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The injection of CO2 at the Ketzin pilot CO2 storage site started in June 2008 and ended in August 2013. During the 62 months of injection, a total amount of about 67 kt of CO2 was injected into a saline aquifer. A third repeat three‐dimensional seismic survey, serving as the first post‐injection survey, was acquired in 2015, aiming to investigate the recent movement of the injected CO2. Consistent with the previous two time‐lapse surveys, a predominantly west–northwest migration of the gaseous CO2 plume in the up‐dip direction within the reservoir is inferred in this first post‐injection survey. No systematic anomalies are detected through the reservoir overburden. The extent of the CO2 plume west of the injection site is almost identical to that found in the 2012 second repeat survey (after injection of 61 kt); however, there is a significant decrease in its size east of the injection site. Assessment of the CO2 plume distribution suggests that the decrease in the size of the anomaly may be due to multiple factors, such as limited vertical resolution, CO2 dissolution, and CO2 migration into thin layers, in addition to the effects of ambient noise. Four‐dimensional seismic modelling based on dynamic flow simulations indicates that a dynamic balance between the newly injected CO2 after the second repeat survey and the CO2 migrating into thin layers and being dissolved was reached by the time of the first post‐injection survey. In view of the significant uncertainties in CO2 mass estimation, both patchy and non‐patchy saturation models for the Ketzin site were taken into consideration.

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Tricyclic antidepressant amitriptyline (AM) has been shown to exert neurotrophic activity on neurons. We thus explored whether AM may aid the neuronal development and protect anesthesia-induced neuro-injury in young spinal cord dorsal root ganglion (DRG) neurons.The DRG explants were prepared from 1-day-old rats. The effect of AM on aiding DRG neural development was examined by immunohistochemistry at dose-dependent manner. AM-induced changes in gene and protein expressions, and also phosphorylation states of tyrosine kinases receptor A (TrkA) and B (TrkB) in DRG, were examined by quantitative real-time polymerase chain reaction and western blot. The effect of AM on attenuating lidocaine-induced DRG neurodegeneration was examined by immunohistochemistry, and small interfering RNA (siRNA)-mediated TrkA/B down-regulation.Amitriptyline stimulated DRG neuronal development in dose-dependent manner, but exerted toxic effect at concentrations higher than 10 M. AM activated TrkA in DRG through phosphorylation, whereas it had little effect on TrkB-signaling pathway. AM reduced lidocaine-induced DRG neurodegeneration by regenerating neurites and growth cones. Moreover, the neuroprotection of AM on lidocaine-injured neurodegeneration was blocked by siRNA-mediated TrkA down-regulation, but not by TrkB down-regulation.Amitriptyline facilitated neuronal development and had protective effect on lidocaine-induced neurodegeneration, very likely through the activation of TrkA-signaling pathway in DRG.