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Direct parenchymal administration of GDNF is robustly neuroprotective and neurorestorative in multiple neurotoxin-based animal models (rat and non-human primate (NHP)) of Parkinson's Disease (PD), suggesting its potential as a therapeutic agent.
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My research program is broadly based in the area of systems neuroscience using animal models (rats and mice) as well as studies in humans; an area of special emphasis is neurocognitive aging.
In both models (rats and mice), we also measured and observed changes in the QTc interval.
Rodent models (rats and mice) have provided important information about the pathogenic mechanisms.
However, laboratory models, rats, and mice are not patients and the glucocorticoid mechanisms leading to effects and adverse effects are manifold.
In humans and laboratory rodent models (rats and mice), the ovaries exhibit age-related dysfunction relatively early in life, with failure noted long before aging-associated changes in other organs are manifest.
Preclinical studies in both small and large animal fracture models (rat, dog, and monkey) have shown that FGF-2 enhances bone repair and induces early healing [ 49].
Therefore, we hypothesize that treatment with AS inhibits mitochondrial dysfunction via an eNOS activation mechanism in injured muscle in CS model rats, and the experiments presented herein are designed to test that hypothesis.
Autophagic cells were observed in cartilage obtained from osteoarthritis (OA) model rats and human OA patients.
Furthermore, we observed autophagic cells in cartilage obtained from OA model rats and human OA patients.
Media from the cultured cancer cell lines, bone marrows, the homogenate of spinal cords of model rats and cancer patient tissue specimens were harvested for formaldehyde assay.
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