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At the current time there is, to the authors' knowledge, no description in the literature of an in vitro model of mechanical joint damage in the rat with experimental models of rat joint disease being surgically induced in vivo [ 7, 8].
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All studies used rats with experimental DM [15 17, 20 22].
To evaluate the effects of osteoporosis induced by glucocorticoid (GIOP) on bone tissue of rats with experimental periodontitis (EP).
Here, we examined the effects of intermittent administration of PTH(1 34) and PTH(7 34) on mineral ion metabolism, bone architecture, and vascular calcification in rats with experimental CKD.
The present study was designed to investigate roles for NF-kappa B and the endogenous H2S producing enzyme cystathionine-beta-synthetase (CBS) signaling pathways in adult rats with experimental diabetes.
In a previous study we observed that parotid glands from rats with experimental periodontitis showed an increase in basal amylase release as a result of an increase in cAMP accumulation induced by PGE2 production.
Enhanced vimentin immunoreactivity was found in the spinal cord of rats with experimental autoimmune encephalomyelitis [28].
Data from urinary bladders of rats with experimental SCI were used in this study.
For example, it was observed that AQP4-specific antibodies promoted NMO-like pathologic changes within the CNS of rats with experimental autoimmune encephalomyelitis (EAE), a myelin-specific T-cell mediated CNS inflammatory disease.
In a prior study we detected expression of VEGF-A in mononuclear cell infiltrates in rats with experimental autoimmune encephalomyelitis (EAE) [22], suggesting that VEGF-A could potentially be expressed in T regulatory cells and/or myelin-specific autoreactive T cells that are enriched in the CNS of MS patients.
We studied the effects of CB1inh in rats with experimental sepsis during anesthesia induction with pentobarbital.
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