Structure determination of Ba5_5 AlF13_{13} by coupling electron, synchrotron and neutron powder diffraction, solid-state NMR and ab initio calculations

International audienceThe room temperature structure of Ba$_5$ AlF$_{13}$ has been investigated by coupling electron, synchrotron and neutron powder diffraction, solid-state high-resolution NMR ($^{19}$F and $^{27}$Al) and first principles calculations. An initial structural model has been obtained from electron and synchrotron powder diffraction data, and its main features have been confirmed by one-and two-dimensional NMR measurements. However, DFT GIPAW calculations of the $^{19}$F isotropic shieldings revealed an inaccurate location of one fluorine site (F3, site 8a), which exhibited unusual long F–Ba distances. The atomic arrangement was reinvestigated using neutron powder diffraction data. Subsequent Fourier maps showed that this fluorine atom occupies a crystallographic site of lower symmetry (32e) with partial occupancy (25%). GIPAW computations of the NMR parameters validate the refined structural model, ruling out the presence of local static disorder and indicating that the partial occupancy of this F site reflects a local motional process. Visualisation of the dynamic process was then obtained from the Rietveld refinement of neutron diffraction data using an anharmonic description of the displacement parameters to account for the thermal motion of the mobile fluorine. The whole ensemble of powder diffraction and NMR data, coupled with first principles calculations , allowed drawing an accurate structural model of Ba$_5$ AlF$_{13}$ , including site-specific dynamical disorder in the fluorine sub-network

Dose- and time-dependence of L-NAME neuroprotection in transient focal cerebral ischaemia in rats

1. In this study the effect of the dose and administration time of N(G)-nitro-L-arginine methyl ester (L-NAME), an NO-synthase inhibitor, in a model of transient focal cerebral ischaemia in rats was investigated. 2. Two injections of L-NAME were given, of 1, 3 and 10 mg kg(−1), 5 min and 3 h after the onset of ischaemia. None of the doses gave any striatal neuroprotection, but 1 and 3 mg kg(−1) L-NAME reduced the infarcted volume in the cortex (by 26%, P<0.01 for 1 mg kg(−1) and 21%, P<0.05 for 3 mg kg(−1)), whereas 10 mg kg(−1) had no neuroprotective effect. 3. Single injections of L-NAME 1 mg kg(−1), given 5 min or 3 h after ischaemia onset, had similar neuroprotective effects on the cortical infarction as did the repeated injections. 4. L-NAME 1 mg kg(−1) given 3, 6 or 9 h after ischaemia induction reduced the cortical infarct volume by 19% (P<0.01) when given 3 h after ischaemia, by 21% (P<0.01) when given at 6 h, and by 16% (P<0.5) when given at 9 h, but had no neuroprotective activity when given 12 h after ischaemia. 5. Thus a low dose of L-NAME is neuroprotective in a model of transient focal ischaemia, with a wide therapeutic window, much larger than that found for MK-801