| 1. |
- Andréasson, Kristofer, et al.
(författare)
-
Faecal calprotectin: a biomarker of gastrointestinal disease in systemic sclerosis.
- 2011
-
Ingår i: Journal of Internal Medicine. - : Wiley. - 1365-2796 .- 0954-6820. ; 270, s. 50-57
-
Tidskriftsartikel (refereegranskat)abstract
- Abstract. Andréasson K, Scheja A, Saxne T, Ohlsson B, Hesselstrand R. (Section for Rheumatology; Section for Gastroenterology and Hepatology, Lund University, Lund, Sweden). Faecal calprotectin: a biomarker of gastrointestinal disease in systemic sclerosis. J Intern Med 2010; doi: 10.1111/j.1365-2796.2010.02340.x. Background. Assessment of gastrointestinal (GI) involvement in systemic sclerosis (SSc) is difficult. Measurement of calprotectin in faeces is a valuable tool for the assessment of inflammatory bowel diseases. Calprotectin is an intracellular protein found in leucocytes and is a potent activator of the innate immune system. Objective. To determine whether faecal calprotectin (F-calprotectin) could serve as a biomarker of GI disease in SSc. Design. In a cross-sectional study, F-calprotectin and plasma calprotectin were measured in patients with SSc using an enzyme-linked immunosorbent assay. F-calprotectin concentrations were evaluated in relation to cineradiography, medical records, laboratory measurements and patients' subjective GI symptoms. Setting. The study was conducted at a tertiary referral centre for SSc. Subjects. The study comprised 81 consecutive patients with SSc. Results. A majority of the patients had pathological levels of F-calprotectin when compared to accepted clinical reference values for healthy adults. F-calprotectin did not correlate with calprotectin levels in plasma. F-calprotectin was associated with the following patient characteristics: pathological cineradiography, history of referral to another clinic because of GI disease, treatment of vitamin or mineral deficiency and use of proton pump inhibitors. We did not find any significant correlation between F-calprotectin and patient-reported GI symptoms. Conclusion. Faecal calprotectin is increased in a majority of patients with SSc. It correlates with objective and clinically important features of GI disease, and faecal concentrations do not vary with plasma concentrations. We suggest that F-calprotectin is a promising objective non-invasive biomarker of GI involvement in SSc.
|
|
| 2. |
- Andréasson, Kristofer, et al.
(författare)
-
Faecal levels of calprotectin in systemic sclerosis are stable over time and are higher compared to primary Sjogren's syndrome and rheumatoid arthritis
- 2014
-
Ingår i: Arthritis Research and Therapy. - : Springer Science and Business Media LLC. - 1478-6362 .- 1478-6354. ; 16:1
-
Tidskriftsartikel (refereegranskat)abstract
- Introduction: Faecal calprotectin (FC) has been proposed to be a biomarker of gastrointestinal (GI) disease in systemic sclerosis (SSc). The purpose of this study was to extend cross-sectional observations and prospectively assess the variability of FC over time in SSc patients. We also aimed to examine FC in relation to immunosuppressive therapy. Finally we wanted to analyse FC in other rheumatic diseases to evaluate the specificity of FC for SSc GI disease. Methods: FC was measured in consecutive patients with SSc, primary Sjogren's syndrome (pSS), rheumatoid arthritis (RA) and in healthy hospital workers. The intraindividual variability of FC in SSc was assessed with intra class correlation (ICC) and. statistics. Associations between FC and objective markers of GI disease and immunosuppressive medication were investigated. Results: FC was associated with micronutrient deficiency and GI pathology as assessed by cineradiography confirming our previous results. FC showed only a limited intra-individual variation in SSc, ICC = 0.69 (95% confidence interval, CI: 0.57-0.78) and kappa = 0.64 (95% CI: 0.56-0.73). Generalised immunosuppression did not have any significant impact on FC. FC was significantly higher in SSc patients compared to patients with pSS or RA as well as compared to healthy subjects. Conclusions: FC is a promising non-invasive biomarker for GI disease in SSc. In view of stable levels over time, FC could be a useful marker when novel, more specific drugs targeting the GI tract in SSc will be introduced.
|
|
| 3. |
- Bartosik, I, et al.
(författare)
-
Correlation between plasma concentrations of calcitonin gene related peptide and pulmonary pressure in patients with systemic sclerosis.
- 2002
-
Ingår i: Annals of the Rheumatic Diseases. - : BMJ. - 1468-2060 .- 0003-4967. ; 61:3, s. 261-263
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To examine plasma levels of calcitonin gene related peptide (p-CGRP) in patients with systemic sclerosis (SSc) and pulmonary hypertension (PH). MATERIAL AND METHODS: Twenty nine patients with SSc, 10 with diffuse form, 18 with limited form and one with overlapping systemic lupus erythematosus were examined. Twelve patients displayed normal systolic pulmonary artery pressure (PAPsyst) < or =30 mm Hg and 17 increased PAPsyst
|
|
| 4. |
- Bartosik, I, et al.
