Multicomponent theory of buoyancy instabilities in magnetized plasmas: The case of magnetic field parallel to gravity

We investigate electromagnetic buoyancy instabilities of the electron-ion plasma with the heat flux based on not the magnetohydrodynamic (MHD) equations, but using the multicomponent plasma approach when the momentum equations are solved for each species. We consider a geometry in which the background magnetic field, gravity, and stratification are directed along one axis. The nonzero background electron thermal flux is taken into account. Collisions between electrons and ions are included in the momentum equations. No simplifications usual for the one-fluid MHD-approach in studying these instabilities are used. We derive a simple dispersion relation, which shows that the thermal flux perturbation generally stabilizes an instability for the geometry under consideration. This result contradicts to conclusion obtained in the MHD-approach. We show that the reason of this contradiction is the simplified assumptions used in the MHD analysis of buoyancy instabilities and the role of the longitudinal electric field perturbation which is not captured by the ideal MHD equations. Our dispersion relation also shows that the medium with the electron thermal flux can be unstable, if the temperature gradients of ions and electrons have the opposite signs. The results obtained can be applied to the weakly collisional magnetized plasma objects in laboratory and astrophysics.Comment: Accepted for publication in Astrophysics & Space Scienc

Search for long-lived neutral particles in pp collisions at s√=13 TeV that decay into displaced hadronic jets in the ATLAS calorimeter

This paper describes a search for pairs of neutral, long-lived particles decaying in the ATLAS calorimeter. Long-lived particles occur in many extensions to the Standard Model and may elude searches for new promptly decaying particles. The analysis considers neutral, long-lived scalars with masses between 5 and 400 GeV, produced from decays of heavy bosons with masses between 125 and 1000 GeV, where the long-lived scalars decay into Standard Model fermions. The analysis uses either 10.8 fb−1 or 33.0 fb−1 of data (depending on the trigger) recorded in 2016 at the LHC with the ATLAS detector in proton–proton collisions at a centre-of-mass energy of 13 TeV. No significant excess is observed, and limits are reported on the production cross section times branching ratio as a function of the proper decay length of the long-lived particles

Angiotensin II type 1 autoantibody induced hypertension during pregnancy is associated with renal endothelial dysfunction

BACKGROUND: Previous investigations suggested that agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA) might mediate a hypertensive response through dysregulation of the endothelin-1 system. AT1-AA induced hypertension was attenuated by the AT1 receptor and/or endothelin-1 type A receptor antagonists. OBJECTIVES: This study was undertaken to determine if AT1-AA induced hypertension was associated with renal endothelial dysfunction. METHODS: We compared the vascular reactivity of renal interlobar arteries from normal pregnant control rats and AT1-AA long-term infused pregnant rats in the presence and absence of endothelin type A (ET(A)) receptor antagonism. Renal endothelial function was tested using isolated renal interlobar arteries in a pressure myograph, which were exposed to acetylcholine or sodium nitroprusside. RESULTS: Vasodilatory responses to the endothelial-dependent agonist acetylcholine were impaired in AT1-AA rats (74 [10]%) compared with normal pregnant controls (95 [5]%, P < 0.05). In the presence of ET(A) receptor antagonism, no differences were observed between controls or the AT1-AA treated group with regard to endothelial-dependent (acetylcholine) relaxation. CONCLUSION: AT1-AA induced hypertension during pregnancy was associated with disparate renal endothelial responses to acetylcholine. The difference in renal vascular responses between AT1-AA and normal pregnant rats was abolished by ET(A) receptor blockade