| 1. |
- Nebel, Daniel, et al.
(författare)
-
1α,25-dihydroxyvitamin D3 promotes osteogenic activity and downregulates proinflammatory cytokine expression in human periodontal ligament cells
- 2015
-
Ingår i: Journal of Periodontal Research. - : John Wiley & Sons. - 0022-3484 .- 1600-0765. ; 50:5, s. 666-673
-
Tidskriftsartikel (refereegranskat)abstract
- Background and ObjectiveThe aim of this study was to assess the impact of 1,25-dihydroxyvitamin D3 (vitamin D3) on osteogenic and inflammatory properties of human periodontal ligament (PDL) cells and investigate underlying mechanisms. Material and MethodsHuman PDL cells, obtained from four subjects, were stimulated with vitamin D3 for 4-48h. The bone markers osteopontin and osteocalcin and proinflammatory cytokine/chemokine expression was determined by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Cytokine and chemokine expression was determined after stimulation with the inflammation promoter lipopolysaccharide (LPS) in the presence or absence of vitamin D3. Alkaline phosphatase activity was assessed using p-nitrophenylphosphate substrate. ResultsTreatment with 30ng/mL of vitamin D3, corresponding to an optimal plasma concentration of vitamin D, for 24h had no effect on PDL cell number and morphology but increased PDL cell osteopontin and osteocalcin mRNA expression by about 70 and 40%, respectively, and, moreover, treatment with vitamin D3 for 48h enhanced PDL cell alkaline phosphatase activity by about two times showing that vitamin D3 exerts pro-osteogenic effects in human PDL cells. Stimulation with LPS (1g/mL) for 4h increased PDL cell interleukin (IL)-6 cytokine and chemokine ligand 1 (CXCL1) chemokine mRNA expression several fold. The LPS-induced increase in IL-6 and CXCL1 transcripts was attenuated by vitamin D3 (30ng/mL). Treatment with vitamin D3 (3-300ng/mL) for 24h reduced the LPS-evoked increase in PDL cell IL-6 protein by about 50%. Vitamin D3 (30ng/mL) had no effect on LPS-induced IL-1 and MCP-1 mRNA expression. ConclusionsVitamin D3 promotes osteogenic differentiation but also downregulates inflammation promoter-induced IL-6 cytokine and CXCL1 chemokine expression in human PDL cells, suggesting that vitamin D3 both stimulates bone regeneration and antagonizes inflammation in human periodontal tissue.
|
|
| 2. |
- Svensson, Daniel, et al.
(författare)
-
Secretory leukocyte protease inhibitor regulates human periodontal ligament cell production of pro-inflammatory cytokines
- 2017
-
Ingår i: Inflammation Research. - : Springer Science and Business Media LLC. - 1023-3830 .- 1420-908X. ; 66:9, s. 823-831
-
Tidskriftsartikel (refereegranskat)abstract
- Objective: Regulation of immune-like cell properties of periodontal ligament (PDL) cells is not understood. We investigate the importance of secretory leukocyte protease inhibitor (SLPI) for production of pro-inflammatory cytokines in human PDL cells. Materials and methods: PDL cells were isolated from teeth extracted for orthodontic reasons. Cellular location of SLPI was investigated by immunocytochemistry. Cytokine transcript and protein expression were assessed by quantitative real-time RT-PCR and Western blotting. SLPI gene activity was knocked-down by siRNA. NF-κB signaling was assessed by measuring IκBα, and phosphorylated p65 and p105 protein expression. Results: PDL cells showed cytoplasmic expression of SLPI. Cellular expression level of SLPI negatively correlated to LPS-induced stimulation of IL-6 and MCP-1. Both SLPI gene activity and protein were reduced by about 70% in PDL cells treated with SLPI siRNA compared to cells treated with non-coding construct. Treatment with SLPI siRNA was associated with up-regulation of both basal and LPS-stimulated IL-6, MCP-1 and TLRs mRNA expression. The up-regulation of MCP-1 transcript in SLPI siRNA-treated cells was confirmed on protein level. SLPI siRNA-treatment enhanced the phosphorylated NF-κB p105 protein expression. Conclusions: SLPI regulates PDL cell pro-inflammatory cytokine expression and modulates NF-κB signaling, suggesting that SLPI governs the immune cell-like properties of PDL cells.
|
|
| 3. |
- Svensson Primus, Robert, 1982-, et al.
