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- Calander, Ann-Marie, 1957, et al.
(författare)
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Impact of staphylococcal protease expression on the outcome of infectious arthritis
- 2004
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Ingår i: Microbes Infect. - : Elsevier BV. - 1286-4579. ; 6:2, s. 202-6
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Tidskriftsartikel (refereegranskat)abstract
- The exoproteases of Staphylococcus aureus have been proposed as virulence factors during S. aureus infections. To investigate this, we used the wild-type S. aureus strain 8325-4 and its mutants devoid of aureolysin, serine protease, and cysteine protease, respectively, in a well-established model of septic arthritis in mice. The inactivation of the exoprotease genes did not affect the frequency or the severity of joint disease. We conclude that in the model of haematogenously spread staphylococcal arthritis, the bacterial proteases studied do not act as virulence factors.
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- Arvidsson, Andreas, et al.
(författare)
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Stroke induces widespread changes of gene expression for glial cell line-derived neurotrophic factor family receptors in the adult rat brain
- 2001
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Ingår i: Neuroscience. - 1873-7544. ; 106:1, s. 27-41
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Tidskriftsartikel (refereegranskat)abstract
- Gene expression for glial cell line-derived neurotrophic factor (GDNF) family ligands and receptors was analyzed with in situ hybridization after two focal ischemic insults of different severities. Focal ischemia was induced in rats by either 30 min or 2 h of middle cerebral artery occlusion (MCAO), causing damage to the striatum only, or involving also the parietal cortex, respectively. We found modest, transient elevation of GDNF mRNA in the dentate granule cell layer. In addition, the number of GDNF mRNA-expressing cells increased in the cortex and striatum after 2 h or 30 min of MCAO, respectively. No changes of neurturin or persephin mRNA expression were detected. Both c-Ret and GFRalpha1 mRNA levels were markedly increased in the ipsilateral cortex outside the ischemic lesion at 6-24 h after the 2-h insult, whereas GFRalpha2 expression was decreased in cortical areas both within and outside the lesion. Similar increases of c-Ret and GFRalpha1 mRNA levels were detected in the striatum, and to a lesser extent, in the cortex following 30 min of MCAO. The 2-h insult also gave rise to transient increases of c-Ret and GFRalpha1 mRNA in hippocampal subregions. Thirty minutes and 2 h of MCAO lead to elevated c-Ret, and GFRalpha1 or GFRalpha2 mRNA expression, respectively, in the ipsilateral ventroposterolateral thalamic nucleus. Both insults induced increased levels of GFRalpha1 mRNA in the subventricular zone of the lateral ventricle.Our data indicate major changes of GDNF family signaling in the forebrain, regulated mainly through altered receptor levels, in the post-ischemic phase. These changes could enhance neuroprotective and neuroregenerative responses both to endogenous and exogenous GDNF ligands.
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- Arvidsson-Lenner, R, et al.
(författare)
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Glycaemic index
- 2004
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Ingår i: Scandinavian Journal of Food and Nutrition. - : Informa UK Limited. - 1748-2976. ; 48:2, s. 84-94
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Tidskriftsartikel (refereegranskat)abstract
- The glycaemic index (GI) concept is based on the difference in blood glucose response after ingestion of the same amount of carbohydrates from different foods, and possible implications of these differences for health, performance and well-being. GI is defined as the incremental blood glucose area (0-2 h) following ingestion of 50 g of available carbohydrates in the test product as a percentage of the corresponding area following an equivalent amount of carbohydrate from a reference product. A high GI is generally accompanied by a high insulin response. The glycaemic load (GL) is the GI×the amount (g) of carbohydrate in the food/100. Many factors affect the GI of foods, and GI values in published tables are indicative only, and cannot be applied directly to individual foods. Properly determined GI values for individual foods have been used successfully to predict the glycaemic response of a meal, while table values have not. An internationally recognised method for GI determination is available, and work is in progress to improve inter- and intra-laboratory performance. Some epidemiological studies and intervention studies indicate that low GI diets may favourably influence the risk of chronic diseases such as diabetes and coronary heart disease, although further well-controlled studies are needed for more definite conclusions. Low GI diets have been demonstrated to improve the blood glucose control, LDL-cholesterol and a risk factor for thrombosis in intervention studies with diabetes patients, but the effect in free-living conditions remains to be shown. The impact of GI in weight reduction and maintenance as well as exercise performance also needs further investigation. The GI concept should be applied only to foods providing at least 15 g and preferably 20 g of available carbohydrates per normal serving, and comparisons should be kept within the same food group. For healthy people, the significance of GI is still unclear and general labelling is therefore not recommended. If introduced, labelling should be product-specific and considered on a case-by-case basis.
