THE DEFECT STRUCTURE OF CALCIA STABILISED ZIRCONIA

EXAFS data comparing the local structural environments of the calcium and zirconium ions in calcia-stabilised zirconia are presented. The Zr data resembles that observed previously for yttria-stabilised zirconia with the zirconium ions tending to be displaced from their centrosymmetric sites and a Zr-O distance of 2.12 Å. These similarities suggest that anion vacancies in this material are also to be found adjacent to Zr4+. The calcium ions are not displaced from their lattice sites but their immediate anion neighbours are highly disordered resulting in at least two Ca-O distances in the radial distribution of the nearest neighbour shell

EXAFS STUDIES OF FLUORITE OXIDES

Many of the unique possibilities of EXAFS as a structural technique are illustrated in the problem of determining the local interactions between defects and anion vacancies in the fluorite oxide systems, yttria stabilised zirconia and Y2O3-doped Bi2O3. From the measured EXAFS on the Y, Zr and Bi absorption edges, it is possible to compare directly the host and dopant cation's different local structural environments. This shows that, in both systems, the Y3+ ions adopt a more ordered and isotropic local environment than the host cation. Both Bi3+ and Zr4+ tend to be displaced from their centrosymmetric sites and the static disorder in the nearest neighbour oxygen shell is comparatively extensive. For yttria-stabilised zirconia, this behaviour can be attributed to ionic relaxations in response to anion vacancies in the Zr-O shell, the anion vacancies being necessary for charge compensation of the trivalent Y3+ ions. The disorder in the Bi2O3 samples is greater than in yttria-stabilised zirconia which can be correlated with the higher anion conductivity in the former. The preference that the host cations exhibit for anisotropic co-ordination geometries can be explained by their high polarisabilities due to the high charge and small size of the Zr4+ ion and the lone electron pair on the Bi3+ ion

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases:subgroup analyses of the RESTART randomised, open-label trial

Background: Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy. Methods: RESTART was a prospective, randomised, open-label, blinded-endpoint, parallel-group trial at 122 hospitals in the UK that assessed whether starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. For this prespecified subgroup analysis, consultant neuroradiologists masked to treatment allocation reviewed brain CT or MRI scans performed before randomisation to confirm participant eligibility and rate features of the intracerebral haemorrhage and surrounding brain. We followed participants for primary (recurrent symptomatic intracerebral haemorrhage) and secondary (ischaemic stroke) outcomes for up to 5 years (reported elsewhere). For this report, we analysed eligible participants with intracerebral haemorrhage according to their treatment allocation in primary subgroup analyses of cerebral microbleeds on MRI and in exploratory subgroup analyses of other features on CT or MRI. The trial is registered with the ISRCTN registry, number ISRCTN71907627. Findings: Between May 22, 2013, and May 31, 2018, 537 participants were enrolled, of whom 525 (98%) had intracerebral haemorrhage: 507 (97%) were diagnosed on CT (252 assigned to start antiplatelet therapy and 255 assigned to avoid antiplatelet therapy, of whom one withdrew and was not analysed) and 254 (48%) underwent the required brain MRI protocol (122 in the start antiplatelet therapy group and 132 in the avoid antiplatelet therapy group). There were no clinically or statistically significant hazards of antiplatelet therapy on recurrent intracerebral haemorrhage in primary subgroup analyses of cerebral microbleed presence (2 or more) versus absence (0 or 1) (adjusted hazard ratio [HR] 0·30 [95% CI 0·08–1·13] vs 0·77 [0·13–4·61]; pinteraction=0·41), cerebral microbleed number 0–1 versus 2–4 versus 5 or more (HR 0·77 [0·13–4·62] vs 0·32 [0·03–3·66] vs 0·33 [0·07–1·60]; pinteraction=0·75), or cerebral microbleed strictly lobar versus other location (HR 0·52 [0·004–6·79] vs 0·37 [0·09–1·28]; pinteraction=0·85). There was no evidence of heterogeneity in the effects of antiplatelet therapy in any exploratory subgroup analyses (all pinteraction>0·05). Interpretation: Our findings exclude all but a very modest harmful effect of antiplatelet therapy on recurrent intracerebral haemorrhage in the presence of cerebral microbleeds. Further randomised trials are needed to replicate these findings and investigate them with greater precision. Funding: British Heart Foundation