| 1. |
- Hildingh, Cathrine, et al.
(author)
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Sense of coherence and experiences of social support and mastery in the early discharge period after an acute cardiac event
- 2008
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In: Journal of Clinical Nursing. - Oxford : Blackwell Publishing. - 0962-1067 .- 1365-2702. ; 17:10, s. 1303-1311
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Journal article (peer-reviewed)abstract
- Aims and objectives: The aim of this study was to examine sense of coherence and experiences of change in social support and mastery from a short-term perspective in patients who had been admitted to hospital with a suspected myocardial infarction.Background: The early discharge period after an acute cardiac event can be a stressful and vulnerable time when psychosocial resources are of the utmost importance. A positive outcome in an encounter with a stressor is thought to be linked to a strong sense of coherence, social support and mastery.Design: A multi-centre survey was conducted in three hospitals in southern Sweden.Methods: The sample was 300, 241 of whom completed the questionnaires; while in hospital and two weeks postdischarge.Results: In the early discharge period a low sense of coherence was found in over 60% of the sample. There was an association between social support and mastery and between sense of coherence and mastery. Differences in social support ratings, with lower ratings two weeks postdischarge, were found among women and persons over 65 years of age.Conclusions: This study adds knowledge about experiences in the early discharge period. Changes in ratings of social support but not in ratings of mastery were found between baseline and two weeks postdischarge.Relevance to clinical practice: Healthcare professionals need to be sensitive to patients’ sense of coherence, mastery and need for social support during the early discharge period. They can help patients to identify adequate support strategies and prevent future potential complications. However, to routinely assess sense of coherence, social support and mastery, there is a need for a simple and useful instrument in clinical practice.
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| 2. |
- Khmaladze, Ia, et al.
(author)
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Mannan induces ROS-regulated, IL-17A-dependent psoriasis arthritis-like disease in mice
- 2014
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In: Proceedings of the National Academy of Sciences of the United States of America. - Washington, DC : National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 111:35, s. E3669-E3678
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Journal article (peer-reviewed)abstract
- Psoriasis (Ps) and psoriasis arthritis (PsA) are poorly understood common diseases, induced by unknown environmental factors, affecting skin and articular joints. A single i.p. exposure to mannan from Saccharomyces cerevisiae induced an acute inflammation in inbred mouse strains resembling human Ps and PsA-like disease, whereas multiple injections induced a relapsing disease. Exacerbation of disease severity was observed in mice deficient for generation of reactive oxygen species (ROS). Interestingly, restoration of ROS production, specifically in macrophages, ameliorated both skin and joint disease. Neutralization of IL-17A, mainly produced by gammadelta T cells, completely blocked disease symptoms. Furthermore, mice depleted of granulocytes were resistant to disease development. In contrast, certain acute inflammatory mediators (C5, Fcgamma receptor III, mast cells, and histamine) and adaptive immune players (alphabeta T and B cells) were redundant in disease induction. Hence, we propose that mannan-induced activation of macrophages leads to TNF-alpha secretion and stimulation of local gammadelta T cells secreting IL-17A. The combined action of activated macrophages and IL-17A produced in situ drives neutrophil infiltration in the epidermis and dermis of the skin, leading to disease manifestations. Thus, our finding suggests a new mechanism triggered by exposure to exogenous microbial components, such as mannan, that can induce and exacerbate Ps and PsA.
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| 3. |
- Shen, Weixing, et al.
(author)
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Protective effects of Wang-Bi tablet on bone destruction in collagen-induced arthritis by regulating osteoclast-osteoblast functions.
