| 1. |
- Aad, G., et al.
(författare)
-
- 2010
-
swepub:Mat__t
|
|
| 2. |
- Aad, G., et al.
(författare)
-
- 2010
-
swepub:Mat__t
|
|
| 3. |
- Aad, G., et al.
(författare)
-
- 2011
-
swepub:Mat__t
|
|
| 4. |
- Aad, G., et al.
(författare)
-
- 2010
-
swepub:Mat__t
|
|
| 5. |
|
|
| 6. |
- Aad, G., et al.
(författare)
-
- 2010
-
swepub:Mat__t
|
|
| 7. |
|
|
| 8. |
- Lewis, R., et al.
(författare)
-
Mapping railway wheel material wear mechanisms and transitions
- 2010
-
Ingår i: Proceedings of the Institution of mechanical engineers. Part F, journal of rail and rapid transit. - 0954-4097 .- 2041-3017. ; 224:F3, s. 125-137
-
Tidskriftsartikel (refereegranskat)abstract
- In order to develop more durable wheel materials to cope with the new specifications being imposed on wheel wear, a greater understanding of the wear mechanisms and transitions occurring in wheel steels is needed, particularly at higher load and slip conditions. The aim of this work was to draw together current understanding of the wear mechanisms, regimes, and transitions (particularly with R8T wheel material) and new tests on R7T wheel material; to identify gaps in the knowledge; and to develop new tools for assessing wear of wheel materials, such as wear maps, that can be used to improve wear prediction. Wear assessment of wheel materials, as well as wear rates, regimes, and transitions, is discussed. Twin disc wear testing, used extensively for studying wear of wheel and rail materials, has indicated that three wear regimes exist for wheel materials: mild, severe, and catastrophic. These have been classified in terms of wear rate and features. Wear rates are seen to increase steadily initially and then level off, before increasing rapidly as the severity of the contact conditions is increased. Analysis of the contact conditions in terms of friction and slip has indicated that the levelling off of the wear rate observed at the first wear transition is caused by the change from partial slip to full slip conditions at the disc interface. Temperature calculations for the contact showed that the large increase in wear rates seen at the second wear transition may result from a thermally induced reduction in yield strength and other material properties. Comparisons made between discs and actual wheels have provided some support for the theories relating to the transitions observed. Wear maps have been produced using the test results to study how individual contact parameters such as load and sliding speed influence wear rates and transitions. The maps are also correlated to expected wheel-rail contact conditions. This improved understanding of wheel wear mechanisms and transitions will help in the aim of eventually attaining a wear modelling methodology reliant on material properties rather than on wear constants derived from testing.
|
|
| 9. |
- Tricoci, Pierluigi, et al.
(författare)
-
Thrombin-receptor antagonist vorapaxar in acute coronary syndromes
- 2012
-
Ingår i: New England Journal of Medicine. - 0028-4793 .- 1533-4406. ; 366:1, s. 20-33
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND:Vorapaxar is a new oral protease-activated-receptor 1 (PAR-1) antagonist that inhibits thrombin-induced platelet activation.METHODS:In this multinational, double-blind, randomized trial, we compared vorapaxar with placebo in 12,944 patients who had acute coronary syndromes without ST-segment elevation. The primary end point was a composite of death from cardiovascular causes, myocardial infarction, stroke, recurrent ischemia with rehospitalization, or urgent coronary revascularization.RESULTS:Follow-up in the trial was terminated early after a safety review. After a median follow-up of 502 days (interquartile range, 349 to 667), the primary end point occurred in 1031 of 6473 patients receiving vorapaxar versus 1102 of 6471 patients receiving placebo (Kaplan-Meier 2-year rate, 18.5% vs. 19.9%; hazard ratio, 0.92; 95% confidence interval [CI], 0.85 to 1.01; P=0.07). A composite of death from cardiovascular causes, myocardial infarction, or stroke occurred in 822 patients in the vorapaxar group versus 910 in the placebo group (14.7% and 16.4%, respectively; hazard ratio, 0.89; 95% CI, 0.81 to 0.98; P=0.02). Rates of moderate and severe bleeding were 7.2% in the vorapaxar group and 5.2% in the placebo group (hazard ratio, 1.35; 95% CI, 1.16 to 1.58; P<0.001). Intracranial hemorrhage rates were 1.1% and 0.2%, respectively (hazard ratio, 3.39; 95% CI, 1.78 to 6.45; P<0.001). Rates of nonhemorrhagic adverse events were similar in the two groups.CONCLUSIONS:In patients with acute coronary syndromes, the addition of vorapaxar to standard therapy did not significantly reduce the primary composite end point but significantly increased the risk of major bleeding, including intracranial hemorrhage. (Funded by Merck; TRACER ClinicalTrials.gov number, NCT00527943.).
|
|
