Experimental discrimination of ion stopping models near the Bragg peak in highly ionized matter

The energy deposition of ions in dense plasmas is a key process in inertial confinement fusion that determines the α-particle heating expected to trigger a burn wave in the hydrogen pellet and resulting in high thermonuclear gain. However, measurements of ion stopping in plasmas are scarce and mostly restricted to high ion velocities where theory agrees with the data. Here, we report experimental data at low projectile velocities near the Bragg peak, where the stopping force reaches its maximum. This parameter range features the largest theoretical uncertainties and conclusive data are missing until today. The precision of our measurements, combined with a reliable knowledge of the plasma parameters, allows to disprove several standard models for the stopping power for beam velocities typically encountered in inertial fusion. On the other hand, our data support theories that include a detailed treatment of strong ion-electron collisions

Proton stopping measurements at low velocity in warm dense carbon

: Ion stopping in warm dense matter is a process of fundamental importance for the understanding of the properties of dense plasmas, the realization and the interpretation of experiments involving ion-beam-heated warm dense matter samples, and for inertial confinement fusion research. The theoretical description of the ion stopping power in warm dense matter is difficult notably due to electron coupling and degeneracy, and measurements are still largely missing. In particular, the low-velocity stopping range, that features the largest modelling uncertainties, remains virtually unexplored. Here, we report proton energy-loss measurements in warm dense plasma at unprecedented low projectile velocities. Our energy-loss data, combined with a precise target characterization based on plasma-emission measurements using two independent spectroscopy diagnostics, demonstrate a significant deviation of the stopping power from classical models in this regime. In particular, we show that our results are in closest agreement with recent first-principles simulations based on time-dependent density functional theory

Spermine attenuates carotid body glomus cell oxygen sensing by inhibiting L-type Ca2+ channels

10 páginas, 7 figuras, 1 tabla.-- et al.An increase in intracellular Ca2+ is crucial to O2 sensing by the carotid body. Polyamines have been reported to modulate both the extracellular Ca2+-sensing receptor (CaR) and voltage-gated Ca2+ channels in a number of cell types. Using RT-PCR and immunohistochemistry, the predominant voltage-gated Ca2+ channels expressed in the adult rat carotid body were L (CaV1.2) and N (CaV2.2)-type. CaR mRNA could not be amplified from carotid bodies, but the protein was expressed in the nerve endings. Spermine inhibited the hypoxia-evoked catecholamine release from isolated carotid bodies and attenuated the depolarization- and hypoxia-evoked Ca2+ influx into isolated glomus cells. In agreement with data from carotid body, recombinant CaV1.2 was also inhibited by spermine. In contrast, the positive allosteric modulator of CaR, R-568, was without effect on hypoxia-induced catecholamine release from carotid bodies and depolarization-evoked Ca2+ influx into glomus cells. These data show that spermine exerts a negative influence on carotid body O2 sensing by inhibiting L-type Ca2+ channels.We thank Amgen, Inc. (grant toDR&PJK), the Spanish Ministerio de Educacion y Ciencia (grant BFU2007-61848 to CG) and Junta de Castilla y Leon (grant VA104A08 to AR) for funding this work.Peer reviewe

Quasi universal blast wave behavior

The two major parameters of shock wave propagation in free air are the space-time diagram and the decay of the peak overpressure as a function of the radial distance. This paper proposes a very simple mathematical function which simulates the space-time diagram and then correlates the peak overpressure. Various applications are presented that validate the proposed functions. In the far field, the asymptotic behaviour is consistent with the physical phenornenon and the similitude laws are preserved. In this manner, the quasi-universal behaviour of shock wave propagation in free air is demonstrated. Very easy-to-use, the proposed functions appear as quasi-universal ones

Effects of the polyamine spermine on arterial chemoreception

Polyamines modulate many biological functions. Here we report a novel inhibitory modulation by spermine of catecholamine release by the rat carotid body and have identified the molecular mechanism underpinning it. We used molecular (RT-PCR and confocal microscopy) and functional (i.e., neurotransmitter release, patch clamp recording and calcium imaging) approaches to test the involvement of: (i) voltage-dependent calcium channels, and; (ii) the extracellular calcium-sensing receptor, CaR, a G protein-coupled receptor which is also activated by polyamines. RT-PCR and immunohistochemistry of isolated carotid bodies revealed that only Cav1.2 and Cav2.2 were expressed in type 1 cells while Cav1.3, Cav1.4, Cav2.1, Cav2.3 and Cav3.1, Cav3.2 and Cav3.3, could not be detected. CaR expression was detected exclusively in the nerve endings. In isolated carotid bodies, the hypoxia-dependent (7% O2 for 10 minutes) and depolarization-evoked catecholamine release were partially suppressed by pre- (and co)-incubation with 500µM spermine. In dissociated type 1 glomus cells intracellular calcium concentration did not change following spermine treatment, but this polyamine did inhibit the depolarisation-evoked calcium influx. Whole-cell patch clamp recordings of HEK293 cells stably transfected with Cav1.2 demonstrated that spermine inhibits this calcium channel. Interestingly, this inhibition was not apparent if the extracellular solution contained a concentration of Ba2 above 2 mM as the charge carrier. In conclusion, spermine attenuates catecholamine release by the carotid body principally via inhibition of Cav1.2. This mechanism may represent a negative feedback, which limits transmitter release during hypoxia