| 1. |
- Brenninkmeijer, C. A. M., et al.
(författare)
-
Civil Aircraft for the regular investigation of the atmosphere based on an instrumented container: The new CARIBIC system
- 2007
-
Ingår i: Atmospheric Chemistry and Physics. - 1680-7324. ; 7:18, s. 4953-4976
-
Tidskriftsartikel (refereegranskat)abstract
- An airfreight container with automated instruments for measurement of atmospheric gases and trace compounds was operated on a monthly basis onboard a Boeing 767-300 ER of LTU International Airways during long-distance flights from 1997 to 2002 (CARIBIC, Civil Aircraft for Regular Investigation of the Atmosphere Based on an Instrument Container, http://www.caribic-atmospheric.com). Subsequently a more advanced system has been developed, using a larger capacity container with additional equipment and an improved inlet system. CARIBIC phase #2 was implemented on a new long-range aircraft type Airbus A340-600 of the Lufthansa German Airlines (Star Alliance) in December 2004, creating a powerful flying observatory. The instrument package comprises detectors for the measurement of O-3, total and gaseous H2O, NO and NOy, CO, CO2, O-2, Hg, and number concentrations of sub-micrometer particles (>4 nm, >12 nm, and >18 nm diameter). Furthermore, an optical particle counter (OPC) and a proton transfer mass spectrometer (PTR-MS) are incorporated. Aerosol samples are collected for analysis of elemental composition and particle morphology after flight. Air samples are taken in glass containers for laboratory analyses of hydrocarbons, halocarbons and greenhouse gases (including isotopic composition of CO2) in several laboratories. Absorption tubes collect oxygenated volatile organic compounds. Three differential optical absorption spectrometers (DOAS) with their telescopes mounted in the inlet system measure atmospheric trace gases such as BrO, HONO, and NO2. A video camera mounted in the inlet provides information about clouds along the flight track. The flying observatory, its equipment and examples of measurement results are reported.
|
|
| 2. |
|
|
| 3. |
- Cegelski, Lynette, et al.
(författare)
-
Small-molecule inhibitors target Escherichia coli amyloid biogenesis and biofilm formation
- 2009
-
Ingår i: Nature Chemical Biology. - : Nature Publishing Group. - 1552-4450 .- 1552-4469. ; 5:12, s. 913-919
-
Tidskriftsartikel (refereegranskat)abstract
- Curli are functional extracellular amyloid fibers produced by uropathogenic Escherichia coli (UPEC) and other Enterobacteriaceae. Ring-fused 2-pyridones, such as FN075 and BibC6, inhibited curli biogenesis in UPEC and prevented the in vitro polymerization of the major curli subunit protein CsgA. The curlicides FN075 and BibC6 share a common chemical lineage with other ring-fused 2-pyridones termed pilicides. Pilicides inhibit the assembly of type1pili, which are required for pathogenesis during urinary tract infection. Notably, the curlicides retained pilicide activities and inhibited both curli-dependent and type 1–dependent biofilms. Furthermore, pretreatment of UPEC with FN075 significantly attenuated virulence in a mouse model of urinary tract infection. Curli and type 1pili exhibited exclusive and independent roles in promoting UPEC biofilms, and curli provided a fitness advantage in vivo. Thus, the ability of FN075 to block the biogenesis of both curli and type 1pili endows unique anti-biofilm and anti-virulence activities on these compounds.
|
|
| 4. |
|
|
| 5. |
- Graslund, S, et al.
(författare)
-
Protein production and purification
- 2008
-
Ingår i: Nature methods. - : Springer Science and Business Media LLC. - 1548-7105 .- 1548-7091. ; 5:2, s. 135-146
-
Tidskriftsartikel (refereegranskat)
|
|
| 6. |
|
|
| 7. |
- Hung, Rayjean J, et al.
(författare)
-
A susceptibility locus for lung cancer maps to nicotinic acetylcholine receptor subunit genes on 15q25
- 2008
-
Ingår i: Nature. - : Nature Publishing Group. - 0028-0836 .- 1476-4687. ; 452:7187, s. 633-637
-
Tidskriftsartikel (refereegranskat)abstract
- Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 x 10(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 x 10(-20) overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to N'-nitrosonornicotine and potential lung carcinogens. A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.
|
|
| 8. |
- Kellen, Eliane, et al.
(författare)
-
Pooled analysis and meta-analysis of the glutathione S-transferase P1 lle 105Val polymorphism and bladder cancer: A HuGE-GSEC review
- 2007
-
Ingår i: American Journal of Epidemiology. - : Oxford University Press (OUP). - 0002-9262 .- 1476-6256. ; 165:11, s. 1221-1230
-
Forskningsöversikt (refereegranskat)abstract
- The glutathione S-transferase P1 genotype (GSTP1) is involved in the inactivation of cigarette smoke carcinogens, and sequence variation in the gene may alter bladder cancer susceptibility. To examine the association between GSTP1lle 105Val and bladder cancer, the authors undertook a meta- and pooled analysis. Summary crude and adjusted odds ratios and corresponding 95% confidence intervals were pooled by using a random-effects model. In the meta-analysis (16 studies, 4,273 cases and 5,081 controls), the unadjusted summary odds ratios for GSTP1 lle/Val and Val/Val compared with GSTP1 lle/lle were 1.54 (95% confidence interval: 1.21,1.99; p < 0.001) and 2.17 (95% confidence interval: 1.27, 3.71; p = 0.005). The association appeared to be the strongest in Asian countries. When the analysis was limited to European descendents (nine studies), the summary odds ratio decreased (odds ratio = 1.24, 95% confidence interval: 1.00, 1.52) (Q = 17.50; p = 0.02). All relevant data previously contributed to the International Study on Genetic Susceptibility to Environmental Carcinogens were pooled (eight studies, 1,305 cases and 1,558 controls). The summary odds ratios were similar to the ones from the meta-analysis. Case-only analyses did not detect an interaction between the GSTP1 genotype and smoking status (never/ever). GSTP1 lle 105Val appears to be associated with a modest increase in the risk of bladder cancer.
|
|
| 9. |
|
|
| 10. |
- McKay, James D., et al.
(författare)
-
Lung cancer susceptibility locus at 5p15.33
- 2008
-
Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 40:12, s. 1404-1406
-
Tidskriftsartikel (refereegranskat)abstract
- We carried out a genome-wide association study of lung cancer (3,259 cases and 4,159 controls), followed by replication in 2,899 cases and 5,573 controls. Two uncorrelated disease markers at 5p15.33, rs402710 and rs2736100 were detected by the genome-wide data (P - 2 x 10(-7) and P = 4 x 10(-6)) and replicated by the independent study series (P = 7 x 10(-5) and P = 0.016). The susceptibility region contains two genes, TERT and CLPTM1L, suggesting that one or both may have a role in lung cancer etiology.
|
|
