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When this team correlated the ability to concentrate urine with renal pathology among individual animals, they observed examples of mice with perfectly normal renal medullas that were functionally equivalent to the ACE null mice in their inability to concentrate urine.
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In this review, we provide examples of mouse models harboring modified endogenous gene(s), generated using the technique commonly referred to as the "knock-in" approach, to exemplify the important and sometimes superior role of this methodology in dermatological research.
Other examples of mouse and rat specific responses include forkhead box Q1 (FOXQ1, HomoloGene ID 7359) and ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2, HomoloGene ID 20333).
Examples of mouse lines with abnormal capacitation include the following: the FGFR dominant negative mouse (Cotton et al., 2006), the Rkip1 knockout (Moffit et al., 2007) and the soluble adenylyl cyclase (sAC) mouse (Hess et al., 2005).
Examples of mouse models with an arrest at metaphase include the Siah1a (Dickins et al., 2002), Cks2 (Spruck et al., 2003) and Mlh1 knockout mice (Eaker et al., 2002).
Few examples of mouse models of mitochondrial disorders, which display a biochemical phenotype but do not present any clinical signs typical of the human pathology, are described in the literature (26, 27).
Examples of mouse models with mtDNA mutations include the Mito-mouse harbouring a heteroplasmic single mtDNA deletion at high mutation load (Inoue et al., 2000), and a mouse model of Leber's hereditary optic neuropathy (LHON) containing the ND6 P25L human mtDNA mutation (Lin et al., 2012).
Examples of mouse models with infertility as a consequence of perturbed endocrine signalling include: a variety of androgen receptor inactivation models (reviewed in (Wang et al., 2009)); the LH and its receptor (Ma et al., 2004; Huhtaniemi et al., 2006); and FSH and its receptor (Abel et al., 2000; Abel et al., 2008).
EMAGE [ 41] is another example of mouse atlas covering gene expression data for anatomical structures corresponding EMAP Anatomy Ontology [ 42].
The different levels of activation (shown are examples of two mice) point to a certain variability in the response to hypoxia between individual mice.
Photographs of examples of treated mice models with 300 kHz of TTFields at low intensities of 5 V/cm and other electrical stimulation parameters are given in (Fig. 2a c) for comparison.
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