Key result
Trypanosoma cruzi infection significantly increased platelet adherence to human endothelial cells compared to controls (P=0.024).
Why the study?
Does Trypanosoma cruzi infection increase platelet adherence and aggregation in preclinical models?
Population
Human umbilical vein endothelial cells and female A/J mice infected with Trypanosoma cruzi
Comparison
Trypanosoma cruzi infection (in vitro and in vivo) vs Uninfected human endothelial cells and…
Design
Preclinical
Follow-up
Up to 12 days post-infection (in mice)
Authors
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May link T. cruzi to endothelial dysfunction in Chagas cardiomyopathy; hypothesis-generating in animal models and requires clinical validation.
Does Trypanosoma cruzi infection increase platelet adherence and aggregation in preclinical models?
p-value: p=0.024
Trypanosoma cruzi infection enhances platelet reactivity and endothelial cell dysfunction, suggesting a potential mechanism for coronary microvascular spasm and cardiomyopathy in Chagas' disease.
Tanowitz et al. (1990) studied Chagas' disease (Trypanosoma cruzi infection). Trypanosoma cruzi infection vs. Uninfected controls was evaluated on Platelet adherence to human endothelial cells (p=0.024). Trypanosoma cruzi infection significantly increased platelet adherence to human endothelial cells compared to controls (P=0.024).
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