| 1. |
|
|
| 2. |
|
|
| 3. |
- Jerndal, Mikael, et al.
(författare)
-
Systematic review and meta-analysis of the efficacy of basic fibroblast growth factor in experimental stroke
- 2009
-
Ingår i: European Stroke conference, Stockholm, Sweden May.
-
Konferensbidrag (refereegranskat)abstract
- Background Basic fibroblast growth factor (bFGF) has been shown to have a potent trophic effect on brain neurons, glia and endothelial cells in both in vitro and in vivo studies and is a candidate drug for treatment of ischemic stroke. Any decision to proceed to clinical trials should be based on an unbiased assessment of all available animal data. This assessment should evaluate the efficacy of the drug as well as the characteristics and limits to that efficacy. We use a systematic approach to assess the evidence for protective effects of bFGF in animal models of focal cerebral ischemia. Methods We have performed a systematic review and meta-analysis of studies describing the efficacy of bFGF in animal models of focal cerebral ischemia where outcome was measured as infarct size or neurological score. Study quality was scored against a quality checklist and certain study characteristics were looked at individually. A random effects model was used and the significance level was set to p<0.001 to allow for multiple comparisons. Results Systematic review identified 21 publications of which 20 report infarct size from 520 animals and 10 report neurological score from 223 animals. bFGF reduced infarct size by 25.7% (95% confidence interval 21.7-29.8%) and improved neurological score by 28.1% (23.0-33.2%). Efficacy was higher with intra-arterial administration which showed a reduction of infarct size by 57.6% (33.8-81.3%, p=9.8E-07). Overall study quality was moderate with a median quality score of 6/11, interquartile range 5-7. Studies that performed blinded assessment of outcome showed lesser efficacy on infarct size reduction than those who did not blind, 20.2% (12.2-28.1) compared to 29.4% (26.7-32.1%, p=0.00073). The use of animals with associated comorbidities was rare, with only 4.4% aged animals and no animals with diabetes or hypertension. Aged animals showed lower effect size with only 4.7% reduction of infarct size (-9.0-18.3%, p=1.0E-05). Conclusion Our study shows that bFGF-1 has efficacy in experimental ischemic stroke. The effect of study quality and bias limits the strength of this conclusion. Further research is needed to test the efficacy in animals with associated co morbidities.
|
|
| 4. |
- Lindén, Sara K., 1974, et al.
(författare)
-
MUC1 limits Helicobacter pylori infection both by steric hindrance and by acting as a releasable decoy.
- 2009
-
Ingår i: PLoS pathogens. - : Public Library of Science (PLoS). - 1553-7374. ; 5:10
-
Tidskriftsartikel (refereegranskat)abstract
- The bacterium Helicobacter pylori can cause peptic ulcer disease, gastric adenocarcinoma and MALT lymphoma. The cell-surface mucin MUC1 is a large glycoprotein which is highly expressed on the mucosal surface and limits the density of H. pylori in a murine infection model. We now demonstrate that by using the BabA and SabA adhesins, H. pylori bind MUC1 isolated from human gastric cells and MUC1 shed into gastric juice. Both H. pylori carrying these adhesins, and beads coated with MUC1 antibodies, induced shedding of MUC1 from MKN7 human gastric epithelial cells, and shed MUC1 was found bound to H. pylori. Shedding of MUC1 from non-infected cells was not mediated by the known MUC1 sheddases ADAM17 and MMP-14. However, knockdown of MMP-14 partially affected MUC1 release early in infection, whereas ADAM17 had no effect. Thus, it is likely that shedding is mediated both by proteases and by disassociation of the non-covalent interaction between the alpha- and beta-subunits. H. pylori bound more readily to MUC1 depleted cells even when the bacteria lacked the BabA and SabA adhesins, showing that MUC1 inhibits attachment even when bacteria cannot bind to the mucin. Bacteria lacking both the BabA and SabA adhesins caused less apoptosis in MKN7 cells than wild-type bacteria, having a greater effect than deletion of the CagA pathogenicity gene. Deficiency of MUC1/Muc1 resulted in increased epithelial cell apoptosis, both in MKN7 cells in vitro, and in H. pylori infected mice. Thus, MUC1 protects the epithelium from non-MUC1 binding bacteria by inhibiting adhesion to the cell surface by steric hindrance, and from MUC1-binding bacteria by acting as a releasable decoy.
|
|
| 5. |
- Lindén, Sara K., 1974, et al.
