This paper focuses on an estimation of light weighting opportunities for the frame structure of commercial road vehicles. This estimation is based on simplified static load cases which play a predominant role for the dimensioning of a frame structure and therefore these simplifications are not putting the general validity of the conclusions into question. A comparison of different materials under this scenario shows that light metals do not show any weight reduction advantage in comparison to steel while a material-independent topology optimization has more weight reduction potential for the frame structure than a simple change of materials. Considering the constraints of part complexity which is directly linked with production and assembly cost, the ladder frame structure has become the current state of the art design. Thus the paper also puts a spotlight on basic rules of node design and vertical load induction in order to keep the weight of such a design as low as possible. Practical examples from manufacturers show that the weight of a commercial vehicle could be reduced by 10% and main parts of the frame structure could be reduced by 30% using high strength steel in combination with innovative production methods like roll forming.

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Spinal cord injury is characterized by different aetiologies, complex pathogenesis, and diverse pathological changes. Current treatments are not ideal, and prognosis is generally poor. After spinal cord injury, neurons die due to various forms of cell death. Among them, ferroptosis causes dysfunction after spinal cord injury, and no existing traditional treatments have been indicated to block its occurrence. Meanwhile, emerging therapies using mesenchymal stem cells, extracellular vesicles, and transcranial magnetic stimulation therapy are promising for reversing spinal cord neuronal ferroptosis after spinal cord injury. However, no definitive studies have demonstrated the effectiveness of these approaches. This review summarizes the existing research on the mechanisms of ferroptosis; ferroptosis after spinal cord injury; treatment of spinal cord injury with mesenchymal stem cells, extracellular vesicles, and transcranial magnetic stimulation; and treatment of ferroptosis using mesenchymal stem cells, extracellular vesicles, and transcranial magnetic stimulation. Inhibiting ferroptosis can promote the reversal of neurological dysfunction after spinal cord injury. In addition, mesenchymal stem cells, extracellular vesicles, and transcranial magnetic stimulation can reverse adverse outcomes of spinal cord injury and regulate ferroptosis-related factors. Thus, it can be inferred that mesenchymal stem cells, extracellular vesicles, and transcranial magnetic stimulation have the potential to inhibit ferroptosis after spinal cord injury. This review serves as a reference for future research to confirm these conclusions.