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Other potential modifiers of lung disease in ATD include NOS3, GSTP1, TNF and IL10.
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Within this locus, Igfbp5 and Igfbp2 are good candidates for cancer modifier of lung tumorigenesis.
Previous work had identified Fn1 gain of function as a modifier of lung branching morphogenesis, associated with gain of cell matrix adhesion relative to the reciprocal repression of E-cadherin cell cell adherence (Sakai et al, 2003).
[20] We chose to evaluate the ABH genes as candidates for modifiers of CF lung disease severity because the role postulated for these polymorphic genes coding for the ABH antigens is thought to be related to host-pathogen interactions; specifically, many pathogens utilize surface glycoproteins in host invasion.
Collectively, we have identified a single polymorphic locus that affects skin and lung tumorigenesis and identify Igfbp5 and Igfbp2 as candidate modifier genes of lung tumorigenesis.
To investigate whether genetic modifiers of cystic fibrosis (CF) lung disease also predispose to congenital bilateral absence of the vas deferens (CBAVD) in association with cystic fibrosis transmembrane conductance regulator (CFTR) mutations.
We now know that one environmental modifier, cigarette smoking, markedly increases the severity of lung disease and that other genetic and environmental modifiers are also involved.
Additionally we studied these effect taking gender, BMI, age and level of lung function into account, which are possible modifiers of these associations.
Baseline interest in lung cancer genetic risk information was a significant modifier of the effect of genetic risk estimate on ΔPR of lung cancer (p = 0.0108).
Recently, a genome-wide analysis investigating genetic modifiers of associations between occupational exposures and lung function combined the GWIS approach with an in silico pathway analysis that indicated the involvement of inflammatory pathways (Liao et al. 2013).
We have also examined them as modifiers of the effects of ozone on lung function (Alexeeff et al. 2007), and we have examined associations with SNPs in metal-processing genes and heart rate variability (Park et al. 2006; Ren et al. 2010).
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