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Multiple proinflammatory mediators, including IL-1, TNF-α, interferon-γ, and MMPs mediate the inflammation of the joints.
Adiposity is associated with enhanced M1 macrophage-dependent production of multiple proinflammatory mediators such as IL-1 β, IL-6, TNF- α, and CXCL10.
Bacterial lipopolysaccharide (endotoxin) triggers acute inflammation, associated with activation of the innate immune system and production of multiple proinflammatory mediators [ 19, 20].
Thus, we have defined WPB, a storage organelle for multiple proinflammatory mediators, as a potential target to control overwhelming inflammation in Gram-positive sepsis and improve tissue oxygenation and hemodynamics.
Our study reinforces the idea that EA and RA have multifaceted properties, including the ability to prevent and/or limit UVB-induced damage, increasing cell viability and decreasing the inflammatory response, through a reduction in multiple proinflammatory mediators and enhancement of the protective IL-10.
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Paneth cells constitute a major component of the innate immune system by producing multiple antimicrobial peptides and proinflammatory mediators.
However, thanks to development of molecular and cellular biology, there are multiple studies which shown that different proinflammatory mediators, such as the cytokines IL-1β and TNFα, could be important in the development of this disease.
During the onset of sepsis, the inflammatory system becomes hyperactive, leading to an overproduction of proinflammatory mediators, which contribute to septic shock, multiple organ failure, and death.
Enhanced expression of proinflammatory mediators in diabetic vasculature may be linked to multiple mechanisms germane to progression of in-stent restenosis, such as smooth muscle cell migration and arterial remodeling.
GBS cell wall preparations and culture supernatants can activate macrophage/monocytes through multiple Toll-like receptors, leading to the release of abundant cytokines and other proinflammatory mediators that contribute to cell and organ dysfunction during sepsis [6], [14] [16].
In addition, high tidal volume ventilation activates proinflammatory mediators into circulation, which may contribute to the progression of multiple organ failure [ 27].
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Justyna Jupowicz-Kozak
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