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The signalling mechanisms that underpin these CXCL12 mediated effects are still to be elucidated but the Rho GTPases, Rac1 and Rac2 has been shown to be required for HSC mobilisation and homing[41].We have no direct evidence that the osteoblastic niche in the PECAM-1−/− mice is abnormal, as normal levels of CXCL12 are present in the bone marrow (Figure 3A).
By contrast, differentiation of the cloacal epithelium in Shh knockout mice is abnormal, a change that is manifested by the absence of Sox2 and aberrant keratin expression.
We have previously shown that mammary gland development in PR-A transgenic mice is abnormal, characterized by extensive ductal growth, lateral branching and loss of basement membrane integrity and cell-cell adhesion [ 6].
Therefore, we conclude that entrainment in Bmal1 brain knockout mice is abnormal under skeleton photoperiods, consistent with the idea that the coherence of phase during entrainment may be compromised.
The E17.5 value in B6 mice is a departure from Murray's law and is outside the range of diameter scaling values reported in the literature (−2.7 to −3.0) (34, 344 44, 61), implying that the intraplacental artery branching pattern in B6 mice is abnormal.
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Germ-free mice are abnormal.
Strikingly however, neuromuscular junctions in Cra1/+ mice are abnormal.
Lastly, we noticed that the response to anaesthesia in Scn8a Clth /Scn8a Clth mice was abnormal.
The shape of the ABR in deaf14 mice was abnormal (Fig. 3C).
In addition, SOD1 G93Adl mice are abnormal in the startle-response test, which the authors introduce as a new assay for use in SOD1 transgenic mice.
The most robust breathing phenotype in RTT mouse models that has been reproducibly observed by different laboratories and in different mouse strains is abnormal variation in respiratory cycle length in room air, including respiratory pauses and periods of tachypnea associated with decreased expiratory time and increased mean breathing frequency (Table 2; supplementary material Table S4).
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