Effectiveness of inhibitors in increasing chloride threshold value for steel corrosion

This investigation was aimed at evaluating the effectiveness of corrosion inhibitors in increasing the chloride threshold value for steel corrosion. Three types of corrosion inhibitors, calcium nitrite （Ca（NO2）2）, zinc oxide （ZnO）, and N,N＇-dimethylaminoethanol （DMEA）, which respectively represented the anodic inhibitor, cathodic inhibitor, and mixed inhibitor, were chosen. The experiment was carried out in a saturated calcium hydroxide （Ca（OH）2） solution to simulate the electrolytic environment of concrete. The inhibitors were initially mixed at different levels, and then chloride ions were gradually added into the solution in several steps. The open-circuit potential （Ecorr） and corrosion current density （lcorr） determined by electrochemical impedance spectra （EIS） were used to identify the initiation of active corrosion, thereby determining the chloride threshold value. It was found that although all the inhibitors were effective in decreasing the corrosion rate of steel reinforcement, they had a marginal effect on increasing the chloride threshold value.

Assessment of early-age cracking of high-performance concrete in restrained ring specimens

High-performance concrete （HPC） is stronger and more durable than conventional concrete. However, shrinkage and shrinkage cracking are common phenomena in HPC, especially early-age cracking. This study assessed early-age cracking of HPC for two mixtures using restrained ring tests. The two mixtures were produced with water/binder mass ratio （mw/mB） of 0.22 and 0.40, respectively. The results show that, with greater steel thickness, the higher degree of restraint resulted in a higher interface pressure and earlier cracking. With steel thickness of 6 mm, 19 mm, and 30 mm, the age of cracking were, respectively, 12 days, 8 days, and 5.4 days with the mw/mB = 0.22 mixture; and 22.5 days, 12.6 days, and 7.1 days with the mw/mB= 0.40 mixture. Cases of the same steel thickness show that the ring specimens with a thicker concrete wall crack later. With the mw/mB = 0.22 mixture, concrete walls with thicknesses of 37.5 mm, 75 mm, and 112.5 mm cracked at 3.4 days, 8.0 days, and 9.8 days, respectively; with the mw/mB = 0.40 mixture, the ages of cracking were 7.1 days, 12.6 days, and 16.0 days, respectively.

Finite element model of reinforcement corrosion in concrete

A nonlinear finite element model （FEM） of the corrosion of steel reinforcement in concrete has been successfully developed on the basis of mathematical analysis of the electrochemical process of steel corrosion in concrete. The influences of the area ratio and the Tafel constants of the anode and cathode on the potential and corrosion current density have been examined with the model. It has been found that the finite element calculation is more suitable for assessing the corrosion condition of steel reinforcement than ordinary electrochemical techniques due to the fact that FEM can obtain the distributions of potential and corrosion current density on the steel surface. In addition, the local corrosion of steel reinforcement in concrete is strengthened with the decrease of both the area ratio and the Tafel constants. These results provide valuable information to the researchers who investigate steel corrosion.

South Galactic Cap u-band Sky Survey(SCUSS):Project Overview

The South Galactic Cap u-band Sky Survey （SCUSS） was established in 2009 in order to provide a photometric input catalog for target selection of the Large Sky Area Multi-Object Fiber Spectroscopic Telescope （LAMOST） project. SCUSS is an international cooperative project between National Astronomical Observatories, Chinese Academy of Sciences, and Steward Observatory at the University of Arizona, using the 90 inch （2.3 m） Bok telescope on Kitt Peak. The telescope is equipped with a prime focus camera that is composed of a mosaic of four 4096 × 4096 CCDs and has a field of view of about 1 deg2. From 2009 to 2013, SCUSS performed a sky survey of an approximately 5000 deg2 field of the South Galactic Cap in u band, including the Galactic anticenter area and the SDSS-IV extended imaging area. The limiting magnitude of SCUSS is deeper than 23 mag （at a signal-to-noise ratio of 5）. In this paper, we briefly describe the goals of this project, method of observations and data reduction, and we also introduce current and potential scientific activities related to the SCUSS project.