(författare)
-
Vascular events are risk factors for anal incontinence in systemic sclerosis: a study of morphology and functional properties measured by anal endosonography and manometry.
- 2014
-
Ingår i: Scandinavian Journal of Rheumatology. - : Informa UK Limited. - 1502-7732 .- 0300-9742. ; 43:5, s. 391-397
-
Tidskriftsartikel (refereegranskat)abstract
- Objectives: To study anal sphincter morphology, anal sphincter pressure, and rectoanal inhibitory reflex (RAIR) in patients with systemic sclerosis (SSc) complicated by anal incontinence (AI) and to investigate possible risk factors for AI in SSc. Method: Nineteen SSc patients with severe AI were investigated using anal endosonography, anal manometry, and rectal manovolumetry. To determine risk factors for AI, disease characteristics of SSc patients with AI were compared with those of 95 SSc patients without AI; there were five matched SSc patients without AI for each SSc patient with AI. Results: The mean (SD) internal sphincter thickness was 1.3 (0.46) mm in patients with AI, which was thinner (p < 0.001) than reference data from healthy individuals whose internal sphincter measured 2.2 (0.45) mm, whereas the external sphincter thickness did not differ. The mean (SD) resting pressure in AI patients was lower than the reference data from healthy individuals [60 (22) vs. 94 (29) mmHg, p < 0.002] whereas the squeeze pressure did not differ. Centromeric antibodies and features of vascular disease [i.e. the presence of pulmonary arterial hypertension (PAH), digital ulcers, pitting scars, or the need for iloprost infusions] were associated with AI whereas fibrotic manifestations [i.e. modified Rodnan skin score (mRss), the diffuse cutaneous SSc (dcSSc) subset, or low vital capacity (VC)] were not. Conclusions: SSc patients with AI have a thin internal anal sphincter and a low resting pressure. Risk factors for AI among SSc patients are centromeric antibodies and vascular disease, which supports the hypothesis that gastrointestinal involvement in SSc is in part a vascular manifestation of the disease.
|
|
| 5. |
|
|
| 6. |
- Chizzolini, C, et al.
(författare)
-
Polarized subsets of human T-helper cells induce distinct patterns of chemokine production by normal and systemic sclerosis dermal fibroblasts
- 2006
-
Ingår i: Arthritis Research and Therapy. - : Springer Science and Business Media LLC. - 1478-6362 .- 1478-6354. ; 8:1
-
Tidskriftsartikel (refereegranskat)abstract
- The role of fibroblasts in inflammatory processes and their cross-talk with T cells is increasingly being recognized. Our aim was to explore the capacity of dermal fibroblasts to produce inflammatory chemokines potentially involved in fibrosis occurring in response to contact with polarized human T cells. Our findings indicate that the program of chemokine production by fibroblasts is differentially regulated depending on the T-helper (Th) cell subset used to activate them. Thus, Th1 and Th2 cells preferentially induced production of IFN-gamma inducible protein (IP)-10 and IL-8, respectively, whereas monocyte chemoattractant protein (MCP)-1 was equally induced by both subsets at mRNA and protein levels. Neutralization experiments indicated that membrane-associated tumour necrosis factor-alpha and IL-1 played a major role in the induction of IL-8 and MCP-1 by Th1 and Th2 cells, whereas membrane-associated lIFN-gamma (present only in Th1 cells) was responsible, at least in part, for the lower IL-8 and higher IP-10 production induced by Th1 cells. The contributions of tumour necrosis factor-alpha, IL-1 and IFN-alpha were confirmed when fibroblasts were cultured separated in a semipermeable membrane from living T cells activated by CD3 cross-linking. We observed further differences when we explored signal transduction pathway usage in fibroblasts. Pharmacological inhibition of c-Jun N-terminal kinase and nuclear factor-kappa B resulted in inhibition of IL-8 mRNA transcription induced by Th1 cells but not that by Th2 cells, whereas inhibition of MEK/ERK (mitogen-activated protein kinase of extracellular signal-regulated kinase/extracellular signal-regulated kinase) and nuclear factor-kappa B resulted in inhibition of MCP-1 mRNA induced by Th2 but not by Th1 cells. Finally, no distinct differences in chemokine production were observed when the responses to T cell contact or to prototypic Th1 and Th2 cytokines were examined in systemic sclerosis versus normal fibroblasts. These findings indicate that fibroblasts have the potential to participate in shaping the inflammatory response through the activation of flexible programs of chemokine production that depend on the Th subset eliciting their response.
|
|
| 7. |
- Chizzolini, C, et al.
