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Because it had already been shown that polymorphisms in TCF7L2 gene were associated with cardiovascular events [16], genotypic information from TCF7L2 was excluded from analysis to assess whether the positive association of combined information happened only because of TCF7L2 influence.
It has been shown that polymorphisms in the adiponectin gene (ADIPOQ) modulate the circulating concentration of adiponectin.
It has recently been shown that polymorphisms in the ABCG2 gene are important predictors for the prognosis of patients with breast cancer treated with tamoxifen [ 75].
It has been shown that polymorphisms in the MBL2 gene, particularly at codon 54 (variant allele B; wild-type allele designated as A), impact upon host susceptibility to Candida infection.
Recently, it has been shown that polymorphisms (collectively termed 'complotype') in complement proteins C3, FB and CFH can be associated with an up to sixfold variation in complement haemolytic activity in vitro 17.
It has recently been shown that polymorphisms in TERC (telomerase RNA component) are associated with CRC risk and increased telomere length (Codd et al, 2010; Houlston et al, 2010; Jones et al, 2012); collectively these data extend the role of genetic variation in telomere elongation mechanisms in defining cancer risk per se.
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The precise effect of vitamin D on AVC is still unknown, although it has been shown that polymorphism of vitamin D receptor is associated with higher prevalence of AVC.
Moreover, it was shown that polymorphisms affecting the CYP3A5 can alter the pharmacokinetics of vincristine, given that this isozyme plays a key role in vincristine elimination.
Nevertheless, recently it was shown that polymorphisms in the CTLA4 gene were correlated with response in melanoma patients (stage IV) receiving anti-CTLA4 treatment [ 25].
Similarly, it was shown that polymorphisms in the TNF promoter and/or the TNF receptor II probably influence response to anti-TNF treatment, as did genetic variations in the interleukin-10 promoter and the Fcγ receptor IIIA [ 9- 12].
It has been shown that genetic polymorphisms in circadian genes may be partially responsible for diurnal preference [ 35].
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