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46 Black carbon and increased PM2.5 exposure, 33 as well as PM10 exposure, 41 have been found to be inversely associated with LINE-1 methylation and both Alu and LINE-1 methylation, respectively, which may impact on lung function or lung function decline.
Conversely, alterations to microRNA expression by co-morbidities may also directly impact lung alveolarization, since, for example, RSV infection itself can alter microRNA expression in human lung cells [41].
As air pollution is also a risk factor for lower lung function in children [20] it may impact on lung function by a vascular mechanism in addition to its direct toxic effects on the lungs.
Although the hypothesis that acute changes in blood coaguability in response to particulate pollution may account for some of the variation in cardio-respiratory disease rates is an established one [18], we consider that the concept that chronic differentials in systemic coagulative activity may impact on lung function is an emerging concept supported by Mendelian randomisation techniques.
Prenatal infections are known to impact lung development.
Variable rates of comorbidities in the different COPD studies may impact genetic associations with lung function (such as the association of diabetes with lower lung function) but the inclusion in genetic analysis of the most diverse group with COPD may increase the likelihood that positive associations are true positive findings.
Recently, the overexpression of p130CAS has been observed in 61.9% of lung cancers suggesting that p130CAS may impact a variety of clinicopathological features of lung cancer and may influence the prognosis of lung cancer patients [ 23].
There are many factors which may impact on delivery of inhaled particles to lung parenchyma.
It has been suggested that the FVL mutation may impact on acute inflammatory responses in the lung [ 29].
Since treatments and prognoses for different pathological subtypes of lung cancer are different, we hypothesized that they may impact mortality, QoL, and medical costs to different degrees.
Thus, a set of SNPs may impact on more than one disease phenotype (e.g., both risk of lung cancer and also the risk of nicotine dependence).
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