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To examine the cellular basis for these alterations in bone, we examined the impact of combined Pkd1 and Kif3a deficiency on cell proliferation, osteoblastic differentiation, and gene expression profiles in cells isolated from calvaria of newborn wild-type, single heterozygous and compound heterozygous Pkd1 and Kif3a deficient mice (Fig. 3).
Increased expression of Fas receptor and lower levels of sFas may provide the basis for these alterations that in turn may promote the rupture of tendons.
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Because of the extended larval period in Xenopus, the molecular basis of these alterations has not been well studied.
Genomic alterations such as aneuploidy indicate a high risk of oral cancer and cancer-related mortality, and the molecular basis of these alterations is largely unknown.
However, the genetic basis for these molecular alterations remains elusive.
These observations provide new insight into the molecular basis for the alterations in neurite outgrowth and axonal viability associated with the CMT disease state.
These findings together strongly implicate PV+ interneurons, driven by enhanced or otherwise aberrant NRG1 ErbB4 signaling, as the basis for the alterations in gamma oscillatory frequency seen in the NRG1tg-type I mice.
The molecular basis for this alteration in RNA-binding properties is proposed to result from the inability of the RNA to induce a change in the structure of the free protein to produce a high-affinity complex.
We also observed that some ACRD cases have a low value for the 5α-THF/THF ratio, indicating enhanced 5β-reductase activity, or concomitant deficiency in 5α-reductase activity, though the basis for this alteration in activity is unknown.
Because epigenetic changes can alter whole-genome expression profiles of various cell types that constitute different tissues and organs, these modifications provide plausible basis for transcriptomic alterations that are associated with various diseases [4], [5].
Therefore, these changes are the basis for important alterations linked to aging [ 11- 15].
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