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Excessive inflammatory process with maladaptive host's immune response leads to organ dysfunctions and death [ 1, 2].
These data suggest that a perturbation of the type I IFN signaling in beta cells may induce an excessive inflammatory process and increased activation of proapoptotic signaling pathways, resulting in increased beta cell inflammation and apoptosis following, for instance, a local viral infection.
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Interestingly, our results from the present study concur with both controlled and excessive inflammatory processes, as well as an antibody receptor gene up-regulation potentially related to an eosinophil response.
Since most of the animals showing increasing IL-10 concentrations had pathomorphological signatures of CBPP, we speculate that the increase in IL-10 is not sufficient to prevent excessive inflammatory processes that shape CBPP lung lesions.
However, local excessive inflammatory and fibrotic processes will cause excessive local collagen deposition.
An excessive inhibition of the inflammatory process could increase the susceptibility to secondary infections related to immune dysfunction [126 129].
An excessive inhibition of the inflammatory process could increase the susceptibility to secondary infections related to immune dysfunction [ 126- 129].
In inflammatory process, the excessive production of inflammatory cytokines causes an unbalanced chondrocyte metabolism leading to the destruction of extracellular matrix and subsequent cartilage degradation [ 40].
Here, from our review of the literature, we suggest that increases in circulating LPS and an excessive generation of ROS are the main actors in the acute inflammatory process generated by excessive AE.
The inflammatory process involves the excessive production of NO, PGs, matrix metalloproteinases, aggrecanases, and cytokines associated with the IL-1 and tumour necrosis factor families [ 5- 9].
Excessive inflammatory and anti-inflammatory responses are involved in the sepsis process [ 1, 2]; many other important biological processes are also involved [ 3– 5].
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