| 1. |
- Armesto, N., et al.
(författare)
-
Heavy-ion collisions at the LHC-Last call for predictions
- 2008
-
Ingår i: Journal of Physics G. - : IOP Publishing. - 0954-3899 .- 1361-6471. ; 35:5, s. 054001-
-
Forskningsöversikt (refereegranskat)abstract
- This writeup is a compilation of the predictions for the forthcoming Heavy Ion Program at the Large Hadron Collider, as presented at the CERN Theory Institute 'Heavy Ion Collisions at the LHC - Last Call for Predictions', held from 14th May to 10th June 2007.
|
|
| 2. |
- Aad, G., et al.
(författare)
-
The ATLAS Experiment at the CERN Large Hadron Collider
- 2008
-
Ingår i: Journal of Instrumentation. - 1748-0221. ; 3:S08003
-
Forskningsöversikt (refereegranskat)abstract
- The ATLAS detector as installed in its experimental cavern at point 1 at CERN is described in this paper. A brief overview of the expected performance of the detector when the Large Hadron Collider begins operation is also presented.
|
|
| 3. |
- Ray, A. K., et al.
(författare)
-
Damage resistance of a thermal barrier coated superalloy used in aero turbine blade under accelerated creep condition
- 2009
-
Ingår i: High Temperature Materials and Processes. - 0334-6455 .- 2191-0324. ; 28:1-2, s. 35-53
-
Tidskriftsartikel (refereegranskat)abstract
- This paper highlights the hot tensile and accelerated creep properties of a thermal barrier coated (TBC) AE 437A alloy used as a candidate blade material in aero engines. Acoustic emission technique has been utilised to characterise the ductile-brittle transition temperature of the bond coat. Results revealed that the DBTT (ductile to brittle transition temperature) of this bond coat is around 923 K, which is in close proximity to the value reported for NiCoCrAlY type of bond coat. Finite element technique used for analysing the equivalent stresses in the bond coat well within the elastic limit, revealed highest order of equivalent stress at 1073 K as the bond coat is ductile above 923 K. The lifetime of the TBC coated superai loy was superior to that of the bare substrate and that oxidation is likely the cause of the reduced life of the bare substrate as compared to the coated substrate while stress rupture or accelerated creep experiments are carried out in an oxidizing environment.. Delamination of the bond coat and that of the TBC at high stresses during accelerated creep was evident. During accelerated creep, the mode of fracture in the substrate at very high stresses was transgranular whereas that at low stresses was intergranular.
|
|
| 4. |
|
|
| 5. |
- Flach, Carl-Fredrik, 1977, et al.
(författare)
-
Broad up-regulation of innate defense factors during acute cholera.
- 2007
-
Ingår i: Infection and immunity. - 0019-9567. ; 75:5, s. 2343-50
-
Tidskriftsartikel (refereegranskat)abstract
- We used a whole-genome microarray screening system (Affymetrix human GeneChips covering 47,000 different transcripts) to examine the gene expression in duodenal mucosa during acute cholera. Biopsies were taken from the duodenal mucosa of seven cholera patients 2 and 30 days after the onset of diarrhea, and the gene expression patterns in the acute- and convalescent-phase samples were compared pairwise. Of about 21,000 transcripts expressed in the intestinal epithelium, 29 were defined as transcripts that were up-regulated and 33 were defined as transcripts that were down-regulated during acute cholera. The majority of the up-regulated genes characterized were found to have an established or possible role in the innate defense against infections; these genes included the LPLUNC1, LF, VCC1, TCN1, CD55, SERPINA3, MMP1, MMP3, IL1B, LCN2, SOCS3, GDF15, SLPI, CXCL13, and MUC1 genes. The results of confirmative PCR correlated well with the microarray data. An immunohistochemical analysis revealed increased expression of lactoferrin in lamina propria cells and increased expression of CD55 in epithelial cells, whereas increased expression of the SERPINA3 protein (alpha1-antichymotrypsin) was detected in both lamina propria and epithelial cells during acute cholera. The expression pattern of CD55 and SERPINA3 in cholera toxin (CT)-stimulated Caco-2 cells was the same as the pattern found in the intestinal mucosa during acute cholera, indicating that the activation of the CD55 and SERPINA3 genes in intestinal epithelium was induced by CT. In conclusion, during acute cholera infection, innate defense mechanisms are switched on to an extent not described previously. Both direct effects of CT on the epithelial cells and changes in the lamina propria cells contribute to this up-regulation.
|
|
| 6. |
- Flach, Carl-Fredrik, 1977, et al.
(författare)
-
Differential expression of intestinal membrane transporters in cholera patients.
- 2007
-
Ingår i: FEBS letters. - : Wiley. - 0014-5793. ; 581:17, s. 3183-8
-
Tidskriftsartikel (refereegranskat)abstract
- Vibrio cholerae causes the cholera disease through secretion of cholera toxin (CT), resulting in severe diarrhoea by modulation of membrane transporters in the intestinal epithelium. Genes encoding membrane-spanning transporters identified as being differentially expressed during cholera disease in a microarray screening were studied by real-time PCR, immunohistochemistry and in a CaCo-2 cell model. Two amino acid transporters, SLC7A11 and SLC6A14, were upregulated in acute cholera patients compared to convalescence. Five other transporters were downregulated; aquaporin 10, SLC6A4, TRPM6, SLC23A1 and SLC30A4, which have specificity for water, serotonin (5-HT), magnesium, vitamin C and zinc, respectively. The majority of these changes appear to be attempts of the host to counteract the secretory response. Our results also support the concept that epithelial cells are involved in 5-HT signalling during acute cholera.
|
|
| 7. |
|
|
