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These observations indicate that successful phagocytosis suppresses pro-inflammatory gene expression in macrophages leading to the concept that impaired efferocytosis in the diabetic wound may be responsible for defective resolution of inflammation.
What if the SAC response of Mlh1−/− oocytes is induced by DNA damage caused by defective resolution of recombination intermediates along chromosome arms?
Pharmacological manipulation of such defective resolution pathways is therefore an attractive avenue for the development of novel proresolution anti-inflammatory treatments (40).
A defective resolution of inflammation has indeed been established in atherosclerosis, and the present study supports this notion in terms of the LXA4 FPR2/ALX pathway.
Thus, taken together, these observations indicate that the stable ERMES-associated mitochondrial constriction sites in gem1Δ cells is a consequence of defective resolution of mitochondrial tips, perhaps as a consequence of altered ER mitochondria contacts.
"In the heart," Frangogiannis said, "defective resolution of inflammation would be expected to be catastrophic," suggesting that it might be optimal to mimic endogenous "stop signals" that suppress inflammation and protect from adverse remodeling.
Similar(54)
However, it has been demonstrated that both inflammatory (M1) and wound healing/profibrotic (M2) populations participate in fibrosis and suggest a requirement for inflammation or defective inflammation resolution in fibrosis pathogenesis [176-179].
These results define a physiological role for the WRN RecQ helicase protein in RAD51-dependent HR and identify a mechanistic link between defective recombination resolution and limited cell division potential, DNA damage hypersensitivity, and genetic instability in human somatic cells (Saintigny et al 2002).
This could result in the persistence of the pro-inflammatory stimuli, prolonged cytokine secretion, a failure in resolution, defective wound healing, granulomatous tissue formation, angiogenesis, fibrosis and scar formation; all of which are hallmarks of the chronic inflammatory phase in CD.
4) The authors claim that the defective ER stress resolution in LRH-1 liver-specific knockout mice is due to the loss of ATF2 phosphorylation in response to ER stress stimuli.
If so, is such effect transmitted through IRE1 or PERK? 4) The authors claim that the defective ER stress resolution in LRH-1 liver-specific knockout mice is due to the loss of ATF2 phosphorylation in response to ER stress stimuli.
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