(författare)
-
Mucin dynamics in intestinal bacterial infection.
- 2008
-
Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 3:12
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Bacterial gastroenteritis causes morbidity and mortality in humans worldwide. Murine Citrobacter rodentium infection is a model for gastroenteritis caused by the human pathogens enteropathogenic Escherichia coli and enterohaemorrhagic E. coli. Mucin glycoproteins are the main component of the first barrier that bacteria encounter in the intestinal tract. METHODOLOGY/PRINCIPAL FINDINGS: Using Immunohistochemistry, we investigated intestinal expression of mucins (Alcian blue/PAS, Muc1, Muc2, Muc4, Muc5AC, Muc13 and Muc3/17) in healthy and C. rodentium infected mice. The majority of the C. rodentium infected mice developed systemic infection and colitis in the mid and distal colon by day 12. C. rodentium bound to the major secreted mucin, Muc2, in vitro, and high numbers of bacteria were found in secreted MUC2 in infected animals in vivo, indicating that mucins may limit bacterial access to the epithelial surface. In the small intestine, caecum and proximal colon, the mucin expression was similar in infected and non-infected animals. In the distal colonic epithelium, all secreted and cell surface mucins decreased with the exception of the Muc1 cell surface mucin which increased after infection (p<0.05). Similarly, during human infection Salmonella St Paul, Campylobacter jejuni and Clostridium difficile induced MUC1 in the colon. CONCLUSION: Major changes in both the cell-surface and secreted mucins occur in response to intestinal infection.
|
|
| 6. |
|
|
| 7. |
- Lindén, Thomas, 1962, et al.
(författare)
-
Plasticitet, kognition och rehabilitering
- 2009
-
Ingår i: Peter-Eriksson-symposiet "Den Stressade Hjärnan", Göteborg, december 2009.
-
Konferensbidrag (övrigt vetenskapligt/konstnärligt)
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
- Mikkelsen, Bent Egberg, et al.
(författare)
-
Promotion of healthy eating in the workplace : a socio-nutritional approach
- 2008
-
Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Purpose: Unhealthy eating and lifestyle as well as low physical activity is a growing problem and are estimated to be among the primary causes for the growth in obesity and overweight among the adult population. In the ‘settings approach’ institutions such as the workplace are seen as arenas in which eating behavioural patterns can be influenced. This arena tends to grow in importance as more companies provide workplace food with increasing nutritional attention and develop not only lunch offers, but also take away offers. However settings based scientific literature has shown that interventions tend to give only modest effect when sustainability of intervention is used as a measure.Methods: The paper is based on a review of literature on workplace healthy eating based projects and research, mainly with focus on Sweden and Denmark carried out in the Good Food at Work project.Results: Important elements in this kind of interventions are management commitment, education, supporting organisational structures, employee participation, and integrated perspective on risk factors at the workplace and the everyday life of employees.Discussion: The paper suggests that a socio nutritional approach to promotion of healthy eating at workplace is needed if workplace interventions are to be successful. It argues that a socio-technical approach (Clausen and Yoshinaka, 2007) where innovation is considered as a multi-stakeholder process in which interaction between the social constitution of the workplace (Seltz & Hildebrandt, 1989), the change agents, and societal influence (Thorsen et al, 2005) play an important role in the shaping of healthy workplace eating.
|
|