(författare)
-
Systemic sclerosis Th2 cells inhibit collagen production by dermal fibroblasts via membrane-associated tumor necrosis factor alpha
- 2003
-
Ingår i: Arthritis and Rheumatism. - : Wiley. - 1529-0131 .- 0004-3591. ; 48:9, s. 2593-2604
-
Tidskriftsartikel (refereegranskat)abstract
- Objective. In systemic sclerosis (SSc; scleroderma), T cells infiltrate organs undergoing fibrotic changes and may participate in dysregulated production of collagen by fibroblasts. The objective of this study was to functionally characterize T cells infiltrating skin lesions in early SSc and investigate their capacity to affect production of type I collagen and interstitial collagenase (matrix metalloproteinase 1 [MMP-1]) by dermal fibroblasts. Methods. Four-color cytometric analysis was used to characterize subset distribution and production of interferon-gamma (IFNgamma) and interleukin-4 (IL-4) in T cell lines generated from the skin of patients with SSc. T cell clones were generated, and their capacity to modulate collagen and MMP-1 production by fibroblasts derived from patients with SSc and from normal individuals was assessed. Neutralizing reagents were used to identify T cell mediators involved in fibroblast modulation. Results. The skin of individuals with early-stage SSc contained T cells preferentially producing high levels of IL-4. Cloned CD4+ Th2-like cells inhibited collagen production by normal fibroblasts. Th2 cell-dependent inhibition was, at least in part, contact-dependent, was essentially mediated by tumor necrosis factor alpha (TNFalpha), and was dominant over the enhancement induced by profibrotic IL-4 and transforming growth factor beta cytokines. The simultaneous induction of MMP-1 production confirmed the specificity of these observations. To be inhibitory, Th2 cells required activation by CD3 ligation. Th2 cells were less potent than were Th1 cells in inhibiting collagen production by normal fibroblasts via cell-to-cell interaction, and SSc fibroblasts were resistant to inhibition. Conclusion. These findings indicate that, despite their production of IL-4, Th2 cells reduce type I collagen synthesis by dermal fibroblasts because of the dominant effect of TNFalpha, and suggest that strategies based on TNFalpha blockade aimed at controlling fibrosis in SSc may be unwise.
|
|
| 8. |
- Erikson, Martin G, et al.
(författare)
-
Från Högskolan i Borås till Humboldt, volym 4
- 2018
-
Rapport (övrigt vetenskapligt/konstnärligt)abstract
- Denna rapport består av åtta kapitel baserade på en seminarieserie om akademiskt ansvar, som arrangerades av Högskolan i Borås under 2015 och 2016. Seminarierna utgjorde den fjärde omgången av de så kallade Humboldtseminarierna, som högskolan arrangerat i olika omgångar sedan 2010. Vid Humboldtseminarierna har aktuella frågor kring akademins möjligheter och utmaningar belysts utifrån olika teman, inte minst kopplat till samhällets förväntningar på forskning och högre utbildning. I det perspektivet blev akademiskt ansvar ett naturligt tema för den fjärde och avslutande omgången av Humboldtseminarierna. Just kopplingen till samhällsnytta är också en röd tråd igenom rapporten. Författarna skriver utifrån skilda erfarenheter som forskare, lärare och akademiska ledare – inte minst är rektorsperspektivet väl företrätt. Ett annat återkommande ämne är kopplingen mellan akademiskt ansvar och akademisk frihet, där ansvaret inte minst bidrar till att legitimera friheten. Kollegialitet är en viktig fråga för flera av författarna, både som princip för kvalitetsstyrning och som beslutsform. Sammantaget visar de olika bidragen att akademiskt ansvar berör många frågor av stor relevans för forskare, lärare, ledare och studenter, men också för intressenter utanför akademin. Där har författarnas bidrag goda möjligheter att ge nya insikter och inspirera till fortsatta diskussioner inom många olika områden.
|
|
| 9. |
- Halldén, Ola, et al.
(författare)
-
Situating the concept of conceptual change
- 2002
-
Ingår i: Reconsidering conceptual change: Issues in theory and practice. - : Kluwer (Dordrecht, Netherlands). - 9781402004940 ; , s. 137-48
-
Bokkapitel (refereegranskat)
|
|
| 10. |
- Halldén, Ola, et al.
(författare)
-
Situating the question of conceptual change
- 2002
-
Ingår i: Reconsidering conceptual change. - Dordrecht : Kluwer. - 9781402004940 ; , s. 137-148
-
Bokkapitel (refereegranskat)abstract
- The contemporary debate regarding the question of conceptual change relates to the learning paradox in Plato’s dialogue Menon, where Menon asks how it is possible to engage in a search for knowledge of something entirely new. How is it possible to change from a commonsense view of a phenomenon into a scientific one that also sometimes goes quite contrary to the commonsense view? Sociocultural analysis dispatch the question by talking of situated cognition and by that ignoring individual cognitions. Constructivist approaches describes cognitive development as an evolution from simple naïve models of a phenomenon to more complex and powerful models, often by implying that the simple models are abandoned in favour of the new ones. Here, another model for conceptual development and conceptual change will be advanced. It is proposed that conceptual development and conceptual change is constituted by a process of a continuous assimilation of new information into an all-embracing model and, simultaneously, a differentiation within this compounded model resulting eventually in different new models. This description that stick to the Piagetian way of describing cognitive development, will be illustrated by means of empirical data from a study of children’s conceptions of the shape of the earth.
|
|
