Prediction of long-term localized corrosion rates in a carbon steel cooling water system is enhanced by metagenome analysis

To predict variation of maximum localized penetration with exposure time, long-term localized corrosion was assessed in an emergency cooling water system composed of two carbon steel pipelines of 700 mm diameter transporting raw river water at flow velocities of 1 m/s and 0.1 m/s. Field tests, visual inspection, ultrasonic testing, BART testing, SEM-EDS and metagenomic analyses were performed to assess the progress of long-term corrosion and determine the influence of microbes in the corrosion process. High corrosion was linked to sulphate reducing bacteria and potentially to methanogenic archaea in the low-velocity pipeline, while moderate corrosion was linked to non-sulphate reducing bacteria in the higher velocity pipeline. Using historical and literature data available as well as our own test results, an empirical model was developed to predict Maximum Localized Penetration change over time to be applied in the ageing management of cooling water systems. Molecular Microbiological Methods in combination with traditional techniques are useful tools in the ageing management of pipelines. By applying the empirical model developed and the approach presented, unexpected through-wall leaking can be avoided, thus, saving costs and assets

Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation

Actin turnover in dendritic spines influences spine development, morphology, and plasticity, with functional consequences on learning and memory formation. In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways. Using in vitro models of neuronal plasticity, such as glycine-induced chemical long-term potentiation (LTP), known to evoke synaptic plasticity, or long-term depolarization block by KCl, leading to homeostatic morphological changes, we show that actin stabilization needed for the enlargement of dendritic spines is dependent on PKD activity. Consequently, impaired PKD functions attenuate activity-dependent changes in hippocampal dendritic spines, including LTP formation, cause morphological alterations in vivo, and have deleterious consequences on spatial memory formation. We thus provide compelling evidence that PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines