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These end-effects are essentially due to the lack of 'future' data for constraining the SV and SA at the model endpoint, and because SV estimates based on annual differences of ground observatory monthly means are available only up to 6 months before the latest available ground observatory data.
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This is a consequence of the model regularization, that forces the SA towards zero at the model endpoints and minimizes time changes in the SA throughout, which is stronger at higher degree.
(underline{underline{Lambda }}_3) involves integration over the full time span of the model, while (underline{underline{Lambda }}_2) involves evaluating the second time derivative only at the model endpoints (t=1997.1) and 2016.6.
(underline {underline {Lambda }}_{3}) involves integration over the full timespan of the model, while (underline {underline {Lambda }}_{2}) involves evaluating the second time derivative only at the model endpoints t=1997.0 and 2015.0.
There was possibly already weak evidence for a pulse around 2013 in CHAOS-4, buthehe sparsity of satellite data in this model after 2010, and the closeness of the pulse to the model endpoint, made interpretation of this feature difficult.
The model endpoint estimates the number of women that will be identified as having GDM, prediabetes and T2D.
The flexibility in changing the cut-off also makes the model endpoint independent.
In 2015 (relatively close to the model endpoint), regularization starts to dominate the solution already above degree 9. We nonetheless choose to present the SA at the core surface also to degree 16, since some information on rapid field changes is possible up to this degree, particularly for epochs more distant from the model endpoints.
This is likely due to the lack of accurate global data close to the model endpoints, forcing modellers to apply unrealistic endpoint conditions that can result in a deterioration of the quality of model secular variation descriptions close to the endpoints.
To avoid this we also minimize at the core surface at the model endpoints t = 1997.0 and 2010.0.
This paper provides an assessment of the toxicological basis of the hormetic dose response relationship including issues relating to its reproducibility, frequency, and generalizability across biological models, endpoints measured and chemical class/physical stressors and implications for risk assessment.
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