Targeting the P2X7 receptor in microglial cells to prevent brain inflammation

Microglial cells are the key innate immune cells in the brain and they are crucial in maintaining brain parenchyma homeostasis.Under physiological conditions,microglial cells assume a ramified morphology with a small cell body and an extensive network of fine processes,which secrete neurotrophic factors and patrol the surroundings in search for pathogens and eliminate cellular debris via phagocytosis.Microglial cells express a repertoire of pattern recognition receptors(PRRs)that enable them to detect diverse danger-associated molecular patterns(DAMPs)released from damaged cells or cells under stress,or pathogen-associated molecular patterns generated by pathogens during infection.

Mechanosensitive Piezo1 channel regulation of microglial cell function and implications to neurodegenerative diseases and neuroinflammation

Microglial cells are the key immunocompetent cells in the central nervous system (CNS) and play a crucial role in CNS health and disease (Paolicelli et al.,2022).Under the homeostatic conditions,microglial cells assume diverse and dynamic states,depending upon interactions with neighboring cells and structures in local contextual settings,continuously patrol brain parenchyma utilizing their highly mobile fine processes,phagocytize protein aggregates,unwanted synapses and cells to maintain CNS health,and secrete neurotrophic factors to support neuronal function (Colonna and Butovsky,2017;Paolicelli et al.,2022).

Melastatin-related transient receptor potential 2 channel in Aβ_(42)-induced neuroinflammation: implications to Alzheimer's disease mechanism and development of therapeutics

Alzheimer’s disease （AD） is an age-related eurodegenerative disease that represents the most common cause of dementia among the elderly people. With the increasingly aging population, AD has presented an overwhelming healthcare challenge to modern society; the World Alzheimer Report 2015 has estimated that 46.8 million people worldwide lived with dementia in 2015 and this number will rise to 74.7 million in 2030 and that the total cost of dementia was 818 billion in US$ in 2015 and will reach two trillion in 2030. Post-mortem studies have identified two histopathological hallmarks in the brains of AD patients; extracellular senile plaque with elevated deposition of amyloid β （Aβ） peptides, and intracellular neurofibrillary tangle composed of hyper-phosphorylated microtubule-associated protein tau.Etiologically, progressive neuronal loss within the cerebral cortex and hippocampus regions of the brain leads to irreversible decline in, and eventually complete loss of, memory and other cognitive functions that afflict AD patients. The widely-accepted amyloid cascade hypothesis for AD pathogenesis holds that accumulation and aggregation of neurotoxic Aβ peptides, due to imbalance of their generation and clearance as a result of changes in genetic makeup, aging and/or exposure to environmental risk factors, is a major and early trigger of AD. This hypothesis has continuously gained support by preclinical and clinical studies （Selkoe and Hardy, 2016）. However, the intensive and costly drug discovery efforts over the past decades based on such a hypothesis have proved extremely frustrating in developing effective therapeutics to treat or slow down the progress of AD, highlighting the need for more research to improve our understanding towards the cellular and molecular mechanisms by which Aβ peptides bring about neurotoxicity and cognitive dysfunction.

Evolutionary trajectory of TRPM2 channel activation by adenosine diphosphate ribose and calcium

Ion channel activation upon ligand gating triggers a myriad of biological events and,therefore,evolution of ligand gating mechanism is of fundamental importance.TRPM2,a typical ancient ion channel,is activated by adenosine diphosphate ribose(ADPR)and calcium and its activation has evolved from a simple mode in invertebrates to a more complex one in vertebrates,but the evolutionary process is still unknown.Molecular evolutionary analysis of TRPM2s from more than 280 different animal species has revealed that,the C-terminal NUDT9-H domain has evolved from an enzyme to a ligand binding site for activation,while the N-terminal MHR domain maintains a conserved ligand binding site.Calcium gating pattern has also evolved,from one Ca^(2+)-binding site as in sea anemones to three sites as in human.Importantly,we identified a new group represented by olTRPM2,which has a novel gating mode and fills the missing link of the channel gating evolution.We conclude that the TRPM2 ligand binding or activation mode evolved through at least three identifiable stages in the past billion years from simple to complicated and coordinated.Such findings benefit the evolutionary investigations of other channels and proteins.