| 1. |
|
|
| 2. |
|
|
| 3. |
- Ronkainen, P. H., et al.
(författare)
-
Postmenopausal hormone replacement therapy modifies skeletal muscle composition and function: a study with monozygotic twin pairs
- 2009
-
Ingår i: J Appl Physiol. - : American Physiological Society. - 8750-7587. ; 107:1, s. 25-33
-
Tidskriftsartikel (refereegranskat)abstract
- We investigated whether long-term hormone replacement therapy (HRT) is associated with mobility and lower limb muscle performance and composition in postmenopausal women. Fifteen 54- to 62-yr-old monozygotic female twin pairs discordant for HRT were recruited from the Finnish Twin Cohort. Habitual (HWS) and maximal (MWS) walking speeds over 10 m, thigh muscle composition, lower body muscle power assessed as vertical jumping height, and maximal isometric hand grip and knee extension strengths were measured. Intrapair differences (IPD%) with 95% confidence intervals (CI) were calculated. The mean duration of HRT use was 6.9 +/- 4.1 yr. MWS was on average 7% (0.9 to 13.1%, P = 0.019) and muscle power 16% (-0.8 to 32.8%, P = 0.023) greater in HRT users than in their cotwins. Thigh muscle cross-sectional area tended to be larger (IPD% = 6%, 95% CI: -0.07 to 12.1%, P = 0.065), relative muscle area greater (IPD% = 8%, CI: 0.8 to 15.0%, P = 0.047), and relative fat area smaller (IPD% = -5%, CI: -11.3 to 1.2%, P = 0.047) in HRT users than in their sisters. There were no significant differences in maximal isometric strengths or HWS between users and nonusers. Subgroup analyses revealed that estrogen-containing therapies (11 pairs) significantly decreased total body and thigh fat content, whereas tibolone (4 pairs) tended to increase muscle cross-sectional area. This study showed that long-term HRT was associated with better mobility, greater muscle power, and favorable body and muscle composition among 54- to 62-yr-old women. The results indicate that HRT is a potential agent in preventing muscle weakness and mobility limitation in older women.
|
|
| 4. |
- Aittoniemi, J, et al.
(författare)
-
Relation among mannose-binding lectin 2 genotype, β-cell autoantibodies, and risk for type 1 diabetes in Finnish children
- 2008
-
Ingår i: Human Immunology. - : Elsevier BV. - 0198-8859 .- 1879-1166. ; 69:2, s. 108-111
-
Tidskriftsartikel (refereegranskat)abstract
- Mannose-binding lectin (MBL) is a key mediator of innate immunity, the insufficiency of which is caused by point mutations in the MBL2 gene. MBL insufficiency is associated with increased susceptibility to infections and certain autoimmune diseases, but its impact in the pathogenesis and risk of type 1 diabetes (T1D) is controversial. We investigated the significance of the MBL2 genotype on the risk of T1D in a Finnish study population comprising 470 diabetic children and 501 controls. Furthermore, the effect of MBL2 gene polymorphism on the emergence of β-cell autoantibodies in 289 unaffected children with human leukocyte antigen-conferred susceptibility to T1D was assessed. MBL genotype had no significant effect on the risk or onset age of T1D. However, children with the biallelic variant genotype reflecting total MBL deficiency tested positive more frequently for ≥3 autoantibodies compared with children with another genotype (odds ratio = 6.0, 95% confidence interval 1.3-28, p = 0.013). In conclusion, the MBL2 genotype did not affect susceptibility to T1D in children, and this finding does not support previous reports implicating a role of the MBL2 genotype as a factor predisposing to T1D. The association of the biallelic variant genotype with positivity for multiple autoantibodies suggests that intermolecular epitope spreading may be linked with impaired clearance of autoantigens as a result of MBL deficiency. © 2008 American Society for Histocompatibility and Immunogenetics.
|
|
| 5. |
- Bonanni, L., et al.
