| 31. |
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| 32. |
- Adler, SS, et al.
(författare)
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Production of phi mesons at midrapidity in root S-NN=200 GeVAu+Au collisions at relativistic energies
- 2005
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Ingår i: Physical Review C (Nuclear Physics). - 0556-2813. ; 72:1
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Tidskriftsartikel (refereegranskat)abstract
- We present the results of phi meson production in the K+K- decay channel from Au+Au collisions at root s(NN) =200 GeV as measured at midrapidity by the PHENIX detector at Brookhaven National Laboratory's Relativistic Heavy Ion Collider. Precision resonance centroid and width values are extracted as a function of collision centrality. No significant variation from the Particle Data Group accepted values is observed, contrary to some model predictions. The phi transverse mass spectra are fitted with a linear exponential function for which the derived inverse slope parameter is seen to be constant as a function of centrality. However, when these data are fitted by a hydrodynamic model the result is that the centrality-dependent freeze-out temperature and the expansion velocity values are consistent with the values previously derived from fitting identified charged hadron data. As a function of transverse momentum the collisions scaled peripheral-to-central yield ratio R-CP for the phi is comparable to that of pions rather than that of protons. This result lends support to theoretical models that distinguish between baryons and mesons instead of particle mass for explaining the anomalous (anti) proton yield.
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| 33. |
- Adler, SS, et al.
(författare)
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Scaling properties of proton and antiproton production in root s(NN)=200 GeV Au+Au collisions
- 2003
-
Ingår i: Physical Review Letters. - 1079-7114. ; 91:17: 172301
-
Tidskriftsartikel (refereegranskat)abstract
- We report on the yield of protons and antiprotons, as a function of centrality and transverse momentum, in Au+Au collisions at rootS(NN)=200 GeV measured at midrapidity by the PHENIX experiment at the BNL Relativistic Heavy Ion Collider. In central collisions at intermediate transverse momenta (1.5
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| 34. |
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| 35. |
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| 36. |
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| 37. |
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| 38. |
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| 39. |
- Vikhorev, PG, et al.
(författare)
-
Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes
- 2017
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Ingår i: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 7:1, s. 14829-
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Tidskriftsartikel (refereegranskat)abstract
- Dilated cardiomyopathy (DCM) is an important cause of heart failure. Single gene mutations in at least 50 genes have been proposed to account for 25–50% of DCM cases and up to 25% of inherited DCM has been attributed to truncating mutations in the sarcomeric structural protein titin (TTNtv). Whilst the primary molecular mechanism of some DCM-associated mutations in the contractile apparatus has been studied in vitro and in transgenic mice, the contractile defect in human heart muscle has not been studied. In this study we isolated cardiac myofibrils from 3 TTNtv mutants, and 3 with contractile protein mutations (TNNI3 K36Q, TNNC1 G159D and MYH7 E1426K) and measured their contractility and passive stiffness in comparison with donor heart muscle as a control. We found that the three contractile protein mutations but not the TTNtv mutations had faster relaxation kinetics. Passive stiffness was reduced about 38% in all the DCM mutant samples. However, there was no change in maximum force or the titin N2BA/N2B isoform ratio and there was no titin haploinsufficiency. The decrease in myofibril passive stiffness was a common feature in all hearts with DCM-associated mutations and may be causative of DCM.
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| 40. |
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