| 1. |
- Horvath, I., et al.
(författare)
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Exhaled breath condensate: methodological recommendations and unresolved questions
- 2005
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Ingår i: Eur Respir J. ; 26:3
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Tidskriftsartikel (refereegranskat)abstract
- Collection of exhaled breath condensate (EBC) is a noninvasive method for obtaining samples from the lungs. EBC contains large number of mediators including adenosine, ammonia, hydrogen peroxide, isoprostanes, leukotrienes, nitrogen oxides, peptides and cytokines. Concentrations of these mediators are influenced by lung diseases and modulated by therapeutic interventions. Similarly EBC pH also changes in respiratory diseases. The aim of the American Thoracic Society/European Respiratory Society Task Force on EBC was to identify the important methodological issues surrounding EBC collection and assay, to provide recommendations for the measurements and to highlight areas where further research is required. Based on the currently available evidence and the consensus of the expert panel for EBC collection, the following general recommendations were put together for oral sample collection: collect during tidal breathing using a noseclip and a saliva trap; define cooling temperature and collection time (10 min is generally sufficient to obtain 1-2 mL of sample and well tolerated by patients); use inert material for condenser; do not use resistor and do not use filter between the subject and the condenser. These are only general recommendations and certain circumstances may dictate variation from them. Important areas for future research involve: ascertaining mechanisms and site of exhaled breath condensate particle formation; determination of dilution markers; improving reproducibility; employment of EBC in longitudinal studies; and determining the utility of exhaled breath condensate measures for the management of individual patients. These studies are required before recommending this technique for use in clinical practice.
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| 2. |
- Janák, K, et al.
(författare)
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Enantiomer-specific accumulation of hexabromocyclododecanes in eggs of predatory birds
- 2008
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Ingår i: Chemosphere. - : Elsevier BV. - 0045-6535. ; 73:1, Supplement 1
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Tidskriftsartikel (refereegranskat)abstract
- The diastereomeric composition of hexabromocyclododecane (HBCD) in eggs of peregrine falcon (Falco peregrinus), white-tailed sea eagle (Haliaeetus albicilla), guillemot (Uria aalge) and common tern (Sterna hirundo) as well as the guillemots’ main prey, herring (Clupea harengus) was determined by reversed-phase chromatography with triple-stage quadrupole mass spectrometric detection (LC–MS–MS). α-HBCD was the predominant diastereomer in all bird species, while in herring, γ-HBCD made a substantial contribution. Two, as yet unidentified diastereomers, were detected in common tern egg. The α-, β- and γ-HBCD (+) and (−) enantiomers were separated using a chiral stationary phase. The enantiomer fractions for α-HBCD differed substantially between different bird species as well as between guillemot and its prey, herring. Total HBCD levels determined by LC–MS–MS were comparable to those previously obtained by GC–MS.
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| 3. |
- Schumann, DM, et al.
(författare)
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The Fas pathway is involved in pancreatic beta cell secretory function
- 2007
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 104:8, s. 2861-2866
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Tidskriftsartikel (refereegranskat)abstract
- Pancreatic β cell mass and function increase in conditions of enhanced insulin demand such as obesity. Failure to adapt leads to diabetes. The molecular mechanisms controlling this adaptive process are unclear. Fas is a death receptor involved in β cell apoptosis or proliferation, depending on the activity of the caspase-8 inhibitor FLIP. Here we show that the Fas pathway also regulates β cell secretory function. We observed impaired glucose tolerance in Fas-deficient mice due to a delayed and decreased insulin secretory pattern. Expression of PDX-1, a β cell-specific transcription factor regulating insulin gene expression and mitochondrial metabolism, was decreased in Fas-deficient β cells. As a consequence, insulin and ATP production were severely reduced and only partly compensated for by increased β cell mass. Up-regulation of FLIP enhanced NF-κB activity via NF-κB-inducing kinase and RelB. This led to increased PDX-1 and insulin production independent of changes in cell turnover. The results support a previously undescribed role for the Fas pathway in regulating insulin production and release.
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