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In the last few years, a series of basic science studies, performed using engineered mice, have contributed important pathophysiologic information about FGF-23 activities.
In addition, knockout mice have contributed significantly to our understanding of the roles of specific molecules and cytokines in these models.
The enhanced levels of ATP and glycogen in serum, muscle, and/or liver of treated mice have contributed to TM-mediate fatigue recovery.
Studies of loss of function situations in mice have contributed to the understanding of epigenetic regulators in early embryonic lineage decisions.
Classical knock-out experiments and tissue-specific conditional mutations in mice have contributed to our understanding of the mechanisms involved in the acquisition of respiratory cell fate.
Cav-1−/− mice have contributed a lot to the understanding of caveolin and caveolae; however, these mice exhibit many chronic vascular alterations, such as pathological angiogenesis and paracellular hyperpermeability.
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For nearly 30 years, the genetic manipulation of laboratory mice has contributed substantially to the development of many fields in medical research and mammalian biology.
The development of selective AR agonists and antagonists, as well as the generation of gene-deficient mice, has contributed to a growing understanding of the cellular and molecular processes that are critically involved in the development of ALI/ARDS.
While powerful genetic engineering tools in the mouse have contributed significantly our understanding of craniofacial development and dysmorphology, forward genetic approaches provide an unbiased means to identify new genes and pathways.
The novel insights into the pathogenesis of these diseases in the mouse have contributed to additional investigations into the underlying pathobiology in humans (Flanagan-Steet et al., 2009; Boonen et al., 2011), and serve as an example of the advances made possible through histopathology phenotyping of seemingly normal knockout mice.
For decades, the deer mouse has contributed to our understanding of population genetics, disease ecology, longevity, endocrinology and behavior.
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