women. In addition, pregnant women had lower basal PBMC-secretion of CCL5/RANTES and higher basal secretion of IL-10 and CCL2/MCP-1. Interestingly, the women with SLE responded similar to pregnancy as did healthy women with lower percentages of CCR2+, CCR5+ and CXCR3+ monocytes. However, they had increased expression of CCR5 on CD16+ monocytes and heightened PBMC-secretion of CCL5/RANTES. In conclusion, our data indicate that monocyte chemokine receptor expression and the chemokine milieu during pregnancy are tightly regulated to support pregnancy.
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  • Forslund, L, et al. (author)
  • Prognostic implications of autonomic function assessed by analyses of catecholamines and heart rate variability in stable angina pectoris.
  • 2002
  • In: Heart. - : BMJ. - 1355-6037 .- 1468-201X .- 0007-0769. ; 87:5, s. 415-22
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: To assess the prognostic impact of autonomic activity, as reflected by catecholamines and heart rate variability (HRV), in patients with stable angina pectoris. DESIGN: Double blind, randomised treatment with metoprolol or verapamil. 24 hour ambulatory ECG, used for frequency domain analyses of HRV, and symptom limited exercise tests at baseline and after one month of treatment. Catecholamine concentrations were measured in plasma (rest and exercise) and urine. SETTING: Single centre at a university hospital. PATIENTS: 641 patients (449 men) with stable angina pectoris. MAIN OUTCOME MEASURES: Cardiovascular (CV) death, non-fatal myocardial infarction (MI). RESULTS: During follow up (median 40 months) there were 27 CV deaths and 26 MIs. Patients who died of CV causes had lower total power and high (HF), low (LF), and very low (VLF) frequency components of HRV. HRV was not altered in patients who suffered non-fatal MI. Catecholamines did not differ between patients with and those without events. Metoprolol increased HRV. Verapamil decreased noradrenaline (norepinephrine) excretion. Multivariate Cox analyses showed that total power, HF, LF, and VLF independently predicted CV death (also non-sudden death) but not MI. LF:HF ratios and catecholamines were not related to prognosis. Treatment effects on HRV did not influence prognosis. CONCLUSIONS: Low HRV predicted CV death but not non-fatal MI. Neither the LF:HF ratio nor catecholamines carried any prognostic information. Metoprolol and verapamil influenced LF, HF, and catecholamines differently but treatment effects were not related to prognosis.
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  • Mattson, Lina, et al. (author)
  • Potential Involvement of Type I Interferon Signaling in Immunotherapy in Seasonal Allergic Rhinitis
  • 2016
  • In: Journal of Immunology Research. - : HINDAWI PUBLISHING CORP. - 2314-8861 .- 2314-7156.
  • Journal article (peer-reviewed)abstract
    • Specific immunotherapy (SIT) reverses the symptoms of seasonal allergic rhinitis (SAR) in most patients. Recent studies report type I interferons shifting the balance between type I T helper cell (Th1) and type II T helper cells (Th2) towards Th2 dominance by inhibiting the differentiation of naive Tcells into Th1 cells. As SIT is thought to cause a shift towardsTh1 dominance, we hypothesized that SIT would alter interferon type I signaling. To test this, allergen and diluent challenged CD4(+) T cells from healthy controls and patients from different time points were analyzed. The initial experiments focused on signature genes of the pathway and found complex changes following immunotherapy, which were consistent with our hypothesis. As interferon signaling involves multiple genes, expression profiling studies were performed, showing altered expression of the pathway. These findings require validation in a larger group of patients in further studies.
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6.
  • Petursdottir, Dagbjort H., et al. (author)
  • Early-Life Human Microbiota Associated With Childhood Allergy Promotes the T Helper 17 Axis in Mice
  • 2017
  • In: Frontiers in Immunology. - : Frontiers Media SA. - 1664-3224. ; 8
  • Journal article (peer-reviewed)abstract
    • The intestinal microbiota influences immune maturation during childhood, and is implicated in early-life allergy development. However, to directly study intestinal microbes and gut immune responses in infants is difficult. To investigate how different types of early-life gut microbiota affect immune development, we collected fecal samples from children with different allergic heredity (AH) and inoculated germ-free mice. Immune responses and microbiota composition were evaluated in the offspring of these mice. Microbial composition in the small intestine, the cecum and the colon were determined by 16S rRNA sequencing. The intestinal microbiota differed markedly between the groups of mice, but only exposure to microbiota associated with AH and known future allergy in children resulted in a T helper 17 (Th17)-signature, both systemically and in the gut mucosa in the mouse offspring. These Th17 responses could be signs of a particular microbiota and a shift in immune development, ultimately resulting in an increased risk of allergy.
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