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- Arvidsson, Yvonne, 1960, et al.
(författare)
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ASK1 resistant neuroblastoma is deficient in activation of p38 kinase.
- 2001
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Ingår i: Cell death and differentiation. - : Springer Science and Business Media LLC. - 1350-9047 .- 1476-5403. ; 8:10, s. 1029-37
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Tidskriftsartikel (refereegranskat)abstract
- Apoptosis Signal-regulating Kinase 1 (ASK1) is known to either induce apoptosis or differentiation in various cell lines of neuronal origin. We analyzed the effect of the constitutively active mutant of ASK1 (ASK1-Delta N) in an adenoviral vector in four neuroblastoma cell lines, two murine, C1300 and NXS2, and two human, SH-SY5Y and IMR-32. Already after 24 h upon infection, C1300 and SH-SY5Y cells arrested in growth when judged by [(3)H]thymidine incorporation, and the majority of the cells demonstrated apoptotic appearance, which was confirmed by DNA-laddering in gel electrophoresis. In contrast, NXS2 and IMR-32 cell lines remained unaffected. Immunoblotting revealed strongly phosphorylated p38 MAPK accompanied by weakly phosphorylated JNK in C1300 and SH-SY5Y, whereas none of these kinases were activated by adenoviruses expressing the kinase negative ASK1 mutant or beta-galactosidase. There was no expression of phosphorylated kinases in IMR-32 cells, but NXS2 showed a faint band of phosphorylated p38 MAPK. Addition of the p38 MAPK specific inhibitor, SB203580, protected C1300 and SH-SY5Y cells from apoptosis induced by ASK1-Delta N. The anti-neoplastic agent, paclitaxel, activates ASK1 and JNK, and promotes the in vitro assembly of stable microtubules. Addition of 10 nM paclitaxel sensitised the NXS2 cell line to ASK1-induced cell death. Our results indicate that ASK1 induces apoptosis in neuroblastoma cells mainly via the p38 MAPK pathway, and resistant neuroblastoma cells can be sensitised to ASK1 by paclitaxel.
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- Faigle, Roland, 1977, et al.
(författare)
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ASK1 inhibits astroglial development via p38 mitogen-activated protein kinase and promotes neuronal differentiation in adult hippocampus-derived progenitor cells.
- 2004
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Ingår i: Molecular and cellular biology. - 0270-7306. ; 24:1, s. 280-93
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Tidskriftsartikel (refereegranskat)abstract
- The mechanisms controlling differentiation and lineage specification of neural stem cells are still poorly understood, and many of the molecules involved in this process and their specific functions are yet unknown. We investigated the effect of apoptosis signal-regulating kinase 1 (ASK1) on neural stem cells by infecting adult hippocampus-derived rat progenitors with an adenovirus encoding the constitutively active form of ASK1. Following ASK1 overexpression, a significantly larger number of cells differentiated into neurons and a substantial increase in Mash1 transcription was observed. Moreover, a marked depletion of glial cells was observed, persisting even after additional treatment of ASK1-infected cultures with potent glia inducers such as leukemia inhibitory factor and bone morphogenetic protein. Analysis of the promoter for glial fibrillary acidic protein revealed that ASK1 acts as a potent inhibitor of glial-specific gene transcription. However, the signal transducers and activators of transcription 3 (STAT3)-binding site in the promoter was dispensable, while the activation of p38 mitogen-activated protein kinase was crucial for this effect, suggesting the presence of a novel mechanism for the inhibition of glial differentiation.
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- Hytönen, Ann-Marie, et al.