- 2019
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In: Journal of Ethnopharmacology. - : Elsevier BV. - 0378-8741 .- 1872-7573. ; 238
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Journal article (peer-reviewed)abstract
- ETHNOPHARMACOLOGICAL RELEVANCE: Wang-bi tablet (WB) consists of 17 traditional Chinese medicines and has been used for treating rheumatoid arthritis (RA) in China for many years, however, its pharmacologic mechanism is not clear.AIM OF STUDY: The aim of this study was to investigate the therapeutic effect of WB on collagen-induced mouse arthritis and explored the underlying mechanism.MATERIALS AND METHODS: DBA/1 mice were used to establish a type II collagen-induced arthritis (CIA) model. From the day of arthritis onset, mice were treated daily by gavage with either total glucosides of paeony (TGP, 0.37 g/kg/d) or WB at a lower (1.11 g/kg/d, WBL) or higher dose of (3.33 g/kg/d, WBH) for 8 weeks. The severity of arthritis, levels of cytokines and the activation of signaling pathways were determined.RESULTS: Our results revealed that WB treatment effectively alleviated inflammatory symptoms and prevented bone erosions and joint destructions. It obviously decreased the serum concentration of pro-inflammatory cytokines TNF-α, IL-6 and IL-17α, while increased the concentration of anti-inflammatory cytokine IL-10. Interestingly, the proportion of splenic Treg cells were increased significantly. In vitro experiments showed that WB inhibited the differentiation of osteoclasts. Consistently, the mRNA levels of tartrate-resistant acid phosphatase (TRAP) and cathepsin K (CtsK), and the activation of NF-κB and JAK-STAT3 signaling pathways in the paws of CIA mice were inhibited by WB treatment. On the other hand, up-regulation of osteogenic genes Runx2, Osterix mRNA, and activation of Wnt/β-catenin signaling pathway along with a decreased receptor activator of nuclear factor κB ligand (RANKL) expression were found in WB treated mice.CONCLUSION: Our results suggest that the therapeutic effect of Wang-bi tablet could be attributed to its inhibitory activity on NF-κB and STAT3 signaling pathway-mediated osteoclast differentiation, and its enhancement on Wnt/β-catenin signaling pathway-mediated osteoblast functions.
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| 4. |
- Adamsson, Viola, et al.
(author)
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Effects of a Nordic diet on cardiovascular and metabolic risk factors in hypercholesterolemic subjects: a randomized controlled study
- 2009
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Conference paper (peer-reviewed)abstract
- Background: Apart from lipid-lowering drugs, dietary changes can also reduce plasma LDL-C concentrations. No studies have been conducted to investigate the clinical effects of a diet with traditional foods originating from the Nordic countries. Method: In a randomised, controlled parallel-group intervention study 88 mildly hypercholesterolemic men and women were randomized to either an ad libitum Nordic diet (ND) or a control diet (CD) for 6 weeks. All meals and foods were provided to the participants in the ND group. Primary outcome measure was LDL-cholesterol, and secondary outcomes were blood pressure, plasma insulin and glucose concentrations. The ND was a high-fibre diet rich in plant foods (fruit, berries, vegetables, root vegetables, whole grain cereals and legumes), vegetable fats (rapeseed oil and nuts) and fatty fish, low-fat milk products, but low in salt, added sugars, saturated fats and red meats. Result: 86 subjects completed the study. Distribution of carbohydrates, fat and protein (E%) in ND was 54, 27, 19, respectively. ND lowered plasma total cholesterol 0.98±0.75 mmol/l (-16%), LDL-C by 0.83±0.67 mmol/l (-21%), HDL-C 0.08±0.23 mmol/l (-5%), including reduced LDL/HDL ratio by -0.42±0.57 (-14%) (all p<0.01 versus controls). Insulin concentrations decreased by 0.51± 2.25 (-9%, p=0.01) and systolic blood pressure by 7±13 mmHg (-5%, P<0.01) compared to controls. Despite diets were eaten ad libitum, body weight decreased by 3.0 kg in the ND (P<0.001). No significant differences were found for diastolic blood pressure, triglycerides or plasma glucose. Conclusion: A Nordic diet improves blood lipid profile, and insulin sensitivity as well as lowering blood pressure to a clinically significant extent in hypercholesterolemic subjects.
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| 5. |
- Teneberg, Susanne, et al.
(author)
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Lactotetraosylceramide, a novel glycosphingolipid receptor for Helicobacter pylori, present in human gastric epithelium
- 2002
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In: Journal of Biological Chemistry. - Bethesda : American Society for Biochemistry and Molecular Biology. - 0021-9258 .- 1083-351X. ; 277:22, s. 19709-19719
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Journal article (peer-reviewed)abstract
- The binding of Helicobacter pylori to glycosphingolipids was examined by binding of 35S-labeled bacteria to glycosphingolipids on thin-layer chromatograms. In addition to previously reported binding specificities, a selective binding to a non-acid tetraglycosylceramide of human meconium was found. This H. pylori binding glycosphingolipid was isolated and, on the basis of mass spectrometry, proton NMR spectroscopy, and degradation studies, were identified as Galβ3GlcNAcβ3-Galβ4Glcβ1Cer (lactotetraosylceramide). When using non-acid glycosphingolipid preparations from human gastric epithelial cells, an identical binding of H. pylori to the tetraglycosylceramide interval was obtained in one of seven samples. Evidence for the presence of lactotetraosylceramide in the binding-active interval was obtained by proton NMR spectroscopy of intact glycosphingolipids and by gas chromatography-electron ionization mass spectrometry of permethylated tetrasaccharides obtained by ceramide glycanase hydrolysis. The lactotetraosylceramide binding property was detected in 65 of 74 H. pylori isolates (88%) Binding of H. pylori to lactotetraosylceramide on thin-layer chromatograms was inhibited by preincubation with lactotetraose but not with lactose. Removal of the terminal galactose of lactotetraosylceramide by galactosidase hydrolysis abolished the binding as did hydrazinolysis of the acetamido group of the N-acetylglucosamine. Therefore, Galβ3GlcNAc is an essential part of the binding epitope.
