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In patients with left main disease or severe LV dysfunction, death was the predominant event.
For example, myocardial ischemia followed by reperfusion typically manifests in microvascular dysfunction, death of myocytes, and myocardial stunning or dysfunction.
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So decreased clearance of amyloid beta increases the number of these amyloid aggregates, which cause neuronal dysfunction and death.
The generated ROS causes cell dysfunction or death when cells are exposed to drugs affecting electron transport in the ETC.
Mishra, S. et al. Human amyloidogenic light chain proteins result in cardiac dysfunction, cell death, and early mortality in zebrafish.
Infection with Bacillus anthracis, the causative agent of anthrax, if untreated can result in rampant bacteraemia, multisystem dysfunction and death.
Wei, M. C. et al. Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death.
Papageorgiou, I. E. et al. TLR4-activated microglia require IFN-? to induce severe neuronal dysfunction and death in situ.
The separate genetic causes still share common pathways to cell dysfunction and death, and these interconnect at several levels.
The mutant amyloidogenic transthyretin protein causes systemic accumulation of amyloid fibrils that results in organ dysfunction and death.
Vesicle accumulation, Golgi disorganization, and alterations of other GM130 functions may account for neuron dysfunction and death.
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