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Thus, targeting bioavailable forms of iron via iron chelation in an energy-deprived context could weaken ferroptosis defences, which would explain the paradoxical clinical worsening in iron chelator trials [33,34]

Therefore, we next performed snRNA-seq on the hearts of mice from both the control and PD-1 inhibitor groups to evaluate the effects of the PD-1 inhibitor on other cardiac cell types and the changes in their transcriptional profiles

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This data correlates well with previous work focusing on PC activation and purification from prothrombin complex concentrate (PCC) in which 5% w/w human thrombin to PC was incubated at 37 C for 3 h to achieve optimum APC generation 13

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