Spatiotemporal blocking of the bouncy particle sampler for efficient inference in state-space models

Abstract: We propose a novel blocked version of the continuous-time bouncy particle sampler of Bouchard-Côté et al. (J Am Stat Assoc 113(522):855–867, 2018) which is applicable to any differentiable probability density. This alternative implementation is motivated by blocked Gibbs sampling for state-space models (Singh et al. in Biometrika 104(4):953–969, 2017) and leads to significant improvement in terms of effective sample size per second, and furthermore, allows for significant parallelization of the resulting algorithm. The new algorithms are particularly efficient for latent state inference in high-dimensional state-space models, where blocking in both space and time is necessary to avoid degeneracy of MCMC. The efficiency of our blocked bouncy particle sampler, in comparison with both the standard implementation of the bouncy particle sampler and the particle Gibbs algorithm of Andrieu et al. (J R Stat Soc Ser B Stat Methodol 72(3):269–342, 2010), is illustrated numerically for both simulated data and a challenging real-world financial dataset

Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen

The aim of this study was to evaluate the effect of acetazolamide on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2). CBF, arterial and jugular venous partial O2 pressure, partial CO2 pressure, pH, and O2 saturation percentage were measured in six patients before and 3 and 20 minutes after intravenous administration of 1 g of acetazolamide. CBF was measured by the intracarotid 133xenon injection technique. In addition, changes in CBF were estimated from the arteriovenous oxygen content difference. CBF increased in all patients after acetazolamide, by approximately 55 and 70% after 3 and 20 min, respectively. The CBF changes were of the same order whether calculated from the 133Xe clearance or from the arteriovenous oxygen differences (A-V)O2. CMRO2, calculated from (A-V)O2 differences and CBF, remained constant. Except for an increase in the venous oxygen saturation, the blood gases remained constant. Acetazolamide, in a dose sufficient to inhibit the erythrocyte carbonic anhydrase (EC 4.2.1.1), thus induced a rapid and marked increase in CBF, leaving CMRO2 unchanged. This effect of acetazolamide on CBF is probably explained by a decrease in brain pH rather than by brain tissue hypoxia due to inhibition of oxygen unloading in the brain capillaries