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Recent studies suggest that autoreactive B cells are important cellular mediators contributing to autoreactive T-cell response diversification via their functions that mediate antigen processing and presentation [ 6, 7].
After peripheral nerve injury, glial cells are initially activated and subsequently generate numerous pro-inflammatory mediators, contributing to the development of neuropathic pain [10, 11].
Inflammation is likely involved, with inflammatory mediators contributing to inhibited preadipocyte differentiation [ 23- 25].
Free radicals can attract inflammatory mediators contributing to a generalized inflammatory response [ 27].
This will allow the analysis of local chemical mediators contributing to the production of bone cancer pain which is difficult to conduct in in vivo mouse models.
This IL-7 is considered to contribute to cartilage destruction indirectly through activation of inflammatory cells that secrete catabolic cartilage-destructive mediators, contributing to joint destruction.
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Cell death and release of proinflammatory mediators contribute to mortality during sepsis.
Because CC chemokines such as eotaxin and RANTES also play critical roles in this phenomenon, it would seem likely that members of both classes of mediators contribute to this response.
While HBP is associated with findings suggestive of increased vascular permeability in human septic shock, this association does not prove causality because many other mediators contribute to human septic ARDS.
Platelets and platelet-derived mediators contribute to arrest bleeding, to clear pathogens directly or indirectly by acting on various steps of the immune response, and to drive vascular/tissue repair by providing matrix building blocks and a multiplicity of signals that remodel matrix, attracting tissue progenitor cells and reconstructing the vascular frame.
This is followed by a second process where insulitis is amplified through interplay between immune cells and β-cells, and third process where inflammatory mediators contribute to prolonged suppression and death of β-cells, or promotion, survival and proliferation of β cells [4].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com