RESUMEN
Natural sand has a loose and porous structure with low strength, and is prone to many geoengineering problems that cause huge losses. In this study, an organic polymer-polymer-fiber blend was used to improve the strength of sand. Using a series of laboratory and numerical simulation tests, researchers have investigated the microdamage behavior of an organic polymer and fiber-treated sand in various types of mechanical tests and explored the improvement mechanism. The results showed that the polymer- and fiber-treated sand enhanced the integrity and exhibited differential damage responses under different test conditions. The increase in polymer content induced uniform force transfer, leading to a wider range of particle motion and crack initiation, whereas the fibers adhered and confined the surrounding particles, inducing an arching force chain and dispersive/buckling cracking. Polymer- and fiber-treated sands increased their energy-carrying capacity and improved their energy release, which affected the damage characteristics. Organic polymers, fibers, and sand particles were wrapped around each other to form an effective interlocking structure, which enhances the integrity and mechanical properties of sand. This study provides novel ideas and methods in the polymer-fiber composite treatment of sand in the microscopic field.
RESUMEN
Oligodendrocytes are the myelin-producing cells of the central nervous system (CNS). A variety of brain disorders from "classical" demyelinating diseases, such as multiple sclerosis, stroke, schizophrenia, depression, Down syndrome and autism, are shown myelination defects. Oligodendrocyte myelination is regulated by a complex interplay of intrinsic, epigenetic and extrinsic factors. Gpr17 (G protein-coupled receptor 17) is a G protein-coupled receptor, and has been identified to be a regulator for oligodendrocyte development. Here, we demonstrate that the absence of Gpr17 enhances remyelination in vivo with a toxin-induced model whereby focal demyelinated lesions are generated in spinal cord white matter of adult mice by localized injection of LPC(L-a-lysophosphatidylcholine). The increased expression of the activated form of Erk1/2 (phospho-Erk1/2) in lesion areas suggested the potential role of Erk1/2 activity on the Gpr17-dependent modulation of myelination. The absence of Gpr17 enhances remyelination is correlate with the activated Erk1/2 (phospho-Erk1/2).Being a membrane receptor, Gpr17 represents an ideal druggable target to be exploited for innovative regenerative approaches to acute and chronic CNS diseases.