Magnesium and its alloys have limited wide applications due to their poor corrosion resistance. In this study, copper coating used as a plating nickel substrate was directly electrodeposited on AZ31 magnesium alloy from copper hydroxide and citrate bath with the addition of fluorine ion and additives using direct current. Copper coating was characterised using scanning electron microscopy (SEM) for observing surface and cross-section morphology of copper coating, by using scratched grid test for examining adhesion strength, by using immersion test for examining corrosion resistance. Observation by SEM showed that copper coating was the typical spherical nodular structure, thus providing uniform and dense appearance of copper coating. Adhesion strength test showed that copper coating was not peeled from AZ31 magnesium alloy when copper coating scratched to form grid was pulled using adhesive tape. Immersion test in 5% (m/v) NaCl solution revealed that copper coating is a protective layer on the AZ31 magnesium alloy.
Perturbed neuronal migration and abnormal axonogenesis have been shown to be implicated in the pathogenesis of autism spectrum disorder (ASD). However, the molecular mechanism remains unknown. Here we demonstrate that dendritic cell factor 1(DCF1) is involved in neuronal migration and axonogenesis. The deletion of dcf1 in mice delays the localization of callosal projection neurons, while dcf1 overexpression restores normal migration. Delayed neurons appear as axon swelling and axonal boutons loss, resulting in a permanent deficit in the callosal projections.Western blot analysis indicates that absence of dcf1 leads to the abnormal activation of ERK signal. Differential protein expression assay shows that PEBP1, a negative regulator of the ERK signal, is significant downregulation in dcf1 KO mice. Direct interaction between DCF1 and PEBP1 is confirmed by Co-immunoprecipitation test, thus indicating that DCF1 regulates the ERK signal in a PEBP1-dependent pattern. As a result of the neurodevelopmental migration disorder, dcf1 deletion results in ASD-like behaviors in mice. This finding identifies a link between abnormal activated ERK signaling, delayed neuronal migration and autistic-like behaviors in humans.
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