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In the study of Barraza-Villarreal et al. (2008), FEV1 was dependent on PM2.5 exposure from the previous 1 5 days.
The relationships between suicide, month of year and change in mean daily sunlight exposure from the previous month were substantively the same as when our measure of sunlight exposure was the mean daily sunlight exposure (see online supplementary tables S1 S3).
While adjusting for month of year removed the risk of sunlight exposure (table 3), adjusting for mean sunlight exposure and change in mean sunlight exposure from the previous month neither removed nor attenuated the relationship between month of year and suicide (table 2).
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All subjects were enrolled prior to the start of the malaria season and therefore infections in the baseline samples most likely represent residual asymptomatic infections resulting from exposure in the previous transmission season.
Several mechanisms may account for our findings of both very acute associations from exposure in the previous 1 8 hr and stronger associations using multiday averaging times.
The outcome of this model is the average difference in parameters (BP, heart rate) throughout the entire exposure (model 2: b2 parameter from the previous model and excluding the b3 parameter in the model when not significant).
Animals were housed in a dark environment for 14 days to clear the effect of light exposure from their previous rearing environment.
The fourth panel shows the subsequent exposure, which reflects the signal from the previous probing with the γ1 subunit antibody, as we had not removed the previous signal.
A subsequent meta-analysis of 10 studies of protracted low-dose occupational and environmental exposures (including the previous estimate from our cohort) estimated a statistically significant dose response association (ERR 0.19, CI (0.07 0.32) per 100 mGy) for leukaemia (excluding CLL) (Daniels and Schubauer-Berigan, 2011).
While the increased lamp2A mRNA levels observed after rotenone exposure agree with the previous findings obtained from in vivo studies using paraquat or 6-OHDA [ 2, 11] and are in line with the knowledge that CMA activation induced by oxidative stress is caused by an increased lamp2A synthesis [ 5], the unchanged lamp2A protein levels are unexpected.
Comparisons are then made to the structural evolution observed after 20 h of exposure from a previous study [1].
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