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They posit that post-operative increases in colonic miR-21 expression may promote tissue injury and the risk of colitis development.
Using this staining technique we could not identify commensal bacteria adhering to the tongue surface in uninfected animals (not shown), suggesting that C. albicans may promote tissue colonization and invasion by normally "innocent" commensals.
Alternatively, certain BCG sub-strains may induce an overwhelmingly intense pro-inflammatory recalled response to mycobacterial antigens that in turn may promote tissue damage independent of the effect of certain susceptibility genotypes.
Accordingly, our in vivo and in vitro evidence implicates that the combinatorial treatment with hMSCs and PACAP may promote tissue debris clearance by the upregulation of galectin-3-positive phagocytes in the injured spinal cord.
A central role for the B lymphocytes in the pathogenesis of RA is supported by the presence of autoantibodies, which are locally produced in the inflamed synovium and may promote tissue inflammation and destruction by forming immune complexes [1].
Changes in vascular permeability may promote tissue edema that may worsen when colloids are administered.
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These senescent cells may also promote tissue remodeling and clearance of the myofibroblasts during wound maturation.
In addition, TNF-α activates phagocytes to produce reactive oxygen intermediates [ 45, 46], which can be toxic to cells like endothelial cells, fibroblasts and leucocytes, and may further promote tissue proteolysis by potentiating the effects of several proteinases, while inactivating proteinase inhibitors [ 47, 48].
However, inflammation that occurs in the absence of an infection, but in response to an injury, so-called sterile inflammation, may promote further tissue damage due to the production of toxic mediators and proteases by recruited immune cells [ 1].
In addition, a recent study found a positive correlation between adipose tissue COL6A3 mRNA and body-mass index in humans and suggested that increased collagen VI expression may promote adipose tissue inflammation [43].
The upregulation of both extracellular matrix proteins and extracellular matrix protein-degrading enzymes by PC indicates that PC may promote synovial tissue repair and regeneration.
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