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a b s t r a c tThe promise of the LaeFeeSi alloys for energy efficient magnetic refrigeration devices stems from a strong magneto-structural transition in the La(Fe,Si) 13 (1:13) phase near room temperature. The formation of the 1:13 phase during rapid solidification was compared in detailed microstructural studies of the wheel-side and free-side surfaces of melt-spun ribbons. On the free-side, clusters of similarlyoriented crystallites are observed; chemical segregation of La, Fe, and Si leads to a nanoscale texturing of a-Fe and LaFeSi. In contrast, equiaxed 1:13 grains~100e400 nm form the microstructure of the wheelside surface, with a minor a-Fe phase precipitated in the matrix. Upon annealing, the 1:13 phase grows via dissolution of the a-Fe phase on the wheel side and a peritectoid reaction from the free side. For longer annealing times, the completion of the peritectoid reaction improves the magnetic entropy change under a magnetic field change of 1.5 T from 12 J/kg K (2 min) to 17 J/kg K (2 h), and increases the Curie temperature of the ribbons from 189 K to 201 K.

Autophagy is an evolutionarily conserved lysosomal degradation pathway that maintains metabolism and homeostasis by eliminating protein aggregates and damaged organelles. Many studies have reported that autophagy plays an important role in spinal cord injury (SCI). However, the spatiotemporal patterns of autophagy activation after traumatic SCI are contradictory. Most studies show that the activation of autophagy and inhibition of apoptosis have neuroprotective effects on traumatic SCI. However, reports demonstrate that autophagy is strongly associated with distal neuronal death and the impaired functional recovery following traumatic SCI. This article introduces SCI pathophysiology, the physiology and mechanism of autophagy, and our current review on its role in traumatic SCI. We also discuss the interaction between autophagy and apoptosis and the therapeutic effect of activating or inhibiting autophagy in promoting functional recovery. Thus, we aim to provide a theoretical basis for the biological therapy of SCI.

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