(författare)
-
Between Grassroots Democracy and Professional Commercialism in Sweden
- 2023
-
Ingår i: Football in the Nordic Countries. - London : Routledge. - 9781003280729 - 9781032249131 ; , s. 64-76
-
Bokkapitel (refereegranskat)abstract
- In the late 19th century, football entered Sweden's coastal cities, such as Malmö, Halmstad and Gothenburg. The sport grew quickly, and the Swedish Football Association (SvFF) was founded in 1904. In the following decades, the popularity of football increased and in the 1950s it was perceived as the national sport of Sweden. However, at that time the sport was non-professional and in practice only for men. In order to keep up with hardening international competition, SvFF overturned the amateur regulations in 1967. Professionalisation was slow due to the lack of revenue but accelerated for male players after the Bosman ruling in 1995. Women's football developed gradually from the 1960s and in 1972 a national league organised by SvFF was formed. Youth football also grew substantially. Despite the differences in resources football became well-established amongst both men and women. However, the tensions between idealism, voluntarism and inclusion on the one hand, and commercialism, professionalism and selection, on the other hand, remain. This is best exemplified by the 51% rule, which states that clubs must be majority-owned by the members. This is hailed by some as a guarantee for democratic football, while others argue that it restricts clubs’ financial development.
|
|
| 4. |
- Aidoukovitch, Alexandra, et al.
(författare)
-
Antimicrobial peptide LL-37 and its pro-form, hCAP18, in desquamated epithelial cells of human whole saliva
- 2020
-
Ingår i: European Journal of Oral Sciences. - : Wiley. - 0909-8836 .- 1600-0722. ; 128:1, s. 1-6
-
Tidskriftsartikel (refereegranskat)abstract
- The antimicrobial peptide LL-37 is active against oral bacteria and has been demonstrated to be present in human saliva, but its distribution in different fractions of saliva is not known. LL-37 is formed from its intracellular pro-form, hCAP18, in an extracellular enzymatic reaction catalyzed by proteinase 3 and kallikrein 5. Here, we prepared cell-containing and cell-free fractions of unstimulated human whole saliva by centrifugation after depolymerization of mucins with dithiothreitol, and measured the levels of hCAP18/LL-37 in these fractions using ELISA. Cellular expression of hCAP18/LL-37 was determined by western blotting and immunocytochemistry. The ELISA analyses demonstrated that both cells and cell-free saliva contained hCAP18/LL-37. Western blot analysis of cell-pellet homogenates showed a strong band corresponding to hCAP18 at the correct molecular weight and a weak band corresponding to LL-37. Phase-contrast and light microscopy revealed that the cells consisted of desquamated epithelial cells. These cells expressed cytoplasmic immunoreactivity for hCAP18/LL-37. The peripheral part of the cytoplasm, corresponding to the plasma membrane, was particularly rich in hCAP18/LL-37 immunoreactivity. No immunoreactivity was observed after omission of the primary antibody. We conclude that desquamated epithelial cells of human whole saliva contain antimicrobial hCAP18/LL-37, suggesting that these cells may take part in the innate immune system by harboring and releasing these peptides.
|
|
| 5. |
- Aidoukovitch, Alexandra, et al.
(författare)
-
Strontium chloride promotes cell proliferation in a human osteoblast cell line
- 2014
-
Rapport (övrigt vetenskapligt/konstnärligt)abstract
- Strontium ranelate (SrRan) is the active component of drugs currently used for reducing the risk of fractures in patients suffering from osteoporosis. Despite extensive use, the underlying mechanisms of action of Sr2+ are not fully understood. In the present study, we assess the impact of SrCl2 on human osteoblast activity and proliferation. Cultures of the human osteoblast-like cell line MG63 were treated for 72 h in presence of 0.1 mM, 1 mM, 5 mM and 10 mM SrCl2 or vehicle, used in control groups. Cells were counted manually using a Bürker chamber. Total protein content was determined by colorimetric analysis performed by a microplate reader using Bio-Rad protein assay. Alkaline phosphatase (ALP) activity was determined enzymatically and normalized to total protein content in each sample. Cell viability was assessed using the MTT assay. Treatment with 5 mM SrCl2 for 72 h enhanced total MG63 cell protein content by 37% compared to controls (p<0.01). A lower concentration (0.1 mM) of SrCl2 had no effect on total protein. Incubation with 5 mM SrCl2 for 72 h increased MG63 cell number by 38% compared to controls (p<0.001). The SrCl2-induced increase in cell number was associated with enhanced (+14% compared to controls, p<0.05) cell viability. Treatment with a higher concentration (10 mM) of SrCl2 enhanced cell number similar to 5 mM SrCl2 (+54% compared to controls, p<0.05). Treatment with 0.1 or 5 mM SrCl2 for 72 h had no effect (p>0.05) on MG63 cell ALP activity, while 1 mM SrCl2 reduced ALP activity as well as total protein content by about 25% compared to controls (p<0.05). The current results demonstrate that treatment with SrCl2 for 72 h, at concentrations higher than 1 mM promotes cell proliferation in human osteoblast-like cells, suggesting that Sr2+ may enhance bone formation through this mechanism.
|
|
| 6. |
- Aidoukovitch, Alexandra, et al.
(författare)
-
The host defense peptide LL-37 is internalized by human periodontal ligament cells and prevents LPS-induced MCP-1 production
- 2019
-
Ingår i: Journal of Periodontal Research. - : Wiley. - 0022-3484 .- 1600-0765. ; 54:6, s. 662-670
-
Tidskriftsartikel (refereegranskat)abstract
- Objective: The human host defense peptide LL-37 both shows antimicrobial effects and modulates host cell properties. Here, we assess the effects of synthesized LL-37 on lipopolysaccharide (LPS)-induced inflammation in human periodontal ligament (PDL) cells and investigates underlying mechanisms. Background: LL-37 has been detected in the periodontal tissues, but its functional importance for PDL cell innate immune responses is not known. Methods: Human PDL cells were obtained from premolars extracted on orthodontic indications. Cellular pro-inflammatory monocyte chemoattractant protein-1 (MCP-1) mRNA expression was determined using quantitative real-time RT-PCR. MCP-1 protein production was assessed by western blot and ELISA. Internalization of LL-37 by PDL cells was visualized by immunocytochemistry. Nuclear factor kappa-light-chain-enhancer of activated B-cell (NF-κB) activity was assessed by western blot of phosphorylated p65, phosphorylated p105, and IκBα proteins. Binding of LL-37 to PDL cell DNA was determined by isolation and purification of DNA and dot blot for LL-37 immunoreactivity. Results: Treatment with LL-37 (1 µmol/L) for 24 hours prevented LPS-induced stimulation of MCP-1 expression analyzed both on transcript and on protein levels. Stimulation with LL-37 (1 µmol/L) for 24 hours had no effect on toll-like receptor (TLR)2 and TLR4 transcript expression, suggesting that LL-37 acts downstream of the TLRs. Preincubation with LL-37 for 60 minutes followed by stimulation with LPS for 24 hours in the absence of LL-37 completely prevented LPS-evoked MCP-1 transcript expression, implying that LL-37 acts intracellularly and not via binding and neutralization of LPS. In PDL cells stimulated with LL-37 for 60 minutes, the peptide was internalized as demonstrated by immunocytochemistry, suggesting an intracellular mechanism of action. LL-37 immunoreactivity was observed both in the cytosol and in the nucleus. Downregulation of LPS-induced MCP-1 by LL-37 was not mediated by reduction in NF-κB activity as shown by unaltered expression of phosphorylated p65, phosphorylated p105, and IκBα NF-κB proteins in the presence of LL-37. Immunoreactivity for LL-37 was observed in PDL cell DNA treated with but not without 0.1 and 1 µmol/L LL-37 for 60 minutes in vitro. Conclusion: LL-37 abolishes LPS-induced MCP-1 production in human PDL cells through an intracellular, NF-κB-independent mechanism which probably involves direct interaction between LL-37 and DNA.
|
|
| 7. |
- Anders, Emma, et al.