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| 6. |
- Bersellini Farinotti, Alex, et al.
(author)
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Cartilage-binding antibodies induce pain through immune complex-mediated activation of neurons
- 2019
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In: Journal of Experimental Medicine. - : Rockefeller University Press. - 1540-9538 .- 0022-1007. ; 216:8, s. 1904-1924
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Journal article (peer-reviewed)abstract
- Rheumatoid arthritis-associated joint pain is frequently observed independent of disease activity, suggesting unidentified pain mechanisms. We demonstrate that antibodies binding to cartilage, specific for collagen type II (CII) or cartilage oligomeric matrix protein (COMP), elicit mechanical hypersensitivity in mice, uncoupled from visual, histological and molecular indications of inflammation. Cartilage antibody-induced pain-like behavior does not depend on complement activation or joint inflammation, but instead on tissue antigen recognition and local immune complex (IC) formation. smFISH and IHC suggest that neuronal Fcgr1 and Fcgr2b mRNA are transported to peripheral ends of primary afferents. CII-ICs directly activate cultured WT but not FcRγ chain-deficient DRG neurons. In line with this observation, CII-IC does not induce mechanical hypersensitivity in FcRγ chain-deficient mice. Furthermore, injection of CII antibodies does not generate pain-like behavior in FcRγ chain-deficient mice or mice lacking activating FcγRs in neurons. In summary, this study defines functional coupling between autoantibodies and pain transmission that may facilitate the development of new disease-relevant pain therapeutics.
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| 7. |
- Tong, D. M., et al.
(author)
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A Shared Epitope of Collagen Type XI and Type II Is Recognized by Pathogenic Antibodies in Mice and Human with Arthritis
- 2018
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In: Frontiers in Immunology. - : Frontiers Media SA. - 1664-3224. ; 9
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Journal article (peer-reviewed)abstract
- Background: Collagen XI (CXI) is a heterotrimeric molecule with triple helical structure in which the alpha 3(XI) chain is identical to the alpha 1(II) chain of collagen II (CII), but with extensive posttranslational modifications. CXI molecules are intermingled in the cartilage collagen fibers, which are mainly composed of CII. One of the alpha chains in CXI is shared with CII and contains the immunodominant T cell epitope, but it is unclear whether there are shared B cell epitopes as the antibodies tend to recognize the triple helical structures. Methods: Mice expressing the susceptible immune response gene A(q) were immunized with CII or CXI. Serum antibody responses were measured, monoclonal antibodies were isolated and analyzed for specificity to CII, CXI, and triple helical collagen peptides using bead-based multiplex immunoassays, enzyme-linked immunosorbent assays, and Western blots. Arthritogenicity of the antibodies was investigated by passive transfer experiments. Results: Immunization with CII or CXI leads to a strong T and B cell response, including a cross-reactive response to both collagen types. Immunization with CII leads to severe arthritis in mice, with a response toward CXI at the chronic stage, whereas CXI immunization induces very mild arthritis only. A series of monoclonal antibodies to CXI were isolated and of these, the L10D9 antibody bound to both CXI and CII equally strong, with a specific binding for the D3 epitope region of alpha 3(XI) or alpha 1(II) chain. The L10D9 antibody binds cartilage in vivo and induced severe arthritis. In contrast, the L5F3 antibody only showed weak binding and L7D8 antibody has no binding to cartilage and did not induce arthritis. The arthritogenic L10D9 antibody bound to an epitope shared with CII, the triple helical D3 epitope. Antibody levels to the shared D3 epitope were elevated in the sera from mice with arthritis as well as in rheumatoid arthritis. Conclusion: CXI is immunologically not exposed in healthy cartilage but contains T and B cell epitopes cross-reactive with CII, which could be activated in both mouse and human arthritis and could evoke an arthritogenic response.
