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Human pancreatic cancer cells may exhibit loss of responsiveness to TGF-β-mediated growth inhibition as a consequence of altered TGF-β expression as well as a result of postreceptor alterations [ 10].
Conversely, alterations in osteoblastogenesis and bone metabolism have been reported as a consequence of altered lamin A/C levels in vitro and in vivo [ 55- 57].
Characteristic changes in the mobile chain end fraction with temperature, in particular its decrease with increasing degree of filling are interpreted as a consequence of altered contour-length fluctuations.
Purkinje neurons and their dendrites, which were not targeted by Cre-mediated recombination of Fgf receptors, were also misplaced in FGFR DKO mice, possibly as a consequence of altered Bergmann glia orientation or reduced granule cell number.
Classically indirect effects of fragmentation have been defined as a consequence of altered ecological interaction within the communities [1], [6], [37].
Because of this association, it appears conceivable that aspects of age-related changes reflect plastic reorganization as a consequence of altered use rather than degenerational processes developing during aging.
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VDR genotypes can play a role as a consequence of altering hormonal status in the course of acromegaly.
However, direct evidence for increasing the concentration of valuable secondary metabolites as a consequence of altering the salinity of the growing environment still remains equivocal.
However, direct evidence of increases in the concentration of valuable secondary metabolites and the antioxidant capacity as a consequence of altering the salinity of the growing environment still remain equivocal.
Our study suggests that VDR FokI genotypes might affect the development of acromegaly and VDR polymorphisms may play a role in the course of acromegaly as a consequence of altering hormonal status.
There are a number of lines of evidence for this; first (and most importantly) Seoane et al. have shown that in colorectal cancer cell lines depletion of C-MYC reduces apoptosis as a consequence of altering the balance of downstream effectors of P53 signalling.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com