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In experimental models, administration of lipoproteins protects against endotoxic shock [5] [7].
In murine arthritis models, administration of sgp130 reduced inflammation [ 28].
In both rabbit models, administration of 130 mg/kg body weight rSP-C surfactant resulted in a far-reaching restoration of gas exchange and compliance.
In all models, administration of osteoprotegerin results in an almost complete protection of the articular bone and disappearance of osteoclasts from the inflamed synovium [ 16, 26- 29].
In animal models, administration of GLP-1 and associated therapies reduced systemic hypertension and albuminuria, and ameliorated renal damage, as verified by histology.
In multiple xenograft models, administration of INK128 alone or in combination with other standard targeted therapy or chemotherapy resulted in antiangiogenic and tumor growth inhibitory effects [107].
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Regueira and colleagues [27] found that in an endotoxemic pig model, administration of NE was associated with an improvement of hepatic mitochondrial respiration and concluded that this effect was probably mediated by a direct effect of NE on liver cells.
In the rat proliferative glomerulonephritis model, administration of PP2 completely abolished the phosphorylation of c-Src and Smad1 and resulted in the amelioration of glomerulosclerosis.
In this model, administration of DSS in the drinking water results in weight loss, intestinal epithelial cell damage and immune-mediated colonic inflammation.
Similar differences were also observed in an arthritis model: in a CIA model administration of IL27 systemically improves the clinical score, while in a proteoglycan-induced arthritis model the lack of WSX1 also improves the clinical scores [39], [40].
Using another murine colitis model, administration of n-3 polyunsaturated fatty acids resulted not only in reduced pathological scores but also an increase of ZO-1 protein expression [56].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com