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ABSTRACTThe consistency of temperature and grain size is crucial to the quality of the continuous casting slab. In order to study the temperature and grain size of the continuous casting slab as influenced by the cooling spray state, a cellular automatic finite element (CAFE) coupled model was developed. The model was validated by low magnification inspection and infrared temperature measurement. The process of continuous casting was simulated by numerical model. Temperature and grain size distribution in the transverse direction of the continuous casting slab can be controlled by adjusting the nozzle arrangement. The effect of different nozzle positions on the temperature field distribution in the second cooling zone of continuous casting was simulated. The optimal nozzle position was selected with the temperature distribution uniformity as the important index. When the optimized nozzle arrangement is selected, the transverse temperature and grain size of the continuous casting slab are more uniform.

The consistency of temperature and grain size is crucial to the quality of the continuous casting slab. In order to study the temperature and grain size of the continuous casting slab as influenced by the cooling spray state, a cellular automatic finite element (CAFE) coupled model was developed. The model was validated by low magnification inspection and infrared temperature measurement. The process of continuous casting was simulated by numerical model. Temperature and grain size distribution in the transverse direction of the continuous casting slab can be controlled by adjusting the nozzle arrangement. The effect of different nozzle positions on the temperature field distribution in the second cooling zone of continuous casting was simulated. The optimal nozzle position was selected with the temperature distribution uniformity as the important index. When the optimized nozzle arrangement is selected, the transverse temperature and grain size of the continuous casting slab are more uniform.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the death of motor neurons. About 10 of ALS cases are inherited (familial), and a large subset of them are caused by mutations in the gene encoding the copper-zinc superoxide dismutase (SOD1). The detection of SOD1-positive inclusions in familial ALS patients suggests the role of SOD1 aggregation underlying the pathology of familial ALS. Although SOD1 mutant proteins are different in structure, stability and activity, they all exhibit a higher aggregation propensity than wild-type SOD1. We here review the recent studies on the role of metallation states and disulfide status in the unfolding, misfolding, and aggregation of SOD1. Investigations of the mechanism of SOD1 aggregation enhance our understanding of onset and progression of ALS and have implications for therapeutic approaches for treating ALS.