(författare)
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Haplotypes of the interleukin-4 receptor alpha chain gene associate with susceptibility to and severity of atopic asthma
- 2004
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Ingår i: Clin Exp Allergy. ; 34:10
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Tidskriftsartikel (refereegranskat)abstract
- Summary Background Development of asthma is likely to depend on a complex interaction between environmental and genetic factors. Several groups have suggested the gene of the IL-4 receptor alpha chain (IL4R) as a candidate gene for the development of asthma, although association with single polymorphisms has shown contradicting results. Objective We chose to analyse IL4R gene haplotypes and assess their possible relevance in susceptibility to asthma and to certain clinical phenotypes. Methods IL4R gene haplotypes were analysed, based on the three markers C-3223T, Q551R and I50V, using the expectation-maximization algorithm, in 170 atopic asthma patients and 350 controls, all adult Swedish Caucasians. Results Our data showed significantly higher levels of soluble IL-4R (sIL-4R) in asthma patients compared with controls (P<0.0001). Furthermore, we showed a significant association between the IL4R haplotype containing the alleles T-3223, V50 and R551 (TVR) of the IL4R gene, and susceptibility to atopic asthma, with a frequency of 6.5% in the patients compared with 1% in the controls (P<0.0005). A subgroup of patients with heterozygous or homozygous state for the T-3223, V50 and R551 alleles, also had lower levels of sIL-4R in their circulation compared with patients with homozygous state in the C-3223, I50 and Q551 alleles (P<0.05) and showed less severe asthma according to lung function test (P<0.05). Analysis of single markers showed the T-3223 IL4R allele to associate with lower serum levels of sIL-4 receptor (P<0.0001) and patients carrying the T allele also had more symptoms of active asthma (wheezing, P<0.01; coughing, P<0.05 and breathing difficulties, P<0.01). Conclusion Our data suggest that asthmatic patients with low levels of sIL-4 receptor may represent a genetically distinct subgroup of atopic asthma. TVR haplotype analyses confirm the importance of IL4R as a candidate gene for susceptibility to asthma. This finding may have implications for the understanding of the pathogenesis of asthma and possibly for the development of more specific therapies.
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| 20. |
- Nilsson Stutz, Liv, 1972-, et al.
(författare)
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Minnet och glömskan av de döda i Skateholm.
- 2004
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Ingår i: <em>Minne och Myt</em>. - Lund : Nordic Academic Press. - 9789189116757 ; , s. 81-98
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Bokkapitel (refereegranskat)
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- Van Neerven, R., et al.
(författare)
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A double-blind, placebo-controlled birch allergy vaccination study: inhibition of CD23-mediated serum-immunoglobulin E-facilitated allergen presentation
- 2004
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Ingår i: Clin Exp Allergy. ; 34:3
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND : The clinical efficacy of specific allergy vaccination (SAV), previously called specific immunotherapy is well documented. The working mechanism of this treatment is not completely known at present. Allergen-specific CD4+ T lymphocytes are activated at extremely low allergen concentrations in vivo possibly as a result of serum IgE-facilitated allergen presentation (S-FAP). Previously, we have shown that this process can be inhibited by long-term birch SAV sera. METHODS : In the present study, we have analysed sera from birch-allergic patients in a randomized double-blind, placebo-controlled clinical trial for their ability to mediate S-FAP. Birch-specific IgE levels were not changed after SAV. Bet v 1-specific IgE levels, however, were significantly decreased (P<0.05) and Bet v 1-specific IgG4 levels were strongly increased after SAV (P<0.001). None of these changes were observed in the placebo group. When the sera were tested for their ability to induce S-FAP, a complete abrogation of this effect was noted in the sera from patients receiving active treatment (P<0.001), but not in the control group. This inhibition of S-FAP seemed to be associated with the reduction in the ratio between Bet v 1-specific IgE and IgG4 antibodies in serum, but a clear correlation could not be demonstrated. CONCLUSION : In conclusion, the present study clearly shows that SAV leads to an inhibition of the S-FAP needed to obtain optimal T cell activation at the low allergen concentrations present in vivo. This novel mechanism may explain the increased allergen threshold levels found in allergen provocation tests and the reduction of late-phase reactions observed after SAV.
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