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As the possibility of a particle traversal through the cytoplasm is much higher than through the nuclei in environmental radiation exposure, the contribution to genotoxic damage from cytoplasmic irradiation should not be ignored in radiation risk estimation.
With regard to quality of exposure, the contribution of material adversity seemed to be dependent on social adversity, whereas social adversity was the exposure domain most consistently and independently related to allostatic load.
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However, there remain knowledge gaps regarding the formation of DNA adducts due to carcinogen exposure and the contribution of endogenous DNA adducts to the total adduct load and the extent of DNA adduction required for effective mutagenesis.
We predict that this is directly related to the cumulative effect of intrauterine environmental exposure, however, the contribution of stochastic events to the observed variation cannot be discounted at this time.
Most primed subjects in Puerto Rico were likely to have had DENV exposure, although the contribution of other flaviviruses or vaccination cannot be excluded (St . LouisEncephalitis virus, West Nile virus, yellow fever vaccination, or Japanese encephalitis vaccination).
The challenge for epidemiology is to separate the effects of different exposures and the contribution of one's genetic profile.
Lastly, an impediment to attracting physicians and other patient-oriented research scientists to the environmental health sciences has been that in many cases research has focused on mechanism based effects of environmental exposures so that the contribution of an environmental exposure to what is seen clinically is not well delineated.
More theoretically oriented research is needed that includes more epidemiological data to understand the independent contributions of the exposure variables beyond the contribution of the established biomedical risk factors, and the possible interplay of the exposure variables and the biomedical variables.
Whereas group 2 VOCs and naphthalene had higher contributions from indoor exposures than outdoor exposures, the source contribution profiles differed depending on the compound (Table 5).
This built-in timer minimalized possible overestimation of program exposure through eliminating the contribution of 'passive' time registration.
Given that, and considering that type 1 pneumocytes (the pulmonary cell type primarily involved in gas exchange in the lung) did not express CYP1A1 in beluga, it is more plausible to conclude that CYP1A1 induction in lung was solely the result of dietary exposure and that the contribution of inhaled contaminants was marginal.
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