(författare)
-
The Open Sustainability Project : A Linked Data Approach to LCA
- 2010
-
Ingår i: LCA X, Bridging Science, Policy, and the Public 2-4 November 2010, Portland, Oregon.
-
Konferensbidrag (refereegranskat)abstract
- The proprietary nature of LCA tools and information limits widespread adoption of sustainability measures. We introduce the Open Sustainability Project(OSP), a Linked Data resource for broadening access to LCA in an effort to increase the transparency and accuracy of environmental impact assessments(2, 9).The OSP applies Free and Open Source Software(FOSS) principles and Linked Data structures to LCA standards and reporting so that communities including students, SME’s and the general public can participate in the assessment and verification of sustainability practices(1,6). The highly flexible data format allows disparate data sources and assessments to be compared along an open standard compliant with ISO 14048 reporting(5, 8, 12).In addition, the OSP makes available a free database of Life Cycle Assessment data using an approach based on Linked Data and RESTful interfaces which supports the development of rich third-party applications for specific user groups and industries(7). This novel combination of linked data and web-based tools is inherently transparent so that LCA practices can be standardized, compared and verified by a broad community.The OSP is an international collaboration between academics, government and industry groups leveraging expertise in LCA, Open Data and web-based tools for sustainability(10). Our first Open Source and Open Data web sustainability tools have confirmed the potential to engage a wider audience, with over two thousand registered users, three thousand environmental assessments performed and over 330,000 page views from more than 75 countries since September 2009(3, 4, 11). The OSP aims to expand reach of LCA through a free and open Application Programming Interface(API) to support distributed development of third-party applications for sustainability assessment through the emerging metrics for social and environmental sustainability(a free LCA "App Store"). These applications are intended to disseminate LCA standards, encourage transparency in environmental reporting and leverage Collective Intelligence in the collection, publication and verification of LCA.The OSP aims to transform LCA into a collaborative process where data collection, analysis, assessment and reporting benefit from the feedback and ideas of a growing worldwide LCA community.
|
|
| 6. |
|
|
| 7. |
- Obase, Y, et al.
(författare)
-
Effects of inhaled corticosteroids on metalloproteinase-8 and tissue inhibitor of metalloproteinase-1 in the airways of asthmatic children
- 2010
-
Ingår i: International archives of allergy and immunology. - : S. Karger AG. - 1423-0097 .- 1018-2438. ; 151:3, s. 247-254
-
Tidskriftsartikel (refereegranskat)abstract
- <i>Background:</i> The effects of corticosteroids on the level and expression of matrix metalloproteinase-8 (MMP-8; collagenase-2) and tissue inhibitors of metalloproteinases (TIMPs) in airway tissue are poorly characterized in vivo. <i>Methods:</i> We compared MMP-8 and TIMP-1 levels in induced sputum and their expression in airway inflammatory cells of healthy children (n = 27) and of children with newly diagnosed asthma with mild (n = 20) or moderate symptoms (n = 19), before and after 6 months of treatment with inhaled budesonide. <i>Results:</i> At baseline, MMP-8 was higher in asthmatic children with moderate symptoms, TIMP-1 was lower and the MMP-8/TIMP-1 ratio was higher in both groups of asthmatic children compared with controls. Inhaled budesonide increased TIMP-1 levels in both groups of asthmatic children and normalized the MMP-8/TIMP-1 ratio, and this paralleled the improvement in forced expiratory volume in 1 s in children with mild symptoms. At baseline, asthmatic children had significantly more MMP-8-positive macrophages than control children, whereas the number of TIMP-1-positive macrophages was almost the same. Budesonide decreased the percentage of MMP-8-positive macrophages and increased that of TIMP-1-positive macrophages; these changes were significant in asthmatic children with mild symptoms. <i>Conclusions:</i> Inhaled budesonide normalized the MMP-8/TIMP-1 ratio in asthmatic children by upregulation of TIMP-1 production and downregulation of MMP-8 production by airway macrophages. This change may be a biochemical marker of an effect on airway inflammation and possibly of an ongoing remodeling process that should be further investigated using biopsy specimens.
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
|
|
