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Our group proposed that ischemia in any of the components of the uteroplacental unit (trophoblast, decidua, fetal membranes, or myometrium) generates paracrine mediators that trigger the premature onset of myometrial contractile activity.
In recent years, there is evidence of the ability of the hemosorption columnsto eliminate cytokines and inflammatory mediators that trigger a cascade reaction of irreversible pathological changes in organs and tissues of the patient [ 1].
It is possible that mosquito saliva could alter cell extravasation by affecting the mediators that trigger cell movement, as evidence from other hematophagous arthropods suggests [7], [8], [9], [10].
Since the host inflammatory response contributes decisively to the pathology caused by Plasmodium infection [2], finding the parasite mediators that trigger inflammation is essential to design new therapeutic strategies that could interfere with the pathological syndromes induced by the disease.
Different mechanisms that regulate apoptosis associated with mediators that trigger or inhibit cell death have led to the development of therapeutic strategies against cancer.
This indicates the presence of crucial mediators that trigger the exchange of growth factors between the participating cells at the tumour invasion field.
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We have identified P. falciparum-derived uric acid as a parasite mediator that triggers inflammation.
With the exception of screening pregnant women for asymptomatic bacteraemia, where antibiotic treatment reduces the risk of infection-mediated preterm birth, little is known of the specific inflammatory mediators that may trigger spontaneous preterm labour.
Accordingly, Hawiger et al.[ 34] observed an increased age-associated circulation of proinflammatory mediators that can trigger the activation and maturation of DC.
LpPLA2 catalyzes the hydrolysis of oxidized phospholipids to lysophosphatidyl choline and oxidized, nonesterified fatty acids, mediators that can trigger inflammatory cell activation and retard clearance of apoptotic cells within the atheroma's necrotic core (4).
So far, we have been unable to identify the mediator(s) that trigger(s) upregulation/activation of the proteasome in ATGL-deficient blood vessels.
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Justyna Jupowicz-Kozak
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