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In summary, platelets might be a forgotten source of mediators that alter heart function during sepsis.
Synovial inflammation (synovitis) is a major contributor to disease progression [ 5- 7] and is responsible for the increased production of catabolic and pro-inflammatory mediators that alter the balance of cartilage matrix degradation and repair, leading to excess production of the proteolytic enzymes responsible for cartilage breakdown [ 6].
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Uroepithelial dysfunction in FIC further led to a peripheral upregulation of neuropeptides and inflammatory mediators that altered bladder afferent soma size and increased input to the central nervous system (CNS) [ 53].
In conclusion, we have identified two new classes of functionally significant gDMRs that appear to be evolutionarily conserved and might be important mediators of the phenotypic effects of pre- and postnatal environmental exposures that alter DNA methylation levels.
Evidence proves that mechanical stress induces acute inflammatory changes that alter the microvascular environment, with studies supporting local release of mediators IL-1β, TNF-α, and expression of chemokines that ultimately promotes leukocyte adhesion and migration [70].
The factors that alter joint mechanosensitivity and promote nociception can be divided into two separate groups: mechanical factors and inflammatory mediators.
These cells are able to release mediators that can alter the secretion and clearance of mucus.
They initiate and augment the innate immunity by forming and releasing pro- or anti-inflammatory mediators that can alter cell differentiation, chemotaxis, and activation of immune cells [ 4].
Whether Bb produces mediators that can directly alter the vascular permeability in vivo has not been investigated.
There are several possible underlying mechanisms for the possible link between O3 exposure and cardiovascular mortality: inflammation of pulmonary tissues, which can induce a spectrum of mediators that also may alter cardiac functions, or irritant-receptor mediated stirritant-receptor mediatedic pathwaystimulationn et al. 2001).
Regarding mediators that might be altered by ApoE mimetic peptides, TNF-α and IL-1β are important pro-inflammatory cytokines activated by NF-κB pathway, which is up-regulated during the pathogenesis of 5-FU-induced mucositis [ 30][ 31].
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