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The observation that full rescue is achieved by adding back only the UGT1A1 gene strongly suggests that the mortality of mutant pups is directly caused by bilirubin toxicity and is not related to other metabolic defects linked to the knockout of the other genes of the Ugt1 cluster.
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Therefore, studying other tissues may reveal defects linked to specific metabolic conditions.
Epidemiological, clinical and experimental evidence strongly link metabolic defects with functional alterations associated with AD pathogenesis.
Insulin resistance, inflammation, and atherogenesis are linked by a common series of metabolic defects, including dyslipidemia and hypercoagulability.
Studies on mice have clearly shown that allowing them to eat only when they are naturally awake, which is at night because they are nocturnal, results in fewer metabolic defects.
All regulate glucose, but they do so by targeting different metabolic defects.
Other metabolic defects may make their appearance only relatively late in life.
The consequences range from stress to metabolic defects, neurodegenerative diseases or even neoplastic transformations [159].
Several metabolic defects, such as phenylketonuria, are associated with autistic symptoms.
PGC-1α knockout mice exhibit multiple metabolic defects, such as obesity, neurodegeneration and cardiomyopathy [9], [10].
The results of the blood chemistry analysis demonstrated that Wwox KO mice had severe metabolic defects.
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CEO of Professional Science Editing for Scientists @ prosciediting.com