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| 8. |
- Nygren, Jens Martin, 1976-, et al.
(author)
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Bone marrow-derived hematopoietic cells generate cardiomyocytes at a low frequency through cell fusion, but not transdifferentiation
- 2004
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In: Nature Medicine. - : Springer Science and Business Media LLC. - 1078-8956 .- 1546-170X. ; 10:5, s. 494-501
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Journal article (peer-reviewed)abstract
- Recent studies have suggested that bone marrow cells might possess a much broader differentiation potential than previously appreciated. In most cases, the reported efficiency of such plasticity has been rather low and, at least in some instances, is a consequence of cell fusion. After myocardial infarction, however, bone marrow cells have been suggested to extensively regenerate cardiomyocytes through transdifferentiation. Although bone marrow-derived cells are already being used in clinical trials, the exact identity, longevity and fate of these cells in infarcted myocardium have yet to be investigated in detail. Here we use various approaches to induce acute myocardial injury and deliver transgenically marked bone marrow cells to the injured myocardium. We show that unfractionated bone marrow cells and a purified population of hematopoietic stem and progenitor cells efficiently engraft within the infarcted myocardium. Engraftment was transient, however, and hematopoietic in nature. In contrast, bone marrow-derived cardiomyocytes were observed outside the infarcted myocardium at a low frequency and were derived exclusively through cell fusion.
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| 9. |
- Varga, Tibor V, et al.
(author)
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Acute and Long-Term Changes in Blood-Borne Biomarkers in Response to Dynamic Standing in Nonambulant Children With Cerebral Palsy
- 2024
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In: Pediatric Exercise Science. - Champaign, IL : Human Kinetics. - 0899-8493 .- 1543-2920. ; 36:1, s. 15-22
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Journal article (peer-reviewed)abstract
- Purpose: To investigate acute and long-term changes in hormonal and inflammatory biomarkers in nonambulant children with cerebral palsy in response to dynamic standing exercise.Methods: Fourteen children with severe cerebral palsy were recruited. Anthropometrics and body composition measures were obtained. Physical activity levels before the study were assessed using hip-worn accelerometry. All children underwent a 30-minute dynamic standing exercise using the Innowalk standing aid. Respiratory data during exercise were collected using indirect calorimetry. Blood samples were collected before and after exercise. Blood samples were also obtained after two 16-week exercise protocols, in a resting state. Hormonal and inflammatory metabolites were measured from blood serum/plasma, and acute and long-term changes in biomarker levels were assessed using Wilcoxon signed-rank tests.Results: Of the 14 children at baseline, all had slightly/moderately/severely elevated C-reactive protein and cortisol levels. C-reactive protein levels were decreased following a 30-minute bout of dynamic standing (before exercise: 53 mg/L [interquartile range: 40-201]; after exercise: 39 mg/L [interquartile range: 20-107]; P = .04).Conclusions: We show that several hormonal and inflammatory biomarkers are dysregulated in children with cerebral palsy. Our preliminary results from a small, but deep-phenotyped prospective cohort indicate acute and long-term alterations of several biomarkers in response to exercise. ©2023 The Authors.
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| 10. |
- Lahore, G. F., et al.
(author)
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Vitamin D3 receptor polymorphisms regulate T cells and T cell-dependent inflammatory diseases
- 2020
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In: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 117:40, s. 24986-24997
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Journal article (peer-reviewed)abstract
- It has proven difficult to identify the underlying genes in complex autoimmune diseases. Here, we use forward genetics to identify polymorphisms in the vitamin D receptor gene (Vdr) promoter, controlling Vdr expression and T cell activation. We isolated these polymorphisms in a congenic mouse line, allowing us to study the immunomodulatory properties of VDR in a physiological context. Congenic mice overexpressed VDR selectively in T cells, and thus did not suffer from calcemic effects. VDR overexpression resulted in an enhanced antigen-specific T cell response and more severe autoimmune phenotypes. In contrast, vitamin D3-deficiency inhibited T cell responses and protected mice from developing autoimmune arthritis. Our observations are likely translatable to humans, as Vdr is overexpressed in rheumatic joints. Genetic control of VDR availability codetermines the proinflammatory behavior of T cells, suggesting that increased presence of VDR at the site of inflammation might limit the antiinflammatory properties of its ligand.
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