| 1. |
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
- Arsene, I. C., et al.
(författare)
-
Rapidity and centrality dependence of particle production for identified hadrons in Cu + Cu collisions at s NN =200 GeV
- 2016
-
Ingår i: Physical Review C - Nuclear Physics. - 0556-2813. ; 94:1
-
Tidskriftsartikel (refereegranskat)abstract
- The BRAHMS collaboration has measured transverse momentum spectra of pions, kaons, protons, and antiprotons at rapidities 0 and 3 for Cu+Cu collisions at sNN=200 GeV. As the collisions become more central the collective radial flow increases while the temperature of kinetic freeze-out decreases. The temperature is lower and the radial flow weaker at forward rapidity. Pion and kaon yields with transverse momenta between 1.5 and 2.5 GeV/c are suppressed for central collisions relative to scaled p+p collisions. This suppression, which increases as the collisions become more central, is consistent with jet quenching models and is also present with comparable magnitude at forward rapidity. At such rapidities, initial state effects may also be present and persistence of the meson suppression to high rapidity may reflect a combination of jet quenching and nuclear shadowing. The ratio of protons to mesons increases as the collisions become more central and is largest at forward rapidities.
|
|
| 11. |
- Raval, NR, et al.
(författare)
-
Synaptic Density and Neuronal Metabolic Function Measured by Positron Emission Tomography in the Unilateral 6-OHDA Rat Model of Parkinson's Disease
- 2021
-
Ingår i: Frontiers in synaptic neuroscience. - : Frontiers Media SA. - 1663-3563. ; 13, s. 715811-
-
Tidskriftsartikel (refereegranskat)abstract
- Parkinson’s disease (PD) is caused by progressive neurodegeneration and characterised by motor dysfunction. Neurodegeneration of dopaminergic neurons also causes aberrations within the cortico-striato-thalamo-cortical (CSTC) circuit, which has been hypothesised to lead to non-motor symptoms such as depression. Individuals with PD have both lower synaptic density and changes in neuronal metabolic function in the basal ganglia, as measured using [11C]UCB-J and [18F]FDG positron emission tomography (PET), respectively. However, the two radioligands have not been directly compared in the same PD subject or in neurodegeneration animal models. Here, we investigate [11C]UCB-J binding and [18F]FDG uptake in the CSTC circuit following a unilateral dopaminergic lesion in rats and compare it to sham lesioned rats. Rats received either a unilateral injection of 6-hydroxydopamine (6-OHDA) or saline in the medial forebrain bundle and rostral substantia nigra (n = 4/group). After 3 weeks, all rats underwent two PET scans using [18F]FDG, followed by [11C]UCB-J on a separate day. [18F]FDG uptake and [11C]UCB-J binding were both lower in the ipsilateral striatal regions compared to the contralateral regions. Using [11C]UCB-J, we could detect an 8.7% decrease in the ipsilateral ventral midbrain, compared to a 2.9% decrease in ventral midbrain using [18F]FDG. Differential changes between hemispheres for [11C]UCB-J and [18F]FDG outcomes were also evident in the CSTC circuit’s cortical regions, especially in the orbitofrontal cortex and medial prefrontal cortex where higher synaptic density yet lower neuronal metabolic function was observed, following lesioning. In conclusion, [11C]UCB-J and [18F]FDG PET can detect divergent changes following a dopaminergic lesion in rats, especially in cortical regions that are not directly affected by the neurotoxin. These results suggest that combined [11C]UCB-J and [18F]FDG scans could yield a better picture of the heterogeneous cerebral changes in neurodegenerative disorders.
|
|