(författare)
-
Globular C1q receptor (p33) binds and stabilizes pro-inflammatory MCP-1 : a novel mechanism for regulation of MCP-1 production and function
- 2018
-
Ingår i: Biochemical Journal. - 0264-6021. ; 475:4, s. 775-786
-
Tidskriftsartikel (refereegranskat)abstract
- The protein gC1qR (globular C1q receptor), also named p33, was originally identified as a binding partner of the globular heads of C1q in the complement system. gC1qR/p33 is abundantly expressed in many cell types, but the functional importance of this protein is not completely understood. Here, we investigate the impact of gC1qR/p33 on the production and function of the pathophysiologically important chemokine monocyte chemoattractant protein-1 (MCP-1) and the underlying molecular mechanisms. Knockdown of gC1qR/p33 negatively regulated the production of MCP-1, but had no effect on the expression of transcript for MCP-1 in human periodontal ligament cells, suggesting a translational/post-translational mechanism of action. Laser scanning confocal microscopy showed considerable cytosolic co-localization of gC1qR/p33 and MCP-1, and co-immunoprecipitation disclosed direct physical interaction between gC1qR/p33 and MCP-1. Surface plasmon resonance analysis revealed a high-affinity binding (KD = 10.9 nM) between gC1qR/p33 and MCP-1. Using a transwell migration assay, we found that recombinant gC1qR/p33 enhances MCP-1-induced migration of human THP-1 monocytes, pointing to a functional importance of the interaction between gC1qR/p33 and MCP-1. An in vitro assay revealed a rapid turnover of the MCP-1 protein and that gC1qR/ p33 stabilizes MCP-1, hence preventing its degradation. We propose that endogenous gC1qR/p33 physically interacts with MCP-1 causing stabilization of the MCP-1 protein and stimulation of its activity in human periodontal ligament cells, suggesting a novel gC1qR/p33-mediated pro-inflammatory mechanism of action.
|
|
| 8. |
- Barker-Ruchti, Natalie, 1971-, et al.
(författare)
-
Don't buy a pig in a poke: Considering challenges of and problems with performance analysis technologies in Swedish men's elite football
- 2021
-
Ingår i: Performance Enhancement and Health. - : Elsevier BV. - 2211-2669. ; 9:1
-
Tidskriftsartikel (refereegranskat)abstract
- During the last decades, technologies to monitor, test and analyze athletes’ performance and health have rapidly developed. At present, global positioning systems (GPS), stadium camcorders, heart rate monitors and mobile applications are prominent performance analysis technologies (PATs) used in most elite sport environments. While PATs is understood as an aid, there is a growing body of literature that points to negative consequences. These negative consequences are concerning and call for research and measures to develop strategies for effective and productive implementation. To achieve this, this article first outlines key challenges and problems of PATs, using sport sociological research on coaching and athletes, historical knowledge of the scientization of training and the changing role of the coach, as well as scientific and experiential knowledge of performance analysis. Our findings show that key challenges and problems occur in a chain of six steps that concern the implementing of PATs: 1. Investment in PATs; 2. Production of performance data; 3. Interpretation of performance data; 4. Communication of performance data; 5. Decision-making based on performance data; and 6. Influence of PATs on coaches and athletes. The article then answers these challenges and problems by outlining recommendations for how sport managers and administrators can prevent buying “a pig in a poke” by acquiring competence about performance analysis and PATs, investing time, and developing effective communication between those working with PATs. © 2021 The Author(s)
|
|
| 9. |
- Crouse, David F., et al.
(författare)
-
The Set MHT
- 2011
-
Ingår i: 14th International Conference on Information Fusion, Fusion 2011; Chicago, IL; 5 July 2011 through 8 July 2011. - 9781457702679
-
Konferensbidrag (refereegranskat)abstract
- Abstract—We introduce the Set MHT, a tracking algorithmthat maintains multiple hypotheses and produces “smooth”estimates without the track coalescence often associated withMinimum Mean Squared Error (MMSE) estimation or thejitter associated with Maximum Likelihood (ML) estimation.It does this by utilizing Minimum Mean Optimal SubpatternAssignment (MMOSPA) estimation techniques coupled with atheoretically-grounded approach for probabilistically determiningthe identities of the state estimates. Unlike traditional MHTalgorithms, the Set MHT does not “forget” uncertainty in targetidentities, i.e. display an unjustifiably high confidence level inthe target identities, as a result of pruning out competinghypotheses. Rather, it uses merging techniques while avoiding theshortcomings of traditional Gaussian mixture reduction trackers.
|
|
| 10. |
|
|
